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

 This week, we will review an article by Dr. David Newman-Toker. Dr. Newman-Toker has been a leader in the movement to change the way patients with sudden onset acute vertigo are evaluated. The primary concern of the physician evaluating these patients is to determine, as best possible, “Is this a stroke versus a benign labyrinthine condition?”

Historically, patients presenting to the Emergency Department (ED) with vertigo are primarily assessed through imaging. Imaging should identify stroke, right? Not so fast.  In the first 48 hours after symptom onset, a Cranial CT scan is only 16% sensitive for detecting stroke in the brainstem or cerebellum, and MRI, though much better, is only 83% sensitive. So, the old adage, “Let’s get an MRI just to be sure” isn’t such a sure bet after all.  Is there a better way?

We have discussed the HINTS protocol in the past, but today I want to review some sensitivity and specificity data that Dr. Newman-Toker has made available. HINTS is a mnemonic for Head Impulse, Nystagmus, and Test of Skew.

 According to Dr. Newman-Toker:

Head Impulse- A normal horizontal Head Impulse test is the single best test to separate a stroke from Vestibular Neuritis (VN),a more common peripheral vestibular cause of acute sudden onset vertigo. He reports that an abnormal Head Impulse test is 85% sensitive and 95% specific for VN.

Nystagmus – If nystagmus is present and is direction changing, this is considered only 38% sensitive, but 92% specific for stroke. By direction changing, we are describing nystagmus that is right beating in gaze right, and left beating in gaze left. Nystagmus associated with VN is direction fixed, meaning it won’t change direction as a result of change in gaze.

Test of Skew – This refers specifically to vertical ocular misalignment (one eye is fixed higher than the other, and can be detected by performing the cover test), and is referred to as “Skew Deviation.” When Skew Deviation is present, it is highly specific (98%) for stroke, but is only 30% sensitive for detecting stroke.

Editors Note and Summary:

When a patient arrives with acute sudden onset spontaneous vertigo, the examiner can take a couple of minutes to assess the patient far faster, far cheaper, and far more accurately than CT scan and even MRI. If the patient has direction fixed nystagmus and a positive Head Impulse test, it is almost certainly a peripheral cause. If the patient has direction changing nystagmus, there is a high probability of stroke. If the patient has Skew Deviation, there is an even higher possibility of stroke. If you see none of the above, you are right back where you started.