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.