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Lacunar infarcts are small lesions (usually < 5 mm in diameter) that occur in the distribution of short penetrating arterioles in the basal ganglia, pons, cerebellum, anterior limb of the internal capsule, and, less commonly, the deep cerebral white matter Lacunar infarcts are associated with poorly controlled hypertension or diabetes and have been found in several clinical syndromes, including contralateral pure motor or pure sensory deficit, ipsilateral ataxia with crural paresis, and dysarthria with clumsiness of the hand The neurologic deficit may progress over 24 36 hours before stabilizing Lacunar infarcts are sometimes visible on CT scans as small, punched-out, hypodense areas, but in other patients no abnormality is seen In some instances, patients with a clinical syndrome suggestive of lacunar infarction are found on CT scanning to have a severe hemispheric infarct Early mortality and risk of stroke recurrence is higher for patients with nonlacunar than lacunar infarcts The prognosis for recovery from the deficit produced by a lacunar infarct is usually good, with partial or complete resolution occurring over the following 4 6 weeks in many instances
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Lastilla M Lacunar infarct Clin Exp Hypertens 2006 AprMay;28(3 4):205 15 [PMID: 16833026]
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2 Cerebral Infarction
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Sudden onset of characteristic neurologic deficit Patient often has history of hypertension, diabetes mellitus, valvular heart disease, or atherosclerosis Distinctive neurologic signs reflect the region of the brain involved
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Thrombotic or embolic occlusion of a major vessel leads to cerebral infarction Causes include the disorders predisposing to transient ischemic attacks (see above) and atherosclerosis of cerebral arteries The resulting deficit depends on the particular vessel involved and the extent of any collateral circulation Cerebral ischemia leads to release of excitatory and other neuropeptides that may augment calcium flux into neurons, thereby leading to cell death and increasing the neurologic deficit
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In the United States, stroke remains the third leading cause of death, despite a general decline in the incidence of stroke in the last 30 years The precise reasons for this decline are uncertain, but increased awareness of risk factors (hypertension, diabetes, hyperlipidemia, cigarette smoking, cardiac
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A Symptoms and Signs
Onset is usually abrupt, and there may then be very little progression except that due to brain swelling Clinical evaluation should always include examination of the heart and auscultation over the subclavian and carotid vessels to determine whether there are any bruits
Nervous System Disorders
CMDT 2008
Table 24 4 Features of the major stroke subtypes
Stroke Type and Subtype Ischemic stroke Lacunar infarct Small (< 5 mm) lesions in the basal ganglia, pons, cerebellum, or internal capsule; less often in deep cerebral white matter; prognosis generally good; clinical features depend on location, but may worsen over first 24 36 hours See text signs vary depending on occluded vessel CT may reveal small hypodensity but is often normal Aspirin; long-term management is to control risk factors (hypertension and diabetes mellitus) Clinical Features Diagnosis Treatment
Carotid circulation obstruction
Noncontrast CT to exclude hemorrhage; CT may be normal during first 6 24 hours of an ischemic stroke, whereas diffusion-weighted MRI is more sensitive; electrocardiography, blood glucose, complete blood count, and tests for hypercoagulable states, hyperlipidemia are indicated; echocardiography or Holter monitoring in selected instances As for carotid circulation obstruction
Select patients for intravenous thrombolytics or intra-arterial mechanical thrombolysis; aspirin (325 mg/d orally) combined with sustainedrelease dipyridamole (200 mg twice daily) is first-line therapy; anticoagulation with heparin for cardioembolic strokes, and sometimes for evolving stroke when no contraindications exist As for carotid circulation obstruction
Vertebrobasilar occlusion Hemorrhagic stroke Spontaneous intracerebral hemorrhage
See text signs vary based on location of occluded vessel Commonly associated with hypertension; also with bleeding disorders, amyloid angiopathy Location: basal ganglia more common than pons, thalamus, cerebellum, or cerebral white matter
Noncontrast CT is superior to MRI for detecting bleeds of < 48 hours duration; laboratory tests to identify bleeding disorder: angiography may be indicated to exclude aneurysm or AVM Do not perform lumbar puncture CT to confirm diagnosis, but may be normal in rare instances; if CT negative and suspicion high, perform lumbar puncture to look for red blood cells or xanthochromia; angiography to determine source of bleed in candidates for treatment CT indicates subarachnoid hemorrhage, and angiography then demonstrates aneurysms; angiography may not reveal aneurysm if vasospasm present
Most managed supportively, but cerebellar bleeds or hematomas with gross mass effect benefit from urgent surgical evacuation
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