spasticity

SPASTICITY

Prashant Makhija

OUTLINE

Introduction- Historical aspects & Epidemiology

Definition

Overview of Pathophysiology

Causes

Assessment

Management

Conclusion

INTRODUCTION The term ‘Spasticity’ is derived from the Greek ‘Spasticos’ &

‘Spaon’ ( to draw or stretch)

Term was first used in English by Good(1829)- describing ‘spastic wryneck’

First recognized by Orthopedic surgeons- Stromeyer (1838) performed subcutaneous tenotomy of contracted extremities

First description given by Little(1843)

A F Thilmann et al. Spasticity: Mechanisms and management. Springer 1993

William John Little himself suffered from Spasticity , treated by Stromeyer

Dedicated his dissertation “Symbolae ad talipedum varum cognoscendum” to the surgeon

Cerebral palsy now known as Little’s disease

A F Thilmann et al. Spasticity: Mechanisms and management. Springer 1993

EPIDEMIOLOGY- Burden of the illness

MS incidence is 4.2 cases per 100,000 and the prevalence is 0.9 per

1000 affects between 37% and 78%

SCI annual incidence of spinal cord injury (SCI) in the US is

approximately 11,000 40%

http://www.mdvu.org/library/disease/spasticity

Stroke the estimated annual incidence of ischemic and hemorrhagic

stroke is 183 per 100,000 approximately 35%

CP prevalence of CP as 3.6 per 1,000 children or about 1 in 278

children more than 90%

TBI at least 5.3 million population, currently have a long-term or

lifelong need for help to perform activities of daily living as a result of a traumatic brain injury

~ 50% http://www.mdvu.org/library/disease/spasticity

DEFINITION

“Spasticity is a motor disorder characterized by a velocity dependent

increase in tonic stretch reflexes (muscle tone) with exaggerated

tendon jerks (phasic stretch reflexes), resulting from

hyperexcitability of stretch reflex, as one component of uppermotor

neuron syndrome” J.W.Lance(1980)

Lance JW (1980) Symposium synopsis. In: Feldman RG,Young RR,Koella WP (eds) Spasticity: disordered motor control. Year Book

Medical Publishers, Chicago

Spasticity- characterstic features

Velocity dependence- increased tone of spasticity is velocity dependent, that is, the faster the stretch, the greater the muscle resistance

‘Clasp-knife’ phenomenon- spastic limb initially resists movement and then suddenly gives way, like the resistance of a folding knife blade

Distribution- differential distribution with antigravity muscles being more affected

Practical Neurology 2012;12:289–298

UMN Syndrome- accompaniments of Spasticity

Positive features Clonus- involuntary rhythmic contractions, response to sudden

sustained stretch, alternate loading and off-loading of muscle spindles

Spasms- sudden involuntary movements involving multiple muscle groups and joints, repetitive and sustained, represent an exaggerated reflex withdrawal response to nociceptive stimuli

Exaggerated tendon reflexes

Babinski sign

Spastic dystonia- tonic muscle overactivity that occurs without any triggers, due to an inability of motor units to cease firing after a voluntary or reflex contraction

Characteristic postures of spastic dystonia shoulder adduction and internal rotation elbow flexion forearm pronation, wrist and elbow flexion hip adduction ankle plantar flexion and inversion

can lead to contractures and deformities causing pain, discomfort

Negative components

Spastic co-contraction- inappropriate activation of antagonistic muscles during voluntary activity. It is due to loss of reciprocal inhibition during voluntary contraction

Motor weakness

Slowed movements

Loss of dexterity


PATHOPHYSIOLOGY Muscle tone visco-elastic properties of muscle neural drive from spinal motor neurons

Control Cortical- motor areas of the cortex facilitate ventromedial reticular

formation Supraspinal descending pathways Inhibitory pathway- dorsal reticulospinal tract, which arises in

the ventromedial reticular formation Excitatory pathways

1) Medial reticulospinal tract- arising in the bulbopontine tegmentum, major pathway

2) Vestibulospinal tract


European Journal of Neurology 2002, 9 (Suppl. 1): 3–9

Mechanisms at Various Levels

Cortical & Supraspinal descending pathways Loss of cortical facilitation of the inhibitory pathway(dorsal

reticulospinal tract) Partial spinal cord lesion, which destroys the inhibitory

pathways but preserves the excitatory fibres Complete spinal cord lesion affecting both inhibitory and

excitatory pathways

Spinal Cord Loss of recurrent inhibition- mediated by motor axon collaterals

and Renshaw cell Loss of reciprocal inhibition- mediated by antagonistic muscle

spindle afferents



Reduced inverse stretch reflex- mediated by Golgi tendon organs Reduced presynaptic inhibition of muscle spindle afferents

Spinal motor neuron Denervation supersensitivity Collateral sprouting

Muscles and joints Shortening of sarcomeres Loss of elastic tissue Fibro-fatty deposits in muscles and tendons



CAUSES

Cerebral palsy

Stroke

Multiple sclerosis

Traumatic Brain injury

Spinal Cord Injury

Anoxia

Neurodegenerative

DISABILITY

Orthopedic deformity such as hip dislocation, contractures, or scoliosis

Impairment of activities of daily living (eg, dressing, bathing, toileting)

Impairment of mobility (eg, inability to walk, roll, sit)

Skin breakdown secondary to positioning difficulties and shearing pressure

Pain

Sleep disturbance

Depression secondary to lack of functional independence

Upper extremity patterns

Adduction and internal rotation of the shoulder

Flexion of the elbow and wrist

Pronation of the forearm

Flexion of the fingers and adduction of the thumb

• PECTORALIS MAJOR • LATISSIMUS DORSI • TERES MAJOR • BICEPS • BRACHIORADIALIS • BRACHIALIS

• PRONATOR TERES AND QUADRATUS

• FLEXOR CARPI RADIALIS AND ULNARIS

• FLEXOR DIGITORUM PROFUNDUS AND SUPERFICIALIS

• ADDUCTOR POLLICIS

Lower extremity patterns

HIP ADDUCTION AND FLEXION

KNEE FLEXION

ANKLE PLANTAR FLEXION OR EQUINOVARUS POSITIONING

• ADDUCTOR MAGNUS • ILIOPSOAS

• HAMSTRINGS (MEDIAL MORE OFTEN THAN LATERAL)

• TIBIALIS POSTERIOR • SOLEUS • GASTROCNEMIUS

Lower extremity patterns

KNEE EXTENSION

EQUINUS AND/OR VALGUS ANKLE

GREAT TOE DORSIFLEXION

• QUADRICEPS FEMORIS

• PERONEUS LONGUS

• EXTENSOR HALLUCIS LONGUS

ADDUCTED/INTERNALLY ROTATED SHOULDER

FLEXED ELBOW PRONATED FOREARM FLEXED WRIST

CLINCHED FIST THUMB IN PALM DEFORMITY STRIATAL TOE EQUINOVARUS

STIFF KNEE FLEXED KNEE ADDUCTED THIGHS

ASSESSMENT

Ashworth and modified Ashworth scales most frequently used clinical methods for estimation of spasticity

G. R. Johnson. Outcome measures of spasticity. European Journal of Neurology 2002, 9 (Suppl. 1): 10–16


Bohannon and Smith found that many of their patients demonstrated levels of spasticity

towards the lower end of the scale

and included an extra category (1+) to render the scale more discrete.

Advantages Simple requires no instrumentation is easy and quick to carry out

Disadvantages interrater reliability worst for plantar flexors- to be due to a shorter lever arm at the

ankle to determine the resistance during the movement

Spasm frequency scores

Created to follow the effect of intrathecal baclofen in patients with spasticity caused by multiple sclerosis and SCL

less optimal for other purposes

Spasticity-assessment: a review. Spinal Cord (2006) 44, 708–722

Journal of Neuroscience Methods. Vol 178, Issue 2, 15 April 2009, Pages 340–344

Waternberg Pendulum Test

Wartenberg Pendulum Test

The patient is seated or lying with the lower leg hanging over the

end of a couch. The examiner then extends the leg to the horizontal position, while the patient is told to relax. The leg is then released and allowed to swing freely under the action of gravity. With the use of electrogoniometers,the swing of the leg about the knee joint may be evaluated

In individuals with spasticity, a reduction of the swing is generally found

the ratio between the initial flexion and the final position of the knee joint measured by goniometers, when the leg has come to a rest


ratio shows a clear correlation to the severity of spasticity as evaluated by the AS

The advantage of the pendulum test is its simplicity, and the more refined quantification of the severity of spasticity that is obtained compared to the AS

Drawbacks- depends crucially on how the person is seated and the ability of the person to relax fully. Furthermore, it may only be used to evaluate spasticity in the knee muscles and it seems not to give any useful information in severe spasticity



Powered oscillation system

Powered oscillation system

Developed by Walsh (1996)

The patient held a simple handle attached to a newly developed electric motor

motor produced flexion/extension of the joint and the apparatus also measured EMG

Walsh showed that, the ability to measure different amplitude and natural frequency of oscillation depending upon joint stiffness


MANAGEMENT

When to treat Not all spasticity requires treatment- inappropriate treatment of

spasticity may lead to loss of function, when spasticity is counterbalancing the effects of paresis

may need to be treated when it causes Pain Difficulty performing ADL Impaired mobility, whether related to ambulation or transfers Poor joint positioning An increased risk for the development of contracture Skin breakdown


Aims to reduce the impact of spasticity to prevent secondary complications

Goals relief of discomfort improved sitting, standing and walking, facilitated activities of

daily living reduced burden of care improved body image and self-esteem prevention of complications


Goal attainment scaling measure of the extent to which treatment goals are achieved intended outcome is graded as

−2: much worse than expected −1: somewhat worse than expected 0: achieved the expected outcome +1: somewhat better than expected +2: much better than expected outcome


Factors influencing treatment

Duration of spasticity

Severity of spasticity

Distribution of spasticity

Success/failure of prior interventions

Current functional status and future goals

Patient's age, preferences, and ability to comply with treatment

Availability of support/caregivers and follow-up therapyRichard D. Zorowitz et al. Spasticity: A Clinical Review. www.medscape.org

MANAGEMENT- KEY ELEMENTS

Identification and elimination of triggers

Non pharmacological interventions Passive movements Exercises Posture & Standing Physical modalities

Medications Oral Injectables

Surgical


Identification and elimination of triggers

Patient and carer education to recognise these triggers is an important part of management

Pressure ulcers Ingrown toenails Skin infections Injuries Constipation Urinary tract infection Urinary tract calculi Deep vein thrombosis Improper seating Ill-fitting orthotics


Passive movements

Passive stretching decreases the excitability of motor neurones and maintains the visco-elastic properties of muscles and joints

Prolonged stretching can help to treat contractures

Stretching can be facilitated by using casts or splints, sometimes used together with botulinum toxin injections

No conclusive evidence whether therapy is effective but no evidence that it is harmful


Exercises improve motor control and cardiovascular fitness in people with

UMN disorders

Posture and standing Standing for about half an hour a day may help to reduce

spasticity weight bearing and standing also help to improve psychological

wellbeing, to improve bone mineral density, facilitate pulmonary drainage and helps bowel and bladder functions

Proper positioning of limbs and trunk is essential to prevent aggravation spasticity and development of contractures

Devices such as splints help to position limbs properly


Physical modalities These physical modalities work through either modulating the

visco-elastic properties of muscles and tendons

Ultrasound Cryotherapy Vibration Shockwave therapy Magnetic stimulation Transcutaneous electrical nerve stimulation (TENS)

limited evidence base to support the use


Medications

Principles of drug therapy Weakness is a side effect of all antispasticity drugs, usually due

to unmasking of underlying UMN weakness

A ‘start low and go slow’ policy limits these unwanted functional effects

reach the maximal tolerated dose for a sufficiently long period before stopping a drug and labeling it as ineffective

Patients not responding to one drug may respond to another


Sudden stopping of even an apparently ‘ineffective’ drug may cause a rebound increase in spasticity. It is better to taper initial drug while simultaneously introducing the second drug.

A combination of two drugs should be tried if the spasticity does not respond to a single agent

It is important to time the doses according to the patient’s activity, care and therapy


Oral agents

Gamma aminobutyric acid (GABA)ergic system Baclofen Gabapentin Benzodiazepines

α-2 adrenergic system Tizanidine

Block calcium release into the muscles Dantrolene

Cannabinoids


BACLOFEN

most widely used oral antispasticity drug Mechanism GABA-B receptor agonist reduces calcium influx ↓s release of excitatory neurotransmitters(glutamate & aspartate) down-regulates activity of 1a sensory afferents, spinal

interneurones & motor neurones

Dose starting - 5 mg thrice daily Maintenance- ↑d by 5–10 mg weekly, until there is an optimal

effect Max- 90–120 mg per day


Adverse effects weakness, drowsiness and dizziness sexual dysfunction& urinary incontinence reduces seizure threshold Abrupt stoppage can provoke rebound spasticity within 48 h Sudden withdrawal may also cause seizures and hallucinations Caution pregnancy- animal studies show impaired sternal

ossification and omphalocele


Benzodiazepines

act on GABA-A receptors

Drowsiness and behavioural side effects limit its use during the daytime

particularly useful to treat spasticity that interferes with sleep

Clonazepam is particularly useful to treat nocturnal spasms

The usual starting dose is 500 mg at night, with a maximum dose of 1 mg


Gabapentin and Pregabalin

useful as adjuncts in treating spasticity associated with pain

Gabapentin - start at 300 mg once daily on day 1, 300 mg twice daily on day 2, then 300 mg thrice daily on day 3, then increased according to the patient’s response in steps of 300 mg every 2–3 days to maximum of 3600 mg daily

Pregabalin- 75 mg twice a day and it can be titrated up to 300 mg twice daily

Adverse effects- weight gain, gastro-intestinal disturbances, confusion, depression and sleep disturbance


Tizanidine

Mechanism α-2 receptor agonist It inhibits excitatory spinal interneurones and tracts from locus

coeruleus Dose Starting dosage is 2 mg at bedtime, increased by 2 mg weekly to

a maximum of 36 mg, divided into 3–4 daily doses Adverse effects dry mouth, gastrointestinal disturbance, hypotension and acute

hepatitis Sudden stopping of tizanidine can lead to a hyperadrenergic

syndrome, characterised by anxiety, tremor, hypertension and tachycardia


Dantrolene

Mechanism blocks calcium release from the sarcoplasmic reticulum and

interferes with excitation–contraction coupling of the skeletal muscle

acts directly on the muscle and so is less sedative

Dose Starting dose is 25 mg daily for the first week, increased in steps

of 25 mg per week to a top dose of 100 mg 3–4 times daily

Adverse effects most important side effect is hepatotoxicity, and so liver function

must be monitored carefully


Cannabinoids

Cannabinoid receptors in dorsal spinal cord, basal ganglia, hippocampus and cerebellum, and these modulate spasticity

Cannabidiol & Nabiximols limited role in managing treatment-resistant spasticity

may be worth trying in patients who are not responding to a combination of two drugs in adequate doses

only 30–40% of people show a response, the treatment effect should be reviewed at 4–6 weeks and continued only if there is an objective improvement

concerns about its long-term effects on cognition, behaviour and mental health


Botulinum toxin

Prepared from the bacterium Clostridium botulinium Mechanism heavy chain of binds to and becomes internalised into presynaptic

nerve endings degrades synaptosomal-associated protein 25, a protein required

for fusion of acetylcholine vesicles to the presynaptic membrane. Inhibits release of acetylcholine, thereby blocking neuromuscular

transmission Reversal effect is reversed by nerve sprouting and reinnervation which

develops over 3-4 months


Usage Particularly useful in the treatment of focal spasticity. Achieves

selective reduction in spasticity with little side effects Electromyography, nerve stimulator or ultrasound can be used to

identify the target muscle Postinjection interventions such as physiotherapy, splinting and

serial casting help to maximise benefits patient should be reassessed 4–6 weeks after the initial injections

to assess the efficacy of the injections If required, further injections should be planned after 3–4 months

Adverse effects muscle weakness, urinary incontinence, falls, fever and pain.

Rarely, the toxin can cause transient dysphagia, even requiring nasogatric feeding


Phenol

Injection of phenol guided by nerve stimulation forobturator nerve for treatment of adductor spasticity

Phenol

Chemical neurolysis 5% concentration injected directly into peripheral nerves cause destruction of

neural tissue by protein coagulation Usage effective in treating spasticity that occurs in large, powerful

muscle groups close to the trunk- thigh adductors blocks to the medial popliteal muscles to aid spastic foot drop, or

obturator nerve blocks either in patients with scissoring gait or to improve perineal hygiene and seating posture

A neurostimulator with a Teflon-coated needle electrode is used for guidance


often has effects lasting many months(~6mths) and can be repeated if necessary

Nerve sprouting may lead to recurrence of spasticity

Adverse effects most trouble some side effect is pain and dysaesthesia; it is

therefore used usually only in people with loss of sensation Other side effects are peripheral oedema, skin sloughing and

wound infection. Phenol also increases the risk of deep venous thrombosis and

leukaemia


Intrathecal baclofen

http://www.google.co.in/url?sa=i&source=images&cd=&cad=rja&docid=RI-jhDYm4jYyGM&tbnid=USEoT8dDmmIlTM:&ved=0CAgQjRwwAA&url=http://www.southeasternspine.com/procedures-treatments/intrathecal-pump-implant/&ei=HbF3UfLDL8HNrQfC-YHoCg&psig=AFQjCNHr5bGKMNgBblgS2Wc62kZWe5VX1w&ust=1366885021864555

Intrathecal baclofen

Indication- for significant lower-limb spasticity which persists despite

adequate treatment with at least two oral antispasticity drugs concomitantly

Principle- Oral baclofen has only very low bioavailability to GABAergic

neurones in the spinal cord administered intrathecally, a relatively small dose of baclofen can

give a high concentration of drug within the spinal cord Patients should initially be screened using a temporary catheter

with an initial test dose is 50 mg


Device comprises a subcutaneous pump which stores and delivers

programmable doses of baclofen through a catheter into the spinal subarchanoid space

can be adjusted to vary the doses delivered, depending on the level of patient activity and needs

Complications procedure related complications- infection, skin erosions,

cerebrospinal fluid leak and seroma formation around the pump Abruptly stopping ITB can cause high fever, confusion, rebound

spasticity and muscle rigidity, similar to neuroleptic malignantsyndrome


Neurosurgical management

for severe spasticity following the failure of noninvasive management (adequate medical and physical therapy)


PERIPHERAL NEUROTOMY

Indications


Procedure It involves microdissection guided by neuro-stimulation at low

intensity Extent of the nerve resection- must be limited to a maximum to

4/5 fibres,over a length of 5 mm, to prevent any regrowth Care must be taken with the sensory fibres, if too many cut in

the sensory peripheral nerve, may induce neurogenic pain

Results(Mertens et al., 180 pts) reduction of spasticity in 82% of cases, with recurrence in only

8% reduction in pain 85%, and a reduction in cutaneous lesions

78% 10% functional improvement, recovery of some ability to walkEuropean Journal of Neurology 9 (Suppl. 1), 35–41


Microsurgical DREZotomy

Principle Modern dorsal rhizotomy is a hyper-selective rhizotomy

At the periphery, the nerve fibres are mixed

Technique of Dorsal Root Entry Zone-otomy (DREZotomy) consists of selective cutting of fibres at the dorsal root zone, including a large area up to the superfcial layers of the posterior grey matter

European Journal of Neurology 9 (Suppl. 1), 35–41


Technique was especially developed for treating neurogenic pain

Spasticity- selectively suppress the nociceptive afferent discharges to the spinal cord

Indication severe and regional spasticity, possibly associated with

chronic intractable pain

Procedure Lesion, max depth 3mm is placed 45° in the ventromedial

direction at dorsal radicular spinal junction



Results (Mertens and Sindou (1998) ) n =151 patients with lower limb spasticity, follow-up 5.6 yrs Decreased hypertonia - 78% Ashworth < 2 Decreased spasms - 88% Increased voluntary mobility - 11% Decreased pain - 82%



Spinal cord stimulation

Principle selective stimulation of the larger fibres in order to inhibit the

activity of the smaller nociceptive fibres and so to decrease the nociceptive input at the level of the spinal cord

level of stimulation was dependent on the topography of the spasticity

electrode must be placed in the posterior epidural space in order to stimulate the dorsal columns

Various authors report improvement varying from 50% to 80% over a period of 2 to 5 yrs, some report no significant improvement

Currently considered as an alternative only if other conservative and surgical treatments do not work



Stratified management approach

European Journal of Neurology 2002, 9 (suppl. 1): 48–52

CONCLUSION

Spasticity is one component of UMN syndrome

Impact of spasticity varies between patients

Not all cases require treatment, useful effects of spasticity must be kept in mind before beginning treatment

Untreated, it can cause significant discomfort and problems to mobility and care

Elimination of triggers and supportive physiotherapy are an important aspect of management

Oral medications should be started at a low dose and gradually titrated

No single drug should be discarded until its maximum dose is reached or if patient develops intolerable side effects

Intervention to be considered in patients with Spasticity resistant to oral medications

THANK YOU

spasticity

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