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3. Neurological System Disorders > Neuro- Concise Version > Flashcards

Neuro- Concise Version Flashcards

1
Q

What is bradykinesia a symptom of? Mutiple answers.
a] ALS
b] HD
c] MS
d] PD

A

a] ALS
d] PD

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2
Q

What is tremors a symptom of? Multiple anwsers.
a] ALS
b] HD
c] MS
d] PD

A

c] MS
d] PD

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3
Q

What is ridigity a symptom of? Multiple answers.
a] ALS
b] HD
c] MS
d] PD

A

b] HD
d] PD

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4
Q

What conditions have fluctuating energies throughout the day ? Multiple answers.

A

PD
ALS
MG

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5
Q

What conditions have symptoms of spasticity and rigidity ?
a] ALS
b] HD
c] PD

A

a] ALS

Primary Lateral Sclerosis: UMN

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6
Q

What conditions can affect swallow and speech ?

A

MG
ALS
HD
GB

dysphasia, dysarthria

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7
Q

What conditions can affect sensory?
a] GBS
b]MG
c] MD
d] ALS
e] HD
f] MS
g] AZ
h] PD

A

a] GBS - impacts pain, texture, heat, B&B
g] AZ- Visual spatial orientation, B&B (middle to late stages)
h] PD- VP/visual processing, B&B

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8
Q

Which conditions are cognition INTACT?

A

GBS
ALS

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9
Q

Prognosis for MG, ALS, HD

A

MG-improves weeks/months after plasma exchange; relapse period ; quadripareis may develop; can be life threatening if respirator muscles are involved

ALS- FATAL; 2- 5yrs

HD-FATAL; progresses over a 15-20 yr period

MG-MAX weakness during first year after diag.

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10
Q

Prognosis for GB, MD, MS

A

GB-
Not fatal/chronic 3-4 yrs
-intial (2-4 wks)
-plateau (few weeks)
-recovery phase (6 months to 2-3 yrs)
Best chance of recovery with early diagnosis

MD-
FATAL; onset childhood/ rarely survives beyond early 20s

  • Duchenne MD (only boys; x-recessive trait;starts in legs/pelvic)
    -w/c by age 12
    -respirator by age 20
    -death by 30
  • Beckers MD (milder symptoms with slower progression)
    -onset age:2-16
    -survives into middle age

MS-
Not fatal; prognosis: 5-10 yrs
* young adults (mostly Caucasians)
* Genetics/cold,flu, viral illness

TYPES:
* RRMS - most common; clear episode, remission
* SPMS -RRMS + neuro. function declines
* PPMS -primary, decline from 1st episode
* PRMS -steadily worsens from onset (w/w/o remissions)

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11
Q

GB

A
  1. Autoimmune disorder where PNS destorys myelin after respiratory illness/gastrointestinal
  2. Rapid onset of symptoms:
    - PAIN
    - FATIGUE
    - tingling/numbness/weakness ascending from feet/hands up to legs and arms; paralysis
    -sensory issues
    -Dilopia, face droop, dysarthria (chew, speak, swallow)
    -respiratory issues if severe (breathing)

NO COGNITIVE/hearing ISSUES

  1. Phases:
    -Initial: onset 2-4 weeks
    -Plateau: few weeks
    -Recovery: 6 months to 1-2 years (3-4 if chronic)

Occurs after upper repiratory/gastroin. viral infection w/i 1-2 wks

PNS

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12
Q

GB-EVAL
Plateau Phase

A
  1. Screen/eval in ICU
  2. Assess PAIN FIRST
  3. Assess sensory such as HEAT
  4. HR/BP/blood clots
  5. Assess communication/env.

WEAKEST, but paralysis is rare

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13
Q

GB-EVAL
Recovery Phase

A
  1. Physical abilities
  2. Focus on mobility
  3. Self-care, etc (inpatient/outpatient/home/work)
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14
Q

GB-INTERVENTION
Plateau Phase

A
  1. AddressPAIN FIRST + FATIGUE + positioning (Skin break down)
  2. swallow screen/communications (EADLs)
  3. Bladder
  4. Passive ROM (gentle/pain free)
  5. Splint to prevent contractures

PAIN/FATIGUE

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15
Q

GB-INTERVENTION
Recovery

A
  1. Focus on occupations (3 Rs) for motivation
    * Roles
    * Rituals
    * Routines
  2. Family support (mental health important for recovery)
  3. EC/fatigue managment
  4. Resistive exercise ( with Joint protection /fatigue)
  5. Mobile arm supports

Work simplification

OT TREAT>PHYSICAL+EMOTIONAL>HOSPITAL>HOME

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16
Q

MG

A
  1. Autoimmune response attacking nicotinic acetylcholine receptors and interferring with synapse at the Neuromuscular junction
  2. Affects **voluntary **movements
  3. Weakness/fatigue (stronger in the morning)
  4. Aspiration/dysphasia
    5.Vision impairment

PNS

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17
Q

MG-Intervention

A
  1. Depends on EVAL results
  2. EC/ monitor fatigue
  3. self-care/exercise ( monitor MMT/strength; report changes )
  4. Vision /fall prevention
  5. Psychosocial /fear of choking, appearance of drooping eyes
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18
Q

MD

A
  1. Progressive degeneration muscle weakness (decline of muscle fibers)
  2. Coritcosteroids used to slow down m. degeneration
  3. Muscle spasm/weakness

PNS

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19
Q

MD-Intervention

A
  1. Rehab FOCUS on maintaining and maximizing FUNCTION
  2. WORK SIMPLIFICATION/EC
  3. Active exercise NO OVEREXERTION & FATIGUE
  4. Coping & maintaining life balance (ENCOURAGE MEANINGFUL ACTIVITIES and PLAY/LEISURE )
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20
Q

ALS

Lou Gehrig’s disease

A
  1. A group of progressive degenerative neuromuscular disease that involves destruction of motor neurons within the spinal cord, brain stem, and motor cortex
  2. occurs when 3-4 regions are invovled:
    * Bulbar - jaw, face, palate, larynx, and tongue
    * Cervical -neck, arm, hand, and diiaphragm
    * Thoracic - back and abdomen
    * Lumbosacral - back abdomen leg and foot
  3. Sporatic and familia (more in males, WWII, genetic)

UMN/LMN

CNS

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21
Q

ALS:
Early Symptoms

A
  1. Focal weakness in arm/leg
  2. Fatigue
  3. Ability to perform ADLs independently

Stage 1 : Clumsiness
Stage 2 : Cannot raise arm
Stage 3 : Easily fatigue when walking

CAN WALK & PERFORM ADLS INDEPENDENTLY

Stages 1-3: Mild, Mod, Severe Weakness

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22
Q

ALS:
Progression

A
  1. W/C dependent (cannot walk)
  2. Muscle atrophy
  3. Weight loss
  4. Spasticity
  5. Fasciculation (twitch of muscules at rest)

Stage 4 :
* MILD weakness in UE
* Can still perform ADLs , but may fatigue easily

Stage 5 :
* Dependent in ADLs
* MODERATE weakness in UE
* Difficulty with weight shift
*Moderate arm function

Stage 5: Mod arm function

W/C dependent

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23
Q

ALS:
End stage

A

Stage 6 :
1. Completely dependent in ADLs and positioning
2. Extreme fatigue
3. Tube feedings and ventilator

Sensory: Eye function, B & B intact

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24
Q

ALS:
Evaluation

A
  1. Middle stage of ALS has more opportunities to benefit from OT
  2. Identify client factors including cultural, social, and spiritual values (which influences ongoing decisions about personal care and life support)
  3. Identify roles
  4. Assessments:
    -COPM
    -ALS Functional Rating Scale
    -Multidimensional Fatigue Inventory
    -Dysphagia screening and testing (report baseline at stage 2); evaluate dysphagia, and recommend appropriate diet (stage 5)
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25
Q

What is the focus of ALS Intervention?

A
  1. Focuses on occupations most important to the indvidual
  2. Focuses on the application of adaptation methods as performance skills decline

adapt to functional activties as d

26
Q

ALS Intervention:
Early Stage

A
  1. EC /work simplification (plan, pace)
  2. AVOID FATIGUE ; breathing exercises
  3. AE/AD /AFO/orthotics ( stage 2 )
  4. May benefit from manual/powered w/c w/ postural support for long distances ( stage 3 )
  5. Work simplifcation (stage 3)
27
Q

ALS intervention:
Progressive Stage

A
  1. Manage PAIN and muscle spasms
    * sling/mobile arm support
    * splint
    * HEAT and massage
  2. AAROM/PROM/ Isometric exercises (stage 4); pressure relief/PROM (stage 5)
  3. Augmented communication device
  4. Psychological support in decisions about extent of life support and medical intervention
  5. Electric hospital bed (stage 5)
  6. EC/ home modifications (stage 4)

Stage 4-5

28
Q

ALS intervention:
End Stage

A
  1. PROM
  2. Sensory stimulation
  3. Educate family on Positioning/skin inspection

SPL for dysphagia and augmentative speech device

Stage 6

29
Q

MS

A
  1. Progressive autoimmune disease in young adults (mostly Caucasians)
  2. Demylination of CNS
  3. Plaques in spinal cord, optic nerves, brainstem/cerebellum
  4. Symptoms:
    *incoordination, ____ ataxia
    * Visual loss:
    - Acuity double vision/diplopia
    - Nystagmas: scanning and tracking
    * Pain/Numbness/ Weakness/ Fatigue
    * Cognition: attention and short-term memory
    * sensorimotor, spasticity, increase reflexes
    * intention tremors

CNS

30
Q

MS:
Evaluation

A
  1. Observe throughout the day
    * MMT- does not accurately reflect degree of weakness
    * schedule around meds
    * Identify performance patterns ( REST PERIOD )
  2. MFS-fatigue/sleep
  3. AMPs; Cog screening
  4. Identify family support
31
Q

MS:
Intervention

A
  1. EC/Fatigue
  2. REST BREAKS
  3. Problem-solving compensatory strategies
  4. Plan and prioritize; delegate; AE

hot temp is a contradiction

32
Q

PD

A
  1. Progressive motor disorder d/t degenerative changes in the basal ganglia (loss of dopamine)
  2. Affects speed and accuracy of motor skills, postural stability, cognition, and affect and expression
  3. Cause is unknown; genetic and environment
33
Q

PD: 4 Cardinal S&S

A
  1. tremor
  2. rigidity
  3. bradykinesia
  4. postural stability
34
Q

rigidity

A
  1. increase tone
  2. may demo cogwheel motions (jerky & sometimes painful with joint mobility)
  3. fatigue d/t increased effort needed to voluntary movement
35
Q

resting tremor

A
  1. early sign: “pill rolling” on one side
  2. worse with stress
36
Q

Bradykinesia

A
  1. Slow movements
  2. Shuffling gait
  3. Difficulty moving from sit to stand
37
Q

Postural stability

A
  1. posural stoop, with a lack of arm swing during mobility and loss of postural refleces
  2. fall risk
38
Q

PD:
Evaluation

A
  1. Interview for brief history
  2. Observe how symptoms affect OP
  3. Assess occupation/preferred activities that have been altered
  4. COPM
  5. Cog screening if warrented

* May experience fluctuating energy levels during the day; symptoms tend to increase just BEFORE the next medication*

39
Q

PD:
Interventions

A
  1. EC/pacing, prioritizing, planning (scheduled bathroom/around meds)
  2. AD/environmental modifications
  3. auditory cues, rhytmic cues, music
  4. mobility techniques
  5. Reduce distractions/avoid multitasking/de-clutter/avoid rushing
  6. Educate caregivers to speak slowly and clearly with simple, 1-step instructions (1 concept at a time)
  7. psychological: hallucination, delusions, psychosis, behavior changes
  8. micrographia/ reduce volume of speech (hypophonia)
  9. PAIN: moist heat, gentle ROM; cold temp. increases stiffness
40
Q

AD

A
  1. Primary dementia of progressive cognitive decline
  2. Accumulation of amyloid-beta senile plaque and tau protein neurofinuillary tangles
41
Q

AD: S&S

A
  1. Impaired memory and executive functioning skills cog.
  2. Impaired speech and language
  3. Agnosia
  4. mood and behavioral changes (wander)
  5. Psychosis, hallucination, behavior changes
  6. Sensory loss
42
Q

AD: Evaluation

A

Early stages:
1. Functional eval of work, home, driving (determine if there is a cognitive deficit), and safety

Later stages:
1. Focus shifts to self-care, mobility, communication, and leisure skills

Determine functional level, context (env. fam support)

43
Q

AD:
Assessments

A

Assessments:
1. Kitchen Task Assessment (KTA) -determing cog skills for cooking
2. Exectuive function test -standarized
3. ACL- determins quality of problem-solving
4. Cognitive Performance Test - identify cognitive deficits that are predictive of functional capacity using several ADL and IADL tasks
5. Assessment of Motor and Process Skills AMPS- Measures motor (posture, mobility, and strength) and process )attentional organizational, and adaptive) skills by using task performance in IADLs
6. Disability Assessment for Dementia (ADA) - uses informant ratings to determine tha bility of indvidual with AD to complete task in both ADL & IADL; determine executive functining skills (intiate, plan, execute).

44
Q

AD: Stage 1

A
  1. Mild loss of memory
  2. difficulty with word choices
  3. repeats self
  4. mild issues with gonosis/praxis

VERY MILD TO MILD COG DECLINE

45
Q

AD: Stage 1
Intervention

A
  1. Help client/caregivers estabilish routine; post it in a central place
  2. Psychological support
  3. Environmental aids-Calendars, appointment book; adapting activities
  4. Communcation training
46
Q

AD: Stage 2

A
  1. Moderate loss of memory (personal history, recent/current events, losing objects)
  2. Supervision slowly increases; no longer employed
  3. Mild impairment in ADLs
  4. Denial, labile moods, anxious, hostile, w/d from activity/social decreases, paranoia
  5. Concentration and problem solving, learning new tasks, visuospatial deficits

MILD TO MOD COG DECLINE

47
Q

AD: Stage 2
Intervention

A
  1. Maintain routines and design environmental support (lists, posters, and pictures) and level of assistance for cues to remember daily routine and important events
  2. Simplify complex tasks
  3. Verbal cues for IADLs and some ADLs
  4. Socalization
  5. Encourage walk, stretching, balance activities
48
Q

AD: Stage 3

A
  1. Progressive memory loss of wel-known amterial; some past history retained
  2. Cannot perform ADLs and IADLs

MOD-MODERATLY SEVERE COG; DIFFICULTIES WITH PHYSICAL STATUS

49
Q

AD: Stage 3
Intervention

A
  1. Managing behavior
  2. Maintain function
  3. Simplify task
  4. Environmental adaptation (perceptual loss)
  5. Rehearse names of camily and others, using pictures
50
Q

AD: Stage 4

A
  1. Severe memory loss (forget family, but recognize famliar people)
  2. Confusion even in familiar surroundings
  3. Gait and balance distubrances
  4. Communication (grunts, single word)
  5. Unable to walk, urinate, eat (SNF)

SEVERE COG DECLINE AND MODERATE TO SEVERE PHYSCIAL DECLINE

51
Q

AD: Stage 4
Intervention

A
  1. Maintain recreation and leisure activities (respite program)
  2. Positioning in bad/ w/c/ skin inspection
  3. AAROM/AROM/PROM
52
Q

AD: Stage 5
Intervention

A
  1. Total A in ADLs and mobility
53
Q

HD

A
  1. genetic hereditary neurological disorder
  2. caused by defective gene on chromosome 4
  3. impacts physical (motor) and mental (mood and thinking) ability
  4. Basal ganglia-motor control/learning, emotion, behavior; cerebral cortex-attention, thought, memory, language
54
Q

HD symptoms

A
  1. slow progression for 15-20 yrs from onset (occurs between age 30-50)
  2. leads to uncontrollable movements of limbs
  3. Brain changes impact mood, esp. depression, irritability, anxiety, and obsessive-compulsive qualities
55
Q

Motor difficulties in HD

A
  1. Chorea/choreiform-rapid, irregular, involuntaryily movements (muscle jerks)
  2. Akathisia-restlessness/fidgety
  3. Dystonia-abnormal sustained posture (muscle spasm in head, trunk, arms)
56
Q

HD: Stage 1

A
  1. 0-8 yrs from onset
  2. can work part-time and needs MIN A for some ADLs
57
Q

HD: Stage 2

A

1.. 3-13 yrs from onset
2.typically unable to work
3. min A in ADLs or MAX A in one area while other basic functions are independent

58
Q

HD: Stage 3

A
  1. 5-16 yrs from onset
  2. unable to work
  3. MAX A for most basic ADLs
59
Q

HD: Stage 4

A
  1. 9-21 yrs from onset
  2. MAX A ADL/IADL
  3. In home care/extended care facility needed
60
Q

HD: Stage 5

A
  1. 11-26 yrs from onset
  2. full time SNF required
  3. chorea becomes hypertonicity, slow movement (bradykinesia), and akinesia present (delayed initation or loss of movement)
61
Q

Overview of HD stages

A
  1. Early stage: still working but maintaining work perfromance gets harder
  2. Middle stage- cognition and gait decrease; descision making, memory, and motor coordination/balance are all impacted
  3. Late stage- long-term care and hospitalization

Other symptoms:
1. dysarthria
2. dysphagia
3. depression
4. high susceptibility to pneumonia

62
Q

HD treatment

A
  1. Enviornmetal mod
  2. safety/fall edu
  3. EC (simplify)
  4. cog strate-(simple step, use lists, cal, labels)
  5. AE to support meal time/FMskills
  6. coping
  7. splints-contractures/positioning

3. Neurological System Disorders (8 decks)

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