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Adult Neuro Exam 2 > Stroke Lecture > Flashcards

Stroke Lecture Flashcards

1
Q

What is the recurrence risk of stroke patients?

A

40%, higher for men

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2
Q

What ages, geographic locations, and races is stroke most prevalent in?

A

Ages 80 +
African American > Hispanic > Caucasian
Most prevalent death from stroke in South eastern US

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3
Q

Risk Factors for stroke

A 
Hypertension
High serum Cholesterol
Obesity
Heavy Alcohol use
Cocaine use
Smoking
Diabetes Mellitus
Heart Disease
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4
Q

Stroke Classifications

A

Thrombotic,
Embolic,
Cerebral Hemorrhage

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5
Q

Thrombotic Stroke (ischemic stroke)

A
  • Caused by ASCHD (atherosclerosis) and HTN
  • “Stroke-in-progress”
  • Transient ischemic attack (indicative of thrombolytic disease, possible vasospasm, transient systemic arterial hypotension)
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6
Q

Thrombotic CVA and TIA medical management

A
  • PREVENTION - most important
  • Goal is to improve circulation ASAP
  • Tissue Plasminogen Activator –> Use within 3 hours of symptoms
  • Anticoagulants
  • Antiplatelets
    Figure 32-16
  • Thromboendarterectomy (carotid, subclavian)
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7
Q

Embolic CVA Pathology

A
  • Sign of cardiac disease
  • Can originate from heart, internal carotid artery, or carotid sinus
  • Branches of MCA most commonly affected (yields poorer outcomes)
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8
Q

What is an embolus?

A

A piece of plaque that has broken off from somewhere else

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9
Q

Medical Management of Embolic CVA

A

Prevention
Long term Anticoagulants
Surgery

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10
Q

Hemorrhagic CVA

A

Causes: HTN, Ruptured saccular aneurysm (berry), AV malformation (ages 10-35 most common)

  • Bleeding displaces midline structures from pressure buildup
  • Blood is reabsorbed over 6-8 months, so function comes back (best recovery)
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11
Q

Medical management of Hemorrhagic CVA

A
  • Prevent and manage hypertension

- Surgery for ruptured aneurysm (with HOB restrictions, 4-6 wks limited activity, and anti-seizure meds)

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12
Q

S/S of CVA common to both sides

A
  • sensory dysfunction (touch, proprioception)
  • visual field defect
  • cognitive impairment
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13
Q

S/S of Right Brain CVA

A
  • Left sided paralysis
  • Perceptual and memory deficits
  • QUICK AND IMPULSIVE BEHAVIOR… dangerous
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14
Q

S/S of Left Brain CVA

A
  • Right sided paralysis
  • Speech and memory deficits
  • Cautious and slow behavior… flaccid R leg = hard time to get WBing through LE because they don’t trust their R LE.
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15
Q

Review textbook

A

Figure 32-26, p 1474, 1455-8

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16
Q

CVA Impairments requiring Medical Management

A

Spasticity, seizures, respiratory dysfuction, trauma (may have fallen), DVT (due to low muscle tone), CRPS and pain

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17
Q

CVA Movement Dysfunction

A
  • Decreased Force production
  • Abnormal synergistic movement (not volitional)
  • Altered ms contraction timing
  • Decreased force regulation
  • Delayed responses
  • Abnormal Tone
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18
Q

CVA Sensory Dysfunction

A
  • Awareness
  • Interpretation
  • Any modality can be affected
  • Visual disturbances are common
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19
Q

CVA Secondary Impairments

A
  • Alignment
  • Mobility
  • Ms and soft tissue length
  • Pain
  • Edema (no muscle pump)
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20
Q

Composite Impairments

A
  • Movement deficits
  • Atypical movements (compensatory mvmts)
  • Undesirable compensation
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21
Q

Orpington Prognostic Scale (OPS)

A
  • Specific to stroke
    < 3.2 Minor (discharge in 3 wks, return to home)
    3.2-5.2 Moderate (eventually home)
    >5.2 Major (d/c to long term care)
    Use during initial eval when neurologically stable!!!
  • Optimal predictive power at 2 weeks post-stroke
  • Scores range from 1.6-6.8
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22
Q

Recovery

A 
Initial functional gains due to
- Reduced cerebral edema
- absorption of damaged tissue
- improved vascular flow
Followed by Neuroplasticity (positive or negative)
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23
Q

Predictors of Motor Function Recovery (UE)

A
  • Initial return of UE movement is predictive of possible full arm recovery
  • Failure to recover some grip strength by 24 days is predictive of no UE recovery at 3 months
  • 30% of patients have no arm recovery
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24
Q

Predictors of Functional Recovery

A

-86% of recovery is predictable at 1 month
Long term:
- 58% regain independence in ADL
- 82% learn to walk

25
Q

Special Considerations Post CVA

A

Vitals

  • SBP : 90-200 mmHG
  • DBP: <110 mmHg
  • HR: 50 - 100 (max during exercise = 140)
  • 90% Respiratory insufficiency
26
Q

Common problems post CVA

A 
Seizure ( Hemorrhagic > ischemic)
Cognitive problems
Dysphagia (trouble swallowing)
Visuospatial and perceptual disturbances
Language deficits (if dominant hemisphere is affected
Aspiration pneumonia
27
Q

Dysphagia

A 
Compensatory Strategies
- Thickening liquids
- chin tuck during swallow
- small sips
Treatment:
- VitalSTIM NMES
- Biofeedback with mirror
- Posture/environmental set up
28
Q

Visuospatial and Perceptual disorders

A
  • Attention deficits and distractibility
  • Homonymous hemianopsia and other visual field cuts
  • Body scheme (somatagnosia) and body image disorders/difficulty with R/L discrimination
  • Depth, distance, or vertical perceptual deficites
29
Q

Agnosia

A

“The inability to recognize familiar objects using one or more of the sensory modalities, while often retaining the ability to recognize the same object using other sensory modalities”

30
Q

Anosognosia

A

“the severe denial, neglect, and lack of awareness of the presence or severity of one’s deficits”

Very common w/ L hemiplegia - R hemisphere stroke

31
Q

Dysarthria

A

Muscle dysfunction leads to impaired verbal communication
- May affect respiration, phonation, articulation, resonance
Treatment: tongue and oral-motor exercises, functional or speaking practice, posture

32
Q

Aphasia

A

DOMINANT hemisphere injury

- Impairs the expression and/or understanding of language

33
Q

Types of Aphasia

A

Broca’s : expressive - hard to talk
Wernicke’s: receptive - word salad - they don’t understand what you are asking.
Global: all funciton
- pt may often be depressed and frustrated. Slow down and try to get them to say something- anything- even if it is not appropriate for situation

34
Q

Apraxia

A

Mild form is DYSPRAXIA
- In pts with parietal lobe injury
“Loss of the ability to execute or carry out skilled movements and gestures, despite having the desire and the physical ability to perform them. The patient is unable to accomplish the task even though the instructions are understood.”

35
Q

Buccofacial or Orofacial Apraxia

A
  • Most common form
  • Inability to carry out facial movements on command
  • Ex: licking lips, whistling, coughing, winking.
    BUT may be able to execute, just not on command (Can see a bubble wand and blow, but not if you tell them to)
36
Q

Limb-kinetic apraxia

A

Inability to make fine, precise movements with an arm or leg

37
Q

Ideomotor Apraxia

A

Inability to make proper movement in response to a verbal command
Ex: Can’t walk over to a table on command, but when asked to “get a cup of coffee” and the pt wants coffee, they will walk

38
Q

Ideational Apraxia

A

Inability to coordinate activities with multiple sequential movements
(Ex: dressing, eating, bathing)

39
Q

Verbal Apraxia

A

Difficulty coordinating mouth and speech movements on command

40
Q

Constructional Apraxia

A

Inability to copy, draw, or construct simple figures

41
Q

Oculomotor Apraxia

A

Difficulty moving the eyes on command

42
Q

Prognosis of Cerebellar stroke

A

Following cerebellectomy - poor
Bilateral < Unilateral
Deep cerebellar nuclei < cortex
- most spontaneous compensation is completed from 6 months - 1 year

43
Q

Treatment of cerebellar stroke

A
  • Postural (core) stability activities for functional tasks
  • Proximal stability activités
  • developmental sequence
  • Decrease the degrees of freedom to allow pt to focus on a particular portion of task
  • Coordination exercises (Frenkel’s)
  • Use proximal jt stability if needed, as well as visual cues
44
Q

Temporary reduction of dysmetria and tremors

A

Controversial: wrist, ankle, and waist weights, weighted utensils and tools
Not controversial: PNF

45
Q

Gait Treatment for Cerebellar Stroke

A
  • Visual cues for placement (mirror and tape)
  • Weights ( controversial)
  • Biofeedback
  • Variety of surfaces, obstacle course
46
Q

Motor learning and Cerebellar dysfunction

A
  • Pts have difficulty with generalization
  • Increase repetitions
  • vary task constraints
  • vary environmental constraints
47
Q

How common is shoulder pain with hemiplegic UE?

A

70-84% of patients, NOT normal

48
Q

How is shoulder subluxation graded?

A

The number of fingers you can fit in the sublimed space

49
Q

Inferior shoulder subluxation

A
  • Lack of active movement
  • Downward rotation of scapula with the glenoid fossa moving vertical to downward
  • loss of passive locking mechanism of the shoulder
  • stretching of the soft tissue and capsule
50
Q

Anterior shoulder subluxation

A
  • New control is usually unbalanced
  • Side bending of head toward more affected side
  • downwardly rotated scapula is pulled superiorly
  • Extension + IR of humerus
51
Q

Superior Shoulder Subluxation

A

Flexion synergy of the UE

  • Elevation of shoulder, scapula elevated and ABD
  • Head of humerus becomes pressed up against acromion
  • Distinct lack of isolated humerus vs scapular movement
  • May lead to impingement
52
Q

Shoulder Impingement

A
  • Marked spasticity
  • superior subluxation
  • muscle imbalance
  • loss of scapulohumeral rhythm
53
Q

Treatment for O/5 Hemiplegic shoulder

A
  • Use sling in standing
  • Estim
  • Awareness of UE with bed mobility
  • PROM with massage for all joints, but limit FL to 90 degrees
  • WB with dome
  • use UE to stabilize objects
54
Q

1-2/5 Hemiplegic shoulder, hypotonia

A
  • PNF scapular patterns
  • Fluidotherapy with physical and mental practice
  • WB (isometric contractions)
  • Sling for standing
  • Estim
55
Q

2-3/5 Hemiplegic shoulder

A
  • Prox> distal strength
  • Have pt use arm for EVERYTHING
  • Distal UE - self ROM, massage, isometrics
  • Proximal UE- AROM, theraband
  • PNF patterns
    WB, Functional tasks (CIMT)
56
Q

0-1/5 prox strength
Modified Ashworth=4
Unable to isolate muscle groups

A 
PROM to maintain shoulder ext
WB with inhib to biceps and facil to triceps
Rhythmic rotation for spasticity
Prone on elbows WB
Scapular retraction
E-stim to triceps
57
Q

What is the Incidence of shoulder hand syndrome?

A

12-25% of pts with UE pain
First signs are hand edema and tenderness, followed by tenderness in shoulder during ROM.
Pain is primarily with movement

58
Q

Mid Stage characteristics of Shoulder- Hand syndrome

A
  • Sympathetic vasomotor changes (warmth, redness, and glossy skin)
  • tropic changes of the fingertips
  • atrophy and contracture
  • Skin changes: cool, cyanotic, damp
  • atrophy of thenar and hypothenar muscles
59
Q

Late Stage shoulder hand syndrome

A
  • Osteoporotic changes occur
  • Few patients will recover at this stage
  • PREVENTION (esp microtrauma)
  • if pain or edema develops, immediately begin a comprehensive program that addresses biomechanics concerns
  • Never push through pain!

Adult Neuro Exam 2 (6 decks)

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