Subcortical Arteriosclerotic Encephalopathy Research Articles

Subcortical arteriosclerotic encephalopathy (Binswanger's disease). Computed tomographic, nuclear magnetic resonance, and clinical correlations.

Twenty-three elderly patients were found to have a consistent pattern of leukoencephalopathy by computed tomography and nuclear magnetic resonance imaging. Eight patients presented with vague, nonspecific symptoms and had no neurologic deficits. The other 15 patients had neurologic deficits that presented in one of three ways: stroke, seven patients; slowly progressive dementia and gait disturbance, five patients; or slowly progressive dementia alone, three patients. Risk factors for arteriosclerosis (hypertension, diabetes) were present in 18 patients (78%). The necropsy of one patient revealed arteriosclerotic vasculopathy characteristic of subcortical arteriosclerotic encephalopathy (SAE) or Binswanger's disease. Subcortical arteriosclerotic encephalopathy may be a relatively common affliction of elderly patients, most of whom have risk factors for arteriosclerosis. The modes of presentation and associated clinical signs are variable, and more than one third may have no neurologic deficit. In some cases SAE overlaps with normal pressure hydrocephalus by clinical and neuroimaging criteria. Some patients with normal pressure hydrocephalus who do not respond to ventricular shunting may actually have SAE.

The identity of lacunar dementia and Binswanger disease

It is postulated here that the dementia occurring in patients with lacunar strokes is due to an ischemic leukoencephalopathy. Severity of the dementia correlates, not with the volume of brain tissue lost from large-artery infarctions, but rather, with the extent of cortex disconnection resulting from demyelination. The term Lacunar Dementia is proposed, instead of the poorly known eponym “Binswanger disease” or the cumbersome descriptive name “subcortical arteriosclerotic encephalopathy”. Clinically, Lacunar Dementia presents with gait difficulties, urinary incontinence, parkinsonian features, pseudobulbar palsy, emotional incontinence and dementia. High-resolution CT scan shows decrease density of frontal and periventricular white matter, without contrast enhancement; ventricular dilatation, and lacunar infarcts. Small-artery disease lipohyalinosis is the cause of the lacunes and the leukoencephalopathy. Since the advent of the high-resolution CT scan, the frequency of lacunar dementia seems to be increasing, in contrast with the number of cases of multi-infarct dementia.

Diffuse white-matter disease in the geriatric population. A clinical, neuropathological, and CT study.

CT findings in 6 autopsy cases of subcortical arteriosclerotic encephalopathy (SAE) are reported. A diffuse area of nonhomogeneous decreased density was observed in the deep white matter of both cerebral hemispheres, together with moderate dilatation of the lateral ventricles and ragged margins. The most characteristic pathological findings at autopsy were a diffuse area of incomplete infarction containing multiple small infarcts as well as cyst formation and marked stenotic atherosclerotic changes in the medullary arteries. Clinical features included patchy mental lapses, frontal-lobe syndromes, minor motor signs, and hypertension. The authors feel that SAE or a similar disease might occur in most cases of multi-infarct dementia.

Subcortical arteriosclerotic encephalopathy: a clinical and radiological investigation.

Subcortical arteriosclerotic encephalopathy (Binswanger's type) was diagnosed in a group of patients with hypertension or arteriosclerosis, who showed acute and subacute neurological deficits, dementia, reduced cerebral blood flow, and white matter low attenuation with mild atrophy and infarcts as the predominant CT scan features. This set of clinical and radiological criteria could be used to make the diagnosis in life, as confirmed neuropathologically in one patient.

Clinical features of subcortical arteriosclerotic encephalopathy (Binswanger disease)

Subcortical arteriosclerotic encephalopathy, a chronic vascular dementia with hydrocephalus, was characterized pathologically in five patients by severe thickening of small vessels and by diffuse regions of white matter loss with gliosis. Lacunar infarcts were also present. The clinical picture in 11 patients was characterized by: (1) persistent hypertension and systemic vascular disease; (2) acute strokes; (3) subacute accumulation of focal neurologic symptoms and signs over weeks to months; (4) long plateau periods; (5) lengthy clinical course; (6) dementia; (7) prominent motor signs and pseudobulbar palsy and; (8) hydrocephalus. The pathogenesis of subcortical arteriosclerotic encephalopathy is unknown; possible mechanisms include diffuse ischemia and fluid transudation with subsequent gliosis related to subacute hypertensive encephalopathy.