Neurologic Conditions Flashcards
Alzheimer’s Disease Anatomical and Physiological Pathology
Progressive neurologic disorder that results in deterioration of neurons that are involved in acetylcholine transmission within the cerebral cortex and subcortical areas.
Alzheimer’s Disease Etiology
Unknown but possibly due to lower levels of neurotransmitters, higher levels of aluminum in the brain tissue, genetic inheritance, autoimmune disease, abnormal processing of amyloid, and virus.
Alzheimer’s Disease Incidence
4.5 million individuals in the US.
Higher incidence in women.
6% of individuals over 65 years and 20% of individuals over 80 years.
Alzheimer’s Disease Clinical Presentation
Early stages: Loss of orientation, word finding difficulties, emotional lability, depression, poor judgment, impaired self-care.
Middle stages: Behavioral and motor problems like aphasia, apraxia, perseveration, agitation, wandering, or violent/socially unacceptable behaviors. Inability to learn, loss of long-term memory.
Late stages: Severe intellectual and physical destruction. Incontinence, inability to speak, seizure activity, functional dependence.
Alzheimer’s Disease Pharmacology
Medications to inhibit acetylcholinesterase, alleviate cognitive symptoms, and control behavioral changes.
Acetylcholinesterase inhibitors include tacrine (Cognex), donepezil (Aricept), and rivastigmine (Exolon)
Alzheimer’s Disease Outcome
Typical course of disease 7-11 years on average.
4th leading cause of death in adults, usually due to infection or dehydration.
Amyotrophic Lateral Sclerosis Anatomical and Physiological Pathology
Chronic degenerative disease that results in UMN and LMN impairments.
Demyelination, axonal swelling, and atrophy within the cortex, which affects LMN structures.
Amyotrophic Lateral Sclerosis Etiology
Unknown but likely due to genetic inheritance, slow acting virus, metabolic disturbances, toxicity of lead and aluminum.
Amyotrophic Lateral Sclerosis Incidence
Risk higher for men.
Usually occurs between 40 and 70 years of age.
Amyotrophic Lateral Sclerosis Clinical Presentation
LMN signs: asymmetric muscle weakness, cramping, and atrophy usually in hands. Muscle weakness due to denervation causes fasciculations, atrophy, and wasting with distal to proximal pattern.
UMN signs: Due to loss of inhibition of the muscle. Incoordination of movement, spasticity, clonus, positive Babinski reflex.
Bulbar involvement shown by dysarthria, dysphagia, and emotional lability.
Fatigue and respiratory paralysis.
Amyotrophic Lateral Sclerosis Pharmacology
Riluzole (Rilutek) to slow disease progression.
Symptomatic pharmacology like anticholinergic, antispasticity, and antidepressant medications.
Amyotrophic Lateral Sclerosis PT Treatment
Focus on quality of life, low-level exercise, ROM, AD and adaptive equipment, w/c prescription, bronchial hygiene, and energy conservation techniques.
Amyotrophic Lateral Sclerosis Outcome
Average course of 2-5 years with 20-30% surviving longer than 5 years.
Death usually occurs from respiratory failure.
Carpal Tunnel Syndrome Anatomical and Physiological Pathology
Compression of the median nerve through carpal tunnel.
Carpal Tunnel Syndrome Structures that Pass Through Tunnel
Median nerve
Flexor digitorum profundus and superficialis tendons
Flexor pollicis longus tendon
Carpal Tunnel Syndrome Etiology
Repetitive use, RA, pregnancy, diabetes, trauma, tumor, hypothyroidism, wrist sprain or fracture, congenital narrowing of the tunnel, vitamin B6 deficiency.
Carpal Tunnel Syndrome Incidence
Usually diagnosed between 35 and 55 years of age.
More common in women.
Carpal Tunnel Syndrome Medical Treatment/Pharmacology
Corticosteroid injections
Methylprednisolone injection proximal to tunnel
Surgical release of carpal ligament and decompression of median nerve if conservative treatment fails
Carpal Tunnel Syndrome PT Treatment
Splinting, carpal mobilization, gentle stretching, work and ADL adaptions. 4-6 weeks of treatment.
Post-surgical treatment includes moist heat with e-stim, iontophoresis, cryotherapy, gentle massage, desensitization of the scar, tendon gliding, AROM. Initially avoid wrist flexion and forceful grasp. After 4 weeks can progress to active wrist flexion, gentle stretching, putty exercise, and light progression of resistance exercises. 6-8 weeks of treatment.
Erb’s Palsy Anatomical and Physiological Pathology
Upper brachial plexus injury of C5-6 nerve roots. Axillary, lateral pectoral, upper and lower subscapular, suprascapular, and partial paralysis of the long thoracic and musculocutaneous nerves. Loss of rotator cuff, deltoid, biceps brachii, brachialis, and coracobrachialis function.
Erb’s Palsy Etiology
Usually due to difficult delivery as a result of a large baby in breech position or prolonged labor with use of forceps. One side of baby’s neck is stretched, which damages nerves.
In adults, usually occurs from stretching, tearing, or other trauma to upper brachial plexus.
Erb’s Palsy Incidence
1 in every 1,000 live births
Erb’s Palsy PT Treatment
Increase active and passive movement and promote use of weak upper extremity for functional activities. Caregiver education for positioning to avoid further traction.
Erb’s Palsy Outcome
Approximately 9 out of 10 recover with conservative treatment. Nerves grow at a rate of 1 inch per month, so it may take several months or years for nerves repaired at cervical level to reach muscles of the hand.
Erb’s Palsy Clinical Presentation
Flaccid paralysis nicknamed “waiter’s tip deformity,” characterized by loss of shoulder function, loss of elbow flexion, loss of forearm supination, and hand positioned in a pinch grip manner.
Guillain-Barre Syndrome Anatomical and Physiological Pathology
Temporary inflammation and demyelination of the peripheral nerves’ myelin sheaths with potential axonal degeneration as a result of autoimmune response.
Guillain-Barre Syndrome Etiology
Autoimmune response to previous respiratory infection, influenza, immunization, or surgery. Also associated with viral infections, Epstein-Barr syndrome (herpes), cytomegalovirus (herpes), bacterial infections.
Guillain-Barre Syndrome Incidence
Can occur at any age, but most common in young adults and adults between their 5th and 8th decades. Incidence slightly greater in males than females and Caucasians than African Americans.
Guillain-Barre Syndrome Clinical Presentation
Motor weakness in a symmetrical, distal to proximal progression, sensory impairment and paresthesia, and possible respiratory paralysis. Lack of DTR and inability to speak or swallow may occur. Peak symptom involvement at 2-4 weeks, followed by a 2-4 week static period, and gradual recovery that can take months to ~2 years.
Guillain-Barre Syndrome Medical/Pharmacologic Treatment
Immunosuppressive and analgesic/narcotic medications.
Cardiac monitoring, plasma exchange, and mechanical ventilation (in 30% of patients).
Guillain-Barre Syndrome PT Treatment
Passive ROM, positioning, light exercise. During acute state, limit overexertion and fatigue to avoid exacerbation of symptoms. In later stages, may include orthotic, wheelchair or AD prescription, exercise and endurance, functional and gait training, progressive respiratory therapy (incentive spirometer).
Guillain-Barre Syndrome Outcome
Most reach full recovery but20% have remaining neurological deficits, and 3-5% die from respiratory complications.
Huntington’s Disease Anatomical and Physiological Pathology
Degeneration and atrophy of the basal ganglia (striatum) and cerebral cortex. Loss of neurons and neurotransmitters leads to decrease ability to modulate movement.
Huntington’s Disease Etiology
Autosomal dominant trait
Huntington’s Disease Incidence
About 25,000 people in the US
Symptoms usually develop between 35 and 55 years
Huntington’s Disease Clinical Presentation
Early stages: choreic movement and mild alteration in personality. Unintentional facial expressions.
Middle stages: ataxic gait, choreoathetoid movements, speech disturbances, mental deterioration.
Late stage: decrease in IQ, dementia, depression, dysphagia, incontinence, inability to ambulate/transfer, rigidity.
Huntington’s Disease Pharmacologic Treatment
Anticonvulsants and antipsychotics. Perphenazine, Haloperidol (Haldol), and Reserpine.
Huntington’s Disease PT Treatment
Mobility and functional activities, trunk stability, relaxation.
Huntington’s Disease Outcome
Fatal 15-20 years after onset
Multiple Sclerosis Anatomical and Physiological Pathology
Demyelination of nerves of the brain and spinal cord and plaque development that leads to decreased nerve conduction.
Multiple Sclerosis Etiology
Unknown, possibly due to genetics, viral infections, and environment.
Multiple Sclerosis Incidence
800,000 cases in US
2x more common in women than males
Onset usually between 20-35 years.
Multiple Sclerosis Clinical Presentation
Visual problems, paresthesias and sensory changes, clumsiness, weakness, ataxia, balance dysfunction, and fatigue.
Relapsing-remitting (85%), secondary progressive, primary progressive, or progressive-relapsing.
Multiple Sclerosis Pharmacologic Treatment
Beta interferons reduce frequency and severity of relapses. Glatiramer acetate (Copaxone, Glatopa). This medication may help block your immune system's attack on myelin
Multiple Sclerosis Outcome
Death usually from secondary complications like disuse atrophy, pressure sores, contractures, renal infection, pneumonia.
Parkinson’s Disease Anatomical and Physiological Pathology
Degeneration of dopaminergic neurons that results in depletion of dopamine production within the basal ganglia. Changes the loop between the basal ganglia and cerebrum, which helps control and modulate voluntary movement.
Parkinson’s Disease Etiology
Unknown; contributing factors may include genetics, toxicity from carbon monoxide, excessive maganese or copper, carbon disulfide, vascular impairment of the striatum, encephalitis, or other neurodegenerative diseases like Huntington’s and Alzheimers.
Parkinson’s Disease Incidence
500,000 individuals affected by Parkinsonism, and 42% diagnosed specifically with Parkinson’s. Most patients between 50 and 79 years old.
Parkinson’s Disease Clinical Presentation
Resting tremor that increases with stress and decreases with rest/sleep, difficulty rolling in bed, balance disturbances, difficulty with fine movements. Rigidity, bradykinesia, difficulty with gait and initiating movements, freezing, masked facial expressions.
Parkinson’s Disease Pharmacological Treatment
Dopamine replacement therapy (levodopa, Sinemet, Madopar), antihistamines, anticholinergics, and antidepressants
Parkinson’s Disease PT Treatment
Maximize endurance, strength and functional mobility. Verbal cueing with visual/oral feedback.
Parkinson’s Disease Outcome
Exacerbation of symptoms and decreased mobility as disease progresses. No significant change in lifespan.
Thoracic Outlet Syndrome Anatomical and Physiological Pathology
Compression and damage to the brachial plexus nerve trunks, subclavian vascular supply, and/or axillary artery.
Thoracic Outlet Syndrome Etiology
Presence of cervical rib, abnormal first rib, postural deviations or changes, body composition, chronic hyperabduction of the arm, hypertrophy or spasms of the scalene muscles, degenerative disorders, and an elongated cervical transverse process.
Thoracic Outlet Syndrome Incidence
Usually occurs between ages 30-40 years
More common in women than men
Thoracic Outlet Syndrome Clinical Presentation
Diffuse pain in arm most often at night, paresthesias in fingers through the UEs, weakness and muscle wasting, poor posture, edema, and discoloration.
Upper plexus involvement: pain reported in neck that may radiate to face and down lateral aspect of forearm into the hand.
Lower plexus involvement: pain reported in back of the neck and shoulder, which will radate over the ulnar distribution to the hand.
Symptoms aggravated with poor posture, lifting activities, and movements overhead.
Thoracic Outlet Syndrome Pharmacology/Medical Treatment
Can use anti-inflammatory agents.
Surgical decompression of bony or fibrotic abnormalities if conservative therapy doesn’t work.
Thoracic Outlet Syndrome PT Treatment
Modification of posture, breathing patterns, positioning in bed and at work, gentle stretching. Strengthening of traps, levator scap, and rhomboids, joint mobs, pain management.
Thoracic Outlet Syndrome Outcome
May be able to return to prior function with PT in 4-8 weeks.
May require surgery if symptoms persist with 3-4 months of PT.
Bell’s Palsy Anatomical and Physiological Pathology
Abnormal pressure on facial nerve, often associated with edema or inflammation (possibly due to tumor or fracture)
Bell’s Palsy Clinical Presentation
Often begins with generalized stiffness or tightness on one side of the face. One-sided facial droop. Sensory and motor deficits, muscles associated with facial expression, eating, and closing eyes and mouth. Decreased taste sensation, altered tear and saliva production, and increased auditory sensitivity.
Bell’s Palsy Pharmacology Treatment
Anti-inflammatory medications to relieve pressure on facial nerve.
Bell’s Palsy PT Treatment
Prevention of long-term deficits due to paralysis-related shortening, weakness, and coordination. Massage, stretching, and heat.
Bell’s Palsy Outcome
Spontaneous recovery may occur in weeks, and full recovery can take up to 6 months. Residual functional deficits is uncommon.
Myesthenia Gravis Anatomical and Physiological Pathology
Autoimmune disorder that causes antibodies to attack nerve receptors on the motor end plate. This results in inefficient nerve transmission of neuromuscular signals.
Myesthenia Gravis Etiology
No known cause but likely due to thymus function abnormalities (tumor or hyperplasia).
Myesthenia Gravis Incidence
Women tend to develop in their 20s and 30s and men develop in their 50s and 60s. Women more affected than men.
Myesthenia Gravis Clinical Presentation
Weakness of skeletal muscles, especially ocular and extremities (proximal > distal), with normal reflexes and sensation. Muscles fatigue rapidly with activity, and rest quickly improves muscle function. Can experience diplopia and ptosis. Can affect facial expression, chewing, swallowing, and speech. Myasthenic crisis is where respiratory muscles experience paralysis and require ventilation.
Myesthenia Gravis Medical/Pharmalogical Treatment
Medication to inhibit acetylcholinesterase to allow acetylcholine to build up at neuromuscular junction.
Corticosteroids to suppress immune system.
Surgical intervention to remove thymus.
plasmapheresis to remove antibodies from blood with acute worsening of symptoms.
Myesthenia Gravis PT Treatment
Strength and endurance training without overexertion. Training for breathing techniques.
Energy conservation techniques.
Myesthenia Gravis Outcomes
Symptoms most severe within first few years of diagnosis. Symptoms plateau or improve after this. Complete remission is rare, but symptoms can be well controlled. Removal in thymus may result in complete remission.
Post-Polio Syndrome Anatomical and Physiological Pathology
Prior history of poliomyelitis, which attacked the anterior horn cells and caused motor nerve degeneration and muscle atrophy. Recovery of strength through collateral sprouting, but increased demands on remaining nerves leads to deterioration over time.
Post-Polio Syndrome Etiology
25-50% of patients with poliomyelitis develop post-polio syndrome.
Post-Polio Syndrome Incidence
Patients with more serious initial onset of poliomyelitis (greater motor involvement) and women are more likely to develop post-polio syndrome.
Post-Polio Syndrome Clinical Presentation
Asymmetric weakness, atrophy, fatigue, and sometimes muscular/joint pain. Weakness can also affect axial muscles and result in difficulty breathing and swallowing. Symptoms appear decades after recovery from poliomyelitis, and weakness progresses slowly over years, interspersed with periods of stability where there is no progression of symptoms.
Post-Polio Syndrome Pharmacological Treatment
Anticholinesterase and intravenous immunoglobin, but they have moderate success.
Post-Polio Syndrome PT Treatment
Overall conditioning, avoiding fatigue or exhaustion. Energy conservation techniques, orthotic and AD device training. Exercise should be performed every other day to allow time to recover.
Post-Polio Syndrome Outcomes
Not life-threatening unless respiratory muscles are involved. Normal lifespan but decreased QOL.
Epilepsy Pathology and Etiology
Due to hypersynchronous neurons in the brain.
No identifiable etiology in about half of the population with epilepsy.
Known conditions due to brain injury, infectious disease (AIDs, meningitis), genetic influence, and developmental disorders (CP).
Epilepsy Clinical Presentation
Mood disturbances, staring, loss of consciousness, uncontrollable jerking of the extremities, stiffening of muscles, and loss of muscle control.
Peripheral Neuropathy Etiology
Usually due to diabetes mellitus. Other causes include advanced age, certain drugs (chemotherapy), alcohol abuse, AIDS, environmental toxins, and inherited neurological conditions.
Peripheral Neuropathy Clinical Presentation
Often starts in distal LEs symmetrically and may progress to hands and more proximal portions of limbs. Numbness, tingling, and pain in “stocking” and “glove” distribution. Loss of position and vibration and ataxia. Muscle weakness and atrophy if motor nerves affected.
If ANS affected, constipation, loss of bowel/bladder control, and orthostatic hypotension.
Trigeminal Neuralgia Pathology and Etiology
Abnormal pressure or irritation of the trigeminal nerve. Due to tumor or swollen blood vessel, irritation of nerve due to conditions that cause demyelination like MS. Possibly due to nerve trauma resulting from recent sinus or oral surgery, stroke, or facial trauma.
Trigeminal Neuralgia Incidence
Most common in women over the age of 50
Trigeminal Neuralgia Clinical Presentation
Typically unilateral and may be episodic or constant. Episodic symptoms are usually sudden onset of pain described as sharp, jolting, stabbing, or shocking. Spasms or tics may occur. Chronic symptoms are described as persistent aching or burning. Triggered by touch or sound with ADLs like shaving or chewing. Symptoms can be progressive and debilitating.
