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Feline dysautonomia is a dysfunction of the autonomic nervous system, the main features of which are dilated pupils, dry mucous membranes, mega‐oesophagus and constipation. The clinical and pathological features, treatment and follow‐up details of 40 cases seen at the University of Glasgow Veterinary School are described. The pathology was demonstrated to be mainly restricted to the autonomic ganglia and neurons in selected cranial nerve nuclei. Less marked changes were also found in neurons of the spinal cord and dorsal root ganglia. Nine cases recovered but this required up to one year and, in some, mild clinical signs persisted. Viral, toxicological and epidemiological studies were unrewarding and the aetiology is presently unknown. The similarities between this condition, grass sickness of horses and dysautonomia in the dog and man are discussed.

Seven cases with tumours localised in the brachial plexus are described. The main clinical features were a progressive lameness in one forelimb with marked muscle atrophy and very obvious but non-localizable pain. A palpable lump in the axilla was present in less than half the cases. Ancillary aids contributed little in the diagnosis except for electrophysiology which gave evidence of neural damage at an early stage of the disease and as such may be the most useful aid to an early diagnosis. Two different pathological entities were observed, the first where the tumour, primarily of neural origin (usually a neurofibrosarcoma), arose within the nerves themselves and the second where the tumours arose in adjacent tissue and involved the plexus by local infiltration. In all cases the prognosis was hopeless because of local infiltration of the tumour and metastases. In the early stages accurate diagnosis can be difficult in the absence of a mass but the possibility should be considered in any case where chronic lameness with obvious non-localizable pain is present in one forelimb.

Increased dosage of the proteolipid protein (Plp) gene causes CNS disease (Pelizaeus-Merzbacher disease [PMD]), which has many similarities to disorders of the PNS associated with duplication of the peripheral myelin protein-22 (PMP22) gene locus. Transgenic mice carrying extra copies of the wild-type Plp gene provide a valid model of PMD. Variations in gene dosage can cause a wide range of phenotypes from severe, lethal dysmyelination through late-onset demyelination. A predilection for different fiber diameters may occur within the various phenotypes with dysmyelination being more obvious in large fibers and late-onset degeneration predominantly affecting small fibers. Although the frequency of apoptotic oligodendrocytes is increased with high gene dosage, the number of mature oligodendrocytes appears adequate. Oligodendrocytes in the dysmyelinated CNS express a range of genes typical of mature cells, yet are unable to assemble sufficient myelin. Oligodendrocytes contain abnormal vacuoles and stain intensely for PLP and other proteins such as MAG. The findings suggest that with high gene dosage much of the PLP, and possibly other proteins, is missorted and degraded in the lysosomal system.