CVA

Question 1

completed stroke

Answer 1

all neurological deficits at onset

Question 2

stroke in evolution

Answer 2

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

Question 3

ischemic strokes

Answer 3

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

Question 4

ischemic strokes - cerebral infarct

Answer 4

actual death of a portion of the brain

Question 5

ischemic penumbra

Answer 5

area surrounding infarcted cerebral tissue

Question 6

ischemic strokes - thrombotic

Answer 6

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

Question 7

ischemic strokes - embolic

Answer 7

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

Question 8

ischemic strokes - lacunar infarcts

Answer 8

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

Question 9

hemorrhagic stroke

Answer 9

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

Question 10

hemorrhagic stroke - intercerebral

Answer 10

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

Question 11

hemorrhagic stroke - subarachnoid

Answer 11

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

Question 12

hemorrhagic stroke - arteriovenous malformation (AVM)

Answer 12

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

Question 13

TIA

Answer 13

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)

Question 14

stroke syndromes

anterior cerebral - distribution

Answer 14

supplies the superior border of the frontal and parietal lobes

Question 15

stroke syndromes

anterior cerebral - patient deficits

Answer 15

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

Question 16

stroke syndromes

middle cerebral - distribution

Answer 16

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

Question 17

stroke syndromes

middle cerebral - patient deficits

Answer 17

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

Question 18

stroke syndromes

vertebrobasilar - patient deficits

Answer 18

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

Question 19

stroke syndromes

vertebrobasilar - distribution

Answer 19

supplies the brainstem and cerebellum

Question 20

stroke syndromes

posterior cerebral - patient deficits

Answer 20

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

Question 21

stroke syndromes

posterior cerebral - distribution

Answer 21

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

Question 22

general risk factors

Answer 22

> 55 yr
males
african americans, pacific islanders & hispanics

Question 23

medical risk factors

Answer 23

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

Question 24

lifestyle risk factors

Answer 24

smoking, obesity, excessive alcohol, drug use & inactivity

Question 25

primary preventable risk factors

Answer 25

HTN; heart disease | lowering diastolic BP by 5-6 mmHg results in a reduction of rick for CVA by 40%

Question 26

activate emergency medical system when:

Answer 26

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

Question 27

characteristics of left hemisphere CVA

Answer 27

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

Question 28

characteristics of right hemisphere CVA

Answer 28

``` 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) ```

Question 29

characteristics of brainstem CVA

Answer 29

``` 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 ```

Question 30

characteristics of cerebellum CVA

Answer 30

``` decreased balance ataxia decreased coordination nausea decreased ability for postural adjustment nystagmus ```

Question 31

clinical findings - | may have some/all/none depends on location & extent of injury

Answer 31

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

Question 32

damage to motor cortex presents

Answer 32

flaccidity first, then spasticity, then impaired postural tone

Question 33

damage to motor cortex presents- | flaccidity first

Answer 33

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

Question 34

damage to motor cortex presents- | spasticity

Answer 34

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

Question 35

how is spasticity graded/documented

Answer 35

modified ashworth scale | 0-4 ordinal scale

Question 36

Modified Ashworth Scale - 0

Answer 36

no increase in muscle tone

Question 37

Modified Ashworth Scale - 1

Answer 37

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

Question 38

Modified Ashworth Scale - 1+

Answer 38

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

Question 39

Modified Ashworth Scale - 2

Answer 39

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

Question 40

Modified Ashworth Scale - 3

Answer 40

considerable increase in muscle tone, passive movement difficult

Question 41

Modified Ashworth Scale - 4

Answer 41

affected part rigid in flexion or extension

Question 42

spasticity/abnormal synergy patterns

Answer 42

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

Question 43

spasticity/abnormal synergy patterns - UE flexion synergy

Answer 43

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

Question 44

spasticity/abnormal synergy patterns - UE extension synergy

Answer 44

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

Question 45

spasticity/abnormal synergy patterns - LE flexion synergy

Answer 45

Hip: flex, abd, ER knee: flex ankle: dflex, inv

Question 46

spasticity/abnormal synergy patterns - LE extension synergy

Answer 46

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

Question 47

Brunnstrom Stages of Recovery- Stage 1

Answer 47

period of flaccidity immediately following acute episode | no movement of limbs can be elicited

Question 48

Brunnstrom Stages of Recovery- Stage 2

Answer 48

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

Question 49

Brunnstrom Stages of Recovery- Stage 3

Answer 49

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)

Question 50

Brunnstrom Stages of Recovery- Stage 4

Answer 50

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)

Question 51

Brunnstrom Stages of Recovery- Stage 5

Answer 51

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

Question 52

Brunnstrom Stages of Recovery- Stage 6

Answer 52

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

Question 53

motor dysfunction - weakness

Answer 53

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

Question 54

motor dysfunction - postural control & balance

Answer 54

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

Question 55

motor dysfunction - ambulation

Answer 55

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

Question 56

motor planning deficits

Answer 56

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

Question 57

sensory impairments

Answer 57

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

Question 58

communication impairments

Answer 58

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

Question 59

aphasia

Answer 59

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

Question 60

broca's aphasia

Answer 60

expressive disorder, difficulty producing speech

Question 61

wernicke's aphasia

Answer 61

receptive disorder, difficulty with language comprehension

Question 62

global aphasia

Answer 62

expressive & receptive disorder

Question 63

dysarthria

Answer 63

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

Question 64

emotional lability R CVA

Answer 64

difficulty controlling emotions; laugh or cry at inappropriate without cause

Question 65

orofacial deficits

Answer 65

``` 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) ```

Question 66

dysphagia

Answer 66

difficulty or inability to swallow foods or liquids

Question 67

respiratory impairments

Answer 67

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%

Question 68

spinal reflex- flexor withdrawl | stimulus & response

Answer 68

stimulus-noxious stimulus applied to the bottom of foot | response-toe extension, ankle dorsiflexion, hip & knee flexion

Question 69

spinal reflex- cross extension | stimulus & response

Answer 69

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

Question 70

spinal reflex- startle | stimulus & response

Answer 70

stimulus- sudden loud noise | response- extension & abduction of UE

Question 71

spinal reflex- grasp | stimulus & response

Answer 71

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

Question 72

brain stem reflex- symmetric tonic neck reflex | response

Answer 72

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

Question 73

brain stem reflex- asymmetric tonic neck reflex | response

Answer 73

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

Question 74

brain stem reflex- tonic labyrinthine reflex | response

Answer 74

prone position facilitates flexion. Supine position facilitates extension

Question 75

brain stem reflex- tonic thumb reflex | response

Answer 75

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

Question 76

deep tendon reflexes

Answer 76

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

Question 77

reflex activity

Answer 77

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

Question 78

associated reactions

Answer 78

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

Question 79

bowel and bladder dysfunction

Answer 79

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

Question 80

incontinence

Answer 80

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

Question 81

associated rxns - souques phenomenon - response

Answer 81

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

Question 82

associated rxns - raimiste phenomenon - response

Answer 82

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

Question 83

associated rxns - homolateral limb synkinesis - response

Answer 83

flexion of the involved UE elicits flexion of the involved LE

Question 84

functional limitations

Answer 84

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

Question 85

common complications

Answer 85

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)

Question 86

secondary/indirect impairments | decreased ROM/contractures

Answer 86

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

Question 87

secondary/indirect impairments | shoulder subluxation/pain

Answer 87

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

Question 88

acute medical mgmt

Answer 88

``` monitor neurologic function prevent dev of secondary complications pharmacologic intervention (tPA helps if w/in 3 hrs) surgical intervention ```

Question 89

``` stroke rehab acute care (<1 mo post CVA) ```

Answer 89

low intensity rehab as soon as stable | shortening LOS

Question 90

stroke rehab | post acute care (1-6 mo post CVA)

Answer 90

moderate to severe residual impairments | team of rehab specialists for comprehensive services

Question 91

stroke rehab | chronic (>6 mo post CVA)

Answer 91

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