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To investigate whether apoptosis contributes to neuronal degeneration in bovine spongiform encephalopathy (BSE), morphological changes consistent with apoptosis were sought and in-situ end labelling (ISEL) was applied, in a series of 20 BSE cases and 10 age-matched normal control cattle. Apoptotic changes were not found in neurons but were occasionally seen in glial cells. Relatively few ISEL-positive neurons were found, but many labelled nuclei were seen in glial cells in certain areas. None of the labelled cells showed morphological features of apoptosis. ISEL+cells occurred in areas of spongÍiform change and other areas of grey matter lacking spongiform change. Some association was found between degree of cellular DNA fragmentation and accumulation of abnormal prion protein (PrPSc). Interestingly, small or moderate numbers of T lymphocytes, not present in the normal central nervous system (CNS), were detected in the CNS parenchyma in most BSE cases. There was a pronounced astrogliosis, but markers of macrophage or microglial activation were only slightly increased. The results indicate that nuclear DNA vulnerability is enhanced in certain neuroanatomical areas in BSE, but evidence that apoptosis plays a role in neuronal loss in BSE was very limited.

Sporadically occurring non‐suppurative encephalitis appears to be a frequent condition of Swiss cattle. Fifty‐one such cases diagnosed over a period of 10 years were examined retrospectively to investigate whether they constituted one or more distinct diseases, and to search for aetiological agents. Three cases were characterised by periventricular granulomatous encephalitis, and most probably represented a different disease, but the remaining 48 cases had disseminated non‐suppurative encephalitis with widespread neuronal changes. Neuronal degeneration was very marked in the hippocampus of 10 cases and in the cerebellar Purkinje cells of 11. It was thought that the latter cases represented morphological variations of the same disease rather than a different disease because of their overlapping morphological features. The 48 cases had the following features in common: the disease had primarily neurological signs affecting mostly adult cattle, it was a sporadic condition, and there was a clear tendency for it to have a subacute to chronic course. Polymerase chain reaction (PCR) amplification for chlamydial DNA was negative except in one of 32 specimens, and immunohistochemistry did not demonstrate the presence of chlamydial antigens either in the one PCR‐positive case or in the other cases examined. Immunohistochemistry for rabies virus, Borna disease virus, and central European tickborne encephalitis virus was negative. In four cases, immunolabelled cells were found in the lesions with antibodies against paramyxovirus antigens.

We examined 103 patients with vestibular neuritis (VN) in a follow-up study (5.7 to 20.5 years, mean 9.8 years). Two patients (1.9%) had developed a second occurrence of VN 29 to 39 months after the first. VN affected the contralateral ear in both and caused less severe distressing vertigo and postural imbalance. Unlike Bell’s palsy and sudden hearing loss, a relapse in the same ear did not occur.