ischemic stroke

Question 1

Incidence and mortality rates for cerebrovascular disease

Answer 1

declining due to lessening stroke severity and better treatment of stroke risk factors

Question 2

Define stroke or cerebrovascular disease

Answer 2

general term that refers to any vascular injury to the brain

Question 3

Define ischemic stroke

Answer 3

ischemic injury to the brain causing a persistent clinical deficit at 24 hours. Even mild residual deficits are classified as strokes. The severity of the deficit is not the determinant, only that the deficit is present at 24 hours.

Question 4

define transient ischemic attacks

Answer 4

ischemic neurological deficits that have completely resolved by 24 hours, regardless of their severity or relative duration (seconds or hours). Some recommend shortening this time period to 1-2hrs, since only short TIAs do not impart any damage to CNS

Question 5

ischemic Stroke time course of presentation

Answer 5

come on rapidly with no warning, headache, or change in consciousness. Deficit most severe at onset, with progressive improvement over seconds, minutes, hours, days and weeks

Question 6

Large vessel ischemia

Answer 6

causes deficits in multiple systems. For example, a typical patient with a large vessel ischemic stroke in the middle cerebral artery territory will have a hemiparesis, a hemi-sensory loss, and a homonymous hemi-anopsia contralateral to the ischemic side of the brain

Question 7

Small vessel ischemia

Answer 7

isolated motor (or isolated sensory) deficit on one side of the body. Caused by occlusion of small penetrating vessels that branch from large arteries and produce lacunar infarctions

Question 8

Multi infarct dementia

Answer 8

Accumulation of multiple lacunar strokes over many years

Question 9

What causes multiple areas of ischemia at one time

Answer 9

hypoperfusion: causes multiple areas of mixed small and/or large vessel infarction. Caused by systemic hypotension, , inadequate perfusion during cardiopulmonary bypass, and isolated major vessel stenosis, multiple emboli showers, vasospasm, hypercoagulation or inflammatory processes

Question 10

Virchows triad

Answer 10

Endothelial disruption, stasis, hypercoagultion

Question 11

risk factors for stroke

Answer 11

Age, men, race, HTN (increases with any increase in BP), lipid disorders, homocysteine elevation, smoking, obesity, physical inactivity, diabetes, alcohol abuse

Question 12

Structural risks for stroke

Answer 12

Atrial fibrillation, CHF, valvular disorders, atrial septal defect (embolus can bypass lung and go to brain), arterial stenosis, dissection or occlusion, infectious endocarditis (infectious embolic stroke or mycotic aneurysm), tumors (atrial myxoma)

Question 13

Causes of Young stroke

Answer 13

vasculopathies, hematological disorders, inflammatory mechanisms, vasospasm

Question 14

What are vasculopathies

Answer 14

Non-inflammatory, non-atherosclerotic hyperplasia of arteries

Question 15

Fibromuscular dysplasia population, what is it, treatment, cause, associations

Answer 15

Women in 30’s-40’s. Hypertrophy of arterial media causing multiple areas of segmental occlusion or stenosis. Renal artery, carotid artery and vertebral artery common. Treated with arterial dilation. No known cause, possibly estrogen or viral? Associated with arterial dissection and intracranial saccular aneurysms

Question 16

Moya Moya- what is it, who gts it, pathology, associations

Answer 16

Non atherosclerotic Focal occlusion of middle cerebral artery. Occurs in children and women in 30-40’s. Pathology is intimal hyperplasia. associated with secular aneurysms and dissection

Question 17

Arterial dissection- what is it, therapy

Answer 17

Results from a tear in the endothelial lining of the artery that allows blood to dissect between the endothelium and the adventitia, in the media of the artery. The occlusion or stenosis of the artery is typically well tolerated, however, emboli from the injured artery can move into the distal artery territory and cause significant strokes. Therapy is with anticoagulation until the dissection heals, although intra-arterial stenting or surgery can have a role.

Question 18

Two types of arterial dissection

Answer 18

Traumatic dissection: Major traumatic injury and direct force to artery. Can happen to anyone. Spontaneous dissection: occurs from normal activities such as swinging golf club. Arteries may be unstable due to other vasculopathies (ie. FMD, marfans, coarctation),

Question 19

Types of hematological disorders that can cause stroke and how are they treated

Answer 19

Familial deficiencies of blood components that help to prevent thrombosis such as deficiencies of Protein C, Protein S, or Antithrombin, or the presence of Factor V Leiden, or Prothrombin Gene, are associated with venous thrombosis, including CNS. Treatment with anticoagulation

Question 20

Malignancies and stroke

Answer 20

can cause a poorly understood hypercoagulable state. Peripheral venous events more common than arterial

Question 21

Sickle cell anemia and stroke

Answer 21

SSA responds to transfusion. The Sickle Cell Trait cells can on occasion ‘sickle’ with dehydration or altitude, but this doesn’t seem to impart any additional risk of stroke or CNS hemorrhage

Question 22

hyperviscosity states and stroke

Answer 22

Protein, elevated hematocrit (60%), thrombocytosis (1,000,000), etc. can generate slowness of flow beyond the pump & pipes ability to compensate.

Question 23

Oral contraceptives and stroke

Answer 23

Causes stroke or venous thrombosis. Migraine/Smokers/OCP increase risk by 25 times

Question 24

Antiphospholipid antibodies and stroke

Answer 24

cause a triad of spontaneous miscarriage, thrombocytopenia, and recurrent large vessel thrombosis, arterial or venous. The mechanism appears to be an attack of the phospholipid membranes in the chorion, platelet, and endothelium, respectively. Treatment involves antithrombotics, anticoag or no treatment

Question 25

Vasculitis and stroke

Answer 25

Can have systemic vasculitis that secondarily affects CNS or isolated CNS vasculitis. Vasculitis has traditionally been considered a manifestation of immunological disorders, but over time, infectious causes are emerging. Varicella-Zoster Virus is increasingly being found in CNS vasculitis.

Question 26

Migraine and stroke

Answer 26

The mechanism of migraine stroke is either vasospasm (sterile serotonin mediated intramural inflammation perhaps mediated through the autonomic nervous system), or increased platelet aggregation that clogs the microcirculation leading to permanent cellular injury. Antiplatelet therapy is usually effective

Question 27

Venous infarctions- causes

Answer 27

The most common cause is major head trauma. Most non-traumatic venous infarction occurs from dehydration, CNS infections, and hypercoagulable states (transient or genetic). Post-partum Sagittal Sinus Thrombosis around days 3-5 is a popular board question

Question 28

Vasospasms causing stroke- causes

Answer 28

sympathometic drugs, severe hypertension, primary vessel irritation (intrathecal drug, catheter contrast, SAH blood) trigger vasospasm that can cause permanent injury.

Question 29

Therapy to prevent recurrent stroke

Answer 29

Treat risk factors (ie. Eat healthy, low stress, etc), aspirin, thienopyridines (Clopidogrel, Prasurgrel, Ticlopidine) and Anticoagulants

Question 30

Anti-platelet therapies

Answer 30

Aspirin: (81mg or 325mg/day). May require H2 blocker or proton pump inhibitor if GI problems. Combo therapy: Clopidogrel plus aspirin is useful after catheter based cardiac re-vascularization, after CNS ischemic event, and long term for arteriopaths. Dipyridamole: available with aspirin combo

Question 31

Anticoagulants

Answer 31

Warfarin: used for atrial fibrillation and patients with mechanical heart valves or CHF. Direct thrombin inhibitors (Dabigatran, Rivaroxiban, and Apixaban): same benefits as warfarin but may be better for lower risk populations and dont work as well for mechanical valves. Injected/IV anticoag: Heparin (AT III, Thrombin), the low molecular weight heparins Enoxaparin & Daltaperin (AT III, Thrombin, Xa), and Argatroban (Thrombin)

Question 32

Geriatric population and anticoags

Answer 32

there is concern that patients over the age of 75 have a higher risk of hemorrhage, so warfarin may not be preferred. Alternatives include aspirin, DTIs, low intensity warfarin. Grading Scales for Atrial Fibrillation like CHADS (points for age, HTN, CHF, DM, Stroke) estimate the benefit/risk ratio.

Question 33

Anticoag vs antiplatelets

Answer 33

Anticoagulation is considered in the patients with a high risk of embolization and large vessel occlusion. For patients with small vessel infarctions, or with low risk of embolization and large vessel occlusion, antiplatelet agents are as useful as anticoagulation, but without the risk.

Question 34

Carotid endarterectomy

Answer 34

Highly beneficial in symptomatic patients with high grade (70-90%) stenosis. Only minimal efficacy in 50-69% stensosis, however asymptomatic patients who undergo carotid endarterectomy plus aspirin and risk factor reduction (with 60% or greater stenosis) benefit.

Question 35

Catheter options for stroke

Answer 35

angioplasty, stent, coil/balloon, embolize, embolectomy

Question 36

BP management after stroke

Answer 36

Most patients have relative hypertension after a stroke that slowly improves over the next 7-10 days. There is little reason to initiate treatment unless the blood pressure is elevated to very high levels.

Question 37

Steps for management of stroke

Answer 37

Fluids (normal saline if not worried about CHF, or dextrose/5% water if not worried about cerebral edema) > tissue plasminogen activator > glucose or glucose (if unstable glucose only )

Question 38

Contraindications of TPA

Answer 38

TPA is contraindicated in patients with abnormal CT scans (indicating stroke has progressed beyond recovery), severe hypertension, coagulation difficulties, or with coma (indicating another diagnosis).

Question 39

Time frame of TPA use following stroke

Answer 39

Within 4.5hrs of incident (IV) or up to 12 hrs (intra-arterial TPA infused into thrombus, used when IV TPA is contraindicated)