Cerebral venous thrombosis (CVT), is the thrombosis of the
intracranial veins or dural sinuses.1 It is a relatively rare disorder,
affecting about 5 persons per million per year with huge regional
variations. It accounts less than 1% of all strokes. It has differential
geographic distribution with a higher incidence in the Asian countries.
In contrast to arterial stroke, thrombosis of the cerebral venous sinuses
and the cerebral cortical veins most often affects children and young
adults. Its presentation is highly variable, etiological factors are diverse
and more heterogeneous making cerebral cortical venous thrombosis
(CVT) a distinctively unique entity. The Virchow’s triad, which compromises the features of
endothelial damage, stasis and hypercoagulability of blood, plays a very
important role in the pathogenesis of cerebral venous sinus thrombosis.
These haemodynamic factors vary with each patient. They may operate
together incidentally or accidentally to produce the clinical
manifestation of cerebral cortical venous sinus thrombosis.
AIM OF THE STUDY :
To study the risk and etiological factors in pathogenesis of Cerebral Venous Thrombosis and the varied clinical presentation in
males.
CONCLUSION : Cerebral venous thrombosis (CVT) which was previously thought
to be an uncommon condition is now being diagnosed frequently due to
increasing awareness and improvement in imaging modalities. Cerebral
venous sinus thrombosis presents with a wide variety of clinical
manifestation, the most common being acute onset headache, seizures,
features of raised intracranial tension and focal neurological deficits not
pertaining to arterial territorial region.
Thrombophilic conditions and hyper oestrogenic states in a
setting of dehydration are known factors postulated in the causation of
CVT. This study, exclusively done in male patients is the first of its kind
to our knowledge from the literature. From the results obtained in this
study, alcoholism, which is very much rampant in this part of Chennai,
seems to be cause for the higher incidence of CVT in males. The
correlations of the various studies quoted from the literature, makes it
plausible to consider folate deficiency in alcoholics with the resultant
hyper homocystinemia as the cause for the hyper coagulability. Further,
in our study group which includes people who are manual labourers,
belonging to low socioeconomic class, pre-existent nutritional deficiency might also contribute to the clinical scenario. Hence these
nutritional deficiencies, which are amenable for correction, if sought
earlier and corrected in the high risk group, might decrease the
incidence of this catastrophic disease.
Further large scale studies are needed to establish a clear
relationship between these factors in our population. Studies are also
needed in the context of treatment with folic acid, methyl cobalamine,
and pyridoxine in the acute setting of CVT. Further studies are also
needed in pregnant and the puerperal women who will also have
decreased folate levels due to increased demand. The appropriate dose
of folic acid needed to overcome these deficient states in various
population subgroups needs to be quantified by further studies
