Age of Onset Matters

I just have the abstract. conclusion: "The current findings of intrinsic differences in tinnitus-related neural activity between the LOT and EOT groups might be applicable for planning individualized treatment modalities according to age of onset. Moreover, differences with regard to the age of tinnitus onset might be a milestone for future studies on onset-related differences in other similar pathologies, such as pain or depression."

LOT : Late Onset Tinnitus.

http://www.ncbi.nlm.nih.gov/pubmed/23415838

 

So they're telling us what we already know - the older you are the worse it gets.

 

Sedley recently identified the heterogenity of tinnitus neural activity and quite a few aspects that need to be addressed, as DeRidder and his colleagues seemed to be presenting tinnitus as largely homogeneous - a fait accompli. This paper seems to barely scratch the surface of the concerns raised.

 

Heres the paper in full - its a heavyweight paper and has a few questions to ponder for the TMS reserachers at Brain2 or whatever its called

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3470708/

 

Actually, I think it's saying that if you get tinnitus for the first time when you're older, it tends to be more severe than if you got tinnitus for the first time when you were younger.

Of course, this is a small sample size and there are always exceptions to the rule so how much we can extrapolate from this I'm not sure.

 

Yes, that's what I meant, if you're older its worse - just like everything else!

 

Louise - Onset of T came on for me at age 70. It was bad enough but after reading all the horror stories on this site and the TMSB forum I am convinced that there are younger people who have it much worse than I. I can still hear pretty well and no other real health problems except for dealing with anxiety and some depression. I will be 72 next month. My doctor tells me I am still in good health. But many times don't feel that way. It doesn't matter what age a person gets T it is a terrible malady to have.

 

Another avenue for research - increased gamma activity reduces rather than causes tinnitus:

Regardless of our model’s correctness, the finding that auditory cortex gamma oscillations are an inhibitory process in tinnitus is an important one; cortical gamma oscillations are known to be generated by the action of gamma-aminobutyric acidergic interneurons (Candin et al., 2009) and to be influenced in vivo by local concentration of gamma-aminobutyric acid (Muthukumaraswamy et al., 2009). These factors are potentially amenable to pharmacological manipulation, and therefore a correct understanding of their role with respect to tinnitus is important for therapeutic exploitation. If our assertion is correct that cholinergic mechanisms influence gamma oscillations in tinnitus, then this might represent a further possible avenue of pharmacological intervention. Our findings suggest that auditory cortex gamma oscillations are not generators of tinnitus, but rather an intrinsic control mechanism that exerts tonic suppression of the phantom auditory percept, and might be augmented to therapeutic effect.

 

And quite a few questions for deRidder et al to ponder here:

Gamma oscillations have been proposed as bases for the perception of tinnitus (Weisz et al., 2007) or, more specifically, for intensity coding (van der Loo et al., 2009; de Ridder et al., 2011a). Increased delta, theta and gamma oscillations in auditory cortex have been reported in several studies of resting-state activity in tinnitus (Weisz et al., 2005, 2007; Ashton et al., 2007; van der Loo et al., 2009; Moazami-Goudarzi et al., 2010; de Ridder et al., 2011b). However, reports of oscillatory changes are controversial in several respects. Firstly, the frequency bands labelled ‘gamma’ in these studies vary hugely from low gamma frequencies under 45 Hz (van der Loo et al., 2009), through narrow ranges such as 50–55 Hz (Weisz et al., 2007) to much wider ranges and higher frequencies (de Ridder et al., 2011b; Ortmann et al., 2011). Outside the field of tinnitus, gamma oscillations in auditory cortex recorded with magnetoencephalography (MEG) can extend to at least 150 Hz (Sedley et al., 2012). Secondly, where auditory gamma oscillations in tinnitus have been identified, they have correlated with tinnitus perceptual features such as laterality in some studies (van der Loo et al., 2009). In Ortmann et al. (2011), however, the correlation appeared to be with hearing loss rather than tinnitus perception. Thirdly, existing evidence is derived from resting-state measurements of tinnitus, which do not permit examination of the dynamic relationship between observed abnormalities and tinnitus perception. Finally, while gamma oscillations have been observed in positive association with tinnitus, and with other types of percept (Tallon-Baudry and Bertrand, 1999), evidence from primary visual cortex shows that they are inversely related to neuronal firing rate and selective attention (Gieselmann and Thiele, 2008; Chalk et al., 2010). At a local circuit level, they are best modelled as having their basis in lateral inhibitory processes and acting to mediate stimulus selectivity (Bathellier et al., 2006; Börgers et al., 2008). Considered alone, these findings raise the possibility that gamma oscillations might even act to suppress tinnitus. We present evidence here that this might be the case.