Introduction
Meniere’s disease (MD) is a multifaceted disorder of the inner ear,
characterized by fluctuating sensorineural hearing loss, episodic
vertigo, tinnitus and aural fullness 1. It is commonly
regarded as a midlife disorder, with an average onset age of 40 to 50
years and an incidence rate of about 513/100,0002. Its
etiology and pathogenesis remain unknown and may be associated with
autoimmune, genetic, neurophysiological, cellular, and molecular
mechanisms. Currently, endolymphatic hydrops(EH) is generally considered
its pathological hallmark3.
According to the 2015 diagnostic criteria, all patients with definited
MD exhibit varying degrees of hearing loss4. A wealth
of clinical data has demonstrated that low-frequency hearing declines in
the early stages of MD, while middle- and high-frequency hearing
gradually deteriorate as the condition progresses5.
The sound is transmitted to the cochlea via the auditory pathway, where
it causes eardrum vibration and activates auditory receptors in the
cochlea. These receptors convert acoustic vibrations into nerve impulses
that travel along the auditory nerve to reach the brain’s auditory
center. Disruption of any aspect within this process may result in
hearing loss. The bipolar cells located in the spiral ganglion serve as
the primary neurons for auditory conduction. Their peripheral processes
are distributed among inner ear hair cells, while their central
processes form the cochlear nerve responsible for transmitting auditory
signals to the brain. Research has demonstrated a strong correlation
between EH and degeneration of spiral ganglion cells within the
cochlea6; Megerian et al. discovered a significant
reduction in the maximum diameter of the auditory nerve in mice with
EH7. We hypothesize that EH plays a significant role
in the development of hearing loss in patients with MD. However, it
remains unclear whether other factors contribute to this condition and
further investigation is warranted.
With the continuous advancement of magnetic resonance technology in
recent years, visualization of EH has gradually become feasible and is
now being applied in clinical practice. Intravenous administration of
contrast agents enables simultaneous imaging of bilateral inner ear
structures while also reflecting blood-labyrinth barrier permeability
through signal intensity ratio of cochlear basal tur8.
Therefore, the signal intensity ratio can serve as a reliable indicator
for permeability estimation and barrier integrity assessment at specific
locations.
The internal auditory canal (IAC) is a crucial component of the inner
ear, characterized by intricate anatomical architecture. It houses vital
blood vessels (labyrinthine artery) and nerves (facial nerve,
vestibulocochlear nerve). In patients with non-sudden sensorineural
hearing loss, Three-dimensional fluid-attenuated inversion recovery
(3D-FLAIR) MRI scanning after intravenous injection of gadolinium
contrast agent reveals higher signal intensity in the IAC bottom on the
affected side compared to the normal side9; this may
be related to the patient’s hearing loss. We hypothesize that a
potential obstruction exists at the IAC bottom, and its destruction may
result in hearing impairment.
All patients diagnosed with definited MD exhibit hearing loss. Our
hypothesis suggests that the IAC bottom may be compromised in these
individuals, yet no research has specifically examined the signal
intensity of this region and its correlation to hearing loss; The
objective of this investigation was to examine whether the signal
intensity of the IAC bottom alters in MD patients following intravenous
administration of gadolinium contrast agent, and to investigate its
correlation with hearing loss.