2Anatomy & physiology
Where the three potentials of the electrocochleogram come from. Master this once and every disease page in the atlas explains itself.
The cochlea makes three electrical signals worth listening to from outside it: the CM cochlear microphonic, the SP summating potential, and the APcompound action potential. ECochG separates them in time and shape. To use it clinically you need to know which cells make each one — because the disease pattern in every condition you'll meet is, at heart, a story about which cells are failing and which are not.
This module works in three layers. The Foundation tier teaches the broad strokes: fluids, hair cells, nerve. The Trainee tier adds the biophysics of mechanoelectrical transduction. The Clinician tier covers the experimental dissections — Pappa 2019, Hutson 2022 — that explain why the SP is so much more subtle than it first looks.[2019, 2022] Toggle the level marker on any heading to fold the relevant prose in or out.
FCochlear fluids and the endocochlear potential
The bony cochlea is a spiral of three parallel ducts. Scala vestibuli and scala tympani contain perilymph, a high-sodium, low-potassium extracellular fluid. Between them runs scala media, the cochlear duct, filled with endolymph— high-potassium, low-sodium, the inverse composition. The two fluids never mix; they're separated by Reissner's membrane on one side and the reticular lamina of the organ of Corti on the other.
The wall between scala media and the bone — the lateral wall — contains the stria vascularis, a vascular epithelial pump that secretes K⁺ into the endolymph and maintains it at a positive +80 mV relative to perilymph. This is the endocochlear potential (EP): the battery that drives every other cochlear signal.[2006, 2008]
Davis's 1965 battery model treats the EP as the supply voltage and the hair-cell transduction channel as a variable resistor. Open the resistor (sound deflects the hair bundle), current flows, and a receptor potential appears across the hair cell. Every potential ECochG records — CM, SP, AP — depends on that current. Strial pathology (loop diuretics, Cx30 mutation, presbyacusis) flattens the EP and collapses every component at once.[1965, 2006]
FThe organ of Corti
Two cell types matter. Inner hair cells (IHCs) form a single row of about 3,500 cells along the spiral; they are the true sensors. Roughly 95% of the cochlear nerve's afferent fibres synapse onto IHCs[1969] — when the brain hears, it is hearing IHCs. Outer hair cells (OHCs) form three rows of about 12,000 cells; they receive only about 5% of afferent innervation and their job is mechanical. They contract and elongate with each cycle of the sound (the protein prestin in their lateral wall is voltage-driven) and this electromotility amplifies basilar-membrane motion 100- to 1000-fold.[2008]
Above the hair-cell stereocilia floats the tectorial membrane. Basilar-membrane displacement shears the stereocilia against it, opening mechanoelectrical transduction (MET) channels at the tips of the stereocilia. K⁺ flows from the endolymph into the cells. The driving force is the EP plus the negative resting potential of the hair cell — together about 150 mV across the apical membrane.[2014]
TMechanoelectrical transduction
FGenerators of CM, SP, and AP
With the fluids and cells in place, the three ECochG components map cleanly onto cellular events:
| Potential | What it is | Generator | Polarity / shape |
|---|---|---|---|
| CM | Cochlear microphonic — an AC signal that mirrors the stimulus waveform | Predominantly outer hair cells, basal turn, via the MET current cycling at the stimulus frequency | Inverts when stimulus polarity inverts. Present even when the auditory nerve is severed.[2017] |
| SP | Summating potential — a sustained DC shift during the stimulus | Multiple sources: OHC + IHC asymmetric MET, plus dendritic and spiking components from the auditory nerve itself | Does not invert with polarity (alternating averaging keeps it). Polarity and magnitude vary with frequency and level.[2019, 2022] |
| AP | Compound action potential — the first synchronous volley of nerve firing | Distal auditory nerve (peripheral fibres of spiral ganglion cells, type I afferents) | Negative-going N1 (≈ 1.5–2.0 ms at high levels), often a smaller N2. Equivalent to ABR wave I.[2014] |
For decades the SP was called "the hair-cell DC potential" and treated as a pure receptor signal. The Fitzpatrick group's elegant pharmacological dissections in 2019 and 2022 showed otherwise. Using furosemide + kanamycin to remove OHCs, then kainic acid to silence the auditory nerve, and finally tetrodotoxin to separate spiking from dendritic components, they isolated four contributors: an OHC component, an IHC component, a dendritic post-synaptic component, and a spiking neural component — with opposite polarities in some conditions.[2019, 2022]This complexity is why the SP varies so unpredictably with frequency and level, and why "elevated SP/AP ratio" can arise from several disease mechanisms — hydrops, third-window shunting, synaptopathy — that look superficially similar but have entirely different biology.
TFrom cell to electrode — the inverse problem
FClinical implications — preview of the disease pages
Six things to anchor before you move on, because every disease page in the atlas leans on them:
- CM present, AP absent means the hair cells are working but neural transmission has failed somewhere between them and the central nervous system. This is the ECochG signature of auditory neuropathy spectrum disorder.[1996, 1998, 2002]
- CM inverts with stimulus polarity; SP and AP do not. This is the test for CM authenticity — if the "CM" doesn't flip when you flip the click, it's stimulus artifact, not biology. The polarity-reversal protocol is the diagnostic manoeuvre that confirms ANSD.[1998]
- SP elevated relative to APclassically indicates endolymphatic hydrops — the basilar membrane is biased into an asymmetric resting position, distorting the MET-current input/output curve and inflating the DC component. This is the basis of ECochG in Ménière's disease.[1999, 2013]
- But SP can also rise from a third-window shunt (superior canal dehiscence) or from synaptopathy unrelated to hydrops. Differentiating these requires the clinical context, not just the ratio.[2015, 2016]
- AP is the same potential as ABR wave I. Its origin is the most distal portion of the auditory nerve, which is why it persists for milliseconds after eighth-nerve section during schwannoma surgery — the generator is peripheral to the cut.[2014]
- Stria pathology flattens everything.Lose the EP, lose the battery; CM, SP, and AP all collapse together. This is why aminoglycoside ototoxicity, loop diuretics, and presbyacusis don't give a clean "SP up, AP down" pattern — they take all three.
The next module, Recording technique, covers how the choice of electrode (tiptrode vs TM vs transtympanic vs intracochlear) and stimulus (click vs tone burst vs chirp) shapes which of these components you can measure cleanly. That decision is the difference between a textbook trace and a noisy mess in clinical practice.