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Neuro Rehab 2 > CVA - 2b Stroke Syndromes > Flashcards

CVA - 2b Stroke Syndromes Flashcards

1
Q

what are common presentations seen specific to a posterior circulation stroke

A

deficits in:
- balance
- brainstem w CNs (funky eye movements, n/v, vertigo)

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2
Q

what is the path of the homunculus from the cerebral cortex

A

down corticospinal tract -> internal capsule -> midbrain and pons and down SC

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3
Q

what structures does ACA specifically supply

A

med and ant portion of cerebral hemispheres (frontal and parietal)

subcortical structures:
- basal ganglia (ant internal capsule, inferior caudate nucleus)
- ant corpus callosum

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4
Q

what role does the basal ganglia play in deficits seen in ACA

A

motor apraxia
- impaired initiation of movement via BG

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5
Q

what is the significance of the ant communicating artery in ACA syndrome

A

more collateral blood flow

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6
Q

most common clinical features to ACA syndrome

A

contra hemiplegia and hemisensory loss LE>UE
parietal cortex = apraxia
prefrontal = abulia
supplemental motor area = expressive aphasia (in L ACA - broca’s aphasia)

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7
Q

what is abulia? how do we treat this?

A

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

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8
Q

what is apraxia

A

problems w motor planning and executing purposeful movements (sequencing problem)
- not attributable to motor, sensory, or peripheral issues

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9
Q

damage to what structures typically lead to apraxia

A

L hemisphere brain damage
- parietal
- BG
- premotor frontal cortex

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10
Q

how does damage to parietal, BG, premotor frontal cortex structures lead to apraxia

A

defect in pathways that contain memory of learned patterns of movement
- pts can’t retrieve models of stored, skilled movements

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11
Q

what is a differential dx for apraxia and what can help w this

A

abulia
- neuropsych consult can help us differientiate

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12
Q

what are 3 types of apraxia and what are the main 2

A
  1. ideomotor **
  2. ideational **
  3. constructional
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13
Q

damage to what structure often results in ideomotor apraxia

A

L parietal

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14
Q

what is ideomotor apraxia

A

unable to imitate movements or produce movement on verbal command
- but can move automatically w habitual movements

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15
Q

damage to what structure results in ideational apraxia

A

L > R parietal

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16
Q

what is ideational apraxia

A

unable to produce movement either on command or automatically

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17
Q

how will someone w ideational apraxia often present outside the apraxia

A

usually very fidgety w things
- not sure what to do w things

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18
Q

what structure results in constructional apraxia

A

R > L parietal

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19
Q

what is constructional apraxia

A

inability to draw pictures or construct simple configurations
ex: draw a clock, assemble something

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20
Q

what artery is the most common site of occlusion

A

MCA

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21
Q

what type of stroke syndrome are we most likely to see and treat

A

MCA
- most common site of occlusion
- low mortality rate

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22
Q

what specific structures does the MCA supply

A

entire lateral aspect of cerebral hemisphere - frontal, temporal, and parietal

subcortical structures:
- post internal capsule
- globus pallidus
- caudate nucleus
- putamen
aka basal ganglia

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23
Q

why are worse outcomes associated w a proximal occlusion of MCA vs distal

A

inc edema and less collaterals available

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24
Q

why do you see global aphasia w MCA and not ACA

A

MCA feeds Wernicke and Broca’s areas
- get both expressive and receptive aphasias

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25
Q

what are the most common clinical features of MCA syndrome

A

contra hemiplegia UE/face > LE
contra sensory loss UE> LE
contra homonymous hemianopsia (HH)
perceptual deficits
aphasia - expressive, receptive, & global
apraxia

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26
Q

what are perceptual deficits that are seen w MCA syndrome

A

unilateral neglect
depth perception
spatial relationships
agnosias

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27
Q

HH vs unilateral neglect

A

HH - sensory deficit
- field cut, no input at all

unilateral neglect
- perceptual deficits
- have visual input, just ignoring it

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28
Q

what is agnosia

A

not knowing
- if you ask them who’s arm (and it is theirs) - they won’t know

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29
Q

what are clinical features specific to L MCA syndrome

A

aphasia
- expressive, receptive, or global depending on area

apraxia
- more common on L hemi than R

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30
Q

what are clinical features specific to R MCA syndrome

A

perceptual deficits
- agnosias
- spatial relations deficits
- unilateral neglect

apraxia

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31
Q

what is HH

A

homonymous hemianopsia

loss of half of field of view on same side in both eyes
- “field cut”

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32
Q

what damage leads to HH

A

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

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33
Q

where is the damage associated w unilateral neglect

A

R parietal lobe lesions
- most commonly somewhere on R hemisphere

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34
Q

what is unilateral neglect

A

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

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35
Q

how would unilateral neglect from a L hemisphere injury present

A

less common
persistent

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36
Q

can a pt spontaneously recover from unilateral neglect?

A

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

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37
Q

what are 5 challenging points of unilateral neglect for PTs

A
  1. anosognosia
  2. heterogeneity
  3. lots of different terms which all mean unilateral neglect
  4. associated w greater risk of falls, poorer functional recovery
  5. can enhance disability associated w hemiparesis
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38
Q

what is anosognosia and what hemisphere is this more common in

A

lack of insight, failure to recognize deficits

R sided strokes

39
Q

what are other terms that mean unilateral neglect

A

hemiagnosia
hemineglect
spatial neglect
hemi-attention
neglect syndrome

40
Q

differences in treating pts w HH vs unilateral neglect

A

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

41
Q

what can often accompany HH

A

visual neglect (often but not always)

42
Q

what are 4 types of neglect

A

visual
auditory
tactile
motor

43
Q

what is motor neglect

A

not moving that side
- could have seen them do spontaneous movement to know they are capable, but not engaging that side in activities

44
Q

how is neglect typically dx

A

observation

45
Q

what are tests that can be used to dx unilateral neglect

A

line bisection test
letter cancellation test
drawing
reading
writing

ecologically valid tests: behavioral inattention test, wheelchair obstacle course

46
Q

who is an asset on the healthcare team to collab w when treating someone w unilateral neglect

A

OTs
- they are more specialized in unilateral neglect

47
Q

what is extinction

A

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

48
Q

what side of the brain is extinction commonly see on

A

L side w perceptual awareness

49
Q

what is aphasia

A

acquired communcation disorder

50
Q

what type of stroke is associated w fluent aphasia

A

wernicke’s
L temporal lobe and MCA

51
Q

what are 2 other terms for fluent aphasia

A

wernicke’s
receptive

52
Q

what deficits and damaged structures are seen in fluent aphasia

A

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

53
Q

what type of stroke results in non-fluent aphasia

A

L frontal lobe w ACA and some MCA

54
Q

what are 2 other terms for non-fluent aphasia

A

broca’s or expressive aphasia

55
Q

what deficits and damaged structures are seen in non-fluent aphasia

A

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

56
Q

what is an important part of treating someone w non-fluent aphasia

A

establish another form of communication
- gestures, point at things, communication board

this is part of why we work w OTs

57
Q

what type of stroke results in global aphasia

A

larger stroke

58
Q

what deficits and damaged structures are seen in global aphasia

A

extensive brain involvement
- comprehension of language and production impaired

59
Q

how does ICA syndrome present

A

a massive infarction
similar to MCA d/t collateral blood flow from Circle of Willis for ACA

60
Q

what are common clinical manifestations of ICA syndrome

A

edema
herniation
coma
death

61
Q

what are the common syndromes sen with posterior circulation

A

posterior cerebral a.
vertebrobasilar a.
complete basilar

62
Q

what does the posterior cerebral artery supply

A

occipital lobe
medial and inferior temporal lobe
upper brainstem, midbrain, and thalamus

63
Q

where is the posterior cerebral artery located anatomically

A

2 terminal branches of basilar artery

64
Q

what are 5 branches of the posterior cerebral artery where infarcts are common

A

thalamic branch
unilateral occipital infarct
bilateral occipital infarct
temporal lobe infarct
unilateral midbrain infarct

65
Q

what is a common feature of a PCA structure and why

A

thalamic pain syndrome
- PCA feeds thalamus and thalamus interprets pain (lots of pain info sent thru here)

66
Q

what is thalamic pain syndrome and what syndrome is this common in

A

feeling pain on contralateral side, can look like neuropathic pain

PCA strokes

67
Q

what is visual agnosia

A

not knowing, spatial awareness issue

68
Q

clinical feature of thalamic branch PCA syndrome

A

contralateral hemianesthesia (thalamic pain syndrome)

69
Q

clinical features of unilateral occipital infarct of PCA

A

contralateral:
- HH
- visual agnosia
- dyslexia w/o agraphia (aka can’t read but can write)

70
Q

clinical feature of bilateral occipital infarct of PCA

A

cortical blindness
- loss of vision d/t visual cortex deficits, eye and pupil remain functional)

71
Q

clinical feature of temporal lobe infarct of PCA

A

memory deficit / amnesia

72
Q

clinical features of unilateral midbrain infarct of PCA

A

Weber’s syndrome
- oculomotor n. palsy (CNIII)
- contralateral hemiplegia

73
Q

what is oculomotor n. palsy and what syndrome is this typically seen in

A

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

74
Q

where are vertebrobasilar arteries (anatomically)

A

vertebral arteries branch off subclavian arteries -> merge near pons to form basilar artery

75
Q

what structures are supplied by vertebrobasilar artery

A

most of brainstem (ie CNs)
cerebellum

76
Q

what are clinical features of vertebrobasilar artery syndromes

A

can produce many different syndromes

ipsi or contralateral
cerebellar deficits
CN deficits
- funky eye movements

77
Q

what is the pathophys of complete basilar syndrome

A

bilateral infarction of pons, typically d/t basilar artery thrombus
- ischemic in nature

sudden catastrophic event

78
Q

what is another term for complete basilar syndrome

A

“locked-in syndrome”

79
Q

what are clinical features of complete basilar syndrome

A

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

80
Q

what is the most common posterior ischemic stroke syndrome

A

PICA syndrome

81
Q

pathophysiology of PICA syndrome

A

lesion of vertebral or posterior inferior cerebellar artery (PICA) of brainstem

82
Q

what are 2 other terms for PICA syndrome

A

lateral medullary syndrome
wallenberg’s syndrome

83
Q

common clinical features of PICA syndrome

A

cerebellar functions
dizziness, vertigo, nystagmus
n/v
dysphagia, hoarseness
LOB w gait instability

impaired contra pain/temp sensation in arm and legs
- spinothalamic tract

84
Q

what are lacuna

A

small terminal vessels perfusing deep gray and white matter

85
Q

pathophysiology of lacunar strokes

A

stroke in one of the small, terminal branches of circle of willis, MCA, vertebral or basilar arteries

86
Q

etiology of lacunar strokes

A

**chronic HTN **
- pushing thrombus thru small vessels

diabetic microvascular dz

87
Q

clinical features of lacunar strokes and prognosis

A

typically impact small area w distinct minor sx

good prognosis - few impairments

88
Q

what are 5 common sites for lacunar syndromes

A
  1. post limb of internal capsule, pyramids, or pons
  2. base of pons
  3. thalamus
  4. anterior limb of internal capsule and adjacent white matter in corona radiata
  5. putamen, globus pallidus
89
Q

sx of lacunar stroke of posterior limb of internal capsule, pyramids, or pons

A

hemiparesis
- no sensory deficit

90
Q

sx of lacunar stroke at base of pons

A

ataxic hemiparesis and dysarthria

91
Q

sx of lacunar stroke at thalamus

A

pure sensory
- contralateral hemisensory loss

92
Q

sx of lacunar stroke at anterior limb of internal capsule and adjacent white matter in corona radiata

A

hemiparesis w apraxia

93
Q

sx of lacunar stroke of putamen, globus pallidus

A

dystonia
choreoathetosis

Neuro Rehab 2 (48 decks)

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