Meniere's disease: histopathology, cytochemistry, and imaging

  title={Meniere's disease: histopathology, cytochemistry, and imaging},
  author={G Ishiyama and Ivan A. Lopez and A R Sepahdari and Akira Ishiyama},
  journal={Annals of the New York Academy of Sciences},
Meniere's disease is a poorly understood, disabling syndrome causing spells of vertigo, hearing fluctuation, tinnitus, and aural fullness. In this paper, we present a review of the histopathology, cytochemistry, and imaging of Meniere's disease. Histopathology is significant for neuroepithelial damage with hair cell loss, basement membrane thickening, and perivascular microvascular damage. Cytochemical alterations are significant for altered AQP4 and AQP6 expression in the supporting cell, and… 
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Vestibular sensory epithelium in Meniere's disease.
Utricle and horizontal semicircular canal ampulla removed during labyrinthectomy from 11 patients with advanced Meniere's disease were studied under light and electron microscope. In light microscopy
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Menière's disease.
Meniere's disease causes recurrent vertigo, hearing loss, tinnitus, and fullness or pressure in the ear, which mainly affects adults aged 40-60 years and episodes can occur in clusters.
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    Archives of neurology
  • 2001
In 1861, Prosper Ménière presented a paper before the French Academy of Medicine in which he described a series of patients with episodic vertigo and hearing loss, and emphasized that vertigo could originate from damage to the inner ear.
Pathophysiology of Ménière's Syndrome: Are Symptoms Caused by Endolymphatic Hydrops?
  • S. Merchant, J. Adams, J. Nadol
  • Medicine
    Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology
  • 2005
Endolymphatic hydrops should be considered as a histologic marker for Ménière's syndrome rather than being directly responsible for its symptoms, consistent with the hypothesis that hydrops resulted from disordered fluid homeostasis caused by disruption of regulatory elements within the spiral ligament.
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