BLOOD-BRAIN-BARRIER DYSFUNCTION IN BINSWANGERS-DISEASE - AN IMMUNOHISTOCHEMICAL STUDY

Binswanger's disease is pathologically characterized by a combination of diffuse cerebrovascular white matter lesions and lacunar infarcts i n the basal ganglia and white matter. Although a blood-brain barrier ( BBB) dysfunction has been implicated in the pathogenesis of these whil e matter (WM)) lesions, few authors have addressed this problem. In th e present study, we describe BBB dysfunction and its regional differen ces in the brains of Binswanger's disease patients. Twelve brains from Binswanger's disease patients (group III) were examined and compared with those from five patients with non-neurological disease (group I) and five cortical in Farct patients without significant WM lesions (gr oup II). Immunohistochemistry was performed for glial fibrillary acidi c protein and vimentin as astroglial cell markers, and for immunoglobu lins, complements and fibrinogen as extravasated serum protein markers . The grading scores for IgG extravasation were significantly higher i n group III as compared to group I, in both the periventricular WM and the subcortical WM (P < 0.01). In group III, the scores in the perive ntricular WM. and subcortical WM were significantly higher than in the subcortical U fibers and cerebral cortex (P < 0.01 for the periventri cular WM; P < 0.001 for the subcortical WM), respectively. Clasmatoden dritic astroglia, which had swollen cell bodies and large cytoplasmic vacuoles with disintegrated processes, incorporated the serum componen ts IgG, IgM, C3d, C1q and fibrinogen, both in the periventricular WM a nd subcortical WM in 5 out of 12 (42%) Binswanger's disease brains. Th ese results indicate that WM lesions in Binswanger's disease are accom panied by BBB dysfunction, although it remains uncertain whether BBB d ysfunction is secondary to either chronic cerebral ischemia or arteria l hypertension.