A review of the primary dysautonomias of domestic animals.

Primary dysautonomias appear to be the result of initial damage to the protein synthetic pathway of a specific neuronal population, but despite detailed morphological study of several species there is, as yet, no indication of the precise lesion or the nature of the causal agent. The very marked similarities between the species with regard to lesion type, distribution, the age group affected and the geographical restrictions of occurrence would suggest a very similar, if not common, aetiology. There is no explanation, however, for the 70 year gap between its appearance in horses and its subsequent occurrence in other species or why it is these species, with very different physiology, habits and habitats, that are affected. No reference could be found in the literature to any infectious agent or toxin causing a similar range of structural effects with a similar species specificity or lesion distribution. Many questions about dysautonomias remain. Why is the lesion distribution so specific? At what level of the synthetic pathway does the primary lesion occur? What are the unusual compounds demonstrated in "acute phase" serum from affected horses; are they a neurotoxic agent(s) and/or its metabolites, or the abnormal product of an affected animal? Why did the experimental ponies which developed autonomic lesions not become ill? When do the clinical signs appear in relation to the occurrence of the primary lesion? Why are adolescent and young adult animals most commonly affected? As the general understanding of neuronal function and the numerous factors which influence it improves, the many subtle distinctions and similarities amongst the myriad sub-populations of neurones will become clearer and common features may emerge which will link the seemingly disparate neuronal types involved in the primary dysautonomias.