Introduction
Hearing loss (HL) after traumatic brain injury (TBI) has been widely reported and is more frequent in males1–11. Motor vehicle collision has been reported as the most frequent etiology of TBI, followed by personal/home accidents2,3,5–7,9,11–14. Some authors reported that there is a high correlation between TBI severity and HL severity8. Similar correlations have been reported with other neurological and cognitive sequelae10,12,14,15–17.
The purpose of this paper is to present one case of profound HL with minimal recovery after a 6-month follow-up period in a 5-year-old female patient who reportedly underwent mild head trauma with no loss of consciousness, no confusion or disorientation, and no other apparent signs of neurological damage.
Case presentation
In July 2021, a 5-year-old female patient was admitted to the pediatric emergency department (PED) of the Hospital General de Mexico in Mexico City. The patient was taken by her mother who reported that she had underwent a mild head trauma on the occipital region while she was playing at home with a ball on the previous night.
The mother watched the incident, and she reported that the patient was able to stand by herself after the fall. The mother reported that there was no loss of consciousness, the patient did not cry, she did not look confused or disoriented, and she did not experience nausea. A few minutes later, the mother noted that the patient was not responding to any sound including very loud noises. The child told her mother: “I cannot hear you.” The next morning the patient was taken to the hospital, and she was admitted to the PED. She underwent a general pediatric examination including a neurological examination which was reported as unremarkable. Neurosurgery and otolaryngological evaluations were performed at the PED. No remarkable findings other than the HL were reported. Imaging procedures were ordered including head computed tomography (CT) scan and magnetic resonance imaging (MRI). She was also referred to the Department of Audiology and Phoniatrics for a complete audiological evaluation. The patient had no family or personal history of HL. Developmental milestones were normal. She was compliant with the examinations. The Audiologist observed that she did not show any behavioral response to oral commands. Speech and language were within normal limits for her age. Only inconsistent typical phonological processes for her age were noted.
Pediatric conditioned play audiometry (CPA) using headphones demonstrated no responses at maximum levels (80-120 dB HL) on any frequency. No responses to speech stimuli were identified either. The patient was indifferent to every sound tested. Immittance testing demonstrated type A tympanograms with the absence of acoustic reflexes. Product distortion otoacoustic emissions (PDOAE) demonstrated no responses.
Brainstem auditory evoked potentials (BAEP) testing demonstrated bilateral absence of all I–V waves when stimuli of 100 dB HL rarefaction clicks were presented monoaurally at a rate of 11 Hz. Moreover, no cochlear microphonics were identified in the recordings.
Imaging procedures including CT scan and MRI were reported as unremarkable (Fig. 1 and Fig. 2). A tapered steroid treatment was suggested. However, the patient did not receive any pharmacological treatment. The patient was discharged to be followed up as an outpatient. Four weeks following the event she was evaluated at the Audiology and Phoniatrics Department. The patient’s mother reported noticing mild improvement in her responses to very loud sounds. A follow-up CPA demonstrated minimal improvement. The right ear thresholds at 500, 1000, and 2000 Hz were found at 86 dB HL. The left ear persisted with the absence of responses. BAEP demonstrated well defined and reproducible waves I–V with prolonged latencies at 90 dB HL on the right ear. No responses were identified on the left ear at the maximum level (Fig. 3 and Fig. 4).
Figure 1. Ears computed tomography scan showing normal anatomy.
Figure 2. Head magnetic resonance imaging with normal anatomy.
Figure 3. Audiometry tests. Profound hearing loss with a slight threshold recovery in the right ear.
Figure 4. Brainstem auditory evoked potentials with a slight recovery in responses of the right ear.
PDOAE persisted with no responses. Hearing aid was indicated to the right ear. The patient was sent to the Department of Speech Pathology for evaluation.
In January 2022 after a 6-month follow-up period, audiometric tests demonstrated no significant changes. The parents reported that they had not been able to purchase the prescribed hearing aid. The patient was admitted to the cochlear implantation (CI) program of the hospital to be evaluated as a candidate. One month after being referred to the CI program, it was not possible to establish contact with the parents for following up. Several attempts to call them by phone were unsuccessful. The hospital records indicated that she had not been scheduled for CI surgery yet. At the time, this article was written no further information concerning the patient’s clinical course had been reported by any of the hospital’s departments.
Discussion
TBI has been recognized as a major public health problem in the pediatric population13. In 2005, an estimated 475,000 events were reported in the population of 0-14 years of age. 2685 of these cases resulted in death, 37,000 were hospitalized, and 435,000 had a visit to Pediatric Emergency Departments for evaluation13. Kozin et al. reported that children with a history of TBI were 2.67 times more likely to report hearing concerns as compared to those without any such history1.
In the US, TBI and HL have been associated frequently. Different hypotheses have been proposed to explain the HL. In some patients with severe TBI, HL is frequently attributed to temporal bone fracture2–7,11. In contrast, a mild head injury usually causes no hearing deficits.
Some authors have reported that mild head trauma usually results in central nervous system sequelae more than hearing disorders12,14,15,17. Some theoretical models have been proposed to explain how the auditory system can be injured by mild head trauma with no evidence of skull fracture. In cases of HL following mild head trauma, the most frequent localization of the trauma is the occipital region. Tension forces applied by the trauma to the auditory system have been reported, especially the cochlear nerves. This statement has been supported by BAEP testing suggesting mild abnormal central conduction times in patients enduring mild head trauma12,14.
Singh et al.2 reported a study of 50 consecutive cases of TBI who were evaluated at the Emergency Department. Sixty-four percent of these cases were motor vehicle accidents, and 8% were domestic accidents. Eighty-six percent of these cases were males. The age group with the most cases was 21-30 years of age (46%), followed by 31-40 years of age (36%). In this report, the youngest group included patients 11-20 years of age accounting for 12% of the cases. Nine temporal bone fractures were demonstrated, seven longitudinal, and two transverse. From these 50 cases, 21 resulted in HL, 5 (23.8%) presented with conductive HL, 9 (42.8%) showed mixed HL, and 7 (33.3%) suffered sensorineural HL.
In 1969, Barber4 studied 110 consecutive cases of TBI. All ages were included in the study group. Audiological and vestibular findings were thoroughly reported. Fifty-four cases presented with a skull fracture. Of the 56 patients without fractures, 39 patients presented with HL. Twenty-three cases demonstrated a sensorineural HL. Six patients presented with a mixed HL. Finally, ten cases were reported as functional hearing loss. A mild head trauma was reported in 42 of these cases. Of these patients, five presented with HL. One case was diagnosed as a sensorineural HL. Four cases were considered functional. The authors concluded that functional HL is the most frequent auditory disorder in cases of mild head trauma.
Bowmana et al.6 described the importance of hearing screening in all children with any kind of head trauma. The report highlighted that HL can be frequently underdiagnosed. They studied 50 children with a history of TBI. The mean age of the patients was 12.6 years. Thirty-two (64%) were male, and 18 were female (36%). Only patients with a Glasgow score of < 13 were included in the study group. Concerning these inclusion criteria, it should be pointed out that this could be considered an inclusion bias. Seventeen cases of HL were detected. Of these, three were conductive hearing losses. Eight patients presented with sensorineural HL. Finally, three cases were reported as unknown sites of lesion. The report mentioned that the severity and mechanism of the head trauma are not reliable predictors of HL. However, a possible relationship between HL the parietooccipital trauma localization was suggested, but no statistically significant association was demonstrated.
Chamyal and Alhluwalia7 studied that 50 consecutive cases of head trauma evaluated at the Emergency Department. Only one patient (2%) was < 10 years of age. The age group including most of the cases was the group including patients 21-30 years of age. Twenty-five patients (50%) were included in this group. Sixty-two percent were cases of mean corpuscular volume. Eleven cases (22%) occurred after a fall. Twenty-two patients (44%) presented with HL. Of these cases, 90% were sensorineural hearing losses, and 10% were conductive.
In another study, Dorman and Morton8 reported that 15% of cases of children with TBI without skull fracture presented with HL. The age range of this study group was 6-16 years of age. The male–female ratio was 2.5:1. Fifty percent of the cases with HL suffered parietooccipital trauma. Thirty-eight of the cases in this study were in the middle cerebral artery, followed by sports injuries (29%). None of the sports injuries presented with HL. Falls were the cause of the trauma in 33% of the cases. Forty-two percent of these cases presented with HL. It should be emphasized that in this report, all cases demonstrated full recovery of hearing thresholds 6 months after the trauma.
Several mechanisms have been reported as possible etiologies of HL without skull fracture including hair cell damage, cochlear nerve ischemia, concussion of neural pathways, sheared, and elongation of axons among others8,12. However, no reliably conclusive data has been reported5,6. Nonetheless, It should be noted that there are reports of the association of TBI with HL, particularly on the parietooccipital area, and without skull fractures2,6,11,14.
Conclusion
From the findings in this case report, it can be concluded that hearing function should be appropriately assessed following any kind of head trauma regardless of the severity. As demonstrated herein, mild head trauma can result in bilateral profound HL. Patients should be closely followed up until auditory function has been recovered to normal levels. Early and adequate auditory intervention would prevent long-term communication sequelae.
Funding
The authors declare that this work was carried out with the authors’ own resources.
Conflicts of interest
The authors declare that they have no conflicts of interest.
Ethical disclosures
Protection of human and animal subjects. The authors declare that no experiments were performed on humans or animals for this study.
Confidentiality of data. The authors declare that no patient data appear in this article. Furthermore, they have acknowledged and followed the recommendations as per the SAGER guidelines depending on the type and nature of the study.
Right to privacy and informed consent. The authors declare that no patient data appear in this article.
Use of artificial intelligence for generating text. The authors declare that they have not used any type of generative artificial intelligence for the writing of this manuscript, nor for the creation of images, graphics, tables, or their corresponding captions.
