Coagulation Activation in Patients With Binswanger Disease

Abstract

These results indicate that the coagulation-fibrinolysis pathway is activated in patients with BD with a subacute aggravation. Coagulation activation may result in the formation of microthrombi and microcirculatory disturbances in the brains of these patients, and thus promote further biological and neurologic insults.

Effects of an Antithrombin Drug in Patients with Subacute Exacerbations of Binswanger Disease.

“…Although there were no fresh lesions on the MRimages of these 4 patients, 1 out of 3 BDpatients with a recent neurological decline had acute lacunar infarctions in our previous study, suggesting a causal relation of microcirculation deficits to neurological decline (7). This is further supported by the observation that neurological decline was frequently accompanied by a recent ischemic lesion in patients with vascular dementia using a more sensitive diffusion-weighted MRimage (15).…”

“…However, in lacunar cerebral infarction, these hemostatic markers are not prominently altered (20)(21)(22). Therefore, the marked increase in the hemostatic markers in BDmay be attributable to a mechanism specific for BD, rather than to incidental lacunar cerebral infarctions (7). In this study, argatroban treatment reduced the levels of the hemostatic markers, with a corresponding improvement in cognitive dysfunction and gait disorders.…”

“…However, the effectiveness of antiplatelet agents remain elusive in small artery diseases such as lacunar cerebral infarctions and white matter lesions. Wehave recently reported activation of the blood coagulation system in BD (6,7). In addition, a correlation between coagulation systemactivation andcerebrovascularwhitematter lesions has been reported in Sneddon syndrome and homocystinuria (8,9).…”

Leukoaraiosis Predicts Cortical Infarct Volume After Distal Middle Cerebral Artery Occlusion

“…5,24 Thus, our data expand on the notion that LA is associated with cerebral pathology beyond its visible aspects on standard neuroimaging 25,26 and together with prior studies provide evidence for the hypothesized link among cortical microvascular rarefaction, chronic hypoperfusion, and decreased ischemic resilience. 3 Additional mechanisms by which LA may modulate ischemic tolerance in remote (cortical) tissue include increased hypercoagulability, 27 platelet activation, 28 and genetic variants implicated in ischemic pathogenesis. 29 Further research is needed to confirm our findings and clarify the potential contribution of such factors.…”

A 55 Year Old Man with Progressive Neurologic Deficits

“…Patients with BD have dementia and various clinical and radiological abnormalities, such as focal cerebrovascular deficits, and subcortical cerebral dysfunction. They also have a variety of vascular risk factors [3][4][5].…”