Puerperal cerebral venous thrombosis: therapeutic benefit of low dose heparin.

Advances in imageology have improved the diagnostic yield of cerebral venous/sinus thrombosis (CVT). However, its management remains a challenge. The present study was carried out to study the role of heparin in CVT. Therapeutic outcome of 150 patients of puerperal CVT manifesting within one month of delivery or abortion, was analyzed. The diagnosis was supported by cranial computed tomography and/or angiography whenever required. Seventy three patients, 46 with non-haemorrhagic infarction and 27 with haemorrhagic infarction, received 2500 units of subcutaneous heparin, three times a day within 24 hours of hospitalization till 30th post partum day or symptomatic relief. Seventy seven patients during the same period, 50 with non-haemorrhagic infarction and 27 with haemorrhagic infarction, who did not receive heparin formed the control group. Repeat CT scans were done when indicated. Among the heparin group, 34 patients made full recovery. There were eight deaths, all among the patients with haemorrhagic lesion. In control group, only 14 patients recovered completely (P=<0.001) and 18 died (P=<0.001). There were no adverse effects of heparin. Low dose heparin is safe and efficacious in puerperal CVT, even in patients with haemorrhagic infarction.

P300 amplitudes vary inversely with continuum of risk in first degree male relatives of alcoholics.

First degree relatives of alcoholics show significantly reduced P300 amplitudes. This phenomenon is though to be a vulnerability marker of alcoholism. Relatives of alcoholics with higher family loading and early onset alcoholism are at greater risk for developing alcoholism. The high risk population may comprise subtypes differentiated by family history and/or age at onset of alcoholism, with differing risks, measurable in terms of the expression of the vulnerability marker. Four groups of alcohol-naive sons/male siblings of alcoholics (n = 64) were studied. The groups were constructed on the permutation of two defining characteristics: high family loading (two or more first degree alcoholic relatives) and early onset alcohol dependence (before 25 years) in the relatives. Comparison of P300 amplitude in an auditory paradigm showed significant inter-group differences as well as progressive increase/normalization of amplitudes from the high loading-early onset group (HR1) to the low loading-late onset group (HR4), with the latter being indistinguishable from a separate group of (control) normals. There were no significant differences of P300 latency among the groups. We conclude that P300 amplitudes vary inversely with the presumed continuum of risk in those at high risk for developing alcoholism.