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Central nervous system susceptibility to viral infection is often age dependent for unclear reasons. In this study, we examined the age-dependent susceptibility of the brain in mumps virus-induced hydrocephalus in hamsters, and evaluated the relationship between neuropathologic features and brain barriers using glial fibrillary acidic protein and zonula occludentes 1 (ZO-1) immunohistochemistry. In a group intracerebrally inoculated with mumps virus at 2 days of age, pathologic findings such as periventricular edema, ependymal cell loss, and ventricular dilation were more prominent and the distribution of mumps virus antigen was wider than in a group inoculated at 30 days of age. ZO-1-immunoreactive tight junctions in the hydrocephalic brains of the 2-day group were severely damaged in the choroid plexus and ependyma, and in white matter capillaries as early as 3 days after inoculation. These changes were not apparent in the hydrocephalic brains of the 30-day group. Prominent cortical dissemination of virus in the 2-day group was related to underdeveloped perivascular glial foot processes in brain parenchyma. Periventricular edema in the 2-day group was linked to ependymal and blood-brain barrier tight-junction permeability. Our results suggest that tight junctions in the early postnatal period are more immature and fragile than in the adult. We concluded that brain susceptibility in mumps virus-induced hydrocephalus is intimately related to the maturity of brain barriers.

We sought to elucidate the pathogenesis of Chiari type I malformation using an experimental model of hydrocephalus produced by inoculating hamsters with mumps virus. Dilatation of the lateral ventricules was detected in all brains inoculated at 2, 10, and 25 days of age. The cerebellum in hamsters inoculated at 2 and 10 days of age showed elongation and flattening of the vermis and protrusion or notching of the uvula. All layers, i.e., the molecular, Purkinje cell, and granular layers, and the white matter were preserved, but had become narrow. Purkinje cells remained normal. Hamsters inoculated at 25 days of age did not develop the cerebellar deformity. Mumps virus antigen was detected in all ependymal cells and in some epithelial cells of the choroid plexus in all hamsters that had been inoculated at 2, 10, or 25 days of age. Results suggest that Chiari type I malformation is caused by two main factors occurring simultaneously, i.e., increasing intracranial pressure and rapid histogenesis of the cerebellar cortex.

To elucidate the pathogenesis of early ventricular dilatation in hydrocephalus, we examined early morphological changes in ependymal layers at the lateral ventricles in suckling hamsters without aqueductal stenosis 5 days after the intracerebral inoculation of mumps virus. Mumps virus antigen was detectable in all ependymal cells. The ependymal cilia had almost disappeared and only the microvilli remained. A number of supraependymal cells were also observed on the surface of the lateral ventricles. Transmission electron microscopy revealed intracytoplasmic viral-like inclusions in the infected ependymal cells. These results suggest that functional and morphological disturbances in infected ependymal cells may cause early ventricular dilatation before aqueductal stenosis occurs.

A 5-year-old male patient with asymptomatic optic neuritis and mumps postinfectious encephalitis or acute disseminated encephalomyelitis is reported. Magnetic resonance imaging (MRI) with a short inversion time inversion recovery sequence was valuable in detecting clinically silent lesions of the unilateral right optic nerve in addition to visual evoked potentials. Evidence of concurrent optic neuritis was useful for detecting more extensive neurological involvement, leading to the diagnosis of mumps postinfectious encephalitis. A systematic MRI study should be performed in children with mumps encephalitis, regardless of appreciable clinical deficits.

Non suppurative periventricular encephalitis and lymphoid infiltration of choroid plexus were induced by intracerebral inoculation of non neuroadapted strains of mumps virus in cercopithecus monkeys. Inflammatory lymphoid infiltration showed an obvious connection with a mild damage of ependymal cells. No signs of neuronal involvement and no inclusions were seen in light microscopy. Proliferation of viral microtubules, though without the typical budding of virions, were visible in ependymal cells in electron microscopy. Subependymal and inflammatory cells which clearly take no part in the virus proliferation were affected by the alteration.