CVA Flashcards
completed stroke
all neurological deficits at onset
stroke in evolution
caused by thrombus that gradually progresses; total neurological deficits are not seen for 1-2 days after onset
ischemic strokes
85% of all CVA’s; hypoxia or decreases O2 to tissue & results from poor blood supply
ischemic strokes - cerebral infarct
actual death of a portion of the brain
ischemic penumbra
area surrounding infarcted cerebral tissue
ischemic strokes - thrombotic
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
ischemic strokes - embolic
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
ischemic strokes - lacunar infarcts
affects deep brain structures (internal capsule, thalamus, basal ganglia, pons); common w/diabetes & HTN; contralateral weakness & sensory loss, ataxia, dysarthra
hemorrhagic stroke
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
hemorrhagic stroke - intercerebral
vessel malformation & integrity of cerebral vessels; cause HTN & aging
hemorrhagic stroke - subarachnoid
bleeding in subarachnoid space; cause- aneurysms (ballooning of a vessel wall) & vascular malformations
hemorrhagic stroke - arteriovenous malformation (AVM)
congenital anomalies that affect circulation of brain; defects weaken vessel walls & can rupture
TIA
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)
stroke syndromes
anterior cerebral - distribution
supplies the superior border of the frontal and parietal lobes
stroke syndromes
anterior cerebral - patient deficits
contralateral weakness & sensory loss primarily in the LE, incontinence, aphasia, apraxia, personality changes
stroke syndromes
middle cerebral - distribution
supplies the surface of the cerebral hemispheres and the deep frontal and parietal lobes
stroke syndromes
middle cerebral - patient deficits
contralateral sensory loss and weakness in the face and UE, less involvement in the LE, homonymous hemianopia
stroke syndromes
vertebrobasilar - patient deficits
cranial nerve involvement (diplopia, dysphagia, dysarthria, deafness, vertigo), ataxia, equilibrium disturbances, headaches, dizziness
stroke syndromes
vertebrobasilar - distribution
supplies the brainstem and cerebellum
stroke syndromes
posterior cerebral - patient deficits
contralateral sensory loss, memory deficits, thalamic pain syndrome, homonymous hemiamopia, visual agnosia, cortical blindness
stroke syndromes
posterior cerebral - distribution
supplies the occipital and temporal lobes, thalamus and upper brain stem
general risk factors
> 55 yr
males
african americans, pacific islanders & hispanics
medical risk factors
previous stroke, TIA, cardiac disease, diabetes, atrial fibrillation & HTN
lifestyle risk factors
smoking, obesity, excessive alcohol, drug use & inactivity
primary preventable risk factors
HTN; heart disease
lowering diastolic BP by 5-6 mmHg results in a reduction of rick for CVA by 40%
activate emergency medical system when:
sudden weakness confusion sudden dimness or loss of vision in one eye difficulty speaking sudden severe headache unexplained dizziness loss of balance difficulty walking
characteristics of left hemisphere CVA
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
characteristics of right hemisphere CVA
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)
characteristics of brainstem CVA
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
characteristics of cerebellum CVA
decreased balance ataxia decreased coordination nausea decreased ability for postural adjustment nystagmus
clinical findings -
may have some/all/none depends on location & extent of injury
spasticity muscle weakness motor planning deficits sensory impairments communication impairments orofacial deficits respiratory impairments reflex activity associated reactions bowel & bladder dysfunction functional limitations
damage to motor cortex presents
flaccidity first, then spasticity, then impaired postural tone
damage to motor cortex presents-
flaccidity first
low muscle tone
inability to generate muscle contraction
transient state
patients develop hypertonicity or spasticity
damage to motor cortex presents-
spasticity
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
how is spasticity graded/documented
modified ashworth scale
0-4 ordinal scale
Modified Ashworth Scale - 0
no increase in muscle tone
Modified Ashworth Scale - 1
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
Modified Ashworth Scale - 1+
slight increase in muscle tone, manifested by a catch, followed by minimal resistance throughout the remainder (less than half) of the ROM
Modified Ashworth Scale - 2
more marked increase in muscle tone through most of the ROM, but affected part easily moved
Modified Ashworth Scale - 3
considerable increase in muscle tone, passive movement difficult
Modified Ashworth Scale - 4
affected part rigid in flexion or extension
spasticity/abnormal synergy patterns
highly stereotypic, obligatory combinations of limb movements or postures
unable to isolate movement; no flexibility of movement for adaptation to task
spasticity/abnormal synergy patterns - UE flexion synergy
scapula: retraction, elevation
shoulder: abd, ER
elbow: flex
forearm: supination
wrist/hand: flex of both
spasticity/abnormal synergy patterns - UE extension synergy
scapula: protraction
shoulder: add, IR
Elbow: ext
forearm: pronation
wrist/hand: flex of both
spasticity/abnormal synergy patterns - LE flexion synergy
Hip: flex, abd, ER
knee: flex
ankle: dflex, inv
spasticity/abnormal synergy patterns - LE extension synergy
hip: ext, add, IR
knee: ext
ankle: pflex, inv
Brunnstrom Stages of Recovery- Stage 1
period of flaccidity immediately following acute episode
no movement of limbs can be elicited
Brunnstrom Stages of Recovery- Stage 2
basic limb synergies or some of their components may appear as associated rxns
minimal voluntary movement responses may be present
spasticity begins to develop
Brunnstrom Stages of Recovery- Stage 3
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)
Brunnstrom Stages of Recovery- Stage 4
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)
Brunnstrom Stages of Recovery- Stage 5
more difficult movement combos are learned as the basic limb synergies lose their dominance over motor acts (synergies are going away)
Brunnstrom Stages of Recovery- Stage 6
with disappearance of spasticity, individual joint movements become possible and coordination approaches normal
as the last recovery step, normal motor function is restored
motor dysfunction - weakness
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
motor dysfunction - postural control & balance
impairments in steadiness, symmetry, dynamic stability, reactive & anticipatory postural control
coordination deficit of poor timing, sequencing & co-contraction contribute
motor dysfunction - ambulation
asymmetric, slow, stiff-knee pattern, foot drop, knee buckle or hyperextension, extension synergy
motor planning deficits
more frequent/prominent in L CVA
poor timing & sequencing
sensory or cerebellar ataxia
apraxia-difficulty performing purposeful movements (sit to stand)
sensory impairments
strokes of parietal lobe
loss of tactile or proprioceptive capabilities (increase risk of falls)
partial loss of sensations
limit motor control
communication impairments
infarcts in frontal & temporal lobes 30% have language dysfunction aphasia dysarthria emotional lability (R CVA)
aphasia
impairment of language comprehension, oral expression & use of symbols to communicate
broca’s aphasia
expressive disorder, difficulty producing speech
wernicke’s aphasia
receptive disorder, difficulty with language comprehension
global aphasia
expressive & receptive disorder
dysarthria
difficulty articulating words as a result of weakness & inability to contro the muscles associated with speech production (muscle strength)
emotional lability R CVA
difficulty controlling emotions; laugh or cry at inappropriate without cause
orofacial deficits
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)
dysphagia
difficulty or inability to swallow foods or liquids
respiratory impairments
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%
spinal reflex- flexor withdrawl
stimulus & response
stimulus-noxious stimulus applied to the bottom of foot
response-toe extension, ankle dorsiflexion, hip & knee flexion
spinal reflex- cross extension
stimulus & response
stimulus-noxious stimulus applied to ball of foot w/ the LE prepositioned in extension
response-flexion & then extension of the opp LE
spinal reflex- startle
stimulus & response
stimulus- sudden loud noise
response- extension & abduction of UE
spinal reflex- grasp
stimulus & response
stimulus-pressure applied to ball of foot or the palm of hand
response-flexion of toes or fingers, respectively
brain stem reflex- symmetric tonic neck reflex
response
flexion of the neck results in flexion of the arms & ext of legs
ext of neck results in ext of arms & flex of neck
brain stem reflex- asymmetric tonic neck reflex
response
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
brain stem reflex- tonic labyrinthine reflex
response
prone position facilitates flexion. Supine position facilitates extension
brain stem reflex- tonic thumb reflex
response
when the involved extremity is elevated above the horizontal, thumb extension is facilitated with forearm supination
deep tendon reflexes
stretch reflex may indicate presence of abnormal tone hypotonia/flaccidity hypertonia/spasticity hyperreflexive early stages-diminished or absent DTR's
reflex activity
spinal & brain stem reflexes may appear following a stroke
clonus, clasp knife, babinski
associated reactions
automatic movements that occur as a result of active or resisted movement in another part of the body
can be misinterpreted as active movement
bowel and bladder dysfunction
incontinence
movement assists in the regulation of bowel function
breathing stimulates peristalsis–if having a hard time breathing it causes bowel problems
incontinence
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
associated rxns - souques phenomenon - response
flexion of the involved arm above 150 facilitates extension and abduction of the fingers
associated rxns - raimiste phenomenon - response
resistance applied to hip abduction or adduction of the uninvolved LE causes similar response in the involved LE
associated rxns - homolateral limb synkinesis - response
flexion of the involved UE elicits flexion of the involved LE
functional limitations
result from loss of motor or sensory function
lose the ability to perform ADL’s
lose the ability to walk
common complications
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)
secondary/indirect impairments
decreased ROM/contractures
UE contractures of elbow, wrist, finger flexors & pronators
LE pflex & inversion contracture
secondary/indirect impairments
shoulder subluxation/pain
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
acute medical mgmt
monitor neurologic function prevent dev of secondary complications pharmacologic intervention (tPA helps if w/in 3 hrs) surgical intervention
stroke rehab acute care (<1 mo post CVA)
low intensity rehab as soon as stable
shortening LOS
stroke rehab
post acute care (1-6 mo post CVA)
moderate to severe residual impairments
team of rehab specialists for comprehensive services
stroke rehab
chronic (>6 mo post CVA)
rehab
60 min for 2-3x/week (financially could be problem)
target flexibility, strength, balance, gait, endurance & UE function
