Risk Factors for Cardiovascular Disease

Differential. The major important condition to separate from these “micropathologies” is occlusion of parent arteries blocking flow in penetrating artery branches. In patients of Asian origin, especially Japan, Korea, and China, small deep infarcts are often caused by occlusive disease of the large intracranial parent arteries. When small deep infarcts are caused by severe occlusive disease of the intracranial large parent arteries, the infarcts are slightly larger, the neurologic signs are slightly worse, and recurrence is more common than in infarcts caused by intrinsic disease of the penetrating arteries.

Clinical Presentations. The most common clinical syndromes caused by lacunar infarction are pure motor hemiparesis (weakness of face, arm, and leg on one side of the body with no sensory, visual, or cognitive abnormalities; pure sensory stroke (hemisensory loss without other signs); dysarthria–clumsy hand syndrome; and ataxic hemiparesis.

CHRONIC SUBCORTICAL VASCULAR DISEASE

Multiple lacunes, white matter gliosis, and atrophy almost always occur together and are accompanied by widespread abnormalities of penetrating small arteries. When severe and clinically evident, this chronic microvasculopathy is often called Binswanger disease. In this condition, the cerebral white matter has confluent areas of soft, puckered, and granular tissue. These areas are patchy and predominate in the occipital lobes and periventricular white matter, especially anteriorly and near the ventricular surface. The cerebellar white matter is also often involved. The ventricles are enlarged, and at times, the corpus callosum is small. The volume of white matter is reduced, but the cortex is generally spared. There are nearly always some lacunes. Microscopic study shows myelin pallor. Usually, the myelin pallor is not homogeneous, but islands of decreased myelination are surrounded by normal tissue. Gliosis is prominent in zones of myelin pallor. The walls of penetrating arteries are thickened and hyalinized, but occlusion of the small arteries is rare. Occasional patients with Binswanger white-matter changes have had amyloid angiopathy and CADASIL as the underlying vascular pathology. In these patients, arteries within the cerebral cortex and leptomeninges are thickened and contain a congophilic substance.

The clinical picture in patients with Binswanger white matter abnormalities is variable. Most patients have abnormal cognitive function and behavior. Most become slow and abulic. Memory loss, aphasic abnormalities, and visuospatial dysfunction are also found. Pseudobulbar palsy, pyramidal signs, extensor plantar reflexes, and gait abnormalities are common. The clinical findings often progress gradually or stepwise, with worsening during periods of days to weeks. Often, there are plateau periods with relative clinical stability. Many patients also have acute lacunar strokes that present clinically with hemiparesis. MRI defines the full extent of white matter involvement and has spatial resolution that allows detection of small lacunar lesions. Diffusionweighted imaging can show even small acute and subacute infarcts with great accuracy.

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