Tinnitus is the perception of sounds with no external acoustic stimulus. Its earliest historic reference is debated, but it is believed to have been a known symptom in ancient Egypt, with its first written reference in the Papyrus Ebers, an Egyptian compilation of medical literature dating back to 1550 B.C.1 In A.D. 980, Avicenna devoted a complete treatise within his Canon of Medicine to otology.2 Within this work, he characterized tinnitus as a ringing sensation resulting from the movement of air inside the ears, occurring in individuals with both strong and weak auditory capabilities.2
In the United States, a cross-sectional study discovered that approximately 2.5 million young people aged 12 to 19 have encountered one or more instances of tinnitus.3 Among this demographic, around 1.6 million individuals experience chronic tinnitus.3 The emotional and psychological impact on those with tinnitus is a potential issue, as untreated tinnitus could lead to indications of depression and anxiety. However, it is worth noting that individuals already suffering from depression and anxiety might somaticize their symptoms through tinnitus and blame their tinnitus as the source of their problems. Treatment of the underlying anxiety or depression by psychiatry and psychology helps those patients to make their tinnitus less annoying.
Fluctuating tinnitus in some patients can be a migraine or central sensitivity disorder phenomenon. In these patients, the activation of the migraine process may lead to a temporary change in hearing and thus increase in tinnitus through the activation of the trigeminal ganglion and altered blood flow to the inner ear.4 This altered blood flow can lead to a decrease in hearing and thus tinnitus.
Another link between migraine/central sensitivity disorder and tinnitus is the increased attention to tinnitus during migraine. We have found that the triggers of the increased loudness of tinnitus in these patients are the same as those seen in migraine headache patients (i.e., stress, poor sleep, diet, etc.). We will explain this link between fluctuating or loud tinnitus and migraine in more detail from an epidemiological and mechanistic perspectives. Finally, we will explain the potential for migraine treatments to be considered in the management and treatment of significantly bothersome and fluctuating tinnitus.
Migraine Is More Common in Patients with Tinnitus and Vice Versa
It has been found that migraine is more common in patients with tinnitus and subjective hearing loss. In an analysis of the National Health and Nutrition Examination Survey (NHANES) database, we found that among 12,962 patients with tinnitus or subjective hearing loss, migraine was reported in 36.6% and 24.5% respectively.5 We also found that patients with tinnitus were more likely to have migraine, and that patients with migraine were more likely to have subjective hearing loss and tinnitus.5 Furthermore, the Hwang, et al. cohort study revealed that among 1,056 patients with migraine, 61.5% of patients with vestibular migraine experienced auditory symptoms with tinnitus being the most common symptom.6 These findings suggest that there may be a mechanistic link between migraine and enhanced attention to the dysregulation of the central auditory pathway in a subpopulation of tinnitus.
How Does Migraine Cause Enhanced Tinnitus Perception?
The primary theory explaining the underlying mechanisms of migraine revolves around the activation of peripheral and central trigemino-vascular system (Figure 1). The trigemino-vascular neurons synapse with blood vessels and release specific neuropeptides and become activated after spreading cortical depression. These neurons secrete cytokines like calcitonin gene-related peptide (CGRP), substance P, neurokinin A, and pituitary adenylate cyclase-activating polypeptide.7,8 This abnormal release of molecules leads to processes such as vasodilation, plasma leakage, and mast cell degranulation. Consequently, this sequence of events creates a persistent state of neuroinflammation in the meninges.9,10 Furthermore, there is a connection between the inner ear (specifically the vestibule and cochlea) and the ophthalmic branch (CN V1) of the trigeminal nerve. Heavy CN V1 innervation of the spiral modiolar artery and the stria vascularis have been found in animal studies.11 Stimulation of CN V1, as would be seen in an active migraine process, was found to cause fluid extravasation in the cochlea within 60 minutes.12 This fluid extravasation in the cochlea, which is likely due to trigeminal nerve inflammation and vasodilation in the inner ear’s circulation, contributes to changes in the cochlea that are associated with the migraine state.13 These neurovascular changes potentially provide an explanation for various cochleovestibular symptoms seen in migraine, including tinnitus, which can occur with hearing disturbance. It appears that the trigeminal innervation of the cochlear vasculature may cause a change in hearing in a migraine activation, which can lead to tinnitus development.
