Searching TinnitusTalk shows that this has come up in the past but may be not quite like this.
If true, I wonder if trigeminal nerve damage can repair itself.
My short version question/hypothesis:
Dental work damage to nerves can cause T because both the auditory and facial (gum) nerves share a common nerve relay (the DNC).
Long version:
I had dental work done (upper molar crown) and then a week later got loud tinnitus.
At first I was thinking it was the dentist's loud drill and the fact that he didn't follow the ATA recommendation of 5 seconds on, 10 seconds off. But I now learned that my hearing is all in the normal range up to 8khz (tinnitus is at 12 khz). For 5 days after the dental work (and before tinnitus), I had massive radiating pain across my upper gum and slight numbness on my upper lip. Then that went away and I got T around day 8. Perhaps nerve damage from the anesthetic needle?
So today "Dr. Google" exposed me to the fact that the trigeminal nerve (which has 3 branches including gums and face) shares a relay (the DCN) which integrates nerve signals from both the trigeminal nerve and the vestibulocochear nerve (auditory nerve).
This document makes the link and suggests that facial nerves can impact a middle ear nerve and T.
Somatic (craniocervical) tinnitus and the dorsal cochlear nucleus hypothesis.
https://www.ncbi.nlm.nih.gov/pubmed/?term=10609479
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 neurological examination. Pure tone and speech audiometry of the 2 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 caused by disinhibition of the ipsilateral dorsal cochlear nucleus. Nerve fibers whose cell bodies lie in the ipsilateral medullary somatosensory nuclei mediate this effect. These neurons receive inputs from nearby spinal trigeminal tract, fasciculus cuneatus, and facial, vagal, and glossopharyngeal nerve fibers innervating the middle and external ear.
CONCLUSIONS: Somatic (craniocervical) modulation of the dorsal cochlear nucleus may account for many previously poorly understood aspects of tinnitus and suggests novel tinnitus treatments.
And in this document, the reverse linkage is described: how middle ear nerve damage can affect the face! (in guinea pigs at least):
Dorsal cochlear nucleus responses to somatosensory stimulation are enhanced after noise-induced hearing loss
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2614620/
Abstract: Multisensory neurons in the dorsal cochlear nucleus (DCN) achieve their bimodal response properties [Shore (2005) Eur. J. Neurosci., 21, 3334–3348] by integrating auditory input via VIIIth nerve fibers with somatosensory input via the axons of cochlear nucleus granule cells [Shore et al. (2000) J. Comp. Neurol., 419, 271–285; Zhou & Shore (2004) J. Neurosci. Res., 78, 901–907]. A unique feature of multisensory neurons is their propensity for receiving cross-modal compensation following sensory deprivation. Thus, we investigated the possibility that reduction of VIIIth nerve input to the cochlear nucleus results in trigeminal system compensation for the loss of auditory inputs. Responses of DCN neurons to trigeminal and bimodal (trigeminal plus acoustic) stimulation were compared in normal and noise-damaged guinea pigs. The guinea pigs with noise-induced hearing loss had significantly lower thresholds, shorter latencies and durations, and increased amplitudes of response to trigeminal stimulation than normal animals. Noise-damaged animals also showed a greater proportion of inhibitory and a smaller proportion of excitatory responses compared with normal. The number of cells exhibiting bimodal integration, as well as the degree of integration, was enhanced after noise damage. In accordance with the greater proportion of inhibitory responses, bimodal integration was entirely suppressive in the noise-damaged animals with no indication of the bimodal enhancement observed in a sub-set of normal DCN neurons. These results suggest that projections from the trigeminal system to the cochlear nucleus are increased and/or redistributed after hearing loss. Furthermore, the finding that only neurons activated by trigeminal stimulation showed increased spontaneous rates after cochlear damage suggests that somatosensory neurons may play a role in the pathogenesis of tinnitus.
If true, I wonder if trigeminal nerve damage can repair itself.
My short version question/hypothesis:
Dental work damage to nerves can cause T because both the auditory and facial (gum) nerves share a common nerve relay (the DNC).
Long version:
I had dental work done (upper molar crown) and then a week later got loud tinnitus.
At first I was thinking it was the dentist's loud drill and the fact that he didn't follow the ATA recommendation of 5 seconds on, 10 seconds off. But I now learned that my hearing is all in the normal range up to 8khz (tinnitus is at 12 khz). For 5 days after the dental work (and before tinnitus), I had massive radiating pain across my upper gum and slight numbness on my upper lip. Then that went away and I got T around day 8. Perhaps nerve damage from the anesthetic needle?
So today "Dr. Google" exposed me to the fact that the trigeminal nerve (which has 3 branches including gums and face) shares a relay (the DCN) which integrates nerve signals from both the trigeminal nerve and the vestibulocochear nerve (auditory nerve).
This document makes the link and suggests that facial nerves can impact a middle ear nerve and T.
Somatic (craniocervical) tinnitus and the dorsal cochlear nucleus hypothesis.
https://www.ncbi.nlm.nih.gov/pubmed/?term=10609479
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 neurological examination. Pure tone and speech audiometry of the 2 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 caused by disinhibition of the ipsilateral dorsal cochlear nucleus. Nerve fibers whose cell bodies lie in the ipsilateral medullary somatosensory nuclei mediate this effect. These neurons receive inputs from nearby spinal trigeminal tract, fasciculus cuneatus, and facial, vagal, and glossopharyngeal nerve fibers innervating the middle and external ear.
CONCLUSIONS: Somatic (craniocervical) modulation of the dorsal cochlear nucleus may account for many previously poorly understood aspects of tinnitus and suggests novel tinnitus treatments.
And in this document, the reverse linkage is described: how middle ear nerve damage can affect the face! (in guinea pigs at least):
Dorsal cochlear nucleus responses to somatosensory stimulation are enhanced after noise-induced hearing loss
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2614620/
Abstract: Multisensory neurons in the dorsal cochlear nucleus (DCN) achieve their bimodal response properties [Shore (2005) Eur. J. Neurosci., 21, 3334–3348] by integrating auditory input via VIIIth nerve fibers with somatosensory input via the axons of cochlear nucleus granule cells [Shore et al. (2000) J. Comp. Neurol., 419, 271–285; Zhou & Shore (2004) J. Neurosci. Res., 78, 901–907]. A unique feature of multisensory neurons is their propensity for receiving cross-modal compensation following sensory deprivation. Thus, we investigated the possibility that reduction of VIIIth nerve input to the cochlear nucleus results in trigeminal system compensation for the loss of auditory inputs. Responses of DCN neurons to trigeminal and bimodal (trigeminal plus acoustic) stimulation were compared in normal and noise-damaged guinea pigs. The guinea pigs with noise-induced hearing loss had significantly lower thresholds, shorter latencies and durations, and increased amplitudes of response to trigeminal stimulation than normal animals. Noise-damaged animals also showed a greater proportion of inhibitory and a smaller proportion of excitatory responses compared with normal. The number of cells exhibiting bimodal integration, as well as the degree of integration, was enhanced after noise damage. In accordance with the greater proportion of inhibitory responses, bimodal integration was entirely suppressive in the noise-damaged animals with no indication of the bimodal enhancement observed in a sub-set of normal DCN neurons. These results suggest that projections from the trigeminal system to the cochlear nucleus are increased and/or redistributed after hearing loss. Furthermore, the finding that only neurons activated by trigeminal stimulation showed increased spontaneous rates after cochlear damage suggests that somatosensory neurons may play a role in the pathogenesis of tinnitus.