Closing the Loop Behind the Cochlea: monitoring and device architecture for slow-growth retrocochlear hearing loss

Hearing assistance is engineered for people whose cochlea has failed and whose auditory nerve still works. It is not engineered for the smaller population whose cochlea is intact and whose nerve is being slowly compressed — by a vestibular schwannoma or a similar lesion of the internal auditory canal — and who are managed by observation over months or years while the hardest question in their care is when to intervene.

This preprint decomposes hearing assistance into eight functional stages and identifies which stage fails for each of four populations. Its central observation is that the ear already contains a feedback loop: auditory nerve fibres drive brainstem neurons whose medial olivocochlear efferents project back onto the outer hair cells and suppress their gain, with otoacoustic emissions as that loop's observable output, measurable from outside the head in minutes. Retrocochlear compression reduces the afferent drive that runs it — the disease opens a loop the body already operates.

A second observation follows. Animal work with selective inner hair cell lesions shows distortion-product emissions essentially unchanged even when 80–100% of inner hair cells are lost, while thresholds in quiet stay near-normal until losses exceed 80%. That insensitivity is usually reported as a limitation of the test. Here it is the specification: a measurement that ignores the nerve is exactly what is needed when the clinical problem is telling the ear apart from the nerve, and the disagreement between emissions and the audiogram becomes the diagnostic content.

Third, cochlear implants carry telemetry able to measure whether a stimulus produced its intended neural response, use it once at fitting, and then operate open-loop — reasonable for a stable deaf ear, wrong for a nerve changing month by month. The control-theoretic residual and its derivatives are proposed as an objective progression marker between clinic visits, where symptom report is weakened by gradual onset and perceptual adaptation.

Further sections cover emission phase gradient rather than amplitude for longitudinal robustness, paired testing of the two hair cell populations, joint vestibular monitoring, acoustic rather than electrical delivery, and a table of where the wall sits for each population. Five of the capabilities discussed exist today and are not novel; they are simply not assembled into a surveillance protocol for this population. An appendix records seven approaches evaluated and not pursued, each with the quantity that closed it.

Preprint, not peer reviewed. Prior-art searching was targeted rather than systematic and was conducted at abstract and extract level. A declaration page states those limits and tags every load-bearing number by provenance — 16 sourced, 7 unverified, 2 assumed, 2 computed — separating decision-relevant quantities from design-relevant ones.

Keywords. vestibular schwannoma; retrocochlear hearing loss; otoacoustic emissions; medial olivocochlear reflex; efferent suppression; contralateral suppression; closed-loop control; cochlear implant telemetry; evoked compound action potential; phase gradient; vestibular evoked myogenic potential; watchful waiting; bone conduction; holonomy