Expanding cerebellar lacunes due to dilatation of the perivascular space associated with Binswanger's subcortical arteriosclerotic encephalopathy.

Abstract

An 80-year-old hypertensive woman developed right hemiplegia and died 24 hours after admission. Neuropathologic examination revealed multiple cerebral infarcts of various ages and diffuse subcortical arteriosclerotic encephalopathy. Clusters of asymptomatic "expanding" lacunes, due to dilatation of the perivascular spaces, were found in both dentate nuclei. These cavities, which presented as space-occupying lesions, were surrounded by a single layer of flattened cells and contained 1 or more sections of normal-looking arterioles. Such a topographic grouping of lacunes in the dentate nucleus has not been described previously. The mechanism of widening of the perivascular compartment remains unclear; its occurrence in a hypertensive patient and its association with typical Binswanger's subcortical arteriosclerotic encephalopathy and severe atherosclerosis with multiple infarcts suggest a common pathophysiologic mechanism possibly including an alteration of the blood-brain barrier.(Stroke 1987;18:1087-1092) C erebral lacunes are usually considered to be old, small, deep cerebral infarcts 12 due to occlusive arterial lesions. 34 However, old hemorrhages can be a cause of lacunes and have been recently reviewed.5 Dilatations of perivascular spaces, well known since the historic paper of Marie 6 and the thesis of Ferrand, 7 have been reemphasized recently as a possible mechanism of genesis of cerebral lacunes. 89To avoid the semantic confusion that surrounds the term cerebral lacune, 10 a new neuropathologic classification has been proposed." 12 Lacunes due to dilatation of the perivascular space are usually asymptomatic. 8 A new type of space-occupying lacune due to dilatation of the perivascular space was described as an "expanding cerebral lacune" by Poirier et al. 9 In this initial report, the thalamo-mesencephalic "expanding lacunes" were responsible for clinical symptoms.In this article, we report a new case of expanding lacune involving the cerebellum with three major points of interest: 1) the lesion was asymptomatic, presenting as an incidental autopsy finding, 2) the topographic grouping of lacunes in the dentate nuclei had never been described, and 3) the lacunes were associated with Binswanger's subcortical arteriosclerotic encephalopathy (SAE) and multiple cerebral infarcts. Such an association in a hypertensive patient suggests com- Received March 5, 1987; accepted June 22, 1987. mon pathogenetic mechanisms as the origin of these various lesions. Report of a CaseAn 80-year-old woman known to be hypertensive for many years had received various antihypertensive treatments. She suffered from left ventricular failure and coronary insufficiency. She was admitted to the hospital on March 8, 1983, because of dyspnea. Blood pressure was 170/100 mm Hg. She became somnolent, then comatose, and developed right hemiparesis 24 hours after admission and died within a few hours. Computed tomography (CT) scan was not obtained.Postmortem examination revealed diffuse and severe atherosclerotic lesions in the thoracic ...

Silent Brain Infarcts

“…For example, the presence or absence of a hyperintense rim around CSFlike lesions on fluid-attenuated inversion recovery images 41 is not always helpful to discriminate small infarcts from dVRS, because astrocytic gliosis have been observed postmortem around large dVRS. 35,42 The use of proton density sequences for separating infarcts from dVRS based on the CSF signal 3 could also be inefficient because both cavitated infarcts and dVRS are filled with fluid. 39,43,44 The imaging analysis of the shape of cavities was recently shown to be crucial in the discrimination of dVRS.…”

Expanding lacunae causing triventricular hydrocephalus

“…The lack of contrast enhancement of the lesions and nearby parenchyma on MR imaging in our cases and in the case reported by Homeyer, et al, [10] however, is at variance with this hypothesis. Moreover, vasculitis was not present in the two other cases of expanding lacunae that have been verified by pathological investigation, [4,7] in which multiple cerebral infarctions and sclerohyalinotic vascular changes secondary to long-standing arterial hypertension were documented. In the case reported by Homeyer, et al, [10] and in our cases, no brain vascular lesion, vascular risk factor, or evidence of systemic vasculitis was present.…”

“…A review of the literature yielded only two other cases of expanding lacunae confirmed by pathological examination, [4,7] in which no clinical correlates of the lesions, located near the caudate and dentate nuclei, respectively, can be found in the brief case history provided. As well, no clinical correlate was found by Ogawa, et al, [17] in two cases of dilated perivascular spaces demonstrated by MR imaging in cerebral hemispheric white matter, although the results of a biopsy sample confirmed one of these cases.…”

“…[19] Because they have only been described by pathologists in three cases, [4,7,18] the clinical correlates of expanding lacunae are unclear. Magnetic resonance (MR) imaging enables an in vivo demonstration of expanding lacunae and contributes to their differential diagnosis, which includes other brain cysts.…”

Perivascular space and neurological disorders

“…However these symptoms do not relate to the locations of PVS, and do not follow the development of clinical symptom of patients [9,[25][26][27] .…”