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Here I will attempt to review the most crucial information I have gleaned over the past few weeks of tinnitus discussion via the internet
1) The Dorsal Cochlear Nucleus Disinhibition Hypothesis (DCND-H)
Both acute and chronic tinnitus subjects (animal and human) display hyperactivity in the dorsal cochlear nucleus (DCN) and/or inferior colliculus (IC), presumably resulting from a loss of inhibitory function in these structures. This hyperactivity has not been observed, or has been observed only weakly, in the auditory brainstem, and has not subsided following ablation of the cochlear nerve; these observations may indicate that the hyperactivity not only registers but also originates centrally.
In noise-induced tinnitus, disinhibition leading to hyperactivity has been shown to result following cochlear damage, suggesting that it may be a central response to alterations in spontaneous input from the auditory periphery. There is some evidence that hyperactivity arises in response to damage to the outer hair cells specifically, and that damage to the corresponding inner hair cells may actually offset the neural instability which produces hyperactivity. Much research in these areas has been led by Dr. James Kaltenbach.
College Essays on Mechanisms of Tinnitus
Dr. Robert Levine has demonstrated that similar patterns of central hyperactivity correlating to unilateral tinnitus can be induced via the somatosensory system (e.g. due to TMJ disorders or whiplash), perhaps indicating a final common pathway for tinnitus and in part explaining the wide variability in individuals apparent susceptibility to noise-induced tinnitus. This hyperactivity model may explain some instances of tinnitus reduction through the use of agents, such as alprazolam (Xanax), which act as agnoists for the inhibitory neurotransmitter GABA, though the GABA agonist baclofen has thus far appeared to have little effect on tinnitus.
) The Edge-Frequency Cortical Reorganisation Hypothesis (EFCR-H)
A related line of thinking is that chronic tinnitus may result from cortical reorganisation following damage to hair cells, in much the same way as phatom pain results from cortical reorganisation following the loss of a limb. Tinnitus subjects demonstrate cortical reorganisation patterns in which the area of the brain corresponding to the frequency region of the tinnitus signal is expanded; a reverse reoganisation is seen in phantom pain patients, for whom the area of the brain corresponding to the amputated limb is often reduced. It is believed that cortical reorganisation results following cochlear damage because the brain rewires itself to receive input from the functional hair cells adjacent to damaged hair cells in the cochlea; the resulting imbalanced signal may produce tinnitus, perhaps by causing and/or maintaining hyperactivity in central auditory structures such as the DCN. Much research in this area has been led by Dr. Herta Flor and associates, and it is worth noting that thus far they have focussed their research on tonal as opposed to noisiform tinnitus.
It remains unclear whether cortical reorganisation and central hyperactivity respectively causes and maintains tinnitus, or whether it shares a common cause or in fact results from the tinnitus signal. It is also unclear exactly what relationship exists between these two phenomena, and how each correlates to inner versus outer hair cell damage.
) Peripheral Involvement in Chronic Tinnitus
Dr.s Alan Lockwood and Richard Salvi examined patients with unilateral tinnitus and found that they displayed neural processing activity on only one side of the brain. A sound presented unilaterally to the cochlea would normally produce bilateral neural activation. As such, these results suggest that regardless of the specific mechanism of tinnitus, the tinnitus signal differs from real sound in its delivery to central auditory structures, and in fact is most probably centrally generated. Peripheral damage merely triggers central generation of tinnitus; it is not the locational source of the tinnitus signal itself. Dr. Hans Zenner has called this type of tinnitus secondary central tinnitus - i.e. tinnitus which is triggered by a peripheral lesion but sustained by centrally generated activity; he distinguishes it from primary central tinnitus, which is triggered by a lesion which is itself central (as in multiple sclerosis).
Despite these findings, debate continues as to whether peripheral signals are in fact the source of tinnitus in a significant number of cases. Dr. Aage Moller, among others, maintains that while severe cases of tinnitus usually appear to have a central, phantom-pain-like origin, milder cases may well be generated at the periphery. It has also been suggested that patient responses to the diuretic furosemide, which appears to suppress peripheral but not central neurotransmitter activity, could be used to distinguish peripheral from central tinnitus. The general anaesthetic lidocaine is often cited as a temporary suppressor of low-pitched tinnitus, and sometimes (with much more variable results) for high-pitched tinnitus, but it appears that researchers have alternately suggested that it works by suppressing peripheral activity (e.g. after perfusion into the inner ear) or by suppressing central activity (e.g. following intravenous infusion).
Dr. Jack Pulec, who does not appear to support the idea of a secondary central tinnitus, has reported a very high success rate in abolishing tinnitus through cochlear neurectomy in cases where the tinnitus signal has been confirmed as having a peripheral source. However, 8 of the 144 patients who obtained abolishment of or substantial relief from tinnitus in his study suffered from endolymphatic hydrops (Menieres disease); many others had tinnitus due to otitis media (4) or otosclerosis/stapedectomy (10). The remaining 1 patients of the 144 who experienced reduction or abolishment of their tinnitus had tinnitus due to trauma or other etiology; as such, the relevance of Dr. Pulecs data for the mechanisms of noise-induced and drug-induced tinnitus remain unclear. It is also worth noting that the sheer destructivenes of the surgery may make its effects unpredictable, and that they may thus provide a poor basis for conclusions regarding tinnitus mechanisms. Most importantly, other studies, such as that undertaken informally by Dr. Jim Chinnis concerning vestibular patients who had complete eighth nerve sections, have indicated a very low rate of tinnitus abolishment with this surgery.
4) Glutamate and Inner Hair Cell Synapses in Hearing Loss and Tinnitus
Another alternate line of thinking, favoured by Dr. Klaus Ehrenberger and associates in Vienna, suggests that some cases of tinnitus are caused by an ongoing destabilisation of glutamate activity at the synapses between inner hair cells and the cochlear nerve. Glutamate is an excitatory neurotransmitter and calcium channel-opener. As such, the glutamate antagonists caroverine and memantine, and also the calcium channel blocker magnesium, have been proposed as potential treatments for tinnitus. Only Dr. Ehrenberger has been able to produce results suggesting success - 48% of 70 patients supposedly obtained a stable, 50%-or-greater reduction in tinnitus following a single administration of intravenous caroverine. Though Dr. Zenner is currently researching memantine, the model of chronic cochlear-synaptic tinnitus is not generally accepted.
That said, there has been some military evidence that magnesium levels may help prevent hearing damage. Indeed, there is considerable evidence that glutamate neurotoxicity is involved in at least some of the hair cell damage which produces acute tinnitus and sometimes permanent hearing damage (which may then lead to the establishment of chronic, secondary central tinnitus). In terms of acute tinnitus, this view is consistent with current thinking on the mechanisms of noise-induced hearing damage. It appears that such damage often occurs due when hair cells overwork to process noise, causing an excessive production of glutamate, which in large quantities can certainly become neurotoxic. It is again unlcear (at least to me) how this theory of damage through glutamate neurotoxicity relates to damage to inner vs. outer hair cells, and whether glutamate neurotoxicity is suggested as causing all noise-induced hearing damage or merely some (e.g. only that which occurs to inner hair cells).
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