Neuro Pathologies Flashcards

1
Q

Alzheimer’s Disease

A
  • progressive neurological disorder results in deterioration and irreversible damage in the cerebral cortex and subcortical areas of the brain
  • neurons that are normally involved with acetylcholine transmission deteriorate within the cerebral cortex of the brain.
  • more common in women and incidence increases over the age of 80
  • changes in higher cortical functions characterized by subtle changes in memory, impaired concentration, and difficulty with new learning.
  • can’t be confirmed until postmortem biopsy to confirm neurofibrillary tangles and amyloid plaques.
  • meds Tacrine (Cognex), donepezil (Aricept), rivastigmine (Exelon)
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2
Q

What is the leading cause of death from someone with Alzheimer’s Disease?

A

Dehydration and infection

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3
Q

Stages of Alzheimer’s Disease

A
  • Early stage: loss of orientation, word finding difficulties, emotional lability, depression, poor judgement, and impaired ability to perform self-care skills
  • Middle stage: behavioral and motor problems such as aphasia, apraxia, perseveration, agitation, and violent or socially unacceptable behavior including wondering
  • End-stage: ability to learn is lost and long-term memory disappears. Severe intellectual and physical destruction. Incontinence, functional dependence, and inability to speak, and seizure acitivity
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4
Q

Amyotrophic Lateral Sclerosis (ALS)

A
  • chronic degenerative disease
  • upper and lower motor neuron impairments
  • etiology unknown. higher incidence in men. 40-70 y/o
  • LMN: asymmetric m weakness, fasciculations, cramping, and atrophy in hands.
  • weakness distal to proximal
  • UMN: incoordination of movement, spasticity, clonus, and positive Babinski reflex
  • will exhibit fatigue, oral motor impairment, motor paralysis, and eventual respiratory paralysis.
  • to confirm diagnosis: EMG or m biopsy
  • Riluzole (Rilutek) to help slow disease process.
  • anticholinergic, antispasticity, and antidepressant
  • PT focus on QOL among other things
  • most likely to die due to decline in respiratory function due to infection or inability to eat. (Death is ~2-5 yr after onset)
  • muscle wasting (amyotrophy) and gliotic hardening (sclerosis) of the anteiror and lateral corticospinal tracts involving UMN and LMN (pg. 160 patho book)
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5
Q

Typical progression of ALS from earliest to latest onset (main ones)

A
  1. fasciculations
  2. loss of dexterity
  3. dysarthria
  4. respiratory failure
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6
Q

Anterior Cord Syndrome

A
  • Incomplete spinal cord lesion which impacts the anterior spinal artery.

*anterior spinal artery supplies blood to the anterior 2/3 of the SC

  • Typically from cervical flexion injury
  • Affects that anterior and lateral corticospinal tracts and spinothalamic tracts…..so…
  • complete loss of motor function and loss of pain and temperature.
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7
Q

Arthrogryposis Multiplex Congenita (AMC)

A
  • non-progressive neuromuscular disease that occurs during the first trimester in utero

*Etiology is unknown

  • Cylinder like extremities with minimal definition, significant and multiple contractures, dislocation of joints, and m atrophy
  • Treatment: to attain maximum level of development through – positioning, stretching, strengthening, splinting, and use of adaptive equipment.
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8
Q

Which intervention(s) would MOST likely be the initial focus of physical therapy for arthrogryposis?

A

Stretching and splinting

Stretching to achieve full range of motion at a contracted joint followed by splinting to maintain the acquired range of motion are the primary intervention strategies for children with arthrogryposis.
Afterwards focus on functional mobility

Arthrogryposis is usually diagnosed at birth when an infant has contractures in two or more body areas. Common areas include the foot, hip, wrist, knee, elbow, and shoulder. There is usually prenatal damage to the anterior horn cells with a decreased number of motor units. Fibrotic tissue limits normal joint development and promotes the development of contractures.

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9
Q

Bell’s Palsy

A
  • acute onset of sensory and motor deficits to the area of the facial nerve due to abnormal pressure on the facial nerve from inflammation/edema
  • Typically from herpes simplex/herpes zoster

*15-45 yr of age.

*Asymmetrical facial appearance with “drooping” of eyelid and mouth, potential for drooling, dryness of eyes, and inability to close the eyelid due to weakness.

  • anti-viral medication, high-dose corticosteroids
  • massage, stretching, and moist heat, biofeedback and NMES

*Some typically resolve in few weeks (mild) but may take up to 6 months

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10
Q

Carpal Tunnel Syndrome

A

*peripheral nerve entrapment of the median nerve under the transverse carpal ligament

  • Flexor digitorum profundus tendons, four flexor digitorum superficialis tendons, and flexor pollicis longus tendon go through here.
  • 35-55 yr; greater in women
  • Risk factors: repetitive use, RA, pregnancy, DM, trauma, tumor, hypothyroidism, and wrist sprain or fracture
  • sensory and paresthesia along median nerve distribution.

*night pain, weakness of hand, m atrophy, decreased grip strength, clumsiness, decreased wrist mobility

*Ape hand caused by atrophy of thenar musculature and first 2 lumbricals. (abductor pollicis brevis)

  • Treatment - corticosteroids injections, splinting, and PT (splinting, mobilization, and gentle stretching)
  • without sx - 4-6 weeks. With sx 6-8 weeks.
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11
Q

Central Cord Syndrome

A
  • incomplete spinal cord lesion caused by cervical hyperextension injury typically that causes bleeding into the central gray matter
  • other contributing factors: cervical spondylosis, narrowing or congenital defect of spinal canal, tumor, RA or syringomyelia
  • over 50 y/o and in men
  • motor loss UE>LE. Most severe distally in UE.
  • Sacral segments are usually unaffected since they are located laterally within the SC
  • Methylprednisolone should be administered within 8 hrs of injury to assist with neurological recovery.
  • CCS is the most common incomplete spinal cord lesion.
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12
Q

Cerebral Palsy

A
  • umbrella term for brain damage occured in utero that is non-progressive.

*Etiology -of oxygen, maternal infections, drug or alcohol abuse, placents abnormalities, toxemia, prolonged labor, prematurity, and p incompatibility. The etiology of acquired cerebral palsy include meningitis, CVA, seizures, and brain injury.

  • Signs and symptoms - demonstrate abnormal muscle tone, impaired modulation of movement, presence of abnormal reflexes, and impaired mobility. (Range from mild to severe)
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13
Q

2 types of cerebral palsy primary motor patterns

A

*Spastic - indicating a lesion in the motor cortex of the cerebrum; upper motor neuron damage
* Athetoid - indicating a lesion involving the basal ganglia

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14
Q

Distribution of involvement of Cerebral palsy motor patterns

A
  • Monoplegia - one extremity
  • Diplegia - bilateral lower extremity involvement, howevel. upper extremities may be affected
  • Hemiplegia - unilateral involvement of the upper and loved extremities
    Quadriplegia - involvement of the entire body
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15
Q

CVA Risk Factors

A
  • Primary: HTN, cardiac disease or arrhythmias, DM, cigarette smoking, TIA
  • Secondary: Obesity, high cholesterol, behavior related to HTN (stress, increase salt intake), physical inactivity, increased alcohol consumption.

*Modifiable: HTN, atherosclerosis, heart disease, DM, elevated cholesterol, smoking, and obesity
HTN is the most prevalent modifiable cause.

  • Non-modifiable: age, race, family hx, and sex.
    Age is the greatest risk for CVA (>65 y/o)
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16
Q

What will you see with a L CVA vs R CVA?

A

L CVA:
- weakness/paralysis on R side
- impaired processing
(difficulty processing communication and processing information in a sequential, linear manner, difficulty with verbal commands)
- heighted frustration
- aphasia
- dysphagia
- motor apraxia
- R hemianopsia
- decreased discrimination b/n L&R

R CVA:
- weakness/paralysis on L side
- poor attention span
- impaired awareness and judgement
- spatial deficits
- memory deficits
- L inattention (neglect)
- decreased abstract reasoning
- emotional lability
- impulsive behavior
- L hemianopsia

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17
Q

Most common artery for CVA?

A

middle

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18
Q

What will you see if a stroke in the brainstem vs cerebellum?

A

Brainstem:
- unstable vital signs
- Decreased consciousness
- decreased ability to swallow
- weakness/paralysis on BOTH sides of the body

Cerebellum:
- decreased balance
- ataxia
- decreased coordination
- nausea
- decreased ability for adjustment
- nystagmus

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19
Q

Diabetic Neuropathy

A
  • direct effect of DM
  • nerve ischemia from direct effects of hyperglycemia (from prolonged exposure to high blood glucose).
  • weakness and sensory disturbances distally in symmetrically.
  • tingling, numbness or pain (especially of the feet)
  • wasting of muscles of the feet or hands “stocking glove” sensory distribution impairment, orthostatic hypotension, weakness, urinary impairments, and significant pain.
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20
Q

Down Syndrome

A

AKA trisomy 21
* Incomplete cell division of the 21st pair of chromosomes. …this results in 47 chromosomes. (Normal odd 46)

  • Advanced maternal age increases the risk of the genetic imbalance
  • S&S: intellectual disability, hypotonia, joint hypermobility, developmental delay, flattened nasal bridge, narrow eyelids with epicanthal folds, small mouth, feeding impairment, flat feet, scoliosis, congenital heart disease, and visual and hearing loss.
  • PT will not accelerate developmental milestones…it will help avoid compensatory patterns with static positions and mobility
  • Exercise is essential for child with Down syndrome in order to avoid inactivity and obesity
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21
Q

Duchenne Muscular Dystrophy

A
  • progressive disorder – absence of gene needed for muscle proteins dystrophin and nebulin. mutation of dystrophin Xp21
  • cell membranes weaken, myofibrils are destroyed, and m contractility is lost.
  • Fat and connective tissue replace muscle
  • Death typically from cardiopulmonary failure before age 25
  • X-linked recessive gene…so the mother is a silent carrier. And only men get it
  • usually diagnosed around 2-5 y/o
  • waddling gait, progressive weakness, disinterest in running, falling, toe walking, excessive lordosis, and pseudohypertrophy of m. , difficulty with stair climbing

*Gowers sign

*is this the one you don’t over work them and you get them a chair sooner rather than later?

  • typically loose ability to ambulate around 10-12 y/o
  • 1/3 have learning disability
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22
Q

Erb’s Palsy

A
  • upper brachial plexus injury/palsy
  • Typically from difficulty deliver (breech position, prolonged labor, large baby, use of forceps) the neck gets stretched and damages the nerves
  • Affects C5-6: axillary, lateral pectoral, upper and lower subscapular, suprascapular, and partial paralysis of the long thoracic and musculocutaneous nerves
  • Loose the rotator cuff, deltoid, brachialis, coracobrachialis, and biceps brachii functions.
  • “Waiter’s tip position”: loss of shld function, loss of elbow flexion, loss of forearm supination, and hand positioned in pinch grip.
  • PT: work on active and passive movement that promotes the use of the weak UE for functional activities.
  • Spontaneous recovery can occur in 3-4 mths. If conservative fails – surgery then splint for 3-4 weeks.
23
Q

Epilepsy

A
  • temporary dysfunction of the brain
  • Conditions that increase risk: genetic influence, head trauma, dementia, CVA, cerebral palsy, DS, and autism
  • S&S: mood disturbances, staring, LOC, uncontrollable jerking of the arms and legs, stiffening of the muscles, and loss of m control.
  • EMG measures the electrical activity of the brain….most common test used to confirm the diagnosis.
  • one seizure doesn’t signal epilepsy
24
Q

Guillain-Barre Syndrome

A
  • temporary inflammation and demyelination of the peripheral nerves myelin sheath. (aka acute polyneuropathy)
  • most common in the young adult pts and again in 5th-8th decades
  • Etiology: autoimmune response to previous respiratory infection, influenza, immunization, or sx. OR viral infections, Epstein-Barr syndrome, SMV, or bacterial infections
  • S&S: (rapidly ascending symmetric motor weakness and distal sensory impairments)
  • motor weakness distal to proximal (distal symmetrical motor impairment)
  • sensory impairment
  • transient paresthesia’s that progresses towards the UE and head.
  • first sign typically paresthesia’s in the toes
  • peaks at 2-4 weeks; but recovery can last from 3-12 months
  • can have life threatening respiratory impairment
  • diagnosed through CSF ( high protein levels and little to no lymphocytes). EMG will have abnormal and slowed conduction
  • Acute: PROM, positioning, and light exercise. Limit overexertion and fatigue to avoid exacerbation of symptoms.
  • majority of pts experience full recover, 20% have remaining neurologic deficits, and 3-5% of pts die from respiratory complications.

After 1 yr 67% have complete recovery, while 20% have significant disability. At 2 yrs 8% still have not recovered.

25
Q

Huntington’s Disease

A
  • degeneration and atrophy of the basal ganglia (striatum) and cerebral cortex. Decrease in quantity and acitivty of GABA and acetylcholine (defect linked to chromosome 4)
  • genetically transmitted as an autosomal dominant trait.
  • Person typically has children prior to symptoms appearing. 35-55 y/o
  • S&S:
  • involuntary choreic movements
  • mild alterations in personality
  • unintentional facial expressions
  • Gait will be ataxic
  • Choreoathetoid movement
  • speech disturbances and mental deterioration
  • Late stage: mental deterioration, decrease in IQ, depression, dysphagia, incontinence, immobility, and rigidity.
  • PT: maximize endurance, strength, balance, postural control, and functional mobility. Focus on motor control.

Pt education on prone lying, stretching, prevention of deformity and contracture and safety with mobility

26
Q

Multiple Sclerosis (MS)

A
  • patches of demyelination that decrease the efficiency of nerve impulses transmission
  • Etiology: proposed slow activating virus initiates the autoimmune response

*Caucasians; 20-35 y/o; women (twice as common); more often in temperate climates

*4 stages/types

27
Q

Types/stages of MS

A

(may need to add clarification)

Relapsing-Remitting MS
- Appearance of full recovery from relapses
- With sequelae/residual deficit after incomplete recovery
- Most common (85%)

Secondary Progressive
- Steady irreversible worsening of neurologic function
- Accumulation of disability
- Further qualifiers (active, not active etc.)

Primary Progressive
- Accumulation of disability from onset of symptoms
- Other subcategories (active, not active etc.)

Progressive Relapsing
- Progressive accumulation of disability
- Clear, acute clinical attacks with or without full recovery

28
Q

Myasthenia Gravis

A
  • autoimmune disease results in neuromuscular junction disorder characterized by progressive m weakness and fatigability on exertion.
  • Antibodies block or destroy the receptor that are needed for acetylcholine uptake and prevents m contraction. (defect of nerve impulses to muscles at NMJ)
  • Associated with: enlarged thymus, DM, RA, lupus, and other immune disorders
  • Cardinal S&S: extreme fatigability and skeletal m weakness that fluctuates over minutes or extended period of time.
  • ocular m typically affected first. 1/2 have ptosis and diplopia
  • dysphagia, dysarthria, and cranial nerve weakness
  • women - 20’s-30’s; men - 50’s-60’s (women are more common)
  • Triggers that make symptoms worse: activity, heat, stress, illness, certain meds, menstruation, and pregnancy.
  • Treatment: acetylcholinesterase inhibitors, corticosteroids, immunosuppressants, thymectomy
  • PT m strength and endurance and energy conservation techniques.

From PTFE test: muscles that contract frequently become weak. Causes ptosis, misalignment of eyes. Other m affected are those that control facial expression, swallowing, proximal limb movements, and respiration.

29
Q

Parkinson’s Disease

A
  • primary degenerative disorder. Characterized by decrease in production of dopamine in the substantia nigra

*unknown etiology

  • 50-79 y/o

*TRAP (tremor [resting], rigidity [“cogwheel” or “lead pipe”], akinesia, postural instability)

  • will first notice tremor or difficulty with rolling over rising from bed or impairment with fine manipulative movements.
  • minimal facial expressions
  • Treatment: dopamine replacement therapy (levodopa, sinemet, madopar)
    maximizing endurance, strength, and functional mobility.
    *v/c and oral/visual feedback.
30
Q

Post-polio syndrome

A
  • individual previously diagnosed with poliomyelitis. (~50% will have post-polio syndrome)
  • Muscle weakness, atrophy, fatigue, and muscular and joint pain
  • primarily affects the muscle affected with poliomyelitis originally.
  • pain and weakness increase with physical activity and exposure to cold
  • Weakness progresses over years and is interspersed with periods of stability
  • No cure
  • PT on energy conservation techniques, avoid fatigue or exhaustions (this worsens symptoms)
31
Q

Prader-Willi Syndrome

A
  • genetic condition that is diagnosed by physical attributes and patterns of behavior rather than genetic testing.
  • Etiology - The causative factor is a partial deletion of chromosome 15.
  • Signs and symptoms -
  • small hands, feet, and sex organs, hypotonia,
  • almond-shaped eyes,
  • obesity, and a
  • constant desire for food.
  • Coordination impairments and intellectual disability.
  • Treatment - PT includes postural control, exercise and fitness, and gross and fine motor skills training.
32
Q

3 types of spina bifida

A
  • Occulta (incomplete fusion of the posterior vertebral arch with no neural tissue protruding),
  • Meningocele (incomplete fusion of the posterior vertebral arch with neural tissue/ meninges protruding outside the neural arch)
  • Myelomeningocele (incomplete fusion of the posterior vertebral arch with both meninges and spinal cord protruding outside the neural arch).
33
Q

Spina Bifida

A
  • congenital neural tube defect. Most common in the lumbar spine

*Etiology: Main one is low levels of folic acid

  • S&S:
  • motor and sensory loss below the vertebral defect
  • hydrocephalus
  • Arnold-Chiari type II malformation
  • Clubfoot
  • Scoliosis
  • Bowel and bladder dysfunction
  • Learning disabilities.
  • The higher the neural lesion the worse the prognosis is for survival.
  • Require surgical intervention to close the lesion and place shunt for hydrocephalus.
  • Approximately 2/3 of children with myelomeningocele have normal intelligence. 1/3 mild intelligence difficulties
  • Prenatal testing of alpha-fetoprotein (AFP)
  • PT family education (positioning, handline, ROM, and therapeutic play)
34
Q

Spinal Muscular Atrophy (SMA)

A
  • progressive degeneration of the anterior horn cell.
  • progressive m weakness and atrophy, diminished or absent DTR, normal intelligence, intact sensation, and end-stage respiratory compromise
  • Treatment - positioning, vestibular and visual stimulation, and access to play

Type 3:
- Acute Infantile SMA (Type 1-Werdnig-Hoffmann disease) - Birth - 2 y/o. Motor degeneration progresses quickly and life expectancy is less than one year.

  • Chronic Childhood SMA (Type 2-Chronic Werdnig-Hoffmann disease) - 6mths - 1yr. Slower progression than infantile SMA. Impairment is steady, however, a child can survive into adulthood.
  • Juvenile SMA (Type 3-Kugelberg-Welander SMA) - 4-17 years of age. Children with juvenile SMA typically survive into adulthood.
35
Q

Thoracic Outlet Syndrome (TOS)

A
  • Causes: cervical rib, abnormal first rib, postural deviations/changes, body composition, chronic hyperabduction of the arm, hyperabduction of the arm, hypertrophy or spasms of the scalene muscle, degenerative disorders, and an elongated cervical TP
  • S&S: diffuse pain in arm at night, paresthesias in the fingers and UE, weakness and muscle wasting, poor posture, edema, and discoloration.
  • If the upper plexus is involved, pain will be reported in the neck that may radiate to the face and may follow the lateral aspect of the forearm into the hand.
  • PT: modification of posture, breathing patterns, positioning in bed and at the work site, and gentle stretching.
36
Q

Trigeminal Neuralgia

A
  • abnormal pression or irritation on the trigeminal nerve (CN V)
  • typically from tumor or swollen blood vessel.
  • commonly seen with demyelination such as MS
  • typically unilateral episodic or constant
  • Episodic: sudden onset of pain (sharp, jolting, stabbing, shock-like).
    Spasms or ticks
    These episodes can be triggered by touch or sound such as ADL such as shaving, chewing, or oral care.
  • Constant/chronic: persistent aching or burning sensations. Still can be triggered like episodic
  • Women over 50 more typical.
37
Q

What will you see if the cerebellum is injured?

A

Motor impairments that affect the ability to perform accurate, smooth, controlled movements.

  • Ataxia, asthenia, dysarthria, dysdiadochokinesia, hypotonia, nystagmus, tremor
38
Q

Common cause of acquired ataxia

A

Alcoholism

39
Q

most common comorbidity present in individuals with Down syndrome?

A

Congenital heart defects

Congenital heart defects are present in approximately half of all children with Down syndrome. Congenital heart problems, respiratory infection, and leukemia are the most common factors associated with morbidity and mortality in childhood. Increased tendency for premature cellular aging and Alzheimer’s disease may account for higher mortality rates in adulthood.

40
Q

Earliest clinical marker of ALS?

A

Fasiculations, muscle cramps, fatigue, weakness, and atrophy.

By the time most individuals report weakness, they have lost approximately 80% of their motor neurons in the areas of weakness

41
Q

Contralateral spastic hemiparesis and sensory loss of the face and upper extremities more than the lower extremities are the main characteristics of a stroke in which artery?

A

Middle cerebral artery

often associated with speech deficits, apraxia, perceptual deficits, and contralateral homonymous hemianopsia.

42
Q

Atlantoaxial subluxation due to ligamentous laxity should be screened for in which neuro pathology?

A

Trisomy 21 - Down Syndrome

Individuals with Down syndrome (trisomy 21) have increased ligamentous laxity, likely from a collagen defect. This can result in pes planus, patellar instability, scoliosis, and atlantoaxial instability.

43
Q

What is the best method to facilitate elbow extension in a patient with hemiplegia?

A

by turning the head to the affected side

The asymmetrical tonic neck reflex produces extension of the affected upper extremity when the patient’s head is turned toward the affected side. This reflex may be present following a CVA and can assist to extend the affected elbow.

44
Q

Atrophy of the thenar eminence and the first and second lumbricals could result from:

A

carpal tunnel syndrome

45
Q

Which factor is most commonly related to cerebral palsy?

A

premature birth

Premature birth is the most common factor in occurrences of cerebral palsy. When an infant is born premature, the blood vessels in the brain are not fully developed and therefore are susceptible to damage from gravitational forces. This may lead to blood vessel rupture and resultant death of brain tissue.

46
Q

Ramsay Hunt Syndrome

A

complication of varicella-zoster virus infections, including chickenpox or shingles (herpes zoster)

Facial nerve palsy with painful rash around ear, face, or mouth.

Affects the facial and vestibular cochlear nerves.

47
Q

A pt with epilepsy should be isolated in therapy….weird to me but okay sure.. to keep it from triggering one

A
48
Q

Most individuals diagnosed with Guillain-Barre syndrome return to their prior level of function within:

A

1 yr

Most individuals diagnosed with Guillain-Barre syndrome (GBS) return to their prior level of function within 1 year. More than two-thirds of individuals report symptoms of an infectious disease two weeks before the onset of GBS symptoms. GBS typically presents with a symmetrical flaccid paralysis progressing from distal to proximal.

49
Q

Which form of multiple sclerosis is characterized by exacerbations that can last days to months and are typically followed by periods of improved function?

A

relapsing remitting

Relapsing remitting multiple sclerosis (MS) represents about 85% of individuals with MS and is characterized by exacerbations that can last days to months and are typically followed by periods of improved function. During remission, function can return to pre-relapse level, but most frequently does not recover fully.

50
Q

Which form of multiple sclerosis is characterized by periods of symptoms and reduction in symptoms followed by a slow, steady progression of increasing disability?

A

secondary progressive

Secondary progressive multiple sclerosis is characterized by a slow, steady progression of increasing disability. Relapses may occur early on, but generally decrease over time. Individuals with relapsing remitting MS typically coverts to the secondary progressive form 10-20 years after diagnosis.

51
Q

Which neurodegenerative disease presents with weakness primarily due to the destruction of acetylcholine receptors in muscle tissue?

A

Myasthenia Gravis

52
Q

When treating an individual with multiple sclerosis it would be most appropriate to conduct sessions that include resistance training at what time?

A

Morning (9 am)

Treatment sessions are best in the morning when the body core temperature tend to be lowest and before fatigue sets in.

Exercising at moderated intensity is recommended to reduce excess fatigue and avoid increasing core body temperature

53
Q

Which macronutrient would be most important to limit in a patient with Parkinson’s disease?

A

Protein

It blocks the effectiveness of the medication Levodopa by competing with it for absorption in the body.

Advised to follow a high calorie, low protein diet with no more than 15% of calories coming from protein.

54
Q

Myasthenia gravis typically affects which muscle group first?

A

Muscles of the eye

Ultimately results in extreme muscular weakness

Initial symptoms are diplopia, ptosis, and squinting of the eye.