The Short Answer Educational content only. Any suspected concussion warrants medical evaluation. Consult vestibular-trained physical therapist, neuro-optometrist, or concussion specialist for individualized guidance. Superior canal dehiscence (SCD) is thinning or absence of bone over the superior semicircular canal creating a "third mobile window" in the inner ear (Silverberg et al., 2020). SCD causes sound and pressure-induced vertigo (Tullio phenomenon, Hennebert sign), hearing changes, autophony, and pulsatile tinnitus. Concussion can trigger symptomatic SCD by disrupting previously compensated dehiscence or through direct head trauma converting subclinical dehiscence to symptomatic. Diagnosis includes cervical VEMP (cVEMP) and ocular VEMP (oVEMP) testing showing reduced thresholds and high-resolution temporal bone CT confirming dehiscence. Treatment includes conservative management with symptom avoidance or middle fossa craniotomy with canal plugging or resurfacing for severe symptoms. SCD is thinning of bone over superior canal. Bone thinning over superior canal. Sound and pressure-induced vertigo characteristic. Sound and pressure vertigo. Concussion can trigger symptomatic SCD. Concussion can trigger symptomatic SCD. SCD Anatomy and Pathophysiology Superior semicircular canal in temporal bone. Superior canal in temporal bone. Bone thinning or absence creates third window. Third window creation. Normal windows: oval and round windows. Normal windows oval and round. Third window allows abnormal fluid movement. Third window abnormal fluid movement. Sound and pressure stimulate vestibular hair cells. Sound and pressure stimulate vestibular hair cells. Congenital thinning common substrate. Congenital thinning common substrate. How Concussion Triggers SCD Symptoms Direct head trauma disrupts compensated dehiscence. Direct head trauma disrupts compensated dehiscence. Barotrauma from impact. Barotrauma from impact. Intracranial pressure changes. Intracranial pressure changes. Fluid dynamics alteration. Fluid dynamics alteration. Previously asymptomatic dehiscence becomes symptomatic. Previously asymptomatic becomes symptomatic. Subclinical dehiscence tips into symptomatic. Subclinical tips into symptomatic. Vestibular Symptoms Tullio phenomenon (sound-induced vertigo). Tullio phenomenon. Hennebert sign (pressure-induced vertigo). Hennebert sign. Vertigo from loud sounds. Vertigo from loud sounds. Vertigo from Valsalva. Vertigo from Valsalva. Vertigo from nose blowing. Vertigo from nose blowing. Vertigo from heavy lifting. Vertigo from heavy lifting. Vertigo from straining. Vertigo from straining. Chronic imbalance. Chronic imbalance. Auditory Symptoms Autophony (hearing own voice loudly). Autophony. Hearing own eye movements. Hearing own eye movements. Hearing own footsteps loudly. Hearing own footsteps loudly. Hearing own heartbeat. Hearing own heartbeat. Pulsatile tinnitus. Pulsatile tinnitus. Sound sensitivity. Sound sensitivity. Air-bone gap on audiometry. Air-bone gap on audiometry. Conductive hyperacusis. Conductive hyperacusis. Diagnostic Testing Cervical VEMP (cVEMP) reduced threshold. cVEMP reduced threshold. Ocular VEMP (oVEMP) increased amplitude. oVEMP increased amplitude. High-resolution temporal bone CT. High-resolution temporal bone CT. Poschl and Stenvers reconstructions. Poschl and Stenvers reconstructions. Audiometry showing air-bone gap. Audiometry air-bone gap. Videonystagmography. Videonystagmography. Fistula test. Fistula test. Treatment Options Conservative management for mild symptoms. Conservative management mild symptoms. Symptom avoidance (loud sounds, straining). Symptom avoidance. Vestibular rehabilitation for compensation. Vestibular rehab for compensation. Middle fossa craniotomy canal plugging. Middle fossa craniotomy canal plugging. Middle fossa craniotomy canal resurfacing. Middle fossa craniotomy canal resurfacing. Transmastoid canal plugging. Transmastoid canal plugging. Round window reinforcement (investigational). Round window reinforcement investigational. Surgical Outcomes 70-90% symptom improvement post-surgery. 70-90% symptom improvement post-surgery. Vestibular symptoms respond well. Vestibular symptoms respond well. Auditory symptoms improve variably. Auditory symptoms improve variably. Sensorineural hearing loss risk 5-10%. Sensorineural hearing loss risk 5-10%. Vestibular compensation over months. Vestibular compensation over months. Supporting Mobility Routine These exercises support recovery through cervical mobility and nervous system regulation. JME 155 Diaphragmatic breathing supports vagal tone and parasympathetic regulation during concussion recovery. 10 breaths every 60-90 minutes. JME 14 Chin tucks reduce upper cervical tension common in concussion injury. 10 repetitions with 5-second holds. JME 1 Cervical rotation supports cerebral blood flow and nervous system regulation. 10 repetitions each direction. JME 150 Thoracic rotation restores breathing depth shallow during concussion recovery. 8 repetitions per direction. Start your 3-day free trial for joint-specific mobility programs that support nervous system regulation through concussion recovery. How is SCD diagnosed after concussion? SCD diagnosis requires characteristic symptoms (sound and pressure-induced vertigo, autophony), reduced cVEMP thresholds, increased oVEMP amplitudes, and dehiscence confirmed on high-resolution temporal bone CT with Poschl and Stenvers reconstructions. Audiometry may show air-bone gap without middle ear pathology. Neuro-otologist evaluation essential. Should I have surgery for SCD after concussion? Surgery indicated for severe symptoms significantly impacting quality of life. Conservative management for mild symptoms. Middle fossa craniotomy with canal plugging or resurfacing standard surgical approach. 70-90% symptom improvement rate. 5-10% sensorineural hearing loss risk. Discuss risks and benefits with neuro-otologist. Can concussion cause SCD or just trigger existing SCD? Concussion typically triggers previously asymptomatic congenital dehiscence rather than creating new SCD. Congenital bone thinning is substrate. Trauma disrupts compensation, converts subclinical to symptomatic. Rarely, severe temporal bone trauma may create traumatic SCD. Most post-concussion SCD represents unmasking of pre-existing dehiscence. What is the third window syndrome? Third window syndrome refers to abnormal opening in inner ear beyond normal oval and round windows. Superior canal dehiscence most common cause. Enlarged vestibular aqueduct, cochlea-facial dehiscence, and posterior canal dehiscence other causes. Third window allows abnormal fluid dynamics and inappropriate stimulation of vestibular hair cells. How do I find an SCD specialist? Neuro-otologist with SCD experience essential. Academic medical centers offer SCD programs. Johns Hopkins, House Ear Institute, University of North Carolina, and others have SCD expertise. Vestibular Disorders Association (VeDA) provides resources. Second opinion recommended before surgery. References Patricios, J. S., et al. (2023). Consensus statement on concussion in sport: the 6th International Conference on Concussion in Sport, Amsterdam, October 2022. British Journal of Sports Medicine, 57(11), 695-711. PubMed Silverberg, N. D., et al. (2020). Management of concussion and mild traumatic brain injury: a synthesis of practice guidelines. Archives of Physical Medicine and Rehabilitation, 101(2), 382-393. PubMed