Vascular Disorders of the Nervous System

Brief, reversible episode of neurologic dysfunction due to focal ischemia

Symptoms typically last <24 hours

5 minutes: irreversible damage

• Most vulnerable areas = hippocampus, neocortex, cerebellum, watershed areas
• 12-48 hours: red dead neurons

• 24-72 hours: necrosis and neutrophils
• 3-5 days: macrophages

1-2 weeks: reactive gliosis + vascular proliferation

>2 weeks: glial scar

Presentation: HA, uncommonly seizure, cerebral edema, well defined neurological deficits, often have antecedent TIAs

• Pathophysiology: plaque
• grows slowly and asymptomatically over years, become symptomatic when a
• thrombosis occludes the remaining narrow lumen, may also give rise to
• emboli

Most are non-hemorrhagic (bland)

Reperfusion may cause hemorrhage(red)

Tx: IV tPA if no CI, permissive HTN, long term antiplatelet therapy

Small strokes that occur in deep brain regions supplied by small arteries

Presentation: often asymptomatic, sx may evolve over hours, may have warning TIAs, four typical syndromes

1. Pure motor hemiplegia: posterior limb of internal capsule

2. Pure somatosensory: thalamic VP nucleus

3. Clumsy hand - dysarthria: paramedian mid pons, least common

4. Ipsilateral hemiparesis - ataxia: basis pontis

Epidemiology: risk factors are diabetes and HTN

• Pathophysiology: arteriolosclerosis
• (fibrocollagenous replacement of smooth muscle in lumen due to
• hemodynamic stress leading to vessel occlusion)
• 

• Pathology: small cavitary lesions ("lake like" space)
• 

Tx: same as atherothrombotic stroke

• Presentation:
• -sudden onset of maximal focal deficit w/o antecedent TIAs.
• -More likely to have HA, seizure and secondary hemorrhage.
• -Evidence of infarcts in other tissues

Pathophysiology: MI leading to mural thrombus, or atrial fibrillation can throw emboli to the brain

Evaluation: EKG, TTE, TEE

Tx: same as atherothrombotic stroke, may include anticoagulation

1. Carotid or vertebral artery dissection (often accompanied by Horner's syndrome)

2. Vasculitides

3. Cardiac valvular disease (vegetations on cardiac valves can form emboli)

4. Emboli from non-cardiac sources (DVT in patients with patent foramen ovale)

5. Migraine (may be due to vasospasm)

6. Meningeal infectious process

7. Stimulant drugs (meth --> vasospasm)

8. Occlusion of cortical veins (patients with hypercoagulable state)

Presentation:  more likely to progress over minutes to hours, HA is common, acute reactive HTN, vomiting

• Pathophysiology:
• -rupture of small vessel walls that have been weakened by arteriolosclerosis
• -expanding hematoma destroys adjacent brain and creates mass effect
• -50% start near putamen

Tx: no tPA, surgical evacuation with cerebellar

Prognosis: worse than ischemic stroke in the short term, better in the long term

1. Cerebral amyloid angiopathy: amyloid (alzheimer's) deposited in vessel walls --> rupture

2. Anticoagulant drugs

3. Brain tumor

4. Vascular malformations (AV malformations)

5. Saccular aneurysm rupture into parenchyma of the brain

Epidemiology: saccular aneurysms are relatively prevalent (2-5%)

Presentation: sudden onset of "worse HA of my life", lethargy, meningismus, maybe LOC of sudden death, "sentinel bleed"

Pathophysiology: aneurysms generally develop at bifurcations of main intracranial arteries, usually in the circle of willis

Tx: emergent head CT +/- LP, clipping or coiling of aneurysm

• Complications:
• -increased risk of rerupture minutes to weeks after
• -increased risk for vasospasm induced ischemic stroke
• -acute hydrocephalus
• -normal pressure hydrocephalus

Often due to aortic disease --> need to check for aortic aneurysm

Infarction typically in territory of spinal artery

Many pts have significant recovery of function

Causes: diabetes, HTN, vasculitides

Presentation: sudden onset of mononeuropathy, often painful

Diabetic third nerve palsy: painful severe lesion of CNIII with sparing of pupillary function