Of all non-auditory sensory systems only the somatosensory system appears to be related to tinnitus (e.g. temporomandibular joint syndrome and whiplash). Purpose: To describe the distinguishing characteristics of tinnitus associated with somatic events and to use these characteristics to develop a neurological model of somatic tinnitus Materials and Methods: Case series Results: Some patients with tinnitus but no other hearing complaints share several clinical features including (1) an associated somatic disorder of the head or upper neck, (2) localization of the tinnitus to the ear ipsilateral to the somatic disorder, (3) no vestibular complaints, and (4) no abnormalities on neurologic examination. Pure tone and speech audiometry of the two ears is always symmetric and usually within normal limits. Based on these clinical features, it is proposed that somatic (craniocervical) tinnitus, like otic tinnitus, is due to disinhibition of the ipsilateral dorsal cochlear nucleus. Nerve fibers...
Tinnitus is the perception of sound in the absence of a physical sound stimulus. It is thought to arise from aberrant neural activity within central auditory pathways that may be influenced by multiple brain centers, including the somatosensory system. Auditory-somatosensory (bimodal) integration occurs in the dorsal cochlear nucleus (DCN), where electrical activation of somatosensory regions alters pyramidal cell spike timing and rates of sound stimuli. Moreover, in conditions of tinnitus, bimodal integration in DCN is enhanced, producing greater spontaneous and sound-driven neural activity, which are neural correlates of tinnitus. In primary auditory cortex (A1), similar auditory-somatosensory integration has been described in the normal system (), where sub-threshold multisensory modulation may be a direct reflection of subcortical multisensory responses (). The present work utilized simultaneous recordings from both DCN and A1 to directly compare bimodal integration across these separate brain stations of the intact auditory pathway. Four-shank, 32-channel electrodes were placed in DCN and A1 to simultaneously record tone-evoked unit activity in the presence and absence of spinal trigeminal nucleus (Sp5) electrical activation. Bimodal stimulation led to long-lasting facilitation or suppression of single and multi-unit responses to subsequent sound in both DCN and A1. Immediate (bimodal response) and long-lasting (bimodal plasticity) effects of Sp5-tone stimulation were facilitation or suppression of tone-evoked firing rates in DCN and A1 at all Sp5-tone pairing intervals (10, 20, & 40ms), and greater suppression at 20ms pairing-intervals for single unit responses.. Understanding the complex relationships between DCN and A1 bimodal processing in the normal animal provides the basis for studying its disruption in hearing loss and tinnitus models.
Different intriguing tinnitus clinical patterns show up this central involvement. Among them, somatic modulation of tinnitus features (intensity, frequency) with specific movements (jaw protrusion, head rotation, muscular contraction, etc.) constitutes a specific sub-type of tinnitus (Levine, ; Abel and Levine, ). Interestingly, lateral gaze has also been shown to interact with ST percept (Coad et al., ). These somatic modulations of ST are putatively supported by the cross-modal wiring and talking between somatosensory and auditory pathways. This has been demonstrated at a sub cortical level (dorsal cochlear nuclei, inferior colliculi) via a trigeminal modulation of auditory function in a behavioral animal model of ST induced by an auditory damage (Shore et al., ). Neuronal pathways, by which the somatic afferences interact with the central auditory pathways, are not ascertained. But animal data (Shore et al., ) support the implication of the dorsal cochlear nucleus, via a trigeminal input, as an important hub for auditory and somatic bimodal interaction especially after cochlear damage (Dehmel et al., ). In humans, jaw protrusion modulation of tinnitus assessed with functional imaging (fMRI) also showed increased activation in cochlear nuclei and inferior colliculi but decreased cerebellar activation when compared to controls (Lanting et al., ). PET data on gaze evoked tinnitus support the hypothesis of the emergence of abnormal links between brainstem systems controlling eye movements and auditory structures (Lockwood et al., ). Moreover an interaction of somatosensory stimulation (TENS) with tinnitus loudness has been reported in tinnitus patients (Vanneste et al., ) and has been interpreted as a clue for the activation of the non-specific extralemniscal pathways ending into parietal cortices (Møller, ). Neural plasticity induced by tinnitus could then interact at many different levels with neural circuitries involved in saccade programming and execution.
Based on these clinical features, it is proposed that somatic (craniocervical) tinnitus, like otic tinnitus, is caused by disinhibition of the ipsilateral dorsal cochlear nucleus.
Modulation of central auditory pathway neurons by multiple non-auditory systems has emerged as a fascinating concept in brain processing (). Observations that the somatosensory system can modulate activity in auditory brain stations like the dorsal cochlear nucleus (DCN), inferior colliculus (), and primary auditory cortex (A1) become clinically relevant since many individuals with tinnitus can alter the pitch and loudness of tinnitus percepts through somatic maneuvers including jaw or neck muscle clenching (; ). Animal studies have demonstrated that DCN pyramidal cells receive somatosensory input from dorsal column and trigeminal brainstem nuclei (; ; ; ; ; ) that can elicit cellular excitation or inhibition (; ; ; ; ). Interestingly, bimodal stimulation with sound and somatosensory activation can facilitate or suppress the firing rates of DCN pyramidal cell neurons to the sound stimulus (; ; ), demonstrating that these neurons are capable of multisensory integration (, ; ; ). Moreover, after noise damage and tinnitus induction, bimodal integration in the DCN is significantly enhanced, leading to large increases in the firing rates of output neurons to higher auditory centers (). Since hyperactivity and neural synchrony are physiologic correlates of tinnitus, bimodal facilitation by the somatosensory system after noise damage may be a major factor in tinnitus generation.
Conclusions: Somatic (craniocervical) modulation of the dorsal cochlear nucleus may account for many previously poorly understood aspects of tinnitus and suggests novel tinnitus treatments.">
Conclusions: Somatic (craniocervical) modulation of the dorsal cochlear nucleus may account for many previously poorly understood aspects of tinnitus and suggests novel tinnitus treatments.