Clinico-radiological profile of CVT patients and its correlation with D-dimer.

Cerebral Venous Thrombosis (CVT) is a well-known disease with diverse clinical presentation and causes. With advances in neuroimaging and changing lifestyles, the clinical profile and causes of CVT are changing. D-dimer has been studied in early diagnosis of CVT with variable results. This prospective study was carried out to assess the clinical profile of CVT and role of D-dimer in early diagnosis of CVT. The study period was from September 2017 to July 2019 and included 32 imaging proven patients of CVT. We also included 32 patients of migraine for assessing D-dimer. Data was collected according to a preformed format. D-dimer was assessed by a rapid semi-quantitative latex agglutination assay. Out of 32 CVT patients, 16(50%) were females. The mean age of the patients was 31.56 ± 14.31 years. Most common clinical features were headache (96.25%), papilloedema (37.5%) and seizures 10 (31.25%). Puerperium was the most common cause of CVT in females. Superior sagittal and transverse sinuses were the most common sinuses to be affected. The sensitivity of D-dimer assay was 81.25% and specificity 62.5%. Cerebral venous thrombosis is a disease with equal predilection among both genders affecting mostly young individuals. Most of the patients present with headache. Puerperium still contributes to majority of the cases. Iron deficiency anaemia needs to be evaluated as an association for CVT. Positive D-dimer should strengthen the suspicion of CVT in patients with acute headache.

Glutamate induces synthesis of thrombogenic peptides and extracellular vesicle release from human platelets.

Platelets are highly sensitive blood cells, which play central role in hemostasis and thrombosis. Platelet dense granules carry considerable amount of neurotransmitter glutamate that is exocytosed upon cell activation. As platelets also express glutamate receptors on their surface, it is pertinent to ask whether exposure to glutamate would affect their signalling within a growing thrombus. In this study we demonstrate that, glutamate per se induced synthesis of thrombogenic peptides, plasminogen activator inhibitor-1 and hypoxia-inducible factor-2α, from pre-existing mRNAs in enucleate platelets, stimulated cytosolic calcium entry, upregulated RhoA-ROCK-myosin light chain/myosin light chain phosphatase axis, and elicited extensive shedding of extracellular vesicles from platelets. Glutamate, too, incited platelet spreading and adhesion on to immobilized matrix under arterial shear, raised mitochondrial transmembrane potential associated with generation of reactive oxygen species and induced activation of AMP-activated protein kinase in platelets. Taken together, glutamate switches human platelets to pro-activation phenotype mediated mostly through AMPA receptors and thus targeting glutamate receptors may be a promising anti-platelet strategy.