title: Lesion localisation: implications for the study of functional effects and mechanisms of action.
abstract: In some toxic neuropathies we see only distal "dying back" of longer and larger diameter axons, the perikaryon appearing to be intact. Some of these are the result of chronic energy deprivation, others are not. In other neuropathies sensory and autonomic neuron cell bodies are damaged without apparent selectivity. Toxic neuropathies often mimic the neurological effects of vitamin deficiencies by causing juxtaposed lesions in the same metabolic pathways. In acute energy deprivation toxic syndromes in the CNS, the pattern of damage is restricted to specific grey centres: there are variations in this pattern according to the site of the metabolic lesion, the species studied, the development of seizures, and other factors. Such toxic responses mimic human and animal disease states, such as Wernicke's encephalopathy and Leigh's disease, both of which are essentially acute energy deprivation syndromes.
authors.affiliation: Toxicology Research Unit, Medical Research Council Laboratories, Carshalton, Surrey, U.K.
authors.forename: J B
authors.initials: JB
authors.lastname: Cavanagh
mesh_terms: D000818:Animals; D004734:Energy Metabolism / Q000187:drug effects*; D006801:Humans; D009536:Niacinamide / Q000031:analogs & derivatives / Q000633:toxicity; D009574:Nitro Compounds / Q000633:toxicity; D010523:Peripheral Nervous System Diseases / Q000139:chemically induced* / Q000378:metabolism; D014899:Wernicke Encephalopathy / Q000378:metabolism*
chemical_list: D009574:Nitro Compounds; D009536:Niacinamide