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Neuro Boards > Neuro Pathology > Flashcards

Neuro Pathology Flashcards

1
Q

Alzheimer’s Disease Brain involvement

A
  • Cerebral Cortex and Subcortical areas
  • Deterioration of neurons involved with ach transmission -Formation of amyeloid plaques and neurofibrillary tangles => further deterioration
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2
Q

AD Etiology

A
  • No exact known cause
  • Risk increases with inc age
  • Higher incidence in women
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3
Q

AD Treatment

A

-Meds to inhibit acetylcholinesterase, alleviate cognitive symptoms and behavioral changes

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4
Q

Common meds for AD

A
  • Tacrine (cognex): cholinergic agent
  • Donepezil (aricept): cholinergic agent
  • Rivastigmine (exelon)
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5
Q

PT management with AD

A
  • Focus on maximizing pt’s remaining function

- Family/caregiver education

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6
Q

Progression of AD (3)

A

1) Initial: change in higher cortical functions (learning new things, memory/concentration)
2) Progression: loss of orientation, rigidity, bradykinesia, shuffling gait, impaired ability to perform self-care
3) End-stage: severe intellectual/physical destruction, incontinence, functional dependence, inability to speed

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7
Q

Amyotrophic Lateral Sclerosis (ALS) Presentation

A
  • Presents with both upper (d/t demyelination of corticospinal and corticobulbar tracts) and LMN (d/t anterior horn cell loss in the SC and motor cranial nerve nuclei in lower brainstem) impairments
  • Rapid degeneration => dennervation of muscle fibers, muscle atrophy, weakness
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8
Q

Amyotrophic Lateral Sclerosis (ALS) Etiology

A
  • unknown exact cause
  • higher incidence in men
  • commonly begins at 40-70 years of age
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9
Q

Amyotrophic Lateral Sclerosis (ALS) signs and symptoms (UMN vs LMN s/sx)

A
  • UMN: incoordination, spasticity, clonus, positive Babinksi
  • LMN: Asymmetric* muscle weakness, fasiculations, cramping, atrophy within the hands.
  • Will exhibit fatigue, oral motor impairment, motor paralysis, and eventual respiratory paralysis
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10
Q

Common meds for Amyotrophic Lateral Sclerosis (ALS) (1)

A

-Riluzole (Rilutek)

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11
Q

PT intervention for ALS

A
  • Focus on quality of life

- Family/caregiver treatment

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12
Q

Bell’s Palsy Presentation

A
  • assymetrical facial involvement
  • Eyelid and mouth drooping
  • Drooling
  • Dry eye
  • Inability to close eye d/t weakness
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13
Q

What nerve is affected with Bell’s Palsy?

A

-Facial Nerve

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14
Q

Bell’s Palsy Etiology

A
  • Herpes simplex/zoster virus thought to be a cause
  • Inflammation within auditory canal injures nerve and => demyelination of the nerve (axonal degeneration if apoxia occurs)
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15
Q

Common (types) of meds for Bell’s Palsy (2)

A
  • Anti-viral meds

- Corticosteroids

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16
Q

PT for Bell’s Palsy

A
  • Less severe cases resolve within 2 weeks with no intervention
  • Stimulation of facial nerve
  • Facial massage/exercise
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17
Q

Carpal Tunnel Syndrome (CTS) signs/symptoms

A
  • Motor and sensory disturbances in median nerve distribution d/t Median Nerve entrapment
  • Paresthesias may radiate into the UE, shoulder, and neck
  • Night pain
  • hand weakness
  • muscle atrophy
  • decreased grip strength/clumsiness
  • decreased wrist mobility
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18
Q

CTS treatement

A
  • splinting
  • ergonomic changes
  • local corticosteroid injections
  • PT
  • Carpel Tunnel release (severe cases)
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19
Q

Types of Cerebellar Disorders (4)

A

1) Congenital Malformations
2) Hereditary ataxias
3) Spinocerebellar ataxias
4) Acquired ataxias

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20
Q

Congenital Malformation

A
  • Type of Cerebellar disorder
  • Manifest early in life, non-progressive
  • Ataxia usually present
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21
Q

Spinocerebellar Ataxia

A
  • Type of Cerebellar Disorder
  • main autosomal dominant ataxia
  • affect multiple areas of the CNS and PNS
  • neuropathy, pyramidal signs, ataxia, and restless leg syndrome
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22
Q

Acquired Ataxias

A
  • Type of Cerebellar Disorder
  • Nondenerative systemic disorder, toxin exposure, or idiopathic in nature
  • i.e. alcoholism, hypothyroidism, and vitE deficiency
23
Q

Hereditary Ataxias

A
  • autosomal dominant
  • Autosomal recessive = Fredrich’s ataxa (gait unsteadiness, upper extremity ataxia, dysarthria, paresis, declined mental function).
24
Q

Cerebellar Disorders s/sx

A
  • depends on affected areas

- ataxia

25
Q

Diabetic Neuropathy Nerve Damage

A

-Microvascular diases combined with effects on nerves from hyperglycemia => nerve ischemia

26
Q

Diabetic Neuropathy s/sx

A
  • Symmetrical pattern of weakness and sensory distrubances (“stocking-glove” distribution)
  • May involve sensory, motor, or autonomic systems
27
Q

Diabetic Neuropathy Treatment

A
  • Monitor blood glucose levels

- PT for pain management, foot care, overall fitness

28
Q

Epilepsy

A
  • Chronic condition where temporary brain dysfunction => seizure
  • Unprovoked and unpredictable
29
Q

Epilepsy etiology

A

-many cases idiopathic

30
Q

Conditions leading to increased risk of Epilepsy (7)

A
  • genetics
  • head injury
  • dementia
  • CVA
  • Cerebral Palsy
  • Down Syndrome
  • Autism
31
Q

Epilespy Treatment

A
  • Antiepileptic meds (major side effects)

- Possible surgical intervention

32
Q

Guillain-Barre Syndrome (GBS) aka Acute Polyneuropathy

A
  • temporary inflammation and demyelination of peripheral nerves due to attack from GBS autoantibodies
  • Peak in frequency in young adults and between 5th-8th decades
33
Q

Etiology of GBS

A

-hypothesized autoimmune response to a previous respiratory infection, influenza, immunization, or surgery

34
Q

GBS s/sx

A
  • motor weakness in distal-proximal progression
  • sensory impairment
  • potential respiratory paralysis (life-threatening)
  • absence of DTRs
  • Inability to speak/swallow
35
Q

Time to peak level of disability with GBS

A

2 to 4 weeks after onset

36
Q

PT treatment with GBS

A
  • pulmonary PT
  • strenghening
  • mobility raining
  • w/c and orthotic prescription
  • AD training
37
Q

Huntington’s Disease (HD) aka Huntington’s Chorea brain involvement

A
  • Degeneration/atrophy of the basal ganglia and cerebral cortex
  • Deficient neurotrasmitters => unable to modulate movement
38
Q

HD etiology

A
  • Autosomal dominant trait linked to chromosome 4

- average age 35-55 years

39
Q

HD s/sx: inital stage

A
  • involuntary choreic movements
  • mild personality changes
  • grimacing/tongue protrusion
  • ataxia with choreathetoid movements
40
Q

HD s/sx: late stage

A
  • mental deterioration
  • decrease in IQ
  • depression
  • dysphagia
  • incontinence
  • immobility/rigidity
41
Q

PT for HD

A

-maximize endurance, strength, balance, postural control, and functional mobility

42
Q

Mutliple Sclerosis (MS) brain involvement

A
  • patches of demyelination in brain and SC
  • subsequent plaque formation
  • evental failure of impulse transmission
43
Q

MS etiology

A
  • unknown, but theorized is an autoimmune repsone from a slow-acting virus combined with genetic and environmental factors
  • highest incidence 20-35 years old
44
Q

MS s/sx

A
  • Periods of relapse and remission
  • initially visual problems
  • parethesias
  • clumsiness/weakness
  • ataxia
  • balance dysfunction
  • fatigue
45
Q

PT for MS

A
  • regulate activity level
  • energy conservation techniques
  • normalize tone
  • balance/gait training
  • core stabilization
  • adaptive/assistive device training
46
Q

Myasthenia Gravis

A
  • autoimmune diease

- antibodies block/destroy ach receptors in synapse and prevent muscle contraction => weakness

47
Q

Myasthenia Gravis etiology

A
  • autoimmne disease associated with an enlarged thymus
  • association with other autoimmune disorders
  • range from mild-severe involvement
48
Q

Myasthenia Gravis s/sx

A
  • remissions and exacerbations
  • extreme fatiguability
  • muscle weakness (occular muscles typically affected first)
  • dysphagia, dysarthrira, and cranial nerve weakness
49
Q

PT for Myasthenia Gravis

A
  • pulmonary intervention
  • energy conservation techniques
  • isometric strengthening exercises
50
Q

Parkinson’s Disease

A
  • degenerative disorder d/t decrease in dopamine production within basal ganglia
  • 50-79 year olds are majority diagnosed
  • PT focuses on strength, endurance, and functional mobility
51
Q

Post-Polio Syndrome

A

-Occurs when compensated reinnervation from Polio fails and results in ongoing muscle denervation

52
Q

PPS s/sx

A
  • Slow and progressive weakness
  • fatigue
  • muscle atrophy
  • pain
  • trouble swallowing
53
Q

PPS treatment

A
  • no deds to alter progression

- lifestyle modification and symptomatic intervention

54
Q

PT for PPS

A
  • encourage supervised exercise
  • functional independence
  • adaptive equipment
  • education

Neuro Boards (18 decks)

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