Cerebrovascular Anatomy, Localizing Vascular Lesions, Stroke Flashcards
common carotid arteries arise from ____ on the L and _____ on the R
the vertebral arteries arise from ______
common carotid arteries arise from aortic arch on the L and brachiocephalic trunk on the right
the vertebral arteries arise from subclavian branches of the aorta, supply posterior circulation (come together to form basilar artery)
describe the vascular territory of the anterior cerebral artery (ACA) and the consequences of an infarction (4)
ACA supplies medial frontal lobe, infarct —>
- contralateral lower extremity weakness (medial primary motor cortex in frontal lobe controls legs)
- contralateral lower extremity sensory loss (medial primary sensory cortex in parietal lobe)
- global abulia (unmotivated state)
- global anterograde amnesia (damage to cingulate cortex)
contralateral lower extremity weakness and sensory loss + anterograde amnesia and lack of motivation = infarct where?
anterior cerebral artery supplies medial frontal lobe, infarct —>
- contralateral lower extremity weakness (medial primary motor cortex in frontal lobe controls legs)
- contralateral lower extremity sensory loss (medial primary sensory cortex in parietal lobe)
- global abulia (unmotivated state)
- global anterograde amnesia (damage to cingulate cortex)
Pt is 76yo M who is taken to the ED by their brother. The brother tells you the patient has been more forgetful than usual and acting withdrawn. The patient is slow to respond to your questioning, and you notice they are dragging their R leg while walking. The brother tells you this is new. CT angiogram reveals an infarct in…
anterior cerebral artery supplies medial frontal lobe, infarct —>
- contralateral lower extremity weakness (medial primary motor cortex in frontal lobe controls legs)
- contralateral lower extremity sensory loss (medial primary sensory cortex in parietal lobe)
- global abulia (unmotivated state)
- global anterograde amnesia (damage to cingulate cortex)
what symptoms may occur with a middle cerebral artery (MCA) infraction? (7)
MCA supplies largest territory in brain (lateral sides), infarct —>
- contralateral hemiparesis via primary motor cortex AND descending motor pathways
- contralateral facial paresis via corticobulbar fibers
- contralateral gaze paresis via frontal eye fields (can’t look away from side of infarct)
- contralateral hemisensory deficits via primary sensory cortex in parietal lobe and ascending pathways
- aphasia via dominant (left) frontal/temporal lobes
- hemi-neglect via non-dominant (right) parietal lobe
- hemianopia (field cut) via damage of both temporal and parietal optic radiations
Pt presents to ED with L-sided weakness and sensory loss of body and face. Where is the infarct most likely, and what are 3 other symptoms you should look for?
middle cerebral artery supplies largest territory in brain (lateral sides), infarct —>
- contralateral hemiparesis via primary motor cortex AND descending motor pathways
- contralateral facial paresis via corticobulbar fibers
- contralateral gaze paresis via frontal eye fields (can’t look away from side of infarct)
- contralateral hemisensory deficits via primary sensory cortex in parietal lobe and ascending pathways
- aphasia via dominant (left) frontal/temporal lobes
- hemi-neglect via non-dominant (right) parietal lobe
- hemianopia (field cut) via damage of both temporal and parietal optic radiations
describe the vascular territory of the posterior cerebral artery (PCA) the and consequences of an infarct (8)
PCA supplies inferior medial temporal lobe and occipital lobe, notably including the thalamus!, infarct —>
- contralateral hemisensory loss via posterior thalamus
- contralateral hemianopia via occipital lobe
- neglect (rare) via non-dominant thalamus (improves more quickly than parietal lobe neglect)
- transcortical aphasia via dominant thalamus (less severe than Broca/Wernicke + intact repetition)
- behavioral abnormalities/ confusion
PCA is also terminal branch of basilar supplying the midbrain, infarct —>
6. contralateral hemiparesis via cerebral peduncle
7. contralateral ataxia via red nucleus
8. ipsilateral CN III palsy
Pt presents to ED with R-sided weakness and sensory loss, R-sided loss of vision, aphasia, confusion, and L-sided CN III palsy. Where is the infarct most likely?
posterior cerebral artery: supplies inferior medial temporal lobe and occipital lobe, notably including the thalamus!, infarct —>
- contralateral hemisensory loss via posterior thalamus
- contralateral hemianopia via occipital lobe
- neglect (rare) via non-dominant thalamus (improves more quickly than parietal lobe neglect)
- transcortical aphasia via dominant thalamus (less severe than Broca/Wernicke + intact repetition)
- behavioral abnormalities/ confusion
PCA is also terminal branch of basilar supplying the midbrain, infarct —>
6. contralateral hemiparesis via cerebral peduncle
7. contralateral ataxia via red nucleus
8. ipsilateral CN III palsy
isolated one-sided ataxia = infarct in which artery?
superior cerebellar artery: supplies anterior cerebellum, infraction causes ipsilateral ataxia (cerebellar fibers double-cross)
describe the vascular territory of the basilar artery and the consequences of infarct
basilar artery supplies pons and some anterior medulla
medial pontine stroke —>
1. contralateral hemiparesis
2. contralateral facial paresis
3. intranuclear ophthalmoplegia
lateral pontine stroke —>
1. ipsilateral facial paresis and sensory loss
2. ipsilateral horizontal gaze paresis
3. contralateral ataxia
4. contralateral hemisensory loss
Pt presents with ataxic hemiparesis on one side… what else should you look for? Where is the infarct?
basilar artery supplies pons and some anterior medulla
medial pontine stroke —>
1. contralateral hemiparesis
2. contralateral facial paresis
3. intranuclear ophthalmoplegia
lateral pontine stroke —>
1. ipsilateral facial paresis and sensory loss
2. ipsilateral horizontal gaze paresis
3. contralateral ataxia
4. contralateral hemisensory loss
describe the vascular territory of AICA and the consequences of infarct (4)
AICA comes off basilar artery, supplies lateral pons, cerebellar peduncles, and anterior inferior cerebellum (duh), infarct —>
- ipsilateral ataxia
- ipsilateral facial sensory loss (trigeminal nucleus)
- ipsilateral Horner’s
- ipsilateral hearing loss (AICA gives rise to labyrinthine artery - VERY rare)
which artery is infarcted in lateral medullary syndrome? what are the symptoms (6)?
PICA infarct —>
- contralateral loss of pain/temp via spinothalamic tract
- ipsilateral ataxia via inferior cerebellar peduncle and vestibular nucleus
- ipsilateral facial sensory loss via trigeminal nucleus
- ipsilateral Horner’s via sympathetics
- taste loss via solitary nucleus
- dysarthria, dysphagia via nucleus ambiguous (donates to CN IX and X)
isolated sensory loss of entire side of body (same side for face and body) = lesion where? what is this structure supplied by?
thalamus, supplied by PCA
will affect CONTRALATERAL side
acute abulia (withdrawn presentation) + R leg weakness + amnesia = lesion where? what is the vascular supply?
medial frontal lobe, supplied by ACA
[on L, contralateral side]
acute left visual field cut + mild apraxia = lesion where? what is the vascular supply?
occipital lobe (optic radiations), supplied by PCA
apraxia = difficulty with skilled movements (ex, using a cellphone), due to damage to thalamus
left visual field cut + left hemi-neglect + right gaze deviation + left spastic hemiparesis + left hemisensory deficits = lesion where? what is the vascular supply?
right fronto-temporo-parietal lobe lesion, supplied by MCA
field cut due to temporo-parietal region, gaze deviation due to frontal eye fields (frontal lobe), sensory deficits and hemi-neglect due to parietal lobe
everything contralateral because you’re at level of cortex (right gaze deviation because frontal eye fields on R help eyes look left)
2 days ago, pt developed sudden posterior R neck pain radiating to the head while lifting weights. 1 hour ago, pt developed acute onset R face numbness, L hemibody numbness, and severe gait instability on the R.
Now, R Horner’s syndrome, trouble swallowing, dysarthria.
Where is the lesion, and what is the vascular supply?
R lateral medulla, supplied by PICA
facial numbness due to damage to CN V, which begins in pons but runs through medulla (don’t get tripped up with that!)
NOT in the pons, because ataxia would be contralateral (coordination fibers have not yet been able to cross in cerebellum)
describe how ischemia causes cytotoxic edema of the brain?
ischemia —> lack of nutrients —> inability to make sufficient ATP —> failure of Na/K ATP pumps —> electrolyte imbalances —> can’t pump out sodium, water follows and rushes into cells —> cytotoxic edema causes cell lysis
how does vasogenic edema of the brain develop?
cerebral autoregulation failure - maximum vasoconstriction is reached/surpassed and hyperperfusion occurs —> tight junctions are opened, plasma escapes into interstitial space
cytotoxic edema vs vasogenic edema of the brain
cytotoxic edema: under perfusion (ischemia) causes failure of Na/K ATP pumps (lack nutrients), water enters neurons and causes edema (—> cell lysis)
vasogenic edema: hyperperfusion causes tight junctions to open and plasma escapes into interstitial space
both are extremes of cerebral auto-regulation failure
how is cerebral perfusion pressure calculated?
CPP (cerebral perfusion pressure) = MAP (mean arterial pressure) - ICP (intracranial pressure)
ICP can be measured with lumbar pressure
if patient is presenting with all the clinical signs of a vascular brain lesion (ex, MCA) but has a normal head CT scan, how should you interpret this?
the brain region is hypo-perfused but not yet ischemic - on the extreme end of its ability to auto-regulate perfusion
if intervention occurs now, brain tissue can be saved!
what are the 5 major syndromes to look for with MCA occlusion?
- aphasia
- contralateral hemiparesis
- contralateral facial droop
- gaze deviation towards lesion
- contralateral field cut (hemianopia)
