Experimentally induced beriberi polyneuropathy in chickens

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Chickens fed with the same composition of diet as our low income beriberi polyneuropathic patients, developed clinical symptoms of thiamine deficiency in 22.3 +/- 6.3 days. There appeared to be a body store of thiamine which is utilized during a period of deficient intake. Haemoglobin content and serum albumin did not change appreciably during thiamine deficiency. The blood thiamine content was low and the thiamine pyrophosphate (TPP) effect increased to more than 25 percent during the development of the beriberi polyneuropathy, which resumed after one week on thiamine tetrahydrofurfuryl disulfide (TTFD) treatment. However, the clinical features gradually improved after about one month. Neurophysiological findings including somatosensory evoked potentials (SSEPs) and neuromorphological studies of the peroneal and sciatic nerves were compatible with a major degree of axonal degeneration and secondary minimal segmental demyelination. We may conclude that the experimentally induced beriberi polyneuropathy in chickens seems a good model for studying these forms of neuropathy in view of diagnosis and treatment.

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Cerebral circulatory disturbances represent the third most frequent cause of death in Western industrialized countries after cardiovascular diseases and neoplasms. With the advent of new diagnostic and therapeutic procedures as, e.g. thrombolysis therapy, cerebral ischemias have become a topic of central importance in clinical neurology. In particular due to the increasing number of available interventional therapies in the carotid artery territory, significantly less attention has been given to the posterior circulation and therefore to vertebrobasilar infarctions. In many instances the described vascular system continues to be only insufficiently evaluated. The great morphologic and clinical variability of the findings further contributes to the difficulty of viewing brainstem infarctions as a nosologic unit.
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