Cerebrovascular Disease Flashcards
What is a TIA?
Sudden, focal neurological deficits which completely resolve within 24 hours
What is a stroke?
Sudden, focal neurological deficits which do not completely resolve within 24 hours
Major risk factors for atherosclerosis (and subsequently CVD)?
HTN, heart disease, DM, smoking, HLD, family history of vascular disease
Minor risk factors for atherosclerosis (and subsequently CVD)?
Obesity, lack of exercise, excessive alcohol consumption
Where do atherosclerotic changes predominate?
At the bifurcation points of large, major cervical and intracranial arteries
What are the two basic mechanisms of ischemic infarction?
Local arterial thrombosis of an atheroma
Embolic arterial occlusions from proximal sources
What structures are supplied by the perforator or lenticulostriate arteries?
Basal ganglia, internal capsule, thalamus, corona radiata
What causes lacunar infarcts?
Thrombosis
What is amaurosis fugax and what causes it?
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
How do vertebrobasilar territory TIAs present?
Cause ischemia of the brain stem, cerebellum, or visual (occipital) cortex, producing ataxia, homonymous hemianopsia, or hemiparesis associated with “crossed” brain stem syndromes
A hemiparesis with greater weakness of the face and upper limb suggests an infarct in the ___.
Pre-central MCA territory
A hemiparesis with greater weakness of the lower limb suggests an infarct in the ___.
Pre-central ACA territory
Sensory deficits limited to the face and upper limb suggest an infarct in the ___.
Post-central MCA
Sensory deficits limited to the lower limb suggest an infarct in the ___.
Post-central ACA
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?
Pure motor hemiplegia (internal capsule)
Ataxic-hemiparesis (corona radiata)
Clumsy hand-dysarthria (basilar pons)
Pure sensory stroke (thalamus)
What are the general etiologic causes of ischemic events?
Pump (heart)
Pipes (blood vessels)
Fluid (blood)
Potential embolic sources leading to TIA or infarcts?
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)
Work-up for TIAs?
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)
Indications for carotid endarterectomy?
Symptomatic atheromatous lesions of 70-99% stenosis at the origin of the ICA
Other treatment options for carotid disease?
Arterial stenting and angioplasty via IV catheters
Medical management of patients with TIAs?
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
First consideration in treating acute ischemic infarction?
IV tPA (thrombolytic drug) if given within 4.5 hours of stroke
Alternative -> endovascular thrombectomy
Contraindications for tPA use?
Hemorrhage on brain CT scan Uncontrollable HTN Extreme hypo- or hyperglycemia Concurrent use of warfarin Increased bleeding risk from recent surgical or invasive procedures
Differences in treatment of large vs. small artery occlusion?
Large - investigate embolic sources (may need warfarin, carotid endarterectomy, interventional procedures, etc.)
Small - antiplatelet drugs and medical therapy
Why is saline without dextrose and potential insulin for controlling glucose important in acute ischemic infarct?
Hyperglycemia is associated with poorer prognosis
How should BP be managed in acute ischemic infarct?
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
Why should warfarin be withheld temporarily in patients with acute stroke due to AFib?
To avoid early complications of cerebral hemorrhage in patients with large acute ischemic infarctions
Who gets antiplatelets in the setting of stroke?
Anyone not getting warfarin
What must be considered if a patient with a recent cerebral infarction develops impaired consciousness in the absence of hypoglycemia?
Increased ICP -> within 3-5 days of an extensive cerebral infarction, brain edema can develop, or even earlier, hemorrhagic transformation can occur
Manage increased ICP?
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)
How does mechanical hyperventilation decrease ICP?
Hypocapnia induces cerebral vasoconstriction -> reduces cerebral blood volume
How does intracranial hemorrhage present and why?
Severe headache, impaired or loss of consciousness, and a focal neurological deficit due to increased ICP
Sudden rupture of arterial blood (arterial BP > ICP)
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 ___.
HTN; head trauma
Management of acute cerebral hemorrhage?
- 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
Most common cause of cerebral hemorrhage?
HTN
___ leads to recurrent lobar hemorrhages usually in the posterior cerebral hemispheres. What causes this?
Cerebral amyloid angiopathy; hereditary condition whereby arterial walls are weakened by amyloid deposits
What are arteriovenous malformations?
Abnormal connection fo cerebral artery to vein, without intervening capillary bed; may enlarge slowly over time -> rupture and hemorrhage
Most common cause of bleeding into the subarachnoid space?
Trauma
Most common cause of SAH in the absence of trauma?
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
Presentation of SAH?
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
While localizing signs are usually absent in SAH, an oculomotor nerve palsy may occur, suggesting a berry aneurysm near what artery?
Posterior communicating artery
Work-up and management of suspected SAH?
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)
