This article discusses an emerging hypothesis linking bothersome tinnitus with migraine-related sensory processing dysfunction.
When evaluating patients with tinnitus, a range of contrasting experiences are noted, from mild, non-bothersome symptoms to those associated with significant distress – broadly corresponding to two main populations. The question becomes, what separates these two groups of patients? Until recently, this phenomenon was somewhat of a mystery. However, in the last few years, we have gained a much better understanding of the cause of bothersome tinnitus and what leads to increased distress in these patients.
An atypical migraine–sensory gating model of bothersome tinnitus
For decades, the dominant story of tinnitus has been straightforward: damage in the cochlea (hair-cell loss or synaptopathy) reduces peripheral input. This leads the central auditory system to compensate by turning up neural ‘gain’, and tinnitus emerges as increased spontaneous activity and reorganisation along the auditory pathway [1]. There is good experimental support for this framework, including animal work showing increased spontaneous firing after noise injury in structures such as the cochlear nucleus, inferior colliculus and auditory cortex [2].
This explanation doesn’t fully account for what clinicians see every day. Why don’t all patients with profound hearing loss have tinnitus? Why do patients with similar hearing thresholds show such different tinnitus severity, including marked fluctuation in loudness or intermittency? Why do some experience periods of complete silence? And why can jaw, neck or facial movement (somatic tinnitus) change tinnitus perception? These ‘real-world’ features point to an additional mechanism beyond cochlear injury alone.
Salience and sensory gating: when the brain stops filtering
This is where the ‘salience network’ and ‘sensory gating’ enter the story [3]. The salience network helps integrate sensory input, bodily state and emotion to decide what deserves attention [3]. Sensory gating is the filtering process that suppresses repetitive or irrelevant signals, so that the brain is not overwhelmed. That is why we are not constantly aware of our shoes on our feet or our shirt on our body. In tinnitus, the evidence points to impaired sensory gating, allowing the tinnitus signal to repeatedly ‘break through’ conscious awareness and remain prioritised [2].
Electrophysiologic and questionnaire-based studies support this link. Auditory evoked potential paradigms (paired stimuli) showed reduced suppression of the second response [4]. This is an objective marker of impaired inhibition, which, when found in tinnitus patients, is correlated with tinnitus severity. Separately, patient-reported sensory gating inventories are higher in decompensated (non-habituated) tinnitus and correlate with emotional distress and loudness [5]. This suggests that for a subset of patients, tinnitus occurs within a broader ‘brain sensitivity’ phenotype rather than being purely an ear and sensorineural hearing loss problem.
Migraine, excitatory gain and central sensitisation
In recent years, ‘migraine’ has been reframed as a sensory processing disorder, not just a headache disorder [1]. At the most fundamental level, migraine represents an excitation-inhibition imbalance in neurotransmitters, resulting in a state of excitatory gain. When this occurs, sensory inputs become amplified from their baseline [6].
We see this clearly in auditory brainstem studies in migraineurs, where there are near-universal deficits in habituation [7]. This refers to neurophysiological habituation in two-click paradigms, where the second click of a pair typically decreases in responsiveness [4]. This neurophysiological habituation deficit is seen clinically as sensory gating deficits, where the brain fails to filter sensory input and, in certain cases, amplifies it. This may manifest clinically as a broader sensory processing disorder. When this occurs over time, the brain starts to remodel such that its baseline responsiveness to sensory stimulus is elevated [4]. This neuroplastic response is known as central sensitisation and is seen in a wide spectrum of disorders. Sensory gating deficits also have downstream consequences on the autonomic response and the salience networks, explaining how both emotional and attentional consequences of tinnitus severity arise.
This sequence of events may represent how cochlear migraine develops. Once the balance between excitation and inhibition shifts, the nervous system becomes more reactive. Sensory responses are not only amplified, but thresholds are lowered via neuroplastic changes (i.e. central sensitisation) [8]. Once this occurs, limbic system activation makes it so that normally innocuous inputs feel urgent and more attention is given to those signals [8].
Epidemiologic work reinforces the association: migraine and tinnitus are more common in one another, and large cohort analyses report increased odds of tinnitus among migraine patients [9]. Notably, many tinnitus patients do not report classic headache histories, yet they may describe ‘atypical’ migraine features. The atypical migraine features include ear pressure, sinus or facial pressure, neck stiffness, head pressure, dizziness or vertigo, hyperacusis, temporomandibular joint (TMJ) symptoms and mental fogginess, among others [10]. The combination of the aforementioned symptoms with tinnitus, fluctuations in tinnitus loudness, and changes in tinnitus severity in response to situational triggers or head, jaw, or neck manipulation can help clinicians recognise a central sensitisation–related tinnitus subtype.
Migraine is increasingly understood as a disorder of sensory processing [1]. Across migraine phenotypes, the brain periodically enters a sensitised state marked by increased neural gain and reduced inhibitory control [1]. In this state, sensory signals become more intrusive and harder to suppress. Indeed, neurophysiological habituation deficits are nearly universal in migraine patients.
This framework hypothesises why unstable (fluctuating) tinnitus consistently tracks classic migraine triggers such as sleep disruption, stress, illness, dehydration, dietary factors, hormonal shifts, weather changes and sensory overload. These triggers do not create new auditory damage. They transiently alter central excitability, shifting the system into a high-gain state that amplifies an existing tinnitus signal [1].
Triggers of bothersome tinnitus
In a brain with migraine physiology, anything that causes small changes in neuroinflammation can cause the cycle of excitation imbalance to occur. These are commonly referred to as triggers. The presentation explicitly groups triggers into familiar migraine categories: stress, sleep changes, diet, hormonal changes and overstimulation (sound, pressure changes, etc.). The ‘threshold’ concept is particularly helpful for counselling: on good days, the brain’s reactivity stays below a symptom threshold; on bad days, stacked triggers push activity above threshold and tinnitus becomes louder or more intrusive.
Peripheral biology still matters: trigeminal pathways and vascular changes
The model doesn’t discard cochlear mechanisms; it adds a second layer. Trigeminal–cochlear connections and neurogenic inflammation are proposed contributors, including vascular permeability changes within the cochlea, potentially explaining ‘fleeting tinnitus’ or sudden shifts in hearing or tinnitus in some patients. Calcitonin gene-related peptide (CGRP)-mediated downstream effects are highlighted as a plausible pathway linking trigeminal activation, vasodilation and sensory hypersensitivity [11].
Treatment implications: match the therapy to the tinnitus subtype
Stable tinnitus with hearing loss may respond best to hearing rehabilitation and sound-based strategies, while recognising that hearing aids are less helpful for certain patterns (e.g. isolated very high-frequency loss or sound-sensitive fluctuating tinnitus).
Table 1: Migraine/central sensitisation subtype of tinnitus that is medically treatable.
Migraine-oriented management is described as layered care: lifestyle and trigger control (including diet), sleep optimisation (treating obstructive sleep apnoea, circadian rhythm disorder, insomnia when present), increased hydration and caffeine elimination, targeted supplements (magnesium glycinate, riboflavin, CoQ10), cognitive behavioural therapy, and medications selected to match comorbidities (e.g. anxiety/depression, hypertension or CGRP-targeted options). Telemedicine treatment of tinnitus, web-based sound therapy and CBT approaches are potential treatments that can be used as scalable adjuncts.
Summary
Patients with tinnitus generally fall into a spectrum ranging from those with mild, non-bothersome tinnitus to those who are highly distressed by it. Traditional models focusing solely on cochlear damage and central gain do not fully explain this disparity. Emerging evidence supports a model in which tinnitus distress is driven by impaired sensory gating and this is the precursor to dysfunction in salience. In this framework, tinnitus is not simply generated but amplified and prioritised by the brain. Fluctuating tinnitus, somatic modulation and concurrent migraine-spectrum symptoms (headache, head pressure, vertigo, sinus/facial pressure, aural fullness, neck stiffness, TMJ symptoms and mental fogginess) point to this subtype. This highlights the importance of addressing triggers such as diet, sleep, stress and other factors that influence central excitability when treating tinnitus and using migraine prophylactic medical therapy for management. Prospective interventional studies are needed to further explore the mechanisms suggested by observations regarding the migraine–tinnitus relationship.
References
1. Lee A, Abouzari M, Akbarpour M, et al. A proposed association between subjective nonpulsatile tinnitus and migraine. World J Otorhinolaryngol Head Neck Surg 2023;9(2):107–14.
2. Norena AJ, Eggermont JJ. Changes in spontaneous neural activity immediately after an acoustic trauma: implications for neural correlates of tinnitus. Hear Res 2003;183(1–2):137–53.
3. Vanneste S, Byczynski G, Verplancke T, et al. Switching tinnitus on or off: An initial investigation into the role of the pregenual and rostral to dorsal anterior cingulate cortices. Neuroimage 2024;297:120713.
4. Finlayson PG, Kaltenbach JA. Alterations in the spontaneous discharge patterns of single units in the dorsal cochlear nucleus following intense sound exposure. Hear Res 2009;256(1–2):104–17.
5. Mohebbi M, Farhadi M, Daneshi A, Mahmoudian S. Toward An Exploration of Habituating to Tinnitus: Perspectives on Sensory Gating. J Am Acad Audiol 2019;30(10):896–903.
6. O’Hare L, Tarasi L, Asher JM, et al. Excitation-Inhibition Imbalance in Migraine: From Neurotransmitters to Brain Oscillations. Int J Mol Sci 2023;24(12):10093.
7. Abouzari M, Tawk K, Lee D, Djalilian HR. Migrainous Vertigo, Tinnitus, and Ear Symptoms and Alternatives. Otolaryngol Clin North Am 2022;55(5):1017–33.
8. Latremoliere A, Woolf CJ. Central sensitization: a generator of pain hypersensitivity by central neural plasticity. J Pain 2009;10(9):895–926.
9. Goshtasbi K, Abouzari M, Risbud A, et al. Tinnitus and Subjective Hearing Loss are More Common in Migraine: A Cross-Sectional NHANES Analysis. Otol Neurotol 2021;42(9):1329–33.
10. Benjamin T, Gillard D, Abouzari M, et al. Vestibular and auditory manifestations of migraine. Curr Opin Neurol 2022;35(1):84–9.
11. Lee EJ, Tsang C, Gutiérrez Pérez ML, et al. Calcitonin gene-related peptide-induced central sensitization: A hypothesis for long COVID symptoms. Med Hypotheses 2025;195:111570.
Declaration of competing interests: HD is the president of the Migraine in Otolaryngology Society, has shares in Elinava Technologies and is an advisor to Finally Quiet!
