Aetiology
The underlying cause of meniere's disease (MD) remains unknown. Some authors, however, believe that in up to 55% of cases, a specific aetiological agent can be identified.[13][14] Among these aetiological agents are allergic responses (especially to food), congenital or acquired syphilis, Lyme disease, hypothyroidism, stenosis of the internal auditory canal, and acoustic or physical trauma.[13] Viral infection and immune-mediated mechanisms affecting the absorption of endolymph have also been implicated.[15] Hereditary factors are thought to play a role in the development of MD.[15] A multi-factorial inheritance may be the best model, leading to endolymphatic malabsorption and subsequent hydrops.[15]
Pathophysiology
Endolymphatic hydrops is thought to be due to over-production or impaired absorption of endolymph. This may occur as a result of one or a combination of the proposed aetiological agents. Some histopathological studies of the temporal bones suggest that, although endolymphatic hydrops is a histological marker for MD, it is not directly responsible for its symptoms.[16] However, studies from 2010 demonstrate through magnetic resonance imaging the central role of endolymphatic hydrops in the pathology of MD.[17]
During the acute attack the excessive endolymphatic fluid pressure causes distension and rupture of Reissner's membrane. This results in the release of potassium-rich endolymph into the perilymphatic space and causes injury to the sensory and neural elements of the inner ear, which manifests clinically as sudden hearing loss, tinnitus, and vertigo. Between attacks, Reissner's membrane may reattach itself, the chemical balance is restored, and symptoms remit.[3] However, some researchers are questioning this theory because membrane ruptures were found post-mortem in temporal bones with no history of vertigo.[16]
Immune-mediated mechanisms have long been implicated in the pathophysiology of MD. This has been supported by the presence of increased levels of immune complexes and the presence of auto-antibodies to structures of the inner ear in patients with MD. Lymphocytes and immunoglobulins have also been found in the endolymphatic sac.[18]
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