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Neuro > CVA > Flashcards

CVA Flashcards

1
Q

completed stroke

A

all neurological deficits at onset

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2
Q

stroke in evolution

A

caused by thrombus that gradually progresses; total neurological deficits are not seen for 1-2 days after onset

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3
Q

ischemic strokes

A

85% of all CVA’s; hypoxia or decreases O2 to tissue & results from poor blood supply

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4
Q

ischemic strokes - cerebral infarct

A

actual death of a portion of the brain

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5
Q

ischemic penumbra

A

area surrounding infarcted cerebral tissue

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6
Q

ischemic strokes - thrombotic

A

atherosclerosis; blood flow reduced limiting O2 to cerebral tissues
variable onset
s/s appear in minutes/days; typically during sleep or upon waking after MI or post-surgical procedure

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7
Q

ischemic strokes - embolic

A

blood clot (solid, liquid, gas) carried to brain; occurs rapidly w/out warning (headache is a common presentation); assoc. w/cardiovascular disease; middle cerebral artery commonly affected

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8
Q

ischemic strokes - lacunar infarcts

A

affects deep brain structures (internal capsule, thalamus, basal ganglia, pons); common w/diabetes & HTN; contralateral weakness & sensory loss, ataxia, dysarthra

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9
Q

hemorrhagic stroke

A

15%; abnormal bleeding in brain due to rupture in blood supply; disruption of O2 to an area & compression from accumulation of blood; 40% of all stroke deaths; HTN could rupture an aneurysm or trauma
s/s severe headache, vomiting, high BP, abrupt onset of symptoms; typically during the day

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10
Q

hemorrhagic stroke - intercerebral

A

vessel malformation & integrity of cerebral vessels; cause HTN & aging

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11
Q

hemorrhagic stroke - subarachnoid

A

bleeding in subarachnoid space; cause- aneurysms (ballooning of a vessel wall) & vascular malformations

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12
Q

hemorrhagic stroke - arteriovenous malformation (AVM)

A

congenital anomalies that affect circulation of brain; defects weaken vessel walls & can rupture

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13
Q

TIA

A

resemble stroke; blood supply temp interrupted; deficits resolve in 24-48 hrs; no residual brain damage or neurological dysfunction; most often in carotid or vertebrobasilar arteries; recurrent indicate thrombotic disease (could have major stroke w/in 1 yr if not treated)

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14
Q

stroke syndromes

anterior cerebral - distribution

A

supplies the superior border of the frontal and parietal lobes

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15
Q

stroke syndromes

anterior cerebral - patient deficits

A

contralateral weakness & sensory loss primarily in the LE, incontinence, aphasia, apraxia, personality changes

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16
Q

stroke syndromes

middle cerebral - distribution

A

supplies the surface of the cerebral hemispheres and the deep frontal and parietal lobes

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17
Q

stroke syndromes

middle cerebral - patient deficits

A

contralateral sensory loss and weakness in the face and UE, less involvement in the LE, homonymous hemianopia

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18
Q

stroke syndromes

vertebrobasilar - patient deficits

A

cranial nerve involvement (diplopia, dysphagia, dysarthria, deafness, vertigo), ataxia, equilibrium disturbances, headaches, dizziness

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19
Q

stroke syndromes

vertebrobasilar - distribution

A

supplies the brainstem and cerebellum

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20
Q

stroke syndromes

posterior cerebral - patient deficits

A

contralateral sensory loss, memory deficits, thalamic pain syndrome, homonymous hemiamopia, visual agnosia, cortical blindness

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21
Q

stroke syndromes

posterior cerebral - distribution

A

supplies the occipital and temporal lobes, thalamus and upper brain stem

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22
Q

general risk factors

A

> 55 yr
males
african americans, pacific islanders & hispanics

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23
Q

medical risk factors

A

previous stroke, TIA, cardiac disease, diabetes, atrial fibrillation & HTN

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24
Q

lifestyle risk factors

A

smoking, obesity, excessive alcohol, drug use & inactivity

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25
Q

primary preventable risk factors

A

HTN; heart disease

lowering diastolic BP by 5-6 mmHg results in a reduction of rick for CVA by 40%

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26
Q

activate emergency medical system when:

A 
sudden weakness
confusion
sudden dimness or loss of vision in one eye
difficulty speaking
sudden severe headache
unexplained dizziness
loss of balance
difficulty walking
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27
Q

characteristics of left hemisphere CVA

A

weakness, paralysis of right side
increased frustration
decreased processing
possible aphasia (expressive, global, receptive)
possible motor apraxia (ideomotor & ideational)
decreased discrimination between L & R
right hemianopsia

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28
Q

characteristics of right hemisphere CVA

A 
weakness, paralysis of left side
left hemianopsia
decreased attention span
decreased awareness & judgement
memory deficits
left inattention or neglect
decreased abstract reasoning
emotional lability
impulsive behaviors
decreased spatial orientation (risk of falls)
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29
Q

characteristics of brainstem CVA

A 
unstable vital signs (where CN's are)
decreased consciousness
decreased ability to swallow
weakness on both sides of the body
paralysis on both sides of the body
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30
Q

characteristics of cerebellum CVA

A 
decreased balance
ataxia
decreased coordination
nausea
decreased ability for postural adjustment
nystagmus
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31
Q

clinical findings -

may have some/all/none depends on location & extent of injury

A 
spasticity
muscle weakness
motor planning deficits
sensory impairments
communication impairments
orofacial deficits
respiratory impairments
reflex activity
associated reactions
bowel & bladder dysfunction
functional limitations
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32
Q

damage to motor cortex presents

A

flaccidity first, then spasticity, then impaired postural tone

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33
Q

damage to motor cortex presents-

flaccidity first

A

low muscle tone
inability to generate muscle contraction
transient state
patients develop hypertonicity or spasticity

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34
Q

damage to motor cortex presents-

spasticity

A

velocity dependent, increased resistance to passive stretch
exaggerated deep tendon reflexes
posturing of extremities: flexion or extension
co-contraction of muscles
synergies: stereotypical movement patterns

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35
Q

how is spasticity graded/documented

A

modified ashworth scale

0-4 ordinal scale

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36
Q

Modified Ashworth Scale - 0

A

no increase in muscle tone

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37
Q

Modified Ashworth Scale - 1

A

slight increase in muscle tone, manifested by a catch & release or by minimal resistance at the end of the range of motion when the affected part is moved in flexion or extension

38
Q

Modified Ashworth Scale - 1+

A

slight increase in muscle tone, manifested by a catch, followed by minimal resistance throughout the remainder (less than half) of the ROM

39
Q

Modified Ashworth Scale - 2

A

more marked increase in muscle tone through most of the ROM, but affected part easily moved

40
Q

Modified Ashworth Scale - 3

A

considerable increase in muscle tone, passive movement difficult

41
Q

Modified Ashworth Scale - 4

A

affected part rigid in flexion or extension

42
Q

spasticity/abnormal synergy patterns

A

highly stereotypic, obligatory combinations of limb movements or postures
unable to isolate movement; no flexibility of movement for adaptation to task

43
Q

spasticity/abnormal synergy patterns - UE flexion synergy

A

scapula: retraction, elevation
shoulder: abd, ER
elbow: flex
forearm: supination
wrist/hand: flex of both

44
Q

spasticity/abnormal synergy patterns - UE extension synergy

A

scapula: protraction
shoulder: add, IR
Elbow: ext
forearm: pronation
wrist/hand: flex of both

45
Q

spasticity/abnormal synergy patterns - LE flexion synergy

A

Hip: flex, abd, ER

knee: flex
ankle: dflex, inv

46
Q

spasticity/abnormal synergy patterns - LE extension synergy

A

hip: ext, add, IR
knee: ext
ankle: pflex, inv

47
Q

Brunnstrom Stages of Recovery- Stage 1

A

period of flaccidity immediately following acute episode

no movement of limbs can be elicited

48
Q

Brunnstrom Stages of Recovery- Stage 2

A

basic limb synergies or some of their components may appear as associated rxns
minimal voluntary movement responses may be present
spasticity begins to develop

49
Q

Brunnstrom Stages of Recovery- Stage 3

A

patient gains voluntary control of the movement synergies
full range of all synergy components does NOT necessarily develop
spasticity has further increased and may become severe
(starting to get mobility back, but then spasticity develops & they struggle again)

50
Q

Brunnstrom Stages of Recovery- Stage 4

A

some movement combos that do not follow the paths of either synergy are mastered first with difficulty, then with more ease
spasticity begins to decline
(moves beyond the patterns)

51
Q

Brunnstrom Stages of Recovery- Stage 5

A

more difficult movement combos are learned as the basic limb synergies lose their dominance over motor acts (synergies are going away)

52
Q

Brunnstrom Stages of Recovery- Stage 6

A

with disappearance of spasticity, individual joint movements become possible and coordination approaches normal
as the last recovery step, normal motor function is restored

53
Q

motor dysfunction - weakness

A

unable to generate normal levels to initiate & control functional movement or to maintain posture
hemiparesis UE>LE
atrophy
reduction in functioning motor units & firing rates
abnormal & inefficient recruitment of motor units

54
Q

motor dysfunction - postural control & balance

A

impairments in steadiness, symmetry, dynamic stability, reactive & anticipatory postural control
coordination deficit of poor timing, sequencing & co-contraction contribute

55
Q

motor dysfunction - ambulation

A

asymmetric, slow, stiff-knee pattern, foot drop, knee buckle or hyperextension, extension synergy

56
Q

motor planning deficits

A

more frequent/prominent in L CVA
poor timing & sequencing
sensory or cerebellar ataxia
apraxia-difficulty performing purposeful movements (sit to stand)

57
Q

sensory impairments

A

strokes of parietal lobe
loss of tactile or proprioceptive capabilities (increase risk of falls)
partial loss of sensations
limit motor control

58
Q

communication impairments

A 
infarcts in frontal & temporal lobes
30% have language dysfunction
aphasia
dysarthria
emotional lability (R CVA)
59
Q

aphasia

A

impairment of language comprehension, oral expression & use of symbols to communicate

60
Q

broca’s aphasia

A

expressive disorder, difficulty producing speech

61
Q

wernicke’s aphasia

A

receptive disorder, difficulty with language comprehension

62
Q

global aphasia

A

expressive & receptive disorder

63
Q

dysarthria

A

difficulty articulating words as a result of weakness & inability to contro the muscles associated with speech production (muscle strength)

64
Q

emotional lability R CVA

A

difficulty controlling emotions; laugh or cry at inappropriate without cause

65
Q

orofacial deficits

A 
CN involvement (brainstem/midbrain)
facial asymmetries
inadequate lip closure
difficulty closing eyes
dysphagia
decreased coordination between eating & breathing (aspirate, which leads to pneumonia-NPO order)
66
Q

dysphagia

A

difficulty or inability to swallow foods or liquids

67
Q

respiratory impairments

A

decreased lung expansion (d vital capacity, d ability to meet O2 demands, i resp rate-shallow breathing - pneumonia)
decreased cough effectiveness
lung volumes are decreased by 30-40%

68
Q

spinal reflex- flexor withdrawl

stimulus & response

A

stimulus-noxious stimulus applied to the bottom of foot

response-toe extension, ankle dorsiflexion, hip & knee flexion

69
Q

spinal reflex- cross extension

stimulus & response

A

stimulus-noxious stimulus applied to ball of foot w/ the LE prepositioned in extension
response-flexion & then extension of the opp LE

70
Q

spinal reflex- startle

stimulus & response

A

stimulus- sudden loud noise

response- extension & abduction of UE

71
Q

spinal reflex- grasp

stimulus & response

A

stimulus-pressure applied to ball of foot or the palm of hand
response-flexion of toes or fingers, respectively

72
Q

brain stem reflex- symmetric tonic neck reflex

response

A

flexion of the neck results in flexion of the arms & ext of legs
ext of neck results in ext of arms & flex of neck

73
Q

brain stem reflex- asymmetric tonic neck reflex

response

A

rotation of the head to the left causes extension of the left arm & leg & flexion of the right arm & leg
rotation of the head to the right causes extension of the left arm & leg & flexion of the left arm & leg

74
Q

brain stem reflex- tonic labyrinthine reflex

response

A

prone position facilitates flexion. Supine position facilitates extension

75
Q

brain stem reflex- tonic thumb reflex

response

A

when the involved extremity is elevated above the horizontal, thumb extension is facilitated with forearm supination

76
Q

deep tendon reflexes

A 
stretch reflex
may indicate presence of abnormal tone
hypotonia/flaccidity 
hypertonia/spasticity
hyperreflexive
early stages-diminished or absent DTR's
77
Q

reflex activity

A

spinal & brain stem reflexes may appear following a stroke
clonus, clasp knife, babinski

78
Q

associated reactions

A

automatic movements that occur as a result of active or resisted movement in another part of the body
can be misinterpreted as active movement

79
Q

bowel and bladder dysfunction

A

incontinence
movement assists in the regulation of bowel function
breathing stimulates peristalsis–if having a hard time breathing it causes bowel problems

80
Q

incontinence

A

inability to control urination
may be seen initially secondary to muscle paralysis or inadequate sensory stimulation to bladder
early weight bearing through bridging or standing can assist in regaining bladder control

81
Q

associated rxns - souques phenomenon - response

A

flexion of the involved arm above 150 facilitates extension and abduction of the fingers

82
Q

associated rxns - raimiste phenomenon - response

A

resistance applied to hip abduction or adduction of the uninvolved LE causes similar response in the involved LE

83
Q

associated rxns - homolateral limb synkinesis - response

A

flexion of the involved UE elicits flexion of the involved LE

84
Q

functional limitations

A

result from loss of motor or sensory function
lose the ability to perform ADL’s
lose the ability to walk

85
Q

common complications

A

altered consciousness (normal, confused, lethargic, coma, obtunded)
seizures
cardiovascular & pulmonary dysfunction
DVT or pulmonary embolus
osteoporosis & fracture risk (fall risk)
cognitive dysfunction (impair in alertness, attn, orientation, memory - impulsivity, decreased insight)
altered emotional status (emotional lability, depression)

86
Q

secondary/indirect impairments

decreased ROM/contractures

A

UE contractures of elbow, wrist, finger flexors & pronators
LE pflex & inversion contracture

87
Q

secondary/indirect impairments

shoulder subluxation/pain

A

shoulder pain
changes in muscle tone, paralysis, poor sensation affect r/c muscles
poor scapular positioning
secondary tightness can develop - adhesive capsulitis
poor handling & positioning

88
Q

acute medical mgmt

A 
monitor neurologic function
prevent dev of secondary complications
pharmacologic intervention (tPA helps if w/in 3 hrs)
surgical intervention
89
Q 
stroke rehab 
acute care (<1 mo post CVA)
A

low intensity rehab as soon as stable

shortening LOS

90
Q

stroke rehab

post acute care (1-6 mo post CVA)

A

moderate to severe residual impairments

team of rehab specialists for comprehensive services

91
Q

stroke rehab

chronic (>6 mo post CVA)

A

rehab
60 min for 2-3x/week (financially could be problem)
target flexibility, strength, balance, gait, endurance & UE function

Neuro (7 decks)

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