Minor head trauma can make a silent canal dehiscence symptomatic

Design

retrospective chart review of a workplace injury database, 1998 to 2025, with audiovestibular testing and CT

Population

12 patients with symptomatic superior semicircular canal dehiscence syndrome after minor head trauma, median age 41

Primary outcome

audiovestibular findings and symptom pattern

Effect

immediate hearing loss in 12 of 12, autophony in 10; affected-ear vHIT gain 0.81 vs 0.92 (P < 0.001); SP/AP 0.40 vs 0.19 (P < 0.001)

Radiological superior semicircular canal dehiscence is a common incidental finding and most of the people who have it never notice. This series drew 12 patients from an Ontario workplace injury database spanning 1998 to 2025 in whom apparently minor head trauma was followed by symptomatic dehiscence syndrome, with CT confirming the bony defect.

Median age was 41. The usual mechanism was a fall, with impact mostly to the temporal region; three had a contrecoup pattern. Every patient had immediate hearing loss. Autophony - hearing one's own voice and body sounds - was immediate in 10, the Tullio phenomenon in six, Hennebert sign in eight and bone conduction hyperacusis in seven. Audiometry showed the classic low-frequency bone conduction supra-thresholds with mild to moderate air conduction loss in seven. Video head impulse testing showed reduced gain in the affected superior canal in every case tested (mean 0.81 against 0.92 contralateral, P < 0.001), and SP/AP ratios were higher on the affected side (0.40 against 0.19, P < 0.001).

The reason to know this is medico-legal as much as clinical. A patient after a minor head injury complaining of hearing their own footsteps, eye movements or heartbeat is usually labelled functional, or attributed to concussion, and the specific triad - autophony, sound-induced or pressure-induced vertigo, and a low-frequency conductive picture with normal middle ear function - points somewhere testable. Ask about autophony explicitly; patients rarely volunteer it because they do not know it is abnormal.

• Ask directly about autophony after head injury - patients do not report it unprompted
• Test for sound- and pressure-induced vertigo (Tullio, Hennebert) at the bedside
• Look for low-frequency bone conduction supra-thresholds with an intact middle ear on audiometry
• Confirm with high-resolution temporal bone CT before attributing symptoms to concussion
• Document the temporal relationship to the injury carefully where compensation is in question

Why it matters

These patients are routinely told their symptoms are post-concussional, and the diagnosis is confirmable with a CT and an audiogram.

Don't overread it

A 12-patient retrospective series from a compensation database; it establishes the clinical picture, not the frequency or the causal link.

The statistics, in plain English

Twelve patients from a workplace compensation database is a case series, not an incidence study - it cannot tell you how often trauma converts a dehiscence into a syndrome, only what the syndrome looks like when it happens. The P values compare affected with contralateral ears within the same patients, which is a strong design for a small sample but says nothing about how well these tests perform in people without the diagnosis. Selection through a compensation database favours patients with documented, attributed injuries.

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