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Comprehensive Neuro Review > Vascular Neurology > Flashcards

Vascular Neurology Flashcards

1
Q

ABCD2 Score What is it for? Components and points?

A

Predicts stroke after TIA Age > 60 (1pt) BP of 140/90 or > (1 pt) Clinical Symptoms (1pt speech w/o weakness, 2 pts focal weakness) Duration (1 pt 10-59min, 2pt 60+min) Diabetes (1pt) 2 day risk of stroke: 0% for 0-1, 1.3% for 2-3, 4.1% for 4-5, 8.1% for 6-7

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2
Q

NIHSS components

A
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3
Q

Wallenberg Syndrome

What region affected?
Vessel?
Structures and corresponding symptoms?

A

Lateral Medulla

PICA off of vertebral artery

  1. Vestibular n. = Vertigo, nystagmus, nausea, vomiting
  2. Descending tract and n. of CN V = ipsilateral facial sensation loss
  3. Spinothalamic tract = pain and temp to contralateral body
  4. 1st order sympathetics = ipsilateral Horner’s (meiosis, anhidrosis, ptosis)
  5. CN IX and X fibers = hoarseness, decreased gag, ipsilateral palate and vocal cord paralysis, dysphagia
  6. Cerebellum and cerebellar tracts = ipsilateral ataxia and lateropulsion
  7. Nucleus solitarius = ipsilateral taste
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4
Q

tPA exclusion criteria

A

Absolute contraindications

  1. Any prior ICH
  2. Severe head trauma last 3 months
  3. Known intracranial malformation or neoplasm
  4. Ischemic stroke < 3 months ago
  5. Aortic arch dissection
  6. Acute internal bleeding or bleeding at a noncompressible site in last 7 days
  7. Diatheses: Platelets < 100K, heparin w/i 48 hours, elevated aPPT, INR >1.7, PT >15
  8. DOAC in last 48 hours - BP > 185 sys or >110 dia - glucose < - INR After 3 hours: - Age >80 - Any AC at all - Hx of diabetes AND stroke - NIHSS >25

Relative Contraindications

  1. Intracranial/spinal surgery last 14 days
  2. Rapidly improving or minor symptoms
  3. Pregnancy
  4. GI or UT hemorrhage w/i 21 days
  5. Seizure at onset
  6. MI w/i 3 months
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5
Q

Thalamic blood supply

Vessels?
Symptoms?

A
  1. Tuberothalamic artery (branch of PCOM) = Anterior thalamus (VA n.)
  2. Thalamoperforating/paramedian artery (PI segment of PCA) = Medial thalamus (DM n.)
    Artery of Percheron = normal variant. Single branch off unilateral P1 supplying bilateral medial thalami
  3. Thalamogeniculate artery (branch of P2 of PCA) = Lateral Thalamus (VL n.)
  4. Posterior choroidal artery (branch of P2 off PCA) = Posterior thalamus (Pulvinar)

Can be effected by CSVT of deep veins as well

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6
Q

Recurrent Artery of Heubner

Origin? Supplies? Risks? Clinical symptoms?

A
  • Deep Branch off ACA
  • Supplies anterior limb of internal capsule, inferior head of the caudate, anterior globus pallidus
  • AT risk w/ ACA aneurysm or clipping
  • Symptoms =
    unilateral = weakness contralateral arm & face. dysarthria. hemichorea.
    bilateral = akinetic mutism.
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7
Q

ACA

Origin?
Supplies?
Infarct Symptoms?

A

Origin: ICA

Supplies:
Pre-and post ACA -> recurrent artery of huebner, deep branches = anterior limb of IC, inferior head of caudate and anterior globus pallidus
- Infarct =
unilateral = weakness contralateral arm & face. dysarthria. hemichorea.
bilateral = akinetic mutism.

Post ACA = anterior 3 quarters of the medial frontal lobe
- Infarct = leg weakness, urinary incontinence (medial micturition center)

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8
Q

MCA

Origin and branches?
Supplies?
Infarct Symptoms?

A

Origin: ICA

Branches:
Superior MCA division supplies lateral and inferior frontal gyri, parietal lobe
- Broca’s, arm and face weakness, eye deviation (FEFs), sensory loss

Inferior MCA division supplies superior temporal lobe, insula

  • Wernicke’s
  • Sensory loss in face and arm
  • Visual defects in contralateral hemifield (optic radiations)

Lenticulostriate branches supply putamen, part of head and body of caudate, external globus pallidus, posterior limb of IC, and corona radiata
- Lacunar infarcts yielding pure sensory or motor syndromes

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9
Q

Parinaud Syndrome

A

Lesion of dorsal midbrain aka quadrigeminal plates (Pineal tumors, midbrain infarcts)

  • Supranuclear paralysis of eye elevation
  • convergence-retraction nystagmus
  • light-near dissociation
  • lid retraction
  • Skew deviation
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10
Q

Anterior Choroidal artery

Origin and branches?
Supplies?
Infarct Symptoms?

A

Origin: ICA just after PCOM

Supplies; Internal segment of globus pallidus, part of posterior limb of internal capsule, part of geniculocalcarine tract, choroid plexus

Symptoms:
hemiplegia
hemianaesthesia and
contralateral hemianopia

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11
Q

Medial Medullary Syndrome

Vessel?
Structures and corresponding symptoms?

A

Vertebral artery or 1+ of its medial branches

  1. Pyramid - contralateral arm and leg
  2. Medial Lemniscus - contralateral sensation/vibration
  3. Hypoglossal fibers - ipsilateral tongue
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12
Q

Millard-Gubler Syndrome

Foville Syndrome

A

MG (AKA Ventral Pontine Syndrome)

  • Corticospinal tracts (pre-decusation) = contralateral arma dn leg hemiparesis
  • Facial n. = ipsilateral facial weakness

Foville Syndrome

  • MG syndrome symptoms
  • Abducens n. = ipsilateral horizontal gaze palsy
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13
Q

Weber vs Benedikt’s Syndrome vs Claude Syndrome

What region infarcted? What structures? Symptoms?

A

Weber
Ventral Midbrain
1. Cerebral Peduncle = Contralateral hemiweakness
2. CNIII Fascicle = CNIII palsy

Benedikt’s:
Ventral mesencephalic tegmentum
1. Ventral red nucleus = contralateral involuntary movements (tremor, choreathetosis)
2. Fascicle of CN III = CNIII palsy

Claude:
Dorsal mesencephalic tegmentum
1. Dorsal red nucleus = Ataxia and tremor (NO chorea)
2. Fascicle of CN III = CNIII palsy

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14
Q

Warfarin-Aspirin Symptomatic Intracranial Disease (WASID) Trial

A

More adverse events but no additional benefit treating severe intracranial stenosis with Warfarin over aspirin.

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15
Q

CHADS2 or CHA2DS2VASc

Use?

Components?

A

Risk Stratification to determine if AC should be used in the setting of Atrial Fibrillation

CHF, HTN, Age >75 (2pts), Diabetes, Stroke/TIA/TE Hx (2 pts), Vascular disease, Age 65-74, Sex category (Female) = Max 9 points

Does not account for chronic kidney disease risk.

Score 0 = Can defer AC. Score 1 = +/- antithrombotics, AC depending. Score > 2 = Offer AC.

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16
Q

SAMPRIS Trial

A

Stenting and Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis trial

Management of symptomatic intracranial stenosis:

  • ASA indefinitely and clopidogrel x 90 days
  • BP control < 140 (130 in diabetics)
  • high dose statin (LDL < 70)
  • Glucose control
  • exercise, stop smoking
17
Q

ASPECTS

A

Alberta Stroke Program Early CT score

Look at CT, subtract 1 point for each area with early changes:

  • 4 deep: Caudate, internal capsule, lentiform nucleus, insular region
  • 6 cortical

10 = normal HCT. 0 = Entire MCA territory. >7 is very bad

18
Q

North American Symptomatic Carotid Endarterectomy Trial

Asymptomatic Carotid Surgery Trial, Asymptomatic Carotid Atherosclerosis Study

A

NASCET (Symptomatic)

Occlusion → Medical management

70-99% symptomatic stenosis → CEA

50-69% → CEA if men, previous strokes, hemispheric symptoms

<50% → Medical management

ACST/ACAS (asymptomatic)

>60% → CEA better than medical management but very high NNT

19
Q

CADASIL

Symptoms
Cause

A

Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy

  • Multiple strokes w/o risk factors, hx of migraines, dementia, family hx
  • Missesense mutation of NOTCH3
20
Q

Gertsmann’s Syndrome

A

Left (Dominant) Parietal Lobe near Angular Gyrus

  1. Finger Agnosia
  2. Right-left confusion
  3. Agraphia
  4. Acalculia
  5. +/- aphasia
21
Q

Lacunar Syndromes

  1. Pure Sensory
    Pure Motor
    Clumsy-Hand Dysarthria
    Ataxic hemiparesis

Cause? Where?

A

Caused by lipohyalinosis of small vessels due to HTN

Pure Sensory → Thalamus, Contralateral sensory
Pure Motor → Posterior limb of IC or ventral pons, contralateral motor
Clumsy Hand Dysarthria → Paramedian Pons, contralateral hand weakness, dysarthria
Ataxic Hemiparesis → Pons, midbrain, or internal capsule, Ataxia out of proportion to weakness

22
Q

Dilated thin-walled vessels, no normal brain tissue, “popcorn” appearance

Name? Cause? Risk?

A

Cavernous malformation
Congenital
Usually incidental, may bleed

23
Q

Thin-walled venous structure, normal brain tissue intervening

Name? Cause? Risk?

A

Venous Angioma
Congenital
Usually benign

24
Q

Abnormally dilated capillaries, normal brain tissue intervening

Name? Cause? Risk?

A

Capillary telangiectasias
Congenital
Usually benign

25
Q

Abnormally dilated vessels, normal brain tissue intervening with parenchymal nidus, A-V communication

Name? Cause? Risk?

A

AV malformation
Congenital
High risk of bleeding

26
Q

Abnormally dilated vessels, normal brain tissue intervening with parenchymal nidus, A-V communication

Name? Cause? Risk?

A

AV malformation
Congenital
High risk of bleeding

27
Q

Balint Syndrome

A

Bilateral Parieto-occipital lesions

  1. inability to perceive the visual field as a whole (simultanagnosia)
  2. difficulty in fixating the eyes (oculomotor apraxia)
  3. inability to move the hand to a specific object by using vision (optic ataxia)
28
Q

Aspirin

A

NSAID - Anti-platelet therapy

Use:

  • should be used in all patients with chronic CAD
  • Antiplatelet naïve patients after stroke

Mechanism of Action:

  • inhibition of platelet aggregation by reducing release of platelet-derived procoagulants and vasoconstrictors
  • stabilizes plaques
  • anti-inflammatory action

Contraindication:

  • allergy
  • gastric bleeding
29
Q

Dabigatran

A

Use:

MoA:

Metab:

Reversal agent: Idarucizumab - small molecule biologic that binds and inactivates dabigatran

30
Q

Simvastatin (Lipitor®)
Atorvastatin (Zocor®)
Lovastatin
Pravastatin
Fluvastatin

A

HMG-CoA Reductase Inhibitors
Lipid Therapy
-statins

Use:
- lower MI and death rates in CAD patients
> high doses are significantly more effective
> no established CHD/CAD goal LDL <130mg/dl
> goal is LDL <100mg/dL in high risk CAD patients (CHD, DM)

  • treat familial lipid disorders

Target and Action:

  1. Stabilize atherosclerotic plaques by decreasing vascular inflammation
  2. improve endothelial cell dysfunction by lowering lipid levels in blood (LDLs)

Side effects:
Statin myositis -

31
Q

Rivaroxiban

A

Factor Xa Inhibitor
Anti-coagulation Therapy

Use:
- Anticoagulation: therapeutic effect in 2-4 hours

Action/Mechanism:

  • Inhibits Factor Xa of the coagulation cascade
  • not reversible, can replete with ***
  • no need for routine monitoring
32
Q

LMWH
I.e. enoxaparin

A

Anticoagulation Therapy
-parin

Uses:

  • Same as UFH, but easier to use as constant monitoring is not usually necessary
  • reduced death in MI patients
  • decreased risk of progression from UA to MI
  • may have better effectiveness than UFH

Mechanism of Action:
- Can bind antithrombin like UFH, but preferentially inhibit Factor Xa

Metabolism

  • 2 subq injections per day based on weight
  • more predictably than UFH, easier to dose
33
Q

Warfarin

A

Vitamin K antagonist
Anticoagulation Therapy

Use:
- Anticoagulation (long-term)
>Venous thromboembolism (DVT, PE)
> Acute Coronary Syndromes (unstable angina, MI)
> Atrial fibrillation
> Post-vascular bypass grafting

  • Keep INR between 2-3 except in mechanical heart valves (INR 2.5-3.5)

Action/Mechanism:

  • inhibits Vitamin K, decreasing Factors 2, 7, 9, 10, and Protein C and S
  • Proteins go first so transient hypercoagulability, bridge with heparin

Side effects:

  • Hemorrhage
  • Skin necrosis
  • Teratogenic

Reversal:
- Reverse with Vitamin K (10h) or FFP (instant)

34
Q

Tissue-type Plasminogen Activator

Ex. Alteplase (tPA), reteplase (rPA), tenecteplase (TNK-tPA)

A

Fibrinolytic Therapy

Use:

  • Treatment of acute MIs caused by complete coronary occlusions due to thrombi
  • must be given ASAP to limit necrosis of heart due to ischemia

Mechanism of Action:

  • activates the natural, circulating plasminogen to make plasmin, which lyses the fibrin found in thrombi and dissolves the clot.
  • preferentially activates plasminogen bound to an already-formed thrombus, limiting systemic fibrinolysis and decreasing bleeding risk compared to streptokinase (SK), which was formerly used.

Metabolism:
- rPA and TNK-tPA are derivatives of tPA with longer 1/2 lives, and can be given as a bolus instead of continuously, making it easier/safer

35
Q

Unfractionated Heparin

A

Anticoagulant Therapy

Mechanism of Action:

  • binds to circulating antithrombin, greatly increasing its effectiveness
  • antithrombin binds and inactivates thrombin, an important component of the coagulation cascade
  • UFH also inhibits Factor Xa, further slowing the coagulation cascade

Uses:

  • improves cardiovascular outcomes in ACS patients
  • prevents progression of UA to MI
  • given during PCI to prevent thrombotic complications, along with GPIIb/IIIa inhibitors ad aspirin

Metabolism:
- high variability, effectiveness must be monitored using aPPT

Comprehensive Neuro Review (13 decks)

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