Ménière's disease: damaged hearing but reduced vertigo

Current thinking is that Ménière’s disease (or, more accurately, Ménière’s syndrome) is a phenotype of unstable or erratic inner ear hearing and vestibular function that arises from failure of one or more of the many inner ear homoeostatic systems that regulate endolymph and perilymph, aff erent and eff erent nerve signalling, and blood fl ow. Clinically, the fl uctuating and progressive sensorineural hearing loss tends to be relatively resistant to treatment (ie, progressive), but the episodic vertigo is usually quite responsive to treatment. The combination of diet and lifestyle adjustments to avoid stressing fragile homoeostatic systems plus diuretic medication to aid with inner ear ionic gradient management can control or eliminate Ménière’s vertigo attacks in over 90% of patients. However, a troublesome group remains: 5–10% of all patients with Ménière’s disease are not responsive to these conservative and medical interventions and need more aggressive treatment. Nowadays, this most often means intratympanic drug treatment. In The Lancet, Mitesh Patel and colleagues present results of a double-blind comparative eff ectiveness trial of intratympanic methylprednisolone (n=30) versus intratympanic gentamicin (n=30) on intractable vertigo attacks in patients with unilateral Ménière’s disease. The two treatments were equally eff ective at reducing vertigo attacks; the mean number of vertigo attacks in the fi nal 6 months compared with the 6 months before the fi rst injection (primary outcome) decreased from 19·9 (SD 16·7) to 2·5 (5·8; 87% reduction) in the gentamicin group and from 16·4 (12·5) to 1·6 (3·4; 90% reduction) in the methylprednisolone group (diff erence –0·9, 95% CI –3·4 to 1·6). Secondary outcomes related to other vestibular symptoms and hearing loss (all p>0·05) were also similar between groups, as was the occurrence of adverse events (three in each group). Intratympanic corticosteroid treatment for Ménière’s disease is based on the supposition that Ménière’s disease symptoms arise from an infl ammatory or other reversible mechanism that could be favourably altered by administration of corticosteroid. Tens or hundreds of inner ear proteins have steroid-binding capability. In fact, it would be startling if administration of corticosteroid to the inner ear didn’t have an eff ect of some kind. But what is the likelihood that application of such a so-called blunt instrument would do more good than harm? We have learned empirically over the past 30 years that intratympanic corticosteroid is safe, producing few side-eff ects and virtually no hearing loss or vestibular damage. It won’t hurt and it might help, so it has become a popular treatment despite the absence of strong evidence of effi cacy. By contrast, gentamicin is a hair cell ototoxin. It is preferentially vestibulotoxic, typically causing much more vestibular than auditory damage. Administration of intratympanic gentamicin to patients with Ménière’s disease is based on the notion that the patient’s vestibular symptoms are due to the damaged and distorted vestibular signals emanating from their damaged ear and that they are better off with no signal than with a damaged and distorted signal. The objective of intratympanic gentamicin is to weaken vestibular signals in the Ménière’s ear to the point at which they are no longer strong enough to generate a vertigo attack. This objective is achieved in about 90% of treated patients. However, there is a price to pay in the form of 1–2 months of, and possibly permanent, disequilibrium and about 20% risk of further hearing loss in the treated ear. Patel and colleagues’ study, by adhering to stringent methods, off ers robust evidence that both of these treatments have substantial effi cacy, with each achieving about 90% reduction of vertigo attacks. Published Online November 16, 2016 http://dx.doi.org/10.1016/ S0140-6736(16)32166-3