LOLOL
Has it occurred to you that it is most likely that the causality is that those who are more likely to get a spike will be the people who will have to have no choice but to "get obsessed with protecting their ears"?
The science suggests that unnecessarily protecting one's ears is a bad practice and can cause further problems. This is why nobody recommends doing it. In fact, experts are very clear about this and warn people not to. There are many stories of people - who when starting to overprotect (do not confuse this with sensible use of protection) - became so dependent that they end up isolating themselves in their homes. Phonophobia can lead to OCD like symptoms where it can become an obsession to protect at all costs. Obviously, this depends on how susceptible one is to this kind of behaviour, but it is common to see individuals getting trapped in their own mind which is why it shouldn't be recommended.
What research are you basing this statement on??
Only a small slice of it:
http://discovermagazine.com/2010/oct/26-ringing-in-the-ears-goes-much-deeper
(I'll post excerpts below each link)
When Schlee compared people who suffer a lot of distress from tinnitus with those who are not much bothered by it, he found that the more distress people felt, the stronger the flow of signals out of the front and back of the brain and into the temporal cortex. This pattern suggests that the network Schlee discovered is important for the full experience of tinnitus. Tinnitus, in other words, extends beyond the ear, beyond a hearing-specialized part of the brain, beyond even any single piece of neural real estate. It is a disease of networks that span the brain.
Clearly the auditory cortex is just an early stop on the journey that sound takes from the outside world to our awareness. Some neurons in the auditory cortex extend branches down to the brain stem, where they link to a pair of regions called the caudate nucleus and putamen. Those regions may be important for processing the signals in several ways, such as categorizing sounds.
Once signals travel from the ear to the auditory cortex, caudate, and putamen, they eventually make their way to regions of the brain that carry out more sophisticated sound information processing: connecting the sounds with memories, interpreting their meaning, giving them emotional significance. It is precisely these regions that Schlee and his colleagues noted were behaving strangely in people with tinnitus. He argues that it is only when signals reach this large-scale network that we become conscious of sounds, and it is only at this stage that tinnitus starts to cause people real torment. Schlee's results suggest that the higher regions of the brain send their own feedback to the auditory cortex, amplifying its false signals. Schlee's model of tinnitus and consciousness could explain some curious observations. Even in bad cases of tinnitus, people can become unaware of the phantom sound if they are distracted. It may be that distractions deprive the errant signals from the auditory cortex of the attention they need to cause real distress. What's more, some of the most effective treatments for tinnitus appear to work by altering the behavior of the front of the brain. Counseling, for example, can make people better aware of the sounds they experience by explaining the brain process that may underlie the disorder, so they can consciously reduce their distress.
https://fullertonhearing.com/2018/02/21/tinnitus-and-emotional-processing-new-study-offers-hope/
Researchers didn't stop there, though. During the second part of the study, the brain activity of those with varying degrees of tinnitus was compared and what researchers found when comparing scans and analyzing participants' initial intake survey responses was surprising. The final report concluded:
"Individuals with lower tinnitus distress may utilize frontal regions to better control their emotional response to affective sounds."
In other words, individuals who reported less effect from their tinnitus during the initial surveys processed emotions more in the
frontal lobe, an area less related to emotion and more tied to cognitive skills. Those more affected by their tinnitus continued to process emotions primarily in the
amygdala. Researchers also pointed out that their findings suggested, "Physical activity may contribute to lower tinnitus severity and greater engagement of the frontal cortices."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5318420/
The "muted" amygdala activation observed in the tinnitus group could reflect an internal modification of emotional response perhaps as a result of successful habituation to emotionally negative sound. This interpretation would predict a heightened amygdala emotional response in individuals with a more clinically bothersome tinnitus.
In support of our first hypothesis we found that the amygdala's response to sound was significantly modulated by emotional valence. That is, compared with neutral sound clips, the amygdala's response to pleasant and unpleasant sound clips was significantly enhanced. This overall "U-shaped" response to pleasantness reflects the same amygdala response pattern found by Irwin et al. (2011) in young adults with normal hearing. Also in agreement with Irwin et al.'s (2011) data, we found no main effect of hemisphere, suggesting a lack of amygdala dominance. However, the distinctive amygdala U-shaped response pattern that has been independently replicated across both studies seems to suggest a genuine neurophysiological difference in amygdala function between sound conditions.
In our exploratory research question which explored whether differential responses could be detected within the three subdivisions of the amygdala, we found that peak activity was most likely to be found in the LB subdivision of the amygdala, and least likely to be found in the CM subdivision of the amygdala. This pattern was consistent across both hemispheres and for both study groups. Within the animal literature, it is well known that the LB nuclei acts as the "gateway" for sensory information to the amygdala, receiving input from both the auditory thalamus and from association areas of the auditory cortex (Bordi and LeDoux, 1992). Support for similar involvement of the LB nuclei when processing emotionally evocative auditory stimuli has been presented in more recent human neuroimaging studies (Ball et al., 2007; Kumar et al., 2012). Kumar et al. (2012) found both the LB and the SF nucleus to encode acoustic features necessary for attributing valence.
https://www.sciencedirect.com/science/article/pii/S0896627310009876
Regardless of its origin, we argue that NAc hyperactivity indicates appraisal of the perceptual relevance of the tinnitus sensation (and/or perhaps the aversiveness of TF-matched stimuli), with the ultimate objective of affecting perception. VmPFC also projects to the
thalamic reticular nucleus (TRN), including its auditory division (Zikopoulos and Barbas, 2006), which is in a position to inhibit (or modulate) communication between auditory cortex and MGN (Figure 5). Thus, inefficient vmPFC output could prevent inhibition of the tinnitus signal at the MGN. As such, positive correlation between the magnitude of vmPFC anomalies and NAc/mHG activity may indicate some preservation of function: those patients with greater amounts/concentrations of GM in vmPFC exhibit less hyperactivity in NAc and mHG, thus reflecting a relatively greater ability of the vmPFC to exert an inhibitory influence on the auditory system.
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0067778
The rGCa values in the bilateral thalamus, the bilateral hippocampus, and the left caudate were positively correlated and those in the left medial superior frontal gyrus and the left posterior cingulate gyrus were negatively correlated with tinnitus loudness. These results suggest that distinct brain regions are responsible for tinnitus symptoms. The regions for distress and depressive state are known to be related to depression, while the regions for tinnitus loudness are known to be related to the default mode network and integration of multi-sensory information.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4623204/
Beyond abnormal basal ganglia connectivity, chronic tinnitus patients also have abnormal patterns of auditory cortical connectivity. A1 has increased coherence with the PHCG, cerebellum, and orbital pre-frontal cortex, a major hub of the default mode network (DMN; Greicius et al., 2003). While not directly related to the striatal gating model, it is possible that increased connectivity between A1 and subregions of the DMN (as well as CH with the DMN) may be related to introspection in this cohort, a function known to be modulated by the DMN (Fransson, 2005). Previous studies have shown that the strength of regional functional connectivity (global cross-correlations of the BOLD signal) for regions of the DMN are related to the amplitude of auditory phantom percepts (Ueyama et al., 2013), though this relationship between A1 and the DMN is not replicated in the current study.
https://lib.ugent.be/fulltxt/RUG01/002/479/794/RUG01-002479794_2018_0001_AC.pdf
https://cdn.elifesciences.org/articles/06576/elife-06576-v1.pdf
Suppose I am crazy, and want to experience pain every time, say, I see a black cat. I don't think that my brain can cause me to have pain for weeks or months at a time, following this random cue.
This is absolutely false. Strong negative and emotional responses, that can lead to a physiological response, can be triggered by any stimulus. This has even been proven with animal studies. There is a technique known as "anchoring" that specifically exploits this vulnerability. Take someone with PTSD for example, if they were involved a bad car accident, they may never be able to sit in a car again because of the reaction of their brain. A person can develop a fear to
anything, and if one strengthens those pathways by reacting each time, then it can easily become a problem. Our thoughts control our endocrine system, so it will feel very real when you have a panic attack.
For some people,
all sound becomes a problem, so using protection, 24/7, is not the right advice. Tinnitus is almost like a form of PTSD for some, which is why we are so averse to sound: we relive the trauma.
And yet - they do. Despite not thinking twice about the episode - because they Know that conversations are too quiet to cause any problems. (If they were worried about the conversation, they wouldn't be having it in the first place.) They first become aware that something is wrong the next morning, as they are waking up. And then it lasts for days or weeks or months.
What?
Back then, it was early after your onset. Thanks to that advice you had healed and now you can enjoy fewer spikes despite more exposure to noise.
What healing? My tinnitus is exactly the same. I luckily dag myself out of a huge hole when I realised I was on the wrong path. I dodged a bullet.
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