Temporal Bone Pathology Secondary to Head Trauma-A Human Temporal Bone Study.
Journal
Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology
ISSN: 1537-4505
Titre abrégé: Otol Neurotol
Pays: United States
ID NLM: 100961504
Informations de publication
Date de publication:
01 09 2021
01 09 2021
Historique:
pubmed:
6
7
2021
medline:
8
10
2021
entrez:
5
7
2021
Statut:
ppublish
Résumé
We hypothesize that following head trauma there is a difference in temporal bone (TB) pathology in cases with and without skull fracture. Although conductive, sensorineural, mixed hearing loss, and TB pathology following head trauma have been reported, to our knowledge, there are no studies that have compared the pathology of the TB in cases with and without skull fracture. We analyzed 34 TBs from donors who had a history of head trauma (20 with skull fracture and 14 without fracture), and 25 age-matched controls without clinical or histological evidence of otologic disorders. We documented the presence and location of TB fracture, ossicular injury, and cochlear hemorrhage and evaluated the loss of spiral ganglion cells and sensory hair cells, damage to the stria vascularis, and the presence of endolymphatic hydrops. We found a significant loss of outer hair cells in the upper basal, lower, and upper middle turns of the cochlea (p = 0.009, =0.019, =0.040, respectively), a significant loss of spiral ganglion cells (p = 0.023), and cochlear hemorrhage predominantly in the basal turns secondary to head trauma. Interestingly, these findings were significantly observed in TBs from donors with a history of head trauma without skull fracture. The greatest damage was to the cochlear basal turn. Our findings suggest that head trauma may result in tonotopic high frequency sensorineural hearing loss. TBs from donors with skull fracture have less pathologic changes than those without.
Sections du résumé
HYPOTHESIS/BACKGROUND
We hypothesize that following head trauma there is a difference in temporal bone (TB) pathology in cases with and without skull fracture. Although conductive, sensorineural, mixed hearing loss, and TB pathology following head trauma have been reported, to our knowledge, there are no studies that have compared the pathology of the TB in cases with and without skull fracture.
METHODS
We analyzed 34 TBs from donors who had a history of head trauma (20 with skull fracture and 14 without fracture), and 25 age-matched controls without clinical or histological evidence of otologic disorders. We documented the presence and location of TB fracture, ossicular injury, and cochlear hemorrhage and evaluated the loss of spiral ganglion cells and sensory hair cells, damage to the stria vascularis, and the presence of endolymphatic hydrops.
RESULTS
We found a significant loss of outer hair cells in the upper basal, lower, and upper middle turns of the cochlea (p = 0.009, =0.019, =0.040, respectively), a significant loss of spiral ganglion cells (p = 0.023), and cochlear hemorrhage predominantly in the basal turns secondary to head trauma. Interestingly, these findings were significantly observed in TBs from donors with a history of head trauma without skull fracture.
CONCLUSION
The greatest damage was to the cochlear basal turn. Our findings suggest that head trauma may result in tonotopic high frequency sensorineural hearing loss. TBs from donors with skull fracture have less pathologic changes than those without.
Identifiants
pubmed: 34224545
doi: 10.1097/MAO.0000000000003192
pii: 00129492-202109000-00049
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e1152-e1159Informations de copyright
Copyright © 2021 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of Otology & Neurotology, Inc.
Déclaration de conflit d'intérêts
The authors disclose no conflicts of interest.
Références
GBD 2016 Traumatic Brain Injury and Spinal Cord Injury Collaborators. Global, regional, and national burden of traumatic brain injury and spinal cord injury, 1990–2016: A systematic analysis for the Global Burden of Disease Study 2016. Lancet Neurol 2019; 18:56–87.
Hyder AA, Wunderlich CA, Puvanachandra P, Gururaj G, Kobusingye OC. The impact of traumatic brain injuries: a global perspective. NeuroRehabilitation 2007; 22:341–353.
Gaw CE, Zonfrillo MR. Emergency department visits for head trauma in the United States. BMC Emerg Med 2016; 16:5.
Taylor CA, Bell JM, Breiding MJ, Xu L. Traumatic brain injury-related to emergency department visits, hospitalizations, and deaths - United States, 2007 and 2013. MMWR Surveill Summ 2017; 66:1–16.
Zaloshnja E, Miller T, Langlois JA, Selassie AW. Prevalence of long-term disability from traumatic brain injury in the civilian population of the United States, 2005. J Head Trauma Rehabil 2008; 23:394–400.
Finkelstein EA, Corso PS, Miller TR. The incidence and economic burden of injuries in the United States. J Epidemiol Community Health 2007; 61:926.
Ishman SL, Friedland DR. Temporal bone fractures: traditional classification and clinical relevance. Laryngoscope 2004; 14:1734–1741.
Chen JX, Lindeborg M, Herman SD, et al. Systematic review of hearing loss after traumatic brain injury without associated temporal bone fracture. Am J Otolaryngol 2018; 39:338–344.
Kong TH, Lee JW, Park YA, Seo YJ. Clinical features of fracture versus concussion of the temporal bone after head trauma. J Audiol Otol 2019; 23:96–102.
Schuknecht HF, Davison RC. Deafness and vertigo from head injury. AMA Arch Otolaryngol 1956; 63:513–528.
Choi MS, Shin SO, Yeon JY, et al. Clinical characteristics of labyrinthine concussion. Korean J Audiol 2013; 17:13–17.
Wittmaack K. Uber die Traumatische Labyrinthdegeneration. Arch f Ohrenh 1932; 131:59–124.
Cureoglu S, Schachern PA, Paul S, Paparella MM, Singh RK. Cellular changes of Reissner's membrane in Meniere's disease: human temporal bone study. Otolaryngol Head Neck Surg 2004; 130:113–119.
Schuknecht HF. Third Edition Schuknecht's Pathology of the Ear. 2010; 34–37.
Monsanto RDC, Schachern P, Paparella MM, Cureoglu S, Penido NO. Progression of changes in the sensorial elements of the cochlear and peripheral vestibular systems: the otitis media continuum. Hear Res 2017; 351:2–10.
Pauler M, Schuknecht HF, White JA. Atrophy of the stria vascularis as a cause of sensorineural hearing loss. Laryngoscope 1988; 98:754–759.
Schuknecht HF, Neff WD, Perlman HB. An experimental study of auditory damage following blows to the head. Ann Otol Rhinol Laryngol 1951; 60:273–289.
Lindquist SE, Schuknecht HF. Stimulation deafness: a study of temporary and permanent hearing losses resulting from exposure to noise and to blast impulses. J Comp Physiol Psychol 1954; 47:406–411.
Cho SI, Gao SS, Xia A, et al. Mechanisms of hearing loss after blast injury to the ear. PLoS One 2013; 8:67618.
Dahiya R, Keller JD, Litofsky NS, et al. Temporal bone fractures: otic capsule sparing versus otic capsule violating clinical and radiographic considerations. J Trauma 1999; 47:1079–1083.
Murakami M, Ohtani I, Aikawa T, Anzai T. Temporal bone findings in two cases of head injury. J Laryngol Otol 1990; 104:986–989.
Shinohara S, Yamamoto E, Saiwai S, et al. Clinical features of sudden hearing loss associated with a high signal in the labyrinth on unenhanced T1-weighted magnetic resonance imaging. Eur Arch Otorhinolaryngol 2000; 257:480–484.
Ferster APO, Cureoglu S, Keskin N, Paparella MM, Isildak H. Secondary endolymphatic hydroops. Otol Neurotol 2017; 38:774–779.
Clark SK, Rees TS. Posttraumatic endolymphatic hydrops. Arch Otolaryngol 1977; 103:725–726.
Yamashita T, Schuknecht HF. Apical endolymphatic hydrops. Arch Otolaryngol 1982; 108:463–466.