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Positional and positioning vertigo and nystagmus.

T Brandt1

  • 1Neurologische Universitätsklinik, Klinikum Grosshadern, München, F.R.G.

Journal of the Neurological Sciences
|January 1, 1990
PubMed
Summary

Positional vertigo syndromes stem from peripheral or central vestibular issues. Benign paroxysmal positioning vertigo, the most common form, involves the posterior semicircular canal.

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Area of Science:

  • Neurology
  • Ophthalmology
  • Otolaryngology

Background:

  • Positional vertigo and nystagmus syndromes arise from peripheral or central vestibular dysfunction.
  • Benign paroxysmal positioning vertigo (BPPV), the most frequent type, results from cupulolithiasis in the posterior semicircular canal.
  • Other causes include buoyancy mechanisms and neurovascular compression of the vestibular nerve.

Purpose of the Study:

  • To differentiate between peripheral and central causes of positional vertigo and nystagmus.
  • To discuss the pathophysiology of various positional vertigo syndromes.
  • To highlight management considerations for disabling positional vertigo.

Main Methods:

  • Review of existing literature on positional vertigo and nystagmus.
  • Categorization of vertigo syndromes based on etiology (peripheral vs. central).
  • Analysis of proposed mechanisms for different positional vertigo subtypes.

Main Results:

  • Peripheral causes include BPPV and buoyancy-related nystagmus.
  • Central positional vertigo is linked to brainstem ischemia or gravitational vector changes.
  • Lesions in central positional vertigo are near the fourth ventricle and vestibular nuclei.

Conclusions:

  • Positional vertigo has diverse etiologies, ranging from canalithiasis to central nervous system involvement.
  • Understanding the underlying mechanism is crucial for appropriate diagnosis and management.
  • Further research is needed for inadequately described entities like disabling positional vertigo.

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