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The histologic changes in the CNS of 10 dogs with epileptiform cramps and psychic alterations are described. Most of the animals had gastroenteritis of apparently diverse aetiology prior to the onset of the nervous signs.The lesions are characterized by bilaterally symmetrical focal necroses in the grey matter. Oedema and proliferation of blood vessels were present to varying extents in individual cases. What is conspicuous is not only the symmetrical localization of the lesions but also the invatiable damage of the rhinencephalon in the broad sense. There was no significant increase of oligo- or astroglia. In almost all cases Ammon's horn and the piriform lobe were simultaneously affected. In addition the olfactory bulbs, septum pellucidum, dorsomedian cortex, and now and then also the lateral cortical layers and basal ganglia might show accompanying lesions. The remaining brain stem and the cerebellum remained almost entirely spared.The aetiology of the lesions described is undetermined. Exogenous intoxication does not appear likely although it cannot be excluded with certainty. The clinical and histologic findings rather suggest the action of diverse pathogenetic factors. These lead to morphologically similar alterations, which may be a consequence of a deficient provision of the brain tissue with oxygen or with nutrient substances.

A histologic study was made of the central nervous system of 108 dogs with neurological illness. One group comprised 71 cases of distemper encephalitis. The second group of 37 cases encompassed toxoplasma encephalitis (14), symmetrical cerebral necrosis (10), reticulosis (6), lymphocytic meningoencephalitis (3), leukoencephalitis (2) and canine viral hepatitis (2).Inclusion bodies can be found in all dogs with distemper encephalitis. In most cases this diagnosis is easy, even without the inclusion bodies. However, detection of inclusions becomes important in cases showing a form of distemper encephalitis atypical with respect to histologic type or localization. In one case each, focal symmetrical necroses and toxoplasmosis-induced lesions were observed in association with distemper infection of the CNS.The regularity with which inclusion bodies can be found in all cases of distemper encephalitis means that in their absence, lesions induced by the distemper virus can be excluded with considerable assurance.The dependence of the density of the inclusion bodies on the type of tissue changes, the histochemical and tinctorial features of the inclusion bodies, the occurrence of lesions in the cerebellar granule cells, and the formation of cell syncytia by glial cells with inclusion bodies are discussed with respect to their specificity for distemper viral infection of the CNS.