Encephalopathy anoxic

Ibrahim et al. 1963). Aiken and Braitman (1989) determined that cyanide has a direct effect on neurons not mediated by its inhibition of metabolism. Consistent with the view that cyanide toxicity is due to the inability of tissue to utilize oxygen is a report that in cyanide-intoxicated rats, arterial p02 levels rose, while carbon dioxide levels fell (Brierley et al. 1976). The authors suggested that the low levels of carbon dioxide may have led to vasoconstriction and reduction in brain blood flow therefore, brain damage may have been due to both histotoxic and anoxic effects. Partial remyelination after cessation of exposure has been reported, but it is apparent that this process, unlike that in the peripheral nervous system, is slow and incomplete (Hirano et al. 1968). The topographic selectivity of cyanide-induced encephalopathy may be related to the depth of acute intoxication and distribution of blood flow, which may result in selected regions of vascular insufficiency (Levine 1969). 

FLAIR) images that affected most severely areas of high vulnerability (cerebellum, hippocampus, thalamus, frontal and parietal cortices) (Singhal et al. 2002). Especially alterations in DWI seemed to correlate well with the distinct neuropathological features of anoxic-ischemic encephalopathy. 

Silva MD, Omae T, Helmer KG, Li F, Fisher M, Sotak CH (2002) Separating changes in the intra- and extracellular water apparent diffusion coefficient following focal cerebral ischemia in the rat brain. Magn Reson Med 48 826-837 Singhal AB, Topcuoglu MA, Koroshetz WJ (2002) Diffusion MRI in three types of anoxic encephalopathy. J Neurol Sci 196 37-40... 

A 31-year-old man developed priapism after taking zuclopenthixol 30 mg/day for 8 days, the dose having been increased to 75 mg the day before, while he was still taking oral carbamazepine 600 mg/day and clora-zepate dipotassium 30 mg/day. He had a history of perinatal anoxic encephalopathy with severe motor sequelae and dyslalia, alcohol dependence, and a personality disorder. On the day before the priapism occurred, he had been physically restrained and given an extra dose of intramuscular clorazepate dipotassium 50 mg. When priapism occurred, all drugs except clorazepate were withdrawn and about 6 hours later the corpora cavernosa were washed and infused with noradrenaline in glucose (8 doses of 40 pg), after which the priapism resolved. 

Burke TG and Mutnick AH (1993) Ventricular fibrillation and anoxic encephalopathy secondary to astemizole overdose. Annals of Pharmacotherapy 9 23-25. 

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