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Cocaine-induced brain damage can be divided into primary neurotoxic effects causing toxic encephalopathy, secondary effects of compromised cerebral blood flow in ischaemic and haemorrhagic stroke, cerebral vasculitis and vasospasm, and tertiary effects due to hypoxia as a result of cardiopulmonary collapse. Toxic leucoencephalopathy mainly affects white matter (WM) tracts serving higher cerebral function, thereby leading to altered personality, attention deficits and memory impairment in mild cases and to dementia, coma and brain death in severe cases. There are numerous legal and illegal substances provoking toxic encephalopathy, which could develop gradually or acutely.1–4 This is, to our knowledge, the first report of fatal cocaine-associated encephalopathy, in a patient who had not taken cocaine previously, assessed by proton nuclear magnetic resonance spectroscopy (1H-MRS).
A 21-year-old man had recurrent episodes of depression. He was found breathing and deeply comatose in a hotel room with injection marks in the left cubital vein. A syringe and a farewell letter were beside him; 14 empty packages with tracks of white powder, later identified as cocaine, were found close by.
On admission he was unresponsive and intubated with intact brain stem reflexes. There was bilateral hyperreflexia and moderately increased muscle tone, but normal plantar reflexes. Blood assays showed mild metabolic acidosis (pH 7.30) with initially elevated liver enzyme concentrations (alanine aminotransferase 530 U/l); rhabdomyolysis (myoglobin 38 000 μg/l) and leucocytosis (17 billions/l); …
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