Abstract

1.) Enzootic ataxia or swayback has been related to Schildcr's disease -- which is of course closely related to disseminated sclerosis -- because of the fact that one sometimes sees in the ataxia of lambs a gelatinous appearance of the white matter (INNES 1939). To be more precise it is the infantile form of Schildcr's disease that has been most frequently cited in this regard (MAc]~A~ i940; WIN]~ELmAN and MooRE 1942; INNES 1943) but INNES and SAUN])EI~S have more recently (1957) stated that "this does not however imply any causal relationship". 2.) Swayback would appear to be a demyelinating disease forming from the pathogenctic point of view part of a generalized disorder -- which may possibly also be local -- involving a disorder of copper metabolism (BE~ETS 1937). It is an attempt to co-ordinate these morphological analogies and the disorders o/ metabolism involved which forms the starting point of the histopathological and biochemical research that we have undertaken as a team in the last five years. In this work we shall only discuss the histopathological findings. Our observations concerning the animals originate in regions as different as those of Thessalonica (Greece) and Reykjavik (Iceland). This is not without interest nor is it unintentional. One must ask oneself wheter there are not differences between the ataxia of lambs observed in England and in Greece and those described in South Africa, in New Zealand andin Australia. Geographical variations can perhaps explain why different observers have published series in which the frequencies and the qualities of the lesions have been very variable. These variations are of such a degree that one sometimes asks oneself whether ~he descriptions do really correspond to identical morbid entities. The first lesions seen by BENN~T (1932) were described as degenerations of fibres in the thoraeo-iumbar spinal cord and in the sciatic and femoral nerves. Some cases with more protracted evolution showed a sclerosis of the spinal cord. These spinal cord lesions were localised, according to STEWART (1932), in the spinocerebellar tracts and in the column of GoU and were accompanied by anomalies of the cells of the column of Clarke in the thoracic cord.

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