DESCRIPTIONA 74-year-old man was brought to emergency services when he was found lying unresponsive in his room. Nearest of the kin reported that his clothes were drenched with sweat and that he was a regular alcohol user who had consumed in excess the previous day. Vital signs were normal. There was decerebrate posturing of limbs with bilateral extensor plantar response. The doll's eye movement and corneal reflexes were preserved. There was no neck stiffness. Random blood sugar at admission was 34 mg/dl, which was corrected with 100 ml 25% dextrose bolus infusion which was maintained with dextrose infusion and glucagon 1 mg intramuscular as injection. His brain CT scan was normal. The spinal tap yielded normal results. The ECG, echocardiogram, four vessels Doppler neck including the aortic arch and Electroencephalogram were normal. MRI of the brain showed hyperintense signals in both hippocampi, right insular, temporal, occipital and frontal cortex in diffusion-weighted images with diffusion restriction in apparent diffusion coefficient mapping suggestive of laminar cortical necrosis. MR angiogram was normal. He did not improve with treatment and succumbed to the illness ( figures 1A, B, C and 2A, B, C).First described in a patient with anoxic encephalopathy, 1 it was found later that laminar cortical necrosis represented cytotoxic oedema affecting a particular layer of cerebral cortex neuropathologically characterised by delayed selective neuronal necrosis and is a consequence of hypoxic-ischaemic encephalopathy, hypoglycaemic encephalopathy, status epilepticus and ischaemic stroke. 2Mechanisms of laminar cortical necrosis are not well elucidated.
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