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
2
Q
postural hypotension
A
when your blood pressure drops when you go from lying down to sitting up, or from sitting to standing
3
Q
deep vein thrombosis (DVT)
A
a blood clot in a deep vein, usually in the leg
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)
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
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
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
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)
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)
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
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
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
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
14
Q
what is guillain-barre syndrome?
A
- nervous system disorder of spinal cord
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
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
- motor weakness or paralysis of limbs
- sensory loss
- muscle atrophy
- respiratory paralysis can require tracheostomy
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
- CN 7, 9, 10
- majority of cases - complete recovery within weeks - months with few residual effects
- can become recurrent and become chronic GBS
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
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
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
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
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
- avoid over fatigue
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
24
Q
etiology of ms
A
- exact cause is unknown; genetics, gender, environmental factors
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
26
Q
symptomology of ms
A
- unpredictable and highly variable symptoms
27
Q
initial symptoms of ms
A
- numbness
- weakness
- vision changes (inflammation of optic nerve)
- gait imbalance or falls
- incontinence
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
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
- behavioral variant frontotemporal dementia
- changes manifest in personality & behavior
- 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
