Neuro -- Vascular/ischemic

Front 1

Describe the typical patterns of subarachnoid hemorrhage that may suggest the location of the ruptured aneurysm.

Back 1

1. Anterior communicating artery: interhemispheric fissure.
2. Posterior communicating artery: ipsilateral basal cisterns.
3. MCA trifurcation: sylvian fissure
4. Basilar tip: interpenduncular fossa, intraventricular
5. PICA: posterior fossa cisterns, intraventricular.

Front 2

What are the complications of subarachnoid hemorrhage?

Back 2

- Communicating hydrocephalus
- Vasospasm leading to infarcts.

Front 3

1. What conditions place a pt at increased risk of aneurysms?
2. What are the common locations of aneurysms?

Back 3

1.
- Adult polycystic kidney disease
- Marfan syndrome
- Ehler's Danlos
- FMD
- Family h/o aneurysm
2.
- ACom = 30-35%
- PCom = 30-35%
- MCA trifurcation = 20%
- Top of basilar artery = 10%
- PICA = 3%
- More distally located aneurysms are associated with trauma and infection.

Front 4

1. What is a giant aneurysm?
2. What are common presentations of a giant aneurysm?
3. What are the imaging findings of giant aneurysm?

Back 4

1. > 2.5cm in diameter. Giant aneurysms most frequently occur in the cavernous and supraclinoid carotid segments.
2.
- Subarachnoid hemorrhage
- Mass effect
- Embolic events related to thrombus formation within the lumen of giant aneurysm.
3.
- Intrinsically dense lesion prior to contrast due to hyperdense thrombus.
- Peripheral/rim calcification.
- On MRI, lamellated thrombus is characteristic.
- Phase artifact can be seen if there is flow within a residual lumen.

Front 5

1. What is a limitation of TOF MRA?

Back 5

1. Methemoglobin within a thrombosed vessel may mimic flow on TOF MRA because of shine through due to clot's intrinsic high signal intensity. However, phase contrast MRA resolve this problem

Front 6

1. What is benign perimesencephalic hemorrhage (perimesencephalic non-aneurysmal subarachnoid hemorrhage)?
2. What are some causes of a negative 4 vessel catheter angiogram?
3. Bleeding in what territory mimics benign perimesencephalic hemorrhage?

Back 6

1.
- Non-aneurysmal subarachnoid hemorrhage. The source of bleeding in PNSH is considered to be venous.
- Hemorrhage is located immediately anterior to the midbrain or within the pre-pontine cistern.
- Absence of intraventricular hemorrhage.
2.
- PNSH
- Occult aneurysms
- Occult arteriovenous malformations
NOTE: Aneurysms and AVMs may be concealed by vasospasm, adjacent hematoma, thrombosis (partial or complete), or small size. Therefore if you have a negative cerebral angiogram in a patient who has had a subarachnoid hemorrhage, angiogram is typically repeated.
3. Aneurysm rupture from the posterior circulation can mimic pattern of benign perimesencephalic hemorrhage in about 10% of cases.

Front 7

1. What are the different types of strokes?
2. What other causes of intracranial hemorrhage?
3. What are the complications of stroke?
4. How many days after an acute stroke is restricted diffusion seen?

Back 7

1. Strokes are broadly divided into ischemic and hemorrhagic. Ischemic strokes in further divided to thrombotic and embolic events.
- Large vessels thromboembolic events (50%)
- lacunar infarcts (25%)
- cardiogenic emboli (15 to 20%)
- vasculitis/vasculopathy (5%)
- subarachnoid hemorrhage leading to vasospasm
- venous infarcts resulting from thrombosis.
2.
- Hypertension
- amyloid angiopathy
- tumors (primary or metastatic)
- vascular malformations
- hemorrhagic stroke/venous infarct
3.
-Hemorrhagic transformation
-brain herniation with secondary infarction and/or hydrocephalus.
4. Reduced diffusion persists for approximately 10 days post infarction.

Front 8

1. What are the clinical findings of stroke in the MCA territory?
2. What are the clinical findings of stroke in the ACA territory?
3. What are the clinical findings of stroke in the PCA territory?
4. What are the clinical findings of stroke in the cerebellum?
5. What are the clinical findings of stroke in the brain stem?

Back 8

1. Contralateral hemiparesis and sensory loss and possibly homonymous hemianopia. Aphasia occurs of infarction is in the dominant hemisphere while confusion neglect occurs at the infarction is in the nondominant hemisphere.
2. Contralateral leg weakness and hemisensory loss.
3. Unilateral PCA infarct results in hemianopia while bilateral involvement results and cortical blindness and memory loss. If the top of the basilar artery is involved, the presentation is thalamic sensory deficits, impaired arousal, and cranial nerve deficits.
4. Ataxia and dysmetria
5. Cranial nerve dysfunction, ataxia, somnolence

Front 9

1. What are the imaging findings of hyperacute stroke (<6 hours)?
2. What are the imaging findings of acute stroke (6-24 hours)?
3. What are the imaging findings of early subacute stroke (1-7 days)?
4. What are the imaging findings of late subacute stroke (1-6 weeks)?
5. What are the imaging findings of chronic stroke (> 6 weeks)?

Back 9

1. HYPERACUTE, less than 6 hours
CT scan:
-Hyperdense MCA
-Subtle obscuration of the insular ribbon
MRI:
-Absent flow void
-abnormalities of diffusion and perfusion

2. ACUTE, 6 to 24 hours
CT scan:
-Loss of the insular ribbon
-obscuration of the lentiform nucleus
-sulcal asymmetry
-loss of gray-white matter differentiation
MRI:
-Sulcal effacement
-T1 hypointensity and T2 hyperintensity in gray matter> white matter

3. EARLY SUBACUTE (1 to 7 days)
- hemorrhagic transformation may occur during this time interval.
- Maximum mass-effect is seen at 3 to 7 days
CT scan:
-Progressive swelling
-onset of parenchymal enhancement
MRI:
-Progressive swelling
-onset of parenchymal and/or meningeal enhancement

4. LATE SUBACUTE (one to 6 weeks)
-swelling present resolves
- contrast enhancement peaks
-fogging effect: refers to increase in density of the infarcted tissue towards isodensity as a consequence of capillary ingrowth, macrophage invasion, and small petechial hemorrhages. Therefore a subacute infarct may be invisible on a nonenhanced CT scan.

5. CHRONIC
-resolution of mass effect
-resolution of parenchymal enhancement
-presence of volume loss
-evidence of Wallerian degeneration

Front 10

1. Under what clinical circumstances do watershed infarctions occur?
2. Where are the watershed regions located?

Back 10

1. Watershed infarction two she occur in the setting of systemic hypotension with a background of pre-existing vascular disease.
2.
-Frontoparietal (ACA-MCA)
-Temporoccipital (MCA-PCA)

Front 11

What is a differential diagnosis of bithalamic hyperintensities?

Back 11

1. Bithalamic infarctions: Secondary to occlusion of small perforating arteries that supply the paramedian thalami bilaterally (arteries of Percheronartery of percheron (common vascular trunk from P1 segment of PCA).
2. Deep venous thrombosis: Look for occlusion of the straight sinus, vein of Galen.
3. Wernicke's encephalopathy:
4. Extra pontine myelinolyses: accompanied by central pontine myelinolysis.
5. Bithalamic tumors

Front 12

1. What is the reason to do perfusion imaging?
2. How is perfusion imaging performed?
3. What 3 parameters are used in perfusion studies?

Back 12

1. Perfusion imaging is done to evaluate the penumbra (tissue at risk for infarction).
2. Monitor the first pass of a contrast agent bolus through the cerebral vasculature. For MRI perfusion, multiple echo-planar images are made with a high temporal resolution.
T2* gradient sequences are used to maximize the susceptibility signal changes.
3.
- Cerebral blood volume
- Cerebral blood flow
- Mean transit time

Front 13

1. What is the sequela of arterial dissection?
2. What is the classic location for an ICA dissection/vertebral artery dissection?
3. What are the imaging findings on MRI?
4. What are the predisposing conditions for development of dissection?

Back 13

1.
-Infarction may occur secondary to a low flow state induced by luminal compromise or vascular thromboembolic events.
-Pseudoaneurysm formation.
2.
- Typical extracranial ICA dissection extends from just beyond the carotid bulb to the level of the carotid canal. Rarely, ICA dissection extends intracranially.
- Vertebral artery dissection typically involves the distal segment extending from C2 to the skull base.
3.
- Narrowed eccentric flow void surrounded by semilunar hyperintense signal that represents intramural hematoma.
4. Marfan syndrome, fibromuscular dysplasia, Ehlers-Danlos syndrome, hypertension, kinking or coiling of the ICA.

Front 14

1. What are the common sites of hypertensive hemorrhage?
2. What is the appearance of remote hypertensive bleeds?
3. What can subacute hematomas be confused with on postcontrast images?

Back 14

1. Hypertensive hemorrhages typically occur in areas supplied by penetrating branches of the middle cerebral artery, posterior cerebral artery, and basilar artery. Therefore, common sites include the putamen (65%), thalamus (20%), pons (10%), cerebellum (5%).
2. Because hematomas dissect brain tissue rather than causing infarction and tissue necrosis, remote hypertensive bleeds typically appear as slitlike cavities with hemosiderin staining.
3. Subacute hematomas may demonstrate ring enhancement and therefore mimicked tumor or abscess on postcontrast images.

Front 15

1. What are the etiologies of anoxia or a severe hypoxic/ischemic insult?
2. Is the gray matter or the white matter more affected by anoxia/ischemia?
3. What are the imaging findings of acute anoxic/severe hypoxic/ischemic injury?
4. What or the imaging findings of chronic anoxic/severe hypoxic ischemic injury?
5. High density of vascular structures in contrast to the hypodense parenchyma in a patient with global anoxic injury may mimic?

Back 15

1.
-Cardiorespiratory arrest
-near drowning
-drug overdose
-status epilepticus
-trauma
2. Since the gray matter is more metabolically active, the cortical gray matter and deep gray matter are affected more profoundly.
3.
-Loss of gray-white matter differentiation
-hypoattenuation of the basal ganglia and cortex
-effacement of cortical sulci and basilar cisterns
-petechial hemorrhage in the cortex and basal ganglia
-" reversal sign": Hemispheric white matter is more dense and cortex. The cerebellum may also demonstrate increased attenuation (white cerebellum sign).
4.
-Global parenchymal volume loss
-shrunken basal ganglia
5. Hyperdensity of the vascular structures and dural reflections in patients with global anoxic injury may mimic subarachnoid or subdural hemorrhage. The hyperdensity is due to venous stasis.

Front 16

1. What are the imaging findings of cavernous malformation? What are they associated with?
2. What is the appearance of venous malformation?
3. What is the appearance of arteriovenous malformation?
4. What is the appearance of capillary telangiectasia?

Back 16

1. Round or multilobulated lesion that shows popcorn pattern of high signal intensity on T1 and T2 weighted images. Surrounding hemosiderin rim with blooming on gradient echo images. Typically no mass effect or edema unless there has been recent hemorrhage. Angiographically occult. Cavernomas are associated with venous malformations.
2. Medusa head appearance of small venous radicles draining into a larger vein which may drain into a subependymal or subpial vein. Adjacent brain may be normal or show gliotic changes. Occult on noncontrast studies. Does not lead to hemorrhage unless associated with cavernoma.
3. Cluster of flow-voids represents the nidus. Adjacent brain is gliotic and may have hemosiderin staining.
4. Only identified on post contrast images as a faint blush usually located in the pons. Gradient echo sequences may show mild hypointensity.

Front 17

What is the differential diagnosis of parenchymal hematoma?

Back 17

1. Hypertensive hemorrhage
2. cavernous malformation
3. underlying neoplasm
4. amyloid angiopathy
trauma
dural sinus thrombosis
aneurysm rupture
coagulopathic hemorrhage

Front 18

1. What are the two types of carotid cavernous fistula?
2. What are the clinical findings of carotid-cavernous fistula?
3. Described the anatomy of the cavernous sinus.
4. What are the imaging findings of carotid-cavernous fistula?

Back 18

1.
Direct carotid-cavernous fistula:
- Fistulous communication between the internal carotid artery itself and the cavernous sinus.
- Usually due to trauma, intracavernous rupture of an ICA aneurysm
- high flow lesions
Indirect carotid cavernous fistula:
- Fistulous communication between meningeal branches of the ICA or the ECA and the cavernous sinus.
- Usually occur spontaneously
- low flow lesions.
2. Pulsatile exophthalmos, bruit, conjunctival chemosis.
3. Cavernous sinus mass he is venous blood from the superior and inferior ophthalmic veins and the sphenoparietal sinus. Blood then flows from the cavernous sinus into the jugular vein via the inferior petrosal sinus. The cavernous sinuses may communicate with each other via the intracavernous sinus and the cavernous sinuses may also communicate with cortical veins.
4.
-Prominent superior ophthalmic vein
-marked dilatation and enhancement of the cavernous sinus
-reversal of blood flow away from the cavernous sinus maybe demonstrate low with phase contrast MR angiography. Flow will be reversed in the superior ophthalmic veins and a dilated cortical veins.
-On angiography: Rapid opacification of the cavernous sinus during the arterial phase.

Front 19

1. What is a dural arteriovenous fistula?
2. What are the imaging findings of DAVFs?
3. What is the most common location of DAVFs?
4. How are DAVFs classified?

Back 19

1. Direct communication b/w DURAL arteries and dilated venules without intervening capillaries. Most are associated with underlying dural sinus thrombosis.
2.
- Multiple enlarged, tortuous vessels found on the surface of the brain.
- WM signal abnormalities may be seen on T2WI due to gliosis from venous HTN.
3. Posterior fossa (the occipital artery).
4. Classified according to their pattern of venous drainage. DAVFs may drain into sinuses, cortical vein, or spinal perimedullary veins.

Front 20

1. Vasculitis occurs under what three settings?
2. What are the imaging findings in vasculitis?
3. Does a negative angiogram or brain bx r/o vasculitis?

Back 20

1.
- Primary angiitis of the CNS (PACNS)
- Complication of rheumatic or vasculitic d/o (SLE, Wegener's)
- Infection/Toxin exposure.
2.
- Multifocal infarcts
- Scattered hypoattenuation on CT/T2 hyperintensity in the deep white matter and cortex.
- +/- parenchymal enhancement
- WM abnormalities may be masslike and mimic neoplasia.
- Segmental narrowing or beading of vessels.
3. Vasculitis involves segments of the brain and thus bx may show false negative results if the bx is not directed to an area of active disease. Also, a negative angiogram does not exclude vasculitis as the vasculitis may involve small vessels not evaluated well with angiogram.

Front 21

1. What arteries are most commonly affected by FMD?
2. What are the three imaging patterns of FMD?
3. How do you distinguish FMD from atherosclerotic disease?
4. What is the DDX of beaded or smooth narrowing of vessels?

Back 21

1. Renal, cervical ICA, and vertebral arteries. Intracranial involvement is rare.
2.
- String of beads: most common pattern consisting of constricting alternating with normal appearing or dilated segments (associated with medial FMD).
- Elongated tubulostenotic pattern.
- Aneurysmal form: eccentric outpouching which may progress to aneurysm formation. It may be difficult to distinguish from atherosclerotic aneurysm or traumatic pseudoaneurysm.
NOTE: the angiographic appearance may evolve over time with transition from a string of beads pattern to an elongated tubulostenotic pattern.
3. FMD typically spares the vascular origins.
4.
- Intracranial aneurysm (20-50%)
- Spontaneous carotid artery dissection
- Carotid artery aneurysm formation.
- Spontaneous arteriovenous fistula.
4.
- Standing waves (regular, evenly spaced appearance with normal caliber b/w areas of constriction)
- Catheter induced spasm (transient)
- Atherosclerosis (typically eccentric, irregular)
- Dissection (typically smooth narrowing)
- Takayasu arteritis: smooth narrowing affecting the large and mid sized vessels.

Front 22

1. What arteries are involved in Takayasu's arteritis?
2. What are the imaging findings?
3. What are the complications?
4. What is the DDX of smooth narrowing of a medium sized artery?

Back 22

1. Affects large- and medium-sized arteries such as aortic arch and its branches.
- Aorta, CCA, subclavian, renal, and pulmonary arteries are typically affected.
2.
- Circumferential vessel wall thickening with reduction in luminal caliber.
- Vascular occlusion may occur resulting in cerebral ischemia/infarction.
- Chronic inflammation may weaken vessel wall resulting in aneurysm.
3.
- Cerebral ischemia/infarction from stenosis/occlusion.
- Renovascular HTN
- Arm claudication
- Aneurysm formation
4. Takayasu arteritis, giant cell arteritis, FMD (fibrostenotic), dissection.

Front 23

1. What is Moyamoya disease?
2. What are the imaging findings?
3. What are the two types of Moyamoya disease?

Back 23

1. Chronic occlusive cerebrovascular d/o leading to progressive stenosis of the arteries of COW. Initially involves the supraclinoid ICA but progressively involves the middle, anterior, and posterior cerebral arteries.
2.
- Enlargement of the lenticulostriate arteries present as multiple flow voids in the deep gray nuclei. On angiography, the markedly hypertrophied lenticulostriate and thalamoperforators result in a "puff of smoke" appearance.
- Leptomeningeal and transdural collaterals may also develop from the ECA.
- Multiple bilateral infarcts of varying ages.
- Parenchymal hemorrhage more common in adults.
3.
- Primary moyamoya disease: idiopathic bilateral stenosis of arteries of COW.
- Secondary Moyamoya: may be related to sickle cell disease, radiation vasculopathy, NF1.

Front 24

Describe the Spetzler and Martin grading system for AVM?

Back 24

Size of nidus:
- Small (< 3 cm): 1
- Moderate(3-6cm): 2
- Large (>6cm): 3

Located in eloquent region:
No: 0
Yes: 1

Venous Drainage:
Superficial: 0
Deep: 1

Front 25

1. What is the role of the vein of Galen?
2. How does the vein of Galen form? What is the etiology of vein of Galen aneurysmal malformation?
3. What is the etiology of vein of Galen aneurysmal dilatation?
4. What are the two types of VGAM?
5. What is the clinical presentation of VAGM?
6. What are the imaging findings of VAGM?

Back 25

1. Vein of Galen serves as a bridge between the deep parenchymal venous system and the venous sinuses.
2. Normally, the paired internal cerebral veins join the most inferior portion of the median prosencephalic vein to form the vein of Galen. If the median prosencephalic vein fails to regress, then it is called vein of Galen aneurysm malfomation (VGAM).
3. Dilatation (not malformation) is typically the result from a parenchymal arteriovenous malformation that drains into a normally formed but dilated vein of Galen.
4. Choroidal or Mural.
- Choroidal VGAM receives bilateral arterial supply from multiple arterial feeders.
- Mural VGAM receives arterial supply from a single artery.
5. High output CHF or hydrocephalus.
- High output CHF is seen in pts with choroidal type VAGM and presents earlier in life.
- Hydrocephalus is seen typically with mural type VAGM. Hydrocephalus is due to mass effect of aneurysm on cerebral aqueduct.
6. Round mass in the quadrigeminal plate cistern. Look for large flow void and phase encoding artifact on MRI. If thrombosed both flow void and phase encoding artifact will be absent.

Front 26

What are the imaging findings in sickle cell disease?

Back 26

- Marrow expansion with calvarial thickening.
- Parenchymal volume loss from multifocal infarctions.
- Moyamoya pattern with narrowing or occlusion of vessels in COW.
- Decrease in SI of basal ganglia on T2WI due to accelerated iron deposition.

Front 27

1. What lobes are affected by venous sinus thrombosis?
2. What are the imaging findings of sinus thrombosis?
3. How is sinus thrombosis treated?

Back 27

1.
- Superior sagittal sinus thrombosis: affects the parasagittal frontal lobes.
- Transverse sinus thrombosis: affects the temporal lobes
- Vein of Galen/straight sinus thrombosis: affects the thalami.
- Retrograde extension of thrombus into cortical and deep medullary veins can also occur and carries a worse prognosis.
2.
- Cord sign on NECT (linear density 2/2 thrombosed sinus)
- Empty delta sign on post-contrast imaging.
- Lack of flow void on T2WI and hyperintensity on T1WI 2/2 metHb.
- Absence of flow related enhancement on TOF MRV. NOTE: On TOF MRV, the T1 shortening effect of metHb can shine through and mimic a patent sinus. In this situation, phase contrast MR venography is helpful as this technique eliminates signal from stationary objects.
3. Sinus thrombosis is treated with heparinization and/or thrombolysis.

Front 28

1. What is the cause of Moya Moya disease?
2. What are the typical angiographic findings in Moya Moya disease?
3. What are the MRI findings?
4. What symptoms does it cause?
5. What is Moyamoya disease associated with?

Back 28

1. Bilateral stenosis or occlusion of the supraclinoid (ICA) that extends to the proximal portions of the ACA and MCA.
2. Angiography shows a "puff of smoke" appearance secondary to numerous collaterals supplying ACA and MCA distribution. Look for anastomosis between leptomeningeal and dural meningeal arteries.
3. MRI findings are associated with chronic ischemic changes -- including atrophy, enlarged ventricles, gliosis.
4. Moyamoya disease results in strokes and/or seizures in children.
5. Associated with Sickle cell disease, Fibromuscular dysplasia, Neurofibromatosis

Front 29

1. What is a cavernoma?
2. Are these lesions seen angiographically?
3. What is the appearance on MRI?

Back 29

1. Vascular malformation consisting of endothelial lined sinusoidal spaces without normal intervening brain.
2. No. Cavernomas are angiographically occult.
lesion
3. Popcorn-like lesions that have mixed signal intensity due to hemorrhage in different stages of evolution.
Complete hemosiderin rim.
Lesions "bloom" on T2* gradient echo and show little or no enhancemnt.
Increased incidence after radiation therapy

Front 30

1. What is sinus precranii?
2. What is the DDX?

Back 30

1.
- Venous sinus located before the cranium. It presents in the pediatric age group as a focal swelling on the scalp. MC in the frontal region.
- Represents an epicranial blood-filled nodule in the scalp that is in communication with an intracranial dural sinus through a dilated diploic vein.
- Therefore, it connects the intracranial and extracranial venous systems.
2. Lipoma, subcutaneous cyst

Front 31

Persistent Trigeminal artery (PTA)

Back 31

- PTA arises from the ICA as it exits the carotid canal and enters the cavernous sinus.
- Connects the ICA to the basilar artery.
- PTA can be of two types:
1) the artery may supply the entire vertebrobasilar system distal to the anastomosis, or
2) the anastomosis may mainly supply the superior cerebellar arteries bilaterally.
- Other persistent arteries that are responsible for communications between the carotid and vertebrobasilar systems are persistent hypoglossal and otic arteries.

Front 32

1. How are AVMs graded?
2. What complications are associated with AVMs?

Back 32

1. Spetzler-Martin system grades on the basis of size (<3 cm or >6), location (eloquent location vs. noneloquent), and venous drainage (deep or superficial).
2. AVM refers to an abnormal tangle of arterioles and venules without an intervening capillary bed.
- Venous HTN leads to enlargement of draining veins
- **Hemorrhage
- Vascular steal: Low resistance shunt steals blood from normally perfused parenchyma leading to ischemia.