CAUSES OF TINNITUS

In some patients the cause remains unexplained (idiopathic) even after thorough examination. These patients make up about 70–80% of cases and probably have a combination of genetic predisposition, minor disorders of the auditory pathways and central hypersensitivity of the brain to non‑existent external stimuli. It is usually associated with sensorineural hearing loss, i.e., hearing impairment due to damage to structures of the inner ear or the auditory nerve. In these patients the tinnitus is benign, meaning it is not dangerous. However, it is necessary to exclude treatable and potentially dangerous causes such as a tumor.

Risk factors for developing tinnitus:

• Long‑term exposure to loud sounds: concerts, industrial noise, loud music through headphones (musicians, workers in noisy environments, etc.), single‑event acoustic trauma (gunshot, explosion) — all of these can cause permanent or temporary hearing loss and excessive neuronal irritation perceived as buzzing or ringing.

• Natural aging/degeneration of auditory cells (presbycusis).

• Infections and inflammations of the middle ear, Eustachian tube dysfunction, ear canal blockage by cerumen (temporary tinnitus), e.g., Lyme borreliosis, syphilis, various viruses (including SARS‑CoV‑2) and bacteria.

• Metabolic diseases: diabetes, elevated cholesterol, vitamin B12 deficiency.

• Increased psychological tension and anxiety lead to increased muscle tone around the head, neck and ears and worsen perception of auditory sensations.

Other possible causes of tinnitus:

• Vascular changes (atherosclerotic changes in the carotid arteries, arteriovenous malformations) and hypertension (high blood pressure) can trigger tinnitus synchronized with the pulse (pulsatile tinnitus).

• Certain medications, e.g., some local anesthetics, antiepileptics (carbamazepine, pregabalin), anti‑inflammatory drugs such as acetylsalicylic acid, sulfasalazine, some antibiotics (gentamicin, azithromycin, erythromycin, tetracyclines, doxycycline, vancomycin), loop diuretics (e.g., furosemide), as well as sildenafil and tadalafil for erectile dysfunction, and many others.

• Head and cervical spine injuries, sudden pressure changes (e.g., during airplane flight).

• Ear causes: earwax impaction, cholesteatoma (expansive non‑neoplastic lesion), foreign body, otitis media, otosclerosis, tympanic membrane perforation.

• Meniere's disease and other inner ear disorders — excessive fluid accumulation increases pressure in the labyrinth and triggers internal sensations of ringing or humming.

• Temporomandibular joint dysfunction, bruxism (teeth grinding).

• Acoustic neuroma (vestibular schwannoma), i.e., a tumor of the auditory nerve.

• Multiple sclerosis — demyelinating plaques affecting the auditory nerve or brain regions involved in auditory processing.

• Vestibular migraine, idiopathic intracranial hypertension or hypotension.

• Autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis.

• Post‑traumatic stress disorder.

• Head and neck tumors exerting pressure on the auditory nerve, pathways or blood vessels.

PRIMARY TINNITUS

Often has an unclear cause and is most commonly associated with sensorineural hearing loss (SNHL). It includes presbycusis and noise‑induced hearing loss. It is thought to be a phantom perception of abnormal neuronal activity in the ear, auditory nerve and central nervous system. It may not bother the patient.

SECONDARY TINNITUS

This type of tinnitus is characterized by sound generated from a source near the ear. It is very rare (about 1% of tinnitus cases). Vascular and neuromuscular causes are more common types of secondary tinnitus. According to guidelines, recommended evaluation includes history, clinical examination, audiometry, imaging studies and laboratory tests.

What is the procedure?

Primary tinnitus and secondary tinnitus

Primary tinnitus often has an unclear cause and is most commonly associated with sensorineural hearing loss (SNHL). It includes presbycusis and noise‑induced hearing loss. It is thought to be a phantom perception of abnormal neuronal activity in the ear, auditory nerve and central nervous system. It may not bother the patient.

Secondary tinnitus is characterized by sound generated from a source near the ear. It is very rare (about 1% of tinnitus cases). Vascular and neuromuscular causes are more common types of secondary tinnitus. Guidelines recommend history taking, clinical examination, audiometry, imaging studies and laboratory tests.

What is the procedure

A patient with primary tinnitus that does not bother them requires no intervention (recommendation of the American Academy of Otolaryngology‑Head and Neck Surgery Foundation). A patient with chronic, bothersome unilateral tinnitus or tinnitus accompanied by hearing deterioration should be examined in an ENT outpatient clinic within weeks and undergo audiological testing.

For unilateral, pulsatile tinnitus associated with asymmetric hearing loss or neurological findings, imaging of the brain/head (CT or MRI) is recommended.

Imaging and tests may include MRI of the brain with or without contrast, CT with angiography in some cases, audiometry via an ENT specialist, and auditory brainstem evoked potentials (BAEP/AEP) in a neurology clinic, together with a clinical neurological examination.

Treatment of tinnitus

Treatment depends on whether the tinnitus bothers the patient and whether a cause is identified. As noted above, in most cases no specific cause is found and no serious condition (e.g., tumor) is detected on thorough examination. If a treatable cause is found (operable tumor, demyelinating plaque in multiple sclerosis, uncontrolled hypertension, etc.), the patient is treated according to recommended protocols.

Somatosensory tinnitus (ST) is thought to arise from altered somatosensory input from the head and neck. Treatment targets dysfunctions of the cervical spine, temporomandibular joint or both — exercises and manual techniques are used. Animal models indicate that connections between brainstem somatosensory and auditory nuclei can alter incoming signals and change the loudness and pitch of existing tinnitus or even generate tinnitus. Changes in central neuronal firing patterns are reflected in tinnitus loudness and pitch. Cervical nerve stimulation in cats implicated mechanoreceptors and proprioception in cranial nerve activity; nociceptors (pain receptors) were not involved. Electron microscopy shows roles for excitatory and inhibitory neurotransmitters and connections to the trigeminal nucleus. In humans, tinnitus has been linked to temporomandibular dysfunction; recommended treatment includes physiotherapy techniques such as manipulation, mobilization and dry‑needling, individualized per patient. Kinesio taping of neck muscles has shown effects in reducing muscle tension and improving proprioception.

TRT (tinnitus retraining therapy) uses daily application of a white‑noise generator for about three months, with or without amplification, combined with counseling.

CBT (cognitive behavioral therapy) helps develop alternative coping strategies to reduce tinnitus perception and improve quality of life. Sound therapy alone or combined with hearing aids is recommended to mask the sound by acoustic stimulation. It is important to treat comorbidities such as depression, anxiety, sleep disorders, memory problems and general instability. Treatments used include SSRIs and sometimes melatonin. Cognitive training can help with memory and concentration deficits. Benzodiazepines are not recommended for tinnitus because of adverse effects and risk of dependence. There is no evidence that ginkgo biloba or nitric oxide preparations are effective. Other methods that have not shown benefit include electrical stimulation, acupuncture, transcutaneous electrical nerve stimulation, bimodal stimulation and hyperbaric oxygen therapy.

Surgical solutions for tinnitus

Surgical treatment, such as microvascular decompression of the vestibulocochlear nerve, may be discussed with a neurosurgeon in patients with proven neurovascular conflict (a vessel contacting or passing near the vestibulocochlear nerve on MRI). This is controversial because the procedure is high‑risk and relatively few patients worldwide have undergone it. A review of the literature found mixed results: in one review of 35 studies with 572 patients, complete symptom resolution after surgery was reported in 28% of tinnitus cases and 32% of vertigo cases; patients with both symptoms experienced relief in 62% of cases, while 11% had more than one complication. Another review of patients with isolated tinnitus for at least five years reported a success rate of about 60% in 43 patients. Overall, the evidence base is limited and the high surgical risk requires careful weighing of risks and benefits; therefore surgery is not routinely recommended even when neurovascular contact is demonstrated.

Conclusion

Tinnitus affects an increasing number of people with age and is not always perceived as bothersome. However, if tinnitus is distressing and occurs in only one ear, or is accompanied by hearing loss, vertigo or other symptoms, medical evaluation is recommended. Assessment and management require a multidisciplinary, multimodal approach. See an ENT specialist for audiometry and, if needed, further evaluation by a neurologist. In my neurology clinic we can add auditory evoked potential testing (AEP, BAEP) to assess possible pathology of the auditory pathway. Auditory pathway lesions (often unilateral) can have various causes, not only tumors but also damage to the auditory apparatus.

Bothersome tinnitus is difficult to treat, and patients are often tempted by unproven methods that can be costly. Be cautious when choosing treatments and always discuss intended therapies with your treating physician.

MUDr. Petra Mištríková, MBA