lower back pain and disorders of intervertebral discs ... · chapter 39 lower back pain and...

C H A P T E R

39Lower Back Pain and Disordersof Intervertebral DiscsLower Back Pain and Disordersof Intervertebral DiscsKeith D. Williams ◆ Ashley L. Park

Epidemiology, •••General disc and spine anatomy, •••

Neural elements, •••Anatomical proportions, •••

Natural history of disc disease, •••Nonspecific lumbar pain, •••

Diagnostic studies, •••Roentgenography, •••Myelography, •••Computed tomography, •••Magnetic resonance imaging, •••Positron emission tomography, •••Other diagnostic tests, •••

Injection studies, •••Epidural cortisone injections, •••

Cervical epidural injection, •••Thoracic epidural injection, •••Lumbar epidural injection, •••

Zygapophyseal (facet) joint injections, •••Cervical facet joint, •••Lumbar facet joint, •••Sacroiliac joint, •••

Discography, •••Lumbar discography, •••Thoracic discography, •••Cervical discography, •••

Psychological testing, •••Cervical disc disease, •••

Signs and symptoms, •••Differential diagnosis, •••Confirmatory testing, •••

Myelography, •••Nonoperative treatment, •••Operative treatment, •••

Removal of posterolateral herniationsby posterior approach (posteriorcervical foraminotomy), •••

Anterior approach to cervical disc, •••Thoracic disc disease, •••

Signs and symptoms, •••Confirmatory testing, •••Treatment results, •••Operative treatment, •••

Costotransversectomy, •••Anterior approach for thoracic disc

excision, •••Thoracic endoscopic disc excision, •••

Lumbar disc disease, •••Signs and symptoms, •••Physical findings, •••Differential diagnosis, •••Confirmatory imaging, •••

Nonoperative treatment, •••Epidural steroids, •••Operative treatment, •••

General principles for open discsurgery, •••

Ruptured lumbar disc excision, •••Microlumbar disc excision, •••Endoscopic techniques, •••Additional exposure techniques, •••Lumbar root anomalies, •••Results of open (micro or standard)

surgery for disc herniation, •••Complications of open disc

excision, •••Dural repair augmented with fibrin

glue, •••Free fat grafting, •••

Chemonucleolysis, •••Spinal instability from degenerative disc

disease, •••Disc excision and fusion, •••Lumbar vertebral interbody fusion, •••

Anterior lumbar interbody fusion, •••Posterior lumbar interbody fusion, •••

Failed spine surgery, •••Repeat lumbar disc surgery, •••

Humans have been plagued by back and leg pain since thebeginning of recorded history. Primitive cultures attributedsuch pain to the work of demons. The early Greeks recognizedthe symptoms as a disease and prescribed rest and massage forthe ailment. The Edwin Smith papyrus, the oldest surgical textdating to 1500 BC, includes a case of back strain. Unfortunately,the text does not include the treatment rendered by the ancientEgyptians. In the fifth century AD, Aurelianus clearly describedthe symptoms of sciatica. He noted that sciatica arose fromeither hidden causes or observable causes, such as a fall, aviolent blow, pulling, or straining. In the eighteenth centuryCotugnio (Cotunnius) attributed the pain to the sciatic nerve.Gradually, as medicine advanced as a science, the number ofspecific diagnoses capable of causing back and leg painincreased dramatically.

Several physical maneuvers were devised to isolate the trueproblem in each patient. The most notable of these is theLasegue sign, or straight leg raising test, described by Forst in1881 but attributed to Lasegue, his teacher. This test wasdevised to distinguish hip disease from sciatica. Althoughsciatica was widespread as an ailment, little was known aboutit because only rarely did it result in death, allowingexamination at autopsy. Virchow (1857), Kocher (1896), andMiddleton and Teacher (1911) described acute traumaticruptures of the intervertebral disc that resulted in death. Thecorrelation between the disc rupture and sciatica was notappreciated by these examiners. Goldthwait in 1911 attributedback pain to posterior displacement of the disc. Oppenheim andKrause in 1909 performed the first successful surgical excisionof a herniated intervertebral disc. Unfortunately, they did not

1955Copyright 2003. Elsevier Science (USA). All Rights Reserved.

#6427 @sunultra1/raid/CLS books/GRP mosby/JOB canale/DIV ch39mktg 7/26/02 303 Pos: 1/74 Pg: 1955 Team:

recognize the excised tissue as disc material and interpreted itas an enchondroma. Oil-contrast myelography was serendipi-tously introduced when iodized poppy seed oil, injected to treatsciatica in 1922, was inadvertently injected intradurally andwas noted to flow freely. Dandy in 1929 and Alajouanine in thesame year reported removal of a ‘‘disc tumor,’’ or chondroma,from patients with sciatica. The commonly held opinion of thattime was that the disc hernia was a neoplasm. Mixter and Barrin their classic paper published in 1934 attributed sciatica tolumbar disc herniation. This report also included a series offour patients with thoracic disc herniations, and four patientswith cervical disc herniations. They suggested surgical treat-ment. Myelography was not used for confirmation of discdisease because of toxicity of the agents used in the years thatfollowed. Myelography was refined with the development ofnonionic contrast media, and the test was combined with CT;however, even this appears to have been supplanted by MRI ofthe spine.

The standard procedure for disc removal was a totallaminectomy followed by a transdural approach to the disc. In1939 Semmes presented a new procedure to remove theruptured intervertebral disc that included subtotal laminectomyand retraction of the dural sac to expose and remove theruptured disc with the patient under local anesthesia. Love inthe same year also described this same technique indepen-dently. This procedure, now the classic approach for theremoval of an intervertebral disc, has been improved with theuse of microscopic and video imaging. Kambin, Onik, andHelms and others have popularized minimally invasivetechniques for selected disc hernias.

As more people were treated for herniated lumbar discs, itbecame obvious that surgery was not universally successful.Over the past several decades, studies of patients with back orleg pain have led to improved treatment of those in whom aspecific diagnosis was possible. Unfortunately, this groupremains the minority of patients who are evaluated for low backor leg pain. Complex psychosocial issues, depression, andsecondary gain are but a few of the nonanatomical problemsthat must be considered when evaluating these patients. Inaddition, the number of anatomical causes for these symptomshas increased as our understanding and diagnostic capabilitieshave increased. In an attempt to identify other causes of backpain Mooney and Robertson popularized facet injections, thusresurrecting an idea proposed originally in 1911 by Goldthwait.Smith et al. in 1963 approached the problem by suggesting aradical departure in treatment—enzymatic dissolution of thedisc by injection of chymopapain. Although this technique isstill used in Europe, it rarely is used in the United Statesbecause of medicolegal concerns.

The anatomical dissections and clinical observations ofKirkaldy-Willis and associates identified pathological pro-cesses associated with or complicating the process of spinalaging as primary causes of disc disease. Additional informationabout this process and its treatment continues to be collected.

A thorough and complete history of all aspects of lumbarspinal surgery was compiled by Wiltse in 1987.

EpidemiologyEpidemiologyBack pain, the ancient curse, is now an international healthissue of major significance. Hult estimated that up to 80% ofpeople are affected by this symptom at some time in their lives.Impairments of the back and spine are ranked as the mostfrequent cause of limitation of activity in people younger than45 years by the National Center for Health Statistics.Physicians who treat patients with spinal disorders andspine-related complaints must distinguish the complaint ofback pain, which several epidemiological studies reveal to berelatively constant, from disability attributed to back pain. In1984, disability was noted by Waddell to be exponentiallyincreasing in the United Kingdom (Fig. 39-1). Conversely, aninsurance industry study revealed a trend toward decreasingclaim rates for low back pain in the United States from 1987 to1995.

Although back pain as a presenting complaint may accountfor only 2% of the patients seen by a general practitioner,Dillane, Fry, and Kalton reported that in 79% of men and 89%of women the specific cause was unknown. Svensson andAndersson noted the lifetime incidence of low back pain to be61% and the prevalence to be 31% in a random sample of 40-to 47-year-old men. They noted that 40% of those reportingback pain also reported sciatica. In women 38 to 64 years of agethe lifetime incidence of low back pain was 66% with aprevalence of 35%. Svensson and Anderson noted psycholog-ical variables associated with low back pain to be dissatisfac-tion with the work environment and a higher degree of worryand fatigue at the end of the workday. The cost to society andthe patient in the form of lost work time, compensation, andtreatment is staggering. Snook reported that Liberty MutualInsurance Company paid $247 million for compensable back

1059585756555453525155

55 60 65 70 75Year

80 85 90 95

Mill

ion

days

(per

yea

r)

Fig. 39-1 Forty-year trends in chronic low back disability.United Kingdom statistics for sickness and invalidity benefits forback incapacities from 1953-1954 to 1993-1994 (based onstatistics supplied by the Department of Social Security). (FromWaddell G: Spine 21:2820, 1996.)

1956 P A R T X I I ◆ The Spine

Copyright 2003. Elsevier Science (USA). All Rights Reserved.


pain in 1980. Because this company represents only 9% of theinsured workers’ compensation market, Webster and Snookestimated the compensable costs of low back pain in the UnitedStates to be $11.1 billion in 1989. They reported that the meancost of each reported claim of low back pain at Liberty Mutualhad increased from $6807 in 1986 to $8321 in 1989, althoughthey suggested that an increase in premiums sold, not anincrease in low back pain claims, was the reason for this rise.More recent data from Liberty Mutual estimates that $8.8billion was paid annually in the United States for claims relatedto low back pain. Of the billions of dollars spent annually in theUnited States because of back complaints, it was estimated thatonly about 39% was spent for medical treatment; the remainingcosts were for disability payments. This did not include thelosses from absenteeism. Although absenteeism because ofback pain varies with the type of work, it rivals the commoncold in total workdays lost.

Saal and Saal noted an 18% incidence of chronic back painin 1135 adults; 80% of those reporting chronic pain did notreport limitation of activity, and fewer than 4% reportedsignificant limitation of activity. Females reported back painmore frequently than males. There were no racial differences,but the lower the educational level of those interviewed thegreater the proportion of those reporting back pain. In 1992Carey et al. interviewed 4437 North Carolinians by telephoneand noted an incidence of 3.9% chronic low back pain. Of thosewho reported having chronic low back pain, 34% said that theywere permanently disabled. These authors concluded thatchronic back pain is common and associated with high costs.In the Netherlands van Doorn noted that the low back paindisability claims for self-employed dentists, veterinarians,physicians, and physical therapists increased 211% from 1977to 1989, and the cost increased 13% over that same time period.Frymoyer and Cats-Baril noted an increase of 2500% in awardsfor back pain disability by the Social Security DisabilityInsurance from 1957 to 1976. They estimated that the total costof low back pain was $25 billion to $100 billion per year, with75% of those costs attributed to the 5% who becamepermanently disabled.

Multiple factors affect the development of back pain.Frymoyer et al. noted that risk factors associated with severelower back pain include jobs requiring heavy and repetitivelifting, the use of jackhammers and machine tools, and theoperation of motor vehicles. They also noted that patients withsevere pain were more likely to be cigarette smokers and hada greater tobacco consumption. In an earlier study Frymoyeret al. noted that patients complaining of back pain reportedmore episodes of anxiety and depression; they also had morestressful occupations. Women with back pain had a greaternumber of pregnancies than those who did not. Jackson,Simmons, and Stripinis noted that adult patients with scoliosisare more likely to have back pain and that the pain persists andprogresses. Deyo and Bass noted a strong relationship betweensmoking and back pain in patients younger than 45 years ofage. They also noted a greater tendency for back pain in thosepatients who were the most obese. Other investigators, how-

ever, have found no relationship between obesity and backpain. Svensson and Anderson associated low back pain withcardiovascular risk factors, including calf pain on exertion,high physical activity at work, smoking, frequent worry,tension, and monotonous work.

The incidence of back pain appears to be constant. Effortsare being made to decrease the physical risk factors that maylead to low back pain. However, as shown by Boos et al.,nonanatomical factors, specifically work perception and psy-chosocial factors, are intimately intertwined with physicalcomplaints. Compounding diagnostic and treatment difficultiesis the high incidence of significant abnormalities demonstratedby imaging studies, which in asymptomatic matched controls isas high as 76%.

General Disc and Spine Anatomy

General Disc and Spine AnatomyThe development of the spine begins in the third week ofgestation and continues until the third decade of life. Forma-tion of the primitive streak marks the beginning of spinaldevelopment, which is followed by the formation of thenotochordal process. This process induces neurectodermal,ectodermal, and mesodermal differentiation.

Somites form in the mesodermal tissue adjacent to theneural tube (neurectoderm) and notochord. They number 42 to44 in humans. The somites begin to migrate in preparation forthe formation of skeletal structures. At the same time, theportion of the somites around the notochord separates into asclerotome with loosely packed cells cephalad and denselypacked cells caudally. Each sclerotome then separates at thejunction of the loose and densely packed cells. The caudaldense cells migrate to the cephalad loose cells of the next morecaudal sclerotome (Fig. 39-2).

The space where the sclerotome separates eventually formsthe intervertebral disc. Vessels that originally were positionedbetween the somites now overlie the middle of the vertebralbody. As the vertebral bodies form, the notochord that is in thecenter degenerates. The only remaining notochordal remnantforms the nucleus pulposus. Pazzaglia, Salisbury, and Byersreviewed the involution of the notochord in fetal andembryonic spines by several histological methods and con-cluded that all chordal cells disappear by early childhood.Notochordal remnants usually are not distinguishable in theadult nucleus pulposus.

The intervertebral disc in adults is composed of the annulusfibrosus and the nucleus pulposus. The annulus fibrosus iscomposed of numerous concentric rings or layers of fibrocar-tilaginous tissue. Fibers in each ring cross diagonally, and therings attach to each other with additional radial fibers. The ringsare thicker anteriorly (ventrally) than posteriorly (dorsally).The nucleus pulposus, a gelatinous material, forms the center ofthe disc. Because of the structural imbalance of the annulus, thenucleus is slightly posterior (dorsal) in relation to the disc as awhole. The discs vary in size and shape with their position inthe spine. Discs also decrease in volume, resulting in a 16% to

C H A P T E R 3 9 ◆ Lower Back Pain and Disorders of Intervertebral Discs 1957



21% loss in disc height after 6 hours of standing or sitting.T2-weighted MRI signals increase as much as 25% after a nightof bed rest. This diurnal variation has been substantiated byBotsford et al. and Paajanen et al.

The nucleus pulposus is composed of a loose, nonoriented,collagen fibril framework supporting a network of cellsresembling fibrocytes and chondrocytes. This entire structure isembedded in a gelatinous matrix of various glucosaminogly-cans, water, and salts. This material usually is under con-siderable pressure and is restrained by the crucible-likeannulus. Inoue demonstrated that the cartilage endplate con-tains no fibrillar connection with the collagen of the sub-chondral bone of the vertebra. This lack of interconnectionbetween the endplate and the vertebra may render the discbiomechanically weak against horizontal shearing forces. Inouealso demonstrated that the collagen fibrils in the outer twothirds of the annulus fibrosus are firmly anchored into thevertebral bodies (Fig. 39-3).

The intervertebral disc in the adult is avascular. Rudert andTillmann were able to demonstrate blood vessels in the annulusuntil the age of 20 years and within the cartilage endplates untilthe age of 7 years. The cells within the disc are sustained bydiffusion of nutrients into the disc through the porous centralconcavity of the vertebral endplate. Histological studies haveshown regions where the marrow spaces are in direct contactwith the cartilage and that the central portion of the endplate ispermeable to dye. Motion and weight-bearing are believed tobe helpful in maintaining this diffusion. The metabolic turnover

of the disc is relatively high when its avascularity is consideredbut slow compared with other tissues. The glycosaminoglycanturnover in the disc is quite slow, requiring 500 days. Inouepostulated that the degeneration of the disc may be promptedby decreased permeability of the cartilage endplate, which isnormally dense.

Fig. 39-2 Schematic representation ofdevelopment of vertebrae and discs. (FromRothman RH, Simeone FA: The spine, vol 1,Philadelphia, 1982, WB Saunders.)

Fig. 39-3 Schematic representation of orientation of fibers indisc and endplate. AF, Annulus fibrosus; NP, nucleus pulposus;CP, cartilaginous plate. (From Inoue H: Spine 6:139, 1981.)




NEURAL ELEMENTSNEURAL ELEMENTSThe organization of the neural elements is strictly maintainedthroughout the entire neural system, even within the conusmedullaris and cauda equina distally. Wall et al. noted that theorientation of the nerve roots in the dural sac and at the conusmedullaris follows a highly organized pattern, with the mostcephalad roots lying lateral and the most caudal lying centrally.The motor roots are ventral to the sensory roots at all levels.The arachnoid mater holds the roots in these positions.

The pedicle is the key to understanding surgical spinalanatomy. The relation of the pedicle to the neural elementsvaries by region within the spinal column. In the cervicalregion, there are seven vertebrae but eight cervical roots.Therefore, accepted nomenclature allows each cervical root toexit cephalad to the pedicle of the vertebra for which it isnamed (e.g., the C6 nerve root exits above or cephalad to the C6pedicle). This relationship changes in the thoracic spinebecause the eighth cervical root exits between the C7 and T1pedicles, requiring the T1 root to exit caudal or below thepedicle for which it is named. This relationship is maintainedthroughout the remaining more caudal segments. Of impor-tance, the naming of the disc levels is different, in that all levelswhere discs are present are named for the vertebral levelimmediately cephalad (i.e., the C6 disc is immediately caudalto the C6 vertebra and disc pathology at that level typicallywould involve the C7 nerve root). In the lumbar spineclassically a similar relationship exists in that disc pathologymost commonly affects the nerve root one segment caudal (e.g.,an L4 disc herniation would be expected to cause L5 rootsymptoms and findings) (Fig. 39-4).

At the level of the intervertebral foramen is the dorsal rootganglion. The ganglion lies within the outer confines of theforamen. Distal to the ganglion three distinct branches arise; themost prominent and important is the ventral ramus, whichsupplies all structures ventral to the neural canal. The secondbranch, the sinu-vertebral nerve, is a small filamentous nervethat originates from the ventral ramus and progresses mediallyover the posterior aspect of the disc and vertebral bodies,innervating these structures and the posterior longitudinalligament. The third branch is the dorsal ramus. This branchcourses dorsally, piercing the intertransverse ligament near the

pars interarticularis. Three branches from the dorsal ramusinnervate the structures dorsal to the neural canal. The lateraland intermediate branches provide innervation to the posteriormusculature and skin. The medial branch separates into threebranches to innervate the facet joint at that level and theadjacent levels above and below (Fig. 39-5).

Pedersen, Blunck, and Gardner noted that the clinicallysignificant function of the sinu-vertebral nerves and theposterior rami is the transmission of pain. The proprioceptivefunctions of these nerves are not known but assumed.

Studies by Bogduk and others demonstrated neural fibers inthe outer layers of the annulus. These fibers are branches of thesinu-vertebral nerve dorsally. Ventral branches arise fromthe sympathetic chain that courses anterolaterally over thevertebral bodies. Rhalmi et al., using histological methods,demonstrated neural elements in all spinal ligaments. In theligamentum flavum the nerve fibers are close to blood vesselsand fat globules.

ANATOMICAL PROPORTIONSANATOMICAL PROPORTIONSVariation in the ratio of the cross-sectional area of the neuralelements to the cross-sectional area of the spinal canal atvarious levels is relatively large. This is particularly true inpatients with developmental stenosis in whom otherwiserelatively minor intrusion into the spinal canal by pathologicalanatomy may cause compression of the neural structures. Manystudies have documented that the changes in the foraminaldimensions increase with flexion and decrease with extension.Also, disc space narrowing causes significant volumetricdecreases in the neural foramen at all levels.

Natural History of Disc Disease

Natural History of Disc DiseaseThe natural process of spinal aging has been studied byKirkaldy-Willis and Hill and by others through observation ofclinical and anatomical data. One theory of spinal degenerationassumes that all spines degenerate and that our current methodsof treatment are for symptomatic relief, not for a cure.

The degenerative process has been divided into threeseparate stages with relatively distinct findings. The first stage

C6

C7

Dorsalramus

Ventralramus

C8

T1

C5

C6

C7

T1

Dorsal rootganglion

L4

S1

L5

L4

L5

Fig. 39-4 Discs are named for vertebrallevel immediately cephalad. Pathologymost commonly affects nerve root onesegment caudal.




is dysfunction, which is seen in those 15 to 45 years of age. Itis characterized by circumferential and radial tears in the discannulus and localized synovitis of the facet joints. Varlotta et al.noted a familial predisposition to lumbar disc herniation inpatients who had disc herniation before the age of 21 years. Inthis group the familial incidence was 32% compared with amatched control group of asymptomatic individuals in whomthe rate was only 7%. A case control study of familialdegenerative disc disease revealed a similar incidence ofdegenerative changes between first-order relatives of those withdocumented lumbar disc herniations and those without such afamily history. However, the first-order relatives did havestatistically significant more severe degenerative change.

The next stage is instability. This stage, found in 35- to70-year-old patients, is characterized by internal disruption ofthe disc, progressive disc resorption, degeneration of the facetjoints with capsular laxity, subluxation, and joint erosion. Thefinal stage, present in patients older than 60 years, isstabilization. In this stage the progressive development ofhypertrophic bone about the disc and facet joints leads tosegmental stiffening or frank ankylosis (Table 39-1).

Each spinal segment degenerates at a different rate. As onelevel is in the dysfunction stage, another may be entering thestabilization stage. Disc herniation in this scheme is considereda complication of disc degeneration in the dysfunction andinstability stages. Spinal stenosis from degenerative arthritis inthis scheme is a complication of bony overgrowth compromis-

ing neural tissue in the late instability and early stabilizationstages. Mayoux-Benhamou et al. noted that a 4-mm collapse ofthe disc produces sufficient narrowing of the foramen tothreaten the nerve.

The stages and progression of degeneration have beenconfirmed by histological studies. Miller, Schmatz, and Schultznoted that disc degeneration progresses histologically as ageincreases. Males were found to have more degeneration thanfemales. L4-5 and L3-4 disc levels showed the greatest degreeof disc degeneration. Urban and McMullin noted that thehydration of disc material decreased with age. The relationshipbetween the change in hydration and swelling pressure wasdependent on the composition of the disc rather than on the ageof the patient or the degree of degeneration. In their study L1-2and L5-S1 discs had the lowest hydration. Yasuma et al. notedprogressive histological changes in the prolapsed discs whencompared with protruded discs. Urovitz and Fornasier wereunable to detect any evidence of autoimmune reaction inhuman disc tissue, but they did detect evidence of the responseto mechanical injury. Using postmyelogram CT scans, Takataet al. found that the cauda equina and affected nerve roots wereswollen in 17 of 28 patients studied. The affected roots returnedto normal size after disc excision. Ziv et al. reported coarselyfibrillated and ulcerated spinal facet joints in young patients,and this finding continued through progressive aging. Thecartilage of the superior facets is thicker and has a higher watercontent than the inferior facets, indicating more frequent

A B

Fig. 39-5 A, Dorsal view of lumbar spinal segment with lamina and facets removed. On left side,dura and root exiting at that level remain. On right side, dura has been resected and root is elevated.Sinu-vertebral nerve with its course and innervation of posterior longitudinal ligament is usuallyobscured by nerve root and dura. B, Cross-sectional view of spine at level of endplate and disc. Notethat sinu-vertebral nerve innervates dorsal surface of disc and posterior longitudinal ligament.Additional nerve branches from ventral ramus innervate more ventral surface of disc and anteriorlongitudinal ligament. Dorsal ramus arises from root immediately on leaving foramen. This ramusdivides into lateral, intermediate, and medial branches. Medial branch supplies primary innervationto facet joints dorsally.




damage. Neumann et al. suggested that the amount of bonetissue in the spine may be functionally related to the structuralproperties of the spinal ligaments.

Long-term follow-up studies of lumbar disc herniations byHakilius in 1970, Weber in 1983, and Seal in 1996 consistentlydocumented several principles, the foremost being thatgenerally symptomatic lumbar disc herniation (which is onlyone of the consequences of disc degeneration) has a favorableoutcome in most patients. This was pointed out by Weber, whonoted that the primary benefit of surgery was early on in thefirst year, but that with time the statistical significance ofthe improvement was lost. In addition, the review by Saalsupported an active care approach, minimizing centrally actingmedications. The judicious use of epidural steroids also issupported. Nonprogressive neurological deficits (except caudaequina syndrome) can be treated nonoperatively with expectedimprovement clinically. If surgery is necessary, it usually canbe delayed 6 to 12 weeks to allow adequate opportunity forimprovement. These principles are consistent with clinicalfindings and treatment practices at this clinic. Clearly, somepatients are best treated surgically, and this is discussed in thesection dealing specifically with lumbar disc herniation.Similar principles are valid regarding cervical disc herniations,which also generally can be treated nonoperatively. Theimportant exceptions are patients with cervical myelopathy,who are best treated surgically.

The natural history of disc disease is one of recurrentepisodes of pain followed by periods of significant or completerelief. Biering-Sørensen and Hilden noted that the memory ofpainful low back episodes was short. At initial evaluation andat 6 months’ follow-up the question of ever having had lowback pain was answered by patients with a yes or no and 84%answered consistently on the two occasions. However, in aquestionnaire at 12 months only two fifths of those interviewedanswered consistently. They questioned the long-term analysisof data from this standpoint and noted that the clinician shouldbe aware of the potential vagueness and unreliability of ahistory of previous back injury.

Before a discussion of diagnostic studies, axial spine painwith radiation to one or more extremity must be considered.

Also, our understanding of certain pathophysiological entitiesmust be juxtaposed to other entities of which we have only arudimentary understanding. It is doubtful if there is any otherarea of orthopaedics in which accurate diagnosis is as difficultor the proper treatment as challenging as in patients withpersistent neck and arm or low back and leg pain, despiteappropriate evaluation and care. Although there are manypatients with clear diagnoses properly arrived at by carefulhistory and physical examination with confirmatory imagingstudies, more patients with pain have absent neurologicalfindings other than sensory changes and have normal imagingstudies or studies that do not support the clinical complaintsand findings. Inability to easily demonstrate an appropriatediagnosis in a patient does not relieve the physician of theobligation to recommend treatment or to direct the patient to asetting where such treatment is available. Careful assessment ofthese patients to determine if they have problems that can beorthopaedically treated (nonsurgically or surgically) is imper-ative to avoid overtreatment as well as undertreatment. Surgicaltreatment can benefit a patient if it corrects a deformity, correctsinstability, or relieves neural compression, or treats a combi-nation of these problems. Obtaining a history and completing aphysical examination to determine a diagnosis that should besupported by other diagnostic studies is a very useful approach;conversely, matching the diagnosis and treatment to the resultsof diagnostic studies, as is done in other subspecialties oforthopaedics, is fraught with difficulty.

As pointed out by Waddell, most patients with nonspecificcomplaints and findings are best treated by their primary carephysicians. For those with significant findings, evaluation andtreatment by a specialist is appropriate. For a small minority ofpatients (although they are responsible for a much moresignificant portion of health care utilization) a multidisciplinaryapproach is best.

NONSPECIFIC LUMBAR PAINNONSPECIFIC LUMBAR PAINNonspecific low back pain occurs at some point in the lives ofmost people. In Western societies a lifetime incidence ofapproximately 80% has been documented. A study of 1389

Table 39-1 Spectrum of Pathological Changes in Facet Joints and Discs and the Interactionof These Changes

Phases of Spinal Degeneration Facet Joints Pathological Result Intervertebral Disc

Synovitis → Dysfunction ← Circumferential tears

Dysfunction Hypermobility ↓ %

Continuing degeneration # Herniation ← Radial tears

InstabilityCapsular laxity → Instability ← Internal disruption

Subluxation → Lateral nerve entrapment ← Disc resorption

StabilizationEnlargement of articular

processes

→&

One-level stenosis

Multilevel spondylosis and

stenosis

←$

Osteophytes

Modified from Kirkaldy-Willis WH, ed: Managing low back pain, New York, 1983, Churchill Livingstone.




adolescents aged 13 to 16 years recorded low back pain innearly 60%. The incidence and severity of this problem hasremained fairly constant since the early 1980s. Appropriatetreatment for what can be at times excruciating pain generallyshould begin with evaluation for significant spinal pathology.This being absent, a brief (1 to 3 days) period of bed rest withinstitution of an antiinflammatory regimen and rapid progres-sion to an active exercise regimen with an anticipated return tofull activity should be expected and encouraged. Diagnosticstudies, including roentgenograms, often are unnecessarybecause they add little information. More sophisticatedimaging with CT scans and MRI or other studies have even lessutility initially. An overdependence on the diagnosis of discherniation occurred with early use of these diagnostic studiesthat show disc herniations in 20% to 36% of normal volunteers.This incidence increased to 76% of asymptomatic controlswhen they were matched to a population at risk for work-related lumbar pain complaints. Imaging guidelines have beenset forth by Bigos et al. (Table 39-2). Generally, patients treatedin this manner improve significantly in 4 to 8 weeks. Patientsshould understand that persistence of some pain is notindicative of treatment failure, necessitating further measures;however, it is important for treating physicians to recognize thatthe longer a person is limited by pain, the less likely is a returnto full activity. Once a patient is out of work for 6 months, thereis only a 50% chance that he will return to his previous job(Fig. 39-6).

For patients who do not respond to treatment regimens,early recognition that other issues may be involved is essential.Careful reassessment of complaints and reexamination for newinformation or findings as well as inconsistencies are necessary.Many studies of occupational back pain have revealed thatdepression, occupational mental stress, job satisfaction, inten-sity of concentration, anxiety, and marital status can be relatedto complaints of pain and disability. The role of these factors ascausal or consequential of the symptoms remains an area ofcontinued study; however, there is certainly some evidence thatthe psychological stresses occur before complaints of pain in

some patients. Another finding that is evident from theliterature is the inability of physicians to detect psychosocialfactors adequately without using specific instruments designedfor this purpose in patients with back pain. In one particularstudy by Grevitt et al. experienced spinal surgeons were able toidentify distressed patients only 26% of the time based onpatient interviews. Given the difficulty of identifying patientswith psychosocial distress, being aware of the high incidence ofincidental abnormal findings on imaging studies underscoresthe need for critical individual review of these studies bytreating physicians. Severe nerve compression demonstrated byMRI or CT correlates with symptoms of distal leg pain;however, mild to moderate nerve compression (Table 39-3),disc degeneration or bulging, and central stenosis do notsignificantly correlate with specific pain patterns.

A review of the pertinent literature reveals that similarpsychological factors are important in patients with neck pain.As confounding as these psychological risk factors are,reasonable and logical measures are available that assist inevaluation and treatment.

Diagnostic StudiesROENTGENOGRAPHYDiagnostic StudiesROENTGENOGRAPHYThe simplest and most readily available diagnostic tests forback or neck pain are anteroposterior and lateral roentgeno-grams of the involved spinal segment. These simple roentgeno-grams show a relatively high incidence of abnormal findings.Ford and Goodman reported only 7.3% normal spine roent-genograms in a group of 1614 patients evaluated for back pain.Scavone, Latshaw, and Rohrer reported a 46% incidence ofabnormal incidental findings in lumbar spine films taken over

100

90

80

70

60

50

40

30

20

10

00 1

Time off work (yr)2

Perc

enta

ge

Fig. 39-6 Diminishing chance of return to work with increasingtime out of work resulting from low back pain (based on data fromClinic Standards Advisory Group). (From Waddell G: Spine21:2820, 1996.)

Table 39-2 Selective Indications forRoentgenography in Acute LowBack Pain

Age >50 yearsSignificant traumaNeuromuscular deficitsUnexplained weight loss (10 pounds in 6 months)Suspicion of ankylosing spondylitisDrug or alcohol abuseHistory of cancerUse of corticosteroidsTemperature ≥37.8° C (100.0° F)Recent visit (within 1 month) for same problem and no

improvementPatient seeking compensation for back pain

Adapted from Deyo RA, Diehl AK: J Gen Intern Med 1:20, 1986.




1 year in a university hospital. Unfortunately, when theseroentgenographic abnormalities are critically evaluated withrespect to the patients’ complaints and physical findings, thecorrelation is very low. Fullenlove and Williams clearlyidentified the lack of definition between roentgenographicfindings in symptomatic, asymptomatic, and operated patients.Rockey et al. and Liang and Komaroff concluded that spinalroentgenograms on the initial visit for acute low back pain donot contribute to patient care and are not cost effective. Theyrecommended that plain roentgenograms be taken only after theinitial therapy fails, especially in patients younger than 45 yearsof age.

There is insignificant correlation between back pain and theroentgenographic findings of lumbar lordosis, transitionalvertebra, disc space narrowing, disc vacuum sign, and clawspurs. In addition, the entity of disc space narrowing isextremely difficult to quantify in all but the operated backs orin obviously abnormal circumstances. Frymoyer et al. in astudy of 321 patients found that only when traction spurs orobvious disc space narrowing or both were present did theincidence of severe back and leg pain, leg weakness, andnumbness increase. These positive findings had no relationshipto heavy lifting, vehicular exposure, or exposure to vibratingequipment. Other studies have shown some relationship be-tween back pain and the findings of spondylolysis, spondylolis-thesis, and adult scoliosis, but these findings also can beobserved in spine roentgenograms of asymptomatic patients.

Special roentgenographic views can be helpful in furtherdefining or disproving the initial clinical roentgenographicimpression. Oblique views are useful in further definingspondylolisthesis and spondylolysis but are of limited use in

facet syndrome and hypertrophic arthritis of the lumbar spine.Conversely, in the cervical spine hypertrophic changes aboutthe foramina are easily outlined. Lateral flexion and extensionroentgenograms may reveal segmental instability. Hayes et al.attempted to identify the pathological level of abnormal lumbarspine flexion, but they found a wide range of motion inasymptomatic patients. They also found that translationalmovements of 2 to 3 mm were frequent, which means that thereis little correlation between abnormal motion and pathologicalinstability. No standards are available to make this distinction.Unfortunately, the interpretation of these views depends onpatient cooperation, patient positioning, and reproducibletechnique. Knutsson, Farfan, Kirkaldy-Willis, Stokes et al.,Macnab, and Bigos are excellent references on this topic. TheFerguson view (20-degree caudocephalic anteroposterior roent-genogram) has been shown by Wiltse et al. to be of value inthe diagnosis of the ‘‘far out syndrome,’’ that is, fifth rootcompression produced by a large transverse process of the fifthlumbar vertebra against the ala of the sacrum. Abel, Smith, andAllen note that angled caudal views localized to areas ofconcern may show evidence of facet or laminar pathologicalconditions.

MYELOGRAPHY

◆ MYELOGRAPHYThe value of myelography is the ability to check all disc levelsfor abnormality and to define intraspinal lesions; it may beunnecessary if clinical and CT findings are in completeagreement. The primary indications for myelography aresuspicion of an intraspinal lesion or questionable diagnosisresulting from conflicting clinical findings and other studies. Inaddition, myelography is of value in a previously operatedspine and in patients with marked bony degenerative changethat may be underestimated on MRI. Myelography is improvedby the use of postmyelography CT scanning in this setting,as well as in evaluating spinal stenosis. Bell et al. foundmyelography more accurate than CT scanning for identifyingherniated nucleus pulposus and only slightly more accuratethan CT scanning in the detection of spinal stenosis. Szyprytet al. found myelography slightly less accurate than MRI indetecting spinal abnormalities.

Several contrast agents have been used for myelography: air,oil contrast, and water-soluble (absorbable) contrast includingmetrizamide (Amipaque), iohexol (Omnipaque), and iopamidol(Isovue-M). Since these nonionic agents are absorbable, thediscomfort of removing them and the severity of the post-myelographic headache have been decreased.

Isophendylate (Pantopaque) was the contrast agent of choicefrom 1944 to the late 1970s (Fig. 39-7). This agent requiredaspiration at the conclusion of the study and was more of ameningeal irritant than the nonionic materials currentlyavailable. Occasionally, older patients are seen with smallamounts of residual Pantopaque within the subarachnoid space.Rarely, patients have severe reactions such as transientparalysis, cauda equina syndrome, or focal neurologicaldeficits.

Table 39-3 Classification for Spinal Nerveand Thecal Sac Deformation

SPINAL NERVE DEFORMATION IN LATERAL RECESSOR INTERVERTEBRAL FORAMEN0—Absent No visible disc material contacting or

deforming nerveI—Minimal Contact with disc material deforming nerve

but displacement less than 2 mmII—Moderate Contact with disc material displacing 2 or

more mm. The nerve is still visible andnot obscured by disc material

III—Severe Contact with disc material completelyobscuring the nerve

THECAL SAC DEFORMATION IN VERTEBRAL CANAL0—Absent No visible disc material contacting or

deforming thecal sacI—Minimal Disc material in contact with thecal sacII—Moderate Disc material deforming thecal sac, antero-

posterior distance of thecal sac ≥7 mmIII—Severe Disc material deforming thecal sac, antero-

posterior distance of thecal sac <7 mm

From Beattie PF, Meyers SP, Strafford P, et al: Spine 25:819, 2000.




Arachnoiditis is a severe complication that has beenattributed on occasion to the combination of isophendylate andblood in the cerebrospinal fluid (CSF). Unfortunately, thisdiagnosis usually is confirmed only by repeat myelography.Attempts at surgical neurolysis have resulted in only short-termrelief and a return of symptoms within 6 to 12 months after theprocedure. Fortunately, time may decrease the effects of thisserious problem in some patients, but progressive paralysishas been reported in rare instances. Arachnoiditis also canbe caused by tuberculosis and other types of meningitis.Arachnoiditis has not been noted to be related to the use ofwater-soluble contrast, with or without injection, in thepresence of a bloody tap. Myelography remains the bestdiagnostic study to evaluate arachnoiditis.

Water-soluble contrast media are now the standard agentsfor myelography (Fig. 39-8). Their advantages includeabsorption by the body, enhanced definition of structures,tolerance, absorption from other soft tissues, and the ability tovary the dosage for different contrasts. Like isophendylate theyare meningeal irritants, but they have not been associated witharachnoiditis. The complications of these agents includenausea, vomiting, confusion, and seizures. Rare complicationsinclude stroke, paralysis, and death. Iohexol and iopamidolhave significantly lower complication rates than metrizamide.The more common complications appear to be related to patienthydration, phenothiazines, tricyclics, and migration of contrastinto the cranial vault. Many of the reported complications canbe prevented or minimized by using the lowest possible dose toachieve the desired degree of contrast. Adequate hydration anddiscontinuation of phenothiazines and tricyclic drugs before,during, and after the procedure should also minimize the

incidence of the more common reactions. Likewise, mainte-nance of at least a 30-degree elevation of the patient’s headuntil the contrast is absorbed also should help prevent reactions.Complete information about these agents and the dosagesrequired is found in their package inserts.

Iohexol (Omnipaque) is a nonionic contrast mediumapproved for thoracic and lumbar myelography. The incidenceof reactions to this medium is low. The most common reactionsare headache (less than 20%), pain (8%), nausea (6%), andvomiting (3%). Serious reactions are very rare and includemental disturbances and aseptic meningitis (0.01%). Goodhydration is essential to minimize the common reactions. Theuse of phenothiazine antinauseants is contraindicated when thismedium is employed. Management before and after theprocedure is the same as for metrizamide.

Air contrast is used rarely and probably should be used onlyin situations in which myelography is mandatory and thepatient is extremely allergic to iodized materials. The resolutionfrom such a procedure is poor. Air epidurography in con-junction with CT has been suggested in patients in whomfurther definition between postoperative scar and recurrent discmaterial is required.

Myelographic technique begins with a careful explanationof the procedure to the patient before its initiation. Hydration ofthe patient before the procedure may minimize postmyelo-graphic complaints. Heavy sedation rarely is needed. Properequipment, including a fluoroscopic unit with a spot filmdevice, image intensification, tiltable table, and televisionmonitoring, is useful. The type of needle selected alsoinfluences the risk of postdural puncture headaches (PDPH),which can be severe. Smaller gauge needles (22 or 25 gauge)

A

Fig. 39-7 A, Anteroposterior roentgenogram of iophendyl-ate (Pantopaque) myelogram showing lumbar disc herniation.B, Oblique roentgenogram showing large L4-5 disc herniation.

B

A

Fig. 39-8 A, Anteroposterior roentgenogram of metrizamidelumbar myelogram showing lumbar disc herniation. B, Obliqueroentgenogram showing large L4-5 disc herniation.

B




have been found to result in a lower incidence of PDPH. Also,use of a Whitacre-type needle with a more blunt tip and sideport opening results in fewer PDPH complaints.

TECHNIQUE 39-1Place the patient prone on the fluoroscopic table. Use of anabdominal pillow is optional. Prepare the back in the usualsurgical fashion. Determine needle placement by thesuspected pathological level. Placement of the needlecephalad to L2-3 is more dangerous because of the risk ofdamaging the conus medullaris.

Infiltrate the selected area of injection with a localanesthetic. Use the smallest-gauge needle that can be wellplaced. If a Whitacre-type needle is used, a 19-gauge needlemay be placed through the skin, subcutaneous tissue, andfascia to form a track, since this relatively blunt needle maynot penetrate these structures well. Midline needle place-ment usually minimizes lateral nerve root irritation andepidural injection. Advance the needle with the bevelparallel to the long axis of the body. Subarachnoidplacement can be enhanced by tilting the patient up toincrease intraspinal pressure and minimize the epiduralspace.

Once the dura and arachnoid have been punctured, turnthe bevel of the needle cephalad. A clear continuous flow ofCSF should continue with the patient prone. Manometricstudies can be performed at this time if desired or indicated.Remove a volume of CSF equal to the planned injectionvolume for laboratory evaluation as indicated by the clinicalsuspicions. In most patients a cell count, differential whitecell count, and protein analysis are performed.

Inject a test dose of the contrast material underfluoroscopic control to confirm a subarachnoid injection. Ifa mixed subdural-subarachnoid injection is suspected,change the needle depth; occasionally a lateral roentgeno-gram may be required to confirm the proper depth. If flowis good, inject the contrast material slowly.

Be certain of continued subarachnoid injection byoccasionally aspirating as the injection continues. The usualdose of iohexol for lumbar myelography in an adult is 10 to15 ml with a concentration of 170 to 190 mg/ml. Higherconcentrations of water-soluble contrast are required ifhigher areas of the spine are to be demonstrated. Consult thepackage insert of the contrast used. The needle can beremoved if a water-soluble contrast (iohexol) is used. Theneedle must remain in place and be covered with a steriletowel if isophendylate is used.

Allow the contrast material to flow caudally for the bestviews of the lumbar roots and distal sac. Make spot films inthe anteroposterior, lateral, and oblique projections. A fulllumbar examination should include thoracic evaluation toabout the level of T7 because lesions at the thoracic levelmay mimic lumbar disc disease. Take additional spot filmsas the contrast proceeds cranially.

If a total or cervical myelogram is desired, allow the

contrast to proceed cranially. Extend the neck and headmaximally to prevent or minimize intracranial migration ofthe contrast medium.

If isophendylate (oil contrast) was used, remove thecontrast medium by extracting through the original needleor a multiholed stylet inserted through the original needle orby inserting another needle if extraction through the firstneedle is difficult. A small amount of medium occasionallyis retained, but remove as much as possible.

If blood is present in the initial tap, abandon theprocedure if oil contrast is to be used. It can be attemptedagain in several days if the patient has no symptoms relatedto the first tap and is well hydrated. If the proper needleposition is confirmed in the anteroposterior and lateral viewsand CSF flow is minimal or absent, suspect a neoplasticprocess. Then place the needle at a higher or lower level asindicated by the circumstances. If attempts to obtain CSFcontinue to fail, abandon the procedure and reevaluate theclinical situation.

The most common technical complications of myelographyare significant retention of contrast medium (oil contrast only),persistent headache from a dural leak, and epidural injection.These problems usually are minor. Persistent dural leaksusually are responsive to a blood patch. With the use of awater-soluble contrast medium, the persistent abnormalitiescaused by retained medium and epidural injection areeliminated.

COMPUTED TOMOGRAPHYCOMPUTED TOMOGRAPHYComputed tomography revolutionized the diagnosis of spinaldisease (Fig. 39-9). Most clinicians now agree that CT is anextremely useful diagnostic tool in the evaluation of spinaldisease.

The current technology and computer software have madepossible the ability to reformat the standard axial cuts in almostany direction and magnify the images so that exact measure-ments of various structures can be made. Software is availableto evaluate the density of a selected vertebra and compareit with vertebrae of the normal population to give a numer-ically reproducible estimate of vertebral density to quantitateosteopenia.

Numerous types of CT studies for the spine are available.These studies vary from institution to institution and evenwithin institutions. One must be careful in ordering the study tobe certain that the areas of clinical concern are included.

Several basic routines are used in most institutions. Themost common routine for lumbar disc consists of making serialcuts through the last three lumbar intervertebral discs. If theequipment has a tilting gantry, an attempt is made to keep theaxis of the cuts parallel with the disc. However, frequentlythe gantry cannot tilt enough to allow a parallel beam throughthe lowest disc space. This technique does not allow demon-




stration of the canal at the pedicles. Another method involvesmaking cuts through the discs without tilting the gantry. Onceagain, the entire canal is not demonstrated, and the lower cutsfrequently have the lower and upper endplates of adjacentvertebrae superimposed in the same view.

The final and most complex method consists of makingmultiple parallel cuts at equal intervals. This allows computerreconstruction of the images in different planes—usuallysagittal and coronal. These reformatted views allow an almostthree-dimensional view of the spine and most of its structures.The greatest benefit of this technique is the ability to seebeyond the limits of the dural sac and root sleeves. Thus thediagnosis of foraminal encroachment by bone or disc materialcan now be made in the face of a normal myelogram. Theproper procedure can be chosen that fits all the pathologicalconditions involved.

Optimal reformatted CT should include enlarged axial andsagittal views with clear notation as to laterality and sequence

of cuts. Several sections of the axial cuts should include thelocal soft tissue and contiguous abdominal contents. Finally, aset of images adjusted for improved bony detail should beincluded for evaluation of the facet joints as well as the lateralrecesses. Naturally this study should be centered on the level ofgreatest clinical concern. The study can be enhanced further ifdone after water contrast myelography or with intravenouscontrast medium. Enhancement techniques are especiallyuseful if the spine being evaluated has been operated onpreviously.

This noninvasive, painless, outpatient procedure can supplymore information about spinal disease than was previouslyavailable with a battery of invasive and noninvasive testsusually requiring hospitalization. Unfortunately, CT does notdemonstrate intraspinal tumors or arachnoiditis and is unable todifferentiate scar from recurrent disc herniation. Bell et al.compared myelography with CT scanning and noted thatmyelography was more accurate. They did not compare the

A

Fig. 39-9 A, CT scan ‘‘scout view’’ of lumbar disc herniation at lumbar disc level showing angledgantry technique. B, CT scan ‘‘scout view’’ of straight gantry technique. C, CT scan of lumbar discherniation at L4-5 disc level showing cross-sectional anatomy with gantry straight. D, CT scan ofL4-5 disc herniation at lumbar disc level showing cross-sectional, sagittal, and coronal anatomyusing computerized reformatted technique. E, CT scan of L4-5 disc herniation at lumbar disc levelshowing cross-sectional anatomy 2 hours after metrizamide myelography. F, CT scan of lumbar discherniation at L4-5 disc level showing cross-sectional anatomy after intravenous injection for greatersoft tissue contrast.

B C

D E F




results of postmyelogram CT scanning. Weiss et al. and Teplickand Haskin in separate reports suggested that the use ofintravenous contrast medium (Fig. 39-9, E) followed by CT canimprove the definition between scar and disc herniation.Myelography is still required to demonstrate intraspinal tumorsand to ‘‘run’’ the spine to detect occult or unsuspected lesions.The development of low-dose metrizamide or iohexol myelog-raphy with reformatted CT done as an outpatient procedureallows a maximum of information to be obtained with aminimum of time, risk, discomfort, and cost.

MAGNETIC RESONANCE IMAGINGMAGNETIC RESONANCE IMAGINGMagnetic resonance imaging (MRI) is the newest technologicaladvance in spinal imaging. This technique uses the interactionof an unpaired electron with an external oscillating electromag-netic field that is changing as a function of time at a particularfrequency. Energy is absorbed and subsequently released byselected nuclei at particular frequencies after excitation withradiofrequency electromagnetic energy. The released energy isrecorded and formatted by computer in a pattern similar to CT.Current MRI techniques concentrate on imaging the proton(hydrogen) distribution present as H2O primarily. The advan-tages of this technique include the ability to demonstrateintraspinal tumors, examine the entire spine, and identifydegenerative discs based on decreased H2O content. Unfortu-nately, the equipment required for this procedure is costly andrequires specially constructed facilities (Fig. 39-10).

Szypryt et al. found MRI slightly better than myelography inthe identification of spinal lesions. The accuracy of MRIin their study was 88% and that of myelography was 75%;

combined accuracy was 94%. MRI is clearly superior in thedetection of disc degeneration, tumors, and infections. MostMRI scans allow evaluation of a complete spinal region (suchas cervical, thoracic, or lumbar) rather than three segments.They also can clearly view areas in the foramen and theparaspinal soft tissues.

MRI is so accurate that a significant number of lesions canbe identified in asymptomatic patients. Gibson et al. found discdegeneration in all symptomatic adolescent patients and in 4of 20 asymptomatic adolescents. Boden et al. found cervicalspinal abnormalities in 14% of asymptomatic patients youngerthan 40 years of age and in 28% of asymptomatic patients overthe age of 40 years. Cervical disc degeneration was found in25% of those younger than 40 years of age and in 60% of those60 years and older. They studied lumbar MRI scans of 67asymptomatic patients and found that 20% of those youngerthan 60 years of age had herniated nuclei pulposi, which werealso present in 36% of those over the age of 60 years.Asymptomatic abnormalities were found in 57% of those 60years of age or older. Lumbar disc degeneration was found in35% of those from 20 to 39 years of age and in 100% of thoseover 50 years of age. Therefore the demonstrated findings mustbe carefully correlated with the clinical impression.

POSITRON EMISSION TOMOGRAPHYPOSITRON EMISSION TOMOGRAPHYPositron emission tomography (PET) and single photonemission CT (SPECT) are other similar techniques that mayoffer additional diagnostic information. Collier et al. and othersreported that SPECT is more sensitive than planar bonescintigraphy in the identification of symptomatic sites inspondylolysis. PET scanners are considered experimental bymost third-party payers at this time. Their use currently islimited to relatively few centers.

Currently, imaging capabilities exceed clinical abilities toidentify the source of pain. However, some patients may havenonanatomical causes for their pain and there is no imaginableexplanation for their symptoms. In these patients, imagingstudies are useful to rule out significant pathology that mayexplain their symptoms, such as with spinal cord tumors,infections, polyradiculopathies, or myeloradiculopathies.

OTHER DIAGNOSTIC TESTSOTHER DIAGNOSTIC TESTSNumerous diagnostic tests have been used in the diagnosis ofintervertebral disc disease in addition to roentgenography,myelography, and CT. The primary advantage of these tests isto rule out diseases other than primary disc herniation, spinalstenosis, and spinal arthritis.

Electromyography is the most notable of these tests. Oneadvantage of electromyography is in the identification ofperipheral neuropathy and diffuse neurological involvementindicative of higher or lower lesions. Electromyography andnerve conduction velocity can be helpful if a patient has ahistory and physical examination suggestive of radiculopathy ateither the cervical or lumbar level with inconclusive imaging

A

Fig. 39-10 Magnetic resonance imaging of lumbar spine.A, Normal T2-weighted image. B, T2-weighted image showingdegenerative bulging and/or herniated discs at L3-4, L4-5, andL5-S1.

B




studies. Macnab et al. reported that denervation of theparaspinal muscles is found in 97% of previously operatedlumbar spines as a result of the surgery. Therefore paraspinalmuscles in a patient with a previous posterior operation usuallyare abnormal and are not a reliable diagnostic finding.

The somatosensory evoked potentials (SSEP) test is anotherdiagnostic tool that can identify the level of root involvement.Unlike electromyography this test can only indicate a problembetween the cerebral cortex and the end organs; the test cannotpinpoint the level of the lesion. This procedure is of benefitduring surgery to avoid neurological damage. Both electromy-ography and SSEP depend on the skill of the technician andinterpreter. Delamarter et al. used cortical evoked potentials tomonitor experimentally induced spinal stenosis. They notedchanges in the cortical response at 25% constriction. This wasthe only change noted in this group. Higher degrees ofconstriction were accompanied by much more significantchanges. The SSEP is an extremely sensitive monitoringtechnique.

Bone scans are another procedure in which positive findingsusually are not indicative of intervertebral disc disease, but theycan confirm neoplastic, traumatic, and arthritic problems in thespine. Various laboratory tests such as a complete blood count,differential white cell count, biochemical profile, urinalysis,and sedimentation rate are extremely good screening pro-cedures for other causes of pain in the spine. Rheumatoidscreening studies such as rheumatoid arthritis latex, antinuclearantibody, lupus erythematosus cell preparation, and HLA-B27also are useful when indicated by the clinical picture.

Some tests that were developed to enhance the diagnosis ofintervertebral disc disease have been surpassed by the moreadvanced technology. Lumbar venography and sonographicmeasurement of the intervertebral canal are two examples.

Injection Studies

Injection StudiesWhenever a diagnosis is in doubt and the complaints appearreal or the pathological condition is diffuse, identification of thesource of pain is problematic. The use of local anesthetics orcontrast media in various specific anatomical areas can beuseful. These agents are relatively simple, safe, and minimallypainful. Contrast media such as diatrizoate meglamine(Hypaque), iothalamate meglumine (Conray), iohexol (Omni-paque), iopamidol, and metrizamide (Amipaque) have beenused for discography and blocks with no reported ill effects.Reports of neurological complications with contrast media usedfor discography and subsequent chymopapain injection are welldocumented. The best choice of a contrast medium fordocumenting structures outside the subarachnoid space is anabsorbable medium with low reactivity because it might beinjected inadvertently into the subarachnoid space. Iohexol andmetrizamide are the least reactive, most widely accepted, andbest tolerated of the currently available contrast media. Localanesthetics such as lidocaine (Xylocaine), tetracaine (Pon-tocaine), and bupivacaine (Marcaine) are used frequently both

epidurally and intradurally. The use of bupivacaine should belimited to low concentrations and low volumes because ofreports of death after epidural anesthesia using concentrationsof 0.75% or higher.

Steroids prepared for intramuscular injection also have beenused frequently in the epidural space with few and usuallytransient complications. Spinal arachnoiditis in years past wasassociated with the use of epidural methylprednisolone acetate(Depo-Medrol). This complication was thought to be caused bythe use of the suspending agent, polyethylene glycol, which hassince been eliminated from the Depo-Medrol preparation. Forepidural injections, we prefer the use of Celestone Soluspan,which is a mixture of betamethasone sodium phosphate andbetamethasone acetate. Celestone Soluspan provides bothimmediate and long-term duration of action, is highly soluble,and contains no harmful preservatives. Isotonic saline is theonly other injectable medium used frequently about the spinewith no reported adverse reactions.

When discrete, well-controlled injection techniques directedat specific targets in and around the spine are used, grading thedegree of pain before and after selective spinal injection ishelpful in determining the location of the pain generator. Thepatient is asked to grade the degree of pain on a 0 to 10 scalebefore and at various intervals after the selective spinalinjection (Box 39-1). If a selective spinal injection done underfluoroscopic control results in a 50% or more decrease in thelevel of pain, which corresponds to the duration of action of theanesthetic agent used, then the target area injected is presumedto be the pain generator.

EPIDURAL CORTISONE INJECTIONSEPIDURAL CORTISONE INJECTIONSEpidural injections in the cervical, thoracic, and lumbosacralspine were developed to diagnose and treat spinal pain.Information obtained from epidural injections can be helpful inconfirming pain generators that are responsible for a patient’sdiscomfort. Structural abnormalities do not always cause painand diagnostic injections can help to correlate abnormalitiesseen on imaging studies with associated pain complaints. Inaddition, epidural injections can provide pain relief during therecovery of disc or nerve root injuries and allow patients toincrease their level of physical activity. Because severe painfrom an acute disc injury with or without radiculopathy often istime-limited, therapeutic injections help to manage pain andmay alleviate or decrease the need for oral analgesics.

Epidural injections were first done in the lumbar region. In1901 the first reports were published of epidural injections ofcocaine for low back pain and sciatica. In 1930 Evans reportedgood results in 22 of 40 patients treated with procaine andsaline injection into the sacral epidural space for unilateralsciatica, and in the early 1950s Robecchi and Capral were thefirst to report epidural injection of cortisone into the first sacralneuroforamen for the treatment of low back pain. The earliestreferences for cervical epidural injections were published byCatchlove and Braha and Shulman et al. No historicalinformation on thoracic epidural injections has been published.




The efficacy of epidural injections is not reliably knownbecause of the lack of well-controlled studies. Inconsistenciesin indications and protocols are striking among reports, andmany epidural steroid injection studies were done withoutfluoroscopic-guided needle placement to confirm correctpositioning, adding another variable to the interpretation of theresults. Nevertheless, more than 40, mostly uncontrolled,studies on more than 4000 patients have been published on theefficacy of lumbar and caudal epidural corticosteroid injec-tions, and according to Bogduk, only 4 recommended againstthe use of lumbosacral epidural corticosteroids in the man-agement of radicular pain in the lumbosacral spine. Kepes andDuncalf calculated the average favorable response rate ob-tained with lumbar epidural steroid injections to be 60%,whereas White calculated the favorable response rate to be75%. Several studies reported the usefulness of transforaminalepidural corticosteroid injections (selective epidural or selec-tive nerve root block) to identify or confirm a specific nerveroot as a pain generator when the diagnosis is not clear basedon clinical evidence.

Few serious complications occur in patients receivingepidural corticosteroid injections; however, epidural abscess,epidural hematoma, durocutaneous fistula, and Cushing syn-drome have been reported as individual case reports. The mostadverse immediate reaction during an epidural injection is avasovagal reaction. Dural puncture has been estimated to occurin 0.5% to 5% of patients having cervical or lumbar epiduralsteroid injections. The anesthesiology literature reported a7.5% to 75% incidence of postdural puncture (positional)headaches, with the highest estimates associated with the use of16- and 18-gauge needles. Headache without dural puncturehas been estimated to occur in 2% and is attributed to airinjected into the epidural space, increased intrathecal pressurefrom fluid around the dural sac, and possibly an undetecteddural puncture. Some of the minor, more common complaintscaused by corticosteroid injected into the epidural space

include nonpositional headaches, fascial flushing, insomnia,low-grade fever, and transient increased back or lowerextremity pain. Epidural corticosteroid injections are contrain-dicated in the presence of infection at the injection site,systemic infection, bleeding diathesis, uncontrolled diabetesmellitus, and congestive heart failure.

We do epidural corticosteroid injections in a fluoroscopysuite equipped with resuscitative and monitoring equipment.Intravenous access is established in all patients with a 20-gaugeangiocatheter placed in the upper extremity. Mild sedation isachieved through intravenous access. We recommend the use offluoroscopy for diagnostic and therapeutic epidural injectionsfor several reasons. Epidural injections performed withoutfluoroscopic guidance are not always made into the epiduralspace or the intended interspace. Even in experienced hands,needle misplacement occurs in up to 40% of caudal and 30% oflumbar epidural injections when done without fluoroscopicguidance. Accidental intravascular injections also can occur,and the absence of blood return with needle aspiration beforeinjection is not a reliable indicator of this complication. In thepresence of anatomical anomalies, such as a midline epiduralseptum or multiple separate epidural compartments, the desiredflow of epidural injectants to the presumed pain generator willbe restricted and remain undetected without fluoroscopy. Inaddition, if an injection fails to relieve pain, it would beimpossible without fluoroscopy to determine whether thefailure was caused by a genuine poor response or by improperneedle placement.

Cervical Epidural InjectionCervical epidural steroid injections have been used with

some success to treat cervical spondylosis associated with acutedisc disruption and radiculopathies, cervical strain syndromeswith associated myofascial pain, postlaminectomy cervicalpain, reflex sympathetic dystrophy, postherpetic neuralgia,acute viral brachial plexitis, and muscle contraction headaches.

BOX 39-1 • Pain Scale and Diary

0 No pain1 Mild pain that you are aware of but not bothered by2 Moderate pain that you can tolerate without medication3 Moderate pain that is discomforting and requires medication4-5 More severe and you begin to feel antisocial6 Severe pain7-9 Intensely severe pain10 Most severe pain; you might contemplate suicide over it

Activity Comments Location of Pain Time Severity of Pain (0 to 10)

From White AH: Back school and other conservative approaches to low back pain, St Louis, 1983, Mosby.




The best results with cervical epidural steroid injections havebeen in patients with acute disc herniations or well-definedradicular symptoms and in patients with limited myofas-cial pain.

◆ Interlaminar Approach

TECHNIQUE 39-2Place the patient prone on a pain management table. We usea low-attenuated carbon fiber table top that allows betterimaging and permits unobstructed C-arm viewing. Foroptimal placement and comfort, place the patient’s face in acervical prone cutout cushion. Cervical epidural injectionsusing a paramedian approach should be done routinely at theC7-T1 interspace unless previous surgery of the posteriorcervical spine has been done at that level, in which case theC6-C7 or T1-T2 level is injected. Aseptically prepare theskin area with isopropyl alcohol and povidone-iodineseveral segments above and below the laminar interspace tobe injected. If the patient is allergic to povidone-iodine, thensubstitute with chlorhexidine gluconate (Hibiclens). Drapethe patient in sterile fashion. Using anteroposterior fluoro-scopic imaging, identify the target laminar interspace. Withthe use of a 27]-gauge needle, anesthetize the skin so thata skin wheal is raised over the target interspace on the sideof the patient’s pain with 1 to 2 ml of 1% preservative-freeXylocaine without epinephrine. To diminish the burningdiscomfort of the anesthetic, mix 3 ml of 8.4% sodiumbicarbonate in a 30-ml bottle of 1% preservative-freeXylocaine without epinephrine. Nick the skin with an18-gauge hypodermic needle. Under fluoroscopic controlinsert and advance a 31⁄2-inch, 22-gauge spinal needle in a

vertical fashion until contact is made with the upper edge ofthe T1 lamina 1 to 2 mm lateral to the midline.

Anesthetize the lamina with 1 to 2 ml of 1%preservative-free Xylocaine without epinephrine. Thenanesthetize the soft tissues with 2 ml of 1% preservative-freeXylocaine without epinephrine as the spinal needle iswithdrawn. Insert a 31⁄2-inch, 18-gauge Tuohy epiduralneedle and advance it vertically within the anesthetized softtissue track until contact is made with the T1 lamina underfluoroscopy. ‘‘Walk off’’ the lamina with the Tuohy needleonto the ligamentum flavum. Remove the stylet from theTuohy needle and attach a 10-ml syringe filled halfway withair and sterile saline. Advance the Tuohy needle into theepidural space using the loss of resistance technique. Onceloss of resistance has been achieved, aspirate to check forblood or spinal fluid. If neither is evident, remove thesyringe from the Tuohy needle and attach a 5-ml syringecontaining 1.5 ml of nonionic contrast dye. Confirmepidural placement by producing an epidurogram withthe nonionic contrast agent (Fig. 39-11). To further con-firm proper placement adjust the C-arm to view the areafrom a lateral perspective. A spot roentgenogram canbe obtained to document placement. Inject a test dose of1 to 2 ml of 1% preservative-free Xylocaine withoutepinephrine and wait 3 minutes. If the patient is withoutcomplaints of warmth, burning, significant paresthesias, orsigns of apnea, place a 10-ml syringe on the Tuohy needleand slowly inject 2 ml of 1% preservative-free Xylocainewithout epinephrine and 2 ml of 6 mg/ml CelestoneSoluspan slowly into the epidural space. If CelestoneSoluspan cannot be obtained, 40 mg/ml of triamcinolone isa good substitute.

Fig. 39-11 Posteroanterior view cervical interlaminar epidurogram demonstrating characteristicC7 to T1 epidural contrast flow pattern.




◆ Transforaminal Approach

TECHNIQUE 39-3Place the patient in a modified lateral decubitus positionwith the painful side up on a pain management table.Aseptically prepare the skin area with isopropyl alcohol andpovidone-iodine several segments above and below theneuroforamen to be injected. Drape the patient in sterilefashion. Identify the foramen level to be injected underfluoroscopy, orienting the beam so that it is slightly tiltedcaudal to cephalad and anterior to posterior to maximizethe view of the neuroforamen. Insert and slowly advance a31⁄2-inch 25-gauge spinal needle until contact is made withthe lower aspect of the superior articular process underfluoroscopy. Stay posterior to the foramen to avoid thevertebral artery. To maximize posterior positioning of thespinal needle bevel, orient the needle notch anteriorly.Orient the C-arm so that the fluoroscopy beam is in ananteroposterior projection. Redirect the spinal needle and‘‘walk off’’ bone into the foramen 3 to 4 mm but no farthermedially than the midpoint of the articular pillar onanteroposterior imaging. Remove the stylet. After a negativeaspiration, inject 0.5 ml of nonionic contrast dye underfluoroscopy. Once an acceptable dye pattern is seen (fillingof the oval neuroforamen and flow of contrast along theexiting nerve root), inject slowly a 1-ml volume, containing0.5 ml of 2% to 4% preservative-free Xylocaine withoutepinephrine and 0.5 ml of 6 mg/ml Celestone Soluspan.

Thoracic Epidural InjectionEpidural steroid injections in the thoracic spine have been

shown to provide relief from thoracic radicular pain secondaryto disc herniations, trauma, diabetic neuropathy, herpes zoster,and idiopathic thoracic neuralgia, although reports in theliterature are few.


TECHNIQUE 39-4A paramedian rather than a midline approach is usedbecause of the angulation of the spinous processes. Place thepatient prone on a pain management table. The preparationof the patient and equipment is identical to that used forinterlaminar cervical epidural injections. Aseptically pre-pare the skin area several segments above and below theinterspace to be injected. Drape the patient in sterile fashion.Identify the target laminar interspace using anteroposteriorvisualization under fluoroscopic guidance. Anesthetize theskin over the target interspace on the side of the patient’spain. Under fluoroscopic control, insert and advance a31⁄2-inch, 22-gauge spinal needle to the superior edge of thetarget lamina. Anesthetize the lamina and the soft tissues asthe spinal needle is withdrawn. Mark the skin with an 18-gauge hypodermic needle and then insert a 31⁄2-inch,18-gauge Tuohy epidural needle and advance it at a 50- to60-degree angle to the axis of the spine and a 15- to 30-degreeangle toward the midline until contact with the lamina ismade. To better view the thoracic interspace, position theC-arm so that the fluoroscopy beam is in the same plane asthe Tuohy epidural needle. ‘‘Walk off’’ the lamina with theTuohy needle into the ligamentum flavum. Remove the styletfrom the Tuohy needle and, using the loss of resistancetechnique, advance it into the epidural space. Once loss ofresistance has been achieved, aspirate to check for blood orspinal fluid. If neither is evident, inject 1.5 ml of nonioniccontrast dye to confirm epidural placement. To furtherconfirm proper placement, adjust the C-arm to view the areafrom a lateral projection (Fig. 39-12). A spot roentgenogramor epidurogram can be obtained. Inject 2 ml of 1%preservative-free Xylocaine without epinephrine and 2 ml of6 mg/ml Celestone Soluspan slowly into the epidural space.

A B

Fig. 39-12 A, Anteroposterior view of thoracic interlaminar epidurogram demonstrating charac-teristic contrast flow pattern. B, Lateral roentgenogram of thoracic interlaminar epidurogram.




Lumbar Epidural InjectionCertain clinical trends are apparent with lumbar epidural

steroid injections. When nerve root injury is associated with adisc herniation or lateral bony stenosis, most patients whoreceived substantial leg pain relief from a well-placed trans-foraminal injection, even if temporary, will benefit fromsurgery for the radicular pain. Patients who do not respond andwho have had radicular pain for at least 12 months are unlikelyto benefit from surgery. Patients with back and leg pain of anacute nature (less than 3 months) respond better to epiduralcorticosteroids. Unless a significant reinjury results in an acutedisc or nerve root injury, postsurgical patients tend to respondpoorly to epidural corticosteroids.


TECHNIQUE 39-5Place the patient prone on a pain management table.Aseptically prepare the skin area with isopropyl alcohol andpovidone-iodine several segments above and below thelaminar interspace to be injected. Drape the patient in asterile fashion. Under anteroposterior fluoroscopy guidance,identify the target laminar interspace. Using a 27]-gaugeneedle, anesthetize the skin over the target interspace onthe side of the patient’s pain with 1 to 2 ml of 1%preservative-free Xylocaine without epinephrine. Insert a31⁄2-inch, 22-gauge spinal needle vertically until contact ismade with the upper edge of the inferior lamina at the targetinterspace, 1 to 2 cm lateral to the caudal tip of the inferiorspinous process under fluoroscopy. Anesthetize the laminawith 2 ml of 1% preservative-free Xylocaine withoutepinephrine. Then anesthetize the soft tissue with 2 ml of

1% Xylocaine as the spinal needle is withdrawn. Nick theskin with an 18-gauge hypodermic needle and then insert a31⁄2-inch, 17-gauge Tuohy epidural needle and advance itvertically within the anesthetized soft tissue track untilcontact with the lamina has been made under fluoroscopy.‘‘Walk off’’ the lamina with the Tuohy needle onto theligamentum flavum. Remove the stylet from the Tuohyneedle and attach a 10-ml syringe filled halfway with air andsterile saline to the Tuohy needle. Advance the Tuohy needleinto the epidural space using the loss of resistancetechnique. Avoid lateral needle placement to decrease thelikelihood of encountering an epidural vein or adjacentnerve root. Remove the stylet once loss of resistance hasbeen achieved. Aspirate to check for blood or spinal fluid. Ifneither is present, remove the syringe from the Tuohy needleand attach a 5-ml syringe containing 2 ml of nonioniccontrast dye. Confirm epidural placement by producing anepidurogram with the nonionic contrast agent (Fig. 39-13).A spot roentgenogram can be taken to document placement.Remove the 5-ml syringe and place on the Tuohy needle a10-ml syringe containing 2 ml of 1% preservative-freeXylocaine and 2 ml of 6 mg/ml Celestone Soluspan. Injectthe corticosteroid preparation slowly into the epidural space.

◆ Transforaminal Approach

TECHNIQUE 39-6Place the patient prone on a pain management table.Aseptically prepare the skin area with isopropyl alcohol andpovidone-iodine several segments above and below the

Fig. 39-13 Anteroposterior and lateral view of lumbar interlaminar epidurogram demonstratingcharacteristic contrast flow pattern.




interspace to the injected. Drape the patient in sterilefashion. Under anteroposterior fluoroscopic guidance, iden-tify the target interspace. Anesthetize the soft tissues overthe lateral border and midway between the two adjacenttransverse processes at the target interspace. Insert a43⁄4-inch, 22-gauge spinal needle and advance it within theanesthetized soft tissue track under fluoroscopy until contactis made with the lower edge of the superior transverseprocess near its junction with the superior articular process.Retract the spinal needle 2 to 3 mm and redirect it towardthe base of the appropriate pedicle and advance it slowly tothe 6-o’clock position of the pedicle under fluoroscopy.Adjust the C-arm to a lateral projection to confirm theposition then return the C-arm to the anteroposterior view.Remove the stylet. Inject 1 ml of nonionic contrast slowly toproduce a perioneurosheathogram (Fig. 39-14). After anadequate dye pattern is observed, inject slowly a 2-mlvolume containing 1 ml of 0.75% preservative-free bupiva-caine and 1 ml of 6 mg/ml Celestone Soluspan.

The S1 nerve root also can be injected using thetransforaminal approach. Place the patient prone on the painmanagement table. After appropriate aseptic preparation,direct the C-arm so that the fluoroscopy beam is in acephalocaudad and lateral-to-medial direction so that theanterior and posterior S1 foramina are aligned. Anesthetizethe soft tissues and the dorsal aspect of the sacrum with 2 to3 ml of 1% preservative-free Xylocaine without epineph-rine. Insert a 31⁄2-inch, 22-gauge spinal needle and advanceit within the anesthetized soft tissue track under fluoroscopyuntil contact is made with posterior sacral bone slightlylateral and inferior to the S1 pedicle. ‘‘Walk’’ the spinalneedle off the sacrum into the posterior S1 foramen to the

medial edge of the pedicle. Adjust the C-arm to a lateralprojection to confirm the position and then return it to theanteroposterior view. Remove the stylet. Inject 1 ml ofnonionic contrast slowly to produce a perineurosheatho-gram. After an adequate dye pattern of the S1 nerve root isobtained, insert a 2-ml volume containing 1 ml of 0.75%preservative-free Marcaine and 1 ml of 6 mg/ml CelestoneSoluspan.

◆ Caudal Approach

TECHNIQUE 39-7Place the patient prone on a pain management table.Aseptically prepare the skin area from the lumbosacraljunction to the coccyx with isopropyl alcohol and povidone-iodine. Drape the patient in sterile fashion. Try to identify bypalpation the sacral hiatus, which is located between the twohorns of the sacral cornu. The sacral hiatus can best beobserved by directing the fluoroscopic beam laterally.Anesthetize the soft tissues and the dorsal aspect of thesacrum with 2 to 3 ml of 1% preservative-free Xylocainewithout epinephrine. Keep the C-arm positioned so thatthe fluoroscopic beam remains lateral. Insert a 31⁄2-inch,22-gauge spinal needle between the sacral cornu at about 45degrees, with the bevel of the spinal needle facing ventrallyuntil contact with the sacrum is made. Using fluoroscopicguidance, redirect the spinal needle more cephalad, hori-zontal and parallel to the table, advancing it into the sacralcanal through the sacrococcygeal ligament and into theepidural space. Remove the stylet. Aspirate to check forblood or spinal fluid. If neither is evident, inject 2 ml ofnonionic contrast dye to confirm placement. Move the C-arminto the anteroposterior position and look for the character-istic ‘‘Christmas tree’’ pattern of epidural flow (Fig. 39-15).If a vascular pattern is seen, reposition the spinal needle andagain confirm epidural placement with nonionic contrastdye. Once the correct contrast pattern is obtained, injectslowly a 10-ml volume containing 3 ml of 1% preservative-free Xylocaine without epinephrine, 3 ml of 6 mg/mlCelestone Soluspan, and 4 ml of sterile normal saline.

ZYGAPOPHYSEAL (FACET) JOINT INJECTIONSZYGAPOPHYSEAL (FACET) JOINT INJECTIONSThe facet joint can be a source of back pain; the exact causeof the pain remains unknown. Theories include meniscoidentrapment and extrapment, synovial impingement, chondro-malacia facetae, capsular and synovial inflammation, andmechanical injury to the joint capsule. Osteoarthritis is anothercause of facet joint pain; however, the incidence of facet jointarthropathy is equal in both symptomatic and asymptomaticpatients. As with other osteoarthritic joints, roentgenographicchanges correlate poorly with pain.

Fig. 39-14 Right L5 selective nerve root injection contrastpattern.




Although the history and physical examination may suggestthat the facet joint is the cause of spine pain, no noninvasivepathognomonic findings distinguish facet joint–mediated painfrom other sources of spine pain. Fluoroscopically guided facetjoint injections therefore are commonly considered the goldstandard for isolating or excluding the facet joint as a source ofspine or extremity pain.

Clinical suspicion of facet joint pain by a spine specialistremains the major indicator for diagnostic injection, whichshould be done only in patients who have had pain for morethan 4 weeks and only after appropriate conservative measureshave failed to provide relief. Facet joint injection proceduresmay help to focus treatment on a specific spinal segment andprovide adequate pain relief to allow progression in therapy.Either intraarticular or medial branch blocks can be used fordiagnostic purposes. Although injection of cortisone into thefacet joint was a popular procedure through most of the 1970sand 1980s, many investigators have found no evidence that thiseffectively treats low back pain caused by a facet joint. Theonly controlled study on the use of intraarticular corticosteroidsin the cervical spine found no added benefit from intraarticularbetamethasone over bupivacaine.

Cervical Facet Joint◆ Medial Branch Block Injection

TECHNIQUE 39-8Place the patient prone on the pain management table.Rotate the patient’s neck so that the symptomatic side isdown. This allows the vertebral artery to be positionedfarther beneath the articular pillar, creates greater accentu-ation of the cervical waists, and prevents the jaw from beingsuperimposed. Aseptically prepare and drape the side to beinjected. Identify the target location using anteroposterior-

directed fluoroscopy. Each cervical facet joint from C3-4 toC7-T1 is supplied from the medial nerve branch above andbelow that joint which curves consistently around the‘‘waist’’ of the articular pillar of the same numberedvertebrae (Fig. 39-16). For example, to block the C6 facetjoint nerve supply, anesthetize the C6 and C7 medialbranches. Insert a 22- or 25-gauge, 31⁄2-inch spinal needleperpendicular to the pain management table and advance itunder fluoroscopic control ventrally and medially untilcontact is made with periosteum. Direct the spinal needlelaterally until the needle tip reaches the lateral margin of thewaist of the articular pillar and then direct the needle untilit rests at the deepest point of the articular pillar’s concavityunder fluoroscopy. Remove the stylet. If there is a negativeaspirate, inject 0.5 ml of 0.75% preservative Marcaine.

Lumbar Facet Joint◆ Intraarticular Injection

TECHNIQUE 39-9Place the patient prone on a pain management table.Aseptically prepare and drape the patient. Under fluoro-scopic guidance, identify the target segment to be injected.Upper lumbar facet joints are oriented in the sagittal(vertical) plane and often can be seen on direct anteropos-terior views, whereas the lower lumbar facet joints,especially at L5-S1, are obliquely oriented and require an

Fig. 39-15 Anteroposterior view of caudal epidurogram dem-onstrating characteristic contrast flow pattern.

g

C2vr

T1

C1

C7

mb

a

tonlaaj

Fig. 39-16 Proper needle placement for posterior approach toC4 and C6 medial branch blocks. Second cervical ganglion (g),third occipital nerve (ton), C2 ventral ramus (C2vr) and lateralatlantoaxial joint (laaj) are noted. (Redrawn from Boduk N: Backpain: Zygapophyseal blocks and epidural steroids. In Cousins MJ,Bridenbaugh PO, eds: Neural blockade in clinical anesthesia andmanagement of pain, ed 2, Philadelphia, 1988, JB Lippincott.)




ipsilateral oblique rotation of the C-arm to be seen. Positionthe C-arm under fluoroscopy until the joint silhouette firstappears. Insert and advance a 22- or 25-gauge, 31⁄2-inchspinal needle toward the target joint along the axis of thefluoroscopy beam until contact is made with the articularprocesses of the joint. Enter the joint cavity through thesofter capsule and advance the needle only a few milli-meters. Capsular penetration is perceived as a subtle changeof resistance. If midpoint needle entry is difficult, redirectthe spinal needle to the superior or inferior joint recesses.Confirm placement with less than 0.1 ml of nonioniccontrast dye with a 3-ml syringe to minimize injectionpressure under fluoroscopic guidance. Once intraarticularplacement has been verified, inject a total volume of 1 ml ofinjectant (local anesthetic with or without corticosteroids)into the joint.

◆ Medial Branch Block Injection

TECHNIQUE 39-10Place the patient prone on a pain management table.Aseptically prepare and drape the patient. Because there isdual innervation of each lumbar facet joint, two medialbranch blocks are required. It is important to remember thatthe medial branches cross the transverse processes belowtheir origin (Fig. 39-17). For example, the L4-5 facet jointis anesthetized by blocking the L3 medial branch at thetransverse process of L4, and the L4 medial branch at thetransverse process of L5. In the case of the L5-S1 facet joint,anesthetize the L4 medial branch as it passes over the L5transverse process and the L5 medial branch as it passesacross the sacral ala. Using anteroposterior fluoroscopicimaging, identify the target transverse process. For L1through L4 medial branch blocks, penetrate the skin using a22- or 25-gauge, 31⁄2-inch spinal needle lateral and superiorto the target location. Under fluoroscopic guidance, advancethe spinal needle until contact is made with the dorsalsuperior and medial aspects of the base of the transverseprocess so that the needle top rests against the periosteum.To ensure optimal spinal needle placement, reposition theC-arm so that the fluoroscopy beam is ipsilateral oblique andthe ‘‘Scotty dog’’ is seen. Position the spinal needle in themiddle of the ‘‘eye’’ of the ‘‘Scotty dog.’’ Slowly inject(over 30 seconds) 0.5 ml of 0.75% Marcaine.

To inject the L5 medial branch (more correctly, the L5dorsal ramus), position the patient prone on the painmanagement table with the fluoroscopic beam in theanteroposterior projection. Identify the sacral ala. Rotate theC-arm 15 to 20 degrees ipsilateral obliquely to maximizeexposure between the junction of the sacral ala and thesuperior process of S1. Insert a 22- or 25-gauge, 31⁄2-inchspinal needle directly into the osseous landmarks approxi-

mately 5 mm below the superior junction of the sacral alawith the superior articular process of the sacrum underfluoroscopy. Rest the spinal needle on the periosteum andposition the bevel of the spinal needle medial and away fromthe foramen to minimize flow through the L5 or S1 foramen.Slowly inject 0.5 ml of 0.75% Marcaine.

◆ Sacroiliac JointThe sacroiliac joint remains a controversial source of primarylow back pain despite validated scientific studies. It often isoverlooked as a source of low back pain because its anatomicallocation makes it difficult to examine in isolation and manyprovocative tests place mechanical stresses on contiguousstructures. In addition, several other structures may refer painto the sacroiliac joint.

The sacroiliac joint, like other synovial joints, moves;however, sacroiliac joint movement is involuntary and iscaused by shear, compression, and other indirect forces.Muscles involved with secondary sacroiliac joint motioninclude the erectae spinae, quadratus lumborum, psoas majorand minor, piriformis, latissimus dorsi, obliquus abdominis,and gluteal. Imbalances in any of these muscles as a result ofcentral facilitation may cause them to function in a shortenedstate that tends to inhibit their antagonists reflexively.

a

a

mb

mb

Fig. 39-17 Posterior view of lumbar spine demonstratinglocation of medial branches of dorsal rami, which innervate lumbarfacet joints (a). Needle position for L3 and L4 medial branchblocks shown on left half of diagram would be used to anesthetizethe L4-5 facet joint. Right half of diagram demonstrates L3-4,L4-5, and L5-S1 intraarticular facet joint injection positions.(Redrawn from Boduk N: Back pain: zygapophyseal blocks andepidural steroids. In Cousins MJ, Bridenbaugh PO, eds: Neuralblockade in clinical anesthesia and management of pain, ed 2,Philadelphia, 1988, JB Lippincott.)




Theoretically, dysfunctional movement patterns may result.Postural changes and body weight also can create motionthrough the sacroiliac joint.

Because of the wide range of segmental innervation (L2-S2)of the sacroiliac joint, there is a myriad of referral zonepatterns. In studies of asymptomatic subjects, the most constantreferral zone was localized to a 3 × 10 cm area just inferior tothe ipsilateral posterior superior iliac spine (Fig. 39-18);however, pain may be referred to the buttocks, groin, posteriorthigh, calf, and foot.

Sacroiliac dysfunction, also called sacroiliac joint mechan-ical pain or sacroiliac joint syndrome, is the most commonpainful condition of this joint. The true prevalence of mediatedpain from sacroiliac joint dysfunction is unknown; however,several studies indicated that it is more common than expected.Because no specific or pathognomonic historical facts orphysical examination tests accurately identify the sacroiliacjoint as a source of pain, diagnosis is one of exclusion.However, sacroiliac joint dysfunction should be considered ifan injury was caused by a direct fall on the buttocks, a rear-endmotor vehicle accident with the ipsilateral foot on the brake atthe moment of impact, a broadside motor vehicle accident witha blow to the lateral aspect of the pelvic ring, or a fall in a holewith one leg in the hole and the other extended outside. Lumbarrotation and axial loading that can occur during ballet or iceskating is another common mechanism of injury. Althoughsomewhat controversial, the risk of sacroiliac joint dysfunctionmay be increased in individuals with lumbar fusion or hippathology. Other causes include insufficiency stress fractures,fatigue stress fractures, metabolic processes, such as depositiondiseases, degenerative joint disease, infection, and inflamma-

tory conditions, such as ankylosing spondylitis, psoriaticarthritis, and Reiter’s disease. The diagnosis of sacroiliac jointpain can be confirmed if symptoms are reproduced upondistention of the joint capsule by provocative injection andsubsequently abated with an analgesic block.

TECHNIQUE 39-11Place the patient prone on a pain management table.Aseptically prepare and drape the side to be injected. Rotatethe C-arm until the medial (posterior) joint line is seen. Usea 27]-gauge needle to anesthetize the skin of the buttock 1to 3 cm inferior to the lowest aspect of the joint. Usingfluoroscopy insert a 31⁄2-inch, 22-gauge spinal needle untilthe needle rests 1 cm above the most posteroinferior aspectof the joint (Fig. 39-19). Rarely, a larger spinal needle isrequired in obese patients. Advance the spinal needle intothe sacroiliac joint until capsular penetration occurs. Con-firm intraarticular placement under fluoroscopy with 0.5 mlof nonionic contrast dye. A spot roentgenogram can be takento document placement. Inject a 2-ml volume containing1 ml of 0.75% preservative-free Marcaine and 1 ml of6 mg/ml Celestone into the joint.

DISCOGRAPHYDISCOGRAPHYDiscography has been used since the late 1940s for theexperimental and clinical evaluation of disc disease in both thecervical and lumbar regions of the spine. Since that timediscography has had a limited but important role in theevaluation of suspected disc pathology.

A B

Fig. 39-18 Pain diagram. A, Patient reported pain diagramconsistent with sacroiliac joint dysfunction. B, Patient reporteddiagram inconsistent with sacroiliac joint dysfunction. (FromFortin JD, Dwyer AP, West S, Pier J: Spine 19:1475, 1994).

Fig. 39-19 Sacroiliac joint injection showing medial (A) andlateral (B) joint planes (silhouettes). Entry into joint is achievedabove most posterior-inferior aspect of joint.




The clinical usefulness of the data obtained from discogra-phy remains controversial. In 1968 Holt published a landmarkstudy that showed a 37% false-positive rate. He concluded thatlumbar discography was an unreliable diagnostic tool. How-ever, Holt’s studies had numerous design flaws, includingsuboptimal imaging equipment, neurotoxic contrast agents,inadequate needle placement, and failure to determine if painresponses were concordant or discordant with patients’ typicalpain patterns. Using modern techniques, Walsh et al. in 1990published a well-controlled prospective study that, unlikeHolt’s study, required an abnormal nucleogram and a con-cordant pain response to indicate a positive provocativediscogram. The investigators of this study found a 0%false-positive rate for discography compared with 37%reported by Holt. These authors concluded that, with currenttechnique and standardized protocol, discography was a highlyreliable test.

In independent studies, Cloward and Smith emphasized thatreproduction of a patient’s pain was the key feature of cervicaldiscography. In 1964 Holt reported that cervical discographyhad no diagnostic value because pain reproduction andfissuring were features of cervical discs in normal volunteers.Later investigative work by Simmons and Segil demonstratedthe importance of discriminating between painful and nonpain-ful discs, while avoiding pain reproduction and disc morphol-ogy as absolute entities. Carrying this idea further, Roth in 1976introduced analgesic cervical discography with the rationalethat once a painful disc is identified, pain relief should occur byinjecting a local anesthetic into the disc. He reported a highsuccess rate for anterior disc excision and fusion using thisform of precision diagnostic testing.

The most important aspect of discography is provocativetesting for concordant pain (that which corresponds to apatient’s usual pain) to provide information regarding theclinical significance of the disc abnormality. Although difficultto standardize, this distinguishes discography from otheranatomical imaging techniques. If the patient is unable todistinguish customary pain from any other pain, the procedureis of no value. In patients who have a concordant responsewithout evidence of a radial annular fissure on discography, CTshould be considered because some discs that appear normal ondiscography show disruption on CT scan.

Indications for lumbar discography include surgical plan-ning of spinal fusion, testing of the structural integrity of anadjacent disc to a known abnormality such as spondylolisthesisor fusion, identifying a painful disc among multiple degener-ative discs, ruling out secondary internal disc disruption orsuspected lateral or recurrent disc herniation, and determiningthe primary symptom-producing level when chemonucleolysisis being considered. Thoracic discography is a useful tool in theinvestigation of thoracic, chest, and upper abdominal pain.Degenerative thoracic disc disease, with or without herniation,has a highly variable clinical presentation, frequently mimick-ing visceral conditions, as well as causing back or musculo-skeletal pain. In the cervical spine, discography is an importantadjunct for diagnosing primary discogenic pain and determin-

ing which disc is affected and will require surgery. Discographyalso may be justified in medicolegal situations to establish adefinitive diagnosis even though treatment may not be plannedon that disc.

Compression of the spinal cord, stenosis of the roots,bleeding disorders, allergy to the injectable material, and activeinfection are contraindications to diagnostic discographyprocedures. Although the risk of complications from discogra-phy is low, potential problems include discitis, nerve rootinjury, subarachnoid puncture, chemical meningitis, bleeding,and allergic reactions. In addition, in the cervical region,retropharyngeal and epidural abscess can occur. Pneumothoraxis a risk in both the cervical and thoracic regions.

◆ Lumbar DiscographyLumbar discography originally was done using a transduraltechnique in a manner similar to myelography with a lumbarpuncture. The difference between lumbar myelography anddiscography was that the needle used for the latter wasadvanced through the thecal sac. The technique later wasmodified, consisting of an extradural, extralaminar approachthat avoided the thecal sac, and it was refined further to enableentry into the L5-S1 disc using a two-needle technique tomaneuver around the iliac crest.

A patient’s response during the procedure is the mostimportant aspect of the study. Pain alone does not determine ifa disc is the cause of the back pain. The concordance of the painin regard to the quality and location are paramount indetermining whether the disc is a true pain generator. A controldisc is necessary to validate a positive finding on discography.

TECHNIQUE 39-12 (Falco)

Place the patient on a procedure or fluoroscopic table. Insertan angiocatheter into the upper extremity and infuseintravenous antibiotics to prevent discitis. Some physiciansprefer to give antibiotics intradiscally during the procedurein lieu of the intravenous route. Place the patient in amodified lateral decubitus position with the symptomaticside down to avoid having the patient confuse the paincaused by the needle with the actual pain on that same side.This position also allows for easier fluoroscopic imaging ofthe intervertebral discs and mobilizes the bowel away fromthe needle path. Lightly sedate the patient with an intra-venous opioid and short-acting benzodiazepine. Prepare anddrape the skin sterilely, including the lumbosacral region.

Under fluoroscopic control, identify the intervertebraldiscs. Adjust the patient’s position or the C-arm so that thelumbar spine is in an oblique position with the superiorarticular process, dividing the intervertebral space in half(Fig. 39-20). Anesthetize the skin overlying the superiorarticular process with 1 to 2 ml of 1% lidocaine if necessary.Advance a single 6-inch spinal needle (or longer, dependingon the patient’s size) through the skin and deeper soft tissuesto the outer annulus of the disc. The disc entry point is just


continuedCopyright 2003. Elsevier Science (USA). All Rights Reserved.


anterior to the base of the superior articular process and justabove the superior endplate of the vertebral body, whichallows the needle to safely pass by the exiting nerve root(Fig. 39-21). Advance the needle into the central third of thedisc, using anteroposterior and lateral fluoroscopic imaging.Confirm the position of the needle tip within the central thirdof the disc with anteroposterior and lateral fluoroscopicimaging. Inject either saline or nonionic contrast dye intoeach disc. Record any pain that the patient experiencesduring the injection as none, dissimilar, similar, or exact inrelationship to the patient’s typical low back pain. Recordintradiscal pressures to assist in determining if the disc is thecause of the pain. Obtain roentgenograms of the lumbarspine upon completion of the study, paying particularattention to the contrast-enhanced disc. Obtain a CT scan ifnecessary to assess disc anatomy further.

An alternative method is a two-needle technique inwhich a 6- or 8-inch spinal needle is passed through ashorter introducer needle (typically 31⁄2 inches in length)into the disc in the same manner as a single needle. Thisapproach may reduce the incidence of infection by allowingthe procedure needle to pass into the disc space without everpenetrating the skin. The introducer needle also may assistin more accurate needle placement, reducing the risk ofinjuring the exiting nerve root. The two-needle approachmay require more time than the single-needle technique, andthe larger introducer needle could cause more pain to thepatient.

The two-needle technique often is used to enter theL5-S1 disc space with one modification. The procedureneedle typically is curved (Fig. 39-22). To bypass the iliaccrest, the introducer needle is advanced at an angle that

places the needle tip in a position that does not line up withthe L5-S1 disc space, which makes it difficult if notimpossible for a straight procedure needle to advance intothe L5-S1 disc. A curved procedure needle, on the otherhand, allows the needle tip to align with the L5-S1 disc asit is advanced towards and into the disc adjusting formalalignment.

◆ Thoracic DiscographyThoracic discography has been refined to provide a techniquethat is reproducible and safe. A posterolateral extralaminar

Fig. 39-21 Disc entry point is just anterior (arrow) to base ofsuperior articular process (s) and just above superior endplate ofvertebral body. (Courtesy Frank JE Falco, MD)

Fig. 39-22 Curved procedure needle (c) passing through straightintroducer needle (n). (Courtesy Frank JE Falco, MD)

Fig. 39-20 Lumbar spine in an oblique position with superiorarticular process (arrow) dividing disc space (d) in half. (CourtesyFrank JE Falco, MD)




approach similar to lumbar discography is used with asingle-needle technique. The significant difference betweenthoracic and lumbar discography is the potential for complica-tions because of the surrounding anatomy of the thoracic spine.In contrast to lumbar discography, which typically is performedin the mid to lower lumbar spine below the spinal cord andlungs, thoracic discography has the inherent risk of pneumo-thorax and direct spinal cord trauma; other complicationsinclude discitis and bleeding.

Essentially the same protocol is used for thoracic discogra-phy as for lumbar discography.


Place the patient in a modified lateral decubitus position onthe procedure table with the symptomatic side down. Beginantibiotics through the intravenous catheter. Alternatively,intradiscal antibiotics may be given during the procedure.Lightly sedate the patient and prepare and drape the skin ina sterile manner.

Using fluoroscopic imaging, identify the intervertebralthoracic discs. Move the patient or adjust the C-armobliquely to position the superior articular process so that itdivides the intervertebral space in half (Fig. 39-23). At thispoint, the intervertebral discs and endplates, subjacentsuperior articular process, and adjacent rib head should be inclear view. The endplates, the superior articular process, andthe rib head form a ‘‘box’’ (Fig. 39-24) that delineates a safepathway into the disc, avoiding the spinal cord and lung.Keep the needle tip within the confines of this ‘‘box’’ whileadvancing it into the annulus.

After proper positioning and exposure, anesthetize theskin overlying the superior articular process with 1 to 2 ml

of 1% lidocaine if necessary. Advance a single 6-inch spinalneedle (a shorter or longer needle can be used, depending onthe patient’s size) through the skin and the deeper soft tissuesinto the outer annulus within the ‘‘box’’ just anterior to thebase of the superior articular process and just above thesuperior endplate. Continue into the central third of the disc,using anteroposterior and lateral fluoroscopic guidance.

Inject either saline or a nonionic contrast dye into eachdisc in the same manner as for lumbar discography. Recordany pain response and analyze for reproduction of con-cordant pain using the same protocol as for lumbardiscography. Obtain roentgenograms and CT imaging of thethoracic spine upon completion of the study.

◆ Cervical DiscographyThe approach to the cervical spine is distinctly different fromthe approaches used for discography of the lumbar and thoracicspine. The cervical spine is approached anteriorly rather thanposteriorly. Complications associated with cervical discogra-phy because of the surrounding anatomy include injury to thetrachea, esophagus, carotid artery, and jugular veins, as well asspinal cord injury and pneumothorax. As with lumbar andthoracic discography, discitis also is a concern in the cervicalspine, although the disc infection often originates from thegram-negative and anaerobic flora of the esophagus as opposedto the gram-positive skin flora seen in lumbar discography.

Traditionally, the approach to the cervical intervertebraldiscs has been via a paralaryngeal route that requires displace-ment of the trachea and esophagus away from the site of entry.A more lateral approach that is gaining popularity bypassesthese structures and does not require such displacement.

Fig. 39-23 Oblique position with superior articular process(arrow) dividing thoracic intervertebral space in half. p, Pedicle.r, rib head. (Courtesy Frank JE Falco, MD)

Fig. 39-24 Thoracic endplates (e), superior articular process (s),and rib head (r) form ‘‘box.’’ (Courtesy Frank JE Falco, MD)




The same protocol for lumbar and thoracic discography isused in cervical discography.


Place the patient supine on the procedure table. Insert anangiocatheter into the upper extremity and begin intrave-nous antibiotic infusion. Alternatively, intradiscal antibioticscan be given during surgery. Sedate the patient and prepareand drape the skin sterilely, including the anterolateralaspect of the neck.

Under fluoroscopic imaging, identify the intervertebraldiscs with aligned endplates and sharp margins of theintervertebral discs. Approach the paralaryngeal area fromthe right, using a finger to displace the esophagus andtrachea to the left and the carotid artery to the right side.With the other hand, insert a 2- or 31⁄2-inch spinal needleover the finger through the skin and into the outer annulusof the disc. Advance the needle into the center of the disc,using anteroposterior and lateral fluoroscopic guidance.

An alternative method is a more lateral approach to thecervical spine using a single needle. This approach mayreduce the incidence of infection by passing the needleposterior to the trachea and esophagus en route to the discspace. Position the patient or the C-arm to place the cervicalspine in an oblique position for optimal foraminal exposureand continue adjusting until the endplates, disc space, anduncovertebral process are in sharp focus (Fig. 39-25). Inserta 2- or 31⁄2-inch needle into the skin and advance it until thetip makes contact with the subjacent uncovertebral process.‘‘Walk off’’ the needle just anterior to the uncovertebralprocess. Advance the needle into the center of the disc, usinganteroposterior and lateral fluoroscopic guidance.

After needle placement with either technique, the rest ofthe procedure is essentially the same as that described forthoracic or lumbar discography. Inject either saline or anonionic contrast dye into each disc. Record any painresponse and analyze for concordance using the sameprotocol employed for lumbar and thoracic discography.Obtain roentgenograms and CT imaging of the cervicalspine upon completion of the study.

Psychological TestingPsychological TestingAs discussed previously in this section, pain in some patients isthe result of nonanatomical causes. Many, but not all, patientsreport the onset of their symptoms after a work-related incident,which may have been relatively minor. Some patients presentacutely, and for these patients treatment as outlined fornonspecific back pain should be followed. It is known thatpatients who do not return to work in 6 months are at increasedrisk for long-term disability. Patients with acute injuries or withhistory of chronic pain require closer evaluation. Increasingevidence suggests that the preeminence of psychosocial factorsover physical variables is responsible for prolonged disability.

Over the past several decades extensive studies have beendone on various evaluation tools for patients with ‘‘abnormalillness behavior.’’ Waddell et al. defined this as ‘‘maladaptiveovert illness-related behavior which is out of proportion to theunderlying physical disease and more readily attributable toassociated cognitive and affective disturbances.’’ Waddell et al.also developed clinical tools designed to detect the presence of‘‘abnormal illness behavior’’ by identifying physical signs orsymptoms and descriptions that are nonorganic in nature. Fivenonorganic signs and seven nonorganic symptom descriptions(Table 39-4) have been identified. Waddell initially describedthese for use in patients with chronic pain and suggested thatthe presence of three signs was required to determine‘‘abnormal illness behavior.’’ Several studies evaluated theability of these signs and symptom descriptions to predictreturn to work but have proved inconclusive; nevertheless, theyappear to be useful in detecting patients at increased risk forpoor outcome with surgical intervention.

The Minnesota Multiphasic Personality Inventory (MMPI)has been used for psychological assessment in many previousstudies and has been demonstrated to be a reasonable predictorof surgical and conservative treatment results regardless of thespinal pathological condition. Unfortunately, the MMPI islengthy and difficult to administer in an orthopaedic clinicalsetting and probably is best given by a psychiatrist orpsychologist. By comparison, the Distress and Risk AssessmentMethod (DRAM) is relatively easily administered and scoredand has been validated in clinical settings with regard topatients with back pain. The DRAM consists of the ModifiedSomatic Perception Questionnaire (MSPQ) and the ZungDepression Index (ZDI). With this simplified method, patients

Fig. 39-25 Foraminal position for performing cervical discog-raphy with anterolateral approach. f, Foramen; v, vertebral body;d, intervertebral disc. (Courtesy Frank JE Falco, MD)




identified as psychologically distressed are three to four timesmore likely to have a poor outcome after any form of treatment.It is our recommendation that some type of formal psycholog-ical evaluation be used preoperatively in patients who havechronic pain but no clear cause of their symptoms; whether theMMPI or the DRAM is used is less important.

The experience at this clinic has been primarily with theMMPI, which we routinely use for assessment of patients whohave symptoms seemingly out of proportion to their anatomicalabnormalities and are being evaluated for surgical treatment,especially spinal fusion. The MMPI is one of the most reliable

and well-documented tests used for this purpose. This test ispredictive of preinjury susceptibility to back injury and thepotential for failure of conservative and surgical treatment.Wiltse and Rocchio demonstrated that elevations of the hysteria(Hs) and hypochondriasis (Hy) T scores above 75 are indicativeof a poor postoperative response (16% good results). Theirstudy evaluated patients treated with chymopapain, and theirclinical results are illustrated in Tables 39-5 and 39-6.

Table 39-5 indicates the rate of good or excellent resultsusing the MMPI test Hs and Hy scores alone in the study byWiltse and Rocchio. Table 39-6 illustrates the lack of statisticalsignificance between the MMPI scores and the presence of thefollowing objective findings: reflex changes, motor weakness,sensory deficits, positive myelogram, positive electromyogram,and elevated CSF protein.

Similar studies of surgically and conservatively treatedpatients have had similar findings. Written reports are helpful,but the raw T score read on the far right or left side of thestandard test result sheet is the simplest guide to postoperativeoutcome. If surgery is necessary in a patient with an elevatedHs or Hy score, then psychiatric or psychological assistancebefore and after the procedure can be helpful, but a poor resultshould be anticipated. Gentry observed a group of patients withobjective evidence of psychological disturbance as indicated bythe MMPI. Those patients who had surgery were less likely toreturn to work, less likely to have a reduction in their pain, andmore likely to have greater disability than similar patientswho did not have surgery. Wiltse and Rocchio recommendedrestraint and conservative treatment in these patients. Elevationof the Hs and Hy scores on the MMPI should be a relativecontraindication to elective spinal surgery.

Additional material on this test can be found in the excellentarticles by Dennis et al., Wiltse and Rocchio, and Southwickand White. Numerous other tests are available, but none hasbeen shown to be as predictive of surgical outcome as the Hsand Hy scores on the MMPI. Riley et al. investigated a MMPI-2and found that the results replicated those of the older MMPI.

Table 39-5 Result Expectancy Relatedto Hs and Hy T Scores on theMMPI Test

Hs and Hy T

Scores

Number

of Patients

Chances of Good

or Excellent

Functional

Recovery (%)

85 and above 10 1075 to 84 32 1665 to 74 31 3955 to 64 36 7254 and below 21 90Prediction from

base rate63 48

From Wiltse LL, Rocchio PD: J Bone Joint Surg 57A:478, 1975.

Table 39-4 Signs and Symptoms forDiagnosis of ‘‘Abnormal IllnessBehavior’’

Nonorganic Signs Organic Signs

Regional disturbances A widespread region of sensorychanges or weakness that isdivergent from acceptedneuroanatomy

Superficial/nonanatomicaltenderness

Tenderness of the skin to lighttouch (superficial) or deep ten-derness felt over a widespreadarea not localized to one struc-ture (nonanatomical)

SimulationAxial loading Low back pain reported with

pressure on the patient’s headwhile standing

Rotation Low back pain reported when theshoulders and pelvis are rotatedin the same plane as the patientstands

DistractionStraight leg raising Inconsistent limitation of straight

leg raising in supine and seatedpositions

Overreaction Disproportionate verbalization,facial expression, muscle ten-sion, collapsing, sweating, andso forth during examination

Nonorganic Symptom Descriptors

1. Do you get pain in your tailbone?2. Do you have numbness in your entire leg (front, side, and

back of leg at the same time?)3. Do you have pain in your entire leg (front, side, and back

of the leg at the same time?)4. Does your whole leg ever give way?5. Have you had any time during this episode when you have

had very little back pain?6. Have you had to go to the emergency room because of

back pain?7. Has all treatment for your back made your pain worse?

From Fritz JM, Wainner RS, Hicks GE: Spine 25:1925, 2000.




Patients with MMPI and MMPI-2 findings of depressed-pathological profile and a conversion V profile reported greaterdissatisfaction with surgical outcome.

Similar outcomes have been noted for nonoperativetreatment of these patients. Gatchel et al. noted similarproblems in patients with acute back pain who were questioned6 months later.

The main problem with the MMPI is that it requires theability to read and comprehend the material. Pincus et al. alsonoted that the MMPI questions may be in line with naturaldisease processes such as rheumatoid arthritis. Patients withchronic diseases may, by the nature of their disease symptoms,have MMPI elevations. Chronic back pain without a specificdisease association should not be considered as similar tochronic disease such as rheumatoid arthritis. Chapman andPemberton noted that the MMPI failed to predict the subjectiveoutcome as reported by patients with chronic back pain whowere in an interdisciplinary pain-management program.

A simple test that is a good screening aid is the paindrawing. The pain drawing correlates well with the Hs and Hyscores. This test also requires some ability to follow simpledirections (Fig. 39-26). Additional information can be found inthe articles by Rainsford, Cairns, and Mooney and by Denniset al. Uden and Landin found that the pain drawing correlatedwell with clinical results. Ohnmeiss reported that the paindrawing remained consistent over 8 months in patients whoreported no change in their symptoms. Also, the intraevaluatorrepeatability was found to be high in this as in other studies.Patients with low Rainsford scores were most likely to havedefinite pathological conditions and those with high Rainsfordscores were least likely to have a demonstrable pathologicalcondition. Cummings and Routan warned that the pain drawingshould not be used to identify areas of somatic disturbance inchronic pain patients.

Cervical Disc Disease

Cervical Disc DiseaseHerniation of the cervical intervertebral disc with spinal cordcompression has been identified since Key detailed thepathological findings of two cases of cord compression by‘‘intervertebral substance’’ in 1838. During the late 1800s andearly 1900s there were many reports of chondromas of thecervical spine. Stookey described the clinical findings and

anatomical location of cervical disc herniation in 1928 butattributed the lesion to a cervical chondroma. Mixter and Barrreported lumbar disc herniation in 1934 and included fourcervical disc protrusions.

The classic approach to discs in this region has beenposteriorly with laminectomy. This approach had been used asa standard exposure for extradural tumors. In 1943 Semmes andMurphey reported four patients in whom cervical disc rupturesimulated coronary disease and introduced the concept thatcervical disc disease usually manifested itself in root symptomsand not cord compression symptoms. Bailey and Badgley,Cloward, and Smith and Robinson in the 1950s popularized theanterior approach coupled with interbody fusion. Robertson in1973, after the initial report by Hirsch in 1960, reported anteriorcervical discectomy without fusion. He showed that simpleanterior disc excision without fusion can give results similar toanterior cervical disc excision with anterior interbody fusion.More recently, Yamamoto et al. reported the long-term (2 to 13year) results of anterior cervical disc excision without fusion.They noted 81% improvement in patients with soft disc herniasbut only 47% improvement in patients with spondylosis; 49%had neck and scapular pain as new postoperative symptoms forthe first 4 weeks after surgery (Table 39-7). Spontaneous fusionwas noted in 79% at 29 months. Currently, anterior cervicaldiscectomy with fusion is the procedure of choice when the discis removed anteriorly to avoid disc space collapse, preventpainful and abnormal cervical motion, and to speed interver-tebral fusion. Foraminotomy is the procedure of choice whenthe disc fragment is removed posteriorly.

In an epidemiological study of acute cervical disc prolapse,Kelsey et al. indicated that cervical disc rupture was morecommon in men by a ratio of 1.4 to 1. Factors associated withthe injury were frequent heavy lifting on the job, cigarettesmoking, and frequent diving from a board. The use ofvibrating equipment and time spent in motor vehicles were notpositively associated with this problem. Participation in sportsother than diving, frequent wearing of shoes with high heels,frequent twisting of the neck on the job, time spent sitting onthe job, and smoking of cigars and pipes were not associatedwith cervical intervertebral disc collapse. Horal reported that40% of the population in Sweden were sometimes affected byneck pain during their lives. Patients with cervical disc diseaseare also likely to have lumbar disc disease. MRI studies haveshown increasing cervical disc degeneration with age.

Table 39-6 Hs and Hy T Scores of Patients with Good or Excellent Results Versus Numberof Preexisting Objective Deficits

Percentage with the No. of Preinjection Objective

Deficits Indicated*

Hs and Hy T scores Number of Patients

Percentage Good

or Excellent Results 1� 2� 3� 4� 5�

75 and over 42 25 95.0 57.5 30.0 7.5 2.5

64 and below 57 87 95.2 64.4 32.6 8.7 2.2

From Wiltse LL, Rocchio PD: J Bone Joint Surg 57A:478, 1975.*X2 <0.001.




The pathophysiology of cervical disc disease is the same asdegenerative disc disease in other areas of the spine. Discswelling is followed by progressive annular degeneration.Frank extrusion of nuclear material can occur as a complicationof this normal degenerative process. Kramer postulated thathydraulic pressure on the disc rather than excessive motionproduces traumatic disc herniation. As the disc degeneration

proceeds, hypermobility of the segment can result in instabilityor degenerative arthritic changes or both. Unlike in the lumbarspine, these hypertrophic changes are predominantly at theuncovertebral joint (uncinate process) (Fig. 39-27). Hypertro-phic changes eventually develop about the facet joints andvertebral bodies. As in lumbar disease, progressive stiffening ofthe cervical spine and loss of motion are the usual result inthe end stages. Hypertrophic spurring anteriorly occasionallyresults in dysphagia. Kang et al. identified the production ofincreased amounts of matrix metalloproteinases, nitric oxide,prostaglandin E2, and interleukin-6 in disc material removedfrom cervical disc hernias. They suggested that these productsare involved in the biochemistry of disc degeneration. Thesesubstances also are implicated in pain production. Thesefindings are similar to those in the lumbar spine. Kauppila andPenttila reported the presence of degenerative changes in thecommon arteries that supply the cervicobrachial area, and theysuggested that impaired blood flow may play a part incervicobrachial disorders.

A

Fig. 39-26 A, Pain drawing and corre-sponding MMPI raw score sheet of patientwith ‘‘conversion V’’ who was unrelievedof pain after disc surgery. B, Pain drawingand corresponding MMPI raw score sheetof patient with normal findings who wasrelieved of pain after disc surgery.

B

Table 39-7 Postoperative Neckor Scapular Pain

Follow-up

Period

Soft

Disc Percentage

Spondy-

losis Percentage

1 month 4/11 36 8/34 531 year 1/11 9 10/29 342 years 0/10 0 6/24 254 years 0/5 0 4/21 19

From Yamamoto I, Ikeda A, Shibuya N, et al: Spine 16:272, 1991.




SIGNS AND SYMPTOMSSIGNS AND SYMPTOMSThe signs and symptoms of intervertebral disc disease are bestseparated into symptoms related to the spine itself, symptomsrelated to nerve root compression, and symptoms of myelopa-thy. Several authors reported that, when the disc is puncturedanteriorly for the purpose of discography, pain is noted in theneck and shoulder. Complaints of neck pain, medial scapularpain, and shoulder pain are therefore probably related toprimary pain about the disc and spine. Anatomical studies haveindicated cervical disc and ligamentous innervations. This hasbeen inferred to be similar in the cervical spine to that of thelumbar spine with its sinu-vertebral nerve. Tamura notedcranial symptoms such as headache, vertigo, tinnitus, andocular problems associated with C3-4 root sleeve defects onmyelography. Dwyer, Aprill, and Bogduk completed a two-stage investigation of the facet joints of the cervical spine aspossible sources of pain. By injecting contrast medium intothe facet joints of normal volunteers under roentgenographic

control to the point of pain production, a topographical mapwas produced. Although the number of volunteers was small,the findings were consistent (Fig. 39-28). The second stage ofthe study included a small number of patients who hadtherapeutic injections based on the location of their pain, as itrelated to the previously constructed pain map. Pain reliefoccurred immediately and completely in 9 of 10 patients whohad had prior evaluation and failed other treatments. These painpatterns are not predicted by accepted dermatomal maps.

Symptoms of root compression usually are associated withpain radiating into the arm or chest with numbness in thefingers and motor weakness. Cervical disc disease also canmimic cardiac disease with chest and arm pain. Usually theradicular symptoms are intermittent and combined with themore frequent neck and shoulder pain.

The signs of midline cervical spinal cord compression(myelopathy) are unique and varied. The pain is poorlylocalized and aching in nature; pain may be only a minorcomplaint. Occasional sharp pain or generalized tingling maybe described with neck extension. This is not unlike theLhermitte sign in multiple sclerosis. The pain can be in both theshoulder and pelvic girdles; it is occasionally associated with ageneralized feeling of weakness in the lower extremities and afeeling of instability.

In patients with predominant cervical spondylosis, symp-toms of vertebral artery compression also may be found. Thesesymptoms consist of dizziness, tinnitus, intermittent blurring ofvision, and occasional episodes of retroocular pain.

The signs of lateral root pressure from a disc or osteophytesare predominantly neurological (Boxes 39-2 to 39-6). Byevaluating multiple motor groups, multiple levels of deep

A

Fig. 39-27 A, Comparison of points at which nerve roots emergefrom cervical and lumbar spine. B, Cross-sectional view of cervicalspine at level of disc (D). Uncinate process (U) forms ventral wallof foramen. Root (N) exits dorsal to vertebral artery (A). (A fromKikuchi S, Macnab I, Moreau P: J Bone Joint Surg 63B:272,1981.)

B

C6-7

C4-5

C2-3

C3-4

C5-6

Fig. 39-28 Composite map of the results in all volunteersdepicting characteristic distribution of pain from facet joints atsegments C2-3 to C6-7. (Redrawn from Dwyer A, Aprill C,Bogduk N: Spine 15:456, 1990.)




tendon reflexes, and sensory abnormalities, the level of thelesion can be localized as accurately as any other lesion in thenervous system. The multiple innervation of muscles cansometimes lead to confusion in determining the exact rootinvolved. For this reason, myelography or other studies donefor roentgenographic confirmation of the clinical impressionusually are helpful.

Rupture of the C4-5 disc with compression of the C5 nerveroot should result in weakness in the deltoid and bicepsmuscles. The deltoid is almost entirely innervated by C5, butthe biceps has dual innervation. The biceps reflex may be

diminished with injury to this nerve root, although it also has aC6 component, and this must be considered. Sensory testingshould show a patch on the lateral aspect of the proximal armto be diminished (Fig. 39-29).

Rupture of the C5-6 disc with compression of the C6 rootcan be confused with other root levels because of dualinnervation of structures. Weakness may be noted in the bicepsand extensor carpi radialis longus and brevis. As mentionedabove, the biceps is dually innervated by C5 and C6, whereasthe long extensors are dually innervated by C6 and C7. Thebrachioradialis and biceps reflexes also may be diminished atthis level. Sensory testing usually indicates a decreasedsensibility over the lateral proximal forearm, thumb, and indexfinger.

Rupture of the C6-7 disc with compression of the C7 rootfrequently results in weakness of the triceps. Weakness of thewrist flexors, especially the flexor carpi radialis, also is moreindicative of C7 root problems. Extensor digitorum communisweakness also can indicate C7 root involvement and may bemore readily apparent because of the normal relative weaknessof this muscle compared to the triceps. Weakness of the flexorcarpi ulnaris usually is caused more by C8 lesions. Asmentioned above, finger extensors also may be weakened inthat they have both C7 and C8 innervation. The triceps reflexmay be diminished. Sensation is lost in the middle finger. C7sensibility is variable because it is so narrow and overlap isprominent. Strong sensibility change can be difficult todocument.

BOX 39-2 • C5 Nerve Root Compression*

Sensory DeficitUpper lateral arm and elbow

Motor WeaknessDeltoidBiceps (variable)

Reflex ChangeBiceps (variable)

*Indicative of C4-5 disc rupture or other pathological condition at thatlevel.


Sensory DeficitLateral forearm, thumb, and index finger

Motor WeaknessBicepsExtensor carpi radialis longus and brevis

Reflex ChangeBicepsBrachioradialis

*Indicative of C5-6 disc herniation or other local pathological conditionat that level.


Sensory DeficitMiddle finger (variable because of overlap)

Motor WeaknessTricepsWrist flexors (flexor carpi radialis)Finger flexors (variable)

Reflex ChangeTriceps

*Indicative of C6-7 disc rupture or other pathological condition at thatlevel.


Sensory DeficitRing finger, little finger, and ulnar border of palm

Motor WeaknessInterosseiFinger flexors (variable)Flexor carpi ulnaris (variable)

Reflex ChangeNone

*Indicative of C7-T1 disc rupture or other pathological condition at thatlevel.

BOX 39-6 • T1 Nerve Root Compression*

Sensory DeficitMedial aspect of elbow

Motor WeaknessInterossei

Reflex ChangeNone

*Indicative of T1-2 disc rupture or other pathological condition at thatlevel.




Rupture between C7 and T1 with compression of the C8nerve root results in no reflex changes. Weakness may be notedin the finger flexors and in the interossei of the hand. Sensibilityis lost on the ulnar border of the palm, including the ring andlittle fingers. Compression of T1 produces weakness of theinterosseus muscles, decreased sensibility about the medialaspect of the elbow, and no reflex changes.

The clinical series of Odom, Finney, and Woodhall notedconsiderable variability in the level of compression and theneurological findings. Change in the triceps reflex was thepredominant reflex change with compression of the sixthcervical root (56%). It also was the predominant reflex changein seventh root compression (64%). Similarly the index fingerwas the predominant digit with sensory change, with evidenceof hypalgesia in both sixth (68%) and seventh (70%) cervicalroot compression.

Care should be taken in the examination of the extremitywhen radicular problems are encountered to rule out moredistal compression syndromes in the upper extremities such asthoracic outlet syndrome, carpal tunnel syndrome, and cubitaltunnel syndrome. The lower extremities should be examinedwith special attention to long tract signs indicative ofmyelopathy.

No tests for the upper extremity correspond with straightleg raising tests in the lower extremity. Davidson, Dunn, and

Metzmaker described the shoulder abduction relief sign. Thiscan be helpful in the diagnosis of cervical root compressionsyndromes. The test consists of shoulder abduction and elbowflexion with placement of the hand on the top of the head. Thisshould relieve the arm pain caused by radicular compression. Itis interesting to note that if this position is allowed to persist fora minute or two and pain is increased, then more distalcompressive neuropathies such as a tardy ulnar nerve syndrome(cubital tunnel syndrome) or primary shoulder pathologicalconditions often are the cause. Viikari-Juntura, Porras, andLaasonen noted that the shoulder abduction, axial compression,and manual axial traction tests are related to disc disease, butthe sensitivity of these tests is low.

Cervical paraspinal spasm and limitation of neck motion arefrequent findings of cervical spine disease but are not indicativeof a specific pathological process. Special maneuvers involvingneck motion can be helpful in the selection of conservativetreatment and identification of pathological processes. Thedistraction test, which involves the examiner placing his handson the occiput and jaw and distracting the cervical spine in theneutral position, can relieve root compression pain but also canincrease pain caused by ligamentous injury. Neck extension andflexion with or without traction can be helpful in selectingconservative therapies.

Patients relieved of pain with the neck extended, with or

Fig. 39-29 C5 neurologicallevel. (After Hoppenfeld S:Physical examination of thespine and extremities, Norwalk,Conn, 1976, Appleton-Century-Crofts.)




without traction, usually have hyperextension syndromes withligamentous injury posteriorly, whereas patients relieved ofpain with distraction and neck flexion are more likely to havenerve root compression caused by either a soft ruptured disc ormost likely hypertrophic spurs in the neural foramina. Painusually is increased in any condition with compression. Onemust be careful before applying compression or distraction tobe sure no cervical instability or fracture is present. One mustalso be careful in interpreting the distraction test to be certainthe temporomandibular joint is not diseased or injured becausedistraction also will increase the pain in this area.

The signs of midline disc herniation are those of spinal cordcompression. If the lesion is high in the cervical region,paresthesias, weakness, atrophy, and occasionally fascicula-tions may occur in the hands. Also present may be a Hoffman’ssign (upper cervical spinal cord) or the inverted radial reflex(typically indicating C5-6 pathology). Most commonly, how-ever, the first and most prominent symptoms are those ofinvolvement of the corticospinal tract; less commonly theposterior columns are affected. The primary signs are sustainedclonus, hyperactive reflexes, and the Babinski reflex. Lesserfindings are varying degrees of spasticity, weakness in the legs,and impairment of proprioception. Equilibrium may be grosslydisturbed, but sense of pain and temperature sense rarely arelost and usually are of little localizing value.

DIFFERENTIAL DIAGNOSISDIFFERENTIAL DIAGNOSISThe differential diagnosis of cervical disc disease is bestseparated into extrinsic and intrinsic factors. Extrinsic factorsgenerally include disease processes extrinsic to the neckresulting in symptoms similar to primary neck problems.Included in this group are tumors of the chest, nervecompression syndromes distal to the neck, degenerativeprocesses such as shoulder and upper extremity arthritis,temporomandibular joint syndrome, and lesions about theshoulder such as acute and chronic rotator cuff tears andimpingement syndromes. Intrinsic problems primarily consistof lesions directly associated with the cervical spine, the mostcommon being cervical disc degeneration with a concomitantcomplication of disc herniation and later development ofhypertrophic arthritis. Congenital factors such as spinalstenosis in the cervical region also may produce symptoms.Primary and secondary tumors of the cervical spine andfractures of the cervical vertebrae also should be considered asintrinsic lesions.

Cervical disc disease has been categorized by Odom et al.into four groups: (1) unilateral soft disc protrusion with nerveroot compression, (2) foraminal spur, or hard disc, with nerveroot compression, (3) medial soft disc protrusion with spinalcord compression, and (4) transverse ridge or cervicalspondylosis with spinal cord compression. Soft disc herniationsusually affect one level, whereas hard disc herniations canaffect multiple levels. Central lesions usually result in cordcompression symptoms, and lateral lesions usually result inradicular symptoms.

Odom et al. reported that most of the soft disc herniations intheir series occurred at the sixth cervical interspace (70%) andfifth cervical interspace (24%). Only six occurred at the seventhinterspace. Foraminal spurs also were found predominantly atthe sixth interspace (48%). The fifth interspace (39%) andseventh interspace (13%) accounted for the remaining levelswhere foraminal spurs were found. They also noted theincidence of medial soft disc protrusion with myelopathy to berare (14 of 246 patients).

Disc material sometimes is extruded into the midline of thespinal canal anteriorly, with compression of the spinal cord andwithout nerve root involvement. Occasionally this is causedby a violent injury to the cervical spine, with or withoutfracture-dislocation, and at times it is associated with imme-diate quadriplegia. However, in some instances the symptomsare progressive and may be suggestive of spinal cord tumor ordegenerative diseases of the spinal cord, such as amyotrophiclateral sclerosis, posterolateral sclerosis, and multiple sclerosis.In most of these ailments no block of the spinal canal has beenreported, and for many years the mechanism causing thecervical cord compression was not understood. However, in therare patients whom we have observed, spinal fluid block couldbe produced by hyperextending the neck, although with theneck in the neutral or flexed position the canal was completelyopen. This finding has been previously reported. It has sincebeen observed that during operation on such patients when theneck is hyperextended, the superior edge of the laminacompresses the cord against the herniated disc, and it istherefore probable that repeated hyperextension of the neckover a period of weeks, months, or years gradually damages thespinal cord.

In view of the disturbances of the spinal fluid dynamics justmentioned, jugular compression should be carried out duringlumbar puncture with the neck in the flexed, neutral, andhyperextended positions. Roentgenographically there is moreoften than not little or no alteration in the cervical curve. MRIusually demonstrates the abnormality without the need formyelography.

CONFIRMATORY TESTINGCONFIRMATORY TESTINGRoentgenographic evaluation of the cervical spine frequentlyshows loss of normal cervical lordosis. Disc space narrowingand hypertrophic changes frequent increase with age but are notindicative of cervical disc rupture. Usually roentgenogramsare most helpful to rule out other problems. Oblique roent-genograms of the cervical spine may reveal foraminalencroachment.

MRI of the cervical spine has rapidly become the majordiagnostic procedure for neck, arm, and shoulder symptoms.Maruyama evaluated the cervical discs in 36 cadavers usingMRI and anatomical dissection and concluded that degenera-tion appeared to parallel T2 low intensity, but the incidence offalse-positive posterior protrusion on MRI was remarkablyhigh. MRI should confirm the objective clinical findings.Asymptomatic findings should be expected to increase with the




age of the patient. Cervical myelography usually is indicatedonly after noninvasive evaluation by MRI fails to reveal thecause or level of the lesion. If MRI is inconclusive,electromyography or nerve conduction velocity may beindicated to demonstrate active radiculopathy before proceed-ing with myelography, especially if the history and physicalexamination are not strongly supportive of the presence ofradiculopathy. Cervical myelography usually is more precisethan lumbar myelography, regardless of the contrast mediumused. Postmyelogram CT scanning with block imaging and thincuts is very helpful.

Cervical discography is a highly controversial techniquewith limited benefits. It is not indicated in frank disc rupture,spondylosis, or spinal stenosis. The primary use is in patientswith persistent neck pain without localized neurologicalfindings in whom standard MRI, myelographic, and CT scanstudies are negative. Some investigators maintain that isolatedpainful discs can be identified in some patients by discography.Certainly a degenerative disc without pain on injection is notthe source of the patient’s complaint. Cervical discographyrequires considerable care and caution. It should be considereda preoperative test in those patients in whom an anterior discexcision and interbody fusion are considered for primary neckand shoulder pain. Assessing the psychosocial well-being of apatient is recommended before proceeding with surgicaltreatment. Great care is required both in the technique andinterpretation if reproducible results are desired. Cervical rootblocks also have been suggested for the localization andconfirmation of symptomatic root compression when used inconjunction with cervical discography. Facet joint injectionsalso should be considered before fusion as a therapeutic as wellas diagnostic procedure.

MyelographyWhen a component of dynamic cord compression is present,

myelography remains a valuable tool, although dynamic MRIhas reduced the role of myelography. Myelography isperformed in the same way as for ruptured lumbar discs exceptthat considerable attention must be paid to the flow of thecolumn of contrast medium with the neck in hyperextended,neutral, and flexed positions. One cannot conclude that spinalcord compression is not present until one is certain that thecephalad flow of the medium is not obstructed with the neckacutely hyperextended. The neck should be hyperextendedcarefully because of the danger of further damage to thespinal cord.

NONOPERATIVE TREATMENTNONOPERATIVE TREATMENTAs discussed earlier, most patients with symptomatic cervicaldisc herniations respond well to nonoperative treatment,including some patients with nonprogressive radicular weak-ness. Reasonably good evidence shows that acute discherniations actually decrease in size over time in the cervicalregion. Many conservative treatment methods for neck pain areused for multiple diagnoses. The primary purpose of the

cervical spine and associated musculature is to support andmobilize the head while providing a conduit for the nervoussystem. The forces on the cervical spine are therefore muchsmaller than on the lower spinal levels. The cervical spine isvulnerable to muscular tension forces, postural fatigue, andexcessive motion. Most nonoperative treatments focus on oneor more of these factors. The best primary treatment is shortperiods of rest, massage, ice, and antiinflammatory agents withactive mobilization as soon as possible. The position of theneck for comfort is essential for relief of pain. The position ofgreatest relief may suggest the offending pathological processor mechanism of injury. Patients with hyperflexion injuriesusually are more comfortable with the neck in extension overa small roll under the neck. No specific position is indicative oflateral disc herniation, although most tolerate the neutralposition best. Patients with spondylosis (hard disc) are mostcomfortable with the neck in flexion.

Cervical traction can be helpful in selected patients. Caremust be exercised in instructing the patient in the proper use ofthe traction. It should be applied to the head in the position ofmaximal pain relief. Traction never should be continued if itincreases pain. The weights should rarely exceed 10 pounds(weight of the head). The proper head halter and duration oftraction sessions should be chosen to prevent irritation of thetemporomandibular joint. Traction applied by a patient-controlled pneumatic force, which is more mobile thanhalter-type units, avoids irritation of temporomandibular joint.Traction also should allow general relaxation of the patient.‘‘Poor man’s’’ traction is a simple method of evaluating theefficacy of cervical traction. It uses the weight of theunsupported head for the traction weight (about 10 pounds).For extension traction, the patient is supine and the head isallowed to gently extend off the examining table or bed. Forflexion the same procedure is repeated in the prone position.The patient continues the exercise in the position that is mostcomfortable for 5 to 10 minutes several times daily.

The postural aspects of neck pain can be treated with morefrequent changes in position and ergonomic changes in thework area to prevent fatigue and encourage good posture.Techniques to minimize or relieve tension also are helpful.

Cervical braces usually limit excessive motion. Like trac-tion, they should be tailored to the most comfortable neckposition. They may be most helpful for patients who are veryactive.

Neck and shoulder exercises are most beneficial as the acutepain subsides. Isometric exercises are helpful in the acutephase. Occasionally, shoulder problems such as adhesivecapsulitis may be found concomitantly with cervical spondy-losis; therefore complete immobilization of the painfulextremity should be avoided.

OPERATIVE TREATMENTOPERATIVE TREATMENTThe primary indications for operative treatment of cervical discdisease are (1) failure of nonoperative pain management,(2) increasing neurological deficit, and (3) cervical myelopathy




that will predictably progress, based on natural history studies.In most patients the persistence of pain is the primaryindication. Intuitively, the level of persistent pain should besevere enough to consistently interfere with the patient’sdesired activity and greater than would reasonably be expectedafter operative treatment. The choice of approach should bedetermined by the position and type of lesion. Soft lateral discsare easily removed from the posterior approach, whereas softcentral or hard discs (central or lateral) probably are best treatedwith an anterior approach. Any controversy that existed relativeto the need for fusion with anterior discectomy essentially hasbeen resolved with long-term follow-up studies of patientswithout fusion, such as that by Yamamoto et al. mentionedpreviously. Osteophytes that were not removed at surgery havebeen shown frequently to be reabsorbed at the level of fusion.The use of a graft also prevents the collapse of the disc spaceand maintains adequate foraminal size.

◆ Removal of Posterolateral Herniationsby Posterior Approach (Posterior CervicalForaminotomy)

TECHNIQUE 39-15With the patient under general endotracheal anesthesia inthe prone position and the face in a Mayfield positioner, flexthe neck to obliterate the cervical lordosis as much aspossible. The upright position for surgery decreases venousbleeding, but concern regarding the possibility of airembolism and cerebral hypoxia in the event of a significantdrop in blood pressure makes us reluctant to recommend itsuse. Usually a slight reverse Trendelenburg position workswell in posterior cervical surgery coupled with carefuldissection to minimize bleeding. The shoulders are retractedinferiorly with tape if roentgenograms of the lower cervicallevels are contemplated.

Appropriately prepare and drape the operative field.Make a midline incision 2.5 cm lower than the interspace tobe explored (Fig. 39-30). Retract the edges of this incisionand the skin will withdraw in a cephalad direction so that thewound becomes properly placed. Divide the ligamentumnuchae longitudinally to expose the tips of the spinousprocesses above and below the designated area. The correctposition is reasonably well ensured by palpation of the lastbifid spine, which usually is the sixth cervical vertebra.However, it should be verified intraoperatively by a markerattached to the spinous process and documented on thelateral cervical spine roentgenogram. Dissect subperi-osteally the paravertebral muscles from the laminae on theside of the lesion and retract them with a self-retainingretractor or with the help of an assistant using a Hibbsretractor.

With a small high-speed drill, grind away the caudal edgeof the lateral portion of the lamina cephalad to theinterspace. Usually minimal bone removal from the

cephalad edge of the lateral portion of the caudal lamina isneeded. Only a small amount of the medial portion of thefacet needs to be removed in most patients. A small Kerrisonrongeur (1 to 2 mm) can be used to enlarge this keyhole asneeded. Sharply excise the ligamentum flavum with a smallKerrison rongeur and identify the nerve root, which iscommonly displaced posteriorly and flattened by pressurefrom the underlying disc fragments. Removal of additionalbone along the dorsal aspect of the foramen and immedi-ately above and below the nerve root often is beneficial atthis point. Once the bony removal has been completed, weprefer to use the operative microscope for the remainder ofthe procedure. This allows more delicate work around theneural elements while minimizing additional bone removaland allows better hemostasis.

The herniated nucleus pulposus most often lies slightlycaudal to the center of the nerve root but occasionallycephalad. Gently retract the nerve root superiorly to exposethe extruded nuclear fragments or a distended posteriorlongitudinal ligament. The nerve root should not beretracted in a caudal direction. If additional exposure isneeded, remove more bone rather than risk nerve root orspinal cord injury from traction on the root. To controltroublesome venous oozing at this point use bipolar cauteryif possible. Otherwise, place tiny pledgets of cotton andthrombin-soaked Gelfoam above and below the nerve root.Take care not to pack the pledgets tightly around the nerve.The nerve root then can be retracted slightly in a cephaladdirection to allow incision of the posterior longitudinalligament over the herniated nucleus pulposus in a cruciatemanner to permit the removal of the disc fragments.

After removal of all visible loose fragments, it isimperative to make a thorough search for additionalfragments, both laterally and medially. It is equallyimportant to be sure that the nerve root is thoroughlydecompressed by inserting a probe in the intervertebralforamen. If the nerve root still seems to be tight, removemore bone from the articular facets until the nerve root iscompletely free. Since recurrence is so rare, do not curetthe intervertebral space. Remove any cotton pledgets andGelfoam after meticulous hemostasis has been achieved.Hemostasis must be complete because postoperative hem-orrhage can produce cord compression and quadriplegia.Close the wound by suturing the fascia to the supraspinousligament with interrupted sutures and then suturing thesubcutaneous layers and skin.

AFTERTREATMENT. Neurological function is closely mon-itored after surgery. Discharge is permitted when the patient canwalk and void. Pain should be controlled with oral medication.Currently most patients are discharged within 24 hours aftersurgery. Radicular pain relief usually is dramatic and prompt,although hypesthesia can persist for weeks or months. Thepatient is allowed to return to clerical work when comfortable




and to manual labor after 6 weeks. As a rule, neither support norphysical therapy is necessary, and the patient’s future activity isnot restricted. Isometric neck exercises, upper extremity range-of-motion exercises, and posterior shoulder girdle exercises canbe useful for patients in whom atrophy or inactivity has beenconsiderable. A soft cervical collar can help relieve immediatepostoperative pain.

Results. In few if any operations in orthopaedic surgery arethe results better than after the removal of a lateral herniatedcervical disc. In the series of 250 operations reported bySimmons there were no deaths or major complicationsinvolving the brain or spinal cord. Three patients had reflexsympathetic dystrophy postoperatively. Two of these com-pletely recovered and one almost so. Two patients continued tohave arm pain after operation and were reexplored during theinitial hospital stay; in each, several more fragments of discwere found and removed. It is assumed that these fragmentswere overlooked at the initial operation. One patient had arecurrent extrusion at the same level. Two other patients had

soft extrusions on the opposite side at another level, alsorequiring a second operation.

Murphey, Simmons, and Brunson analyzed the results in aseries of 150 patients who returned questionnaires concerningthe success or failure of the operation. They were asked to statethe percentage of benefit they derived from the procedure(Table 39-8), whether they were performing the same work asthey had done preoperatively, and if not, whether the change ofwork had resulted from neck trouble. Approximately 90% hadextremely good results, and there were none who were notsignificantly improved, as the data concerning work doneconfirm. Only 7 (6%) of the 125 patients who answered thispart of the questionnaire found a change of work necessarybecause of neck trouble.

Anterior Approach to Cervical DiscSmith and Robinson in 1955 were the first to recommend

an anterior approach to the cervical spine in the treatmentof cervical disc disease. They described an anterolateraldiscectomy with interbody fusion (Fig. 39-31). This pro-

A

Fig. 39-30 Technique of removal of disc between fifth and sixth cervical vertebrae. A, Midlineincision extending from spinous process of fourth cervical vertebra to that of first thoracic vertebra.B, Paraspinal muscles have been dissected from laminae and retracted laterally. Hole is to be drilledwith Hudson burr (see text). C, Ligamentum flavum is being dissected. D, Defect measuring about1.3 cm has been made (see text) to expose nerve root and lateral aspect of dura. E, Nerve root hasbeen separated from nucleus and retracted superiorly to expose herniated disc. F, Longitudinalligament has been incised, and loose fragment of nucleus is being removed.

BC

D

E F




cedure attained widespread acceptance and application afterCloward in 1958 modified the procedure and introduced newinstrumentation.

Three basic techniques are used for anterior cervical discexcision and fusion. The Cloward technique involves making around hole centered at the disc space. A slightly larger, roundiliac crest plug is then inserted into the disc space hole. TheSmith-Robinson technique involves inserting a tricortical plugof iliac crest into the disc space after removing the disc andcartilaginous endplate. The graft is inserted with the cancellousside facing the cord (posterior). Bloom and Raney modified thistechnique by fashioning the tricortical graft to be thicker in itsmidportion and then inserting the graft with the cancellousportion facing anteriorly. The Bailey-Badgley technique in-volves the creation of a slot in the superior and inferiorvertebral bodies. This technique is most applicable to recon-struction when one or more vertebral bodies are excised fortumor, stenosis, or other extensive pathological conditions.Simmons and Bhalla modified this technique by using akeystone graft that increases the surface area of the graft by30% and allows more complete locking of the graft. Bio-mechanically, the Smith-Robinson technique provides thegreatest stability and least risk of extrusion, compared to theCloward or Bailey-Badgley type fusions.

White et al. reported relief of pain in 90% of 65 patientsundergoing anterior cervical spine fusion for spondylosis withthe technique of Smith and Robinson. Analysis of 90 patientswith anterior cervical discectomies and fusion for cervicalspondylosis with radiculopathy using the Cloward techniqueshowed good or excellent results in 82% in the study by Jacobs,Krueger, and Levy. These investigators did not use discogra-phy. Others also have found that discography does notstatistically improve the results. The Smith-Robinson techniqueis used almost exclusively at this clinic for anterior cervicaldiscectomy procedures.

The choice of right- or left-sided approach to the cervicalspine is somewhat controversial. The right side of the neck ispreferred by some right-handed surgeons because of the ease ofdissection. The reported increased risk of recurrent laryngealnerve trauma when operating on the right is not judged by those

who use it to be a significant deterrent to choosing thisexposure. Exposure from the left is more inconvenient for aright-handed surgeon but decreases the risk of recurrentlaryngeal nerve injury. This nerve on the left consistentlydescends with the carotid sheath and exits from the carotidsheath and vagus nerve intrathoracically. The nerve thencourses under the arch of the aorta and ascends in the neckbeside the trachea and esophagus. The course of the nerve onthe right is not as consistent. The nerve usually descends withthe carotid sheath and then loops around the subclavian arteryand ascends between the trachea and esophagus. Occasionallythe right recurrent laryngeal nerve exits the carotid sheath earlyand crosses anteriorly behind the thyroid. A large series ofanterior cervical procedures implicated the endotracheal tubein combination with self-retaining retractors as the cause of

Type I (50.9) KP/cm2

Type II (41.6) KP/cm2

Anteroposterior

Anteroposterior

Type III (35.2) KP/cm2

Anteroposterior

Lateral

Lateral

Lateral

Fig. 39-31 Types of anterior cervical fusion. A, Smith-Robinsonfusion. B, Cloward fusion. C, Bailey-Badgley fusion. D, Bloom-Raney modification of Smith-Robinson fusion. (A to C redrawnfrom White AA, Jupiter J, Southwick WO, Panjabi MM: ClinOrthop 91:21, 1973; D redrawn from Bloom MH, Raney FL:J Bone Joint Surg 63A:602, 1981.)

A

B

C

D

Table 39-8 Results of Removal of LateralHerniated Discs in CervicalRegion (Patient’s Estimateof Percent Improvement)

Relief (%)

Patients

Improved (%)

Number

of Patients

95-100 65.3 9890-94 23.3 3575-89 8.0 1250-74 3.3 5Total 100.0 150

Murphey F, Simmons JCH, Brunson B: J Neurosurg 38:679, 1973.




recurrent laryngeal nerve injuries. The recommendation madewas to deflate the cuff of the endotracheal tube after retractorplacement to allow the tip of the tube to reposition itself. Thissignificantly decreased the incidence of recurrent laryngealnerve palsy in a series of 600 patients. See Chapter 36 for acomplete description of anterior cervical discectomy andfusion.

Anterior Foraminotomy. Recently there have been severalreports of microsurgical anterior foraminotomy to treatunilateral foraminal nerve compression from soft disc hernia-tions or uncovertebral joint degenerative change. Verbiest firstdescribed this technique; Jho reported a modification, andJohnson reported a small clinical series. This technique appearsto allow adequate decompression of the ventral aspect of theforamen unilaterally while removing the lateral portion of thedisc, thus preserving the remaining disc. The long-term resultsare not yet available to compare this technique with anteriordiscectomy with fusion. We do not have any clinical experiencewith this technique.

◆ Microsurgical Anterior Cervical Foraminotomy

TECHNIQUE 39-16 (Jho)

After anesthesia has been administered by means ofendotracheal intubation, place the patient supine, with abolster placed behind both shoulders to maintain gentleextension of the cervical spine. Position the head with themidline upright. Gently pull both shoulders caudally and fixwith tape for a good lateral view of the cervical spine onintraoperative roentgenogram. Do not use a cervical tractiondevice. Prepare the anterior neck with antiseptic solutionand drape.

Make a 3- to 5-cm long transverse incision in a skincrease ipsilateral to the radiculopathy. The first two thirdsof the incision should be medial to the sternocleidomas-toid muscle and the remainder should be lateral to themedial border of that muscle. Incise the subcutaneoustissue and platysma muscle along the line of the skinincision. Cleanly undermine the loose connective tissuelayer under the platysma muscle to provide space in whichto work. Use a combination of sharp and blunt dissectionto access the anterior column of the cervical spine. Keepthe carotid artery and the sternocleidomastoid musclelateral and the strap muscle, trachea, and esophagusmedial. Open the prevertebral fascia and expose the anteriorcolumn of the cervical spine. Confirm the correct levelroentgenographically.

Use an anterior cervical discectomy retractor system toexpose the ipsilateral longus colli muscle (Fig. 39-32, A).Use only smooth-tipped retractor blades to avoid injury tothe trachea and esophagus medially and the carotid arteryand vagus nerve laterally. Use the operating microscope atthis stage and excise the medial portion of the longus collimuscle to expose the medial parts of the transverse

processes of the upper and lower vertebrae (Fig. 39-32, B).Expose the vertebral artery anterior to the C7 transverseprocess. When operating at C6-7 take care not to injure thevertebral artery while removing the medial portion ofthe longus colli muscle. For operations above C6-7, thevertebral artery is not exposed purposely at this point.

Once the medial parts of the transverse processes ofthe upper and lower vertebrae have been identified, theipsilateral uncovertebral joint between them can be seen.The interface of the uncovertebral joint is angled approxi-mately 30 degrees cephalad from the horizontal line of theintervertebral disc. Make a sharp vertical incision of the discat the medial margin of the ipsilateral uncovertebral joint toprevent inadvertent internal disruption of the remainingdisc. While drilling the bone, repeated sharp cutting of thedeeper disc may be required. Remove the thin layer of discmaterial located at the uncovertebral joint.

Drill between the transverse processes of the uncoverte-bral joint using a high-speed microdrill attached to an angledhandpiece (Fig. 39-32, B). To prevent injury to the vertebralartery, leave the thin cortical bone attached to the liga-mentous tissue covering the medial portion of this artery.Continue drilling down to the posterior longitudinal liga-ment (Fig. 39-32, C). While drilling posteriorly, gentlyincline medially. When the posterior longitudinal ligamentis exposed, a piece of thin cortical bone remains attachedlateral to the ligamentous tissue covering the vertebralartery. Dissect the lateral remnant of the uncinate processfrom the ligamentous tissue and fracture it at the base of theuncinate process (Fig. 39-32, D). Further dissect it from thesurrounding soft tissue and remove it. The vertebral arterycan be identified by its pulsation between the transverseprocesses of the vertebrae. Drilling at the base of theuncinate process must proceed cautiously because the nerveroot lies just behind it. After the uncinate process becomesloosened at its base, remove the remaining thin bone of theuncinate process by fracturing it from its base rather than bycontinued drilling. Once the remaining piece of uncinateprocess is removed, the compressed nerve root will bedistended forward by bone decompression (Fig. 39-32, E).The size of the hole that is made by drilling at theuncovertebral joint usually is approximately 5 to 8 mm widetransversely and 7 to 10 mm wide vertically. If there is noruptured herniated disc fragment behind the posteriorlongitudinal ligament, this will end the nerve rootdecompression.

At this point the posterior longitudinal ligament stillcovers the nerve root and the lateral margin of the spinalcord. If the disc fragment has ruptured through the posteriorlongitudinal ligament, the tail of the disc material will bevisible. Remove this disc fragment at this time. To avoidoverlooking a hidden disc fragment, use a no. 15 blade knifeor micro scissors to incise the ligament and remove anyfragment with a 1- or 2-mm foot-plated bone punch. The




ipsilateral one third to one half of the spinal cord is thusexposed and the nerve root can be seen laterally as it exitsbehind the vertebral artery (Fig. 39-32, F).

Jho reported excision of the posterior longitudinalligament in selected cases because it is unlikely that ahidden ruptured disc fragment could be present withoutdisruption of this ligament. Removal of the ligament some-times is complicated by epidural bleeding. If the ligamentis not removed, the procedure is much simpler and theoperating time is shorter. If epidural bleeding occurs duringremoval of the posterior longitudinal ligament, use bipolarcoagulation. To avoid any potential compressive materialcoming into contact with the nerve root or spinal cord, donot use hemostatic agents. Although epidural bleedingusually is not a problem, removing the posterior longitudinalligament is the most difficult part of this procedure. The discwithin the intervertebral space remains untouched andpreserved.

Close the platysma with interrupted 3-0 absorbablestitches and approximate the skin with subcuticular sutures.The operation can be performed at multiple levels. To

minimize postoperative incisional pain, inject a fewmilliliters of local anesthetic subcutaneously.

Thoracic Disc DiseaseThoracic Disc DiseaseThe thoracic spine is the least common location for discpathology. C.A. Key has been credited with the first report of aspinal cord injury caused by thoracic disc herniation, whichappeared in 1838 in the Guy’s Hospital Report. In the earlytwentieth century several reports of enchondromata, chondro-mata, or echondromata appeared. In their study in 1934 Mixterand Barr included four patients with a thoracic location of theherniated nucleus pulposus. Of the four patients in this series,three were treated operatively and one nonoperatively. Thepatient with nonoperative treatment died soon after diagnosis.Of the surgical group, two had complete paraplegia postopera-tively. The third surgical patient died several months later forunknown reasons. These three were treated with posteriorlaminectomy. This initial report not only described the con-dition, but also revealed some of the difficulties of treatment.

A

Fig. 39-32 Anterior foraminotomy.(Redrawn from Johnson JP, Filler AG,McBride DQ, Batzdorf U: Spine 25:906,2000.)

B C

D E




Since the 1960s many other approaches have been describedand validated through clinical experience. It is apparent thatposterior laminectomy has no role in the surgical treatment ofthis problem. Other posterior approaches, such as costotrans-versectomy, have good indications. Fessler and Sturgill, as wellas Vanichkachorn and Vaccaro, chronicled the history andtreatment evolution for thoracic disc disease.

Symptomatic thoracic disc herniations remain relativelyrare, with an estimated incidence of 1 in 1,000,000 persons peryear. They represent 0.25% to 0.75% of the total incidence ofsymptomatic disc herniations. The most common age of onsetis between the fourth and sixth decades. As with the other areasof the spine, the incidence of asymptomatic disc herniations ishigh. Wood et al. reviewed MRI studies in 90 asymptomaticpatients and found thoracic disc abnormalities in 73%. Ofthese, 37% had frank herniations and 29% showed cordcompression. At a mean follow-up of 26 months with repeatMRI of some of these patients none had become symptomatic.Also, Wood et al. noted that small herniations often increased,whereas the larger herniations often regressed. Operativetreatment of thoracic disc herniations is indicated in the rarepatient with acute disc herniation with myelopathic findingsattributable to the lesion, especially progressive neurologicalsymptoms.

SIGNS AND SYMPTOMSSIGNS AND SYMPTOMSFortunately, the natural history of symptomatic thoracic discdisease is similar to that in other areas, in that symptoms andfunction typically improve with conservative treatment andtime. However, the clinical course can be quite variable, and ahigh index of suspicion must be maintained to make the correctdiagnosis. The differential diagnosis for the symptoms ofthoracic disc herniations is fairly extensive and includesnonspinal causes occurring with the cardiopulmonary, gastro-intestinal, and musculoskeletal systems. Spinal causes ofsimilar symptoms can occur with infectious, neoplastic,degenerative, and metabolic problems within the spinal columnas well as the spinal cord.

Two general patient populations have been documented inthe literature. The smaller group of patients is younger and hasa relatively short history of symptoms, often with a history oftrauma. Typically, an acute soft disc herniation with either acutespinal cord compression or radiculopathy is present. Outcomegenerally is favorable with operative or nonoperative treatment.The larger group of patients has a longer history, often morethan 6 to 12 months of symptoms, which result from chronicspinal cord or root compression. Disc degeneration, often withcalcification of the disc, is the underlying process.

Pain is clearly the most common presenting feature ofthoracic disc herniations. There appear to be two patterns ofpain: one is axial and the other is bandlike radicular pain alongthe course of the intercostal nerve. The T10 dermatomal levelis the most commonly reported distribution, regardless of thelevel of involvement. This is a band extending around the lowerlateral thorax and caudally to the level of the umbilicus. This

radicular pattern is more common with upper thoracic andlateral disc herniations. Some axial pain often occurs with thispattern as well. Associated sensory changes of paresthesiasand dysesthesia in a dermatomal distribution also occur.(Fig. 39-33). High thoracic discs (T2 to T5) can presentsimilarly to cervical disc disease with upper arm pain,paresthesias, radiculopathy, and even Horner’s syndrome.Myelopathy also may occur. Complaints of weakness, whichmay be generalized by the patient, typically involving bothlower extremities present in the form of mild paraparesis. Thepresence of sustained clonus, a positive Babinski sign, andwide-based and spastic gait are all signs of myelopathy. Boweland bladder dysfunction occur in only about 15% to 20% ofthese patients. The neurological evaluation of patients withthoracic disc herniations must be meticulous because there arefew localizing findings. Abdominal reflexes, cremasteric reflex,dermatomal sensory evaluation, rectus abdominis contractionsymmetry, lower extremity reflex, strength, and sensory exami-nations, as well as determination of long tract findings, are allimportant.

CONFIRMATORY TESTINGCONFIRMATORY TESTINGPlain roentgenograms are of some help to evaluate traumaticinjuries and to determine potential osseous morphologicalvariations that may help to localize findings, especially onintraoperative films, if these become necessary. MRI is the mostimportant and useful imaging method to demonstrate thoracicdisc herniations. In addition to the disc herniation, neoplastic orinfectious pathology can be seen. The presence of intraduralpathology, including disc fragments, also usually is demon-strated on MRI. The spinal cord signal may indicate the

T4

T8

T10

T12

Fig. 39-33 Sensory dermatomes of trunk region. (Redrawn fromKlein JD: Clinical evaluation of patients with spinal disorders. InGarfin SR, Vaccaro AR, eds: Orthopaedic knowledge update:spine, Rosemont, Ill, 1997, American Academy of OrthopaedicSurgeons.)




presence of inflammation or myelomalacia as well. Despite allthese advantages, MRI may underestimate the thoracic discherniation, which often is calcified and thus has low signalintensity on T1 and T2 sequences.

Myelography followed by CT scanning also can be usefulin evaluating the bony anatomy, as well as more accuratelyassessing the calcified portion of the herniated thoracic disc.Regardless of the imaging methods used, the appearance andpresence of a thoracic disc herniation must be carefullyconsidered and correlated with the patient’s complaints anddetailed examination findings.

TREATMENT RESULTSTREATMENT RESULTSAs mentioned previously, nonoperative treatment usually iseffective. Brown reported that 63% of patients improved usinga combination of nonoperative treatments. A specific regimencannot be recommended for all patients; however, the prin-ciples of short-term rest, pain relief, antiinflammatory agents,and progressive directed activity restoration appear mostappropriate. These measures generally should be continued atleast 6 to 12 weeks if feasible. If neurological deficits progressor present as myelopathy, or if pain remains at an intolerablelevel, surgery should be recommended. The initial procedurerecommended for this lesion was posterior thoracic laminec-tomy and disc excision. At least half of the lesions have beenidentified as being central, making the excision from thisapproach extremely difficult, and the results were somewhatdisheartening. Most series reported fewer than half of thepatients improving, with some becoming worse after posteriorlaminectomy and discectomy. Most recent studies suggest thatlateral rachiotomy (modified costotransversectomy) or ananterior transthoracic approach for discectomy produces con-siderably better results with no evidence of worsening after theprocedure. Video-assisted thoracic surgery (VATS) has beenused in several series to successfully remove central thoracicdisc herniations without the need for a thoracotomy or fusion.Bohlman and Zdeblick reported the results of anterior thoracicdisc excision in 19 patients: 16 patients had excellent or goodresults, and 3 had fair or poor results. Pain was relieved in 10,decreased in 8, and unchanged in 1. None had worsening ofneurological symptoms. Regan, BinYashay, and Mack reporteda series of 29 thoracoscopic disc excisions with 76% sat-isfactory results.

OPERATIVE TREATMENTOPERATIVE TREATMENTThe best surgical approach for these lesions depends on thespecific characteristics of the disc herniation, as well as on theparticular experience of the surgeon. Simple laminectomyreally has no role in the treatment of thoracic disc herniations.Posterior approaches, including costotransversectomy, trans-pedicular approach, and the lateral extracavitary approach,have all been used successfully. Anterior approaches viathoracotomy, a transsternal approach, or VATS also have beenused successfully (Fig. 39-34).

◆ CostotransversectomyCostotransversectomy is probably best suited for thoracic discherniations that are predominantly lateral or herniations that aresuspected to be extruded or sequestered. Central discherniations are probably best approached transthoracically.Some surgeons have recommended subsequent fusion after discremoval anteriorly or laterally.

TECHNIQUE 39-17The operation usually is done with the patient under generalanesthesia with a cuffed endotracheal tube or a Carlen tubeto allow lung deflation on the side of approach. Place thepatient prone and make a long midline incision or a curvedincision convex to the midline centered over the side ofinvolvement. Expose the spine in the usual manner out tothe ribs. Remove a section of rib 5 to 7.5 cm long at the levelof involvement, taking care to avoid damage to theintercostal nerve and artery. Carry the resection into thelateral side of the disc, exposing it for removal. Additionalexposure can be made by laminectomy and excision of thepedicle and facet joint. Fusion is unnecessary unless morethan one facet joint is removed. Close the wound in layers.

AFTERTREATMENT. The aftertreatment is similar to that forlumbar disc excision without fusion (Technique 39-21).

◆ Anterior Approach for Thoracic Disc ExcisionBecause of the relative age of patients with thoracic discruptures, special care must be taken to identify those withpulmonary problems. In these patients the anterior approachcan be detrimental medically, making a posterolateral approachsafer. Patients with midline protrusions probably are besttreated with the transthoracic approach to ensure complete discremoval.

TECHNIQUE 39-18The operation is done with the patient under generalanesthesia, using a cuffed endotracheal tube or Carlen tubefor lung deflation on the side of the approach. Place thepatient in a lateral recumbent position. A left-sided anteriorapproach usually is preferred, making the operative pro-cedure easier. Make a skin incision along the line of the ribthat corresponds to the second thoracic vertebra above theinvolved intervertebral disc except for approaches to theupper five thoracic segments, where the approach is throughthe third rib. Choose the skin incision by inspection of theanteroposterior roentgenogram. Cut the rib subperiosteallyat its posterior and anterior ends and then insert a ribretractor. Save the rib for grafting later in the procedure. Onecan then decide on an extrapleural or transpleural approachdepending on familiarity and ease. Exposure of the thoracicvertebrae should give adequate access to the front andopposite side. Dissect the great vessels free of the spine.




Ligate the intersegmental vessels near the great vessels andnot near the foramen. One should be able to insert the tip ofa finger against the opposite side of the disc when thevascular mobilization is complete. Exposure of the interver-tebral disc without disturbing more than three segmentalvessels is preferable to avoid ischemic problems in thespinal cord. In the thoracolumbar region strip the diaphragmfrom the eleventh and twelfth ribs. The anterior longitudinalligament usually is sectioned to allow spreading of theintervertebral disc space. Remove the disc as completelyas possible if fusion is planned. The use of the operating

microscope or loupe magnification eases the removal of thedisc near the posterior longitudinal ligament. Use curets andnibbling instruments to remove the disc up to the posteriorlongitudinal ligament. Then place a finger on the oppositeside of the disc to avoid penetration when removing discmaterial on the more distant side. Carefully inspect theposterior longitudinal ligament for tears and extrudedfragments. Remove the posterior longitudinal ligament onlyif necessary. Significant bleeding can occur if the venousplexus near the dura is torn. After removal of the disc, stripthe endplates of their cartilage. Make a slot in one vertebral

A

LaminectomyFig. 39-34 Exposure of thoracic disc provided by standard lami-nectomy (A), transpedicular approach (B), costotransversectomyapproach (C), lateral extracavitary approach (D), and anterolateralthoracotomy (E). (Redrawn from Fessler RG, Sturgill M: Surg Neurol49:609, 1998.)

Transpedicular Costotransversectomy

Lateral extracavitary

Transthoracic

B C

D E




body and a hole in the body on the opposite side of the discspace to accept the graft material. Make the hole largeenough to accept several sections of rib, but make the slotlarge enough to accept only one rib graft at a time. Theninsert iliac, tibial, or rib grafts into the disc space. Tiethe grafts together with heavy suture material when themaximal number of grafts have been inserted. Close thewound in the usual manner and employ standard chestdrainage. As an alternative, if fusion is not desired a morelimited resection using the operating microscope can bedone. After the vascular mobilization, resect the rib head toallow observation of the pedicle and foramen caudal to thedisc space. The pedicle can be removed with a high-speedburr and Kerrison rongeurs, thus exposing the posterolateralaspect of the disc. This allows careful, blunt development ofthe plane ventral to the dura with removal of the discherniation and preservation of the anterior majority of thedisc, as well as limiting the need for fusion. A similartechnique using VATS is described in Technique 39-19.

The transthoracic approach removing a rib two levelsabove the level of the lesion can be used up to T5. Thetransthoracic approach from T2 to T5 is best made byexcision of the third or fourth rib and elevation of thescapula by sectioning of attachments of the serratus anteriorand trapezius from the scapula. The approach to the T1-2disc is best made from the neck with a sternal splittingincision.

AFTERTREATMENT. Postoperative care is the same as for athoracotomy. The patient is allowed to walk after the chesttubes are removed. Extension in any position is prohibited. Abrace or body cast that limits extension should be used if the

stability of the graft is questionable. The graft usually is stablewithout support if only one disc space is removed. Postopera-tive care is the same as for anterior corpectomy and fusion ifmore than one disc level is removed. If no fusion is done, thepatient is mobilized as pain permits without a brace.

◆ Thoracic Endoscopic Disc ExcisionMicrosurgical and endoscopic surgical techniques are beingapplied to the anterior excision of thoracic disc herniation.Rosenthal et al. and Horowitz et al. first performed theseprocedures on cadavers to perfect the technique. Because thesemethods are highly technical, they should be performed by asurgeon who is proficient in this technique and in the use ofendoscopic equipment and with the assistance of an experi-enced thoracic surgeon. Ideally the procedure should be doneon cadavers or live animals first. Regan et al. also described thistechnique, with different portal positions.

TECHNIQUE 39-19 (Rosenthal et al.)

(Figs. 39-35 and 39-36)Place the patient in the left lateral decubitus position toallow a right-sided approach and displacement of the aortaand heart to the left. Insert four trocars in a triangularfashion along the middle axillary line converging on the discspace. Introduce a rigid endoscope with a 30-degree opticangle attached to a video camera into one of the trocars,leaving the other three as working channels. Deflate the lungusing a Carlin tube or similar method. Split the parietalpleura starting at the medial part of the intervertebral spaceand extending up to the costovertebral process. Preserve andmobilize the segmental arteries and sympathetic nerve outof the operating field. Drill away the rib head and lateral

I

S

S

A

1 2 3

4

M

Fig. 39-35 Position on operating tableand operating room setup. Surgeons (S)and nurse with instruments (I) stand infront of patient. Monitor (M) placed atback. ‘‘Working channels’’ (1,2,3) con-verge toward spine. Channel for opti-cal system (4) situated ventrally. (FromRosenthal D, Rosenthal R, de Simone A:Spine 19:1087, 1994.)




portion of the pedicle. Remove the remaining pedicle withKerrison rongeurs to improve exposure to the spinal canal.Removing the superior posterior portion of the vertebracaudal to the disc space allows safer removal of the discmaterial, which then can be pulled anteriorly and inferiorlyaway from the spinal canal to be removed. Use endoscopicinstruments for surgery in the portals. Remove the discposteriorly and the posterior longitudinal ligament, restrict-ing bone and disc removal to the posterior third of theintervertebral space and costovertebral area to maintainstability. Insert chest tubes in the standard fashion and setthem to water suction; close the portals.

AFTERTREATMENT. The patient is rapidly mobilized astolerated by the chest tubes. Discharge is possible once thechest tubes have been removed and the patient is ambulat-ing well.

Lumbar Disc DiseaseSIGNS AND SYMPTOMSLumbar Disc DiseaseSIGNS AND SYMPTOMSAlthough back pain is common from the second decade of lifeon, intervertebral disc disease and disc herniation are mostprominent in otherwise healthy people in the third and fourth

decades of life. Most people relate their back and leg pain to atraumatic incident, but close questioning frequently reveals thatthe patient has had intermittent episodes of back pain for manymonths or even years before the onset of severe leg pain. Inmany instances the back pain is relatively fleeting and isrelieved by rest. This pain often is brought on by heavyexertion, repetitive bending, twisting, or heavy lifting. In otherinstances an exacerbating incident cannot be elicited. The painusually begins in the lower back, radiating to the sacroiliacregion and buttocks. The pain can radiate down the posteriorthigh. Back and posterior thigh pain of this type can be elicitedfrom many areas of the spine, including the facet joints,longitudinal ligaments, and the periosteum of the vertebra.Radicular pain, on the other hand, usually extends below theknee and follows the dermatome of the involved nerve root.

The usual history of lumbar disc herniation is of repetitivelower back and buttock pain, relieved by a short period of rest.This pain is then suddenly exacerbated by a flexion episode,with the sudden appearance of leg pain much greater than backpain. Most radicular pain from nerve root compression causedby a herniated nucleus pulposus is evidenced by leg pain equalto, or in many cases much greater than, the degree of back pain.Whenever leg pain is minimal and back pain is predominant,great care should be taken before making the diagnosis of asymptomatic herniated intervertebral disc. The pain from discherniation usually is intermittent, increasing with activity,especially sitting. The pain can be relieved by rest, especially inthe semi-Fowler position, and can be exacerbated by straining,sneezing, or coughing. Whenever the pattern of pain is bizarreor the pain itself is constant, a diagnosis of symptomaticherniated disc should be viewed with some skepticism.

Other symptoms of disc herniation include weakness andparesthesias. In most patients the weakness is intermittent,variable with activity, and localized to the neurological level ofinvolvement. Paresthesias also are variable and limited to thedermatome of the involved nerve root. Whenever thesecomplaints are generalized, the diagnosis of a simple unilateraldisc herniation should be questioned.

Numbness and weakness in the involved leg and occasion-ally pain in the groin or testicle can be associated with a highor midline lumbar disc herniation. If a fragment is large or theherniation is high, symptoms of pressure on the entire caudaequina can be elicited. These include numbness and weaknessin both legs, rectal pain, numbness in the perineum, andparalysis of the sphincters. This diagnosis should be theprimary consideration in patients who complain of sudden lossof bowel or bladder control. Whenever the diagnosis of a caudaequina syndrome or acute midline herniation is suspected,evaluation and treatment should be aggressive.

PHYSICAL FINDINGSPHYSICAL FINDINGSThe physical findings in back pain with disc disease arevariable because of the time intervals involved. Usuallypatients with acute pain show evidence of marked paraspinalspasm that is sustained during walking or motion. A scoliosis or

Fig. 39-36 Endoscopic removal of thoracic disc. Horizontalview at T6 level. Patient is in left lateral decubitus position.A, Right lung (collapsed). B, Heart and pericardium. C, Esoph-agus. D, Aorta. E, Forceps and endoscope. F, Left lung. (FromRosenthal D, Rosenthal R, de Simone A: Spine 19:1087, 1994.)




a list in the lumbar spine may be present, and in many patientsthe normal lumbar lordosis is lost. As the acute episodesubsides, the degree of spasm diminishes remarkably, and theloss of normal lumbar lordosis may be the only telltale sign.Point tenderness may be present over the spinous process at thelevel of the disc involved, and in some patients pain may extendlaterally.

If there is nerve root irritation, it centers over the length ofthe sciatic nerve, both in the sciatic notch and more distallyin the popliteal space. In addition, stretch of the sciatic nerve atthe knee should reproduce buttock, thigh, and leg pain (i.e.,pain distal to the knee). A Lasegue sign usually is positive onthe involved side. A positive Lasegue sign or straight leg raisingshould elicit buttock or leg pain distal to the knee or both on theside tested. Occasionally if leg pain is significant the patientwill lean back from an upright sitting position and assume thetripod stance to relieve the pain. Contralateral leg painproduced by straight leg raising should be regarded aspathognomonic of a herniated intervertebral disc. The absenceof a positive Lasegue sign should make one skeptical of thediagnosis, although older individuals may not have a positiveLasegue sign. Likewise, inappropriate findings and inconsis-tencies in the examination usually are nonorganic in origin (seediscussion of nonspecific back pain). If the leg pain haspersisted for any length of time, atrophy of the involved limbmay be present, as demonstrated by asymmetrical girth of thethigh or calf. The neurological examination will vary asdetermined by the level of root involvement (Boxes 39-7 to39-9). Smith et al. examined the motion of the spinal roots incadavers. They observed 0.5 to 5 mm of linear motion and 2%to 4% strain on the nerves at L4, L5, and S1. With increasedstrain, the roots moved lateral to the pedicle.

Unilateral disc herniation between L3 and L4 usuallycompresses the fourth lumbar root as it crosses the disc beforeexiting at the L4 intervertebral foramen. Pain may be localizedaround the medial side of the leg. Numbness may be presentover the anteromedial aspect of the leg. The tibialis anteriormay be weak as evidenced by inability to heel walk. Thequadriceps and hip adductor group, both innervated from L2,L3, and L4, also may be weak and, in extended ruptures,

atrophic. Reflex testing may reveal a diminished or absentpatellar tendon reflex (L2, L3, and L4) or tibialis anteriortendon reflex (L4). Sensory testing may show diminishedsensibility over the L4 dermatome, the isolated portion ofwhich is the medial leg (Fig. 39-37), and the autonomous zoneof which is at the level of the medial malleolus.

Unilateral disc herniation between L4 and L5 results incompression of the fifth lumbar root. Fifth lumbar rootradiculopathy should produce pain in the dermatomal pattern.Numbness, when present, follows the L5 dermatome along theanterolateral aspect of the leg and the dorsum of the foot,including the great toe. The autonomous zone for this nerve isthe dorsal first web of the foot and the dorsum of the third toe.Weakness may involve the extensor hallucis longus (L5),gluteus medius (L5), or extensor digitorum longus and brevis(L5). Reflex change usually is not found. A diminished tibialisposterior reflex is possible but difficult to elicit.

With unilateral rupture of the disc between L5 and S1 thefindings of an S1 radiculopathy are noted. Pain and numbnessinvolve the dermatome of S1. The S1 dermatome includes thelateral malleolus and the lateral and plantar surface of the foot,occasionally including the heel. There is numbness over thelateral aspect of the leg and, more important, over the lateralaspect of the foot, including the lateral three toes. The

BOX 39-7 • L4 Root Compression*

Sensory DeficitPosterolateral thigh, anterior knee, and medial leg

Motor WeaknessQuadriceps (variable)Hip adductors (variable)

Reflex ChangesPatellar tendonTibialis anterior tendon (variable)

*Indicative of L3-4 disc herniation or pathological condition localized tothe L4 foramen.

BOX 39-8 • L5 Root Compression*

Sensory DeficitAnterolateral leg, dorsum of the foot, and great toe

Motor WeaknessExtensor hallucis longusGluteus mediusExtensor digitorum longus and brevis

Reflex ChangeUsually noneTibialis posterior (difficult to elicit)

*Indicative of L4-5 disc herniation or pathological condition localized tothe L5 foramen.

BOX 39-9 • S1 Root Compression*

Sensory DeficitLateral malleolus, lateral foot, heel, and web of fourth and

fifth toes

Motor WeaknessPeroneus longus and brevisGastrocnemius-soleus complexGluteus maximus

Reflex ChangeTendo calcaneus (gastrocnemius-soleus complex)

*Indicative of L5-S1 disc herniation or pathological condition localizedto the S1 foramen.




autonomous zone for this root is the dorsum of the fifth toe.Weakness may be demonstrated in the peroneus longus andbrevis (S1), gastrocnemius-soleus (S1), or gluteus maximus(S1). In general, weakness is not a usual finding in S1radiculopathy. Occasionally, mild weakness may be demon-strated by asymmetrical fatigue with exercise of these motorgroups. The ankle jerk usually is reduced or absent.

Massive extrusion of a disc involving the entire diameter ofthe lumbar canal or a large midline extrusion can produce painin the back, legs, and occasionally perineum. Both legs may beparalyzed, the sphincters may be incontinent, and the anklejerks may be absent. Tay and Chacha in 1979 reported that thecombination of saddle anesthesia, bilateral ankle areflexia, andbladder symptoms constituted the most consistent symptoms ofcauda equina syndrome caused by massive intervertebral discextrusion at any lumbar level. In these instances a cystomet-rogram may show bladder denervation.

More than 95% of the ruptures of the lumbar intervertebraldiscs occur at L4 or L5. Ruptures at higher levels in manypatients are not associated with a positive straight leg raisingtest. In these instances, a positive femoral stretch test can behelpful. This test is carried out by placing the patient prone andacutely flexing the knee while placing the hand in the poplitealfossa. When this procedure results in anterior thigh pain, the

result is positive and a high lesion should be suspected. Inaddition, these lesions may occur with a more diffuseneurological complaint without significant localizing neurolog-ical signs.

Often the neurological signs associated with disc diseasevary over time. If the patient has been up and walking for aperiod of time, the neurological findings may be much morepronounced than if he has been at bed rest for several days, thusdecreasing the pressure on the nerve root and allowing thenerve to resume its normal function. In addition, variousconservative treatments can change the physical signs of discdisease.

Comparative bilateral examination of a patient with backand leg pain is essential in finding a clear-cut pattern of signsand symptoms. It is not uncommon for the evaluation tochange. Adverse changes in the examination may warrant moreaggressive therapy, whereas improvement of the symptomsor signs should signal a resolution of the problem. Earlysymptoms or signs suggestive of cauda equina syndrome orsevere or progressive neurological deficit should be treatedaggressively from the onset. McLaren and Bailey warn that thecauda equina syndrome is more frequent when disc excision isperformed in the presence of an untreated spinal stenosis at thesame level.

Fig. 39-37 L4 neurological level. (AfterHoppenfeld S: Physical examination ofthe spine and extremities, Norwalk, Conn,1976, Appleton-Century-Crofts.)




DIFFERENTIAL DIAGNOSISDIFFERENTIAL DIAGNOSISThe differential diagnosis of back and leg pain is extremelylengthy and complex. It includes diseases intrinsic to the spineand those involving adjacent organs but causing pain referred tothe back or leg. For simplicity, lesions can be categorized asbeing extrinsic or intrinsic to the spine. Extrinsic lesionsinclude diseases of the urogenital system, gastrointestinalsystem, vascular system, endocrine system, nervous system notlocalized to the spine, and the extrinsic musculoskeletal system.These lesions include infections, tumors, metabolic distur-bances, congenital abnormalities, and the associated diseases ofaging. Intrinsic lesions involve those diseases that ariseprimarily in the spine. They include diseases of the spinalmusculoskeletal system, the local hematopoietic system, andthe local neurological system. These conditions include trauma,tumors, infections, diseases of aging, and immune diseasesaffecting the spine or spinal nerves.

Although the predominant cause of back and leg pain inhealthy people usually is lumbar disc disease, one must beextremely cautious to avoid a misdiagnosis, particularly giventhe high incidence of disc herniations present in asymptomaticpatients as discussed previously. Therefore a full physicalexamination must be completed before making a presumptivediagnosis of herniated disc disease. Common diseases that canmimic disc disease include ankylosing spondylitis, multiplemyeloma, vascular insufficiency, arthritis of the hip, osteopo-rosis with stress fractures, extradural tumors, peripheralneuropathy, and herpes zoster. Infrequent but reported causes ofsciatica not related to disc hernia include synovial cysts, ruptureof the medial head of the gastrocnemius, sacroiliac jointdysfunction, lesions in the sacrum and pelvis, and fracture ofthe ischial tuberosity.

CONFIRMATORY IMAGINGCONFIRMATORY IMAGINGAlthough the diagnosis of a herniated lumbar disc can besuspected from the history and physical examination, imagingstudies are necessary to rule out other causes, such as a tumoror infection. Plain roentgenograms are of limited use in thediagnosis because they do not show disc herniations or otherintraspinal lesions, but they can demonstrate infection, tumors,or other anomalies and should be obtained, especially if surgeryis planned. Currently, the most useful test for diagnosing aherniated lumbar disc is MRI. Since the advent of MRI,myelography is used much less frequently, although in somesituations it may help to demonstrate subtle lesions. Whenmyelography is used, it should be followed with a CT scan.

NONOPERATIVE TREATMENTNONOPERATIVE TREATMENTThe number and variety of nonoperative therapies for back andleg pain are overwhelming. Treatments range from simple restto expensive traction apparatus. All these therapies are reportedwith glowing accounts of miraculous ‘‘cures’’; unfortunately,

few have been evaluated scientifically. In addition, the naturalhistory of disc disease is characterized by exacerbations andremissions with eventual improvement regardless of treatment.Finally, several distinct symptom complexes appear to beassociated with disc disease. Few if any studies have isolatedthe response to specific and anatomically distinct diagnoses.

The simplest treatment for acute back pain is rest. Deyo,Diehl, and Rosenthal reported that 2 days of bed rest werebetter than a longer period. Biomechanical studies indicate thatlying in a semi- Fowler position (i.e., on the side with the hipsand knees flexed) with a pillow between the legs should relievemost pressure on the disc and nerve roots. Muscle spasm can becontrolled by the application of ice, preferably with a massageover the muscles in spasm. Pain relief and antiinflammatoryeffect can be achieved with nonsteroidal antiinflammatorydrugs (NSAIDs). Most acute exacerbations of back painrespond quickly to this therapy. As the pain diminishes, thepatient should be encouraged to begin isometric abdominal andlower extremity exercises. Walking within the limits of comfortalso is encouraged. Sitting, especially riding in a car, isdiscouraged. Malmivaara et al. compared the efficacy of bedrest alone, back extension exercises, and continuation ofordinary activities as tolerated in the treatment of acute backpain. They concluded that continuation of ordinary activitieswithin the limits permitted by pain led to a more rapid recovery.

Education in proper posture and body mechanics is helpfulin returning the patient to the usual level of activity after theacute exacerbation is eased or relieved. This education can takemany forms, from individual instruction to group instruction.Back education of this type is now usually referred to as ‘‘backschool.’’ Although the concept is excellent, the quality andquantity of information provided may vary widely. The work ofBergquist-Ullman and Larsson and others indicates that patienteducation of this type is extremely beneficial in decreasing theamount of time lost from work initially but does little todecrease the incidence of recurrence of symptoms or length oftime lost from work during recurrences. Certainly thecombination of back education and combined physical therapyis superior to placebo treatment. Cohen et al. reviewed 13studies on group back education and concluded that theevidence was insufficient to recommend group education.A study by Galm et al. regarding sacroiliac joint dysfunction inpatients with image-proven herniated nucleus pulposus andsciatica but without motor or sensory deficits found that 75%improved with respect to sciatic and back pain with intensivephysiotherapy.

Numerous medications have been used with varied results insubacute and chronic back and leg pain syndromes. The currenttrend appears to be moving away from the use of strongnarcotics and muscle relaxants in the outpatient treatment ofthese syndromes. This is especially true in the instances ofchronic back and leg pain where drug habituation and increaseddepression are frequent. Oral steroids used briefly can bebeneficial as potent antiinflammatory agents. The many typesof NSAIDs also are helpful when aspirin is not tolerated or is




of little help. Numerous NSAIDs are available for the treatmentof low back pain. When depression is prominent, moodelevators such as amitriptyline can be beneficial in reducingsleep disturbance and anxiety without increasing depression. Inaddition, amitriptyline also decreases the need for narcoticmedication.

Physical therapy should be used judiciously. The exercisesshould be fitted to the symptoms and not forced as an absolutegroup of activities. Patients with acute back and thigh paineased by passive extension of the spine in the prone positioncan benefit from extension exercises rather than flexionexercises. Improvement in symptoms with extension isindicative of a good prognosis with conservative care. On theother hand, patients whose pain is increased by passiveextension may be improved by flexion exercises. Theseexercises should not be forced in the face of increased pain.This may avoid further disc extrusion. Any exercise thatincreases pain should be discontinued. Lower extremityexercises can increase strength and relieve stress on the back,but they also can exacerbate lower extremity arthritis. The truebenefit of such treatments may be in the promotion of goodposture and body mechanics rather than of strength. Hansenet al. compared intensive, dynamic back muscle exercises,conventional physiotherapy (manual traction, flexibility, iso-metric and coordination exercises, and ergonomics counseling),and placebo-control treatment in a randomized, observer blindtrial. Regardless of the method used, patients who completedtherapy reported a decrease in pain. However, physiotherapyappeared to have better results in men, and intensive backexercises gave better results in women. Patients with hardphysical occupations responded better to physiotherapy,whereas patients with sedentary occupations responded betterto intensive back exercises.

Numerous treatment methods have been advanced for thetreatment of back pain. Some patients respond to the use oftranscutaneous electrical nerve stimulation (TENS). Others dowell with traction varying from skin traction in bed with 5 to 8pounds to body inversion with forces of over 100 pounds. Backbraces or corsets may be helpful to other patients. Ultrasound anddiathermy are other treatments used in back pain. The scientificefficacy of many of these treatments has not been proved. Inaddition, all therapy for disc disease is only symptomatic.

EPIDURAL STEROIDS

◆ EPIDURAL STEROIDSThe epidural injection of a combination of a long-acting steroidwith an epidural anesthetic is an excellent method ofsymptomatic treatment of back and leg pain from discogenicdisease and other sources. Most studies show a 60% to 85%short-term success rate that falls to a 30% to 40% long-term(6-month) good result rate. The local effect of the steroids hasbeen shown to last at least 3 weeks at a therapeutic level. In awell-controlled study Berman et al. found that the best resultswere obtained in patients with subacute or chronic leg pain withno prior surgery. They also found that the worst results were in

patients with motor or reflex abnormalities (12% to 14% goodresults). A negative myelogram also was associated with abetter result. Cuckler et al. in a double-blind, randomized studyof epidural steroid treatment of disc herniation and spinalstenosis found no difference in the results at 6 months betweenplacebo and a single epidural injection. Our experienceparallels that of Berman et al. We agree that epidural steroidsare not a cure for disc disease, but they do offer relativelyprolonged pain relief without excessive narcotic intake ifconservative care is elected. Hopwood and Abram observedthat factors associated with poor surgical outcome also wereassociated with a poor outcome from epidural steroid injection.These factors included lower educational levels, smoking, lackof employment, constant pain, sleep disruption, nonradiculardiagnosis, prolonged duration of pain, change in recreationalactivities, and extreme values on psychological scales.

In experienced hands the complication rate from thisprocedure should be small. White, Derby, and Wynne reportedthat the most common problem is a 25% rate of failure to placethe material in the epidural space. Renfrew et al. and el-Khouryet al. observed that the use of fluoroscopic control dramaticallydecreased the failure rate. Another technique-related problem isintrathecal injection with inadvertent spinal anesthesia. Otherreported complications include transient hypotension, difficultyin voiding, severe paresthesias, cardiac angina, headache, andtransient hypercorticoidism. Kushner and Olson reportedretinal hemorrhage in several patients who had epidural steroidinjection for chronic back pain. They recommended carefulconsideration of this procedure in patients who have bleedingproblems and in patients who have only one eye. DeSio et al.reported facial flushing and generalized erythema in patientsafter epidural steroid injection. The most serious complicationreported was bacterial meningitis. The total complication ratein most series is about 5%, and the complications are almostalways transient.

This procedure is contraindicated in the presence ofinfection, neurological disease (such as multiple sclerosis),hemorrhagic or bleeding diathesis, cauda equina syndrome, anda rapidly progressive neural deficit. Rapid injections of largevolumes or the use of large doses of steroid also can increasethe complication rate. The exact effects of intrathecal injectionof steroids are not known. This technique must be used only inthe low lumbar region. We prefer to abort the procedure if abloody tap is obtained or if CSF is encountered.

We prefer to do the procedure in a room equipped forresuscitation and with the capability to monitor the patient. Thisprocedure lends itself well to outpatient use, but the patientmust be prepared to spend several hours to recover from theblock. Methylprednisolone (Depo-Medrol) is the usual steroidinjected. The dosage may vary from 80 to 120 mg. Theanesthetics used may include lidocaine, bupivacaine, orprocaine. Our current protocol is to inject the patient threetimes. These injections are made at 7- to 10-day intervals. Thisensures at least one good epidural injection and decreases thevolume of material injected at each procedure.




TECHNIQUE 39-20 (Brown)

The equipment needed includes material for an appropriateskin preparation, sterile rubber gloves, a 31⁄2-inch, 20-gaugeor 22-gauge disposable spinal needle (45-degree blunt- orcurve-tipped epidural needles are preferred), several dispos-able syringes, bacteriostatic lidocaine, and methylpredniso-lone acetate, 40 mg/ml. The injection may be done with thepatient in the sitting or lateral decubitus position. Anesthe-tize the skin near the midline. Advance the needle until theresistance of the ligamentum flavum is encountered. Thenattach a syringe and slowly advance the needle whileapplying light pressure on the syringe. When the epiduralspace is encountered, the resistance is suddenly lost and theepidural space will accommodate the air. Remove thesyringe and inspect the needle opening for blood or spinalfluid. If there is no flow out of the needle, then inject 3 mlof 1% lidocaine or other appropriate anesthetic. This maybe preceded or followed by the chosen dosage ofmethylprednisolone.

Several variations also can be used. Some physicians usea sterile balloon to indicate the proper space. Others use the‘‘disappearing drop’’ technique, which involves placing adrop of sterile saline over the hub of the needle. When theepidural space is entered, the drop disappears. Caudalinjection also is used, but this may require larger volumes towash the steroid up to the involved level. This method issafer but less reliable than an injection at L4-5.

OPERATIVE TREATMENTOPERATIVE TREATMENTIf nonoperative treatment for lumbar disc disease fails, the nextconsideration is operative treatment. Before this step is taken,the surgeon must be sure of the diagnosis. The patient must becertain that the degree of pain and impairment warrants such astep. Both the surgeon and the patient must realize that discsurgery is not a cure but may provide symptomatic relief. Itneither stops the pathological processes that allowed theherniation to occur nor restores the back to a normal state. Thepatient must still practice good posture and body mechanicsafter surgery. Activities involving repetitive bending, twisting,and lifting with the spine in flexion may have to be curtailed oreliminated. If prolonged relief is to be expected, then somepermanent modification in the patient’s lifestyle may benecessary.

The key to good results in disc surgery is appropriate patientselection. The optimal patient is one with predominant, if notonly, unilateral leg pain extending below the knee that has beenpresent for at least 6 weeks. The pain should have beendecreased by rest, antiinflammatory medication, or evenepidural steroids but should have returned to the initial levelsafter a minimum of 6 to 8 weeks of conservative care. Somemanaged care plans now insist on a trial of physiotherapy. Thework of Hansen et al. is indicative of the problems with such

requirements, not only because of gender and occupationvariations in response to physiotherapy and intensive backexercises, but also because no therapy appeared to have thesame or better results. Physical examination should revealsigns of sciatic irritation and possibly objective evidence oflocalizing neurological impairment. CT, lumbar MRI, ormyelography should confirm the level of involvement consis-tent with the patient’s examination.

Surgical disc removal is mandatory and urgent only in caudaequina syndrome with significant neurological deficit, espe-cially bowel or bladder disturbance. All other disc excisionsshould be considered elective. This should allow a thoroughevaluation to confirm the diagnosis, level of involvement, andthe physical and psychological status of patient. Frequently, ifthere is a rush to the operating room to relieve pain withoutproper investigation, both the patient and physician later regretthe decision.

Regardless of the method chosen to treat a disc rupturesurgically, the patient should be aware that the procedure ispredominantly for the symptomatic relief of leg pain. Patientswith predominant back pain may not be relieved of their majorcomplaint—back pain. Spangfort, in reviewing 2504 lumbardisc excisions, found that about 30% of the patients complainedof back pain after disc surgery. Failure to relieve sciatica wasproportional to the degree of herniation. The best results of99.5% complete or partial pain relief were obtained when thedisc was free in the canal or sequestered. Incomplete herniationor extrusion of disc material into the canal resulted in completerelief for 82% of patients. Excision of the bulging or protrudingdisc that had not ruptured through the annulus resulted incomplete relief in 63%, and removal of the normal orminimally bulging disc resulted in complete relief in 38%,which is near the stated level for the placebo response.Likewise, the incidence of persistent back pain after surgerywas inversely proportional to the degree of herniation. Inpatients with complete extrusions the incidence was about 25%,but with minimal bulges or negative explorations the incidencerose to over 55% (Figs. 39-38 and 39-39).

General Principles for Open Disc SurgeryMost disc surgery is performed with the patient under

general endotracheal anesthesia, although local anesthesia hasbeen used with minimal complications. Patient positioningvaries with the operative technique and surgeon. To position thepatient in a modified kneeling position, a specialized frame orcustom frame modified from the design of Hastings is popular.Positioning the patient in this manner allows the abdomen tohang free, minimizing epidural venous dilation and bleeding(Fig. 39-40). A head lamp allows the surgeon to direct light intothe lateral recesses where a large proportion of the surgery maybe required. The addition of loupe magnification also greatlyimproves the identification and exposure of various structures.Some surgeons also use the operative microscope to furtherimprove visibility. The primary benefit of the operatingmicroscope compared with loupes is the view afforded the




assistant. Roentgenographic confirmation of the proper level isnecessary. Care should be taken to protect neural structures.Epidural bleeding should be controlled with bipolar electrocau-tery. Any sponge, pack, or cottonoid patty placed in the woundshould extend to the outside. Pituitary rongeurs should bemarked at a point equal to the maximal allowable disc depth toprevent accidental biopsy of viscera or aorta. Considerable

research has gone into techniques to prevent epidural fibrosis.Hoyland et al. noted dense fibrous connective tissue aboutpreviously operated nerve roots. They also found fibrillarforeign material within the scar in 55% of patients. This findingshould remind the surgeon to minimize the use of cottonpatties. The placement of autogenous fat appears to be areasonable although not foolproof or complication-free tech-

Fig. 39-38 Percentage relief of sciatica with type of disc herniation. (From Spangfort E: ActaOrthop Scand Suppl 142:1, 1972.)

A B

Fig. 39-39 Types of disc herniation. A, Normal bulge. B, Pro-trusion. C, Extrusion. D, Sequestration.

C D

Fig. 39-40 Kneeling position for lumbar disc excision allowsabdomen to be completely free of external pressure.




nique of minimizing postoperative epidural fibrosis. Commer-cially available products may reduce scar volume, but clinicalbenefit remains uncertain.

◆ Ruptured Lumbar Disc Excision (Open Technique)

TECHNIQUE 39-21After thoroughly preparing the back, identify the spinousprocesses of L3, L4, L5, and S1 by palpation. Make amidline incision 5 to 8 cm long, centered over the interspacewhere the disc herniation is located. Incise the supraspinousligament; then, by subperiosteal dissection, strip the muscles

from the spinous processes and laminae of these vertebraeon the side of the lesion. Retract the muscles either with aself-retaining retractor or with the help of an assistant andexpose one interspace at a time. Verify the location with aroentgenogram so that no mistake is made regarding theinterspaces explored. Secure hemostasis with electrocautery,bone wax, and packs. Leave a portion of each packcompletely outside the wound for ready identification.

Denude the laminae and ligamentum flavum with a curet(Fig. 39-41). Commonly the lumbosacral interspace is largeenough to permit exposure and removal of a herniatednucleus pulposus without removal of any bone. If not,

A

Fig. 39-41 Technique of lumbar disc excision. A, With lamina and ligamentum flavum exposed,use curet to remove the ligamentum flavum from inferior surface of lamina. Kerrison rongeur is usedto remove bone. B, Elevate ligamentum flavum at upper corner and carefully dissect it back toexpose dura and epidural fat below. Patties should be used to protect dura during this procedure.C, Expose dura and root. Remove additional bone if there is any question about adequacy ofexposure. D, Retract nerve root and dural sac to expose disc. Inspect capsule for rent and extrudednuclear material. If obvious ligamentous defect is not visible, then carefully incise capsule of disc.If disc material does not bulge out, press on disc to try to dislodge herniated fragment. E, Carefullyremove disc fragments. It is safest to avoid opening pituitary rongeur until it is inserted into discspace. F, After removing disc, carefully explore foramen, subligamentous region, and beneath durafor additional fragments of disc. Obtain meticulous hemostasis using bipolar cauterization.

B

C

D

EF




remove a small part of the inferior margin of the fifth lumbarlamina. Exposure of the disc at higher levels usuallyrequires removal of a portion of the inferior lamina. Thin theligamentum flavum using a pituitary rongeur to remove thesuperficial layer. Detach the ligamentum from its cephalador caudad laminar attachment using a small curet. Use careto keep the cutting edges of the curet directed posteriorly tominimize the chance of dural laceration. Using an angledKerrison rongeur, preferably one with a thin foot plate andappropriate width, remove the detached ligamentum later-ally and preserve the more medial ligamentum. Keep theKerrison rongeur oriented parallel to the direction of thenerve root to minimize the risk of root injury, and the rootwill be more posterior than is normal due to the dis-placement caused by the herniated disc fragment. Analternative technique that can be used with good lighting andmagnified visual aid is to divide the ligamentum parallelwith its fibers using a no. 11 blade knife. Once the fullthickness of the ligamentum has been divided, bluntlyextend the division across the interspace with a Penfield 4dissector and remove the lateral portion of the ligamentum.The lateral shelving portion of the ligamentum should beexcised, often with a portion of the medial inferior facet togain access to the lateral aspect of the nerve root. Next,retract the dura medially and identify the nerve root. If theroot is compressed by a large extruded fragment, itcommonly will be displaced posteriorly. Retract the nerveroot, once identified, medially so that the underlyingextruded fragment or bulging posterior longitudinal liga-ment can be seen. Occasionally the nerve root adheres to thefragment or to the underlying ligamentous structures andrequires blunt dissection from these structures. If theposition of the root is not known for certain, remove thelamina posterior to the root and medial to the pedicle untilthe root is clearly identified. Bipolar cautery on a low settingcan be used to coagulate the epidural veins and maintainhemostasis. Gelfoam and small cottonoids also are useful.Take care to minimize packing about the nerve root. Retractthe root or dura, identify any bleeding vein, and cauterize itwith a bipolar cautery. Earlier insertion of cotton patties maywell displace fragments from view. The underlying discshould be clearly visible at this time.

Gently retract the nerve with a Love root retractor or ablunt dissector, thus exposing the herniated fragment orposterior longitudinal ligament and annulus. If an extrudedfragment is not seen, carefully palpate the posteriorlongitudinal ligament and seek a defect or hole in theligamentous structures. A microblunt hook can be used forthis. If no obvious abnormality is detected, follow the rootaround the pedicle or even outside the canal in search offragments that may have migrated far laterally. Additionalsearching in the root axilla helps ensure that fragments thathave migrated inferiorly are not missed. If the expectedpathology is not found, obtain another roentgenogram witha blunt dissector at the level of the disc to be certain of the

proper level and review preoperative imaging studies toconfirm proper sidedness.

If the herniated fragment is especially large, it is muchbetter to sacrifice a portion of the facet to obtain a morelateral exposure than to risk injury to the root or caudaequina by excessive medial retraction. With such a lateralexposure the nerve root usually can be elevated, and theherniated fragment can be teased from beneath the nerveroot and cauda equina, even when the fragment is largeenough to block the entire canal. If the fragment is verylarge as with cauda equina lesions typically, a bilaterallaminectomy is preferred to allow safer removal. If the disccannot be teased from under the root, make a cruciateincision in the disc laterally. Gently remove disc fragmentsuntil the bulge has been decompressed to allow gentleretraction of the root over the defect.

If the herniation is upward or downward, further removalof bone from the lamina and facet edges may be required.The herniated nucleus pulposus may be covered by a layerof posterior longitudinal ligament or may have rupturedthrough this structure. In the latter event, carefully lift theloose fragments out by suction, blunt hook, or pituitaryforceps. If the ligament is intact, incise it in a cruciatefashion and remove the loose fragments. The tear or hole inthe annulus should then be identifiable in most instances.The cavity of the disc can be entered through this hole, oroccasionally the hole may need to be enlarged to allowinsertion of the pituitary forceps. Remember that theanterior part of the annulus is adjacent to the aorta, venacava, or iliac arteries and veins and that one of thesestructures can be injured if one proceeds too deeply.Remove other loose fragments of nucleus pulposus with thepituitary forceps and remove additional nuclear materialalong with the central portion of the cartilaginous plates,both above and below as necessary.

When placing instruments into the disc space do notpenetrate beyond a depth of 15 mm to avoid injury to theanterior viscera. Then carry out a complete search foradditional fragments of nucleus pulposus, both inside andoutside the disc space. Additional fragments commonlymigrate medially beneath the posterior longitudinal liga-ment but outside the annulus and can easily be missed. Thenremove all cotton pledgets and control residual bleedingwith Gelfoam and bipolar cautery. Forcefully irrigate anyloose fragments from the disc space using a syringe with aspinal needle placed into the disc space under direct visionuntil no fragments are returned with the irrigating solution.Close the wound routinely with absorbable sutures in thesupraspinous ligament and subcutaneous tissue. Variousabsorbable sutures are most commonly used in routine skinclosure. Staples are avoided for patient comfort.

AFTERTREATMENT. Neurological function is closely mon-itored after surgery. The patient is allowed to turn in bed at willand to select a position of comfort such as a semi-Fowler




position. Pain should be controlled with oral medication.Muscle relaxants are used postoperatively as well. Bladderstimulants can be used to assist voiding. The patient is allowedto stand with assistance on the evening after surgery to go to thebathroom. Discharge is permitted when the patient is able towalk and void. Currently most patients are discharged within24 hours after surgery. Isometric abdominal and lowerextremity exercises are started. The patient is instructed tominimize sitting and riding in a vehicle. Increased walking ona daily basis is recommended. Lifting, bending, and stoopingare prohibited for the first several weeks. As the patient’sstrength increases, gentle isotonic leg exercises are started.

Between the fourth and sixth postoperative week, backschool instruction is resumed or started, provided that pain isminimal. Lifting, bending, and stooping are gradually restartedafter the sixth week. Increased sitting is allowed as painpermits, but long trips are to be avoided for at least 4 to 6weeks. Lower extremity strength is increased from the eighth totwelfth postoperative weeks. Patients with jobs requiring muchwalking without lifting are allowed to return to work within 2to 3 weeks. Patients with jobs requiring prolonged sittingusually are allowed to return to work within 4 to 6 weeksprovided minimal lifting is required. Patients with jobsrequiring heavy labor or long periods of driving are not allowedto return to work until 6 to 8 weeks and then to a modified duty.Some patients with jobs requiring exceptionally heavy manuallabor may have to permanently modify their occupation or seeka lighter occupation. Keeping the patient out of work beyond3 months rarely improves recovery or pain relief.

◆ Microlumbar Disc ExcisionMicrolumbar disc excision has replaced the standard openlaminectomy as the procedure of choice for herniated lumbardisc. This procedure can be done on an outpatient basis andallows better lighting, magnification, and angle of view with amuch smaller exposure. Because of the limited dissectionrequired there is less postoperative pain and a shorter hospitalstay. Zahrawi reported 103 outpatient microdiscectomies,noting 88% excellent and good results in the 83 who responded.Newman reported 75 conventional laminectomies done on anoutpatient basis and noted 2 complications unrelated to theprocedure or the outpatient setting. Kelly et al. noted lesspulmonary morbidity and temperature elevation in patientsafter microlumbar discectomy. Numerous other investigatorssuch as Silvers, Zahrawi, Lowell et al., and Moore et al.reported excellent results with low morbidity and early returnto activity using microlumbar disc excision. Williams, theoriginator of the term, questioned its current usage, since theconcept of the technique has changed over the years.

Microlumbar discectomy requires an operating microscopewith a 400-mm lens, special retractors, a variety of small-angled Kerrison rongeurs of appropriate length, micro instru-ments, and preferably a combination suction–nerve rootretractor. The procedure is performed with the patient prone. Avacuum pack is molded around the patient, and an inflatablepillow is positioned under the abdomen and is removed after

evacuation of the vacuum pack. Alternatively, the Andrew’stype frame previously described can be used. The microscopecan be used from skin incision to closure. However, the initialdissection can be done under direct vision. A lateralroentgenogram is taken to confirm the level.

TECHNIQUE 39-22 (Williams, Modified)

Make the incision from the spinous process of the uppervertebra to the spinous process of the lower vertebra at theinvolved level. This usually results in a 1-inch (2.5-cm) skinincision (Fig. 39-42). Maintain meticulous hemostasis withelectrocautery as the dissection is carried to the fascia.Incise the fascia at the midline using electrocautery. Theninsert a periosteal elevator in the midline incision. Usinggentle lateral movements separate the deep fascia andmuscle subperiosteally from the spinous processes andlamina. Obtain a lateral roentgenogram with a metal clampattached to the spinous process to verify the level. Now,using a Cobb elevator gently sweep the remaining muscularattachments off in a lateral direction exposing the interlami-nar space and the edge of each lamina. Meticulouslycauterize all bleeding points. Insert the microlumbarretractor into the wound and adjust the microscope. Identifythe ligamentum flavum and lamina. Use a pituitary rongeurto remove the superficial leaf of the ligamentum. Using a no.15 blade with the microscope, carefully incise the thinnedligamentum flavum superficially. Then use a Penfield no. 4dissector to perforate the ligamentum. Minimal force shouldbe used in this maneuver to prevent penetration of the dura.Once the ligamentum is open, use a 45-degree Kerrisonrongeur to remove the ligamentum flavum laterally. Thelamina, facet, and facet capsule should remain intact.However, one must remove the ligamentum flavum andbone from the lamina as needed to clearly identify the nerveroot. Once identified, carefully mobilize the root medially;this may require some bony removal. Gently dissect thenerve free from the disc fragment to avoid excessive tractionon the root. Bipolar cautery for hemostasis is very helpful.Once mobilized, retract the root medially. Maintain theorientation of the Kerrison parallel to that of the nerve rootat all times. Once identified, the nerve root can be gentlymobilized and retracted medially. Then make an extraduralexploration using a 90-degree hook. In large herniations thenerve root appears as a large, white, glistening structure andcan easily be mistaken for a ruptured disc. Follow the rootto the pedicle if necessary to be certain of its location. Thesmall opening and magnification can make the edge of thedural sac appear as the nerve root. When using bipolarcautery make sure only one side is in contact with the nerveroot to avoid thermal injury to the nerve. Also, when usinga Kerrison rongeur for bone or ligamentum removal, orientit parallel to the course of the nerve root as much as possibleto minimize the risk of nerve root or dural injury. Epiduralfat is not removed in this procedure. Insert the suction–nerveroot retractor, with its tip turned medially under the nerveroot, and hold the manifold between the thumb and index

continued




finger. With the nerve root retracted, the disc will now bevisible as a white, fibrous, avascular structure. Small tearsmay be visible in the annulus under the magnification. Nowenlarge the annular tear with a Penfield no. 4 dissector andremove the disc material with the microdisc forceps. Do not

insert the instrument into the disc space beyond the angle ofthe jaws, which usually is about 15 mm, to minimize the riskof anterior perforation and vascular injury. Remove theexposed disc material. Do not curet the disc space. Inspectthe root and adjacent dura for disc fragments. Irrigate the

A B

L3

L4

L5

Ilium

Sacrum

Fig. 39-42 Microlumbar disc excision. A, Position ofskin incision for microlumbar disc excision. B, Entranceof epidural space by penetration of ligamentum flavum.C, Removal of ligamentum flavum with Kerrison rongeur.D, Dilation of annular defect before removal of disc frag-ment. E, Decompression of disc hernia by repeated smallevacuations with discectomy forceps. (Redrawn fromCauthen JC: Lumbar spine surgery, Baltimore, 1983,Williams & Wilkins.)

Spinousprocess

Lamina

Penfield no. 4dissectorLigamentum

flavumSpinousprocess

Facet jointcapsule

Lamina

Micro 45-degree angleKerrison rongeurLigamentum

flavumSpinousprocess

LaminaLamina

LaminaLamina

Penfield no. 4 dissector(into opening in HNP)

Nerveroot

Facet

Suctionretractor

Disc forceps

Nerves

VertebraDisc

Spinous process

Nerveroot

Suctionretractor

C D

E




disc space using a lock syringe and 18-gauge spinal needleinserted into the disc space. Obtain meticulous hemostasis.If the expected pathology is not found, review preoperativeimaging studies for level and sidedness. Also obtain a repeatroentgenogram with a metallic marker at the disc level toverify the level. Be aware of bony anomalies that may alterthe numbering of the vertebrae on imaging studies. Closethe fascia and the skin in the usual fashion, using absorbablesutures.

AFTERTREATMENT. Postoperative care is similar to thatafter standard open disc surgery. Typically this procedure isdone on an outpatient basis. Injecting the paraspinal muscleson the involved side with Bupivacaine 0.5% with epinephrineat the beginning of the procedure and additional Bupivacaineat the conclusion aids patient mobilization immediatelypostoperatively.

Endoscopic TechniquesEndoscopic techniques have been developed over the past

several years with the purported advantage of shortenedhospital stay and faster return to activity. These techniquesgenerally are variations of the microdiscectomy techniqueusing an endoscope rather than the microscope and differenttypes of retractors. Thus far the purported advantages have notbeen demonstrated. This remains another alternative technique.Each system is somewhat unique, and the reader is referred tothe technique guide of the various manufacturers for details.The basic principles remain the same as with microdiscectomy.

Additional Exposure TechniquesA large disc herniation or other pathological condition such

as lateral recess stenosis or foraminal stenosis may require agreater exposure of the nerve root. Usually the additionalpathological condition can be identified before surgery. If theextent of the lesion is known before surgery, the properapproach can be planned. Additional exposure includeshemilaminectomy, total laminectomy, and facetectomy. Hemi-laminectomy usually is required when identifying the root isa problem. This may occur with a conjoined root. Totallaminectomy usually is reserved for patients with spinalstenoses that are central in nature, which occurs typically incauda equina syndrome. Facetectomy usually is reserved forforaminal stenosis or severe lateral recess stenosis. If more thanone facet is removed, then a fusion should be considered inaddition. This is especially true in the removal of both facetsand the disc at the same interspace in a young, active personwith a normal disc height at that level.

On rare occasions disc herniation has been reported to beintradural. An extremely large disc that cannot be dissectedfrom the dura or the persistence of an intradural mass afterdissection of the disc should alert one to this potential problem.Excision of an intradural disc requires a transdural approach,which increases the risk of complications from CSF leak andintradural scarring.

A disc that is far lateral may require exposure outside thespinal canal. This area is approached by removing theintertransverse ligament between the superior and inferiortransverse processes lateral to the spinal canal. The disc herniausually is anterior to the nerve root that is found in a mass offat below the ligament. A microsurgical approach or a per-cutaneous approach are good methods for dealing with thisproblem. Maroon et al. also recommended discography toconfirm the lesion before surgery. Epstein noted little differencebetween lateral intertransverse exposure, facetectomy, and amore extensive hemilaminectomy with medial facetectomy.Donaldson et al. recommended the lateral approach after firstfinding the root medially and dissecting laterally down to aprobe on top of the root (Fig. 39-43), and Strum et al.recommended an anterolateral approach.

Lumbar Root AnomaliesLumbar nerve root anomalies (Figs. 39-44 to 39-47) are

more common than may be expected, and they rarely arecorrectly identified with myelography. Kadish and Simmonsidentified lumbar nerve root anomalies in 14% of 100 cadaverexaminations. They noted nerve root anomalies in only 4% of100 consecutive metrizamide myelograms. They identified fourtypes of anomalies. Type I is an intradural anastomosis betweenrootlets at different levels. Type II is an anomalous origin of thenerve roots. They separated this type into four subtypes:(1) cranial origin, (2) caudal origin, (3) combination of cranialand caudal origin, and (4) conjoined nerve roots. Type III is anextradural anastomosis between roots. Type IV is the extraduraldivision of the nerve root. The surgeon must be aware of thepossibility of anomalous roots hindering the disc excision. Thismay require a wider exposure. Sectioning of these roots resultsin irreversible neurological damage. Traction on anomalousnerve roots has been suggested as a cause of sciatic symptomswithout disc herniation.

L5

L4 L4 root

L4-L5 disc

Fig. 39-43 Lateral approach for discectomy. L4 foraminotomyallows exposure of root. (Redrawn from Donaldson WF et al: Spine18:1264, 1993; original by P Gretsky.)




Results of Open (Micro or Standard) Surgeryfor Disc HerniationNumerous retrospective and some prospective reviews of

open disc surgery are available. The results of these series varygreatly with respect to patient selection, treatment method,evaluation method, length of follow-up, and conclusions. Goodresults range from 46% to 97%. Complications range fromnone to over 10%. The reoperation rate ranges from 4% to over20%. The detailed studies of Spangfort, Weir, and Rish aresuggested for more detailed analysis. A comparison betweentechniques also reveals similar reports.

Several points do stand out in the analysis of the results oflumbar disc surgery. Patient selection appears to be extremelyimportant. Several studies noted that a low educational level issignificantly related to poor results of surgery. The works ofWiltse and Rocchio, and Gentry indicate that valid results of theMMPI (hysteria and hypochondriasis T scores) are very goodindicators of surgical outcome regardless of the degree of thepathological condition. The extremely detailed work of Weirsuggests that the duration of the current episode, the age of thepatient, the presence or absence of predominant back pain,the number of previous hospitalizations, and the presence orabsence of compensation for a work injury are factors affectingfinal outcome. Spangfort’s work also indicates that the softerthe findings for disc herniation clinically and at the time ofsurgery, the lower the chance for a good result.

Complications of Open Disc ExcisionThe complications associated with standard disc excision

and microlumbar disc excision are similar. Spangfort’s series(Table 39-9) of 2503 open disc excisions lists a postoperativemortality of 0.1%, a thromboembolism rate of 1.0%, apostoperative infection rate of 3.2%, and a deep disc spaceinfection rate of 1.1%. Postoperative cauda equina lesions

developed in five patients. Laceration of the aorta or iliac arteryalso has been described as a rare complication of this operation.Rish, in a more recent report with a 5-year follow-up, noted atotal complication rate of 4% in a series of 205 patients. Themajor complication in his series involved a worseningneuropathy postoperatively. There was one disc space infection

Fig. 39-44 Type I nerve root anomaly: intradural anastomosis.(From Kadish LJ, Simmons EH: J Bone Joint Surg 66B:411, 1984.)

A B

Fig. 39-45 Type II: anomalous origin of nerve roots. A, Cranialorigin. B, Caudal origin. C, Closely adjacent nerve roots. D, Con-joined nerve roots. (From Kadish LJ, Simmons EH: J Bone JointSurg 66B:411, 1984.)

C D

Fig. 39-46 Type III nerve root anomaly: extradural anastomosis.(From Kadish LJ, Simmons EH: J Bone Joint Surg 66B:411, 1984.)




and one wound infection. Dural tears with CSF leaks,pseudomeningocele formation, CSF fistula formation, andmeningitis also are possible but are more likely after re-operation. The complications of microlumbar disc excisionappear to be lower than with standard laminectomy. Alexanderreviewed patients who had sustained incidental durotomy at thetime of disc surgery and found no perioperative morbidity orcompromise of results if the dura was repaired. They noted a4% incidence of this complication in 450 discectomies.

The presence of a dural tear or leak results in the potentiallyserious problems of pseudomeningocele, CSF leak, andmeningitis. Eismont, Wiesel, and Rothman suggested five basicprinciples in the repair of these leaks (Fig. 39-48):

1. The operative field must be unobstructed, dry, and wellexposed.

2. Dural suture of a 4-0 or 6-0 gauge with a tapered orreverse cutting needle is used in either a simple orrunning locking stitch. If the leak is large or inaccessible,

a free fat graft or fascial graft can be sutured to the dura.Fibrin glue applied to the repair also is helpful but willnot seal a significant leak.

3. All repairs should be tested by using the reverseTrendelenburg position and Valsalva maneuvers.

4. Paraspinous muscles and overlying fascia should beclosed in two layers with nonabsorbable suture used in awatertight fashion. Drains should not be used.

5. Bed rest in the supine position should be maintained for4 to 7 days after the repair of lumbar dural defects. Alumbar drain should be placed if the integrity of theclosure is questionable.

The development of headaches on standing and a stormypostoperative period should alert one to the possibility of anundetected CSF leak. This can be confirmed by MRI studies.

The presence of glucose in drainage fluid is not a reliablediagnostic test. On rare occasions a pseudomeningocele hasbeen implicated as a cause of persistent pain from pressure ona nerve root by the cystic mass.

◆ Dural Repair Augmented with Fibrin GlueDural repair can be augmented with fibrin glue. Pressure testingof a dural repair without fibrin glue reveals that the dura is ableto withstand 10 mm of pressure on day 1 and 28 mm on day 7.With fibrin glue the dura is able to withstand 28 mm on day 1and 31 mm on day 7. Fibrin glue also can be used in areas oftroublesome bleeding or difficult access for closure such as theventral aspect of the dura.

TECHNIQUE 39-23Mix 20,000 U of topical thrombin and 10 ml of 10 calciumchloride. Draw the mixture up into a syringe. In anothersyringe, draw 5 U of cryoprecipitate and inject equalquantities of each onto the dural repair or tear. Allow theglue to set to the consistency of ‘‘Jello’’ (Box 39-10).Commercially available kits also are available.

Free Fat GraftingFat grafting for the prevention of postoperative epidural

scarring has been suggested by Kiviluoto; Jacobs, McClain,and Neff; and Bryant, Bremer, and Nguyen. The study byJacobs et al. indicated that free fat grafts were superior toGelfoam in the prevention of postoperative scarring. Thecurrent rationale for free fat grafting appears to be the pos-sibility of making any reoperation easier. Unfortunately, thebenefit of reduced scarring and its relationship to the preventionof postoperative pain have not been established, neither has theincreased ease of reoperation in patients in whom fat graftingwas performed. Caution should be taken in applying a fat graftto a large laminar defect because this has been reported to resultin an acute cauda equina syndrome in the early postoperativeperiod. We currently reserve the use of a fat graft (or fascialgrafts) for dural repairs and small laminar defects where thegraft is supported by the bone. A study by Jensen et al. found

Fig. 39-47 Type IV nerve root anomaly: extradural division.(From Kadish LJ, Simmons EH: J Bone Joint Surg 66B:411, 1984.)

Table 39-9 Complications of Lumbar DiscSurgery

Complication Incidence (%)

1. Cauda equina syndrome 0.22. Thrombophlebitis 1.03. Pulmonary embolism 0.44. Wound infection 2.25. Pyogenic spondylitis 0.076. Postoperative discitis 2.0 (1122 patients)7. Dural tears 1.68. Nerve root injury 0.59. Cerebrospinal fluid fistula *

10. Laceration of abdominal vessels *11. Injury to abdominal viscera *

Modified from Spangfort EV: Acta Orthop Scand Suppl 142:65, 1972.*Rare occurrence (numbers 10 and 11 not identified in Spangfort’s study butreported elsewhere).




that fat grafts decreased the dural scarring but not radicular scarformation. The clinical outcome was not improved.

The technique of free fat grafting is straightforward. At theend of the procedure, just before closing, take a large piece ofsubcutaneous fat and insert it over the laminectomy defect. If

the patient is thin, a separate incision over the buttock may berequired to get sufficient fat to fill the defect.

CHEMONUCLEOLYSISCHEMONUCLEOLYSISChemonucleolysis has been used in the United States for morethan 30 years. The enzyme was released for general use by theFood and Drug Administration (FDA) in December of 1982.Before its release in the United States it was used extensivelyin Europe and Canada. A wealth of experimental and clinicalinformation exists concerning the technique and the enzyme.Specific guidelines have been suggested by the FDA regardingthe use of the enzyme in the United States. The initialenthusiasm for the use of chymopapain has all but vanished inthe United States; however, the use of this enzyme is stillpopular in Europe and elsewhere, with therapeutic resultssimilar to surgery.

Because of the disclosure of neurological sequelae and othercomplications, the original guidelines issued in January of 1983were radically changed. Those interested in performing thetechnique should contact the pharmaceutical companies that

Fig. 39-48 A, Illustration of duralrepair using running-locking duralsuture on taper or reverse-cutting,one-half-circle needle. A smaller-sized suture should be used. Useof suction with sucker and smallcotton pledgets is essential to pro-tect nerve roots while operative fieldis kept dry of CSF. B, Single duralstitches can be used to achieveclosure, each suture end being leftlong. Second needle then is attachedto free suture end, and ends of su-ture are passed through piece ofmuscle or fat, which is tied downover repaired tear to help to achievewatertight closure. Whenever duralmaterial is inadequate to allowclosure without placing excessivepressure on underlying neuraltissues, free graft of fascia or fascialata, or freeze-dried dural graft,should be secured to margins ofdural tear using simple sutures ofappropriate size. C, For small duraldefects in relatively inaccessibleareas, transdural approach can beused to pull small piece of muscleor fat into defect from inside out,thereby sealing CSF leak. Cen-tral durotomy should be largeenough to expose defect from duralsac. Durotomy is then closed instandard watertight fashion. (FromEismont FJ, Wiesel SW, Roth-man RH: J Bone Joint Surg 63A:1132, 1981.)

B

AC

BOX 39-10 • Fibrin Glue

INGREDIENTSTwo vials of topical thrombin, 10,000 U each10 ml of calcium chloride5 U of cryoprecipitateTwo 5-ml syringesTwo 22-gauge spinal needles

INSTRUCTIONSDo not use saline that comes with thrombinMix thrombin and calcium chlorideDraw mixture into syringeDraw cryoprecipitate into second syringeApply equal amounts to area of needAllow to set to a ‘‘Jello’’ consistency




produce the drug for information regarding training andcertification in the technique. Treating physicians also areencouraged to frequently check the package insert accompa-nying the drug and the information bulletins sent out by theFDA and the pharmaceutical companies regarding any newchanges in the protocol or use of the enzyme. Careful patientselection and proficiency in performing this procedure aremandatory.

The indications for the use of chemonucleolysis are thesame as for open surgery for disc herniation. Fraser reported theresults of 60 patients treated for lumbar disc herniation in a2-year double-blind study of chemonucleolysis. At 2 years 77%of the patients treated with chymopapain were improved,whereas only 47% of the saline injection group were improved.At 2 years from injection 57% of the chymopapain group werepain-free compared with 23% of the placebo group. Numerousother studies of the efficacy of the drug place the good orexcellent results between 40% and 89%, which is comparableto the clinical reports for open surgery (Table 39-10).Tregonning et al. reviewed 145 patients who had receivedchymopapain injection and 91 patients who had laminectomy at10-year follow-up and concluded that the surgically treatedgroup had slightly better results than the chymopapain group.Javid compared 100 patients who had laminectomy with 100patients who had chemonucleolysis and reported that patientswho had received chymopapain had better results with respectto 6-month overall improvement, short-term improvement innumbness and motor strength, and longer improvement insensory status. Also, chymopapain was significantly lessexpensive than laminectomy. Nordby and Wright reviewed 45clinical studies of chymopapain and laminectomy. Theyconcluded that chemonucleolysis was somewhat less effectivethan open disc excision, but it did avoid the trauma of surgeryand postoperative fibrosis.

As with open disc surgery, this technique is not applicable inall lumbar disc herniations. The use of the drug is limited to thelumbar spine. The patient optimally has predominantlyunilateral leg pain and localized neurological findings con-sistent with confirmatory testing with MRI, CT, or myelogra-

phy. Patients with moderate lateral recess or foraminal stenosismay worsen after the procedure because of collapse of the discspace and narrowing of the foraminal opening. Large discherniations may not shrink sufficiently to result in relief ofsymptoms, and sequestered discs may be untouched by theenzyme. Smith et al. reported cauda equina syndromes in threepatients after chymopapain was injected after a myelogramrevealed a complete block.

Chymopapain injection is specifically contraindicated inpatients with a known sensitivity to papaya, papaya derivatives,or food containing papaya, such as meat tenderizers. Othercontraindications include severe spondylolisthesis, severe,progressive neurological deficit or paralysis, and evidence ofspinal cord tumor or a cauda equina lesion. The enzyme cannotbe injected in a patient who has been previously injected,regardless of the level injected. Use of chymopapain is limitedto the lumbar intervertebral discs. Relative contraindicationsinclude allergy to iodine or iodine contrast material, use of theenzyme in a previously operated disc, patients with elevatedallergy studies such as radioallergosorbent (RAST), Chymo-Fast, and skin testing with the drug, and patients with a severeallergic history, especially with a previous anaphylactic attack.

Spinal Instability from DegenerativeDisc DiseaseSpinal Instability from DegenerativeDisc DiseaseFarfan defined spinal instability (caused by degenerative discdisease) as a clinically symptomatic condition without newinjury, in which a physiological load induces abnormally largedeformations at the intervertebral joint. Biomechanical studieshave revealed abnormal motion at vertebral segments withdegenerative discs and the transmission of the load to the facetjoints. Numerous attempts at roentgenographic definition ofspinal instability with disc disease have resulted in morecontroversy than agreement as to a standard method ofmeasurement. The method described by Knutsson is simple andrelatively efficient in determining anteroposterior motion. The

Table 39-10 Results and Complications of Chemonucleolysis and Open Disc Excision

Results (percent)

Technique Year

No.

Performed Excellent

Partial/

Good None Worse Complications Reoperation

Persistent

Back Pain

Open Disc

Semmes 1955 1440 53.6 43.3 1.7 1.4 NA 6.3

Spangfort 1972 2503 76.9 17.0 5.0 0.5 8.0 31.5

Weir 1979 100 73.0 22.0 3.0 1.0 NA NA

Rish 1984 57 74.0 17.0 9.0 4.0 18.0

Chemonucleolysis

Illinois trial 1982 273 90.0 10.0 1.1

Javid 1983 40 82.0 18.0

Nordby 1983 641 55.0 25.0 20.0 NA NA




fourth edition of the American Medical Association Guide tothe Evaluation of Permanent Impairment defined instability asan anterior slip of 5 mm or more in the thoracic or lumbar spine(Fig. 39-49, A) or a difference in the angular motion of twoadjacent motion segments more than 11 degrees from T1 to L5and motion greater than 15 degrees at L5-1 compared with L4-5(Fig. 39-49, B). There is little controversy as to the surgicaltreatment of lumbar spinal instability and spinal fusion of theunstable segments. The type of fusion performed and theindications for fusion are areas of controversy.

The major problem in spinal instability is the correlation ofthe patient’s symptoms of giving way, catching, and predomi-nant back pain to the roentgenographic identification ofinstability. Other factors such as concomitant spinal stenosis,disc herniation, and psychological problems only complicateany evaluation of spinal instability. Currently the decision forsurgery for clinically significant lumbar spine instability causedby degenerative disc disease should be made on an individualpatient basis with all the factors and risks weighed carefully.

DISC EXCISION AND FUSIONDISC EXCISION AND FUSIONThe necessity of lumbar fusion at the same time as disc excisionwas first suggested by Mixter and Barr. In the first 20 years aftertheir discovery the combination of disc excision and lumbarfusion was common. More recent data comparing disc excisionalone with the combination of disc excision and fusion byFrymoyer et al. and others indicate that there is little if anyadvantage to the addition of a spinal fusion to the treatment ofsimple disc herniation. These studies do indicate that spinalfusion increases the complication rate and lengthens recovery.The indications for lumbar fusion should be independent of theindications for disc excision for sciatica.

LUMBAR VERTEBRAL INTERBODY FUSIONLUMBAR VERTEBRAL INTERBODY FUSIONAnterior lumbar intervertebral fusion (ALIF) and posteriorlumbar intervertebral fusion (PLIF) have been suggested asdefinitive procedures for lumbar disc disease. Biomechanicallythe lumbar interbody fusion offers the greatest stability. Italso eliminates the disc segment as a further source of pain.The primary problems are the more involved and poten-tially dangerous dissection, the risk of graft extrusion, andpseudarthrosis.

Most series of these fusions include a significant number ofsalvage procedures and complex pathological conditions, thusmaking direct comparison with primary disc surgery difficult.The routine use of such procedures for simple lumbar discherniation with sciatica is not justified.

Most often, different types of grafts are taken from the iliaccrest; however, hollow, perforated cylinders filled withautologous bone are now available for use in posterior andanterior lumbar intervertebral fusion. These cylinders are notindicated for spondylolisthesis greater than grade 1, osteopenia,malignancy, or gross obesity. Kuslich and Dowdle reported98% fusion at one level anteriorly and 89% fusion at two levelswith a slightly better functional improvement than the fusionrates using this device. This device also can be introduced bya percutaneous, laparoscopic anterior approach. The laparo-scopic approach requires a team consisting of a laparoscopicgeneral surgeon, spine surgeon, anesthesiologist, cameraoperator, scrub nurse, circulating nurse, and a radiologytechnician. It is strongly advised that the team attend a courseon this technique or observe several cases before attemptingsuch a procedure.

◆ Anterior Lumbar Interbody Fusion

TECHNIQUE 39-24Place the patient supine on a radiolucent operating table.Support the lumbar spine with a rolled sheet or inflatablebag. Prepare and drape the patient’s abdomen from upperchest to groin, leaving the iliac crests exposed for obtainingbone grafts. Expose the lumbar spine through a transab-dominal or retroperitoneal approach as desired. Mobilize thegreat vessels over the segment to be excised. Ligate themedian artery and vein at the bifurcation of the aorta toprevent tearing this structure when exposing the disc at L4-5or L5-S1.

Identify and inspect all major structures before and afterdisc excision and fusion. Use anteroposterior fluoroscopy toconfirm the proper disc level. Then incise the anteriorlongitudinal ligament superiorly or inferiorly over the edgeof the vertebral body. Elevate the ligament as a flap ifpossible. Next remove the annular and nuclear material ofthe disc. The use of magnification can be beneficial as thedissection nears the posterior longitudinal ligament. Re-move all nuclear material from the disc space.

A

Fig. 39-49 Loss of motion segment integrity. A, Translation.B, Angular motion. (From American Medical Association:Guide to the evaluation of permanent impairment, ed 4, Chicago,1993, AMA.)

B




Techniques for fusion vary. Some prefer to use dowelgrafts to fill the space. Others prefer to use tricortical iliacgrafts (Fig. 39-50). Obtain the grafts from the iliac crest asdescribed for anterior cervical fusions (Chapter 36). Preparethe graft area for the desired grafting technique. We prefertricortical grafts for this fusion. Good results using fibulargrafts and banked bone also have been reported. Prepare thevertebrae by curetting the endplates to cancellous boneposteriorly. Then carefully make a slot in the vertebra toaccommodate the grafts; use an osteotome slightly largerthan the width of the disc space for this purpose and directthe cut toward the inferior vertebral body. Try to leave theupper and lower lips of the vertebral bodies intact. Removeenough tricortical iliac bone to allow insertion of at leastthree individual grafts. Fashion the grafts to fit snugly in thespace with a laminar spreader in place. Insert the grafts sothat the cancellous portions face the decorticated endplates.The grafts should be 3 to 4 mm shorter than theanteroposterior diameter of the vertebral body. Impact thegrafts and seat them behind the anterior rim of the vertebralbodies. Usually three such grafts can be inserted. Addadditional cancellous chips around the grafts. Suture theanterior longitudinal ligament. Close the retroperitoneumand abdomen in the usual manner.

AFTERTREATMENT. The patient is allowed to sit as soon aspossible. Extension of the lumbar spine is prohibited for at least6 weeks. Bracing or casting is left to the discretion of thesurgeon after considering the stability of the grafts andreliability of the patient.

◆ Posterior Lumbar Interbody Fusion

TECHNIQUE 39-25 (Cloward)

Position the patient in the prone or kneeling position asdesired. Expose the spine through a midline incisioncentered over the level of the pathological condition. Stripthe muscle subperiosteally from the lamina bilaterally. Insertthe laminar spreader between the spinous processes at thelevel of pathological findings. Open and remove theligamentum flavum from the midline laterally. Enlargethe opening laterally by removing the lower one third of theinferior facet and the medial two thirds of the superior facet(Fig. 39-51, A). The upper lamina also can be thinned byundercutting to increase the anteroposterior diameter of thecanal. Retract the lower nerve root and dura to the midlineand protect it with the self-retaining nerve root retractor.Cauterize the epidural vessels with bipolar cautery. Cut outthe disc and vessels over the annulus laterally. Remove as

A

Fig. 39-50 Anterior lumbar intervertebral fusion (ALIF) can be performed using tricortical iliaccrest graft (A) or fibular grafts (B). (A from Ruge D, Wiltse LL: Spinal disorders: diagnosis andtreatment, Philadelphia, 1977, Lea & Febiger; B from Wiltse LL: Instr Course Lect 28:207, 1979.)

B




much disc material as possible (Fig. 39-51, B). Remove athin layer of the endplates posteriorly. Repeat this processon the opposite side. Remove the remaining anterior edgesof the endplates to the anterior longitudinal ligament. Thismust be done under direct vision to avoid injury to the greatvessels. Prepare a surface of bleeding cancellous bone onboth vertebral bodies. Obtain tricortical iliac crest grafts aspreviously noted from the posterior iliac crest. (Clowardused frozen human cadaver bone grafts.) Shape the grafts tobe slightly shorter and the same height or slightly higherthan the disc shape. Tamp the first graft in place and lever itmedially to allow insertion of the remaining grafts. Repeatthe procedure on the opposite side (Fig. 39-51, C). Removethe laminar spreader and check the graft for stability.Close the wound in the usual fashion.

AFTERTREATMENT. Aftertreatment is the same as forlumbar discectomy (p. ••••). Early walking is encouraged.

Failed Spine Surgery

Failed Spine SurgeryOne of the greatest problems in orthopaedic surgery andneurosurgery is the treatment of failed spine surgery. Numerous

reasons for the failures have been advanced. The best resultsfrom repeat surgery for disc problems appear to be related tothe discovery of a new problem or identification of a previouslyundiagnosed or untreated problem. Waddell et al. suggestedthat the best results from repeat surgery occur when the patienthad experienced 6 months or more of complete pain relief afterthe first procedure, when leg pain exceeded back pain, andwhen a definite recurrent disc could be identified. Theyidentified adverse factors such as scarring, previous infection,repair of pseudarthrosis, and adverse psychological factors.Similar factors were identified by Lehmann and LaRocca andFinnegan et al. Satisfactory results from reoperation have beenreported to be from 31% to 80%. Patients should expectimprovement in the severity of symptoms rather than completerelief of pain. As the frequency of repeat back surgeriesincreases, the chance of a satisfactory result drops precipi-tously. Spengler et al. and Long et al. observed that the majorcause of failure is improper patient selection.

The recurrence or intensification of pain after disc surgeryshould be treated with the usual conservative methods initially.If these methods fail to relieve the pain, the patient should becompletely reevaluated. Frequently a repeat history andphysical examination will give some indication of the problem.Additional testing should include psychological testing, my-elography, MRI to check for tumors or a higher disc herniation,and reformatted CT scans to check for areas of foraminal

A B

Fig. 39-51 Posterior lumbar in-terbody fusion technique. A, Bilat-eral laminotomy with preservationof facets. Control of epiduralhemorrhage. Dipolar or insulatedcoagulation forceps are used on leftside. On right side, epidural hem-orrhage is controlled by impactedsurgical tampons. Impacted surgi-cal tampons also push nerve rootmedially and expose disc spacewithout need for nerve root retrac-tor. B, After intervertebral rimsare removed, cleavage of disc at-tachment to cortical plate is identi-fied. Curved, up-bite curet is usedto remove concave centrum oflower cartilaginous plate. Thendetached large chunks of discmaterial are removed with rongeur.C, Medial graft advancement withsingle chisel. (From Cauthen JC:Lumbar spine surgery, Baltimore,1983, Williams & Wilkins.)

C




stenosis or for lateral herniation. The use of the differentialspinal, root blocks, facet blocks, and discograms also can helpidentify the source of pain. The presence of abnormalpsychological test results or an abnormal differential spinalshould serve as a modifier to any suggested treatment indicatedby the other testing. Satisfactory nonoperative treatment of thisproblem should be attempted before additional surgery isperformed, provided that this surgery is elective. A distinct,surgically correctable, anatomical problem should be identifiedbefore surgery is contemplated. The surgery should be tailoredspecifically to the anatomical problem(s) identified.

REPEAT LUMBAR DISC SURGERY

◆ REPEAT LUMBAR DISC SURGERYThe technique of repeat lumbar disc surgery at the same leveland side as the previous procedure is nearly the same as forinitial surgery. The procedure is longer and involves moremeticulous dissection.

TECHNIQUE 39-26Approach the spine using the method described previously.Identify normal tissue first. Use a curet to carefully removescar from the edges of the lamina. Then remove additionalbone as necessary to expose normal dura. Identify thepedicles superiorly and inferiorly if there is any question ofposition and status of the root. Carry the dissection from thepedicles to identify each root. This will allow thedevelopment of a normal plane between the dura and scar.Maintain meticulous hemostasis with bipolar cautery. Thenremove disc material as indicated by the preoperativeevaluation. Meticulously check the roots, dura, and posteriorlongitudinal ligament after removal of the offending discherniation. Spinal fusion is not performed unless an unstablespine is created by the dissection or was identifiedpreoperatively as a correctable and symptomatic problem.

AFTERTREATMENT. Aftertreatment is the same as for discexcision (p. ••••).

ReferencesHISTORYAlajouanine TH: From the presidential address for Professor Jean Cauchoix

before the annual meeting of the International Society for the Study ofthe Lumbar Spine, San Francisco, June 1978.

Aurelianus C: Acute diseases and chronic diseases, Chicago, 1950,University of Chicago Press.

Barr JS, Hampton AO, Mixter WJ: Pain low in the back and ‘‘sciatica’’ dueto lesions of the intervertebral discs, JAMA 109:1265, 1937.

Catchlove RF, Braha R: The use of cervical epidural nerve blocks in themanagement of chronic head and neck pain, Can Anaesth Soc J 31:188,1984.

Cotugnio D: Treatise on the nervous sciatica or nervous hip gout, London,1775, J Wilkie.

Dandy WE: Loose cartilage from the intervertebral disc simulating tumorof the spinal cord, Orthop Surg 19:1660, 1929.

de Seze S: Sciatique ‘‘banale’’ et disques lombo-sacres, Presse Med51-52:570, 1940.

de Seze S: Histoire de la sciatique, Rev Neurol 138:1019, 1982.Dyck P: Lumbar nerve root: the enigmatic eponyms, Spine 9:3, 1984.

Elsberg CA: Experiences in spinal surgery: observations upon 60laminectomies for spinal disease, Surg Gynecol Obstet 16:117, 1913.

Forst JJ: Contribution a l’etude clinique de la sciatique, thesis, Lyon,France, 1881.

Goldthwait JE: The lumbosacral articulations: an explanation of manycases of ‘‘lumbago,’’ ‘‘sciatica,’’ and paraplegia, Bost Med Surg J164:365, 1911.

Hall GW: Neurologic signs and their discoverers, JAMA 95:703, 1930.Kepes ER, Duncalf D: Treatment of backache with spinal injections of local

anesthetics, spinal and systemic steroids: a review, Pain 22:33, 1985.Kirkaldy-Willis WH, Hill RJ: A more precise diagnosis for low-back pain,

Spine 4:102, 1979.Kocher T: Die Verlitzungen der Wirbelsaule Zurleich Als Beitrag zur

Physiologic des Menschichen Ruchenmarks, Mitt Grenzgeb Med Chir1:415, 1896.

Lasegue C: Considerations sur la sciatique, Arch Gen Med 2:558, 1864.Love JG: Removal of intervertebral discs without laminectomy, Proc Staff

Meet Mayo Clin 14:800, 1939.Middleton GS, Teacher JH: Extruded disc at T12-L1 level: microscopic

exam showed it to be nucleus pulposus, Glasgow Med J 76:1, 1911.Middleton GS, Teacher JH: Injury of the spinal cord due to rupture of an

intervertebral disc during muscular effort, Glasgow Med J 76:1, 1911.Mixter WJ, Barr JS: Rupture of the intervertebral disc with involvement of

the spinal canal, N Engl J Med 211:210, 1934.Murphy PL, Volinn E: Is occupational low back pain on the rise? Spine

24:691, 1999.Oppenheim H, Krause F: Ueber Einklemmung bzw. Strangulation der

Cauda equina, Deutsche Med Wochenschr 35:697, 1909.Robinson JS: Sciatica and the lumbar disk syndrome: a historic perspective,

South Med J 76:232, 1983.Semmes RE: Diagnosis of ruptured intervertebral discs without contrast

myelography and comment upon recent experience with modifiedhemilaminectomy for their removal, Yale J Biol Med 11:433, 1939.

Shulman M, Joseph NJ, Haller CA: Effect of epidural and subarachnoidinjections of a 10% butamben suspension, Reg Anesth 15:142, 1990.

Sjoqvist O: The mechanism of origin of Lasegue’s sign, Acta Psych Neurol46(suppl):290, 1947.

Smith L, Garvin PJ, Gesler RM, et al: Enzyme dissolution of the nucleuspulposus, Nature 198:1131, 1963.

Sugar O: Charles Lasegue and his ‘‘Considerations on Sciatica,’’ JAMA253:1767, 1985.

Virchow R: Untersuchunger uber die Enwickelung die Schadeigrunder,Berlin, 1857, G Reimer.

Waddell G: Low back pain: a twentieth-century health care enigma, Spine21:2820, 1996.

Wiltse LL: History of lumbar spine surgery. In White AA, ed: Lumbar spinesurgery: techniques and complications, St Louis, 1987, Mosby.

EPIDEMIOLOGYAndersson GBJ: Epidemiologic aspects of low-back pain in industry, Spine

6:53, 1981.Andersson GBJ, Svensson HO, Oden A: The intensity of work recovery in

low back pain, Spine 8:880, 1983.Biering-Sorensen F, Hilden J: Reproducibility of the history of low-back

trouble, Spine 9:280, 1984.Buckle PW, Kember PA, Wood AD, Wood SN: Factors influencing

occupational back pain in Bedfordshire, Spine 5:254, 1980.Carey TS, Evans A, Haler N, et al: Care-seeking among individuals with

chronic low back pain, Spine 20:312, 1995.Damkot DK, Pope MH, Lord J, Frymoyer JW: The relationship between

work history, work environment, and low-back pain in men, Spine 9:395,1984.

Deyo RA, Bass JE: Lifestyle and low-back pain: the influence of smokingand obesity, Spine 14:501, 1989.

Dillane JB, Fry J, Kalton G: Acute back syndrome: a study from generalpractice, Br Med J 2:82, 1966.

Frymoyer JW, Cats-Baril WL: An overview of the incidences and costs oflow back pain, Orthop Clin North Am 22:263, 1991.

Frymoyer JW, Newberg A, Pope MT, et al: Spine radiographs in patientswith low-back pain: an epidemiological study in men, J Bone Joint Surg66A:1048, 1984.

Frymoyer JW, Pope MT, Clements JH, et al: Risk factors in low-back pain:an epidemiological survey, J Bone Joint Surg 65A:213, 1983.

Grabias S: Current concepts review: the treatment of spinal stenosis, J BoneJoint Surg 62A:308, 1980.




Gyntelberg F: One-year incidence of low back pain among male residentsof Copenhagen aged 40-59, Dan Med Bull 21:30, 1974.

Harreby M, Nygaard B, Jessen T, et al: Risk factors for low back pain ina cohort of 1389 Danish school children: an epidemiologic study, EurSpine J 8:444, 1999.

Hult L: The Munkfors investigation, Acta Orthop Scand Suppl 16:1, 1954.Jackson RP, Simmons EH, Stripinis D: Incidence and severity of back pain

in adult idiopathic scoliosis, Spine 8:749, 1983.Johnsson K, Willner S, Pettersson H: Analysis of operated cases with

lumbar renal stenosis, Acta Orthop Scand 52:427, 1981.Kelsey JL, White AA III: Epidemiology and impact of low-back pain, Spine

5:133, 1980.Knutsson F: The instability associated with disk degeneration in the lumbar

spine, Acta Radiol 25:593, 1944.Kostuik JP, Bentivoglio J: The incidence of low-back pain in adult

scoliosis, Spine 6:268, 1981.Manning DP, Shannon HS: Slipping accidents causing low-back pain in a

gearbox factory, Spine 6:70, 1981.Middleton GS, Teacher JH: Injury of the spinal cord due to rupture of an

intervertebral disc during muscular effort, Glasgow Med J 76:1, 1911.Mooney V, Robertson J: The facet syndrome, Clin Orthop 115:149, 1976.Nachemson AL: Prevention of chronic back pain: the orthopaedic challenge

for the 80s, Bull Hosp Jt Dis 44:1, 1984.Riihimaki H, Tola S, Videman T, Hanninen K: Low-back pain and

occupation: a cross-sectional questionnaire study of men in machineoperating, dynamic physical work and sedentary work, Spine 14:204,1989.

Ryden LA, Molgaard CA, Bobbitt S, Conway J: Occupational low-backinjury in a hospital employee population and epidemiologic analysis ofmultiple risk factors of a high-risk occupational group, Spine 14:315,1989.

Sandover J: Dynamic loading as a possible source of low-back disorders,Spine 8:652, 1983.

Snook SH: The costs of back pain in industry, Spine: State of the ArtReviews 2:11, 1987.

Snook SH, Webster BS: The cost of disability, Clin Orthop 221:77, 1987.Svensson HO, Andersson GBJ: Low back pain in 40- to 47-year-old men:

work history and work environment factors, Spine 8:272, 1983.Svensson HO, Andersson GBJ: The relationship of low-back pain, work

history, work environment and stress: a retrospective cross-sectionalstudy of 38- to 64-year-old women, Spine 14:517, 1989.

Svensson HO, Vedin A, Wilhelmsson C, Andersson GBJ: Low-back pain inrelation to other diseases and cardiovascular risk factors, Spine 8:277,1983.

Troup JDG, Martin JW, Lloyd DC: Back pain in industry: a prospectivesurvey, Spine 6:61, 1981.

van-Doorn JW: Low back disability among self-employed dentists,veterinarians, physicians, and physical therapists in The Netherlands: aretrospective study over a 13-year period (N 1,119) and an earlyintervention program with 1-year follow-up (N 134), Acta Orthop ScandSuppl 263:1, 1995.

Waddell G, Main CJ, Morris EW, et al: Chronic low-back pain,psychological distress, and illness behavior, Spine 9:209, 1984.

Webster BS, Snook SH: The cost of compensable low back pain, J OccupMed 32:13, 1990.

Webster BS, Snook SH: The cost of 1989 workers’ compensation low backpain claims, Spine 19:1111, 1994.

Weisz GM: Lumbar spinal canal stenosis in Paget’s disease, Spine 8:192,1983.

White AWM: Low back pain in men receiving workmen’s compensation:a follow-up study, Can Med Assoc J 101:61, 1969.

Wilder DG, Woodworth BB, Frymoyer JW, Pope MH: Vibration and thehuman spine, Spine 7:243, 1982.

GENERAL DISC AND SPINE ANATOMYAdams MA, Hutton WC: The mechanical function of the lumbar

apophyseal joints, Spine 8:327, 1983.Bogduk N: The clinical anatomy of the cervical dorsal rami, Spine 7:319,

1982.Bogduk N: The innervation of the lumbar spine, Spine 8:286, 1983.Bogduk N, Engel R: The menisci of the lumbar zygapophyseal joints: a

review of their anatomy and clinical significance, Spine 9:454, 1984.Bogduk N, Macintosh JE: The applied anatomy of the thoracolumbar

fascia, Spine 9:164, 1984.

Bose K, Balasubramaniam P: Nerve root canals of the lumbar spine, Spine9:16, 1984.

Botsford DJ, Esses SI, Ogilvie-Harris DJ: In vivo diurnal variation inintervertebral disc volume and morphology, Spine 15:935, 1994.

Crock HV: Normal and pathological anatomy of the lumbar spinal nerveroot canals, J Bone Joint Surg 63B:487, 1981.

de Peretti F, Hovorka I, Ganansia P, et al: The vertebral foramen: a reportconcerning its contents, Surg Radiol Anat 15:287, 1993.

Hasue M, Kikuchi S, Sakuyama Y, Ito T: Anatomical study of theinterrelation between lumbosacral nerve roots and their surroundingtissues, Spine 8:50, 1983.

Inoue H: Three-dimensional architecture of lumbar intervertebral discs,Spine 6:139, 1981.

Jayson MIV: Compression stresses in the posterior elements and pathologicconsequences, Spine 8:338, 1983.

Kikuchi S, Hasue M, Nishiyama K, Ito T: Anatomical and clinical studiesof radicular symptoms, Spine 9:23, 1982.

King AG: Functional anatomy of the lumbar spine, Orthopedics 6:1588,1983.

Kirkaldy-Willis WH: The relationship of structural pathology to the nerveroot, Spine 9:49, 1984.

Knutsson F: The instability associated with disc degeneration in the lumbarspine, Acta Radiol 25:593, 1944.

Mayoux-Benhamou MA, Revel M, Aaron C, et al: A morphometric studyof the lumbar foramen: influence of flexion-extension movements and ofisolated disc collapse, Surg Radiol Anat 11:97, 1989.

Miller JAA, Haderspeck KA, Schultz AB: Posterior element loads inlumbar motion segments, Spine 8:331, 1983.

Neumann P, Keller T, Ekstrom L, et al: Structural properties of the anteriorlongitudinal ligament: correlation with lumbar bone mineral content,Spine 18:637, 1993.

Paajanen H, Lehto I, Alanen A, et al: Diurnal fluid changes of lumbar discsmeasured indirectly by magnetic resonance imaging, J Orthop Res12:509, 1994.

Pazzaglia UE, Salisbury JR, Byers PD: Development and involution of thenotochord in the human spine, J R Soc Med 82:413, 1989.

Pedersen H, Blunck CFJ, Gardner E: The anatomy of lumbosacral posteriorrami and meningeal branches of spinal nerves (sinu-vertebral nerves),J Bone Joint Surg 38A:2377, 1956.

Postacchini F, Urso S, Ferro L: Lumbosacral nerve-root anomalies, J BoneJoint Surg 64A:721, 1982.

Rhalmi S, Yahia LH, Newman N, Isler M: Immunohistochemical study ofnerves in lumbar spine ligaments, Spine 18:264, 1993.

Rudert M, Tillman B: Lymph and blood supply of the human intervertebraldisc: cadaver study of correlations to discitis, Acta Orthop Scand 64:37,1993.

Rydevik B, Brown MD, Lundborg G: Pathoanatomy and pathophysiologyof nerve root compression, Spine 9:7, 1984.

Spencer DL, Irwin GS, Miller JAA: Anatomy and significance of fixationof the lumbosacral nerve roots in sciatica, Spine 8:672, 1983.

Wall EJ, Cohen MS, Abitbol J, Garfin SR: Organization of intrathecal nerveroots at the level of the conus medullaris, J Bone Joint Surg 72A:1495,1990.

Wilder DG, Pope MH, Frymoyer JW: The functional topography of thesacroiliac joint, Spine 5:575, 1980.

Young A, Getty J, Jackson A, et al: Variations in the pattern of muscleinnervation by the L5 and S1 nerve roots, Spine 8:616, 1983.

Ziv I, Maroudas C, Robin G, Maroudas A: Human facet cartilage: swellingand some physiochemical characteristics as a function of age. II. Agechanges in some biophysical parameters of human facet joint cartilage,Spine 18:136, 1993.

NATURAL HISTORY OF DISC DISEASEBiering-Sørensen F, Hilden J: Reproducibility of the history of low-back

trouble, Spine 9:280, 1984.Gibson MJ, Szypryt EP, Buckley JH, et al: Magnetic resonance imaging of

adolescent disc herniation, J Bone Joint Surg 69B:699, 1987.Goldthwait E: Low-back lesions, J Bone Joint Surg 19:810, 1937.Hakelius A: Prognosis in sciatica: a clinical follow-up of surgical and

nonsurgical treatment, Acta Orthop Scand 129(suppl):1, 1970.Jackson RP, Simmons EH, Stripinis D: Incidence and severity of back pain

in adult idiopathic scoliosis, Spine 8:749, 1983.Jayson MIV: Compression stresses in the posterior elements and pathologic

consequences, Spine 8:338, 1983.




Kelsey JL, Githens PB, White AA III, et al: An epidemiologic study oflifting and twisting on the job and risk for acute prolapsed lumbarintervertebral disc, J Orthop Res 2:61, 1984.

Kirkaldy-Willis WH, Hill RJ: A more precise diagnosis for low-back pain,Spine 4:102, 1979.

Matsui H, Kanamori M, Ishihara H, et al: Familial predisposition forlumbar degenerative disc disease, Spine 23:1029, 1998.

Miller JAA, Schmatz C, Schultz AB: Lumbar disc degeneration: correlationwith age, sex and spine level in 600 autopsy specimens, Spine 13:2173,1988.

Pope MH, Bevins T, Wilder DG, Frymoyer JW: The relationship betweenanthropometric, postural, muscular, and mobility characteristics of malesage 18-55, Spine 10:644, 1985.

Roland M, Morris R: A study of the natural history of back pain. I.Development of a reliable and sensitive measure of disability in low-back pain, Spine 8:141, 1983.

Rydevik B, Brown MD, Lundborg G: Pathoanatomy and pathophysiologyof nerve root compression, Spine 9:7, 1984.

Saal JA: Natural history and nonoperative treatment of lumbar discherniation, Spine 21:2S:1996.

Sandover J: Dynamic loading as a possible source of low-back disorders,Spine 8:652, 1983.

Takata K, Inoue S, Takahashi K, Ohtsuka Y: Swelling of the cauda equinain patients who have herniation of a lumbar disc: a possible pathogenesisof sciatica, J Bone Joint Surg 70A:3361, 1988.

Urban JPG, McMullin JF: Swelling pressure of the lumbar intervertebraldiscs: influence of age, spinal level, composition, and degeneration,Spine 13:2179, 1988.

Urovitz EP, Fornasier VL: Autoimmunity in degenerative disk disease: ahistopathologic study Clin Orthop 142:215, 1979.

Varlotta GP, Brown MD, Kelsey JL, Golden AL: Familial predisposition forherniation of a lumbar disc in patients who are less than twenty-one yearsold, J Bone Joint Surg 73A:124, 1991.

Weber H: Lumbar disc herniation: a controlled, prospective study with tenyears of observation, Spine 8:131, 1983.

Yasuma T, Koh S, Okamura T, Yamauchi Y: Histological changes in aginglumbar intervertebral discs, J Bone Joint Surg 72A:220, 1990.

DIAGNOSTIC STUDIESAbel MS, Smith GR, Allen TNK: Refinements of the anteroposterior

angled caudad view of the lumbar spine, Skeletal Radiol 7:113,1981.

Abraham SR, Tedeschi AA, Partain CL, Blumenkopf B: Differentialdiagnosis of severe back pain using MRI, South Med J 81:487, 1988.

Alemohammad S, Bouzarth WF: Intracranial subdural hematoma followinglumbar myelography: case report, J Neurosurg 52:256, 1980.

Amundsen P: Cervical myelography with Amipaque: seven years’experience, Radiology 21:282, 1981.

Angiari P, Crisi G, Merli GA: Aphasia and right hemiplegia after cervicalmyelography with metrizamide: a case report, Neuroradiology 26:61,1984.

Asztely M, Kadziolka R, Nachemson A: A comparison of sonographyand myelography in clinically suspected spinal stenosis, Spine 8:885,1983.

Barrow DL, Wood JH, Hoffman JC Jr: Clinical indications for computer-assisted myelography, Neurosurgery 12:47, 1983.

Beattie PF, Meyers SP, Stratford P, et al: Associations between patientreport of symptoms and anatomical impairment visible on lumbarmagnetic resonance imaging, Spine 25:819, 2000.

Bell GR, Rothman RH, Booth RE, et al: A study of computer-assistedtomography. II. Comparison of metrizamide myelography and computedtomography in the diagnosis of herniated lumbar disc and spinal stenosis,Spine 9:552, 1984.

Birney TJ, White JJ, Berens D, Kuhn G: Comparison of MRI anddiscography in the diagnosis of lumbar degenerative disc disease,J Spinal Disord 5:417, 1992.

Blade J, Gaston F, Montserrat E, et al: Spinal subarachnoid hematoma afterlumbar puncture causing reversible paraplegia in acute leukemia: casereport, J Neurosurg 58:438, 1983.

Bobest M, Furo I, Tompa K, et al: 1H nuclear magnetic resonance study ofintervertebral discs: a preliminary report, Spine 11:709, 1986.

Boden SD, Davis DO, Dina TS, et al: Abnormal magnetic-resonance scansof the lumbar spine in asymptomatic subjects: a prospective investiga-tion, J Bone Joint Surg 72A:403, 1990.

Boden SD, McCowin PR, Davis DO, et al: Abnormal magnetic-resonancescans of the cervical spine in asymptomatic subjects, J Bone Joint Surg72A:1178, 1990.

Boos N, Rieder R, Schade V, et al: The diagnostic accuracy of magneticresonance imaging, work perception, and psychosocial factors inidentifying symptomatic disc herniations, Spine 20:2613, 1995.

Brem SS, Hafler DA, Van Uitert RL, et al: Spinal subarachnoid hematoma:a hazard of lumbar puncture resulting in reversible paraplegia, N EnglJ Med 304:1020, 1981.

Charles MF, Byrd SE, Cohn ML, Huntington CT: Metrizamide com-puter tomography of the postoperative lumbar spine, Orthop Rev 11:49,1982.

Coin CG: Cervical disk degeneration and herniation: diagnosis bycomputerized tomography, South Med J 77:979, 1984.

Collier BD, Johnson RP, Carrera GF, et al: Painful spondylolysis orspondylolisthesis studied by radiography and single-photon emissioncomputed tomography, Radiology 154:207, 1985.

Deburge A, Benoist M, Boyer D: The diagnosis of disc sequestration, Spine9:496, 1984.

Delamarter RB, Bohlman HH, Dodge LD, Biro C: Experimental lumbarspinal stenosis: analysis of the cortical evoked potentials, microvascu-lature, and histopathology, J Bone Joint Surg 72A:110, 1990.

Delamarter RB, Leventhal MR, Bohlman HH: Diagnosis of recurrentlumbar disc herniation vs postoperative scar by gadolinium-DTPA-enhanced magnetic resonance imaging (unpublished data).

Dvonch V, Scarff T, Bunch WH, et al: Dermatomal somatosensoryevoked potentials: their use in lumbar radiculopathy, Spine 9:291,1984.

Edelstein WA, Schenck JF, Hart HR, et al: Surface coil magnetic resonanceimaging, JAMA 253:828, 1985.

Eisen A, Hoirch M: The electrodiagnostic evaluation of spinal root lesions,Spine 8:98, 1983.

Eldevik OP: Side effects and complications of myelography with water-soluble contrast agents, J Oslo City Hosp 32:121, 1982.

Esses SI, Moro JK: The value of facet joint blocks in patient selection forlumbar fusion, Spine 18:185, 1993.

Fager CA: Evaluation of cervical spine surgery by postoperativemyelography, Neurosurgery 12:416, 1983.

Firooznia H, Benjamin V, Kricheff II, et al: CT of lumbar spine discherniation: correlation with surgical findings, Am J Roentgenol 142:587,1984.

Fitzgerald RH, Reines HD, Wise J: Diagnostic radiation exposure in traumapatients, South Med J 76:1511, 1983.

Ford LT, Goodman FG: X-ray studies of the lumbosacral spine, South MedJ 10:1123, 1966.

Frymoyer JW, Newberg A, Pope MH, et al: Spine radiographs in patientswith low-back pain: an epidemiological study in men, J Bone Joint Surg66A:1048, 1984.

Fullenlove TM, Williams AJ: Comparative roentgen findings in symptom-atic and asymptomatic backs, Radiology 63:572, 1957.

Gibson MJ, Buckley J, Mulholland RC, Worthington BS: The changes inthe intervertebral disc after chemonucleolysis demonstrated by magneticresonance imaging, J Bone Joint Surg 68B:719, 1986.

Gibson MJ, Szypryt EP, Buckley JH, et al: Magnetic resonance imaging ofadolescent disc herniation, J Bone Joint Surg 69B:699, 1987.

Glasauer FE, Alker G: Metrizamide enhanced computed tomography: anadjunct to myelography in lumbar disc herniation, Comput Radiol 7:305,1983.

Greenberg RP, Ducker TB: Evoked potentials in the clinical neurosciences,J Neurosurg 56:1, 1982.

Gulati AN, Guadognoli DA, Quigley JM: Relationship of side effects topatient position during and after metrizamide lumbar myelography,Radiology 141:113, 1981.

Haldeman S: The electrodiagnosis evaluation of nerve root function, Spine9:42, 1984.

Harrington H, Tyler HR, Welch K: Surgical treatment of post-lumbarpuncture dural CSF leak causing chronic headache: case report,J Neurosurg 57:703, 1982.

Haughton VM, Eldevik OP, Magnaes B, Amundsen P: A prospectivecomparison of computed tomography and myelography in the diagnosisof herniated lumbar disks, Radiology 142:103, 1982.

Hayes MA, Howard TC, Gruel CR, Kopta JA: Roentgenographicevaluation of lumbar spine flexion-extension in asymptomatic individu-als, Spine 14:327, 1989.




Hemminghytt S, Daniels DL, Williams AL, Haughton VM: Intraspinalsynovial cysts: natural history and diagnosis by CT, Radiology 145:375,1982.

Herkowitz HN, Romeyn RL, Rothman RH: The indications for metriza-mide myelography: relationship with complications after myelography,J Bone Joint Surg 65A:1144, 1983.

Herkowitz HN, Wiesel SW, Booth RE Jr, Rothman RH: Metrizamidemyelography and epidural venography: their role in the diagnosis oflumbar disc herniation and spinal stenosis, Spine 7:55, 1982.

Hirschy JC, Leue WM, Berninger WH, et al: CT of the lumbosacral spine:importance of tomographic planes parallel to vertebral endplate, AmJ Roentgenol 136:47, 1981.

Holt EP Jr: The question of lumbar discography, J Bone Joint Surg50A:720, 1968.

Howie DW, Chatterton BE, Hone MR: Failure of ultrasound in theinvestigation of sciatica, J Bone Joint Surg 65B:144, 1983.

Hudgins WR: Computer-aided diagnosis of lumbar disc herniation, Spine8:604, 1983.

James AE Jr, Partain CL, Patton JA, et al: Current status of magneticresonance imaging, South Med J 78:580, 1985.

Jepson K, Nada A, Rymaszewski L: The role of radiculography in themanagement of lesions of the lumbar disc, J Bone Joint Surg 64B:405,1982.

Johansen JP, Fossgreen J, Hansen HH: Bone scanning in lumbar discherniation, Acta Orthop Scand 51:617, 1980.

Kambin P, Nixon JE, Chait A, Schaffer JL: Annular protrusion:pathophysiology and roentgenographic appearance, Spine 13:671, 1988.

Kapoor W, Hemmer K, Herbert D, Karpf M: Abdominal computedtomography: comparison of the usefulness of goal-directed vs non-goal-directed studies, Arch Intern Med 143:249, 1983.

Kelsey JL, Githens PB, Walter SD, et al: An epidemiological study ofacute prolapsed cervical intervertebral disc, J Bone Joint Surg 66A:907,1984.

Kieffer SA, Cacyorin ED, Sherry RG: The radiological diagnosis ofherniated lumbar intervertebral disk: a current controversy, JAMA251:1192, 1984.

Kikuchi S, Macnab I, Moreau P: Localisation of the level of symptomaticcervical disc degeneration, J Bone Joint Surg 63B:272, 1981.

Killebrew K, Whaley RA, Hayward JN, Scatliff JH: Complications ofmetrizamide myelography, Arch Neurol 40:78, 1983.

Liang M, Komaroff AL: Roentgenograms in primary care patients withacute low back pain: a cost-effectiveness analysis, Arch Intern Med142:1108, 1982.

MacGibbon B, Farfan HF: A radiologic survey of various configurations ofthe lumbar spine, Spine 4:258, 1979.

Macnab I: The traction spur: an indicator of segmental instability, J BoneJoint Surg 53A:663, 1971.

Macnab I, Cuthbert H, Godfrey CM: The incidence of denervation of thesacrospinales muscles following spinal surgery, Spine 2:294, 1977.

Macnab I, St Louis EL, Grabias SL, Jacob R: Selective ascendinglumbosacral venography in the assessment of lumbar disc herniation,J Bone Joint Surg 58A:1093, 1976.

Macon JB, Poletti CE: Conducted somatosensory evoked potentials duringspinal surgery. I. Control conduction velocity measurements, J Neuro-surg 57:349, 1982.

Macon JB, Poletti CE, Sweet WH, et al: Conducted somatosensory evokedpotentials during spinal surgery. II. Clinical applications, J Neurosurg57:354, 1982.

MacPherson P, Teasdale E, MacPherson PY: Radiculography: is routine bedrest really necessary? Clin Radiol 34:325, 1983.

Meador K, Hamilton WJ, El Gammal TAM, et al: Irreversible neurologiccomplications of metrizamide myelography, Neurology 34:817, 1984.

Moufarrij NA, Hardy RW Jr, Weinstein MA: Computed tomographic,myelographic, and operative findings in patients with suspectedherniated lumbar discs, Neurosurgery 12:184, 1983.

Paleari GL, Ballarati P, Gambrioli PL, Paleari M: Recent progress invertebral body section roentgenography in the study of the pathology ofthe lumbar vertebrae, Ital J Orthop Traumatol 8:109, 1982.

Raskin SP, Keating JW: Recognition of lumbar disk disease: comparison ofmyelography and computed tomography, Am J Roentgenol 139:349,1982.

Risius B, Modic MT, Hardy RW Jr, et al: Sector computed tomographicspine scanning in the diagnosis of lumbar nerve root entrapment,Radiology 143:109, 1982.

Rockey PH, Tompkins RK, Wood RW, Wolcott BW: The usefulness ofx-ray examinations in the evaluation of patients with back pain, J FamPract 7:455, 1978.

Scavone JG, Latshaw RF, Rohrer GV: Use of lumbar spine films: statis-tical evaluation of a university teaching hospital, JAMA 246:1105,1981.

Schelkun SR, Wagner KF, Blanks JA, Reinert CM: Bacterial meningitisfollowing Pantopaque myelography: a case report and literature review,Orthopedics 8:74, 1985.

Schutte HE, Park WM: The diagnostic value of bone scintigraphy inpatients with low back pain, Skeletal Radiol 10:1, 1983.

Schwarzer AC, Aprill CN, Derby R, et al: The relative contributions of thedisc and zygapophyseal joint in chronic low back pain, Spine 19:801,1994.

Shima F, Mihara K, Hachisuga S: Angioma in the paraspinal musclescomplicated by spinal epidural hematoma: case report, J Neurosurg57:274, 1982.

Siddiqi TS, Buchheit WA: Herniated nerve root as a complication of spinaltap: case report, J Neurosurg 56:565, 1982.

Siqueira EB, Kranzler LI, Schaffer L: Intraoperative myelography:technical note, J Neurosurg 58:786, 1983.

Smith GR: Nerve root cut-off on metrizamide-enhanced computerizedtomography, South Med J 79:553, 1986.

Smith SE, Darden BV, Rhyne AL, Wood KE: Outcome of unoperateddiscogram-positive low back pain, Spine 20:1997, 1995.

Steiner RE: Nuclear magnetic resonance: its clinical application, J BoneJoint Surg 65B:533, 1983.

Stokes IAF, Wilder DG, Frymoyer JW, Pope MH: Assessment of patientswith low-back pain by biplanar radiographic measurement of interver-tebral motion, Spine 6:233, 1981.

Szypryt EP, Twining P, Wilde GP, et al: Diagnosis of lumbar discprotrusion, J Bone Joint Surg 70B:717, 1988.

Tchang SPK, Howie JL, Kirkaldy-Willis WH, et al: Computed tomographyversus myelography in diagnosis of lumbar disc herniation, J Can AssocRadiol 33:15, 1982.

Teplick JG, Haskin ME: Intravenous contrast-enhanced CT of thepostoperative lumbar spine: improved identification of recurrent diskherniation, scar, arachnoiditis, and diskitis, Am J Roentgenol 143:845,1984.

Tibrewal SB, Pearcy MJ: Lumbar intervertebral disc heights in normalsubjects and patients with disc herniation, Spine 10:452, 1985.

Waddell G, McCulloch JA, Kummel E, Venner RM: Nonorganic physicalsigns in low-back pain, Spine 5:117, 1980.

Weiss T, Treisch J, Kazner E, et al: CT of the postoperative lumbar spine:the value of intravenous contrast, Neuroradiology 28:241, 1986.

Whelan MA, Gold RP: Computed tomography of the sacrum. I. Normalanatomy, Am J Roentgenol 139:1183, 1982.

Whelan MA, Hilal SK, Gold RP, et al: Computed tomography of thesacrum. II. Pathology, Am J Roentgenol 139:1191, 1982.

Wiesel S, Tsourmas N, Feffer HL, et al: A study of computer-assistedtomography. I. The incidence of positive CAT scans in an asymptomaticgroup of patients, Spine 9:549, 1984.

Wilberger JE Jr, Pang D: Syndrome of the incidental herniated lumbar disc,J Neurosurg 59:137, 1983.

Williams AL, Haughton VM, Daniels DL, Thornton RS: CT recogni-tion of lateral lumbar disk herniation, Am J Roentgenol 139:345,1982.

Williams PC: Reduced lumbosacral joint space: its relation to sciaticirritation, JAMA 99:1677, 1932.

Wiltse LL, Guyer RD, Spencer CW, et al: Alar transverse processimpingement of the L5 spinal nerve: the far-out syndrome, Spine 9:31,1984.

Winston K, Rumbaugh C, Colucci V: The vertebral canals in lumbar discdisease, Spine 9:414, 1984.

Witt I, Vestergaard A, Rosenklint A: A comparative analysis of x-rayfindings of the lumbar spine in patients with and without lumbar pain,Spine 9:298, 1984.

Wood KB, Garvey TA, Gundry C, Heithoff KB: Magnetic resonanceimaging of the thoracic spine: evaluation of asymptomatic individuals,J Bone Joint Surg 77A:1631, 1995.

INJECTION STUDIESAhlgren EW, Stephen R, Lloyd EAC, McCollum DE: Diagnosis of pain

with a graduated spinal block technique, JAMA 195:125, 1966.




Angtuaco EJC, Holder JC, Boop WC, Binet EF: Computed tomographicdiscography in the evaluation of extreme lateral disc herniation,Neurosurgery 14:350, 1984.

Benoist M, Ficat C, Baraf P, Cauchoix J: Postoperative lumbarepiduro-arachnoiditis: diagnostic and therapeutic aspects, Spine 5:432,1980.

Berman AT, Garbarino JL, Jr, Fisher SM, Bosacco SJ: The effects ofepidural injection of local anesthetics and corticosteroids on patientswith lumbosciatic pain, Clin Orthop 188:144, 1984.

Bogduk N, Long DM: The anatomy of the so-called ‘‘articular nerves’’ andtheir relationship to facet denervation in the treatment of low-back pain,J Neurosurg 51:172, 1979.

Bromley JW, Varma AO, Santoro AJ, et al: Double-blind evaluation ofcollagenase injections for herniated lumbar discs, Spine 9:486, 1984.

Brooks S, Dent AR, Thompson AG: Anterior rupture of the lumbosacraldisc: report of a case, J Bone Joint Surg 65A:1186, 1983.

Brown FW: Management of discogenic pain using epidural and intrathecalsteroids, Clin Orthop 129:72, 1977.

Colhoun E, McCall IW, Williams L, Pullicino VNC: Provocationdiscography as a guide to planning operations on the spine, J Bone JointSurg 70B:267, 1988.

Cuckler JM, Bernini PA, Wiesel SW, et al: The use of epidural steroids inthe treatment of lumbar radicular pain: a prospective, randomized,double-blind study, J Bone Joint Surg 67A:63, 1985.

Debaene A: Anatomo-radiological considerations about lumbar discogra-phy: an experimental study, Neuroradiology 17:77, 1979.

Deburge A, Benoist M, Rocolle J: La chirurgie dans les echecs de lanucleolyse des hernies discales lombaires, Rev Chir Orthop 70:637,1984.

De La Porte C, Siegfried J: Lumbosacral spinal fibrosis (spinalarachnoiditis): its diagnosis and treatment by spinal cord stimulation,Spine 8:593, 1983.

Destouet JM, Bilula LA, Murphy WA, Monsees B: Lumbar facet jointinjection: indication, technique, clinical correlation, and preliminaryresults, Radiology 145:321, 1982.

Dory MA: Arthrography of the lumbar facet joints, Radiology 140:23,1981.

Eisenstein SM, Parry CR: The lumbar facet arthrosis syndrome, J BoneJoint Surg 69B:3, 1987.

Eng RHK, Seligman SJ: Lumbar puncture-induced meningitis, JAMA245:1456, 1981.

Fortin JD, Dwyer AP, West S, Pier J: Sacroiliac joint: pain referral mapsupon applying a new injection/arthrography technique. I. Asymptomaticvolunteers, Spine 19:1475, 1994.

Fox AJ: Lumbar discography: a dissenting opinion letter, J Can AssocRadiol 34:88, 1983.

Fraser RD, Osti OL, Vernon-Roberts B: Discitis after discography, J BoneJoint Surg 69B:26, 1987.

Ghia JN, Duncan GH, Teeple E: Differential spinal block for diagnosis ofchronic pain, Compr Ther 8:55, 1982.

Ghormley RK: Low back pain with special reference to the articular facetswith presentation of an operative procedure, JAMA 101:1773, 1933.

Goldthwait E: Low-back lesions, J Bone Joint Surg 19:810, 1937.Green PWB, Burke AJ, Weiss CA, Langan P: The role of epidural cortisone

injection in the treatment of diskogenic low back pain, Clin Orthop153:121, 1980.

Hauelsen DC, Smith BS, Myers SR, Pryce RL: The diagnostic accuracy ofspinal nerve injection studies, Clin Orthop 198:179, 1985.

Hodgkinson A: Neck pain localization by cervical disc stimulation andtreatment by anterior interbody fusion, J Bone Joint Surg 52B:789,1970.

Hoffman GS, Ellsworth CA, Wells EE, et al: Spinal arachnoiditis. Whatis the clinical spectrum? II. Arachnoiditis induced by Pantopaque/autologous blood in dogs, a possible model for human disease, Spine8:541, 1983.

Holt EP: The fallacy of cervical discography, JAMA 188:799, 1964.Jackson RP, Jacobs RR, Montesano PX: Facet joint injection in low-back

pain: a prospective statistical study, Spine 13:966, 1988.Johnson RG: Does discography injure normal discs? An analysis of repeat

discograms, Spine 14:424, 1989.Johnson RG, Macnab I: Localization of symptomatic lumbar pseudoar-

throses by use of discography, Clin Orthop 197:164, 1985.Kahanovitz N, Arnoczky SP, Sissons HA, et al: The effect of discography

on the canine intervertebral disc, Spine 11:26, 1986.


Laun A, Lorenz R, Agnoli AL: Complications of cervical discography,J Neurosurg Sci 25:17, 1981.

Lownie SP, Ferguson GG: Spinal subdural empyema complicating cervicaldiscography, Spine 14:1415, 1989.

Macnab I: Negative disc exploration: an analysis of the causes ofnerve-root involvement in sixty-eight patients, J Bone Joint Surg53A:891, 1971.

Macnab I, Grabias SL, Jacob R: Selective ascending lumbosacralvenography in the assessment of lumbar-disc herniation: an anatomicalstudy and clinical experience, J Bone Joint Surg 58A:1093, 1976.

Merriam WF, Stockdale HR: Is cervical discography of any value? EurJ Radiol 3:138, 1983.

Milette PC, Melanson D: A reappraisal of lumbar discography, J Can AssocRadiol 33:176, 1982.

Murtagh FR: Computed tomography and fluoroscopy guided anesthesiaand steroid injection in facet syndrome, Spine 13:6686, 1988.

Nachemson A: Lumbar discography: where are we today? Spine 14:555,1989.

Quinnell RC, Stockdale HR: The significance of osteophytes on lumbarvertebral bodies in relation to discographic findings, Clin Radiol 33:197,1982.

Quinell RC, Stockdale HR: Flexion and extension radiography of thelumbar spine: a comparison with lumbar discography, Clin Radiol34:405, 1983.

Quinell RC, Stockdale HR, Harmon B: Pressure standardized lumbardiscography, Br J Radiol 53:1031, 1980.

Roth DA: Cervical analgesic discography: a new test for the definitivediagnosis of the painful disk syndrome, JAMA 235:1713, 1976.

Sachs BL, Vanharanta M, Spirey MA et al: Dallas discogram description:a new classification of CT/discography in low back disorders, Spine12:287, 1987.

Schellhas KP, Pollei SR, Dorwart RH: Thoracic discography: a safe andreliable technique, Spine 19:2103, 1994.

Shinomiya K, Nakao K, Shindoh S, et al: Evaluation of cervicaldiskography in pain origin and provocation, J Spinal Disord 6:422,1993.

Simmons EH, Segil CM: An evaluation of discography in the localizationof symptomatic levels in discogenic disease of the spine, Clin Orthop108:57, 1975.

Simmons JW, Aprill CN, Dwyer AP, Brodsky AE: A reassessment of Holt’sdata on: ‘‘The question of lumbar discography,’’ Clin Orthop 237:120,1988.

Skubic JN, Kostuik JP: Thoracic pain syndromes and thoracic discherniation. In Frymoyer JN, ed: The adult spine: principles and practice,New York, 1991, Raven Press.

Smith GW: The normal cervical diskogram, Am J Radiol 81:1006, 1959.Smith GW, Nichols P: The technic of cervical discography, Radiology

68:718, 1957.Stambough JL, Booth RE Jr, Rothman RH: Transient hypercorticism after

epidural steroid injection: a case report, J Bone Joint Surg 66A:1115,1984.

Sussman BJ, Bromley JW, Gomez JC: Injection of collagenase forherniated lumbar disk: initial clinical report, JAMA 245:730, 1981.

Tajima T, Furukawa K, Kuramochi E: Selective lumbosacral radiculogra-phy and block, Spine 5:68, 1980.

Teeple E, Scott DL, Ghia JN: Intrathecal normal saline without preservativedoes not have a local anesthetic effect, Pain 14:3, 1982.

Walsh TR, Weinstein JN, Spratt KF, et al: Lumbar discography in normalsubjects: a controlled, prospective study, J Bone Joint Surg 72A:1081,1990.

White AH, Derby R, Wynne G: Epidural injections for the diagnosis andtreatment of low-back pain, Spine 5:78, 1980.

Wilkinson HA: Field block anesthesia for lumbar puncture, JAMA 249:2177, 1983 (letter).

Yasuma T, Ohno R, Yamauchi Y: False-negative lumbar discograms:correlation of discographic and histological findings in postmortem andsurgical specimens, J Bone Joint Surg 70A:1279, 1988.

PSYCHOLOGICAL TESTINGBarnes D, Smith D, Gatchel RJ, Mayer TG: Psychosocioeconomic

predictors of treatment success/failure in chronic low-back pain patients,Spine 14:427, 1989.




Bigos SJ, Battie MC, Spengler DM, et al: A prospective study of workperceptions and psychosocial factors affecting the report of back injury,Spine 16:1, 1991.

Carron H, DeGood DE, Tait R: A comparison of low back pain patients inthe United States and New Zealand: psychosocial and economic factorsaffecting severity of disability, Pain 21:77, 1985.

Chapman SL, Pemberton JS: Prediction of treatment outcome fromclinically derived MMPI clusters in rehabilitation for chronic low backpain, Clin J Pain 10:267, 1994.

Cohen CA, Foster HM, Peck EA III: MMPI evaluation of patients withchronic pain, South Med J 76:316, 1983.

Colligan RC, Osborne D, Swenson WM, Offord KP: The aging MMPI:development of contemporary norms, Mayo Clin Proc 59:377, 1984.

Cummings GS, Routan JL: Accuracy of the unassisted pain drawings bypatients with chronic pain, J Orthop Sports Phys Ther 8:391, 1987.

Dennis MD, Greene RL, Farr SP, Hartman JT: The Minnesota MultiphasicPersonality Inventory: general guidelines to its use and interpretation oforthopedics, Clin Orthop 150:125, 1980.

Dennis MD, Rocchio PO, Wiltse LL: The topographical pain representationand its correlation with MMPI scores, Orthopedics 5:433, 1981.

Deyo RA, Diehl AK: Measuring physical and psychosocial function inpatients with low-back pain, Spine 8:635, 1983.

Deyo RA, Walsh NE, Schoenfeld LS, Ramamurthy S: Studies of theModified Somatic Perceptions Questionnaire (MSPQ) in patients withback pain: psychometric and predictive properties, Spine 14:507,1989.

Feyer AM, Herbison P, Williamson AM, et al: The role of physical andpsychological factors in occupational low back pain, Occup EnvironMed 57:116, 2000.

Fritz JM, Wainner RS, Hicks GE: The use of nonorganic signs andsymptoms as a screening tool for return-to-work in patients withacute low back pain, Spine 25:1925, 2000.

Gatchel RJ, Polatin PB, Kinney RK: Predicting outcome of chronic backpain using clinical predictors of psychopathology: a prospective analysis,Health Psychol 14:415, 1995.

Gentry WD: Chronic back pain: does elective surgery benefit patients withevidence of psychologic disturbance? South Med J 75:1169, 1982.

Gentry WD, Shows WD, Thomas M: Chronic low back pain: a psycho-logical profile, Psychosomatics 15:174, 1974.

Grevitt M, Pande K, O’Dowd J, Webb J: Do first impressions count? Acomparison of subjective and psychologic assessment of spinal patients,Eur Spine J 7:218, 1998.

Herron LD, Pheasant HC: Changes in MMPI profiles after low-backsurgery, Spine 7:591, 1982.

Leavitt F, Garron DC, McNeill TW, Whisler WW: Organic status,psychological disturbance, and pain report characteristics in low-back-pain patients on compensation, Spine 7:398, 1982.

Linton SJ: A review of psychological risk factors in back and neckpain, Spine 25:1148, 2000.

Long CJ, Brown DA, Engelberg J: Intervertebral disc surgery:strategies for patient selection to improve surgical outcome,J Neurosurg 52:818, 1980.

Ohnmeiss DD: Repeatability of pain drawings in a low back painpopulation, Spine 25:980, 2000.

Pincus T, Callahan LF, Bradley LA, et al: Elevated MMPI scores forhypochondriasis, depression and hysteria in patients with rheumatoidarthritis reflect disease rather than psychological status, Arthritis Rheum29:1456, 1986.

Rainsford AO, Cairns D, Mooney V: The pain drawing as an aid to thepsychologic evaluation of patients with low-back pain, Spine 1:127,1976.

Riley JL, Robinson ME, Geisser ME, Wittmer VT: Multivariate clusteranalysis of the MMPI-2 in chronic low-back pain patients, Clin J Pain9:248, 1993.

Riley JL, Robinson ME, Geisser ME, et al: Relationship between MMPI-2cluster profiles and surgical outcome in low-back pain patients, J SpinalDisord 8:213, 1995.

Simmonds MJ, Kumar S, Lechelt E: Psychosocial factors in disabling lowback pain: cause or consequences? Dis Rehab 18:161, 1996.

Southwick SM, White AA: The use of psychological tests in the evaluationof low-back pain, J Bone Joint Surg 65A:560, 1983.

Uden A, Landin LA: Pain drawing and myelography in sciatic pain, ClinOrthop 216:124, 1987.

Waddell G, McCullouch JA, Kummel E, et al: Nonorganic physical signsin low-back pain, Spine 5:117, 1980.

Wiltse LL, Rocchio P: Preoperative psychological tests as predictors ofsuccess of chemonucleolysis in the treatment of the low-back syndrome,J Bone Joint Surg 57A:478, 1975.

CERVICAL DISC DISEASEAldrich F: Posterolateral microdiscectomy for cervical monoradiculopathy

caused by posterolateral soft cervical disc sequestration, J Neurosurg72:370, 1990.

Aprill C, Dwyer A, Bogduk N: Cervical zygapophyseal joint pain patternsII: a clinical evaluation, Spine 15:458, 1990.

Bailey RW, Badgley CE: Stabilization of the cervical spine by anteriorfusion, J Bone Joint Surg 42A:565, 1960.

Bernardo KL, Grubb RL, Coxe WS, Roper CL: Anterior cervical discherniation: case report, J Neurosurg 69:134, 1988.

Bloom MH, Raney FL: Anterior intervertebral fusion of the cervical spine:a technical note, J Bone Joint Surg 63A:842, 1981.

Boden SD, McCowin PR, Davis DO, et al: Abnormal magnetic-resonancescans of the cervical spine in asymptomatic subjects, J Bone Joint Surg72A:1178, 1990.

Braun IR, Pinto RS, De Fillip GJ, et al: Brain stem infarction due tochiropractic manipulation of the cervical spine, South Med J 76:1507,1983.

Cloward RB: The treatment of ruptured lumbar intervertebral discs byvertebral body fusion. I. Indications, operative technique, after care,J Neurosurg 10:154, 1953.

Cloward RB: The anterior approach for removal of ruptured cervical discs,J Neurosurg 15:602, 1958.

Cosgrove GR, Theron J: Vertebral arteriovenous fistula following anteriorcervical spine surgery: report of two cases, J Neurosurg 66:297, 1987.

Davidson RI, Dunn EJ, Metzmaker JN: The shoulder abduction test in thediagnosis of radicular pain in cervical extradural compressive monora-diculopathies, Spine 6:441, 1981.

Dwyer A, Aprill C, Bogduk N: Cervical zygapophyseal joint pain patterns.I. A study in normal volunteers, Spine 453, 1990.

Farley ID, McAfee PC, Davis RF, Long DM: Pseudarthrosis of the cervicalspine after anterior arthrodesis, J Bone Joint Surg 72A:1171, 1990.

Garcia A: Cervical traction, an ancient modality, Orthop Rev 13:429,1984.

Griffith SL, Zogbi SW, Guyer RD, et al: Biomechanical comparison ofanterior instrumentation for the cervical spine, J Spinal Disord 8:429,1995.

Hirsch D: Cervical disc rupture: diagnosis and therapy, Acta Orthop Scand30:172, 1960.

Horal J: The clinical appearance of low back disorders in the city ofGothenburg, Sweden: comparisons of incapacitated probands withmatched controls, Acta Orthop Scand Suppl 116:1, 1969.

Jacobs B, Krueger EG, Levy DM: Cervical spondylosis with radiculopathy:results of anterior diskectomy and interbody fusion, JAMA 211:2135,1970.

Jenis L, Leclair WJ: Late vascular complication with anterior cervicaldiscectomy and fusion, Spine 19:1291, 1994.

Jho: Microsurgical anterior cervical foraminotomy for radiculopathy: a newapproach to cervical disc herniation, J Neurosurg 84:155, 1996.

Johnson JP, Filler AG, McBride DQ, Batzdorf U: Anterior cervicalforaminotomy for unilateral radicular disease, Spine 25:905, 2000.

Kang JD, Georgescu HI, McIntryre LL, et al: Herniated cervicalintervertebral discs spontaneously produce matrix metalloproteinases,nitric oxide, interleukin-6, and prostaglandin EW, Spine 20:2373, 1995.

Kauppila LI, Penttila A: Postmortem angiographic study of degenerativevascular changes in arteries supplying the cervicobrachial region, AnnRheum Dis 53:94, 1994.

Kelly MF, Spiegel J, Rizzo KA, Zwillenberg D: Delayed pharyngoesoph-ageal perforation: a complication of anterior spine surgery, Ann OtolRhinol Laryngol 100:201, 1991.

Kelsey JL, Githens PB, Walter SD, et al: An epidemiological study of acuteprolapsed cervical intervertebral disc, J Bone Joint Surg 66A:907, 1984.

Key CA: On paraplegia depending on the ligaments of the spine, Guy’sHosp Rep 7:1737, 1838.

Kikuchi S, Hasue M, Nishiyama K, Ito T: Anatomical and clinical studiesof radicular symptoms, Spine 9:23, 1984.


Koop SE, Winter RB, Lonstein JE: The surgical treatment of instability ofthe upper part of the cervical spine in children and adolescents, J BoneJoint Surg 66A:403, 1984.




Kramer J: Pressure dependent fluid shift in the intervertebral disc, OrthopClin North Am 8:211, 1977.

Lindsey RW, Newhouse KE, Leach J, Murphy MJ: Nonunion followingtwo-level anterior cervical discectomy and fusion, Clin Orthop 223:155,1987.

Lunsford LD, Bissonette DJ, Jannetta PJ, et al: Anterior surgery for cervicaldisc disease. I. Treatment of lateral cervical disc herniation in 253 cases,J Neurosurg 53:1, 1980.

Maruyama Y: Histological, magnetic resonance imaging, and discographicfindings on cervical disc degeneration in cadaver spines: a comparativestudy, Nippon Seikeigeka Gakkai Zasshi 69:1102, 1995.

Murphey F, Simmons JCH, Brunson B: Surgical treatment of laterallyruptured cervical discs: a review of 648 cases, 1939 to 1972, J Neurosurg38:679, 1973.

Naito M, Kurose S, Oyama M, Sugioka Y: Anterior cervical fusion with theCaspar instrumentation system, Int Orthop 17:73, 1993.

Odom GL, Finney W, Woodhall B: Cervical disk lesion, JAMA 166:23,1958.

O’Laoire SA, Thomas DGT: Spinal cord compression due to prolapse ofcervical intervertebral disc (herniation of nucleus pulposus), J Neurosurg59:847, 1983.

Pennecot GF, Gouraud D, Hardy JR, Pouliquen JC: Roentgenographicalstudy of the stability of the cervical spine in children, J Pediatr Orthop4:346, 1984.

Rainer JK: Cervical disc surgery: a historical review, J Tenn Med Assoc77:12, 1984.

Rath WW: Cervical traction: a clinical perspective, Orthop Rev 13:430,1984.

Riley LH: Surgical approaches to the anterior structures of the cervicalspine, Clin Orthop 91:16, 1973.

Robertson JT: Anterior removal of cervical disc without fusion, ClinNeurosurg 20:259, 1973.

Robinson JS: Sciatica and the lumbar disc syndrome: a historic perspective,South Med J 76:232, 1983.

Roda JM, Gonzalez C, Blazquez, MG, et al: Intradural herniated cervicaldisc: case report, J Neurosurg 57:278, 1982.

Rosenorn J, Hansen EB, Rosenorn MA: Anterior cervical discectomy withand without fusion, J Neurosurg 59:252, 1983.

Semmes RE, Murphey F: The syndrome of unilateral rupture of the sixthcervical intervertebral disk, with compression of the seventh nerve root:a report of four cases with symptoms simulating coronary disease, JAMA121:1209, 1943.

Sherk HH, Watters WC III, Zeiger L: Evaluation and treatment of neckpain, Orthop Clin North Am 13:439, 1982.

Simmons EH, Bhalla SK: Anterior cervical discectomy and fusion: aclinical and biomechanical study with eight-year follow-up, with a noteon discography: technique and interpretation of results by WP Butt,J Bone Joint Surg 51B:225, 1969.

Simmons JCH: Rupture of cervical intervertebral discs. In Edmonson AS,Crenshaw AH, eds: Campbell’s operative orthopaedics, ed 6, St Louis,1980, Mosby.

Smith GW, Robinson RA: Anterior lateral cervical disc removal andinterbody fusion for cervical disc syndrome, Bull Johns Hopkins Hosp96:223, 1955.

Stookey B: Cervical chrondroma, Arch Neurol Psychol 20:275, 1928.Tamura T: Cranial symptoms after cervical injury: aetiology and treatment

of the Barre-Lieou syndrome, J Bone Joint Surg 71B:282, 1989.Verbeist H: A lateral approach to the cervical spine: technique and

indications, J Neurosurg 28:191, 1968.Viikari-Juntura E, Porras M, Laasonen EM: Validity of clinical tests in the

diagnosis of root compression in cervical disc disease, Spine 14:253,1989.

Welsh LW, Welsh JJ, Chinnici JC: Dysphagia due to cervical spine surgery,Ann Otol Rhinol Laryngol 96:112, 1987.

White AA, Jupiter J, Southwick WO, Panjabi MM: An experimental studyof the immediate load-bearing capacity of three surgical constructionsfor anterior spine fusions, Clin Orthop 91:21, 1973.

White AA, Southwick WO, DePonte RJ, et al: Relief of pain by anteriorcervical spine fusion for spondylosis: a report of sixty-five cases, J BoneJoint Surg 55A:525, 1973.

Whitecloud TS: Management of radiculopathy and myelopathy by theanterior approach: the cervical spine, Philadelphia, 1983, JB Lippincott.

Yamamoto I, Ikeda A, Shibuya N, et al: Clinical long-term results ofanterior discectomy without interbody fusion for cervical disc disease,Spine 16:272, 1991.

THORACIC DISC DISEASEAntoni N: Fall av kronisk rotkompression med ovanlig orsak, hernia nuclei

pulposi disci intervertebralis, Sv Lakartidn 28:436, 1931.Bohlman HH, Zdeblick TA: Anterior excision of herniated thoracic discs,

J Bone Joint Surg 70A:1038, 1988.de Looze MP, Toussaint HM, van Dieen JH, Kemper HC: Joint moments

and muscle activity in the lower extremities and lower back in lifting andlowering tasks, J Biomech 26:1067, 1993.

Fessler RG, Sturgill M: Review: complications of surgery for thoracic discdisease, Surg Neurol 49:609, 1998.

Gajdosik RL, Albert CR, Mitman JJ: Influence of hamstring length on thestanding position and flexion range of motion of the pelvic angle, lumbarangle, and thoracic angle, J Orthop Sports Phys Ther 20:213, 1994.

Hochman MS, Pena C, Ramirez R: Calcified herniated thoracic discdiagnosed by computerized tomography: case report, J Neurosurg 52:722, 1980.

Horowitz MB, Moossy JJ, Julian T, et al: Thoracic discectomy usingvideo-assisted thoracoscopy, Spine 19:1082, 1994.

Love JG, Kiefer EJ: Root pain and paraplegia due to protrusions of thoracicintervertebral disks, J Neurosurg 15:62, 1950.

Maiman DJ, Larson SJ, Luck E, El-Ghatit A: Lateral extracavity approachto the spine for thoracic disc herniation: report of 23 cases, Neurosurgery14:178, 1984.

Martucci E, Mele C, Martella P: Thoracic intervertebral disc protrusion,Ital J Orthop Traumatol 10:333, 1984.

Milgrom C, Finestone A, Lev B, et al: Overexertional lumbar and thoracicback pain among recruits: a prospective study of risk factors andtreatment regimens, J Spinal Disord 6:187, 1993.

Naunheim KS, Barnett MG, Crandall DG, et al: Anterior exposure of thethoracic spine, Ann Thorac Surg 57:1436, 1994.

O’Leary PF, Camins MB, Polifroni NV, Floman Y: Thoracic disc disease:clinical manifestations and surgical treatment, Bull Hosp Jt Dis 44:27,1984.

Omojola MF, Cardoso ER, Fox AJ, et al: Thoracic myelopathy secondaryto ossified ligamentum flavum: case report, J Neurosurg 56:448, 1982.

Panjabi MM, Krag MH, Dimnet JC, et al: Thoracic spine centers of rotationin the sagittal plane, J Orthop Res 1:387, 1984.

Regan JJ, Ben-Yishay A, Mack MJ: Video-assisted thoracoscopic exci-sion of herniated thoracic disc: description of technique and prelim-inary experience in the first 29 cases, J Spinal Disord 11:183, 1998.

Ridenour TR, Haddad SF, Hitchon PW, et al: Herniated thoracic disks:treatment and outcome, J Spinal Disord 6:218, 1993.

Rogers MA, Crockard HA: Surgical treatment of the symptomaticherniated thoracic disk, Clin Orthop 300:70, 1994.

Rosenthal D, Rosenthal R, de Simone A: Removal of a protruded thoracicdisc using microsurgical endoscopy, a new technique, Spine 19:1087,1994.

Sekhar LN, Jannetta PJ: Thoracic disc herniation: operative approaches andresults, Neurosurgery 12:303, 1983.

Stone JL, Lichtor T, Banerjee S: Intradural thoracic disc herniation, Spine19:1281, 1994.

Vaccaro AR, Rizzolo SJ, Allardyce TJ, et al: Placement of pedicle screwsin the thoracic spine. I. Morphometric analysis of the thoracic vertebrae,J Bone Joint Surg 77A:1193, 1995.

Vaccaro AR, Rizzolo SJ, Balderston RA, et al: Placement of pedicle screwsin the thoracic spine. II. An anatomical and radiographic assessment,J Bone Joint Surg 77A:1200, 1995.

Vanichkachorn JS, Vaccaro AR: Thoracic disk disease: diagnosis andtreatment, J Am Acad Orthop Surg 8:159, 2000.

LUMBAR DISC DISEASE: ETIOLOGY, DIAGNOSIS,AND CONSERVATIVE TREATMENTAlcoff J, Jones E, Rust P, Newman R: Controlled trial of imipramine for

chronic low back pain, J Fam Pract 14:841, 1982.American Medical Association: Guides to the evaluation of permanent

impairment, ed 4, Chicago, 1993, American Medical Association.Atkinson JH, Kremer EF, Garfin SR: Psychopharmacological agents in the

treatment of pain, J Bone Joint Surg 67A:337, 1985.Basmajian JV: Acute back pain and spasm: a controlled multicenter trial of

combined analgesic and antispasm agents, Spine 14:438, 1989.Bell GR, Rothman RH: The conservative treatment of sciatica, Spine 9:54,

1984.Bergquist-Ullman M, Larsson U: Acute low back pain in industry: a

controlled prospective study with special reference to therapy andconfounding factors, Acta Orthop Scand Suppl 170:1, 1977.




Berman AT, Garbarino JL, Fisher ST, Bosacco SJ: The effects of epiduralinjection of local anesthetics and corticosteroids on patients withlumbosciatic pain, Clin Orthop 188:144, 1984.

Bernard TN, Kirkaldy-Willis WH: Recognizing specific characteristics ofnonspecific low back pain, Clin Orthop 217:266, 1987.

Berwick DM, Budman S, Feldstein M: No clinical effects of back schoolsin an HMO: a randomized prospective trial, Spine 14:338, 1989.

Bigos SJ, Battie MC: Acute care to prevent back disability: ten years ofprogress, Clin Orthop 221:121, 1987.

Blower PW: Neurologic patterns in unilateral sciatica: a prospective studyof 100 new cases, Spine 6:175, 1981.

Bostman OM: Body mass index and height in patients requiring surgery forlumbar intervertebral disc herniation, Spine 18:851, 1993.

Cauthen C: Lumbar spine surgery, Baltimore, 1983, Williams & Wilkins.Christodoulides AN: Ipsilateral sciatica on femoral nerve stretch test is

pathognomonic of an L4-5 disc protrusion, J Bone Joint Surg 71B:88,1989.

Clarke NMP, Cleak DK: Intervertebral lumbar disc prolapse in children andadolescents, J Pediatr Orthop 3:202, 1983.

Cohen JE, Frank JW, Bombardier C, Guillemin F: Group educationinterventions for people with low back pain: an overview of theliterature, Spine 19:1214, 1994.

Cuckler JM, Bernini PA, Wiesel SW, et al: The use of epidural steroids inthe treatment of lumbar radicular pain, J Bone Joint Surg 67A:63, 1985.

de Seze S: Sciatique ‘‘banale’’ et disques lombo-sacres, La Presse Medicale51-52:570, 1940.

de Seze S: Histoire de la sciatique, Rev Neurol 138:1019, 1982.DeSio JM, Kahn CH, Warfield CA: Facial flushing and/or generalized

erythema after epidural steroid injection, Anesth Analg 80:617, 1995.Deyo RA: Conservative therapy for low back pain: distinguishing useful

from useless therapy, JAMA 250:1057, 1983.Deyo RA, Diehl AK, Rosenthal M: How many days of bed rest for acute

low back pain: a randomized clinical trial, N Engl J Med 315:1064,1986.

Deyo RA, Walsh NE, Martin DC, et al: A controlled trial of transcutaneouselectrical nerve stimulation (TENS) and exercise for chronic low backpain, N Engl J Med 322:1627, 1990.

el-Khoury GY, Ehara S, Weinstein JN, et al: Epidural steroid injection: aprocedure ideally performed with fluoroscopic control, Radiology168:554, 1988.

Estridge MN, Rouhe SA, Johnson NG: The femoral stretching test: avaluable sign in diagnosing upper lumbar disc herniations, J Neurosurg57:813, 1982.

Fairbank JCT, O’Brien JP: The iliac crest syndrome: a treatable cause oflow-back pain, Spine 8:220, 1983.

Farfan HF: The torsional injury of the lumbar spine, Spine 9:53, 1984.Fisher RG, Saunders RL: Lumbar disc protrusion in children, J Neurosurg

54:480, 1981.Friberg O: Clinical symptoms and biomechanics of lumbar spine and hip

joint in leg length inequality, Spine 8:643, 1983.Galm R, Frohling M, Rittmeister M, Schmitt E: Sacroiliac joint dysfunction

in patients with imaging-proven lumbar disc herniation, Eur Spine J7:450, 1998.

Giles LGF, Taylor JR: Low back pain associated with leg length inequality,Spine 6:510, 1981.

Grabel JD, Davis R, Zappulla R: Intervertebral disc space cyst simulatinga recurrent herniated nucleus pulposus, J Neurosurg 69:137, 1988.

Hansen FR, Bendix T, Skov P, et al: Intensive, dynamic back-muscleexercises, conventional physiotherapy, or placebo-control treatmentof low-back pain: a randomized, observer-blind trial, Spine 18:98:1993.

Hazard RG, Fenwick JW, Kalisch SM, et al: Functional restoration withbehavioral support: a one-year prospective study of patients with chroniclow-back pain, Spine 14:157, 1989.

Herron LD, Pheasant HC: Prone knee-flexion provocative testing forlumbar disc protrusion, Spine 5:65, 1980.

Hopwood MB, Abram SE: Factors associated with failure of lumbarepidural steroids, Reg Anesth 18:238, 1993.

Kikuchi S, Hasue M, Nishiyama K, et al: Anatomical and clinical studiesof radicular symptoms, Spine 9:23, 1984.


Klier I, Santo M: Low back pain as presenting symptoms of chronicgranulocytic leukemia, Orthop Rev 11:111, 1982.

Kosteljanetz M, Bang F, Schmidt-Olsen S: The clinical significance ofstraight-leg raising (Lasegue’s sign) in the diagnosis of prolapsed lumbardisc: interobserver variation and correlation with surgical findings, Spine13:393, 1988.

Kostuik JP, Bentivoglio J: The incidence of low-back pain in adultscoliosis, Spine 6:268, 1981.

Kushner FH, Olson JC: Retinal hemorrhage as a consequence of epiduralsteroid injection, Arch Ophthalmol 113:309, 1995.


Malmivaara A, Hakkinen U, Aro T, et al: The treatment of acute low backpain—bed rest, exercises, or ordinary activity? N Engl J Med 332:1786,1995.

Melleby A, Kraus H: Chronic back pain: use of a YMCA-developedexercise regimen, J New Develop Clin Med 5:75, 1987.

Miller A, Stedman GH, Beisaw NE, Gross PT: Sciatica caused by anavulsion fracture of the ischial tuberosity, J Bone Joint Surg 69A:143,1987.

Nachemson AL: Prevention of chronic back pain: the orthopaedic challengefor the 80s, Bull Hosp Jt Dis 44:1, 1984.

Natchev E, Valentino V: Low back pain and disc hernia: observation duringauto-traction treatment, Manual Med 1:39, 1984.

Offierski CM, Macnab I: Hip-spine syndrome, Spine 8:316, 1983.Onel D, Tuzlaci M, Sari H, Demir K: Computed tomographic investiga-

tion of the effect of traction on lumbar disc herniations, Spine 14:82,1989.

Pheasant H, Bursk A, Goldfarb J, et al: Amitriptyline and chronic low-backpain: a randomized double-blind crossover study, Spine 8:552, 1983.

Postacchini F, Urso S, Tovaglia V: Lumbosacral intradural tumourssimulating disc disease, Int Orthop 5:283, 1981.

Ramamurthi B: Absence of limitation of straight leg raising in provedlumbar disc lesion: case report, J Neurosurg 52:852, 1980.

Renfrew DL, Moore TE, Kathol ME, et al: Correct placement of epiduralsteroid injections: fluoroscopic guidance and contrast administration,Am J Neuroradiol 12:1003, 1991.

Robinson JS: Sciatica and the lumbar disk syndrome: a historic perspective,South Med J 76:232, 1983.

Saag KG, Cowdery JS: Spine update: nonsteroid anti-inflammatory drugs:balancing benefits and risks, Spine 13:1530, 1994.

Saal JA, Saal JS: Nonoperative treatment of herniated lumbar intervertebraldisc with radiculopathy and outcome study, Spine 14:431, 1989.

Sandover J: Dynamic loading as a possible source of low back disorders,Spine 8:652, 1983.

Shiqing X, Quanzhi Z, Dehao F: Significance of the straight leg raising testin the diagnosis and clinical evaluation of lower lumbar intervertebraldisc protrusion, J Bone Joint Surg 69A:517, 1987.

Simmons JW, Dennis MD, Rath D: The back school: a total backmanagement program, Orthopedics 7:1453, 1984.

Smith SA, Massie JB, Chesnut R, Garfin SR: Straight leg raising:anatomical effects on the spinal nerve root without and with fusion,Spine 18:992, 1993.

Solheim LF, Siewers P, Paus B: The piriformis muscle syndrome: sciaticnerve entrapment treated with section of the piriformis muscle, ActaOrthop Scand 52:73, 1981.

Sprangfort E: Lasegue’s sign in patients with lumbar disc herniation, ActaOrthop Scand 42:459, 1971.

Tay EC, Chacha PB: Midline prolapse of a lumbar intervertebral disc withcompression of the cauda equina, J Bone Joint Surg 61B:43, 1979.

Tonelli L, Falasca A, Argentieri C, et al: Influence of psychic distress onshort-term outcome of lumbar disc surgery, J Neurosurg Sci 27:237,1983.

Troup JDG: Straight leg raising (SLR) and the qualifying tests for increasedroot tension: their predictive value after back and sciatic pain, Spine6:526, 1981.

Ueyoshi A, Shima Y: Studies on spinal braces with special reference to theeffects of increased abdominal pressure, Int Orthop 9:255, 1985.

Verta MJ Jr, Vitello J, Fuller J: Adductor canal compression syndrome,Arch Surg 119:345, 1984.

Waddell G: A new clinical model for the treatment of low-back pain, Spine12:632, 1987.

Waddell G, Main CJ, Morris EW, et al: Chronic low-back pain, psychologicdistress, and illness behavior, Spine 9:209, 1984.

Waddell G, McCullouch JA, Kummel E, et al: Nonorganic physical signsof low-back pain, Spine 5:117, 1980.




Ward NG: Tricyclic antidepressants for chronic low-back pain: mecha-nisms of action and predictors of response, Spine 11:661, 1986.


Weise MD, Garfin SR, Gelberman RH, et al: Lower-extremity sensibilitytesting in patients with herniated lumbar intervertebral discs, J BoneJoint Surg 67A:1219, 1985.

Weitz EM: The lateral bending sign, Spine 6:388, 1981.White AA III, Gordon SL: Synopsis: workshop on idiopathic low-back

pain, Spine 7:141, 1982.White AH, Derby R, Wynne G: Epidural injections for the diagnosis and

treatment of low-back pain, Spine 5:78, 1980.White AH, Taylor LW, Wynne G, Welch RB: Appendix: a diagnostic

classification of low-back pain, Spine 5:83, 1980.Willner S: Effect of a rigid brace on back pain, Acta Orthop Scand 56:40,

1985.Yoganandan N, Maiman DJ, Pintar F, et al: Microtrauma in the lumbar

spine: a cause of low back pain, Neurosurgery 23:162, 1988.Zaleske DJ, Bode HH, Benz R, Krishnamoorthy KS: Association of

sciatica-like pain and Addison’s disease: a case report, J Bone Joint Surg66A:297, 1984.

LUMBAR DISC DISEASE: SURGICAL TREATMENTAND RESULTSAdams CB: ‘‘I’ve torn it: how to repair it,’’ Br J Neurosurg 9:201, 1995.Balderston RA, Gilyard GG, Jones AA, et al: The treatment of lumbar

disc herniation: simple fragment excision versus disc space curettage,J Spinal Disord 4:22, 1991.

Blaauw G, Braakman R, Gelpke GJ, Singh R: Changes in radicular functionfollowing low-back surgery, J Neurosurg 69:649, 1988.

Blower PW: Neurologic patterns in unilateral sciatica: a prospective studyof 100 new cases, Spine 6:175, 1981.

Bradford DS, Garcia A: Lumbar intervertebral disk herniations in childrenand adolescents, Orthop Clin North Am 2:583, 1971.

Bryant MS, Bremer AM, Nguyen TQ: Autogeneic fat transplants in theepidural space in routine lumbar spine surgery, Neurosurgery 13:367,1983.

Capanna AH, Williams RW, Austin DC, et al: Lumbar discectomy—percentage of disc removal and detection of anterior annulus perforation,Spine 6:610, 1981.

Carruthers CC, Kousaie KN: Surgical treatment after chemonucleolysisfailure, Clin Orthop 165:172, 1982.

Castellvi AE, Goldstein LA, Chan DPK: Lumbosacral transitionalvertebrae and their relationship with lumbar extradural defects, Spine9:493, 1984.

Cauthen C: Lumbar spine surgery, Baltimore, 1983, Williams & Wilkins.Chow SP, Leong JCY, Yau AC: Anterior spinal fusion for deranged lumbar

intervertebral disc: a review of 97 cases, Spine 5:452, 1980.Clarke NMP, Cleak DK: Intervertebral lumbar disc prolapse in children and

adolescents, J Pediatr Orthop 3:202, 1983.Crawshaw C, Frazer AM, Merriam WF, et al: A comparison of surgery and

chemonucleolysis in the treatment of sciatica: a prospective randomizedtrial, Spine 9:195, 1984.

Crock HV: Normal and pathological anatomy of the lumbar spinal nerveroots, J Bone Joint Surg 63B:487, 1981.

Delamarter RB, Leventhal MR, Bohlman HH: Diagnosis of recurrentlumbar disc herniation vs postoperative scar by gadolinium-DTPAenhanced magnetic resonance imaging (unpublished data).

Di Lauro L, Poli R, Bortoluzzi M, Marini G: Paresthesias after lumbar discremoval and their relationship to epidural hematoma, J Neurosurg57:135, 1982.

Donaldson WF, Star MJ, Thorne RP: Surgical treatment for the far lateralherniated lumbar disc, Spine 18:1263, 1993.

Dvonch V, Scarff T, Bunch WT, et al: Dermatomal somatosensory evokedpotentials: their use in lumbar radiculopathy, Spine 9:291, 1984.

Ebeling U, Kalbarcyk H, Reulen HJ: Microsurgical reoperation followinglumbar disc surgery: timing, surgical findings, and outcome in 92patients, J Neurosurg 70:397, 1989.

Ebersold MJ, Quast LM, Bianco AJ: Results of lumbar discectomy in thepediatric patient, J Neurosurg 67:643, 1987.

Eie N, Solgaard T, Kleppe H: The knee-elbow position in lumbar discsurgery: a review of complications, Spine 8:897, 1983.

Eismont FJ, Wiesel SW, Rothman RH: The treatment of dural tearsassociated with spinal surgery, J Bone Joint Surg 63A:1132, 1981.

Epstein JA, Carras R, Ferrar J, et al: Conjoined lumbosacral nerve roots,J Neurosurg 55:585, 1981.

Epstein NE: Different surgical approaches to far lateral lumbar discherniations, J Spinal Disord 8:383, 1995.

Epstein NE: Evaluation of varied surgical approaches used in themanagement of 170 far-lateral lumbar disc herniations: indications andresults, J Neurosurg 83:648, 1995.

Fisher RG, Saunders RL: Lumbar disc protrusion in children, J Neurosurg54:480, 1981.

Floman Y, Wiesel SW, Rothman RH: Cauda equina syndrome presenting asa herniated lumbar disc, Clin Orthop 147:234, 1980.

Flynn JC, Price CT: Sexual complications of anterior fusion of the lumbarspine, Spine 9:489, 1984.

Frymoyer JW, Hanaley EN, Howe J: A comparison of radiographic findingsin fusion and nonfusion patients ten or more years following lumbar discsurgery, Spine 5:435, 1979.

Garrido E, Rosenwasser RH: Painless footdrop secondary to lumbar discherniation: report of two cases, Neurosurgery 8:484, 1981.

Getty CJM, Johnson JR, Kirwan E, Sullivan MF: Partial undercuttingfacetectomy for bony entrapment of the lumbar nerve root, J Bone JointSurg 63B:330, 1981.

Greenberg RP, Ducker TB: Evoked potentials in the clinical neurosciences,J Neurosurg 56:1, 1982.

Hastings DE: A simple frame of operations of the lumbar spine, Can J Surg12:251, 1969.

Hoyland JA, Freemont AJ, Denton J, et al: Retained surgical swab debrisin post-laminectomy arachnoiditis and peridural fibrosis, J Bone JointSurg 70B:659, 1988.

Hurme M, Torma AT, Einola S: Operated lumbar disc herniation:epidemiological aspects, Ann Chir Gynaecol 72:33, 1983.

Jacobs RR, McClain O, Neff J: Control of postlaminectomy scar formation:an experimental and clinical study, Spine 5:223, 1980.

Jane JA, Haworth CS, Broaddus WC, et al: A neurosurgical approach tofar-lateral disc herniation, J Neurosurg 72:143, 1990.

Jensen TT, Asmussen K, Berg-Hansen E-M, et al: First-time operation forlumbar disc herniation with or without free fat transplantation, Spine21:1072, 1996.

Kadish L, Simmons EH: Anomalies of the lumbosacral nerve roots andanatomical investigation and myelographic study, J Bone Joint Surg66B:411, 1984.

Kahanovitz N, Viola K, Muculloch J: Limited surgical discectomy andmicrodiscectomy: a clinical comparison, Spine 14:79, 1989.

Kambin P: Lumbar discectomy, surgical technique. Paper presented at theAmerican Academy of Orthopaedic Surgeons Course, St Louis, May1996.

Kataoka O, Nishibayashi Y, Sho T: Intradural lumbar disc herniation:report of three cases with a review of the literature, Spine 14:529,1989.

Kelly RE, Dinner MH, Lavyne MH, Andrews DW: The effect of lumbardisc surgery on postoperative pulmonary function and temperature: acomparison study of microsurgical lumbar discectomy with standardlumbar discectomy, Spine 18:287, 1993.

Key JA: Intervertebral-disk lesions in children and adolescents, J BoneJoint Surg 32A:97, 1950.

Kikuchi S, Hasue M, Nishiyama K, et al: Anatomical and clinical studiesof radicular symptoms, Spine 9:23, 1984.


Kiviluoto O: Use of free fat transplants to prevent epidural scar formation:an experimental study, Acta Orthop Scand Suppl 164:1, 1976.

Kostuik JP, Harrington I, Alexander D, et al: Cauda equina syndrome andlumbar disc hernia, J Bone Joint Surg 68A:386, 1986.

Kuslich SD, Dowdle JA: Two-year follow-up results of the BAK interbodyfusion device. Proceedings of the Ninth Annual Meeting of the NorthAmerican Spine Society, Oct 1994.

Leavitt F, Garron DC, Whisler WW, D’Angelo CM: A comparison ofpatients treated by chymopapain and laminectomy for low back painusing a multidimensional pain scale, Clin Orthop 146:136, 1980.

Leong JCY, Chun SY, Grange WJ, Fang D: Long-term results of lumbarintervertebral disc prolapse, Spine 8:793, 1983.

Lewis PJ, Weir BKA, Broad RW, Grace MG: Long-term prospective studyof lumbosacral discectomy, J Neurosurg 67:49, 1987.

Lindholm TS, Pylkkanen P: Discitis following removal of intervertebraldisc, Spine 7:618, 1982.




Lowell TD, Errico TJ, Fehlings MG, et al: Microdiskectomy for lumbardisk herniation: a review of 100 cases, Orthopedics 18:985, 1995.

Macnab I: Management of low back pain. In Ahstrom JP Jr, ed: Currentpractice in orthopaedic surgery, St Louis, 1973, Mosby.


Macon JB, Poletti CE: Conducted somatosensory evoked potentials duringspinal surgery. I. Control, conduction velocity measurements, J Neuro-surg 57:349, 1982.

Macon JB, Poletti CE, Sweet WH, et al: Conducted somatosensory evokedpotentials during spinal surgery. II. Clinical applications, J Neurosurg57:354, 1982.

Maroon JC, Kopitnik TA, Schulhoff LA, et al: Diagnosis and microsurgicalapproach to far-lateral disc herniation in the lumbar spine, J Neurosurg72:378, 1990.

Moore AJ, Chilton JD, Uttley D: Long-term results of microlumbardiscectomy, Br J Neurosurg 8:319, 1994.

Mullen JB, Cook WA Jr: Reduction of postoperative lumbar hemilaminec-tomy pain with Marcaine, J Neurosurg 51:126, 1975.

Nachemson AL: Prevention of chronic back pain: the orthopaedic challengefor the 80s, Bull Hosp Jt Dis Orthop 44:1, 1984.

Nakano N, Tomita T: Results of surgical treatment of low back pain: acomparative study of the anterior and posterior approach, Int Orthop4:101, 1980.

Neidre A, Macnab I: Anomalies of the lumbosacral nerve roots, Spine8:294, 1983.

Newman MH: Outpatient conventional laminotomy and disc excision,Spine 20:353, 1995.

Nielsen B, deNully M, Schmidt K, Hansen RI: A urodynamic study ofcauda equina syndrome due to lumbar disc herniation, Urol Int 35:167,1980.

Onik G, Helms CA: Automated percutaneous lumbar diskectomy, AmJ Roentgenol 156:531, 1991.

Pasztor E, Szarvas I: Herniation of the upper lumbar discs, Neurosurg Rev4:151, 1981.

Pau A, Viale ES, Turtas S, Zirattu G: Redundant nerve roots of the caudaequina, Ital J Orthop Traumatol 4:95, 1984.

Posner I, White AA III, Edwards WT, Hayes WC: A biomechanical analysisof the clinical stability of the lumbar and lumbosacral spine, Spine 7:374,1982.

Postacchini F, Urso S, Ferro L: Lumbosacral nerve-root anomalies, J BoneJoint Surg 64A:721, 1982.

Rechtine GR, Reinert CM, Bohlman HH: The use of epidural morphine todecrease postoperative pain in patients undergoing lumbar laminectomy,J Bone Joint Surg 66A:1, 1984.

Rish BL: A critique of the surgical management of lumbar disc disease ina private neurosurgical practice, Spine 9:500, 1984.

Ruggieri F, Specchia L, Sabalat S, et al: Lumbar disc herniation: diagnosis,surgical treatment, and recurrence: a review of 872 operated cases, ItalJ Orthop Traumatol 14:15, 1988.

Semmes RE: Diagnosis of ruptured intervertebral discs without contrastmyelography and comment upon recent experience with modifiedhemilaminectomy for their removal, Yale J Biol Med 11:433, 1939.

Silvers HR: Microsurgical versus standard lumbar discectomy, Neurosur-gery 22:837, 1988.

Smith RV: Intradural disc rupture: report of two cases, J Neurosurg 55:117,1981.

Solgaard T, Kleppe H: Long-term results of lumbar intervertebral discprolapse, Spine 8:793, 1983.

Solheim LF, Siewers P, Paus B: The piriformis muscle syndrome: sciaticnerve entrapment treated with section of the piriformis muscle, ActaOrthop Scand 52:73, 1981.

Spangfort EV: The lumbar disc herniation: a computer-aided analysis of2504 operations, Acta Orthop Scand Suppl 142:1, 1972.

Spencer DL, Irwin GS, Miller JA: Anatomy and significance of fixation ofthe lumbosacral nerve roots in sciatica, Spine 8:672, 1983.

Spengler DM: Lumbar discectomy: results with limited disc excision andselective foraminotomy, Spine 7:604, 1982.

Spengler DM, Freeman CW: Patient selection for lumbar discectomy: anobjective approach, Spine 4:129, 1979.

Techakapuch S, Bangkok T: Rupture of the lumbar cartilage plate into thespinal canal in an adolescent, J Bone Joint Surg 63A:481, 1981.

Vaughan PA, Malcolm BW, Maistrelli GL: Results of L4-L5 disc excisionalone versus disc excision and fusion, Spine 13:690, 1988.

Waddell G, Main CJ, Morris EW, et al: Chronic low-back pain, psychologicdistress, and illness behavior, Spine 9:209, 1984.

Waddell G, Reilly S, Torsney B, et al: Assessment of the outcome of lowback surgery, J Bone Joint Surg 70B:723, 1988.

Wayne SJ: A modification of the tuck position for lumbar spine surgery: a15-year follow-up study, Clin Orthop 184:212, 1984.


Weinstein J, Spratt KF, Lehmann T, et al: Lumbar disc herniation: acomparison of the results of chemonucleolysis and open discectomy afterten years, J Bone Joint Surg 68A:43, 1986.

Weinstein JN, Scafuri RL, McNeill TW: The Rush-Presbyterian–St. Luke’slumbar spine analysis form: a prospective study of patients with ‘‘spinalstenosis,’’ Spine 8:891, 1983.

Weir BKA: Prospective study of 100 lumbosacral discectomies, J Neuro-surg 50:283, 1979.

Weise MD, Garfin SR, Gelberman RH, et al: Lower-extremity sensibilitytesting in patients with herniated lumbar intervertebral discs, J BoneJoint Surg 67A:1219, 1985.

Wilberger JE Jr, Pang D: Syndrome of the incidental herniated lumbar disc,J Neurosurg 59:137, 1983.

Wilkinson HA, Baker S, Rosenfeld S: Gelfoam paste in experimentallaminectomy and cranial trephination: hemostasis and bone healing,J Neurosurg 54:664, 1981.

Williams RW: Microlumbar discectomy: a conservative surgical approachto the virgin herniated lumbar disc, Spine 3:175, 1978.

Williams RW: Microcervical foraminotomy: a surgical alternative forintractable radicular pain, Spine 8:708, 1983.

Williams RW: Microdiskectomy—myth, mania, or milestone? An 18-yearsurgical adventure, Mt Sinai J Med 58:139, 1991.

Yong-Hing K, Reilly J, de Korompay V, Kirkaldy-Willis WH: Preventionof nerve root adhesions after laminectomy, Spine 5:59, 1980.

Zahrawi F: Microlumbar discectomy (MLD), Spine 13:358, 1988.Zahrawi F: Microlumbar discectomy: is it safe as an outpatient procedure?

Spine 19:1070, 1994.Zamani MH, MacEwen GD: Herniation of the lumbar disc in children and

adolescents, J Pediatr Orthop 2:528, 1982.

CHEMONUCLEOLYSISAbdel-Salam A, Eyres KS, Cleary J: A new paradiscal injection technique

for the relief of back spasm after chemonucleolysis, Br J Rheumatol31:491, 1992.

Agre K, Wilson RR, Brim M, McDermott DJ: Chymodiactin postmarketingsurveillance: demographic and adverse experience data in 29,075patients, Spine 9:479, 1984.

Alexander AH: Debate: resolved—chemonucleolysis is the best treatmentof the recalcitrant acute herniated nucleus pulposus: what’s new andwhat’s true in the Napa Valley. Paper presented March 14, 1985.

Apfelbach HW: Technique for chemonucleolysis, Orthopedics 6:1613,1983.

Barach EM, Nowak RM, Lee TG, Tomlanovich MC: Epinephrine fortreatment of anaphylactic shock, JAMA 251:2118, 1984.

Battit GE: Anaphylaxis associated with chymopapain injections, JAMA253:977, 1985.

Benoist M, Bonneville JF, Lassale B, et al: A randomized, double-blindstudy to compare low-dose with standard-dose chymopapain in thetreatment of herniated lumbar intervertebral discs, Spine 18:28, 1993.

Benoist M, Deburge A, Heripret G, et al: Treatment of lumbar discherniation by chymopapain chemonucleolysis: a report on 120 patients,Spine 7:613, 1982.

Bernstein IL: Adverse effects of chemonucleolysis, JAMA 250:1167,1983.

Boumphrey FRS, Bell GR, Modic M, et al: Computed tomographyscanning after chymopapain injection for herniated nucleus pulposus: aprospective study, Clin Orthop 219:120, 1987.

Bradford DS, Cooper KM, Oegema TR, Jr: Chymopapain, chemonucleol-ysis, and nucleus pulposus regeneration, J Bone Joint Surg 65A:1220,1983.

Brown MD, Tompkins JS: Pain response post-chemonucleolysis or discexcision, Spine 14:321, 1989.

Burkus JS, Alexander AH, Mitchell JB: Evaluation and treatment ofchemonucleolysis failures, Orthopedics 11:1677, 1988.

Carruthers CC, Kousaie KN: Surgical treatment after chemonucleolysisfailure, Clin Orthop 165:172, 1982.




Castro WH, Halm H, Jerosch J, et al: Long-term changes in the mag-netic resonance image after chemonucleolysis, Eur Spine J 3:222,1994.

Crawshaw C, Frazer AM, Merriam WF, et al: A comparison of surgery andchemonucleolysis in the treatment of sciatica: a prospective randomizedtrial, Spine 9:195, 1984.

Dolan P, Adams MA, Hutton WC: The short-term effects of chymopapainon intervertebral discs, J Bone Joint Surg 69B:422, 1987.

Eguro H: Transverse myelitis following chemonucleolysis: report of a case,J Bone Joint Surg 65A:1328, 1983.

Fraser RD: Chymopapain for the treatment of intervertebral disc herniation:the final report of a double-blind study, Spine 9:815, 1984.

Garreau C, Dessarts I, Lassale B, et al: Chemonucleolysis: correlation ofresults with the size of the herniation and the dimensions of the spinalcanal, Eur Spin J 4:77, 1995.

Grammer LC, Ricketti AJ, Schafer MF, Patterson R: Chymopapain allergy:case reports and identification of patients at risk for chymopapainanaphylaxis, Clin Orthop 188:139, 1984.

Hall BB, McCulloch JA: Anaphylactic reactions following the intradiscalinjection of chymopapain under local anesthesia, J Bone Joint Surg65A:1215, 1983.

Hill GM, Ellis EA: Chemonucleolysis as an alternative to laminectomy forthe herniated lumbar disc, Clin Orthop 225:229, 1987.

Hoogland T, Scheckenbach C: Low-dose chemonucleolysis combined withpercutaneous nucleotomy in herniated cervical disks, J Spinal Disord8:228, 1995.

Javid MJ: Chemonucleolysis versus laminectomy: a cohort comparison ofeffectiveness and charges, Spine 20:2016, 1995.

Kato F, Mimatsu K, Kawakami N, Miura T: Changes seen on magneticresonance imaging in the intervertebral disc space after chemonucleol-ysis: a hypothesis concerning regeneration of the disc after chemonu-cleolysis, Neuroradiology 34:267, 1992.

Kato F, Mimatsu K, Kawakami N, et al: Serial changes observed bymagnetic resonance imaging in the intervertebral disc after chemonu-cleolysis: a consideration of the mechanism of chemonucleolysis, Spine17:934, 1992.

Leavitt F, Garron DC, Whisler WW, D’Angelo CM: A comparison ofpatients treated by chymopapain and laminectomy for low back painusing a multidimensional pain scale, Clin Orthop 146:136, 1980.

Maciunas RJ, Onofrio BM: The long-term results of chymopapain: ten-yearfollow-up of 268 patients after chemonucleolysis, Clin Orthop 206:37,1986.

McCulloch JA: Chemonucleolysis: experience with 2000 cases, ClinOrthop 146:128, 1980.

McCulloch JA, Ferguson JM: Outpatient chemonucleolysis, Spine 6:606,1981.

Moneret-Vautrin DA, Feldmann L, Kanny G, et al: Incidence and riskfactors for latent sensitization to chymopapain: predictive skin-pricktests in 700 candidates for chemonucleolysis, Clin Exp Allergy 24:471,1994.

Nachemson AL, Rydevik B: Chemonucleolysis for sciatica: a criticalreview, Acta Orthop Scand 59:56, 1988.

Naylor A, Earland C, Robinson J: The effect of diagnostic radiopaque fluidsused in discography on chymopapain activity, Spine 8:875, 1983.

Nordby EJ, Wright PH: Efficacy of chymopapain in chemonucleolysis: areview, Spine 19:2578, 1994.

Nordby EJ, Wright PH, Schofield SR: Safety of chemonucleolysis: adverseeffects reported in the United States, 1982-1991, Clin Orthop 293:122,1993.

Oegema TR Jr, Swedenberg S, Johnson SL, et al: Residual chymopapainactivity after chemonucleolysis in normal intervertebral discs in dogs,J Bone Joint Surg 74A:831, 1992.

Parkinson D: Late results of treatment of intervertebral disc disease withchymopapain, J Neurosurg 59:990, 1983.

Shields CB, Reiss SJ, Garretson HD: Chemonucleolysis with chymopa-pain: results in 150 patients, J Neurosurg 67:187, 1987.

Simmons JW, Stavinoha WB, Knodel LC: Update and review ofchemonucleolysis, Clin Orthop 183:51, 1984.

Smith S, Leibrock LG, Gelber BR, Pierson EW: Acute herniated nucleuspulposus with cauda equina compression syndrome following chemo-nucleolysis: report of three cases, J Neurosurg 66:614, 1987.

Strum PF, Armstrong GW, O’Neil DJ, Belanger JM: Far lateral lumbar discherniation treated with an anterolateral retroperitoneal approach: reportof two cases, Spine 17:363, 1992.

Suguro T, Oegema TR, Bradford DS: Ultrastructural study of the short-termeffects of chymopapain on the intervertebral disc, J Orthop Res 4:281,1986.

Tregonning GD, Transfeldt EE, McCulloch JA, et al: Chymopapain versusconventional surgery for lumbar disc herniation: 10-year results oftreatment, J Bone Joint Surg 73B:481, 1991.

Tsay YG, Jones R, Calenoff E, et al: A preoperative chymopapainsensitivity test for chemonucleolysis candidates, Spine 9:764, 1984.

van Leeuwen RB, Hoogland PH: CT examination of 91 patients afterchemonucleolysis, Acta Orthop Scand 62:128, 1991.

Wakano K, Kasman R, Chao EY, et al: Biomechanical analysis of canineintervertebral discs after chymopapain injection: a preliminary report,Spine 8:59, 1983.

Weinstein J, Spratt KF, Lehmann T, et al: Lumbar disc herniation: acomparison of the results of chemonucleolysis and open discectomy afterten years, J Bone Joint Surg 68A:43, 1986.

Weitz EM: Paraplegia following chymopapain injection: a case report,J Bone Joint Surg 66A:1131, 1984.

Whisler WW: Anaphylaxis secondary to chymopapain, Orthopedics 6:1628, 1983.

Willis J, ed: Chymopapain administration procedures modified, FDA DrugBull 14:14, 1984.

PERCUTANEOUS LUMBAR DISCECTOMYBlankstein A, Rubinstein E, Ezra E, et al: Disc space infection and vertebral

osteomyelitis as a complication of percutaneous lateral discectomy, ClinOrthop 225:234, 1987.

Davis GW, Onik G: Clinical experience with automated percutaneouslumbar discectomy, Clin Orthop 238:98, 1989.

Goldstein TB, Mink JH, Dawson EG: Early experience with automatedpercutaneous lumbar discectomy in the treatment of lumbar discherniation, Clin Orthop 238:77, 1989.

Graham CE: Percutaneous posterolateral lumbar discectomy: an alternativeto laminectomy in the treatment of backache and sciatica, Clin Orthop238:104, 1989.

Hijikata S: Percutaneous nucleotomy: a new concept of technique and 12years’ experience, Clin Orthop 238:9, 1989.

Kahanovitz N, Viola K, Goldstein T, Dawson E: A multicenter analysis ofpercutaneous diskectomy, Spine 15:713, 1990.

Kahanovitz N, Viola K, McCullough J: Limited surgical diskectomy andmicrodiskectomy: a clinical comparison, Spine 14:79, 1989.

Kambin P, Brager MD: Percutaneous posterolateral discectomy: anatomyand mechanism, Clin Orthop 223:145, 1987.

Kambin P, Gellman H: Percutaneous lateral discectomy of the spine, ClinOrthop 174:127, 1983.

Kambin P, Schaffer JL: Percutaneous lumbar discectomy: review of 100patients and current practice, Clin Orthop 238:24, 1989.

Maroon JC, Onik G, Sternau L: Percutaneous automated discectomy: a newapproach to lumbar surgery, Clin Orthop 238:64, 1989.

Monteiro A, Lefevre R, Pieters G, Wilment E: Lateral decompression of apathological disc in the treatment of lumbar pain and sciatica, ClinOrthop 238:56, 1989.

Morris J: Percutaneous discectomy, Orthopedics 11:1483, 1988.Onik G, Helms CA, Ginsburg L: Percutaneous lumbar discectomy using a

new aspiration probe, Am J Radiol 144:1137, 1985.Onik G, Maroon J, Davis GW: Automated percutaneous discectomy at the

L5-S1 level: use of a curved cannula, Clin Orthop 238:71, 1989.Schreiber A, Suezawa Y, Leu H: Does percutaneous nucleotomy with

discoscopy replace conventional discectomy? Eight years of experienceand results in treatment of herniated lumbar disc, Clin Orthop 238:35,1989.

Schweigel J: Automated percutaneous discectomy: comparison withchymopapain. In Automated percutaneous discectomy, San Francisco,1988, University of California Press.

Shepperd JAN, James SE, Leach AB: Percutaneous disc surgery, ClinOrthop 238:43, 1989.

Stern MB: Early experience with percutaneous lateral discectomy, ClinOrthop 238:50, 1989.

Wilson D, Harbaugh R: Microsurgical and standard removal of protrudedlumbar disc: a comparative study, Neurosurgery 8:422, 1986.

COMPLICATIONS OF LUMBAR SPINE SURGERYBenoist M, Ficat C, Baraf P, Cauchoix J: Postoperative lumbar epiduro-

arachnoiditis: diagnostic and therapeutic aspects, Spine 5:432, 1980.




Bryant MS, Bremer AM, Nguyen TQ: Autogeneic fat transplants in theepidural space in routine lumbar spine surgery, Neurosurgery 13:367,1983.

Caplan LR, Norohna AB, Amico LL: Syringomyelia and arachnoiditis,J Neurol Neurosurg Psychiatr 53:106, 1990.

Choudhury AR, Taylor JC: Cauda equina syndrome in lumbar disc disease,Acta Orthop Scand 51:493, 1980.

Di Lauro L, Poli R, Bortoluzzi M, Marini G: Paresthesias after lumbar discremoval and their relationship to epidural hematoma, J Neurosurg57:135, 1982.

Eismont FJ, Wiesel SW, Rothman RH: The treatment of dural tearsassociated with spinal surgery, J Bone Joint Surg 63A:1132, 1981.

Floman Y, Wiesel SW, Rothman RH: Cauda equina syndrome presenting asa herniated lumbar disc, Clin Orthop 147:234, 1980.

Javid MJ, Nordby EJ, Ford LT, et al: Safety and efficacy of chymopapain(Chymodiactin) in herniated nucleus pulposus with sciatica: results of arandomized, double-blind study, JAMA 249:2489, 1983.

Jones AA, Stambough JL, Balderson RA, et al: Long-term results of lumbarspine surgery complicated by unintended incidental durotomy, Spine14:443, 1989.

May ARL, Brewster DC, Darling RC, et al: Arteriovenous fistula followinglumbar disc surgery, Br J Surg 68:41, 1981.

Mayer PJ, Jacobsen FS: Cauda equina syndrome after surgical treatment oflumbar spinal stenosis with application of free autogenous fat graft: areport of two cases, J Bone Joint Surg 71A:1090, 1989.

McLaren AC, Bailey SI: Cauda equina syndrome: a complication of lumbardiscectomy, Clin Orthop 204:143, 1986.

Nielsen B, deNully M, Schmidt K, Hansen RI: A urodynamic study ofcauda equina syndrome due to lumbar disc herniation, Urol Int 35:167,1980.

Puranen J, Makela J, Lahde S: Postoperative intervertebral discitis, ActaOrthop Scand 55:461, 1984.

Salander JM, Youkey JR, Rich NM, et al: Vascular injury related to lumbardisc surgery, J Trauma 24:628, 1984.

Shaw ED, Scarborough JT, Beals RK: Bowel injury as a complication oflumbar discectomy: a case report and review of the literature, J BoneJoint Surg 63A:478, 1981.

Zide BM, Wisoff JH, Epstein FJ: Closure of extensive and complicatedlaminectomy wounds: operative technique, J Neurosurg 67:59, 1987.

FAILED SPINE SURGERYBlaauw G, Braakman R, Gelpke GJ, Singh R: Changes in radicular function

following low-back surgery, J Neurosurg 69:649, 1988.Cauthen C: Lumbar spine surgery, Baltimore, 1983, Williams & Wilkins.Ebeling U, Kalbarcyk H, Reulen HJ: Microsurgical reoperation following

lumbar disc surgery: timing, surgical findings, and outcome in 92patients, J Neurosurg 70:397, 1989.

Finnegan WJ, Fenlin JM, Marval JP, et al: Results of surgical interventionin the symptomatic multiply operated back patient, J Bone Joint Surg61A:1077, 1979.

Frymoyer JW, Hanaley EN, Howe J: A comparison of radiographic findingsin fusion and nonfusion patients ten or more years following lumbar discsurgery, Spine 5:435, 1979.

Lehmann TR, LaRocca AS: Repeat lumbar surgery: a review of patientswith failure from previous lumbar surgery treated by spinal cordexploration and lumbar spinal fusion, Spine 6:615, 1981.

Long DM, Filtzer DL, BenDebba M, Hendler NH: Clinical features of thefailed-back syndrome, J Neurosurg 69:61, 1988.

Nakano N, Tomita T: Results of surgical treatment of low back pain: acomparative study of the anterior and posterior approach, Int Orthop4:101, 1980.

Quimjian JD, Matrka PJ: Decompression laminectomy and lateral spinalfusion in patients with previously failed lumbar spine surgery,Orthopedics 2:563, 1988.

Spengler DM, Freeman C, Westbrook R, Miller JW: Low-back painfollowing multiple lumbar spine procedures: failure of initial selection?Spine 5:356, 1980.

Tria AJ, Williams JM, Harwood D, Zawadsky JP: Laminectomy with andwithout spinal fusion, Clin Orthop 224:134, 1987.




lower back pain and disorders of intervertebral discs ... · chapter 39 lower back pain and...

Documents