Cerebrovascular Disease

Question 1

What is a TIA?

Answer 1

Sudden, focal neurological deficits which completely resolve within 24 hours

Question 2

What is a stroke?

Answer 2

Sudden, focal neurological deficits which do not completely resolve within 24 hours

Question 3

Major risk factors for atherosclerosis (and subsequently CVD)?

Answer 3

HTN, heart disease, DM, smoking, HLD, family history of vascular disease

Question 4

Minor risk factors for atherosclerosis (and subsequently CVD)?

Answer 4

Obesity, lack of exercise, excessive alcohol consumption

Question 5

Where do atherosclerotic changes predominate?

Answer 5

At the bifurcation points of large, major cervical and intracranial arteries

Question 6

What are the two basic mechanisms of ischemic infarction?

Answer 6

Local arterial thrombosis of an atheroma

Embolic arterial occlusions from proximal sources

Question 7

What structures are supplied by the perforator or lenticulostriate arteries?

Answer 7

Basal ganglia, internal capsule, thalamus, corona radiata

Question 8

What causes lacunar infarcts?

Answer 8

Thrombosis

Question 9

What is amaurosis fugax and what causes it?

Answer 9

Monocular blindness in which a “lowered dark shade” then gradually lightens up; one type of carotid territory TIA involving the ophthalmic artery or its retinal branches

Question 10

How do vertebrobasilar territory TIAs present?

Answer 10

Cause ischemia of the brain stem, cerebellum, or visual (occipital) cortex, producing ataxia, homonymous hemianopsia, or hemiparesis associated with “crossed” brain stem syndromes

Question 11

A hemiparesis with greater weakness of the face and upper limb suggests an infarct in the ___.

Answer 11

Pre-central MCA territory

Question 12

A hemiparesis with greater weakness of the lower limb suggests an infarct in the ___.

Answer 12

Pre-central ACA territory

Question 13

Sensory deficits limited to the face and upper limb suggest an infarct in the ___.

Answer 13

Post-central MCA

Question 14

Sensory deficits limited to the lower limb suggest an infarct in the ___.

Answer 14

Post-central ACA

Question 15

Infarcts from small artery occlusions may cause one of the “classic” lacunar syndromes or no symptoms at all if the lesion involves a more “silent” part of the brain. What are some fo these syndromes?

Answer 15

Pure motor hemiplegia (internal capsule)
Ataxic-hemiparesis (corona radiata)
Clumsy hand-dysarthria (basilar pons)
Pure sensory stroke (thalamus)

Question 16

What are the general etiologic causes of ischemic events?

Answer 16

Pump (heart)
Pipes (blood vessels)
Fluid (blood)

Question 17

Potential embolic sources leading to TIA or infarcts?

Answer 17

Endocardial clot associated with an acute MI
Poorly contracting L ventricle
L atrial clot created during AF
Infected or septic emboli from endocarditis
Venous clots in adults with PFOs (R->L atrium)

Question 18

Work-up for TIAs?

Answer 18

If younger or lacking stroke risk factors -> work-up for coagulopathy or non-atherosclerotic causes of ischemia

If typical risk factors -> echocardiogram (cardiac sources of emboli), U/S of the cervical ICA or other arterial imaging (MRA, CTA, catheter angiography)

Question 19

Indications for carotid endarterectomy?

Answer 19

Symptomatic atheromatous lesions of 70-99% stenosis at the origin of the ICA

Question 20

Other treatment options for carotid disease?

Answer 20

Arterial stenting and angioplasty via IV catheters

Question 21

Medical management of patients with TIAs?

Answer 21

If chronic AF -> warfarin (target INR 2.5) if no contraindications exist

All other patients -> antiplatelet agents (aspirin 50-325 mg daily, clopidogrel 75 mg daily, or aspirin 25 mg/dipyridamole 200 mg BID), statins (even in the absence of hyperlipidemia), control fo BP, DM, smoking cessation

Question 22

First consideration in treating acute ischemic infarction?

Answer 22

IV tPA (thrombolytic drug) if given within 4.5 hours of stroke

Alternative -> endovascular thrombectomy

Question 23

Contraindications for tPA use?

Answer 23

Hemorrhage on brain CT scan
Uncontrollable HTN
Extreme hypo- or hyperglycemia
Concurrent use of warfarin
Increased bleeding risk from recent surgical or invasive procedures

Question 24

Differences in treatment of large vs. small artery occlusion?

Answer 24

Large - investigate embolic sources (may need warfarin, carotid endarterectomy, interventional procedures, etc.)

Small - antiplatelet drugs and medical therapy

Question 25

Why is saline without dextrose and potential insulin for controlling glucose important in acute ischemic infarct?

Answer 25

Hyperglycemia is associated with poorer prognosis

Question 26

How should BP be managed in acute ischemic infarct?

Answer 26

In the absence of symptoms from hypertensive encephalopathy, mild to moderate BP elevations can be observed without treatment If using TPA, BP must be maintained below 185/110; IV antihypertensives like labetolol may be needed for BP >220/120

Question 27

Why should warfarin be withheld temporarily in patients with acute stroke due to AFib?

Answer 27

To avoid early complications of cerebral hemorrhage in patients with large acute ischemic infarctions

Question 28

Who gets antiplatelets in the setting of stroke?

Answer 28

Anyone not getting warfarin

Question 29

What must be considered if a patient with a recent cerebral infarction develops impaired consciousness in the absence of hypoglycemia?

Answer 29

Increased ICP -> within 3-5 days of an extensive cerebral infarction, brain edema can develop, or even earlier, hemorrhagic transformation can occur

Question 30

Manage increased ICP?

Answer 30

Mechanical hyperventilation to a pCO2 of 30-35 (if intubated) Intermittent IV boluses of mannitol or hypertonic saline NOT corticosteroids (in this setting -> they do counteract elevated ICP from tumor or infection)

Question 31

How does mechanical hyperventilation decrease ICP?

Answer 31

Hypocapnia induces cerebral vasoconstriction -> reduces cerebral blood volume

Question 32

How does intracranial hemorrhage present and why?

Answer 32

Severe headache, impaired or loss of consciousness, and a focal neurological deficit due to increased ICP Sudden rupture of arterial blood (arterial BP > ICP)

Question 33

A deeply located hemorrhage suggests ___ as the cause, while more superficial hemorrhages at the poles of the frontal, temporal, or occipital lobes often occur from ___.

Answer 33

HTN; head trauma

Question 34

Management of acute cerebral hemorrhage?

Answer 34

- Observe in the ICU or stroke unit - Dx with non-contrast head CT - Check INR if patient takes warfarin; other blood tests for a bleeding disorder warrant checking if the cause of hemorrhage is unclear or if non-traumatic bleeding is occurring elsewhere - Infusion of platelets or plasma clotting factors when indicated - UDS (cocaine or other sympathomimetics can increase BP and cause cerebral hemorrhage) - Control BP and increased ICP - Surgical evacuation only for worsening cerebellar hemorrhages

Question 35

Most common cause of cerebral hemorrhage?

Answer 35

HTN

Question 36

___ leads to recurrent lobar hemorrhages usually in the posterior cerebral hemispheres. What causes this?

Answer 36

Cerebral amyloid angiopathy; hereditary condition whereby arterial walls are weakened by amyloid deposits

Question 37

What are arteriovenous malformations?

Answer 37

Abnormal connection fo cerebral artery to vein, without intervening capillary bed; may enlarge slowly over time -> rupture and hemorrhage

Question 38

Most common cause of bleeding into the subarachnoid space?

Answer 38

Trauma

Question 39

Most common cause of SAH in the absence of trauma?

Answer 39

Ruptured congenital berry aneurysm, which arise in the circle of Willis at the base of the brain, especially anteriorly; risk of rupture beyond 7-10 mm

Question 40

Presentation of SAH?

Answer 40

May have sentinel headache or warning leak from mild to moderate bleeding Worse headache of my life (due to increased ICP and meningeal irritation) Nuchal rigidity and meningeal signs, often with N/V, impaired consciousness

Question 41

While localizing signs are usually absent in SAH, an oculomotor nerve palsy may occur, suggesting a berry aneurysm near what artery?

Answer 41

Posterior communicating artery

Question 42

Work-up and management of suspected SAH?

Answer 42

Non-con CT (blood in the cisterns and sulci around the base of the brain) If CT is normal, LP is necessary to exclude -> xanthochromia, consistent blood from tube to tube Emergent angiography (preferably conventional catheter angiography for optimal imaging) to locate the aneursm, occlude with intravascular coils or surgical clipping Monitor/treat cerebral vasospasm with hypertensive therapy (pressors to preserve cerebral blood flow) Oral nimodipine also improves patient outcome (probably neuroprotective)