Psychopathology of Tinnitus


The aim of this article is to show that tinnitus is secondary to an aberrant brain-ear circuitry affected by disorders such as mood, anxiety, and alcohol and substance abuse as well as executive dysfunction, migraine, sleep and stress. By treating these comorbidities, tinnitus tends to improve.

Tinnitus is the perception of noise in the absence of any corresponding sound


Pharmacological treatment of tinnitus

TABLE. Pharmacological treatment of tinnitus

Tinnitus is the perception of noise in the absence of any corresponding sound source. Physicians and patients tend to immediately assume that this disorder is mainly localized at the level of the auditory system. In the case of idiopathic tinnitus, patients are told that there is no treatment and they just need to “learn to live with it.” The aim of this article is to show that tinnitus is secondary to an aberrant brain-ear circuitry affected by disorders such as mood, anxiety, and alcohol and substance abuse as well as executive dysfunction, migraine, sleep and stress. By treating these comorbidities, tinnitus tends to improve.


A 55-year old man (MR) presents with bilateral tinnitus and high-frequency sensorineural hearing loss. MR has a complex developmental history including global developmental delay, traumatic brain injury at the age of 5, and dyslexia diagnosed at age 16. MR works part-time as a train operator and is exposed to high levels of acoustic trauma. His brain MRI scan reveals an incidental finding of volume loss within the bilateral parietal lobes. He denies any significant decline in cognitive functioning. However, in the context of a language-based learning disability, he continues to struggle with several aspects of language, including problems with articulation, reading, writing, and spelling, consistent with his baseline.

MR reports no difficulty carrying out his job responsibilities and is fully independent for all activities of daily living. His mental status is consistent with expectations for an individual with a language-based learning disability, including deficits across several aspects of language. He also exhibits select weakness in aspects of the executive domain that overlap heavily with language functions, including sequencing, word generation, and retrieval of unstructured verbal information.

The causes of his difficulties, although likely neurodevelopmental, were exacerbated by additional salient factors, such as tinnitus that in turn is directly related to and worsening a lack of restorative sleep due to sleep apnea and a split shift work schedule, as well as a history of alcohol use. The goal of the evaluation and management of this patient was to treat his comorbid conditions, decreasing his perception of tinnitus. It was recommended that he use ear protection, wear sound cancellation devices, and taper off alcohol. He receives mindfulness training and cognitive behavioral therapy for dyslexia and attentional difficulties. A low dose of sertraline is started for anxiety and melatonin and continuous positive airway pressure (CPAP) for sleep regulation.


Tinnitus is described as ringing, roaring, hissing, or pulsatile. It is classified as subjective and objective. Objective tinnitus is very rare and consists of a sound heard by both the patient and the physician such as arterial bruits, venous hums, and palatal and stapedial myoclonus. Subjective tinnitus is the most common and is only appreciated by the patient. It affects 50 million people in the US. About 0.5% to 2% of people request urgent medical assistance either for acute unbearable tinnitus or for chronic tinnitus that worsened suddenly. The number one culprit of tinnitus is hearing loss.

Causes and differential diagnosis of tinnitus

There is no standard diagnostic criterion for tinnitus. Self-report is the base for determining tinnitus presence. In a subset of psychiatric patients (eg, with schizophrenia) tinnitus may be confused with auditory hallucinations.

The causes of tinnitus could be peripheral or central. Peripheral causes usually involve cochlear pathologies associated with hearing loss (eg, noise-induced hearing loss or Meniere disease), acoustic neuroma or vestibular nerve damage due to infection, an autoimmune disorder, or diabetes. Central causes of tinnitus include stroke, demyelinating lesions, traumatic brain injury, and arteriovenous malformations. Other causes of tinnitus include the use of ototoxic drugs and neck trauma.

Pathophysiologically, tinnitus is understood as the result of an adaptive mechanism to a diminished input: when the neural output stemming from the cochlea is weakened, the auditory system automatically compensates the loss by augmenting its gain. In such situations, tinnitus is compared to that of phantom limb pain. Indeed, a strong positive correlation between the amount of cortical reorganization and the subjective strength of tinnitus was found in a study by Muhlnickel and colleagues.1 Other theories have also been described that are non-adaptive in nature and connect tinnitus to the somatosensory system or the hypothalamic-pituitary axis, specifically cortisol.

Interestingly in tinnitus, many brain areas are affected beyond the auditory system and pathway. In fact, electrophysiological data show that various electroencephalogram (EEG) abnormalities involving different brain areas are associated with tinnitus. Particularly, quantitative EEG showed unilateral localized focus of high frequency activity over the temporal lobe auditory cortex in tinnitus patients. Other areas involved in tinnitus include the anterior cingulate cortex, dorsal lateral prefrontal cortex, insula, supplementary motor area, orbitofrontal cortex, parahippocampus, posterior cingulate cortex, and the precuneus.

Imaging studies also showed involvement of certain regions including auditory structures (auditory brain stem, medial geniculate nucleus, primary and secondary auditory cortex and temporo-parietal association areas) as well as cortical and subcortical areas found on positron emission tomography (PET) scan and functional MRI (amygdala, hippocampus, anterior cingulate, and orbitofrontal cortex).2

Comorbid psychiatric symptoms and syndromes

Alcohol consumption has been described as a risk factor for tinnitus; however, most results have not been significant. There is very limited literature on the relationship between tinnitus and substance use, and most results are inconclusive. However, it is still recommended that patients abstain from substance use including alcohol and tobacco because of their negative effects on overall health.

Affective disorders: there is a high prevalence of depressive disorder in tinnitus patients; in fact, a decrease in depression was associated with a decrease in tinnitus3

• Anxiety disorder: along with depression, anxiety is more prevalent among the tinnitus clinical population4

• Personality disorders: tinnitus distress is associated with high neuroticism, low extraversion, high stress reaction, higher alienation, worse social closeness, worsened well-being, lower self-control, lower psychological acceptance, type D personality, and externalized locus of control5

• Psychosis: patients with tinnitus have higher scores on paranoid ideation, psychoticism, and hostility6

• Somatoform disorder: findings from the World Health Organization indicate that 42% of the patients with somatization disorder had tinnitus with autonomic arousal as a common link7

• Cognitive impairment: tinnitus affects executive function and attention; patients also have slower cognitive processing speed and longer reaction times on brain speed test8

• Stress: emotional exhaustion is a strong predictor of the severity of tinnitus; exposure to high stress has the same incidence of tinnitus as exposure to occupational noise9; some people report that their first awareness of tinnitus coincides with a stressful event such as divorce, accident, surgery, loss of employment, or illness in the family

• Sleep: insomnia is a common complaint in tinnitus patients, in particular difficulty falling asleep; obstructive sleep apnea is a key factor to screen for during an evaluation for tinnitus10; achieving restorative sleep is a key element of tinnitus management.

Impact on quality of life/level of distress

The Tinnitus Handicap Inventory (THI) is a good tool to assess the impact of tinnitus on quality of life and patients’ progress. Patients with tinnitus appear to have poorer quality of life compared with people who do not have tinnitus, notably in those with disabling hearing loss. Reported consequences include anxiety, concentration difficulties, depression, and irritability.

Similarly, reducing tinnitus intensity has a direct impact on the improvement in patients’ quality of life. It is interesting to note that children’s quality of life is affected less by tinnitus. Although children experience tinnitus, they complain about it less frequently. It could be that children adjust better and quicker to the tinnitus or that they consider tinnitus to be a more normal event and distract themselves with other activities, thereby ignoring it more easily.

Treatment strategies

Ideally, the treatment of tinnitus consists of treating the underlying etiology. This includes stopping an ototoxic drug and treating arteriovenous malformations or strokes. In the case of dysfunction of the cervical spine or the temporomandibular joint, manipulations, exercises, occlusion adjustments, and trigger point treatment can improve tinnitus severity. If the tinnitus is caused by a tumor, stereotactic radiosurgery or microscopic decompression may be needed.

Most patients are affected by chronic idiopathic tinnitus. In these cases, a comprehensive evaluation should be conducted to identify comorbidities such as depression, anxiety, alcohol and substance abuse as well as insomnia. By treating these comorbidities, tinnitus severity might decrease.

Auditory therapeutic measures. For tinnitus associated with hearing loss or deafness, hearing aids are used; a cochlear implant may be indicated. Acoustic simulation during sleep has also been shown to reduce tinnitus intensity and improve patients’ quality of life.11

Pharmacotherapy. Psychiatric medications such as anxiolytics, antidepressants, mood stabilizers, and antipsychotics may also be used (Table). Benzodiazepines such as alprazolam, midazolam, and clonazepam are effective treatments and decrease the amplitude of tinnitus. This treatment carries multiple complications with addiction, cognitive difficulties, and gait disturbances in the elderly population.

Antidepressants such as nortriptyline, sertraline, and duloxetine have been shown to be beneficial in studies.12 It is recommended that bupropion be avoided in patients because its activating dopaminergic effect could worsen the tinnitus. Mirtazapine should be avoided as it could increase tinnitus perception.

Mood stabilizers and/or anticonvulsants have been investigated in the treatment of tinnitus. Carbamazepine, valproic acid, and gabapentin have shown some benefit.13 Mood stabilizers are mainly used when tinnitus is comorbid with bipolar disorder, seizure disorder, or migraine.

Antipsychotics should be used as a last resort unless patients have a comorbid psychotic disorder. Antipsychotics have been found helpful in moderate to severe obsessive-compulsive disorders worsening tinnitus and for short-term treatment of hyperacusis.

Psychotherapy. Cognitive behavioral therapy (CBT) is the most studied nonpharmacological treatment. It is the treatment of choice as it targets anxiety and improves patients’ quality of life.14 Mindfulness and meditation reduce the stress response state and in turn decrease the distress associated with tinnitus.

Other interventions. Patients who received acupuncture treatments reported benefit compared with the control group that received sham treatment with fake needles.15 When the tinnitus is associated with sensorineural hearing loss, especially if unilateral, cochlear implantation may be indicated.

Brain stimulation. Both low frequency and high frequency repetitive trans-cranial magnetic stimulation to the auditory cortex was studied in patients with tinnitus and showed promising results. Other areas studied are the frontal and parietal regions, as well as the dorsal cochlear nucleus, the inferior colliculus, and the medial geniculate body of the thalamus.16

Epidural stimulation has been shown to be safe and effective in small trials.17 Deep brain stimulation, although not used specifically for tinnitus but rather for other approved indications (eg, movement disorders) has shown benefit in patients who have comorbid tinnitus.18


We currently know that tinnitus is an aberrant brain-ear circuitry. The work-up consists of a thorough history and physical exam including a cognitive assessment. Urgent referrals should be made when tinnitus is pulsatile or associated with neural deficits (facial weakness or paralysis), unexplained sudden hearing loss, vestibular symptoms, or otalgia and drainage.

In the case of tinnitus without the symptoms described above, other comorbidities such as psychiatric symptoms, stress, sleep, and trauma should be assessed and treated. There is no single treatment for tinnitus, and the goal is to target associated distress with CBT to decrease the perception of tinnitus and improve the patient’s quality of life.


Dr Chemali is Director, Neuropsychiatry Clinics; Director, Behavioral Neurology-Neuropsychiatry Fellowship; Director, Global Implementation Program in Neuropsychiatry, Behavioral and Social Sciences; Associate Professor, Harvard Medical School, Massachusetts General Hospital, Boston, MA. Dr Nehme is Psychiatry Fellow, Consult-Liaison Psychiatry, Cambridge Health Alliance, Cambridge, MA. The authors report no conflicts of interest concerning the subject matter of this article.


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2. Landgrebe M, Langguth B, Rosengarth K, et al. Structural brain changes in tinnitus: grey matter decrease in auditory and non-auditory brain areas. Neuroimage. 2009;46:213-218.

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7. Hiller W, Janca A, Burke KC. Association between tinnitus and somatoform disorders. J Psychosom Res. 1997;43:613-624.

8. Das SK, Wineland A, Kallogjeri D, et al. Cognitive speed as an objective measure of tinnitus. Laryngoscope. 2012;122:2533-2538.

9. Baigi A, Oden A, Almlid-Larsen V, et al. Tinnitus in the general population with a focus on noise and stress: a public health study. Ear Hear. 2011;32:787-789.

10. Koo M, Hwang JH. Risk of tinnitus in patients with sleep apnea: A nationwide, population-based case control study. Laryngoscope. 2017;127:2171-2175.

11. Drexler D, Lopez-Paullier M, Rodio S, et al. Impact of reduction of tinnitus intensity on patients’ quality of life. Int J Audiol. 2016;55:11-19.

12. Chang JP, Wu CC. Serotonin-norepinephrine reuptake inhibitor treatment for tinnitus and depression. J Clin Psychopharmacol. 2012;32:729.

13. Hoekstra CE, Rynja SP, van Zanten GA, et al. Anticonvulsants for tinnitus. Cochrane Database Syst Rev. 2011;(7):CD007960.

14. Hesser H, Weise C, Westin VZ, et al. A systematic review and meta-analysis of randomized controlled trials of cognitive-behavioral therapy for tinnitus distress. Clin Psychol Rev. 2011;31:545-553.

15. Rogha M, Rezvani M, Khodami AR. The effects of acupuncture on the inner ear originated tinnitus. J Res Med Sci. 2011;16:1217-1223.

16. van Zwieten G, Smit JV, Jahanshahi A, Temel Y, Stokroos RJ. Tinnitus: is there a place for brain stimulation? Surg Neurol Int. 2016;7(Suppl 4):S125-S129.

17. De Ridder D, Vanneste S, Menovsky T, et al. Surgical brain modulation for tinnitus: the past, present and future. J Neurosurg Sci. 2012; 56:323-340.

18. Auffret M, Rolland B, Deheul S, et al, for the CAMTEA team. Severe tinnitus induced by off-label use baclofen. Ann Pharmacother. 2014;48:656-659.

19. Smith PF, Zheng Y, Darlington CL. Revisiting baclofen for the treatment of severe chronic tinnitus. Front Neurol. 2012;3:34.

20. Azevedo AA, Figueiredo RR. Tinnitu treatment with acamprosate: double-blind study. Braz J Otorhinolarygol. 2005;71:618-623.

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