2Where the lesion sits

FFour places hearing can fail

Trace the path of sound and there are four broad sites where it can break down. A conductive lesion in the outer or middle ear stops sound reaching a healthy cochlea — usually treatable, and not implant territory. A sensory lesion destroys the hair cells of the organ of Corti. A neural lesion damages the spiral-ganglion neurons or the auditory nerve. And a central lesion lies above the nerve, in the brainstem or cortex. The same degree of hearing loss can come from any of them.

FTSensorineural — two zones, one label

The term sensorineural bundles the sensory and the neural together, because the routine audiogram cannot separate them: both produce a loss with no air–bone gap. But biologically they are different. A pure sensory loss — dead hair cells over a living nerve — is the textbook implant case. A neural loss damages the very cells the implant must stimulate. One label, two prospects.

TWhere the implant enters

The reason the distinction is not academic is the implant's point of entry. A cochlear implant injects its signal at the spiral ganglion, downstream of the hair cells and upstream of the brainstem. Everything between the eardrum and the ganglion — the middle ear, the cochlear fluids, the hair cells — is simply bypassed. That is why a sensory lesion is no obstacle. But the ganglion itself, the nerve, and the central pathway are not bypassed; if the lesion sits there, the implant cannot route around it.

CWhy the distinction decides outcome

This single geometric fact — entry at the ganglion — organises every cause that follows. As we go through them, the recurring question is the same: does this disease damage the cochlea (which the implant bypasses) or the neural elements (which it depends on), or both? Causes that stay upstream tend to implant well; causes that reach the ganglion or nerve are the hard cases. The chapter is, in effect, a tour of where each disease lands on the spectrum you have just seen.