Tinnitus: From Traditional Concept to Challenges to Loosen the Gordian Knot

Abstract

Tinnitus is a distressing symptom that affects 15% of the population. Persistent tinnitus can interfere with an individual’s ability to perform usual daily activities and can prevent individuals from getting enough sleep. Tinnitus can cause considerable psychological distress and can be incapacitating (9). Causes of tinnitus include aging, exposure to loud environmental noise, stiffening of the middle ear bones, Meniere disease, labyrinthitis, otitis media, mastoiditis, acoustic schwannomas, ototoxic drugs, and head injuries. The facts that there are many different forms of tinnitus with different, often multiple causes and that the pathophysiology is poorly understood are obstacles to finding effective treatments. Neurosurgeons are generally unfamiliar with long-term management of tinnitus. If a patient complains of persistent tinnitus, the neurosurgeon usually rules out tinnitus of vascular flow origin such as dural arteriovenous fistula and carotid stenosis. Exclusion of a small acoustic schwannoma is also important. When no organic abnormalities are found, the neurosurgeon usually sends the patient to an otolaryngologist for further management. Most otolaryngologists never send the patient back for neurosurgical treatment. Some neurosurgeons have performed microvascular decompression of the cochlear nerve for intractable tinnitus (2, 6, 13, 16). Various audiometric tests have been developed over the years to identify vascular compression of the eighth cranial nerve preoperatively. Many of these tests are no longer in use. Vascular decompression for tinnitus is less successful than vascular decompression for trigeminal neuralgia or hemifacial spasm. Improvement may take up to 1 year. The most likely explanations of failure are that vascular compression, although present, was not the cause of the patient’s tinnitus or that changes of the central nervous system by prolonged peripheral injury were irreversible. Drug treatments for tinnitus are aimed at either the cochlea using intratympanic injections of gentamicin, dexamethasone, or lidocaine or the brain. Benzodiazepines and anticonvulsants have been used, and antidepressants have been introduced more recently. This strategy resembles medical treatment of neuropathic pain in which, following almost complete abandonment of peripheral nerve blocks, antiepileptic drugs and antidepressants play an important role. The mechanism of neuropathic pain is considered to be neuroplastic changes of sensory functions in the central nervous system after small lesioning in the pain pathway, and some types of tinnitus can be a result of deafferentation in the auditory mechanisms. Despite significant recent progress in understanding of neural mechanisms of tinnitus, neurosurgeons seem to be uninvolved in the treatment of this condition. In late 1990s, Jeanmonod, a Swiss neurosurgeon, and his group proposed a hypothesis of thalamocortical dysrhythmia syndrome to explain various forms of positive symptoms after lesioning of the nervous system (7, 11, 12, 17). These positive symptoms include neuropathic pain, tinnitus, abnormal movements, epilepsy, and certain neuropsychiatric disorders. With electroneurophysiologic recordings during stereotactic operations, Jeanmonod found thalamocortical dysrhythmia phenomena in patients with positive symptoms. Since then, with the development of imaging and electrophysiologic studies such as functional magnetic resonance imaging (fMRI) and transcranial magnetic stimulation (TMS), various functional abnormalities in the brain have been identified in patients with tinnitus. Tinnitus is accompanied by a change in the tonotopic map of the auditory cortex (1). There is a highly positive association between the subjective intensity of tinnitus and the amount of shift in tinnitus frequency in the auditory cortex (i.e., the amount of cortical reorganization). This cortical reorganization can be shown by fMRI. A brain network involving limbic and other nonauditory