Meniere’s disease was first described by Prosper Meniere in the 1800s. Up until that time, vertigo was thought to be the result of epileptic type seizures. Meniere was the first to publicly suggest that the inner ear was the cause of the collection of symptoms including hearing loss and vertigo, but he thought that they were the result of a hemorrhage of the inner ear. For those interested in a detailed history regarding Dr. Meniere, see the excellent article by Dr. Robert Baloh, published in 2001.

 There have been many theories ascribed to the causes of Meniere’s symptoms. We discussed one plausible theory last week involving a blockage of one of the ducts connecting different fluid filled chambers within the inner ear. There has been a widely accepted similar theory around for years, where it was suspected that a different duct connecting to the endolymphatic sac could become blocked. This theory led to a long standing surgical technique used to treat Meniere’s disease where a shunt is created to offer an alternative fluid pathway for the inner ear fluid (endolymph).

Others have suggested that Meniere’s disease is not the result of a blockage at all, but rather an over production of endolymph by the stria vascularis, while others have theorized that Meniere’s episodes could involve disrupted blood flow to the labyrinth, an allergic response or an immune system response. Most recently, it has been suggested that Meniere’s disease may be a variant of migraine. Many believe that a variety of abnormalities, including those listed above, may be responsible for the hearing loss and vertigo symptoms, and that there is not one single cause to be found.

 Obviously, there is a lot of work to be done to understand this condition before we can offer early effective treatments.

Photo courtesy of Yamane et al


It seems like a high percentage of my posts here relate to Meniere’s disease.  So many questions, with very few definite answers. There are many theories as to what causes the triad of symptoms (vertigo, tinnitus, hearing loss) associated with a Meniere’s episode, and many treatment options available. If you think about it, if any one theory explained all aspects of the disease, or if there was solid evidence to support a theory, we may not have so many alternative theories. Let’s explore some of the more popular theories, and see where the evidence leads us.

I will start with the most recent entry. Yamane and colleagues in Japan have published two papers in the past few years proposing a novel theory on Meniere’s disease, with some impressive supporting evidence. First, a quick review: the labyrinth (balance part of the inner ear) is a series of interconnected chambers and tunnels. There are motion sensors in each of the chambers and tunnels. When you move your head, the inner ear fluid (endolymph) lags behind and stimulates these sensors, sending messages to the brain regarding the speed and direction of head movement. The key word here is “interconnected.” One theory is that the endolymph flows throughout these chambers and tunnels, and more than one theory about Meniere’s disease suggests that the disease may be caused by a blockage somewhere in the labyrinth, causing endolymph to build up (sort of a “mini-dam”). There are some very narrow points where different chambers in the labyrinth connect.

So, what could be blocking these narrow points? Yamane suggests that otoconia dislodged from the saccule may find its way into the narrow opening between the saccule and the cochlea (the hearing part of the inner ear). This narrow path is known as the Reuniting Duct.

As discussed by Yamane, we are quite confident that BPPV is the result of otoconia being dislodged from the utricle, gravitating into one of the semi-circular canals. Why would one think that the saccule does not also discharge excess otoconia at times? And where does that saccular otoconia go? And, is there any evidence to support this theory?

Yamane performed 3D CT scanning of the labyrinth in a series of people with definite Meniere’s disease in one ear, and compared those findings to the opposite healthy ear as well as ears of people that do not and never had Meniere’s disease. They were looking specifically at the reuniting duct to see if appeared open or blocked. They found that the reuniting duct appeared blocked in one third (37%) of the affected ears in patients with Meniere’s disease, but only in 10% of the opposite healthy ears. In the group of patients with no history of Meniere’s disease, they found no (0%) blockages.

They summarize their article hypothesizing whether opening or widening these narrow points that are susceptible to blockage may be an effective treatment for Meniere’s disease. This theory has yet to be tested.



Photo courtesy of Yamane et al