JOURNAL ARTICLE
REVIEW

Positional and positioning vertigo and nystagmus

T Brandt
Journal of the Neurological Sciences 1990, 95 (1): 3-28
2187057
Positional and positioning vertigo and nystagmus syndromes can be attributed to either peripheral or central vestibular dysfunction. The most common form is benign paroxysmal positioning vertigo which is caused by cupulolithiasis into the posterior semicircular canal. Other labyrinthine manifestations such as positional alcohol nystagmus, positional nystagmus with macroglobulinaemia and "heavy water" or glycerol ingestion occur because of a specific gravity differential between the cupula and the endolymph (buoyancy mechanism). Neurovascular compression of the vestibular nerve may be a causative factor for "disabling positional vertigo" which is an insufficiently described entity. Hesitation is highly justifiable since retromastoid craniectomy for microvascular decompression is the recommended management. Central positional vertigo is either induced by head movements which result in a transient ischaemia of the ponto-medullary brainstem, or by a change in head position relative to the gravitational vector. The latter is comprised of at least three forms: positional downbeat nystagmus (nodulus), positional nystagmus without concurrent vertigo, and positional vertigo with nystagmus. The site of the lesion is always near the fourth ventricle and the vestibular nuclei. The most probable explanation for the positional response is a vestibular tone imbalance caused by disinhibition of the vestibular reflexes on perception, eye, head and body position.

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