A loud sound presented to either ear elicits a bilateral contraction of the stapedius muscle, which pulls the stapes posteriorly and stiffens the ossicular chain. The change in middle-ear stiffness — about 0.02 to 0.10 mmho — is measurable by the same probe used for tympanometry. By presenting the stimulus to one ear while measuring the admittance change in either the same ear (ipsilateral reflex) or the opposite ear (contralateral reflex), and by sweeping the stimulus level until the reflex first appears, we obtain four numbers: the acoustic reflex threshold (ART) for each of the four conditions.
These four numbers are remarkably diagnostic. The reflex arc runs:
A lesion anywhere along this pathway produces a distinctive pattern of present, absent, or elevated reflexes that localises the lesion better than the audiogram alone. The ipsi vs contra distinction discriminates between brainstem (the contra pathway crosses) and peripheral lesions.
What the test looks like
In each of four conditions, the audiologist plays a 1- to 2-second pure tone (or noise) at increasing levels — typically 500, 1000, 2000, 4000 Hz — and watches for an admittance shift time-locked to the stimulus. The lowest stimulus level that reliably produces a shift is the acoustic reflex threshold for that condition. Normal ARTs sit between 70 and 100 dB HL — well above conversational speech, well below painful levels.
scenario:
Normal — reflexes present bilaterally at 70–100 dB HL. The four-condition reflex pattern is one of the most informative single tests in audiology: a small table of four numbers (or "absent" entries) can distinguish among cochlear, conductive, retrocochlear, and brainstem pathology. The reflex itself is a brainstem-mediated reflex that requires intact cochlea, auditory nerve, brainstem (cochlear nucleus → superior olivary complex → facial nucleus), facial nerve, and stapedius muscle. A break anywhere produces a distinctive pattern.
The four-condition matrix
The diagnostic power lies in patterns across the four conditions, not in any single threshold.
Normal pattern
All four reflexes present at 70–100 dB HL. The complete pathway, peripheral structures, brainstem crossover, and effectors are intact. Note that the reflexes are useful but not diagnostic alone; you can have mild cochlear losses with normal reflex thresholds and normal hearing with elevated reflex thresholds.
Conductive loss (left)
Left ipsi: absent. Left contra (probe L, stim R): absent. Right ipsi: present. Right contra (probe R, stim L): absent.
A left conductive loss breaks the test in two ways:
Probe-ear effect. Any time the probe is in the left ear, even a perfectly normal stapedius contraction would not produce a measurable admittance change — the conductive pathology is blocking the very thing the probe is trying to measure. So both “probe L” entries (ipsi-L and contra-L) become absent regardless of which ear is stimulated.
Stimulus-ear effect. When the stimulus is presented to the left ear, the conductive loss attenuates the sound before it reaches the cochlea, so the stimulus level needed to elicit a reflex is elevated by the size of the conductive loss — often beyond the audiometer’s output limit, giving “absent” thresholds for left-stimulus conditions.
The result is the table above: only ipsi-R and contra-L (probe R, stim L) are both absent for a reason — and the cross-pattern (both pathways involving the left ear are absent) is the unmistakable signature of left middle-ear conductive pathology.
In bilateral conductive losses all four reflex conditions become absent — even an inferred-conductive diagnosis is straightforward from this complete absence combined with a bilateral type-As or type-B tympanogram and an audiometric air-bone gap.
Cochlear loss (left, with recruitment)
Left ipsi: present at slightly reduced sensation level. Left contra: similarly present at reduced SL. Right ipsi: normal. Right contra: normal.
A cochlear loss elevates the patient’s audiometric threshold but also produces recruitment — abnormally rapid loudness growth above threshold. The reflex (which is driven by loudness, not by absolute sound level) therefore stays elicitable at a stimulus level that is only modestly elevated. Crucially, the sensation level at which the reflex fires — that is, the difference between the reflex threshold and the audiometric threshold — narrows. Where a normal-hearing person needs ~85 dB SPL (≈ 85 dB SL above their 0 dB HL threshold), a cochlear-impaired listener with a 50 dB HL threshold may have a reflex at 85 dB HL — a sensation level of only 35 dB. This reduced SL gap is the classical cochlear reflex pattern: the Metz test for recruitment, named for Otto Metz who first described it in 1952.
Left ipsi: absent or markedly elevated. Left contra: absent. Right ipsi: present. Right contra: present.
A retrocochlear lesion (most often a vestibular schwannoma growing on the auditory or vestibulocochlear nerve) interrupts the afferent limb of the reflex specifically when the stimulus is presented to the affected ear. The pattern can look similar to a conductive loss on the same side, but the tympanograms are normal, the audiograms typically show high-frequency loss without an air-bone gap, and the audiologist therefore knows to look behind the cochlea.
A second retrocochlear sign is acoustic reflex decay: even if the reflex is elicited, the contraction cannot be sustained. A normal stapedius can maintain contraction for at least 10 seconds at a 10-dB-above-threshold stimulus. A retrocochlear lesion fatigues quickly — the contraction visibly drops by 50% or more within 5 seconds. Tested at 500 and 1000 Hz, reflex decay has historically been one of the most sensitive (though not specific) screens for vestibular schwannoma before MRI became routine.
Brainstem (intra-axial) lesion
Left ipsi: present. Right ipsi: present. Left contra: absent. Right contra: absent.
The contralateral reflex pathway crosses the brainstem in the trapezoid body (the same crossing fibres carry the ILD/ITD signals that produce binaural localisation — see Hearing 6.2 — The superior oliverefresher →). A lesion in the trapezoid body — multiple sclerosis plaques, brainstem stroke, pontine glioma — preferentially disrupts the contralateral pathways while leaving the ipsilateral arcs (which do not cross) intact. The resulting pattern of bilateral absent contralateral reflexes with intact ipsilateral reflexes is one of the most specific brainstem signs available without imaging.
⏳The history— The acoustic reflex
The stapedius contraction in response to loud sound was described as a curious anatomical observation in the 19th century by Hensen (1878) — visible through a perforated drum in cadaver experiments. Lüscher (1929) showed that it occurred in live human ears via stroboscopic observation.
Clinical use came with Otto Metz’s 1946 monograph that founded clinical immittance audiometry. Metz observed that hearing-impaired patients with recruitment showed reflex thresholds at much smaller sensation levels than their audiometric thresholds would predict; he proposed the Metz test as a recruitment indicator in 1952. The pattern still bears his name.
The four-condition decision matrix is owed to James Jerger (1972). Jerger systematised the use of ipsi/contra threshold patterns to localise lesions — and crucially, he showed that the contralateral reflex selectively fails in brainstem lesions, a finding that has remained one of the strongest acoustic-reflex predictions across fifty years of imaging-confirmed retrospective studies.
The role of reflex testing has shrunk somewhat in the imaging era — MRI now diagnoses what reflex decay used to screen for — but reflex testing remains the fastest, cheapest, most universally available localising tool in audiology. A reflex panel takes about three minutes, is non-invasive, and produces a pattern interpretable across the entire central auditory pathway. As Jerger put it in a much-cited 1980 review: “the reflex pattern is the audiologist’s neurological exam.”
The next and final lesson of this chapter steps back from acute pathology to the everyday: why most normal-population patients show a slightly negative TPP after a cold, after a flight, or after a swim in cold water.