Otopathologic Changes in the Cochlea following Head Injury without Temporal Bone Fracture

Abstract

Objective Hearing loss following temporal bone (TB) fracture may result from direct transection of the middle and inner ear. The pathophysiology of hearing loss due to head injury without TB fracture, however, is not well understood. Few reports describe otopathologic findings. Herein, we investigate the pathologic findings of patients who sustained a head injury without evidence of a TB fracture. Study Design Otopathology study. Setting Otopathology laboratory. Subjects Subjects with a history of head injury without TB fracture. Methods The TBs of patients with head injury were evaluated by light microscopy. Inner ear anatomy was evaluated, including counts of spiral ganglion cells (SGCs), hair cells, pillar cells, atrophy of the stria vascularis, and the presence of endolymphatic hydrops. SGC counts were compared with those of historical age-matched controls. Results All cases (N = 6 TBs) had evidence of inner ear pathology. Of the 6 cases, 2 (33%) had severe loss of hair cells in all 3 turns of the cochlea, and 4 (67%) cases demonstrated moderate to severe loss at the basal turn of the cochlea. Four cases had scattered atrophy of the stria vascularis, and 3 (50%) had cochlear hydrops. The number of total SGCs was decreased, with an average 53% loss (range, 25%-79%) as compared with controls. The SGC count loss was evenly distributed along Rosenthal's canal. Conclusions Patients with a history of head injury without TB fracture demonstrate inner ear pathology. Further studies are necessary to determine if otopathology findings are directly attributable to trauma.

Patient‐reported auditory handicap measures following mild traumatic brain injury

“…In terms of peripheral auditory etiologies, the diagnosis of labyrinthine concussion has been used since the turn of the 20th century to describe auditory symptoms in the absence of a temporal bone fracture . Recently published human otopathologic studies have demonstrated distinct histologic changes in patients following head injury, including loss of hair and spiral ganglion cells . Limited mid–20th century animal experiments on labyrinthine concussion noted a range of potential causes, including inner ear hemorrhage, traveling pressure wave, obstruction of the endolymphatic sac, and stretching of the cochlear nerve .…”

“…[52][53][54][55] Recently published human otopathologic studies have demonstrated distinct histologic changes in patients following head injury, including loss of hair and spiral ganglion cells. 56 Limited mid-20th century animal experiments on labyrinthine concussion noted a range of potential causes, including inner ear hemorrhage, traveling pressure wave, obstruction of the endolymphatic sac, and stretching of the cochlear nerve. [57][58][59][60][61] Furthermore, emerging evidence over the past decade points to cochlear synaptopathy (also known as hidden hearing loss) as a potential etiology for auditory dysfunction after noise trauma, resulting in difficulty hearing in noise, hyperacusis, and tinnitus.…”

Peripheral Vestibular System Histopathologic Changes following Head Injury without Temporal Bone Fracture

“…The inclusion and exclusion criteria were similar to a previous cochlear otopathologic study from our group. 27 The study was approved by the Massachusetts Eye and Ear Infirmary Institutional Review Board.…”

Contralateral sensorineural deafness in the absence of temporal bone fractures: an ignored entity in traumatic brain injury

“…The prevalence of ipsilateral SNHL with associated temporal bone fractures in TBI ranges from 14% to 67%. 1 Direct anatomic disruption of the auditory nerve, the inner ear sensory neuro-epithelium, injury to the brainstem (at inferior colliculi) or brain parenchyma (temporal lobe contusions) are reasons postulated. 1,2 Contralateral SNHL is often overlooked, reported only a handful and the causes remain elusive.…”

“…1 Direct anatomic disruption of the auditory nerve, the inner ear sensory neuro-epithelium, injury to the brainstem (at inferior colliculi) or brain parenchyma (temporal lobe contusions) are reasons postulated. 1,2 Contralateral SNHL is often overlooked, reported only a handful and the causes remain elusive. A high index of suspicion is needed for timely diagnosis which if delayed or ignored may deny a patient of the possible recovery only to suffer a permanent handicap.…”