Interpretation of levels of strontium-90 in human bone.

Poiyneuritiis-Miller BMRITIsH 1225that high circulating levels of isoniazid based on this inherited metabolic variation induce neuropathy, as do the high levels of circulating nitrofurantoin sometimes encountered in the chemotherapy of chronic kidney infections in the presence of renal failure.But in the case of isoniazid the genetically deter- mined basis of the toxic circulating levels is especially remark- able, and may have implications for other kinds of poisoning where familial susceptibility has been observed.Thalidomide neuropathy is an example from the field under discussion.Other types of toxic neuropathy are at present the subject of active biochemical study, though the results so far obtained have thrown less light on the general problems concerned than in the two instances mentioned above.Morphological and physiological investigations present fewer intrinsic difficulties than attempts to unravel chemical pathogenesis, especially since we have so little certain knowledge of the intimate chemistry of the normal peripheral nervous system, but the biochemical approach undoubtedly has greater potentialities in relation both to aetiology and to ultimate therapeutic possibilities. SummaryAlthough polyneuritis is usually regarded as a disorder of nerve fibres, these fibres are in fact the long processes of neurones situated in the spinal cord and posterior root ganglia.Some polyneuritic lesions primarily affect the nerve fibre at intervals along its length.In others peripheral dying back of the fibre results from damage to the neurone itself.In a third group its myelin sheath is disproportionately affected.The current contributions of electrophysiological investiga- tion, tissue biopsy, and animal experiment to the study of peripheral nerve lesions are discussed, and a brief account is given of the application of concepts drawn from these fields to some of the commoner clinical forms of neuropathy.