A condition that has resolved cannot be the ongoing cause of a symptom that has not. If migraines were in fact
the main driving factor of the worker's ear pain, as the Opinion concludes, the resolution of the migraines
should have produced resolution of the ear pain. It has not. Dr. Abdalkhani's own record identifies this
contradiction directly, naming the WCB audiologist's attribution and setting it against the observed clinical
course, This is not the worker's argument alone: it is the independent clinical observation of the treating ENT
specialist who examined him five months after the Opinion was written, once enough time had passed for the
two conditions to be distinguished by their actual course rather than by their coincidence in January.

3. The Actual Mechanism: Tensor Tympani and TMJ Dysfunction

Neither the Opinion nor the TELUS Health submission explains why acoustic trauma and acoustic shock were
the only two mechanisms considered. Both are inner-ear mechanisms triggered by single, high-intensity events.
Neither has been proposed by any treating specialist as the injury pathway in this case, and, as Section 2
establishes, neither was ever the worker's claim.

The specialists who have actually examined the worker identify a different, and more ordinary, pathway:

Sustained noise exposure acting as a physical and psychological stressor, producing a tension-based muscular

and autonomic cascade — specifically involving the tensor tympani muscle and the temporomandibular joint
~ rather than direct cochlear damage.

Source: Dr. Idris Samad. MD, FRCSC, Otolaryngology — Head and Neck Stagery, consultation report, May 27, 2026.

“Impression: Left ear pain, likely secondary to masseter muscle inflammation and temporomandibular joint
dysfunction. Loud noise exposure from work.may have been an exacerbating factor causing muscle tension

related issues. No apparent otologic pathology. Normal hearing without significant concern,” — Dr 1 Samad,
May 27, 2026

Dr: Samad's examination found mild tenderness on palpation of the left temporomandibular joint and masseter
muscle, a jaw click on wide opening, and signs of bruxism, alongside microscopically normal ears and normal
hearing. His conclusion — referred ear pain from a tension-based TMJ and masseter Process, exacerbated by
the noise exposure ~— is a coherent, examined, physiological explanation for the worker's ear pain that the
acoustic-trauma/acoustic-shock framework in both submissions never considers, because it is not an
audiological mechanism at all.

The worker's reported nocturnal symptoms are consistent with this picture: physical spasms affecting the neck
and hands approximately every thirty seconds for the first four hours of sleep, contributing to measurable neck
tension and requiring sedating medication to manage, A mechanism confined to “was the sound loud enough to
damage the cochlea” does not account for, and was never asked to account for, this autonomic and muscular
presentation.

\ third, independent specialist reaches the same conclusion

Dr. Abdatkhani examined the worker on July 16, 2026, independently of Dr. Samad, with the benefit of an
interval otoscopic and audiometric re-check. His findings confirm Dr. Samad's: normal otoscopy, normal
audiometry, and an assessment of “left ear canal pain, likely muscular or neurological in origin” with a
“possible TMJ component.” An MRI of the internal auditory canal and a sleep study, both ardered by Dr.
Samad, remain outstanding and will be provided as addendum evidence once complete.

Saurce: Dr. Arman Abdalkhani, MD, FRCSC, Van City Ear, Nose & Throat, consultation report, July 16, 2026.

Three specialists have now examined the worker independently — an otolaryngologist in May,.a neurologist
and pain specialist in June, and a second otolaryngologist in July — and none has proposed acoustic trauma or
acoustic shock as the injury mechanism. All three have identified some combination of muscular, neurological,
and temporomandibular findings. The Opinion's audiological framework has not been contradicted by a
difference of clinical opinion; it has simply never been the framework any. treating specialist applied.

Delayed onset supports this mechanism; it does not undermine it

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