CORE Stroke and Vascular Anatomy Flashcards

1
Q

Central Sulcus

The central sulcus separates the ______ strip (______ lobe) from the _______ cortex (_______ lobe).

How do you find the central sulcus on the sagittal plane?

How do you find central sulcus on the axial plane?

A
  • The central sulcus separates the motor strip (frontal lobe) from the sensory cortex (parietal lobe).
  • To find the central sulcus, follow the cingulate sulcus posteriorly on a slightly off midline sagittal. The cingulate sulcus connects to the marginal ramus. Directly anterior to the marginal ramus is the paracentral lobule, which contains both the motor strip and the sensory cortex.
  • On an axial image, the central sulcus forms a characteristic upside down omega. The corresponding region of the motor strip, just anterior to the, controls the hand.
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2
Q

What are the segments of the Internal Carotid Artery?

Include important branches off of the ICA and off what specific segment

A
  • Cervical (C1): does not branch within the neck.
  • Petrous (C2): Fixed to bone as the ICA enters the skull base, so a cervical carotid dissection is unlikely to extend intracranially.
  • Lacerum (C3): No branches.
  • Cavernous (C4): The meningohypophyseal trunk arises from the cavernous carotid to supply the pituitary, tentorium, and dura of the clivus. The inferolateral trunk also arises from C4 to supply the 3rd, 4th, and 6th cranial nerves, as well as the trigeminal ganglion.
  • Clinoid segment (C5): The carotid rings are two dural rings that mark the proximal and distal portions of the clinoid segment of the ICA. The carotid rings prevent an inferiorly located aneurysm from causing intracranial subarachnoid hemorrhage with rupture.
  • Supraclinoid (C6 Ophthalmic -C7 Communicating): gives off several key arteries:
    • The ophthalmic artery supplies the optic nerve. It takes off just distal to the distal carotid ring in 90% of cases and can be used as a landmark for the distal ring. Aneurysms located superior to this ring can result in subarachnoid hemorrhage. Given this risk, these aneurysms are treated more aggressively than aneurysms located proximal to the distal dural ring, which are contained.
    • The posterior communicating artery (P-comm) is an anastomosis to the posterior circulation. A fetal posterior cerebral artery (PCA) is a variant supplied entirely by the ipsilateral ICA via an enlarged P-comm.
    • The anterior choroidal artery supplies several critical structures, despite its small size. It supplies the optic chiasm, hippocampus, and posterior limb of the internal capsule.
  • MNEMONIC: CPLCCOC
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3
Q

What are the persistent fetal connections of the anterior and posterior circulation?

Include origin, what it feeds, and location of each.

Which one is most common? Clinical significance? Angiographic appearance? What are the two types of this most common one?

A
  • Trigeminal: cavernous carotid, top of basilar, suprasellar cistern
    • A persistent trigeminal artery is the most common persistent carotid-basilar connection and has an association with aneurysms.
    • The persistent trigeminal artery courses adjacent to the trigeminal nerve. Angiography shows a characteristic trident or tau sign on the lateral view due to the artery’s branching structure.
    • Saltzman type I connects to the basilar artery while Saltzman type II connects to the superior cerebellar artery.
  • Otic: petrous carotid, mid-basilar, internal auditory canal
  • Hypoglossal: high cervical internal carotid at the skull base, intracranial vertebrobasilar circulation, hypoglossal canal
  • Proatlantal type 1: low internal carotid, cranial and cervical vertebrobasilar circulation, C2 level.
  • Proatlantal type 2: external carotid, cranial and cervical vertebrobasilar circulation, C2 level.MNEMONIC: PPHOT (this is upside down from above but goes along with mnemonic for segments of ICA - CPLCCOC)
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4
Q

Circle of Willis (COW)

Name it all baby

What are all the critical small arteries arising from the COW? Provide origin and the structures it feeds.

A
  • The anterior choroidal artery is the most distal branch of the internal carotid artery and supplies the optic chiasm, hippocampus, and posterior limb of the internal capsule.
  • The A1 segment of the anterior cerebral artery travels above the optic nerves and give off the recurrent artery of Heubner, which supplies the caudate head and anterior limb of the internal capsule. The A1 segment also gives rise to the medial lenticulostriate perforator vessels, which supply the medial basal ganglia.
  • Just outside the circle of Willis, the middle cerebral artery gives rise to the lateral lenticulostriate perforator vessels to supply the lateral basal ganglia including the lateral putamen, external capsule, and the posterior limb of the internal capsule.
  • The posterior communicating artery travels between the optic tract and the 3rd cranial nerve, giving off anterior thalamoperforator vessels. A P-comm aneurysm may cause cranial nerve III palsy due to local mass effect.
  • The posterior cerebral artery gives off thalamoperforators to supply the thalamus. Artery of Percheron is a variant where there is a dominant thalamic perforator supplying the ventromedial thalami bilaterally and the rostral midbrain, arising from a P1 PCA segment. An artery of Percheron infarct will result in bilateral ventromedial thalamic infarction, with or without midbrain infarction (the infarct may be v-shaped if the midbrain is involved). Deep venous thrombosis may also result in bilateral thalamic infarcts.
    • MNEMONIC - recurrent artery of Huebner comes off A1 while artery of Percheron comes off of the PCA.
    • Medial lenticulostriates perforator vessels come off ACA while lateral lenticulostriate vessles come off MCA (makes sense anatomically).
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5
Q

What are the Circle of Willis anatomic variants?

Normal COW anatomy is seen in approximately what percent of the time?

In what scenario can you have an isolated ICA?

A
  • Normal circle of Willis anatomy is only seen approximately 25% of the time.
  • Hypoplastic (34%) or absent (rare) PCOM.
  • Fetal PCA (~20%): PCA supplied by ICA
  • Hypoplastic P1: pretty similar to fetal PCA
  • Hypoplastic (10%) or absent (rare) A1
  • Absent ACOM (5%)
  • Azygous ACA (3%): associated with holoprosencephaly
  • Double of Plexiform ACOM: associated with aneurysms.
  • Can have a fetal origin of PCA and absent A1 = anatomically isolated ICA = restricted potential collateral blood flow!
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6
Q

Vascular Arterial Territories

Name it all baby!

A
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7
Q

ACA Distribution

A
  • Anterior cerebral artery (ACA) distribution. Shaded areas of these axial diagrams, arranged in sequence from base to vertex, outline the territory of the ACA including the medial lenticulostriate (orange), callosal (blue), and hemispheric branches (green).
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8
Q

MCA Distribution

A
  • Middle cerebral artery (MCA) distribution. This diagram of the axial sections, arranged in sequence from base to vertex, outlines the MCA distribution with the lateral lenticulostriate (orange) and hemispheric branches (green).
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9
Q

PCA Distribution

A
  • Posterior cerebral artery (PCA) distribution. Axial diagrams arranged in sequence from base to vertex outline supply from the PCA, the thalamic and midbrain perforators (orange), callosal (blue), and hemispheric branches (green).
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10
Q

Segmental Anatomy of the MCA

Describe extent each segment.

Where is the transition from the M1 to the M2 segment?

A
  • Although the transition from M1 to M2 is technically defined as the upward point of deflection into the Sylvian fissure, in practical terms, the pre-bifurcation MCA is often called M1 and the post-bifurcation MCA is called M2.
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11
Q

Segmental Anatomy of the ACA

What are the segments and branches of the ACA?

Where does the recurrent artery of Huebner arise from? What does it supply?

A
  • The recurrent artery of Heubner arises most commonly from the A1 segment of the ACA, proximal to the anterior communicating artery. The recurrent artery of Heubner supplies the head of the caudate and the anterior limb of the internal capsule.
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12
Q

Imaging of Stroke

  • The goal of stroke _______ is to determine who would benefit from therapy.
  • The goal of stroke ________ is to restore perfusion to the brain.
  • Discuss the American Heart Association guidelines for early management of adults with ischemic stroke (2018).
A
  • The goal of stroke imaging is to determine who would benefit from therapy.
  • The goal of stroke therapy is to restore perfusion to the brain.
  • Administer IV tPA within 3 hrs of last known normal (up to 4.5 hrs in some patients)
  • NCCT and glucose check prior to IV tPA
  • For patients who may be candidates for mechanical thrombectomy a CT angio or MRA is done.
  • Patients ≥18 years should undergo mechanical thrombectomy with a stent retriever if they have minimal prestroke disability, have a causative occlusion of the internal carotid artery or proximal middle cerebral artery, have a National Institutes of Health stroke scale score of ≥6, have a reassuring noncontrast head CT (ASPECT score of ≥6), and if they can be treated within 6 hours of last known normal.
  • In selected acute stroke patients within 6-24 hours of last known normal who have evidence of a large vessel occlusion in the anterior circulation -> get diffusion imaging to see if the patient is a candidate for mechanical thrombectomy.
  • In selected acute stroke patients within 6-16 hours of last known normal who have a large vessel occlusion in the anterior circulation and meet other DAWN or DEFUSE 3 eligibility criteria, mechanical thrombectomy is recommended (6-24 hours is reasonable).
  • Administration of aspirin is recommended in acute stroke patients within 24-48 hours after stroke onset.
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13
Q
  • Some institutions add additional exclusion criteria for administration of intravenous tPA, although these additional criteria are not a part of the AHA guidelines. What are the three additional exclusion criteria?
A
  1. Individuals with a large (greater than 1/3 MCA territory) infarct may be excluded from IV tPA.
  2. Occlusion of the distal internal carotid artery and proximal MCA and ACA (a T-shaped occlusion) may preclude treatment with Iv tPA.
  3. Absence of a penumbra of salvageable brain that represents at least 20% of the region of abnormal perfusion may preclude treatment with Iv tPA.
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14
Q

Perfusion Stroke Imaging

What is the goal of perfusion imaging?

What in the world is a penumbra?

The penumbra has how much perfusion (mL/100g tissue per minute) vs how much in the normal gray matter?

What is the infarct core?

A
  • The goal of perfusion imaging is to characterize the ischemic penumbra, which is the area of vulnerable brain adjacent to the infarct core that may also become infarcted without intervention.
  • The penumbra does receive some perfusion, but at a reduced rate compared to normal brain.
  • Perfusion of the penumbra is <20 mL/100 g tissue per minute in physiologic studies, compared to >60 mL/100 g tissue per minute for normal gray matter. Such a low rate of perfusion causes cellular dysfunction and produces a neurologic deficit, which may be restored with therapy.
  • The infarct core is usually dead tissue, which generally cannot recover even after therapy.
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15
Q

NCCT Imaging of Acute Stroke

Why do we do NCCT to eval hyperacute infarcts? Whats the main purpose?

The sensitivity of NCCT for stroke?

What imaging findings can you see on NCCT in hyperacute stroke?

What window should one evaluate hyperacute stroke on NCCT?

A
  • Noncontrast CT is the initial test of choice for evaluation of hyperacute infarct when the patient presents within the Iv tPA time window (3 hours, or 4.5 hours at some institutions).
  • The main purpose of a noncontrast CT is to exclude patients who would be harmed by thrombolytic therapy, most importantly to exclude those with hemorrhage.
  • Noncontrast CT in the hyperacute stage is relatively insensitive to detect early infarction compared to MRI. Subtle loss of gray-white differentiation in the insula or basal ganglia may be present on CT, thought to be due to decreased cerebral blood volume.
  • The insular ribbon sign describes the loss of gray-white differentiation in the insula. The gray-white junction becomes most conspicuous at very narrow stroke windows (window 30/level 30).
  • Obscuration of the lentiform nucleus (putamen and globus pallidus) is caused by loss of gray-white differentiation at the border of the lentiform nucleus and the posterior limb of the internal capsule.
  • The hyperdense artery sign describes the direct visualization of the acute intravascular thrombus, most commonly seen in the MCA. The hyperdense artery sign is specific for ischemia when seen, but relatively insensitive (seen in approximately one-third of cases). Some authors suggest that the presence of the hyperdense artery sign portends a worse prognosis.
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16
Q

MR Imaging of Acute Stroke

What is the most sensitive sequence to detect acute stroke?

What do you see on FLAIR imaging?

What is the MRI correlate to the hyperdense artery sign?

A
  • For the initial evaluation, diffusion sequences can detect acute infarction with high sensitivity within minutes of symptom onset. DWI is more sensitive than FLAIR in the detection of hyperacute stroke.
  • T2 FLAIR prolongation (hyperintensity) - most apparent 6-72 hrs
  • GRE blooming artifact represents intraluminal thrombus and is the MRI correlate to the hyperdense artery sign that can be seen on CT.
17
Q

Evolution of Infarction

What are the phases?

Describe diffusivity, T2 hyperintensity, mass effect, and enhancement, when appropriate.

A
  • Hyperacute (0-6 hrs) - primary MR abnormality is reduced diffusivity
  • Acute (6-72 hrs) - reduced diffusion, cortical T2 hyperintensity, increasing mass effect.
  • Early subacute (1.5-5 days) - less restricted diffusion, T2 hyperintensity extends to white matter, mass effect peaks
  • Late subacute (5 days - 2 wks) - diffusivity normalizes, gyral enhancement, resolution of mass effect.
  • Chronic - increased diffusivity, cystic encephalomalacia, no mass effect
18
Q

Hyperacute Infarct

Timeline?

What are the molecular occurrences within minutes of critical ischemia?

What is the most sensitive imaging modality?

Diffusion is reduced in an acute infarct for what 2 reasons?

FLAIR appearance of hyperacute infarct?

Perfusion imaging findings?

A
  • 0–6 hours (Note - same timeline as hyperacute hematoma)
  • Within minutes of critical ischemia, the sodium-potassium ATPase pump that maintains the normal low intracellular sodium concentration fails. Sodium and water diffuse into cells, leading to cell swelling and cytotoxic edema.
  • Calcium also diffuses into cells, which triggers cascades that contribute to cell lysis.
  • By far the most sensitive imaging modality for detection of hyperacute infarct is MRI diffusion-weighted imaging. DWI hyperintensity and ADC map hypointensity reflect reduced diffusivity, which can be seen within minutes of the ictus.
  • Diffusion is reduced in an acute infarct by two factors:
    • Shift from extracellular to intracellular water due to Na/K ATPase pump failure.
    • Increased viscosity of infarcted brain due to cell lysis and increased extracellular protein.
  • FLAIR may be normal. Subtle hyperintensity may be seen on FLAIR images in the hyperacute stage. These changes are seen less than two-thirds of the time within the first six hours.
  • Perfusion shows decreased cerebral blood volume of the infarct core, with or without a surrounding region of decreased cerebral blood flow, which represents the penumbra.
19
Q

Acute Infarct

Timeline?

What is this phase characterized by?

What is there an increased risk of during this phase? Why?

Imaging appearance?

FLAIR, DWI, Perfusion findings?

A
  • 6 hours–72 hours (note - same timeline as acute hematoma)
  • The acute infarct phase is characterized by an increase in vasogenic edema and mass effect. Damaged vascular endothelial cells cause leakage of extracellular fluid and increase the risk of hemorrhage.
  • On imaging, there is increased sulcal effacement and mass effect. The mass effect peaks at 3-4 days, which is an overlap time between the acute and early subacute phases.
  • MRI shows hyperintensity of the infarct core on T2-weighted images, best seen on FLAIR. The FLAIR abnormality is usually confined to the gray matter. DWI continues to show restricted diffusion.
  • There may be some arterial enhancement, due to increased collateral flow.
  • Perfusion images most commonly show an increase in the size of the infarct core with the resultant decrease in the size of the penumbra.
20
Q

Early Subacute Infarct

Timeline?

What happens to blood flow to the region of infarct?

Mass effect?

FLAIR appearance? Contrast this to acute stage.

ADC, DWI and perfusion findings?

A
  • 1.5 days–5 days
  • In the early subacute phase, blood flow to the affected brain is re-established by leptomeningeal collaterals and ingrowth of new vessels into the region of infarction.
  • The new vessels have an incomplete blood-brain barrier, causing a continued increase in vasogenic edema and mass effect, which peaks at 3-4 days.
  • MR imaging shows marked hyperintensity on T2-weighted images involving both gray and white matter (in contrast to the acute stage, which usually involves just the gray matter).
  • The ADC map becomes less dark or even resolves if there is extensive edema; however, the DWI images typically remain bright due to underlying T2 shine through.
  • Perfusion imaging shows continued expansion of the infarct core and further reduction in the ischemic penumbra.
21
Q

Late Subacute Infarct

Timeline?

This phase is characterized by what?

Key imaging finding? How to differentiate this with a tumor?

What is the “2-2-2” rule?

DWI, ADC, T2 appearances?

A
  • 5 days–2 weeks
  • The subacute phase is characterized by resolution of vasogenic edema and reduction in mass effect.
  • A key imaging finding is gyriform enhancement, which may occasionally be confused for a neoplasm. Unlike a tumor, however, a subacute infarction will not typically demonstrate both mass effect and enhancement simultaneously. Enhancement can be seen from approximately 6 days to 6 weeks after the initial infarct. The enhancement of a subacute infarct has also been described by the “2-2-2” rule, which states that enhancement begins at 2 days, peaks at 2 weeks, and disappears by 2 months.
  • DWI may remain bright due to T2 shine through, although the ADC map will either return to normal or show increased diffusivity.
22
Q

Chronic Infarct

What happens molecularly during the chronic stage of infarcts?

Infarct involvement of the corticospinal tract may lead to what image finding? These changes are first seen when?

DWI appearance?

Instead of encephalomalacia, what else can occur? Histologic and MR appearance of this?

A
  • In the chronic stage of infarction, cellular debris and dead brain tissue are removed by macrophages and replaced by cystic encephalomalacia and gliosis.
  • Infarct involvement of the corticospinal tract may cause mass effect, mild hyperintensity on T2-weighted images, and eventual atrophy of the ipsilateral cerebral peduncle and ventral pons due to Wallerian degeneration. These changes can first be seen in the subacute phase, with atrophy being the predominant feature in the chronic stage.
  • DWI has usually returned to normal in the chronic stage.
  • Occasionally, cortical laminar necrosis can develop instead of encephalomalacia.
  • Cortical laminar necrosis is a histologic finding characterized by deposition of lipidladen macrophages after ischemia that manifests on imaging as hyperintensity on both T1- and T2-weighted images.