Audiological Damage After Traumatic Brain Injury

Why comprehensive evaluation matters for recovery and restoring quality of life

Shahrzad Cohen, Au.D., M.S., CH-TM, ABA-C, CBIS

After a traumatic brain injury, a patient may hear tones in a quiet booth yet remain unable to fully understand speech in noise, tolerate ordinary sounds, maintain balance, or efficiently remember details of spoken information. The audiogram is essential—but it is only the beginning of the evaluation.

Traumatic brain injury (TBI), including concussion or mild TBI (mTBI), can disrupt hearing, vestibular function, postural control, and central auditory processing. Additionally, it can lead to comorbidities such as tinnitus perception, which can negatively affect overall daily communication activities and the patient’s quality of life.

Symptoms may include peripheral hearing loss, tinnitus, sound intolerance, episodic vertigo, chronic disequilibrium, impaired speech perception in noise, increased listening effort, and difficulty retaining spoken information. Importantly, these conditions may persist despite clinically normal pure-tone thresholds.

A Multisystem Injury

TBI is often discussed in terms of headache, memory, mood, vision, and executive function. Yet hearing and balance complaints are also common and may substantially prolong disability. A contemporary review estimated that approximately 34 percent to 50 percent of patients with mTBI experience sensorineural hearing loss, tinnitus, or vestibular symptoms such as vertigo and postural imbalance (Harris et al., 2024). In a landmark clinical sample, Lew et al. (2007) found higher rates of hearing loss and tinnitus complaints among patients with blast-related TBI than among those with non-blast injuries. These data do not imply that every post-TBI symptom arises from the same lesion; rather, they demonstrate the breadth of structures and networks that may be affected.

The auditory and balance systems depend on tightly coordinated peripheral and central pathways. Trauma may injure the tympanic membrane or ossicular chain, cochlear hair cells, synapses between inner hair cells and auditory-nerve fibers, the auditory nerve, brainstem timing pathways, thalamocortical networks, auditory cortex, vestibular end organs, ocular-motor pathways, cerebellum, or the brain’s multisensory integration systems. Diffuse axonal injury and altered neural timing can disturb communication between these regions even when structural imaging is unrevealing. The clinical phenotype therefore varies widely and may evolve as the patient encounters more demanding environments.

Tinnitus: The Persistent Internal Signal

Tinnitus is one of the most frequently reported auditory symptoms after head injury. It may begin immediately or become apparent later, and it may be unilateral, bilateral, intermittent, constant, tonal, broadband, or pulsatile. Possible contributors include cochlear injury, altered auditory-nerve input, central gain changes, somatosensory influences from the cervical spine or temporomandibular region, medication effects, stress, and sleep disruption. Blast exposure and repeated TBI appear to increase risk (Yurgil et al., 2016).

The clinical impact of tinnitus cannot be inferred from its loudness alone. For some patients, it becomes an attentional and emotional stressor that disrupts sleep, concentration, communication, and work. Its burden may be magnified by post-traumatic stress disorder, anxiety, depression, pain, or cognitive fatigue (Moring et al., 2018). Assessment should therefore include laterality, onset and injury chronology, pulsatile characteristics, somatic modulation, tinnitus pitch and loudness measures when appropriate, and a validated outcome measure such as the Tinnitus Functional Index or Tinnitus Handicap Inventory. Sudden hearing loss, objective or pulsatile tinnitus, focal neurologic findings, or new unilateral symptoms require appropriate medical referral.

The Multidimensional Burden of Tinnitus After TBI

Tinnitus deserves active evaluation and treatment because its consequences extend beyond perception of sound. It can interact with nearly every domain already vulnerable after brain injury. Important negative effects include:

• Reduced sleep length
• Reduced sleep quality
• Speech-processing disturbance
• Increased listening effort
• Attention and concentration difficulty
• Auditory working-memory strain
• Emotional distress
• Reduced sound tolerance
• Restricted participation and quality of life

These associations are clinically important, but should not be interpreted as proof that tinnitus is the sole cause of every symptom. Hearing loss, brain injury, vestibular dysfunction, pain, medications, sleep disorders, mood, and cognitive impairment may contribute simultaneously. The audiologist’s task is to define the tinnitus-specific burden while identifying interacting conditions that require coordinated care.

Tinnitus Should Be Treated

Treatment is warranted even when the tinnitus sound cannot be completely eliminated. The evidence-based goal is to reduce its intrusiveness, distress, attentional capture, and functional interference. A successful outcome may include longer and more restorative sleep, lower anxiety, less listening effort, improved communication confidence, better concentration, greater sound tolerance, and return to valued activities.

Treatment options may include:

• A nightly treatment system
• Individualized education and counseling
• Environmental sound enrichment and customized sound therapy
• Cognitive behavioral therapy
• Tinnitus retraining therapy or progressive tinnitus management
• Bimodal neuromodulation for appropriately selected patients
• Management of hyperacusis
• Treatment of contributing otologic, neurologic, cervical, temporomandibular, sleep, migraine, pain, or behavioral-health conditions

Care should be based on candidacy, evidence, contraindications, patient goals, and validated outcome measures rather than a one-size-fits-all device recommendation.

Hearing Loss: Conductive, Sensorineural, Mixed—and Hidden

Head trauma can produce conductive hearing loss through tympanic-membrane perforation, hemotympanum, ossicular-chain disruption, or temporal-bone fracture. Sensorineural loss may result from cochlear concussion, labyrinthine injury, acoustic trauma accompanying a blast, vascular compromise, or injury to the auditory nerve and central pathways. Mixed loss can occur when peripheral mechanisms coexist. A systematic review concluded that hearing loss following TBI without temporal-bone fracture is clinically significant but remains incompletely characterized (Chen et al., 2018).

Routine pure-tone audiometry remains necessary because it identifies threshold loss and guides medical and rehabilitative decisions. However, conventional testing from 250 through 8000 Hz measures detection of simple tones in quiet; it does not directly measure the fidelity of suprathreshold neural coding, binaural integration, temporal resolution, auditory attention, or real-world speech understanding. Extended-high-frequency testing, otoacoustic emissions, immittance and acoustic reflexes, speech recognition, and—when clinically indicated—electrophysiologic measures can reveal information not captured by the threshold audiogram.

Vertigo Attacks: Episodic Disorientation After Injury

Vertigo is the illusion of movement—often spinning, tilting, rocking, or being pulled. After TBI, episodic vertigo may arise from benign paroxysmal positional vertigo (BPPV), labyrinthine concussion, perilymphatic fistula or third-window disorders, migraine-associated mechanisms, central vestibular injury, or less commonly other otologic or neurologic causes. Trauma can dislodge otoconia and precipitate BPPV, sometimes affecting more than one canal or both ears. Because positional vertigo is frequently treatable, careful positional testing is essential when medically appropriate.

Not every vertigo attack is peripheral. Central ocular-motor abnormalities, post-traumatic migraine, medication effects, orthostatic intolerance, and visually induced dizziness can produce overlapping complaints. The history should define timing, duration, triggers, auditory accompaniments, headache features, visual sensitivity, falls, nausea, and neurologic symptoms. Acute severe vertigo with new focal neurologic signs, inability to stand, sudden hearing loss, or severe headache warrants urgent medical evaluation.

General Imbalance: When Multiple Sensory Systems No Longer Agree

Many patients do not describe true spinning. Instead, they report unsteadiness, veering, motion sensitivity, or disequilibrium while turning the head. Balance depends on integration of vestibular, visual, and somatosensory information, followed by accurate central weighting and motor responses. TBI can disturb any component of this system. Chronic TBI research has linked dizziness and imbalance to reduced postural stability, particularly during tasks that demand greater use of vestibular and visual input (Taylor et al., 2022).

Vestibular test results are heterogeneous. In veterans with chronic dizziness after mTBI or blast, Akin et al. (2022) reported vestibular abnormalities in approximately one third of participants, with otolith-related abnormalities more frequent than horizontal semicircular-canal abnormalities. Normal results on one vestibular test therefore do not exclude impairment elsewhere. Evaluation may require video-oculography, positional testing, video head-impulse testing, caloric or rotational-chair testing, cervical and ocular vestibular-evoked myogenic potentials, dynamic visual acuity, and postural-stability assessment. Findings must be integrated with vision, migraine, cervical, autonomic, neurologic, orthopedic, and psychological factors.

Auditory Processing Disorder: Hearing the Words but Losing the Message

Central auditory processing refers to how the nervous system analyzes and uses acoustic information. After TBI, a person may struggle to separate a speaker from background noise, combine information arriving at the two ears, follow rapid speech, recognize degraded speech, localize sound, or retain multistep verbal instructions. These complaints are especially apparent in restaurants, meetings, classrooms, vehicles, and group conversations—settings that are not represented by word recognition in quiet.

Behavioral and electrophysiologic studies support persistent central auditory changes after mTBI. Long-term research has identified abnormal performance on behavioral and electrophysiological central auditory measures in some individuals with mTBI (Buriti et al., 2022). Studies of blast-exposed service members have likewise documented auditory-processing difficulty despite clinically normal hearing, particularly on demanding speech and temporal tasks (Gallun et al., 2016; Saunders et al., 2015). More recent evidence continues to show altered central auditory processing after TBI and reinforces the need for tests that challenge binaural, temporal, and degraded-speech processing (Lichtenstein et al., 2025).

Interpretation requires care. Auditory processing performance is influenced by attention, language, memory, fatigue, sleep, mood, and test-taking endurance—all of which may also be affected by TBI. These influences do not make the listening complaint less real; they make interdisciplinary assessment more important. The audiologist should identify the auditory demands that fail, compare patterns across tests, monitor fatigue, and coordinate with neuropsychology and speech-language pathology when cognitive-linguistic factors may contribute.

Normal Hearing Thresholds Do Not Mean Normal Auditory Function

All of the problems discussed in this article—including tinnitus, sound intolerance, episodic vertigo, chronic imbalance, speech-in-noise difficulty, increased listening effort, and central auditory-processing dysfunction—may exist in the presence of normal pure-tone hearing thresholds. A normal audiogram means that soft tones were detected within the conventional test range under quiet, controlled conditions. It does not establish normal cochlear synaptic function, central neural timing, binaural processing, speech perception in noise, vestibular function, auditory memory, or everyday communication ability.

Theodoroff et al. (2021) emphasized that concussion-management guidelines often overlook tinnitus, noise sensitivity, and difficulty understanding speech in complex environments. In blast-exposed populations with average pure-tone thresholds in the normal range, decreased sound tolerance and functional auditory problems may still be present (Theodoroff et al., 2019). Grant et al. (2021) similarly reported increased risk for abnormal auditory task performance associated with blast exposure even among service members without substantial threshold elevation. Consequently, stopping the evaluation after “normal hearing” is documented can leave the primary disability unexplained and untreated.

Evaluating Beyond the Simple Audiogram to Restore Function & Quality of Life

The purpose of comprehensive assessment is not merely to name abnormalities; it is to connect findings to formulate a comprehensive, multidisciplinary treatment plan that emphasizes restoration of function and improves the patient’s quality of life over the years. Depending on the profile, management may include:

• Medical or neuro-otologic treatment of structural injury, sudden loss, BPPV, migraine, or other identified conditions
• Hearing aids, remote microphones, and assistive listening technology to improve audibility and signal-to-noise ratio
• Tinnitus technology-based treatment, counseling, sound therapy, cognitive behavioral approaches, and combination treatment plans when appropriate
• Auditory rehabilitation targeting speech in noise, temporal processing, localization, compensatory strategies, and communication-partner training
• Environmental modification, written reinforcement, paced information, preview/review strategies, and reduced competing noise
• Vestibular rehabilitation, gaze-stability exercises, balance therapy, habituation, and graded return to visually complex environments
• Coordination with otology, neurology, neuropsychology, speech-language pathology, optometry/ophthalmology, physical therapy, occupational therapy, behavioral health, and primary care

Treatment must be individualized. A patient with normal thresholds but poor speech-in-noise performance may benefit more from communication technology and auditory rehabilitation than from amplification alone. A patient with BPPV may improve rapidly after canalith repositioning, while another with combined vestibular, visual, migraine, and central deficits may require staged interdisciplinary care. Repeat outcome measures should document whether treatment improves participation, safety, listening effort, dizziness, tinnitus distress, and quality of life.

Clinical and Rehabilitation Implications

Auditory deficits can masquerade as inattention, memory failure, irritability, avoidance, or lack of effort. A patient who cannot reliably encode speech in noise cannot be expected to remember it accurately later. A patient whose visual and vestibular signals conflict may avoid stores, driving, exercise, or work environments because those spaces provoke symptoms. When these difficulties are recognized as sensory and neural consequences of injury, rehabilitation becomes more precise, and the patient’s experience becomes more understandable.

TBI care should therefore include routine screening questions about tinnitus, sound sensitivity, hearing in noise, vertigo, imbalance, oscillopsia, falls, and fatigue during listening. A positive screen should lead to comprehensive audiological and/or vestibular evaluation—not reassurance based solely on a normal threshold audiogram. This approach is particularly important after blast exposure, repeated concussion, temporal-bone or ear trauma, or persistent post-concussive symptoms.

TBI can change how a person detects, interprets, tolerates, and remembers sound—and how the brain uses vestibular, visual, and somatosensory information to maintain orientation and balance. Tinnitus, hearing loss, vertigo attacks, general imbalance, and auditory processing disorder may occur alone or in combination. Some abnormalities are peripheral, some central, and many reflect interaction across systems. A simple audiogram is indispensable, but it cannot answer the full clinical question. Comprehensive, functionally oriented assessment gives patients the best opportunity for accurate diagnosis, targeted rehabilitation, and meaningful return to communication, mobility, work, and daily life.

Dr. Shahrzad Cohen, Au.D., M.S., CH-TM, ABA-C, CBIS, is a Board-Certified Audiologist and Certified Brain Injury Specialist whose clinical work focuses on tinnitus, hearing loss, and auditory dysfunction following traumatic brain injury. She is the founder of Hearing Loss Solutions and Auditory Processing Centers Corporations in Sherman Oaks, Calif.

References

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