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Neuro > Cerebrovascular Anatomy, Localizing Vascular Lesions, Stroke > Flashcards

Cerebrovascular Anatomy, Localizing Vascular Lesions, Stroke Flashcards

1
Q

common carotid arteries arise from ____ on the L and _____ on the R

the vertebral arteries arise from ______

A

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)

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2
Q

describe the vascular territory of the anterior cerebral artery (ACA) and the consequences of an infarction (4)

A

ACA supplies medial frontal lobe, infarct —>

  1. contralateral lower extremity weakness (medial primary motor cortex in frontal lobe controls legs)
  2. contralateral lower extremity sensory loss (medial primary sensory cortex in parietal lobe)
  3. global abulia (unmotivated state)
  4. global anterograde amnesia (damage to cingulate cortex)
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3
Q

contralateral lower extremity weakness and sensory loss + anterograde amnesia and lack of motivation = infarct where?

A

anterior cerebral artery supplies medial frontal lobe, infarct —>

  1. contralateral lower extremity weakness (medial primary motor cortex in frontal lobe controls legs)
  2. contralateral lower extremity sensory loss (medial primary sensory cortex in parietal lobe)
  3. global abulia (unmotivated state)
  4. global anterograde amnesia (damage to cingulate cortex)
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4
Q

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 The brother tells you the patient has been more forgetful than usual and acting withdrawn.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…

A

anterior cerebral artery supplies medial frontal lobe, infarct —>

  1. contralateral lower extremity weakness (medial primary motor cortex in frontal lobe controls legs)
  2. contralateral lower extremity sensory loss (medial primary sensory cortex in parietal lobe)
  3. global abulia (unmotivated state)
  4. global anterograde amnesia (damage to cingulate cortex)
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5
Q

what symptoms may occur with a middle cerebral artery (MCA) infraction? (7)

A

MCA supplies largest territory in brain (lateral sides), infarct —>

  1. contralateral hemiparesis via primary motor cortex AND descending motor pathways
  2. contralateral facial paresis via corticobulbar fibers
  3. contralateral gaze paresis via frontal eye fields (can’t look away from side of infarct)
  4. contralateral hemisensory deficits via primary sensory cortex in parietal lobe and ascending pathways
  5. aphasia via dominant (left) frontal/temporal lobes
  6. hemi-neglect via non-dominant (right) parietal lobe
  7. hemianopia (field cut) via damage of both temporal and parietal optic radiations
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6
Q

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?

A

middle cerebral artery supplies largest territory in brain (lateral sides), infarct —>

  1. contralateral hemiparesis via primary motor cortex AND descending motor pathways
  2. contralateral facial paresis via corticobulbar fibers
  3. contralateral gaze paresis via frontal eye fields (can’t look away from side of infarct)
  4. contralateral hemisensory deficits via primary sensory cortex in parietal lobe and ascending pathways
  5. aphasia via dominant (left) frontal/temporal lobes
  6. hemi-neglect via non-dominant (right) parietal lobe
  7. hemianopia (field cut) via damage of both temporal and parietal optic radiations
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7
Q

describe the vascular territory of the posterior cerebral artery (PCA) the and consequences of an infarct (8)

A

PCA supplies inferior medial temporal lobe and occipital lobe, notably including the thalamus!, infarct —>

  1. contralateral hemisensory loss via posterior thalamus
  2. contralateral hemianopia via occipital lobe
  3. neglect (rare) via non-dominant thalamus (improves more quickly than parietal lobe neglect)
  4. transcortical aphasia via dominant thalamus (less severe than Broca/Wernicke + intact repetition)
  5. 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

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8
Q

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?

A

posterior cerebral artery: supplies inferior medial temporal lobe and occipital lobe, notably including the thalamus!, infarct —>

  1. contralateral hemisensory loss via posterior thalamus
  2. contralateral hemianopia via occipital lobe
  3. neglect (rare) via non-dominant thalamus (improves more quickly than parietal lobe neglect)
  4. transcortical aphasia via dominant thalamus (less severe than Broca/Wernicke + intact repetition)
  5. 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

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9
Q

isolated one-sided ataxia = infarct in which artery?

A

superior cerebellar artery: supplies anterior cerebellum, infraction causes ipsilateral ataxia (cerebellar fibers double-cross)

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10
Q

describe the vascular territory of the basilar artery and the consequences of infarct

A

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

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11
Q

Pt presents with ataxic hemiparesis on one side… what else should you look for? Where is the infarct?

A

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

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12
Q

describe the vascular territory of AICA and the consequences of infarct (4)

A

AICA comes off basilar artery, supplies lateral pons, cerebellar peduncles, and anterior inferior cerebellum (duh), infarct —>

  1. ipsilateral ataxia
  2. ipsilateral facial sensory loss (trigeminal nucleus)
  3. ipsilateral Horner’s
  4. ipsilateral hearing loss (AICA gives rise to labyrinthine artery - VERY rare)
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13
Q

which artery is infarcted in lateral medullary syndrome? what are the symptoms (6)?

A

PICA infarct —>

  1. contralateral loss of pain/temp via spinothalamic tract
  2. ipsilateral ataxia via inferior cerebellar peduncle and vestibular nucleus
  3. ipsilateral facial sensory loss via trigeminal nucleus
  4. ipsilateral Horner’s via sympathetics
  5. taste loss via solitary nucleus
  6. dysarthria, dysphagia via nucleus ambiguous (donates to CN IX and X)
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14
Q

isolated sensory loss of entire side of body (same side for face and body) = lesion where? what is this structure supplied by?

A

thalamus, supplied by PCA

will affect CONTRALATERAL side

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15
Q

acute abulia (withdrawn presentation) + R leg weakness + amnesia = lesion where? what is the vascular supply?

A

medial frontal lobe, supplied by ACA

[on L, contralateral side]

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16
Q

acute left visual field cut + mild apraxia = lesion where? what is the vascular supply?

A

occipital lobe (optic radiations), supplied by PCA

apraxia = difficulty with skilled movements (ex, using a cellphone), due to damage to thalamus

17
Q

left visual field cut + left hemi-neglect + right gaze deviation + left spastic hemiparesis + left hemisensory deficits = lesion where? what is the vascular supply?

A

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)

18
Q

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?

A

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)

19
Q

describe how ischemia causes cytotoxic edema of the brain?

A

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

20
Q

how does vasogenic edema of the brain develop?

A

cerebral autoregulation failure - maximum vasoconstriction is reached/surpassed and hyperperfusion occurs —> tight junctions are opened, plasma escapes into interstitial space

21
Q

cytotoxic edema vs vasogenic edema of the brain

A

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

22
Q

how is cerebral perfusion pressure calculated?

A

CPP (cerebral perfusion pressure) = MAP (mean arterial pressure) - ICP (intracranial pressure)

ICP can be measured with lumbar pressure

23
Q

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?

A

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!

24
Q

what are the 5 major syndromes to look for with MCA occlusion?

A
  1. aphasia
  2. contralateral hemiparesis
  3. contralateral facial droop
  4. gaze deviation towards lesion
  5. contralateral field cut (hemianopia)
25
Q

what are 2 types of stroke that can occur with large vessel disease of the carotid artery (atherosclerosis)?

A
  1. piece of clot breaks off and enters brain —> small, localized infarct (more common)
  2. artery narrows to the point of hypoperfusion, affecting most sensitive parts of brain - the watershed zone between MCA and ACA —> “string of pearls” appearance of hyperintensities on diffusion weighted MRI
26
Q

which symptoms will you NOT see with lacunar strokes?

A

lacunar stories = small vessel disease, milder symptoms and affect SUBcortical regions

therefore, will NOT see cortical deficits such as aphasia, neglect, field cuts

can see pure sensory loss (thalamus), pure motor loss (internal capsule), sensorimotor loss (thalamo-capsule), or ataxia hemiparesis (pons)

27
Q

what are the 4 presentations of lacunar strokes, and where is the origin of each?

A
  1. pure sensory loss = thalamus
  2. pure motor loss = internal capsule
  3. sensorimotor loss = thalamo-capsule
  4. ataxia hemiparesis = pons
28
Q

what is the pathogenesis of lacunar (small vessel) vs large vessel strokes?

A

small vessel (lacunar) due to lipohyalinosis: thickened media with fibrinoid material narrowing the lumen of small arteries

large vessel due to atherosclerosis: plaque buildup in large arteries

29
Q

how does cardioembolic ischemic stroke appear on radiographic imaging (2 possibilities)?

A

most often due to atrial fibrillation/cardiopathy, most dangerous mechanism of ischemic stroke (highest annual rate of stroke recurrence)

radiographic imaging shows either
1. large zone of infarct (large hyperintensity)
2. small infarcts (small hyperintensities) in multiple vascular territories (shower of embolisms)

30
Q

what are the 4 possible mechanisms of ischemic stroke?

A
  1. large vessel (atherosclerosis)
  2. small vessel, aka lacuna (lipohyalinosis)
  3. embolic (ex, cardioembolic due to A-fib)
  4. hypercoagulable state
    [5. unknown cause]

*note, cardioembolic carries highest risk of stroke recurrence

31
Q

how does presentation of hemorrhagic stroke differ from that of ischemic stroke? (generally speaking, how will you tell it apart?)

A

hemorrhagic strokes expand very quickly, causing hydrocephalus and increased ICP (mass effect!) —> patients will present with headache, lethargy, N/V, confusion

32
Q

how can small vessel disease cause hemorrhagic (rather than ischemic) stroke?

A

HTN (risk factor) —> rupture of small penetrating arterioles (Charcot-Bouchard aneurysms) —> intraparenchymal (deep/subcortical) hemorrhage

presents with subcortical symptoms due to injury of basal ganglia, thalamus, pons, cerebellum

33
Q

pt >60yo w/ dementia who develops multiple lobar micro-hemorrhages =

A

cerebral amyloid angiopathy (CAA): amyloid deposits in leptomeningeal and cortical arterioles

can detect amyloid deposits with Congo red staining of arteriolar walls!

Neuro (50 decks)

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