Abstract

Introduction: Cerebral venous thrombosis is mostly an uncommon but severe
thrombotic manifestation which has a high mortality rate, has the potential to end in
disability and the greater tendency of recurrence. There are some coagulation
abnormalities such as gain-of-function mutations in the genes that encodes factor V
(factor V Leiden) and prothrombin3 are presented with an increased risk of cerebral
vein thrombosis4-6 whereas there are no data currently reported on the role of
hyperhomocysteinemia as a risk factor for cerebral venous thrombosis. High plasma
levels of total homocysteine (tHcy) result from the connection between genetic and
acquired determinants. Cerebral venous thrombosis is one of the commonest causes of
stroke as far as Indian population is concerned. CVST usually predisposes in the state
of pregnancy and puerperium. The pathological hallmark that is reported in CVST is
haemorrhagic infarction. CVST predominantly occur in the young individuals and can
present with a broad spectrum of clinical manifestations which include headache,
altered sensorium, seizures, focal neurological deficits, papilloedema and cranial nerve
palsies. Headache is the most frequent and often the first reported clinical
manifestation. Homocysteine (Hcy) is a sulfhydryl amino acid compound that is
generated from protein breakdown and the essential amino acid methionine as it is
metabolized to cysteine. Hcy can be broken down in two pathways. When there is in
excess methionine, Hcy is directed to transulphuration pathway where it is irreversibly
conjugated to cysteine. Hcy can also be remethylated in a methionine conserving
pathway and this pathway requires folic acid and MTHFR.