CVA - 2b Stroke Syndromes Flashcards
what are common presentations seen specific to a posterior circulation stroke
deficits in:
- balance
- brainstem w CNs (funky eye movements, n/v, vertigo)
what is the path of the homunculus from the cerebral cortex
down corticospinal tract -> internal capsule -> midbrain and pons and down SC
what structures does ACA specifically supply
med and ant portion of cerebral hemispheres (frontal and parietal)
subcortical structures:
- basal ganglia (ant internal capsule, inferior caudate nucleus)
- ant corpus callosum
what role does the basal ganglia play in deficits seen in ACA
motor apraxia
- impaired initiation of movement via BG
what is the significance of the ant communicating artery in ACA syndrome
more collateral blood flow
most common clinical features to ACA syndrome
contra hemiplegia and hemisensory loss LE>UE
parietal cortex = apraxia
prefrontal = abulia
supplemental motor area = expressive aphasia (in L ACA - broca’s aphasia)
what is abulia? how do we treat this?
no motor drive
- even if have motor and sensory capacity, no will to initiate movement –> poorer outcomes
flat affect
benefit from a neuropsych eval -> use pharm to improve initiation
what is apraxia
problems w motor planning and executing purposeful movements (sequencing problem)
- not attributable to motor, sensory, or peripheral issues
damage to what structures typically lead to apraxia
L hemisphere brain damage
- parietal
- BG
- premotor frontal cortex
how does damage to parietal, BG, premotor frontal cortex structures lead to apraxia
defect in pathways that contain memory of learned patterns of movement
- pts can’t retrieve models of stored, skilled movements
what is a differential dx for apraxia and what can help w this
abulia
- neuropsych consult can help us differientiate
what are 3 types of apraxia and what are the main 2
- ideomotor **
- ideational **
- constructional
damage to what structure often results in ideomotor apraxia
L parietal
what is ideomotor apraxia
unable to imitate movements or produce movement on verbal command
- but can move automatically w habitual movements
damage to what structure results in ideational apraxia
L > R parietal
what is ideational apraxia
unable to produce movement either on command or automatically
how will someone w ideational apraxia often present outside the apraxia
usually very fidgety w things
- not sure what to do w things
what structure results in constructional apraxia
R > L parietal
what is constructional apraxia
inability to draw pictures or construct simple configurations
ex: draw a clock, assemble something
what artery is the most common site of occlusion
MCA
what type of stroke syndrome are we most likely to see and treat
MCA
- most common site of occlusion
- low mortality rate
what specific structures does the MCA supply
entire lateral aspect of cerebral hemisphere - frontal, temporal, and parietal
subcortical structures:
- post internal capsule
- globus pallidus
- caudate nucleus
- putamen
aka basal ganglia
why are worse outcomes associated w a proximal occlusion of MCA vs distal
inc edema and less collaterals available
why do you see global aphasia w MCA and not ACA
MCA feeds Wernicke and Broca’s areas
- get both expressive and receptive aphasias
what are the most common clinical features of MCA syndrome
contra hemiplegia UE/face > LE
contra sensory loss UE> LE
contra homonymous hemianopsia (HH)
perceptual deficits
aphasia - expressive, receptive, & global
apraxia
what are perceptual deficits that are seen w MCA syndrome
unilateral neglect
depth perception
spatial relationships
agnosias
HH vs unilateral neglect
HH - sensory deficit
- field cut, no input at all
unilateral neglect
- perceptual deficits
- have visual input, just ignoring it
what is agnosia
not knowing
- if you ask them who’s arm (and it is theirs) - they won’t know
what are clinical features specific to L MCA syndrome
aphasia
- expressive, receptive, or global depending on area
apraxia
- more common on L hemi than R
what are clinical features specific to R MCA syndrome
perceptual deficits
- agnosias
- spatial relations deficits
- unilateral neglect
apraxia
what is HH
homonymous hemianopsia
loss of half of field of view on same side in both eyes
- “field cut”
what damage leads to HH
vascular lesions or tumors of optic tract (MCA or circle of willis) or visual cortex (PCA) can cause contra HH
ex: L hemi injury = R visual field of each eye is damaged
where is the damage associated w unilateral neglect
R parietal lobe lesions
- most commonly somewhere on R hemisphere
what is unilateral neglect
inability to report, respond or orient to stimuli in contralesional space
- not d/e primary sensory or motor deficits
difficulty maintaining internal map or image or other spatial knowledge of objects on that side of space
how would unilateral neglect from a L hemisphere injury present
less common
persistent
can a pt spontaneously recover from unilateral neglect?
spontaneous recovery can occur in early stages of recovery
- but up to 75% of pt have persisting neglect
need intense therapy and repetitive training to start to attend to body or environment
what are 5 challenging points of unilateral neglect for PTs
- anosognosia
- heterogeneity
- lots of different terms which all mean unilateral neglect
- associated w greater risk of falls, poorer functional recovery
- can enhance disability associated w hemiparesis
what is anosognosia and what hemisphere is this more common in
lack of insight, failure to recognize deficits
R sided strokes
what are other terms that mean unilateral neglect
hemiagnosia
hemineglect
spatial neglect
hemi-attention
neglect syndrome
differences in treating pts w HH vs unilateral neglect
HH - most are aware that they are missing part of their world
- easier to treat and recover
unilateral neglect - don’t know they are missing something
both are risk for falls and safety impairments
what can often accompany HH
visual neglect (often but not always)
what are 4 types of neglect
visual
auditory
tactile
motor
what is motor neglect
not moving that side
- could have seen them do spontaneous movement to know they are capable, but not engaging that side in activities
how is neglect typically dx
observation
what are tests that can be used to dx unilateral neglect
line bisection test
letter cancellation test
drawing
reading
writing
ecologically valid tests: behavioral inattention test, wheelchair obstacle course
who is an asset on the healthcare team to collab w when treating someone w unilateral neglect
OTs
- they are more specialized in unilateral neglect
what is extinction
difficulty in reporting a contralesional stimulus when it occurs simultaneously w a correctly reported ipsilesional stimulus
- attend to one side more
ex: R side lesion, if 1 stimulus can identify on L, if 2 stimuli simultaneously will only identify it on R side
what side of the brain is extinction commonly see on
L side w perceptual awareness
what is aphasia
acquired communcation disorder
what type of stroke is associated w fluent aphasia
wernicke’s
L temporal lobe and MCA
what are 2 other terms for fluent aphasia
wernicke’s
receptive
what deficits and damaged structures are seen in fluent aphasia
auditory association cortex in L lateral temporal lobe impaired
- auditory comprehension impaired
could talk in complete sentence but answer will be nonsensical bc can’t perceive info appropriately
what type of stroke results in non-fluent aphasia
L frontal lobe w ACA and some MCA
what are 2 other terms for non-fluent aphasia
broca’s or expressive aphasia
what deficits and damaged structures are seen in non-fluent aphasia
premotor area of L frontal lobe damaged
- flow of speech slow, word-finding difficulties, comprehension intact
impacts ms of speech
- understand what you said but can’t form the words to form the sentence
what is an important part of treating someone w non-fluent aphasia
establish another form of communication
- gestures, point at things, communication board
this is part of why we work w OTs
what type of stroke results in global aphasia
larger stroke
what deficits and damaged structures are seen in global aphasia
extensive brain involvement
- comprehension of language and production impaired
how does ICA syndrome present
a massive infarction
similar to MCA d/t collateral blood flow from Circle of Willis for ACA
what are common clinical manifestations of ICA syndrome
edema
herniation
coma
death
what are the common syndromes sen with posterior circulation
posterior cerebral a.
vertebrobasilar a.
complete basilar
what does the posterior cerebral artery supply
occipital lobe
medial and inferior temporal lobe
upper brainstem, midbrain, and thalamus
where is the posterior cerebral artery located anatomically
2 terminal branches of basilar artery
what are 5 branches of the posterior cerebral artery where infarcts are common
thalamic branch
unilateral occipital infarct
bilateral occipital infarct
temporal lobe infarct
unilateral midbrain infarct
what is a common feature of a PCA structure and why
thalamic pain syndrome
- PCA feeds thalamus and thalamus interprets pain (lots of pain info sent thru here)
what is thalamic pain syndrome and what syndrome is this common in
feeling pain on contralateral side, can look like neuropathic pain
PCA strokes
what is visual agnosia
not knowing, spatial awareness issue
clinical feature of thalamic branch PCA syndrome
contralateral hemianesthesia (thalamic pain syndrome)
clinical features of unilateral occipital infarct of PCA
contralateral:
- HH
- visual agnosia
- dyslexia w/o agraphia (aka can’t read but can write)
clinical feature of bilateral occipital infarct of PCA
cortical blindness
- loss of vision d/t visual cortex deficits, eye and pupil remain functional)
clinical feature of temporal lobe infarct of PCA
memory deficit / amnesia
clinical features of unilateral midbrain infarct of PCA
Weber’s syndrome
- oculomotor n. palsy (CNIII)
- contralateral hemiplegia
what is oculomotor n. palsy and what syndrome is this typically seen in
impact ability for eye to move and pupillary functions
common sx:
- paresis of eye ADD, upward and downward gaze
- if pupil also affected -> eye typically dilated and light reflexes altered
Weber’s Syndrome
- feature of unilateral midbrain infarct of PCA
where are vertebrobasilar arteries (anatomically)
vertebral arteries branch off subclavian arteries -> merge near pons to form basilar artery
what structures are supplied by vertebrobasilar artery
most of brainstem (ie CNs)
cerebellum
what are clinical features of vertebrobasilar artery syndromes
can produce many different syndromes
ipsi or contralateral
cerebellar deficits
CN deficits
- funky eye movements
what is the pathophys of complete basilar syndrome
bilateral infarction of pons, typically d/t basilar artery thrombus
- ischemic in nature
sudden catastrophic event
what is another term for complete basilar syndrome
“locked-in syndrome”
what are clinical features of complete basilar syndrome
acute hemiparesis -> rapidly progress to tetraplegia
lower bulbar paralysis
- CNs V - XII
progress to anarthria (mutism)
horizontal eye movements impaired
consciousness and sensation intact
vertical eye movements and blinking intact
- how communicate
what is the most common posterior ischemic stroke syndrome
PICA syndrome
pathophysiology of PICA syndrome
lesion of vertebral or posterior inferior cerebellar artery (PICA) of brainstem
what are 2 other terms for PICA syndrome
lateral medullary syndrome
wallenberg’s syndrome
common clinical features of PICA syndrome
cerebellar functions
dizziness, vertigo, nystagmus
n/v
dysphagia, hoarseness
LOB w gait instability
impaired contra pain/temp sensation in arm and legs
- spinothalamic tract
what are lacuna
small terminal vessels perfusing deep gray and white matter
pathophysiology of lacunar strokes
stroke in one of the small, terminal branches of circle of willis, MCA, vertebral or basilar arteries
etiology of lacunar strokes
**chronic HTN **
- pushing thrombus thru small vessels
diabetic microvascular dz
clinical features of lacunar strokes and prognosis
typically impact small area w distinct minor sx
good prognosis - few impairments
what are 5 common sites for lacunar syndromes
- post limb of internal capsule, pyramids, or pons
- base of pons
- thalamus
- anterior limb of internal capsule and adjacent white matter in corona radiata
- putamen, globus pallidus
sx of lacunar stroke of posterior limb of internal capsule, pyramids, or pons
hemiparesis
- no sensory deficit
sx of lacunar stroke at base of pons
ataxic hemiparesis and dysarthria
sx of lacunar stroke at thalamus
pure sensory
- contralateral hemisensory loss
sx of lacunar stroke at anterior limb of internal capsule and adjacent white matter in corona radiata
hemiparesis w apraxia
sx of lacunar stroke of putamen, globus pallidus
dystonia
choreoathetosis
