Ménière's Timeline

Advances Over the Last 165 Years

1861
Prosper Ménière's theory emerges

Prosper Ménière proposes that vertigo, tinnitus, and fluctuating hearing loss originate from the inner ear, not the brain.

1938
Expanded
Endolymphatic Hydrops is discovered

Hallpike & Cairns (England) and Yamakawa (Japan) independently identify cochleosaccular endolymphatic hydrops as the pathological hallmark of Ménière’s disease.

Mid 20th Century
Expanded
Theories & surgical approaches take shape

Growing anatomical knowledge leads to theories involving autonomic dysregulation and other systemic causes

Development of early surgical interventions such as:

Late 20th Century
Sub Label
Medical therapies expand

Physicians begin to prescribe new practices and medications to reduce inner‑ear fluid pressure, including diuretics, low‑sodium dietsBetahistine (not in the U.S.), intratympanic gentamicin for vertigo control, and intratympanic steroids to preserve hearing

2010s
Sub Label
Targeted drug delivery & clinical trials are introduced

Rise of intratympanic steroid formulations (e.g., OTO‑104) with multiple Phase 3 trials

Gentamicin vs. steroid trials refine treatment strategies for refractory vertigo

2020s
Sub Label
Precision medicine & new therapeutics emerge
Advanced Imaging

High‑resolution MRI now allows in vivo visualization of endolymphatic hydrops, shifting Ménière’s from a purely clinical diagnosis to one with objective imaging criteria.

Phenotype‑Based Classification

Modern research segments Ménière’s patients into distinct subtypes based on vestibular aqueduct/  endolymphatic sac morphology, age of onset, gender, and bilateral vs. unilateral involvement.

New Drug Development

Ebselen (SPI‑1005) enters Phase 3 trials as a promising anti‑inflammatory/antioxidant therapy.

Ongoing trials explore serotonin–norepinephrine reuptake inhibitors, novel steroid delivery systems, and antiviral approaches (e.g., Famvir)

Understanding of Disease Mechanisms are Refined

Consensus grows that Ménière’s involves failure of inner‑ear fluid homeostasis, with multiple potential pathways rather than a single cause.