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RITE > Cerebrovascular > Flashcards

Cerebrovascular Flashcards

1
Q

1) Ocular apraxia

(the inability to move the eyes volitionally, also known as sticky fixation)

2) Optic ataxia

(the inability to reach for a target under visual guidance in the absence of primary visual deficits)

3) Simultanagnosia

Inability to perceive visual fields as a whole

A

BALINT’s syndrome

-Lesion in the parietal/occipital junction BILATERAL (such as seen in posterior watershed infarcts)

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2
Q

Alexia without agraphia

A
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3
Q

Artery involved?

Ipsilateral tongue weakness

—Hypoglossal Nerve

Contralateral hemiparesis w/ facial sparing

—Pyramid

Contralateral loss of position & vibration

—Medial Lemniscus

A

Anterior spinal artery = Medial Medullary Syndrome

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4
Q

Mollaret’s Triangle

-Lesion along this circuit causes what?

A

Palatal myoclonus

  • Red nucleus, inferior olive, dentate nucleus of cerebellum
  • Dentate-rubro-thalamic pathway; Ventrolateral nucleus of the thalamus

The Triangle of Guillain-Mollaret consists of the 1) Red Nucleus to the 2) Inferior Olive via the central tegmental tract to the 3) Dentate Nucleus of the cerebellum via climbing fibers through the inferior cerebellar peduncle then back to the Red Nucleus via the superior cerebellar peduncle.

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5
Q

What artery supplies the anteroinferior portion of the caudate, putamen, and anterior limb of internal capsule?

A

Recurrent Artery of Heubner

-arises from A1 segment of anterior cerebral artery

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6
Q

What artery is occluded here?
What symptoms do you expect this patient to have?

A

Anterior Cerebral Artery

  • Contralateral Leg weakness of UMN type
  • Contralateral Leg sensory loss
  • Behavioral Problems (frontal lobe)
  • Incontinence
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7
Q

What artery(ies) caused this infarct?

A

Recurrent Artery of Heubner

Comes off A1 segment of ACA

Supplies

  1. Anterior inferior caudate
  2. Putamen
  3. Anterior limb of IC
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8
Q

Where is the aneurysm?

A

Left Anterior Cerebral Artery (anterior to genu of corpus callosum)

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9
Q

What is the likely cause of the hemorrhage?

  • Amyloid Angiopathy
  • Ruptured ACA aneurysm
  • Hypertension
  • Melanoma
A

Intraparenchymal frontal hemorrhage due to rupture ACA aneurysm that was coiled

  • SAH w/ small focal infarcts due to vasospasm
  • Most concerning complication – complete effacement of the sulci supratentorially & basal cisterns -> will lead to herniation and death if not emergently treated
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10
Q

This is:

  • L MCA dissection
  • L MCA aneurysm
  • Anatomical variant
  • Occluded R ICA
A

Anatomical variant of both ACA originating from LICA

RPCA originates from anterior circulation – (fetal origin)

No aneurysm or stenosis

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11
Q
A

MRA of COW - Axial
•1 - Anterior Cerebral

  • 2 – Middle Cerebral
  • 3 – Posterior Cerebral
  • 4 – Basilar
  • 5 – Vertebral
  • 6 – Internal Carotid
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12
Q
A

MRA of COW - Coronal
•1 - Anterior Cerebral

  • 2 – Middle Cerebral
  • 3 – Posterior Cerebral
  • 4 – Basilar
  • 5 – Vertebral
  • 6 – Internal Carotid
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13
Q
  • L ICA aneurysm
  • No flow in basilar artery
  • R MCA dissection
  • Basilar artery dissection
A

No flow in basilar artery

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14
Q
  • High grade prox L MCA stenosis
  • R carotid body tumor
  • No flow in basilar artery
  • Dolichoectatic basilar artery
A

High grade proximal MCA stenosis (loss of flow signal in proximal L MCA)

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15
Q
A

Near occlusion of superior sagittal sinus

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16
Q
A

B symmetric, parasagittal, cortical & BG venous infarctions due to thrombosis of superior sagittal sinus & deep cerebral veins

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17
Q
A

Sagittal sinus venous thrombosis – infarction w/ hemorrhage over an area of extensive cortex & in underlying white matter

*venous thrombosis assoc w/ hypercoaguable state & severe dehydration

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18
Q
A

Thrombus in Vein of Galen & Straight sinus – abnormal hyperintensity on T1 & axial proton density images; hemorrhagic infarction in B thalami

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19
Q
A

Aneurysm of vein of Galen

Time of flight – blood backing up into the posterior region of SSS which is dilated

20
Q
A

Vein of Galen aneurysm

Congenital anomaly

21
Q

64YOM was involved in a MVA and complained of neck pain. A conventional angriogram was performed. How should the man be treated?

  • Anticoagulation
  • Carotid Endarterectomy
  • Antiplatelet Therapy
  • Nothing
A

Proximal internal carotid artery has a rounded stump w/ no distal flow -> occlusion b/c of atheroslerosis

Proximal ICA occlusion from ulcerated plaque. NOT dissection or total occlusion of L ICA-> No surgery

Accident did NOT cause the findings

22
Q

64YOM was involved in a MVA and complained of neck pain. A conventional angriogram was performed. How should the man be treated?
•Anticoagulation
•Carotid Endarterectomy
•Antiplatelet Therapy
•Nothing

A

Anticoagulation

Dissection = “flame shaped” stump of ICA

23
Q

Which of the following conditions is associated w/ spontaneous dissections?
•Fibromuscular Dysplasia
•DIC
•FVL
•PFO
•Vasculitis

A

Fibromuscular Dysplasia

24
Q
A

Fibromuscular Dysplasia

String of beads

Characteristically FMD extends from C1-2 to entrance of ICA into petrous carotid canal; 1/3 are assoc. w/ intracranial aneurysms - can have spontaneous dissection

25
Q

The medial & anterior nucleus of the thalamus is supplied by what arteries?
•Thalamoperforating
•Thalamogeniculate
•Inferior Thalamic
•Postero-medial choroidal

A

Thalamoperforating

26
Q

72YOM presents w/ acute onset of L facial numbness, vertigo, ataxia, & L Horner’s syndrome

Where is the lesion?
•Left lateral pons
•Left medial medulla
•Left lateral medulla
•Right lateral medulla
•Right medial medulla
•Right lateral pons

What is the name of this syndrome?

What artery is involved?

What other clinical deficits do you expect to see?

A

Left lateral medulla

Lateral Medullary / Wallenberg

PICA or Vertebral

Other deficits:
•Contralateral Deficits in Pain & Temp in Body
•Ipsilateral Deficits in Pain & Temp in Face
•Dysphagia, Hoarseness, decreased gag reflex
•Ipsilateral ataxia
•Vertigo, nystagmus, N/V
•Ipsilateral Horner’s
•Palatal myoclonus

27
Q

73YOM w/ HTN & DM presents w/ RUE & RLE weakness. You open his mouth and boy does he have a bad case of Halitosis! DANG! But you notice his tongue deviates to the L. What other symptom might he have?

  • Decreased R body proprioception
  • Decreased L body proprioception
  • Right gaze palsy
  • Right sided hearing loss
A

Medial Medullary Syndrome

(Anterior spinal artery)

Decreased R body proprioception

Signs & Symptoms
–Ipsilateral tongue weakness
•Hypoglossal Nerve
–Contralateral hemiparesis w/ facial sparing
•Pyramid
–Contralateral loss of position & vibration
•Medial Lemniscus

28
Q

72YOM presents w/ acute onset of hearing loss, N/V, L facial numbness, vertigo, ataxia, & L Horner’s syndrome. What artery is most likely involved?
•A - PICA
•B - Vertebral Artery
•C – AICA
•D – Basilar Artery
•E – Anterior Spinal
•F – A&B

A

C- AICA

Lateral Inferior or Caudal Pontine Infarct

•AICA Infarct
–Hearing loss
–+ some Lateral Medullary syndrome signs

•PICA / Lateral Medullary Syndrome
–No hearing loss
–No weakness

•Labyrinthine artery
–Branch of AICA
–Hearing loss only

29
Q

77YOM presents w/ acute onset of L face & R body weakness, diplopia w/ a L 6th nerve palsy. Where is the lesion?

  • Midbrain
  • Pons
  • Medulla
  • Frontal lobe
  • There are two lesions
A

Pons

Millard Gubler Syndrome
•Ipsilateral lateral rectus weakness
•Ipsilateral facial weakness
•Contralateral hemiplegia (crossed hemiplegia)

30
Q

65YOM presents w/ acute onset of L sided weakness, sensory loss & an incomplete L homonymous hemianopsia. The artery occluded is:
•Right ACA
•Right PCA
•Right recurrent artery of Heubner
•Right anterior choroidal artery
•Right posterior choroidal artery

A

Anterior Choroidal Artery

•Supplies
–Internal Capsule
•Motor / Sensory
–Medial Temporal Lobes
–LGN of thalamus
•Incongruent Homonymous Hemianopsia

31
Q

Patient is blind but denies it.

What is this called?
Where is the lesion?

A

Anton’s syndrome (denial of blindness)

  • B medial occipital lobes usually from B PCA infarcts
  • Trauma to optic nerve w/ associated bifrontal lobe contusions
32
Q

Patient cannot read but can write.
What is this called?
Where is the infarct?
What other findings do you expect this patient to have?
•A- Complete R homonymous hemianopsia
•B- Color anomia
•C - Color blindness
•D - Cortical blindness
•E - Denial of blindness
•F - A&B
•G - A,B,&C
•H – All of the above

A

Alexia without agraphia

L dominant PCA infarct (splenium of corpus callosum)

R homonymous hemianopsia and Color anomia

33
Q

An ICA aneurysm is found in the cavernous sinus. What other signs or symptoms do you expect the patient to have?

A
  • Diplopia upon horizontal gaze
  • Diplopia upon vertical gaze
  • Abnormal facial sensation in the forehead
  • Abnormal facial sensation in the cheek
34
Q
A

RCVS

35
Q

One of your patients has an SAH and is more difficult to arouse the next AM. Determine the patient’s GCS…
•Opens eyes to voice
•Utters inappropriate words
•Obeys commands

A

12

36
Q

How old is this hemorrhage?
A. 5 hours
B. 2 days
C. 20 days
D. 2 months

A

20 days old

Methemoglobin – bright on T 1 & T2 occur after 4 days

Hemosiderin – gray on T1 & dark on T2 occurs during 2nd or 3rd weeks.

T2 – Bright

T1 – Bright

“BaBy”

-> 1-3 weeks (20 days)

37
Q

What blood product is this?
•Oxyhemoglobin
•Deoxyhemoglobin
•Methemoglobin
•Hemosiderin

A

Methemoglobin

(Bright on T2 and T1 = “BaBy”)

38
Q

47YOF presents with increasing confusion. 1 week ago she developed a sudden worst headache of her life. What is the probability that a CT scan will detect a SAH?
•100%
•90%
•75%
•50%
•25%

A

50%

39
Q

47YOF presents with increasing confusion. 1 week ago she developed a sudden worst headache of her life.

You decide to complete the work-up with a lumbar puncture. If this is a SAH and symptoms began 1 week ago, what is the probability of detecting xanthochromia via spectrophotometry?
•100%
•90%
•70%
•50%
•25%

A

100%

40
Q

What therapy is best suited to prevent future strokes in patients with sickle cell disease?
•Aspirin
•Warfarin
•Heparin
•Chronic Infusion Therapy

A

Chronic Infusion Therapy

Cerebrovascular disease occurs in 25% of sickle cell disease. 80% of events occur before age 15, most are caused by a progressive cerebral vasculopathy that can be partially arrested by chronic transfusion therapy to keep hemoglobin S below 30%. Most events are thrombotic.

41
Q

Patient had suffered from an acute stroke. You notice a rash on his abdomen & lower extremities. He also has a hx of kidney & heart disease. What is the treatment?
•Anti-platelet therapy
•Anti-coagulation
•Enzyme replacement
•Chronic infusion therapy

A

Enzyme replacement

Fabry’s Disease

Deficiency in Alpha galactosidase A

42
Q

CADASIL

  1. What does it stand for?
  2. Name gene mutation (incl which chromosome)
  3. Clinical features
  4. Imaging findings
  5. Skin biopsy findings
A
  1. Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts & Leukoencephalopathy
  2. Hereditary small-vessel dis 2/2 NOTCH 3 gene mutation Chrom 19
  3. TIAs/strokes most common (subcortical, Ø traditional vasc risk factors )
    Migraine w aura
    Cognitive deficits
    Psych disturbances
    Apathy, depression
    Sz, less common
    Onset in 50s
    Multiple affected family members
  4. Diffuse subcortical WM hyperintensities T2/FLAIR
    Lacunar infarcts; BG, thalamus, pons
    Anterior temporal lobe & external capsule hyperintensities
  5. Skin biopsy-Granular osmiophilic material (GOMs) within the vascular basal lamina of arteries, arterioles, and precapillaries on EM
43
Q

What is this?

What is the largest risk factor for this?

A

massive basal ganglionic hemorrhage with rupture into the ventricular system.

common for hypertensive intracerebral hemorrhage. Hypertension is a major risk factor for this type of hemorrhage

44
Q
A

The lesion is seen in the cortex of the gyri to the right of midline in this coronal section and is

typical example of laminar necrosis due to hypoxic/ischemic injury.

45
Q
A

A 1.6 x 0.9 cm mass is seen that represents a saccular aneurysm of the L internal carotid artery that projects medially.

Can treat with endovascular coil

46
Q
A

The gross findings are those of a remote hemorrhagic stroke.

Microscopically, the blood vessels of the meninges and superficial cortex showed amorphous eosinophilic material indicative of cerebral amyloid angiopathy.

47
Q

Patient presents with inability to write, right-left disorientation, acalculia, and finger agnosia.

  1. What is this syndrome called?
  2. Where is the lesion?
A

Gerstmann’s syndrome
=agraphia, finger agnosia, right-left disorientation, acalculia

Dominant (usually left) inferior parietal lobe (includes supramarginal and angular gyri)

RITE (16 decks)

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