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clinical conditions > Exam 11: Progressive & Degenerative CNS > Flashcards

Exam 11: Progressive & Degenerative CNS Flashcards

1
Q

autonomic dysreflexia

A

a potentially life-threatening syndrome involving an abnormal, overreaction of your autonomic nervous system to painful sensory input

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2
Q

postural hypotension

A

when your blood pressure drops when you go from lying down to sitting up, or from sitting to standing

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3
Q

deep vein thrombosis (DVT)

A

a blood clot in a deep vein, usually in the leg

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4
Q

long term issues with spinal cord injury

A
  • contractures & spasticity
    • splinting, positioning, use of AE, tenodysis splint
  • frequent infections: UTI, pneumonia, cellulitis
  • decubitus ulcers (pressure ulcers)
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5
Q

support for decreased abdominal muscles

A
  • abdominal binder
    • assists with trunk control
    • supports organs to decrease risk of digestive issues/ hernias
    • assists with bp management
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6
Q

spinal cord bowel and bladder management

A
  • bowel stim programs
  • self-catheterization vs. indwelling catheter
  • self-catheterization
  • UTIs
    • increase in spasticity, fevers, increased fatigue
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7
Q

non-cognitive impairment disorders

A
  • Amyotrophic Lateral Sclerosis (ALS)
  • Guillain Barre Syndrome
  • Post-polio syndrome or post viral syndrome
  • aging with a spinal cord injury
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8
Q

cognitive impairment disorders

A
  • Alzheimer’s Disease
  • Dementias
  • Lewy Body Disease
  • Parkinson’s Disease
  • Multiple Sclerosis (less cog. impair.)
  • other brain degeneration (PSP, CBD)
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9
Q

what is amyotrophic lateral sclerosis?

A
  • Lou Gehrig’s Disease
  • rapidly progressive neuromuscular disease systematically destroys the body’s functional capabilities
  • men 2x more likely than women
  • 40-60 yr old onset (av. 58, young as 16)
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10
Q

etiology of ALS

A
  • unknown
  • attacks spinal cord (at all levels eventually, not brain)
  • starts low on spinal cord and works way up
  • sporadic: most common - no genetic link, possible environmental factors
  • familial: only one parent needs to carry the gene
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11
Q

symptomology of ALS

A
  • affects voluntary muscles
  • upper motor neurons (at all levels)
    • spasticity & stiffness
    • hyperactive reflexes
    • fasciculations (twitching)
  • lower motor neurons (at all levels)
    • weakness
    • hypotonicity
    • atrophy
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12
Q

early & progressive symptoms of ALS

A
  • early
    • difficulty walking
    • difficulty with fine motor tasks and picking up objects
  • progressive
    • weakness spreads to muscle groups of limbs, neck, trunk - eventually becoming flaccid
  • speech deficits
  • dysphagia
  • respiratory problems as result of failing respiratory muscles
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13
Q

ALS prognosis

A
  • terminal condition (20-48 mo)
  • cognition is preserved, but in some cases there may be fronal/ temporal dementia processes
  • death results from respiratory complications
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14
Q

what is guillain-barre syndrome?

A
  • nervous system disorder of spinal cord
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15
Q

etiology of GBS

A
  • acute inflammatory condition involving the spinal nerve roots, peripheral nerves, and in some cases, selected cranial nerves
  • rapid onset (12-24 hrs)
  • often follows a viral illness, immunization or surgery
  • male = female
  • any age
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16
Q

symptomology of GBS

A
  • pain and tenderness of muscles
  • weakness
  • decreased deep tendon reflexes
  • progressive symptoms
    • motor weakness or paralysis of limbs
      • progresses from LE to UE & trunk
  • sensory loss
  • muscle atrophy
  • respiratory paralysis can require tracheostomy
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17
Q

GBS prognosis

A
  • variable
  • severe cases
    • CN 7, 9, 10
      • difficulty speaking, swallowing, and breathing
    • involvement of vital centers in the medulla
      • respiratory failure requiring tracheostomy or assisted ventilation
  • majority of cases - complete recovery within weeks - months with few residual effects
  • can become recurrent and become chronic GBS
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18
Q

what is post-polio syndrome?

A
  • polio is a contagious viral disease that affects the motor neurons in spinal cord + motor nuclei in brainstem
  • flaccid paralysis that affects LE, accessory muscles of respiration, and muscles that promote swallowing
  • sensory roots and sensation are intact
  • no known cure
  • deformities caused by asymmetrical pulling of muscles (paralysis), pain, fractures
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19
Q

etiology of PPS

A
  • patients who had polio earlier in life are now experiencing additional weakness and other disabling symptoms years after the initial disease
  • increased weakness of muscles that were previously affected by the polio infection
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20
Q

symptomology of PPS

A
  • fatigue
  • slowly progressing muscle weakness
  • muscular atrophy
  • joint pain
  • increasing skeletal deformities such as scoliosis
  • severity depends on degree of residual weakness and disability resulting from the original episode of polio
    • mild polio = mild PP symptoms
    • severe polio = greater weakness and greater loss of function with PPS
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21
Q

PPS prognosis

A
  • effective remedies aim to prevent muscle fatigue, improve body mechanics, conserve energy
  • typically, patients who adjust their lifestyles experience improvements of symptoms & stabilization of function
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22
Q

non-cognitive disorder impact on occupational performance

A
  • progressive
  • increasingly debilitating
  • increased dependence on others for ADLs & IADLs
  • compensatory strategies
    • AE
  • energy conservation
    • avoid over fatigue
      • pacing, successful use of compensatory strategies, AE, ADL assistive devices, home/work modifications
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23
Q

what is multiple sclerosis?

A
  • immunologic or autoimmune disease of the CNS
    • body attacks myelin sheath around the brain/ spinal cord neurons
  • characterized by demyelination in white matter, gray matter, and axons in multiple sites
    • scar tissue/ plaques decrease ability of axon to conduct impulses
    • can affect visual, motor, sensory, cognitive, psychological, bowel/ bladder systems
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24
Q

etiology of ms

A
  • exact cause is unknown; genetics, gender, environmental factors
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25
Q

prevalence with ms

A
  • most common non-traumatic neurodegenerative disorder among adults 40+
  • diagnosed in middle-age
  • 1% of pop. +
  • higher in parts of country with ethnic groups
  • f > m
  • european ancestry
  • relatives with ms
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26
Q

symptomology of ms

A
  • unpredictable and highly variable symptoms
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27
Q

initial symptoms of ms

A
  • numbness
  • weakness
  • vision changes (inflammation of optic nerve)
  • gait imbalance or falls
  • incontinence
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28
Q

progressive symptoms of ms

A
  • muscle weakness/fatigue
  • ataxia
  • fatigue
  • hypoesthesia/ paresthesia
  • pain
  • optic neuritis or diplopia
  • dysarthria
  • dysphagia
  • difficulties with bowel/ bladder control
  • varying degrees of cognitive impairment
  • depression
  • impulsivity
  • lability
  • temp. control issues
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29
Q

types/ patterns of ms

A
  • benign MS-non-progressive MS
  • relapsing remitting - non-progressive
  • relapsing remitting - progressive MS
  • primary progressive MS
30
Q

prognosis of ms

A
  • progressive
  • gradually increasing disability
  • no significant effect on life expectancy (could live 50+ yrs w/ disability)
31
Q

OT role of MS

A
  • teach compensatory strategies to deal with symptoms:
    • energy conservation, work simplification, cognitive strategies, falls prevention, caregiver education, positioning, feeding, splints, ROM, coping strategies, etc.
32
Q

what is parkinson’s disease?

A
  • characterized by degeneration in dopaminergic pathways (basal ganglia)
    • dopamine: neurotransmitter that transports signals to motor control areas
    • dopaminergic neurons deteriorate quickly, decreasing amount of dopamine production, resulting in impairments
33
Q

etiology of pd

A
  • exact cause is unknown… combo of genetic & environmental factors believed to be contributors
  • previous serious and recurrent TBIs
  • diet
  • exposure to herbicides/ pesticides
34
Q

symptomology of pd

A
  • two variations:
    • tremor dominant & nontremor non-dominant
  • symptom complex: parkinsonism
35
Q

primary symptoms of pd

A
  • bradykinesia
    • resting tremor
    • “pill-rolling” tremor
  • muscle rigidity
  • festinating gait
36
Q

secondary symptoms of pd

A
  • gait disturbance
    • flexed forward posture, shuffling steps, impaired balance, reduced arm-swing
  • dexterity and coordination difficulties
  • tremors
  • micrographia
  • cognitive impairments
  • muffled speech
  • poor balance
  • fatigue
  • oculomotor impairments
  • problems with oral musculature
    • drooling, dysphagia, monotone speech/ low vol.
  • problems w/ bowel/ bladder control
  • depression
  • dementia
37
Q

3 phases of pd

A
  • preclinical period
  • prodromal period
  • symptomatic period
38
Q

preclinical period of pd

A

neurons degenerate, but no symptoms

39
Q

prodromal period of pd

A
  • lasts months or years
  • generalized symptoms
40
Q

symptomatic period of pd

A
  • classic motoric symptoms followed by non-motor symptoms
41
Q

prognosis of pd

A
  • highly variable
  • slow progressive disease
  • 15-20 yrs before entering most severe stages
  • loss of function is not a linear progression; periods of improvement intermixed with periods of exacerbation
  • no cure
  • medical management concentrates on symptom control through medication
42
Q

what is delirium

A
  • disturbance in attention (reduced level of arousal) with decreased ability to focus, sustain or shift attention
  • change in cognition
    • memory loss/confusion, disorientation, hallucinations/paranoid thoughts, language, perceptual disturbance
  • rapid onset; fluctuating symptoms
  • lasts hrs-days
  • usually resides when medical condition clears
43
Q

etiology of delirium

A
  • caused by underlying medical condition
    • fever, infection, medication, surgery, traumatic event, drugs/ alcohol
  • risk factors:
    • multiple medications, extremes of age, presence of underlying cognitive condition
  • prevalence:
    • difficult due to left untreated
44
Q

prognosis/ progression of delirium

A
  • altered sleep wake patterns
  • perceptions altered
  • decreased attention
  • memory impairment
  • motor issues
  • rapid onset
  • 48 hrs after onset
  • patterns or intervals of lucid mixed with confusion
  • sundowning (symptoms worse at night)
  • brief duration: days to weeks
  • outcomes can result in recovery to death
44
Q

signs & symptoms of delirium

A
  • prodromal symptoms (before onset & full symptom appearance)
    • restlessness, anxiety, sleep disturbances, irritability
44
Q

subtypes of neurocognitive disorders

A
  • alzheimer’s disease
  • vascular dementia
  • NCD with lewy bodies
  • frontotemporal dementia
  • normal pressure hydrocephalus
  • progressive supranuclear palsy
  • corticobasilar degeneration
44
Q

etiology/ risk factors of delirium

A
  • no one perfect biological marker
  • known risk factors
    • age, genetics (early onset, DS), environmental factors, women have greater risk
  • potential contributing factors (pg. 175)
44
Q

what is alzheimer’s disease

A
  • most common form of dementia
  • progressive & significant deterioration of intellectual, social, and occupational functioning
  • 6th leading cause of death is U.S.
  • significant cost to healthcare system
45
Q

etiology of AD

A
  • exact cause is unknown
  • definitive diagnosis can only be done through brain autopsy
    • eval. to diagnose AD: recent history of mental/ behavioral symptoms, physical exam., neuropsychological tests, CT/MRI scans
46
Q

signs & symptoms of AD

A

most common early sign is difficulty remembering newly learned information
- early signs are often mistaken for normal aging
- frequently repeating statements, misplacing items, difficulty finding names for familiar objects, mood swings

47
Q

additional behavior changes of AD

A
  • difficulty performing familiar tasks
  • disorientation to time and place
  • poor or decreased judgment
  • problems w/ abstract thinking
  • change in mood or behavior
  • change in personality
  • loss of initiative
48
Q

stages of AD

A
  • mild (MCI)
  • moderate
  • severe
49
Q

stage I (MCI) of AD

A
  • 2-3 years
  • complex attention
  • executive function
  • learning & memory
  • language
  • perceptual motor abilities
  • social cognition
50
Q

Stage II moderate/ middle stage of AD

A
  • 2-10 years
  • loss of short-term memory
  • invent words
  • difficulty remembering familiar faces
  • psychiatric symptoms increase and behavioral changes arise
  • disorientation to time & place
  • wandering & agitation
  • assistance needed for basic ADLs, dependent for IADLs
51
Q

stage III severe late stage of AD

A
  • 1-3 years, can last 8-12
  • dependent for basic ADLs
  • memory is so poor that no one is recognizable
  • bowel/ bladder incontinence
  • dysphagia
  • immobile and stays in bed/chair
    • at risk for contractures, pressure ulcers, UTIs, pneumonia, and infection
52
Q

prognosis of AD

A
  • no cure
  • can live 8-10 yrs, as long as 20 after diagnosis
  • eventually leads to coma & death
53
Q

early onset vs. late onset of AD

A
  • progresses similarly
  • early onset: 35
  • late onset: 65+
54
Q

what is frontotemporal dementia?

A
  • progressive cell degeneration in the brain’s frontal lobe or temporal lobes
  • impairments in planning and judgment; emotions, speaking and understanding speech; certain movements
55
Q

categories of symptoms for frontotemporal dementia

A
  1. behavioral variant frontotemporal dementia
    • changes manifest in personality & behavior
  2. primary progressive aphasia
    • affects language and behavior
    • semantic dementia/ progressive nonfluent aphasia
56
Q

symptoms of frontotemporal dementia

A
  • socially inappropriate behaviors
  • loss of mental flexibility; appears memory impaired
  • language problems
  • difficulty with thinking and concentration
  • hyperorality, hypersexuality
57
Q

other progressive brain degeneration diseases

A
  • corticobasal degeneration (CBD): shakiness, lack of coordination, muscle rigidity & spasms
  • progressive supranuclear palsy (PSP): walking and balance problems, frequent falls and muscle stiffness
58
Q

prognosis for CBD & PSP

A
  • progressive
  • much variation from one person to another, all typically become mute and bed-bound
  • 6-8 years, can be 2-20 of survival
59
Q

what is lewy body dementia?

A
  • lewy bodies are microscopic neuronal inclusion bodies within the cytoplasm of a cell
  • often misdiagnosed as alzheimer’s/ parkinson’s diseases
60
Q

etiology of lewy body dementia

A
  • cause is unknown
  • more psychiatric disturbance, including hallucinations
  • hallucinations are often pleasant
  • mood disturbance is common
61
Q

symptoms of lewy body dementia

A
  • similar to PD
  • unique - often includes fluctuations between confusion and lucidity, visual hallucinations, and parkinsonism (tremors & rigidity)
  • REM sleep behavior disorder - acting out dreams, kicking and thrashing
62
Q

prognosis of lewy body dementia

A
  • no treatment that can slow or stop the brain cell damage
  • duration: 5-6 yrs, can be 2-20
  • initially affects frontal lobe, then spreads to parietal and temporal lobes
63
Q

what is vascular dementia?

A
  • decline in thinking skills as a result of damage to the brain caused by problems with cerebral circulatory system
  • symptoms begin suddenly, following CVA
  • multiple small CVAs, brain mass shrinks, vessels harden and brain does not receive nutrition
64
Q

etiology of vascular dementia

A
  • high bp
  • previous TIAs, stroke or heart attacks
  • caused by one or more strokes - large infarcts or small lacunar strokes
65
Q

symptoms of vascular dementia

A
  • vary widely - depending on area of brain damaged
  • memory loss may or may not be a significant symptom
    • changes in executive function
  • sudden post-stroke changes
    • confusion, disorientation, receptive/ expressive aphasia, vision loss
66
Q

what is normal pressure hydrocephalus?

A
  • fluid builds in ventricles, lower pressure than typical hydrocephalus
  • for best results, must be caught quickly
  • will typically use a shunt to decrease fluid NPH
67
Q

symptoms of NPH

A
  • more sudden onset of symptoms compared to dementia (1-2 weeks)
    • incontinence, rapid cognitive changes, decreased balance with falls)
68
Q

what is huntington’s disease

A
  • recessive gene
  • child has a 50% chance of getting it, able to find out in advance
  • early symptoms are psychiatric, then movement disorders, athetosis, chorea, large tremors, spasticity

clinical conditions (16 decks)

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