LACUNAR STROKES

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Lacunar strokes are small, ischemic strokes in the distribution of small penetrating arteries of the circle of Willis (lenticulostriate, thalamoperforate) and paramedian branches of the basilar artery. The common locations of lacunes are internal capsule, basal ganglia, thalamus, and pons. They account for about 20% of all ischemic strokes.

When to Suspect Lacunar Stroke

• Arm and leg are equally affected (motor or sensory deficit).
• Motor and/or sensory deficit that is not associated with higher cortical function abnormalities: aphasia, apraxia, astereognosis, agraphesthesia.
• Dense neurological deficit associated with normal repeated head CT scan.

Major Risk Factors for Lacunar Infarcts

  1. Hypertension.
  2. Diabetes.
  3. Hypercholesterolemia.
  4. Aging.
  5. Smoking.

Five Common Clinical Lacunar Syndromes

1. Pure motor stroke: posterior limb of internal capsule or pons infarct. The most common form. Weakness of ipsilateral face, arm, and leg.
2. Pure sensory stroke: thalamic infarct. Sensory deficit in face, arm, and leg.
3. Sensorimotor: posterior limb of internal capsul or thalamus. Weakness and numbness of face, arm and leg.
4. Ataxic-hemiparesis: pons or internal capsule infarct. Ipsilateral limb weakness and ataxia, disproportionate to the weakness.
5. Dysarthria—clumsy hand: pons or internal capsule infarct. Ipsilateral facial weakness, with mild arm weakness and dysarthric speech. The least common of these five. Workup for lacunar stroke is same as stroke (see Table 1). Cerebral angiogram generally is not indicated unless carotid endarterectomy is considered. Prognosis of lacunar stroke is generally good. Treatment is same as other
ischemic strokes with the exception of anticoagulation (heparin/warfarin), which is rarely indicated.

EMBOLIC STROKE

When to Suspect Embolic (as opposed to thrombotic) Stroke
• Patient presents with sudden and fixed neurological deficit, particularly during the daytime and activity.
• Rapid resolution of neurological deficit (sudden onset and offset).
• Stroke associated with headache, seizure, or altered mental status.
• Stroke occurs in young adult.
• Stroke occurs in the distribution of two or more major blood vessels of the brain (not in distribution of penetrating blood vessel).
• Hemorrhagic infarct on head CT scan.
• Patient presents with acute isolated neurological deficits such as aphasia or visual field defect.
• Stroke occurs in a patient who has strong history of heart disease but weak history of atherosclerosis (documented by history and diagnostic tests).
Strong history of heart disease includes: atrial fibrillation, valvular disease, myocardial infarction, cardiomyopathy, prosthetic valves, ventricular hypokinesia or dilatation, cardiac thrombus, atrial myxoma, and patent foramen
ovale (paradoxical embolization).

CAUSES OF SPONTANEOUS INTRACEREBRAL HEMORRHAGE

• Ruptured cerebral aneurysm or arteriovenous malformations.
• Hypertensive hemorrhage: pons, putamen basal ganglia, thalamic.
• Drugs: cocaine, amphetamines, phenylpropanolamine.
• Anticoagulant: warfarin.
• Thrombocytopenia or other coagulopathies.
• Cerebral amyloid angiopathy: an elderly patient presents with recurrent lobar hemorrhage (leading cause after hypertension).
• Central nervous system (CNS) vasculitis.
• Metastasis: melanoma, renal cell carcinoma, lung cancer, choriocarcinoma.

Caveat: The location of the hemorrhage is helpful in establishing the
cause. Head CT scan is superior to magnetic resonance imaging in detecting
an intracerebral hemorrhage. You must determine the cause of hemorrhage. Consult a neurosurgeon because many hematomas can be evacuated; surgical evacuation of cerebellar hemorrhage can be life-saving. You may consider treating the elevated blood pressure more aggressively in hemorrhagic stroke. Stabilize airway and treat raised intracranial pressure. Prognosis depends on location and size of hemorrhage and age of the patient.

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