[The acute vestibular paralysis (author's transl)]

Acute vestibular paralysis may not be considered as a nosologic entity but as a syndrome. Symptomatology (vertigo, spontaneous and provoked vestibular nystagmus, absence of cochlear signs) shows an uniform picture. The results of the caloric test as well as the nystagmic responses induced by galvanic stimulation and the development of central vestibular compensation however indicate that the site of the lesion is not only confined to the labyrinth but may also occur at the level of the peripheral neuron or even the vestibular nuclei. Etiology and pathology are still vague. Our own clinical observations as well as the scarce data in literature about morphological and experimental studies suggest in a way that vascular and infectious disorders are of importance as primary releasing factors. Hypothetically, vestibular loss of function may either be caused by a disturbance of labyrinthine microcirculation, initiated in a great majority of cases by infection, or by a direct lesion of the peripheral neuron as well as the vestibular nuclei. Retrolabyrinthine lesions may be due to menigoencephalitis, caused by a neurotropic virus or other infectious agents such as Toxoplasma gondii. Acute vestibular paralysis should be strictly distinguished from vestibular neuronitis. While vestibular paralysis is a syndrome, vestibular neuronitis must be considered as a nosologic entity, including a lesion of the peripheral neuron as well as evidence of an infectious event.