Abstract

It is postulated that mumps virus gains entry into the cochlea from the parotid gland retrogradely through the ipsilateral lymphatics, accounting for ipsilateral sensorineural deafness. In bilateral deafness, besides causing neurolabyrinthitis, it is hypothesised that auditory; 'neuronitis', akin to vestibular neuronitis, may be an additional causative factor which spares the vestibular neurones. In this instance the mumps virus presumably acts on a toxic or allergic basis (sensitization), bringing about 'neuronitis' with a selective 'cochleotoxic' action, rather than neuritis. Acoustic neuritis is likely to affect both the components of the statoacoustic nerve. Meningitis or meningoencephalitis are other alternative known causes of involvement of the acoustic nerve, intracranially/extracranially, or the infection may travel down from the C.S.F. through the cochlear aqueduct into the cochlea causing the deafness. Quite often there is ipsilateral sensorineural deafness associated with mumps. Deafness has been detected even in the cases of subclinical (inapparent) mumps corroborated only by serologilcal evidence of previous attack of mumps, 90% of the 30 cases, observed by the author over the last 30 years, had audiologically established ipsilateral sensorineural deafness. A putative explanation is offered for its ipsilaterality. In about 30% of the moderately deaf cases SISI was positive and in most of them discrimination score for speech was 90-100% indicating cochlear pathology. Vestibular function tests were within normal limits in all the author's cases. Mumps is caused by paramyxovirus and once suffered, a life-long immunity is usually conferred. 25% of the cases are subclinical or inapparent and 80-90% of an adult population has serological evidence of previous attack of mumps. Usually, unilateral deafness or rarely a bilateral one is associated with mumps (Shambaugh, 1976, Harrison, 1994); infrequently there is bilateral involvement (Lindsay et al, 1960, Prasad 1963). Sudden deafness in mumps has also been recorded (Friedmann, 1974). There is slight or no loss of vestibular response ~ (Shambaugh, 1967) and Lindsay et al (1960) found in a case of 5 years old boy degeneration of cochlear duct and organ o f corti and mild degeneration and loss of neurones of the spiral ganglion (limited to the basal coil) and atrophy of the stria vascularis, in both the ears. In this case labyrinthine symptoms developed three weeks after the clinical diagnosis, No damage in' the vestibular part has been mentioned. So it appears that it has a clear predilictien for the cochlear part of the labyrinth and the statoacoustic nerve. Ylikoski et al (1981) observed extensive reduction of nerve fibres in the osseous spiral lamina and neurone cell bodies in the spiral ganglion (70 to 85% of the cells were destroyed) following mechanical destructive lesion to the labyrinth and in one case no detectable ganglion cells were found. This appears to be retrograde degeneration upto the spiral ganglion does not take place to any significant extent, if at all.

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