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Brain Power: Adam and Victor's Neurology > Cerebrovascular > Flashcards

Cerebrovascular Flashcards

1
Q

What level of cerebral blood flow causes an infarction almost regardless of its duration?

A

Below 10-12 ml/100g/min

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2
Q

What is the usual level of cerebral blood flow?

A

55ml/100mg/min

12-23 slow EEG

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3
Q

What molecular mechanisms lead to cell death in ischemia?

  1. Failure of ATP
  2. Free radical formation
  3. Excitatory neurotransmitters
A
  1. Failure of ATP production –> lactic acid accumulation
  2. Formation of free radicals –> peroxidation and disruption of the outer cell and mitochondrial membranes
  3. Glutamate and aspartate releaed by ischemic cells cause intracellular influx of Na and Ca
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4
Q

What are Hollenhorst plaques?

A

Crystalline cholesterol sloughed off from an atheromatous ulcer

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5
Q

What is the size range of the arteries occluded in lacunar strokes? And what is the size range of the cavities that they produce?

A

50-200 microns

3-15 mm in diameter

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6
Q

What are the 3 kinds of lacunar infarctions?

A
  1. Fibrohyaloid arteriolar sclerosis
  2. Atherosclerosis of a large trunk vessel that occludes the origin of these same vessels
  3. Emboli of small arteries
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7
Q

List the most common location of lacunes in descending order of frequency

A
  1. Putamen and Caudate nuclei
  2. Thalamus
  3. Basis pontis
  4. Internal capsule
  5. Deep in the central hemispheral white matter

Mnemonic: Going down then going up

COMPARE WITH MOST COMMON LOCATION FOR ICH:

  1. Putamen and adjacent internal capsule 50%!
  2. Lobar hemorrhage!!!!
  3. Thalamus
  4. Cerebellar hemisphere
  5. Pons

Mnemonic: Just going down

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8
Q

What locations are associated with the following lacunar stroke syndromes?

  1. Pure motor hemiplegia
  2. Pure sensory stroke
  3. Clumsy hand-dysarthria
  4. Ipsilateral hemiparesis-ataxia
A
  1. Internal capsule or adjacent corona radiata
  2. Lateral thalamus or adjacent parietal white matter
  3. Paramedian midpons on the opposite side of the clumsy hand
  4. Pons, midbrain, internal capsule
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9
Q

How to differentiate pontine lacune from supratentorial lacune?

A

Sparing of the face and the presence of ipsilateral paresis of the conjugate gaze

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10
Q

According to the NASCET and ECST what degree of stenosis necessitates carotid endarterectomy?

A

70-80%

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11
Q

What is the most common symptom of hyperperfusion syndrome from carotid endarterectomy?

A

Unilateral severe headache

Other: Headache, Focal deficits, Seizures, Brain edema, Brain hemorrhage

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12
Q

T or F: Asymptomatic carotid stenosis of more than 60-70% in men may benefit from sugery in terms of stroke reduction.

A

T

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13
Q

What percentage of embolic infarcts develop seizures?

A

10

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14
Q

What is AKA arteriosclerosis dementia?

A

Binswanger subcortical leukoencephalopathy

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15
Q

How much stroke is prevented by atorvastatin according to the SPARCL trial?

A

3%

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16
Q

What is the Raeder syndrome?

A

ICA dissection syndrome composed Ipsilateral Horner syndrome + Unilateral headache

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17
Q

What is the most common origin of vertebral artery dissection?

A

C1-C2 where it is mobile but tethered

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18
Q

What arterial dissection can cause SAH?

A

Vertebral artery

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19
Q

What are the two components of Moyamoya?

A
  1. Cerebral rete mirabile: small anastomotic vessels around and distal to the circle of Willis
  2. Segmental stenosis or occlusion of the terminal intracranial parts of both internal carotid arteries
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20
Q

What are the 3 main components of Binswanger disease?

A

Dementia, pseudobulbar state, gait disorder

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21
Q

What are the top differentials for ischemic stroke in the young?

A

Dissection
Drugs (Contraceptives and Shabu)
APAS
PFO

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22
Q

What is the hispathology of the thrombotic vessel in a patient with a stroke?

A

Nodular intimal hyperplasia of eccentric distribution with increased mucopolysaccharides and replication of the internal lamina

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23
Q

What percentage of primary intracerebral hemorrhages are multiple?

A

2%

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24
Q

What are the most common sites for hypertensive hemorrhages?

A
  1. Putamen and adjacent internal capsule 50%!
  2. Lobar hemorrhage!!!!
  3. Thalamus
  4. Cerebellar hemisphere
  5. Pons

COMPARE WITH MOST COMMON SITES FOR LACUNAR INFARCTION

  1. Putamen and Caudate nuclei
  2. Thalamus
  3. Basis pontis
  4. Internal capsule
  5. Deep in the central hemispheral white matter
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25
Q

What is the spot sign?

A

Appearance of contrast within the hemorrhage during the CT angiography, associated with a high rate of hematoma expansion

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26
Q

What part of the hematoma causes it to become bright on T1 and dark on T2?

A

Formation of deoxyhemoglobin and methemoglobin

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27
Q

What is the term used to describe the arteriolar wall in hypertensive patients with bleeds?

A

Segmental lipohyalinosis

Primary HTN hemorrhages are also associated with the flase aneurysm Charocot Bouchard

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28
Q

What is the risk of rupture for unruptured aneurysms?

A

25mm 10%

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29
Q

Identify which age period the following CVD occur:

  1. MELAS
  2. etat marbe: Cardiorespiratory failure and generalized ischemia
  3. Binswanger disease
  4. Unilateral cerebral infarction
A
  1. Infancy and childhood
  2. Perinatal and postnatal circulatory disorders
  3. Late Adult
  4. Prenatal
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30
Q

What component of the LP conferes the most risk for stroke?

A

LDL followed by TG

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31
Q

What are the top 3 sites for atheromatous plaques?

A
  1. ICA at the origin from the common carotid artery
  2. cervical part of the vertebral arteries at the junction to form the basilar
  3. in the stem or at the bifurcation of the MCA
  4. Proximal PCA
  5. Proximal ACA
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32
Q

What is a more common cause of stroke atherothrombosis or embolism?

A

Embolism

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33
Q

What is the critical residual lumen in the ICA before stroke occurs?

A

<2mm (Normal size is 5-10mm of the ICA)

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34
Q

What comprises the CHA2DS2-VASC scoring?

A 
Congestive heart failure
Hypertension
Age >65 
>75 2 points
Diabetes
Sex
Stroke 2 points
Peripheral or coronary disease
35
Q

What is the risk for stroke with a patient with PFO?

A

2% if with septal aneurysm it balloons to 15%

36
Q

What is the mechanism for stroke in Osler Weber Rendu disease?

A

Pulmonary shunts results in conduits for stroke to the brain

37
Q

Prior to CNS symptoms how do fat emboli present?

A

Pulmonary symptoms followed by dermal petechial hemorrhages

38
Q

What is the 5 year risk of stroke for TIA patients?

39
Q

What is the ABCD score?

A 
Age >= 60 1pt
Blood pressure >=140/90 1 pt
Clinical
Hemiparesis 2pts
Speech impairment without weakness 1 pt
Duration
>60 2 pts
10-59 1 pt
<10 0 pt
Diabetes 1 pt
40
Q

A bruit at the angle of the jaw is indicative of?

A

Occlusion at the proximal internal carotid artery

41
Q

Enumerate the sturctures affected and symptoms

  1. Nothnagel
  2. Parinaud
  3. Avellis
  4. Jackson
A
  1. Tectum of midbrain, superior cerebellar peduncles, cranial nerves 3 and/or 4: frozen eyes, ataxia
  2. No accomodation, no upward gaze, light near dissociation of pupils, eyelid retraction, Convergence retraction nystagmus
  3. Tegmentum of medulla (10, spinothalamic, sympathetic fibers): soft palate, vocal cord and contralateral anesthesia
  4. Avellis plus tongue paralysis
42
Q

What is the most common mechanism for the formation of lacunes?

A

Fibrohyalinoid arteriolar sclerosis

43
Q

T or F about fibromuscular dysplasia

  1. Most are male
  2. Radiologic picture is made up of irregular string of beads or a tubular narrowing
  3. Symptomatic arteries are treated with endarterectomy
A
  1. F
  2. T
  3. F– they are excised if symptomatic and observed if not
44
Q

What is the Raeder syndrome and what pathology is it associated with?

A

Ipsilateral horner and unilateral headache associated with dissection

45
Q

The string sign and the double lumen sign both pertain to?

A

Carotid artery dissection

46
Q

What are the pathological findings in dissection?

A

Cystic medial necrosis and disorganizatino of the media and internal elastic lamina

47
Q

Where is the most common location of vertebral artery dissection?

A

As it originates in the C1-C2 segment of the vessel where it is mobile but tethered

48
Q

What is the treatment for dissection?

A

Steroids for the pain

Anticoagulation for several weeks or months

49
Q

What is the angiographic picture of Moya2?

A

Segmental stenosis or occlusion of the terminal intracranial parts of both ICAs + small anastomototic vessels at the base of the brain around and distal to the circle of Willis

50
Q

What is the most common initial manifestaiton of Moya2 in older individuals?

51
Q

What layer of the vessel is affected by Moya2?

A

Intima

Similar to vessels of patients with OCP related strokes

52
Q

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is associated with what kind of headache? Also what the characteristic location of the lesions?

A

Migraine.

Anterior temporal lobes

53
Q

T or F Protein C Protein S and antithrombin 3 levels are depressed after stroke so detected abnormalities NEED TO BE CONFIRMED MONTHS LATER AND IN THE ABSENCE OF ANTICOAGULATION

54
Q

What gene is affected in CADASIL?

55
Q

Chronic basal meningitis include the ff:

A
  1. TB men
  2. Fungal med
  3. Meningovascular syphillis
56
Q

What layer of the vessel is affected in women who take oral contraceptives?

A

Internal Elastic Lamina: nodular intimal hyperplasia

Similar to moya2

57
Q

What conditions further predispose women on OCPs to stroke?

A
  1. Smoking
  2. age over 35 years old
  3. Migraine
58
Q

What dose of OCPs give a preponderance to stroke?

A

High dose estrogen pills 0.5mg

59
Q

A spinal tap is enough to rule out SAH if the tap is taken AT LEAST how many minutes from the index event?

A

30 minutes

60
Q

Several days after aneurysmal rupture occurs what modalities can be relied upon to say that an SAH really occured?

A

MRI flair and CSF with xanthochromia after centrifugation

61
Q

Why is MRA not recommended for localizing aneurysms?

A

It only shows the basal vessels and the first branches. Distal aneurysms will not be seen.

62
Q

What time does delayed plegia and other deficits because of focal vasospasm appear in patients with SAH?

A

3-10 days post ictus

63
Q

What is the critical velocity of blood flow is vasospasm probably occuring?

64
Q

Match the location of the aneurysm:

  1. 3rd nerve palsy
  2. Transient paresis of both lower extremities
  3. Hemiplegia or aphasia
  4. Retained consciousness with akinetic mutism
A
  1. Pcomm
  2. Acomm
  3. First major bifurcation of the MCA
  4. Acomm
65
Q

Terson syndrome is?

A

Unilateral preretinal Subhyaloid hemorrhage on the side of the SAH

66
Q

What are the first clinical manifestations of AVM?

A

50% SAH
30% Seizure
20% Headache

67
Q

What is the spletzer martin grade?
5cm aneurysm
Non eloquent area
With deep venous drainage

A 
0-3cm 1
3-6cm 2
6cm or more 3
Eloquent 1
Deep venous drainage 1

Grade 1-2 Surgical
Grade 3 Embolization with surgery
Grade 4-5 NOT surgical

68
Q

What is the ideal size for radiosurgery

A

<3cm but effects at 18-24 months!

69
Q

What is the definition of dural AVF

A

Nidus of abnormal arteries and veins the AV shunting contained completely in the leaflets of the dura. Arteries are dural arterial vessels from the ICA while the drainage is to the dural venous sinus

70
Q

What dural AVF’s are at risk for bleeding?

A

Those at the anterior cranial fossa and tentorial incisura

71
Q

What is the risk for bleeding and rebleeding in brainstem cavernomas?

A

B 5%

R 30%

72
Q

What is the most common cerebral vascular malformation?

A

Deep venous anomaly; caput medusa draining into a small collecting vein

73
Q

How does giant cell temporal arteritis cause blindness?

A

Involvement of the ophthalmic artery

74
Q

What is the treatment for giant cell temporal arteritis that can prevent blindness?

A

Prednisone 50-75mg per day

75
Q

What is the rate of brain involvement with PAN and Churg Strauss angiitis?

76
Q

What are the 2 neurologic manifestations of Wegener Granulomatosis?

A
  1. Mononeuropathy multiplex

2. Multiple craniopathies from direct extension of nasal sinus granulmoas into the skull base

77
Q

What are the two main CNS manifestations of SLE that resemble MS?

A
  1. Longitudinally extensive myelopathy

2. White matter changes “lupus sclerosis”

78
Q

What kind of cocaine causes CVD bleed? Infarct?

A

Bleed: cocaine hydrochloride
Infarct: Alkaloid form or crack cocaine

79
Q

What is the triad of Bechet disease?

Neuro symptoms include: CN palsies, meningoencephalitis, venous occlusion

A
  1. Relapsing iridiocyclitis
  2. Recurrent genital ulcers
  3. Recurrent oral ulcers
80
Q

What part of the brain is affected in thrombosis of:

  1. Labbe
  2. Trolard
A
  1. Superior temporal lobe

2. Parietal cortex

81
Q

What is the usual dominant transverse sinus found in more than half of individuals?

A

Right; 1/4 are symmetric

82
Q

Bilateral thalamic infarct can be from what form of CVD?

A

Venous infarct of the deep cerebral vein (Vein of Galen)

83
Q

Identify the deficits

  1. Anton’s sydnrome
  2. Balint’s syndrome

A. Bilateral PCA
B. PCA-MCA Borderzone

#Bilateral visual loss with denial of blindness and confabulations or visual hallucinations
@ Optic ataxia, oculomotor ataxia, simultagnosia

Brain Power: Adam and Victor's Neurology (19 decks)

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