Fifty four patients of tuberculous meningitis, diagnosed by a standard protocol were followed up for a mean period of 9 months, with periodic assessment of laboratory tests for liver function. A total of 23 patients (42.6%: 10 males and 13 females) developed hepatic dysfunction and 7 of these (30.4%) developed clinical jaundice. Derangement of liver functions was noted in the first month after starting the treatment. Of the various risk factors, a low body mass index and low serum albumin were possible predictors, while presence of increased intracranial tension, previous exposure to anti-tuberculous therapy and presence of extraneural tuberculosis and tuberculous emerged as possible protective factors. Age, sex, basal metabolic rate, concurrent anticonvulsant medication, other laboratory and clinical paremeters were insignificant risk factors.

This prospective uncontrolled study was done to evaluate the role of acetazolamide as an adjunct in the treatment of partial and secondarily generalized seizures. Fourteen out of 15 patients responded to addition of acetazolamide. The mean follow up was 14.86 months. Three patients subsequently developed tolerance. The only side effect noted was paresthesia of limbs not disabling enough to stop the drug. Acetazolamide is a useful adjunct, in the management of partial and secondarily generalized seizures.

Cryptococcal meningitis is an uncommon cause of multiple cranial nerve palsies. This case report illustrates one such case of cryptococcal meningitis clinically manifesting with extensive cranial nerve involvement in an HIV seronegative individual. Histology revealed infiltration of the cranial nerves by cryptococci causing axonal disruption with secondary demyelination in the absence of any evidence of inflammation or vasculitis. We believe that axonal damage underlies the pathogenesis of cranial nerve involvement in cryptococcal meningitis.

A 49 year old woman presented with one year's history of dysarthria and ataxia. She had 3 attacks of falciparum malaria in the past and developed features of cerebellar dysfunction on the seventh day after the third attack was cured. All three episodes were diagnosed on the basis of positive peripheral blood films for asexual stages of Plasmodium falciparum. The illness reached its peak in two weeks and remained static thereafter. Delayed cerebeller syndrome following falciparum malaria is usually a self-limiting illness with complete recovery (delayed reversible post-malaria cerebellar syndrome). This case illustrates another variety of delayed post-malaria cerebellar syndrome in which cerebellar dysfunction is persistent (delayed persistent post-malaria cerebella syndrome). This could be considered a type of post-malaria neurological syndrome described in the past.

This 50 year old housewife reported with severe right sided orbital and temporal pain. The clinical examination revealed right third cranial nerve paresis with ptosis and small sized pupil, (Reader's syndrome - Group I). Cerebral angiogrpahy revealed a giant, partially thrombosed aneurysm of the right internal carotid artery. Her facial pain was relieved by carotid ligation. Intracranial internal carotid aneurysms rarely cause paratrigeminal syndrome of Raeder. The mechanism of facial pain and ocular synpathetic involvement is discussed.