pta 120 pathophysiology week 7-nervous system. discuss anatomic structures and physiologic...

PTA 120Pathophysiology

Week 7-Nervous System

Discuss anatomic structures and physiologic processes related to the neurological system.

Discuss physical effects of aging on the

body. Explain the difference between the gate

control and endogenous opiate theories of pain.

Objectives

Arnold-Chiari Malformation Autism Spectrum Disorder Cerebral Palsy Alzheimer’s Disease Amyotrophic Lateral Sclerosis Cerebral Vascular Accident

Pathological Conditions

Transient Ischemic Attack Creutzfeldt-Jacob Disease Dementia Epilepsy Guillain-Barré Syndrome Huntington’s Disease Multiple Sclerosis Drowning

Objectives

Peripheral Neuropathy Parkinson’s Disease Post-polio Syndrome Spinal Cord Injury Traumatic Brain Injury

Objectives

Pathology for the Physical Therapist Assistant, Ch. 7

Physical Therapy Clinical Handbook for PTAs

Textbooks

Copyright 2009 Walters Kluwer Health / Lippincott Williams & Wilkins

CNS develops from the neural tube that becomes the brain and spinal cord

The opening of the neural tube becomes the ventricles

Four chambers within the brain Filled with cerebrospinal fluid

CNS Development

Copryright 2009 Walters Kluwer Health / Lippincott Williams & Wilkins

Sensory input Gathers information about stimuli occurring

inside the body and outside in the environment. Integration

Processes and interprets sensory input and decides if action is needed.

Motor output Responds to integrated stimuli by activating

muscles or glands.

Functions of the Nervous System

From: Stillerman (Ed), Modalities for Massage and Bodywork, Elsevier, St Louis, 2008, in press.

Aging of the Nervous System

Physiologic Change Functional Effect

Nerve cell degeneration and decrease in cerebral blood flow (about 20% reduction between ages 50-80)

Reduced response time and decreased reflexes; loss or increased sensitivity to pain, which increases injury risk; decreased tolerance to heat or cold; decreased balance and coordination; altered gait

Decrease in neurotransmitters Increased potential for dementing processes

“An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” - Merskey, 1986

Perception is influenced by levels of attention, anxiety, arousal, suggestibility, fatigue, overall health, as well as influences from culture, religion, and past experiences.

Pain

Sensory Receptors Free Nerve Endings Nociceptors

Mechanoreceptors Thermoreceptors Chemoreceptors

Pain Pathway

A Delta Fibers/ 1st response Myelinated nerve fiber Quick response time Localized sharp sensation Short duration

C Fibers/2nd response Nonmyelinated nerve fiber Slow response time Non-localized dull sensation Longer duration

Pain Pathway

Sensory Receptor Dorsal Root Ganglion/Spinal Cord

Contains cell bodies of A and C fibers Synapse Site for A and C fibers A fibers enter spinal cord crossover and

connect to Spinothalamic tract C fibers synapse with interneurons in order to

connect to Spinothalamic tract Spinothalamic Tract

Ascending Pain Pathway

Brainstem (Autonomic Nervous System) Reticular Formation (arousal system) Influences changes in blood pressure, heart

rate and respiration Thalamus (relay station)

Receives and sorts sensory information sending them to particular areas of the cortex for interpretation

Cortex Interprets location, type of sensation, intensity and

amount of pain

Pain Pathway

1st Order Neuron A and C cell bodies in dorsal root ganglion

2nd Order Neuron A and C axons located in the dorsal horn of the

spinal cord Cross the midline in order to join the spinothalamic

tract 3rd Order Neuron

Located in parietal lobe of cortex Registers and interprets sensory information

Pain Pathway

Cortex Thalamus and Hypothalamus Midbrain/Medulla

Site in which the descending pathway synapses with ascending pathways

Spinal Cord 2nd Site in which the descending pathway

synapses with ascending pathways

Descending Pain Pathway

Function of Descending Pain Pathway Modulate the intensity of pain perception Inhibit the intensity of pain perception

Opiate nerve receptors Located in afferent nerve endings of 1st Order

Neurons and cell bodies in 2nd Order Neurons Block or inhibit pain transmission

Descending Pain Pathway

Inflammatory response Releases histamine, bradykinin, serotonin,

prostaglandins Edema -> pressure on nerves

Produces reaction in muscles -> spasm -> splinting mechanism to prevent movement

Pain production and response

Release of endogenous opiates - activities that stimulate the release and can produce analgesia, such as exercise, laughter, acupuncture, relaxation, electrical stimulation

Gate control theory – pain impulses must outnumber pain inhibiting factors for the “gate” to open to the brain; biofeedback used

Pain Control Theories

Visual Analog Scale (VAS) Visual Pain Drawing/Anatomical Pain Drawing Numeric Pain Rating Scale (NPRS) McGill Pain Questionnaire Dolorimeters/Pressure Algometers Facial Expressions Influence on daily living

Pain Assessments

Description Structural defect of the cerebellum and skull in

the developing fetus Blockage of CSF circulation in skull and spinal

cord Pressure on the spinal cord from cerebellum

through foramen magnum Three types, with Type I being the mildest and

Type III the most severe Can be accompanied by myelomeningocele

Arnold – Chiari Malformation

Etiology Unknown Genetic within families Chromosomes 9 and 15


Signs and Symptoms Dizziness Muscle weakness, paralysis Decreased sensation Headaches and vision deficits Decreased balance and coordination


Treatment No cure Surgical correction to restore CSF flow


Dependent upon level of severity Early childhood intervention to

address developmental delays and family education

Balance and coordination training

Physical Therapy Intervention for Arnold-Chiari Malformation

"Autism is a complex developmental disability that typically appears during the first three years of life and is the result of a neurological disorder that affects the normal functioning of the brain, impacting development in the areas of social interaction and communication skills.” – Autism Society of America

Autism Spectrum Disorder

Also known as ASD or PDD (Pervasive Developmental Disorder)

Encompasses a wide range of neurodevelopmental disorders (autism, Asperger syndrome, Rett syndrome, childhood disintegrative disorders, and pervasive developmental disorders (PDD-NOS)

Incidence is 1 in 150 children, as many as 1 in 94 boys; growing at a rate of 10-17 percent per year


Etiology Not completely understood, with a

combination of both genetic and environmental factors

Environmental factors may possibly be heavy metals, viral infections, toxic chemical exposure

Abnormal serotonin levels


Signs and Symptoms Little or no eye contact Physical and emotional distance from others;

failure to develop social attachments Insistence on sameness; resistance to change Difficulty in expressing needs; uses gestures or

pointing instead of words Repeating words or phrases in place of normal,

responsive language; echolalia


Often self-stimulates; spins objects, flaps hands

Laughing, crying, showing distress for reasons not apparent to others

Inappropriate attachments to objects Uneven gross/fine motor skill level Can be non responsive to verbal cues May perform above average on memory or

spatial tasks 1/4 - 1/3 have IQ>70


Treatment Medications if necessary to reduce depression,

anxiety, obsessive-compulsive behavior, other behavioral issues, seizures

Family counseling Behavior therapy Team approach with neurologist, therapist,

psychiatrist, psychologist, teachers


Address developmental delays Help child develop more normal

movement patterns Reeducation in motor planning Balance and coordination training

Physical Therapy Intervention for Autism Spectrum Disorder

Description Group of motor disorders caused by cerebral

damage during fetal life, birth or early childhood

Brain involvement is irreversible and not progressive

Symptoms vary from mild to extremely severe Difficulties with function as person grows

Cerebral Palsy

Classification By functional skills

The Gross Motor Function Classification System By muscle tone

Spastic / high tone Athetoid Ataxic Mixed

Cerebral Palsy

Etiology Damage to the cerebrum resulting from:

Inadequate blood flow (ischemia) Reduced oxygen supply (hypoxia or anoxia) Brain abnormalities Congenital genetic defects Hypoglycemia Traumatic brain injury Meningitis

Cerebral Palsy

Cerebral Palsy

Signs and Symptoms Related to motor

functions Lack of coordination,

exaggerated reflexes Contractures Drool excessively Difficulty swallowing

Complications can include seizures and mental retardation

Treatment Education on prevention during pregnancy Medications based upon characteristic of the

disease Surgery for tissue release, dorsal rhizotomy Intrathecal baclofen for hypertonicity Team approach including therapists,

physicians, and teachers is very important

Cerebral Palsy

Goal is to maximize independence and potential through strengthening. stretching, and mobility, with use of assistive devices if appropriate. Education of the family or caregivers is extremely important.

Physical Therapy Intervention for Cerebral Palsy

Description Progressive degenerative disease of the brain Destroys cerebral cortex neurons Leads to dementia 500,000 new cases diagnosed each year

Alzheimer’s Disease

Etiology Exact cause unknown Risk increased with advancing age, genetics,

atherosclerosis Plaques and amyloid accumulate in brain

tissue -> neurofibrils break down and become tangled -> nerve impulse transmission prevented -> function of sections on the cerebral cortex destroyed

Neurofibrillary tangles detectable at autopsy


Signs and Symptoms Loss of memory, inability to concentrate,

impairment of reasoning, apathy, personality changes

Warning signs: memory loss, problems with language, disorientation, difficulty completing familiar tasks, distorted judgment, problems with abstract thinking, misplacing things, mood, behavior, and personality changes


Treatment Prevention including healthy diet, higher

education Medications Stem cell research Massage Supportive environment, and long term care



From Chabner DE: The language of medicine, ed 8, 2007, Saunders.


From Alzheimer’s Association

Goal is to maintain functional independence for as long as possible by encouraging activity, as the disease may lead to inactivity due to the cognitive restrictions. Strengthening, balance activities training, and modalities for pain relief are helpful. Due to the patient’s cognitive status, the therapist must use short, clear, and concise instructions.

Physical Therapy Intervention for Alzheimer’s Disease

Description Also called Lou Gehrig’s Disease or ALS Degeneration and demyelination of motor

neurons Leads to general paralysis and immobility;

progresses rapidly, with death usually in 3 - 10 years

Intelligence and sensations not affected Mainly occurs between 40 and 60 years of age,

with men > women; 1 case per 100,000

Amyotrophic Lateral Sclerosis

Etiology Cause unknown; genetics involved in 5 – 10 %

of cases Genetics 5 - 10% Possibly viral, metal or mineral exposure,

autoimmune disease High glutamate concentration in CSF causes

destruction of neurons


Signs and Symptoms Begins with weakness and atrophy of hands,

forearms, legs and eventually spreading to rest of the body

Severe fatigue Paralysis Difficulty with speech, chewing, swallowing,

breathing


Treatment Medications to control muscle spasms Assistance with breathing including

intermittent positive pressure ventilation (IPPV) or tracheostomy

Gene therapy possibly leading to development of medication to treat and delay symptoms

Speech therapy to assist with feeding


Goal is to maintain independence and functional independence for as long as possible

Work on functional mobility, including wheelchair evaluation and training if needed

Home modifications and assistive devices Strengthening and stretching Low-impact aerobic exercise Breathing exercises, postural drainage, chest PT

Physical Therapy Intervention for Amyotrophic Lateral Sclerosis

Description Also called CVA, a stroke, or a “brain attack” Sudden disruption in cerebral blood flow, with

death of brain tissue leading to irreversible brain damage

Symptoms last more than 24 hours Men > women Leading cause of disability and 3rd leading

cause of death in the US

Cerebrovascular Accident

Etiology Smoking is a leading cause Hemorrhagic CVA

Aneurysm ruptures -> blood seeps into surrounding tissue and creates pressure -> symptoms dependent upon which area of the brain is affected

Ischemic CVA Atherosclerosis leads to an embolus (blood clot) ->

clot travels and blocks a smaller blood vessel in the brain -> lack of oxygen leads to brain tissue necrosis


Signs and Symptoms Reflect portions of brain affected Severe headache, seizure activity, personality

changes Visual disturbances, unequal pupils Speech difficulty, difficulty understanding

others Sudden weakness; unilateral paralysis and

neglect Numbness, tingling, or burning Coma, loss of consciousness, death


Treatment Immediate medical attention, within 90

minutes after onset of symptoms Anticoagulants for ischemic type Control of hypertension and brain bleeds for

hemorrhagic type Reduce hypertension and blood cholesterol,

anticoagulants or antiplatelet treatment


Long-term medical treatment Quit smoking, reduce alcohol consumption Decrease weight Medications including low-dose daily aspirin, flu

and pneumonia vaccines Surgery


Description Brief episode of impaired brain functioning due

to a temporary reduction of blood flow Individual remains conscious Complete recovery in 24 hours with no residual

dysfunction; > 24 hours is a CVA Can indicate development of CVA or stroke Etiology, signs and symptoms, and treatment

are the same as those of a CVA

Transient Ischemic Attack

May begin in ICU if indicated for bed mobility and range of motion, progressing to strengthening exercises and ambulation as tolerated.

Training on how to use the affected and neglected extremities.

Gait training and adaptive equipment as necessary.

Follow precautions very closely – ch. 7, pg 313

Physical Therapy Intervention for Cerebrovascular Accident

Description CJD, one form is “Mad Cow Disease” Group of degenerative disorders Sporadic, hereditary, acquired, variant Fatal Onset after 60 years of age Between 200 – 300 cases in U.S. annually 85% of affected have the sporadic form

Creutzfeld-jacob disease

Etiology Sporadic form

Unknown cause, or direct contact with infected transplant organs and grafts

Hereditary form Autosomal gene Spontaneous mutation of the PRNP gene (makes

proteins that transports copper and protects neurons) Prion protein builds up -> neurons destroyed ->

extensive brain damage


Signs and Symptoms Dementia – rapid and progressive Severe mental impairments – personality

changes, judgment deficits Depression, insomnia Motor deficits – decreased coordination,

weakness, myoclonus, speech deficits, immobility

Blindness and coma at end stage


Treatment Alleviate symptoms Medications to reduce pain and myoclonus


Maintain mobility as long as possible with strengthening exercises and assistive devices as necessary

Treat within patient’s tolerance

Physical Therapy Intervention for Creutzfeld-Jacob Disease

Description Types include: Lewy body, senile, vascular, and

dementias precipitated by other diseases Progressive brain deterioration Decline of mental facilities (thinking,

remembering, communicating) Affect a wide age range

Dementia (Non-Alzheimer’s)

Etiology Buildup of Lewy body proteins which decreases

dopamine and acetylcholine Vascular disease resulting in ischemia Toxic substances, certain medications,

exposure to heavy metals Smoking and exposure to secondhand smoke Advancing age


Signs and Symptoms Begins with forgetfulness then loss of memory Personality disintegration, disorientation,

general loss of cognitive abilities Parkinson-like motor deficits Depression, aimless wandering

Treatment Dependent upon causative factors Medications and reminiscence therapy


Treatment is aimed at the neurological and musculoskeletal manifestations, and must be adjusted due to the patient’s cognitive status by using short instructions and a familiar location.

Work on stretching, strengthening, endurance, balance and coordination, as well as ambulation may be indicated.

Physical Therapy Intervention for Dementia

Description Epilepsy and epileptic syndromes Explosive episodes of uncontrolled and

excessive electrical activity in the brain which results in multiple involuntary muscle contractions

Diagnosis of epilepsy requires 2 seizures occur without a known cause

Seizure Disorders

Etiology Abnormalities within the neurons or with the

balance of the neurotransmitters, which cause the neurons to be triggered all at one time

Unknown, possibly genetic factors involved Head trauma or brain tumors Infections, high fevers

Seizure Disorders

Cerebrovascular disturbances Chemical imbalances Drug or alcohol withdrawal Stress

Seizure Disorders

Signs and Symptoms Uncontrolled muscular contractions; convulsions Absence seizures – “petit mal”, with brief loss of

consciousness, staring Atonic – temporary loss of muscle tone, collapses Myoclonic / myotonic – jerking and twitching Simple partial – emotion and sensation changes Complex partial – altered level of consciousness,

staring, twitching

Seizure Disorders

Treatment Prescribed medications acting on

neurotransmitters Vagal nerve stimulation Surgery to remove the affected area of brain Ketogenic diet, gene therapy, stem cell

research

Seizure Disorders

Treatment is aimed at the injuries or conditions resulting from the seizure, such as fractures or developmental delays. Treatment may include work on mobility, stretching, strengthening and balance.

It is important to be aware of seizure precautions if a patient has had a prior neurological injury.

Physical Therapy Intervention for Seizure Disorders

Description Rapidly progressing inflammatory disease in

which the immune system affects the neural tissue

1-2 people per 100,000 affected worldwide Etiology

Unknown Related to autoimmune response preceding

viral infection or immunization

Guillain-Barré Syndrome

Signs & Symptoms Numbness or tingling in feet and hands Followed by progressive muscle weakness

beginning in legs and traveling up the trunk, down the arms to the face, usually bilaterally, with possible complete paralysis

Vision, speech, and breathing may be impaired Absent deep tendon reflexes High level of proteins in the cerebrospinal fluid


Treatment No known cure Plasmapheresis to reduce the autoimmune

response and remove toxins Intravenous immunoglobulin to restore

immune defenses Manage symptoms of dehydration and skin

breakdown Psychological support for patient and family


Treatment follows the pace of peripheral nerve recovery, and usually begins with patient and family education in range of motion exercises to prevent contractures, progressing through wheelchair training or ambulation with assistive devices, strengthening, and balance and coordination activities. It is important not to overfatigue a patient.

Physical Therapy Intervention for Guillain-Barré Syndrome

Description Autosomal dominant degenerative disorder Caused by mutation of the gene which

produces huntingtin protein Motor disturbances, mental deterioration,

abnormal behavior Slow progression from 10 - 30 years before

death, symptoms appear in the 30s and 40s 1 in 20,000 in U.S. affected

Huntington’s Disease


Etiology Genetic mutation on

the fourth chromosome -> long version of HTT gene (responsible for huntingtin protein) -> breaks into segments -> segments build up in brain neurons

Signs and Symptoms Chorea - involuntary, purposeless, rapid or

jerky motions of the arms and face Dystonia – increased muscle tone, involuntary

movements with rotation Myoclonus – involuntary twitching and spasm Movement tics – brief muscular spasms on the

face Parkinson – like movements – rigidity and

tremors


Speech and swallowing difficulties Mental and emotional deterioration and

dementia

http://www.youtube.com/watch?v=kINXIjs_V3M&feature=related




Treatment No successful medications to cure or prevent,

so aimed at controlling both motor and psychiatric symptoms

Botulism toxin injections, deep brain stimulation, stem cell transplants

Psychological support Speech therapy for feeding and

communication Occupational therapy for activities of daily

living


Treatment focuses on maintaining independence for as long as possible through strength, flexibility, and endurance training; progressing through wheelchair training or ambulation with assistive devices, as well as education regarding fall prevention and energy conservation techniques for both the patient and the family.

Physical Therapy Intervention for Huntington’s Disease

Description Autoimmune disorder. chronic Progressive demyelination of neurons of the brain,

spinal cord, cranial nerves Periods of remissions and exacerbations Women > men (at least 2:1); onset between teens - 50

years old Both relapsing-remitting (most common) and primary

progressive Exacerbations related to stress, heat, fatigue,

infections

Multiple Sclerosis (MS)

Etiology Genetic defect reducing the ability of T-cells to

turn off the immune response -> autoimmune attack on the myelin -> scar tissue causes plaques which build up in spinal cord and brain -> disruption of brain function and neural transmission

Higher prevalence in countries further from the equator; viruses and concentration of sex hormones may trigger the disease


Signs and Symptoms Demyelination causes the primary symptoms

Paresthesias, vision disturbances, progressive muscle weakness, cognitive impairments, and bladder and bowel dysfunctions

Secondary symptoms result from primary symptoms

Tertiary symptoms include social and psychological functioning


Treatment Team approach including physicians,

psychologists, social workers, physical therapists, occupational therapists, speech therapists, and family

Medications to reduce the development of new brain lesions and slow down disease progression


Treatment focuses on maintaining mobility and the quality of life, as well as reducing fatigue through strengthening (including resistance training if fatigue can be avoided), stretching, aerobic exercise, and education regarding fall prevention and energy conservation techniques. Standardized tests are frequently used to monitor progress.

Physical Therapy Intervention for Multiple Sclerosis

Description Primary respiratory impairment from

submersion in a liquid “Near-drowning” term discontinued Fifth leading cause of death in U.S. > 8000 deaths annually; 1500 are children For every 1 death = 4 hospitalized, 14 in ER

Drowning

Etiology Adults

Water sports Diving Alcohol consumption Other diseases / disorders Men > women; ages 15 – 24

Drowning

Children Swimming pools Bathtubs; girls > boys; under age 4 35% fatal; 33% some neurological impairment;

11% severe impairment

Factors affecting recovery Amount of time in the water Water temperature; cold water = damage may

be slowed down

Drowning

Signs and Symptoms Immediate

Altered vital signs, hypothermia Tachycardia, bradycardia Anxiety, dyspnea, tachypnea Hypoxia Metabolic acidosis Altered level of consciousness Cardiopulmonary arrest

Drowning

Long term results Effects range from none to severe Anoxia of the brain, extensive brain damage Pulmonary damage from aspiration; ARDS Pulmonary edema, pneumonia

Can result in death Seizures, coma, changes in mental status

Drowning

Treatment PREVENTION!

Fenced areas, supervision, groups vs. alone, no alcohol, childproofing

Rescue attempt; rescue breathing; neck in neutral

Activate EMS; hospital Long-term rehabilitation Speech therapy or occupational therapy involved

for swallowing and feeding disorders

Drowning

Treatment focuses on neurological rehabilitation, including NDT, functional movement, positioning to prevent pressure ulcers and assist with breathing.

Physical Therapy Intervention for Drowning

Description Disease of the peripheral nerves Affects motor, sensory, autonomic systems > 20 million affected; more common in older

adults

Peripheral Neuropathy

Etiology Unknown; inherited Diabetes mellitus, Guillain-Barre Alcoholism Autoimmune diseases Kidney failure, thyroid dysfunction, cancer Environmental toxins; Infections Long-term medications Vitamin B deficiency, malnutrition


Signs and Symptoms Sudden or gradual, > in distal lower

extremities Mild to severe and debilitating Pain during regeneration of nerves Weakness and atrophy, fasciculations,

cramping Altered sensation: “Glove” distribution,

vibratory, touch, pressure, temperature, numbness, kinesthetic


Decreased balance, coordination, mobility Decreased weight bearing -> bone

degeneration Hypotension -> dizziness, poor balance Facial muscle weakness -> swallowing, eating

difficulties Bowel / intestinal symptoms Can result in skin breakdown, amputation


Treatment Team approach Treat underlying cause Lifestyle changes Medications to decrease pain Orthopedic shoes


Treatment begins with PT evaluation of muscle strength, skin sensation. The treatment plan may include orthotics, wound care, prevention of contractures, gait training, balance training, strengthening, endurance, and patient education.

Physical Therapy Intervention for Peripheral Neuropathy

Description Progressive, degenerative neurologic disorder Produces syndrome of abnormal movements Basal ganglia undergo degenerative changes▪ Dopamine▪ Regulates voluntary movements, emotions,

mood, motivation

Parkinson’s Disease

Etiology Primary ▪ Idiopathic origins

Secondary ▪ Traced to another cause or pathologic event▪ Infection▪ Trauma▪ Tumors▪ Atherosclerosis▪ Drug use


Signs and Symptoms Tremors – “pill-rolling” Cogwheel rigidity Slowness of voluntary movements Postural abnormalities Dystonia Propulsive gait Decreased balance


Masklike appearance of the face Muffled speech Difficulty with chewing and swallowing

http://www.youtube.com/watch?v=_L_WF6gv5BI&playnext=1&list=PL10AF05605106C2D6




Treatment Incurable Prescribed medications to slow the

development of dopamine, or anticholinergic medications

Surgery Deep brain stimulation, stem cell implantation Speech therapy for speaking and swallowing Occupational therapy for activities of daily

living


Treatment focuses on addressing the patient’s functional problems and pain relief. Range of motion exercises, strengthening, balance training, gait training, and instruction in use of assisted devices are all used to maximize the patient’s mobility.

Physical Therapy Intervention for Parkinson’s Disease

Description Seen in some patients who have had

poliomyelitis earlier in life Appears an estimate of 35 years after infection Exhibited in 28.5 to 64% of previous polio

patients Increased occurrence due to polio epidemic in

1940s and 1950s

Post-polio syndrome

Etiology Actual cause is unknown Motor neurons not affected in the original

infection -> overused -> overworked and stressed -> neuron death -> autoimmune response to neuron death

Post-polio syndrome

Signs and Symptoms Develop slowly Weakness and decreased muscular endurance,

“post-polio progressive muscular atrophy” Fatigue, loss of energy, myalgia Decreased concentration, mental exhaustion Respiratory, speech, and swallowing problems Joint problems, inflammation; leads to

decreased mobility and function

Post-polio syndrome

Treatment No cure Medications not effective Manage physical effects of weakness through

lifestyle changes

Post-polio syndrome

Energy conservation techniques including rest and use of a wheelchair

Low-impact aerobic program Strengthening program without

fatiguing

Physical Therapy Intervention for Post-polio Syndrome

Description Damage to the vertebrae, neural tissue Loss of movement and sensation distal to

injury site Quadriplegia or paraplegia Men > women 4:1; ages 15 - 25 12,000 new cases each year in the U.S.

Spinal Cord Injury

Etiology Primary injury from trauma, including motor

vehicle accidents, sports, falls, and violence Possible fracture or dislocation -> damage to

spinal cord and blood vessels -> damage to neuronal and glial cells

Secondary effects include ischemia, inflammation, delayed cell death, production of free radicals -> more damage to neural and glial cells -> scarring

Spinal Cord Injury

Spinal Cord Injury

Signs and Symptoms Immediate phase

Lasts up to 2 hours after the injury Spinal shock, with no movement, sensations, or

reflexes below the level of the injury Edema in the spinal cord -> hemorrhage and

death of gray and white matter cells -> ischemia of spinal cord

Spinal Cord Injury

Acute phase From 2 – 48 hours after injury Hemorrhage continues -> increased inflammation and

edema -> free radical production -> damaged tissue -> immune system response -> neural and glial cell damage

Sub acute phase From 2 days – 2 weeks after injury Phagocytes clean-up debris and destroy myelin ->

scarring -> barrier for axon regeneration

Spinal Cord Injury

Intermediate phase From 2 weeks – 6 months after injury Scarring matures -> axon regeneration

Chronic phase From 6 months – the end of lifetime At 1-2 years, symptoms and deficits occurs Bone density loss, pressure ulcers, depression,

suicidal thoughts, hostility, substance abuse

Spinal Cord Injury

Treatment Immediate

Immobilization and decompression of spinal cord Position changes, wound care Medications and light therapy to decrease

inflammation, stem cell research Surgery

Once injury healed Rehabilitation to maximize independence, prevent

complications

Spinal Cord Injury

Treatment focuses not only compensatory movements, but also on recovery. Strategies include functional electrical stimulation and passive range of motion, progressing to more active strengthening and balance training. Treatment also includes transfer training, wheelchair training, and gait training as necessary.

Physical Therapy Intervention for Spinal Cord Injuries

Description Also known as a head injury, with external

forces affecting brain function Impairment of cognition and physical function

which can be temporary or permanent Men > women 2:1; ages 15 – 24 5.3 million in US have long-term effects 1.4 million seen in the emergency room yearly

Traumatic Brain Injury (TBI)

Etiology Trauma from falls, motor vehicle accidents, direct

blows, as with sports Open injuries - meninges are breached and the

brain is exposed Closed head injuries

Epidural or subdural hematoma occurs -> blood creates pressure on brain tissue -> ischemia of brain tissue

Edema of brain tissue -> diffuse pressure on brain -> increased intracranial pressure



Coup – contrecoup injury The brain hits one part

of the brain as well as the directly opposing part of the brain

Creates a shearing effect

Signs and Symptoms Mild to severe range Loss of consciousness, seizures, coma, death Headaches, dizziness, nausea and vomiting Altered cognition, changes in personality or

emotions, retrograde or posttraumatic amnesia, post-traumatic stress disorder

Glasgow Coma Scale


Treatment Maintaining oxygen levels in the brain, blood

pressure control Surgery to remove particles Medications for long-term effects such as

spasticity and other complications


Treatment will begin in the ICU and continue throughout the patient’s life if necessary. Strategies include passive range of motion, progressing to more active strengthening with transfer training, wheelchair training, and gait training as necessary. It is very important to be aware of the patient’s cognitive deficits in order to communicate with and teach the patient appropriately.

Physical Therapy Intervention for Traumatic Brain Injuries

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