Labyrinthine concussion refers to labyrinthine injury without temporal bone fracture in cases of closed head injury, sometimes accompanied by labyrinthine fenestration rupture. According to statistics, 40% of patients with brain concussion exhibit labyrinthine symptoms.

bubble_chart Etiology

During head trauma with acceleration, the displacement of auditory and vestibular end receptors due to inertia, as well as strong shock waves transmitted through the skull to the inner ear, are the direct causes of labyrinthine concussion. A sudden increase in cerebrospinal fluid pressure during head trauma can elevate the perilymph pressure through transmission via the cochlear aqueduct or the base of the internal auditory canal, leading to rupture of the labyrinthine membranes (round window membrane and/or oval window annular ligament). During explosions or slaps to the ear, a sudden rise in local air pressure in the external auditory canal or nasopharynx can also transmit inward through the middle ear, causing the labyrinthine windows to implode inward.

bubble_chart Clinical Manifestations

The main symptoms include sensorineural deafness, tinnitus, nystagmus, and balance disorders. When otoliths deposit on the cupula of the posterior semicircular canal, known as cupulolithiasis, it can lead to typical benign paroxysmal positional vertigo. These symptoms are often accompanied by concussion-related manifestations and psychiatric symptoms. Some patients may recover their hearing, and vestibular symptoms generally disappear within a year. If hearing and vertigo frequently fluctuate, the possibility of a perilymphatic fistula due to labyrinthine window rupture should be considered. In such cases, typical cochlear deafness is often present, and symptoms of cochlear and vestibular dysfunction may worsen with increased physical activity, as more perilymph leaks. Suprathreshold auditory function tests, fistula tests, positional tests, and Romberg's sign may yield positive results, while vestibular function tests often show varying degrees of decline. In recent years, surgical exploration and histopathological examinations of surgical specimens, along with other otoneurological tests, have demonstrated that vestibular dysfunction following head trauma is not limited to the labyrinth. Lesions at the junction of the eighth cranial nerve and the brainstem or within the brainstem itself account for approximately 50% of cases. Therefore, when diagnosing labyrinthine concussion, further determination of the injury site is necessary.

The treatment for labyrinthine concussion can follow the principles of managing brain concussion. Bed rest for 1–2 weeks is recommended, with sedatives and analgesics administered as needed, and intravenous fluids provided if necessary.

For cases with labyrinthine window rupture, bed rest is advised with the head elevated at 30%. Activities or actions that may increase intracranial pressure, such as nose blowing, severe coughing, or straining during bowel movements, should be avoided. If symptoms continue to worsen or do not improve after one week of bed rest, tympanotomy may be considered. Once a window membrane rupture is confirmed, immediate repair should be performed.