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Transient Ischemic Attack
Brief, reversible episode of neurologic dysfunction due to focal ischemia
Symptoms typically last <24 hours
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Stroke General Time Course
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
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Atherothrombotic Infarction
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
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Lacunar Infarction
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
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Infarction due to cardiac emboli
- 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
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Less common causes of ischemic stroke
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)
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Hypertensive Intracerebral Hemorrhage
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
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Intracerebral hemorrhage due to less common causes
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
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Subarachnoid hemorrhage due to ruptured saccular aneurysm
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
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Ischemic infarct of spinal cord
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
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Ischemic infarct of peripheral nerve
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
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