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Acute intermittent porphyria presenting with short duration of gastrointestinal symptoms followed by rapidly progressive fulminant neurological syndrome during first attack is relatively uncommon. It is a neurological emergency and mimics many other psychiatric and medical disorders and can be fatal if it remains undiagnosed and untreated. Further, specific treatment in the form of Heme arginate is not universally available and very costly, so high clinical suspicion and early diagnosis and management of acute attack and prevention of further attacks are very important. We report a series of six cases who presented with convulsion and/or polyneuropathy early in the course of disease to highlight this fact.

Human brucellosis, more specifically neurobrucellosis, is a less commonly reported disease in India; although, animal brucellosis and seroprevalence in specific areas is well reported. We are reporting 4 cases of neurobrucellosis presenting as meningoencephalitis. Diagnosis was confirmed by serological test and agglutination titre was > 1:320 in all the patients. All these patients had close contact with animals and history of raw milk ingestion was present in 3 cases. The aim of presenting these cases is to create awareness among physicians while treating meningitis in persons, engaged in occupations related to brucellosis or having a history of ingestion of raw milk or milk product.

Brainstem auditory evoked potentials (BAEP) and somatosensory evoked potentials (SSEP) were recorded in 10 patients of heatstroke. Glasgow coma scale was used to assess level of consciousness. Values of either BAEP and/or SSEP were abnormal in all patients. Most consistent abnormalities of BAEP were delayed peak, latency of wave III & V and delayed IPL of III-V & I-V. The most consistent abnormality of SSEP were delayed absolute peak, latency of N20 and delayed IPL of N13-N20 (CCT). Distorted N20 was observed in 40 percent patients. The delay in conduction of electrical activities throughout the central nervous system in the patients, resulting in abnormal values of either BAEP and/or SSEP probably due to cerebral oedema with extensive parenchymatous degeneration of cells in brain, either from hyperpyrexia per se or from petechial haemorrhage in the brain, as reported on autopsy material by earlier workers.