Role of Attention in the Generation and Modulation of Tinnitus

http://www.sciencedirect.com/science/article/pii/S0149763413001784

Lots of interesting reading.

Increased neural synchrony, which may play a crucial role in the generation of tinnitus percepts, is a further neural correlate of tinnitus that may result from neuroplastic mechanisms (Eggermont and Roberts, 2004,Weisz et al., 2007a and Weisz et al., 2007b). Following hearing loss and diminished intracortical inhibition, cortical neurons in the regions affected by hearing loss begin to discharge in phase locked patterns (Seki and Eggermont, 2003 and Noreña and Eggermont, 2003) likely mediated by their lateral connections or by other shared inputs such as rhythmic local field potentials arising from recurrent corticothalamic activity disinhibited by hearing loss (Llinas et al., 2005). Subsequently such cortical network activity may be forged into larger functional assemblies by spike-timing dependent plasticity (STDP) in the cortical hearing loss region (cf. Yao and Dan, 2001), giving rise to tinnitus sounds.

Changes in spontaneous activity (occurring either intrinsically in the auditory cortex or conveyed from subcortical auditory structures) induced by cochlear damage could provide a substrate for the development of such network activity. If this process continues unabated over a period of time, chronic functional changes may result in a tinnitus that is dependent wholly on central mechanisms and resistant to therapeutic intervention (Noreña and Farley, 2013). Although it is not known whether STDP or some other neuroplastic process is involved, a progression to dependence on central mechanisms has been described in subcortical auditory nuclei following cochlear damage induced by noise trauma. In the inferior colliculus (IC) of guinea pigs increased spontaneous activity induced by cochlear damage is reduced by stimulating olivocochlear efferents or by cochlear ablation up to about 6 weeks after noise trauma, demonstrating that in its early stage IC hyperactivity is at least partially dependent on continued afferent input from the ear (Mulders et al., 2010). However, after about 8 weeks cochlear ablation no longer had any effect on IC hyperactivity, indicating a transition to mechanisms intrinsic to the IC or in auditory regions projecting to this structure had occurred over this time window (Mulders and Robertson, 2011 and Robertson et al., 2013).

 

So @tomm, would this mean that Tinnitus becomes an intrinsic mechanism or chronic after 8 weeks and it's resolution becomes much more difficult?

 

That's what this 1 study indicates. I've seen others talk about 3, 6 and 8 months before it gets more internalised. I think I posted another one with a different figure recently.

Example:
After cochlear damage induced by noise trauma cholinergic activity in the ventral (VCN) and dorsal (DCN) cochlear nucleus is upregulated for up to 2 months (the longest duration studied), suggesting a role for this pathway in adaptations that occur in hearing loss (Jin et al., 2006, Kaltenbach and Zhang, 2007 and Meidinger et al., 2006).

 

There have been so many studies but also cases of so many people having their T go away. I'm hopeful that these studies are not accurate.

 

"Going away" might mean habituated and no longer hearing it. Having the tinnitus precept obliterated from our brains is something different.

What studies are you referencing? In general, no one knows exactly when the precept becomes chronic, but the study @tomm sites does provide some insight. thanks @tomm

Is is interesting that Autifony is targeting 18 months. That suggests a large window. I wonder what data influenced this cut off date?

(https://clinicaltrials.gov/ct2/show/NCT02315508?term=tinnitus&rank=85)

 

I think people would know the difference between habituation and T going away. Or Not?

 

Also what type of "therapeutic intervention" are they suggesting? Brain therapies should also work, e.g., Trobalt. They must mean cochlear interventions.

I don't. Many people get tinnitus (mild cases), and it means nothing to them. They really don't focus on it. Because they are not focusing on it, it becomes easier for the brain to "shut it down." By "shut it down," I mean the brain is still misfiring in the auditory brain stem (DCN, VCN) and perhaps mid-brain areas, i.e., the inferior colliculus (IC), but the precept is no longer transmitted to the conscious areas of the brain, the prefrontal cortex. The prefrontal cortex is critical to our awareness. Of particular importance are the DLPFC and the VLPFC to tinnitus awareness. That said, scientists still don't know "all the pieces" regarding tinnitus awareness: e.g., how the auditory cortex, lower and mid brain structures, and limbic system affect awareness.

For the DLPFC and tinnitus awareness (specifically, loudness which is correlated with awareness) see, for example, this study:

Exp Brain Res. 2013 Apr;226(1):25-31. doi: 10.1007/s00221-013-3406-7. Epub 2013 Jan 12.
Comparing immediate transient tinnitus suppression using tACS and tDCS: a placebo-controlled study.
Vanneste S1, Walsh V, Van De Heyning P, De Ridder D.
Author information
Abstract
Tinnitus is an auditory phantom percept with a tone, hissing, or buzzing sound in the absence of any objective physical sound source. Two forms of low-intensity cranial electrical stimulation exist for clinical and research purposes: transcranial direct current stimulation (tDCS) and transcranial alternating current stimulation (tACS). In a recent study, it was demonstrated that a single session of tDCS over the dorsolateral prefrontal cortex (DLPFC) (anode over right DLPFC) yields a transient improvement in subjects with chronic tinnitus and that repeated sessions can possibly be used as a treatment. In the present study, the effect of a single-session individual alpha-modulated tACS and tDCS applied at the DLPFC bilaterally is compared with tinnitus loudness and tinnitus annoyance. A total of fifty tinnitus patients were selected and randomly assigned to the tACS or tDCS treatment. Our main result was that bifrontal tDCS modulates tinnitus annoyance and tinnitus loudness, whereas individual alpha-modulated tACS does not yield a similar result. This study provides additional insights into the role of DLPFC in tinnitus modulation as well as the intersection between tinnitus and affective/attentional processing.

Reference:

http://www.ncbi.nlm.nih.gov/pubmed/23314693​