I have sometimes seen the idea that tinnitus has a genetic basis for development in some of the papers I have breezed over.
Both of my parents have tinnitus (my mother has two forms, regular and pulsate) and since I was a baby I was prone to common ear infections. While I have not uncovered any twin studies (the common research method for determining whether a disease has a genetic basis or not) on the matter. Twin studies are effective (usually in the case of monozygotic or single egg twins) in determining this because if one monozygotic twin has one disorder and the other one has the same disorder in, say, 68% of the cases, then it strongly suggests a genetic basis for that disorder and its heritability.
In regards to tinnitus, the comorbidity of tinnitus and depress is about twice as high compared to the general population. Neuroimaging studies have shown that those with tinnitus has grey matter (neuron reduction) in areas of the brain's limbic system (the emotion center of the frontal lobe) have some reduction. Those with tinnitus tend to have a smaller left hippocampus (among other areas), but this same thing is observed in those with major depression, anxiety disorders, PTSD, and so forth.
Josef Raushecker's 2010 study that showed a massive loss in tissue volume in the ventral-medial-prefrontal cortex (vmPFC) was believed to be related to the failure of certain thalamic areas (specifically the MGN and TRN) to suppress a tinnitus signal from reaching consciousness. This led to a "gate keeping" theory of tinnitus pathology and formation, and drew more attention to the role of the limbic system in tinnitus. While I disagree with Rauschecker that the limbic system plays a primary role in tinnitus development, I think it does have effect on personal affect (emotional state) and coping ability. I refute his idea of the limbic system and thalamus "gate keeper" on the basis that antidepressants that boost serotonin fail to restore this alleged "gate keeper" mechanism. A study from last year even suggested serotonin could worsen tinnitus by further agonizing hyperactivity in the dorsal cochlear nucleus (DCN).
So where does this fit into my post? Those who have under-active limbic systems (or overactive, as the amygdala [a brain region associated with fear and fight or flight responses] is hyperactive in depression and stays that way after the depression subsides), or genetic predisposition to such phenomenons such as under-active serotonin, dopamine, and norepinephrine production may have less down regulation of these feelings of dread. Some people with short alleles of the serotonin transporter gene are more at risk for depression and anxiety. People with less stable basilar membranes (the inner ear cochlear structure that displaces itself to generate action potentials, converting sound from mechanical sound waves into neurological energy to be read) may be more prone to losing their hearing and have less resilient hair cells.
All of these neurobiological factors are complicated to combine together. In some sense it creates a "chicken vs. egg" scenario. Do dysfunctional changes in the brain's limbic system come before or after tinnitus onset? Does being more neurotic lead to the development of tinnitus more often if people are more depressed, anxious, and demonstrate cognitive biases that direct their attention primarily towards negative things (as mine does from what you all have seen)?
Is there a genetic bases for tinnitus? It can obviously happen to anyone, but why do some get it with hearing loss while others can go deaf without it developing?
What do you guys think?
Both of my parents have tinnitus (my mother has two forms, regular and pulsate) and since I was a baby I was prone to common ear infections. While I have not uncovered any twin studies (the common research method for determining whether a disease has a genetic basis or not) on the matter. Twin studies are effective (usually in the case of monozygotic or single egg twins) in determining this because if one monozygotic twin has one disorder and the other one has the same disorder in, say, 68% of the cases, then it strongly suggests a genetic basis for that disorder and its heritability.
In regards to tinnitus, the comorbidity of tinnitus and depress is about twice as high compared to the general population. Neuroimaging studies have shown that those with tinnitus has grey matter (neuron reduction) in areas of the brain's limbic system (the emotion center of the frontal lobe) have some reduction. Those with tinnitus tend to have a smaller left hippocampus (among other areas), but this same thing is observed in those with major depression, anxiety disorders, PTSD, and so forth.
Josef Raushecker's 2010 study that showed a massive loss in tissue volume in the ventral-medial-prefrontal cortex (vmPFC) was believed to be related to the failure of certain thalamic areas (specifically the MGN and TRN) to suppress a tinnitus signal from reaching consciousness. This led to a "gate keeping" theory of tinnitus pathology and formation, and drew more attention to the role of the limbic system in tinnitus. While I disagree with Rauschecker that the limbic system plays a primary role in tinnitus development, I think it does have effect on personal affect (emotional state) and coping ability. I refute his idea of the limbic system and thalamus "gate keeper" on the basis that antidepressants that boost serotonin fail to restore this alleged "gate keeper" mechanism. A study from last year even suggested serotonin could worsen tinnitus by further agonizing hyperactivity in the dorsal cochlear nucleus (DCN).
So where does this fit into my post? Those who have under-active limbic systems (or overactive, as the amygdala [a brain region associated with fear and fight or flight responses] is hyperactive in depression and stays that way after the depression subsides), or genetic predisposition to such phenomenons such as under-active serotonin, dopamine, and norepinephrine production may have less down regulation of these feelings of dread. Some people with short alleles of the serotonin transporter gene are more at risk for depression and anxiety. People with less stable basilar membranes (the inner ear cochlear structure that displaces itself to generate action potentials, converting sound from mechanical sound waves into neurological energy to be read) may be more prone to losing their hearing and have less resilient hair cells.
All of these neurobiological factors are complicated to combine together. In some sense it creates a "chicken vs. egg" scenario. Do dysfunctional changes in the brain's limbic system come before or after tinnitus onset? Does being more neurotic lead to the development of tinnitus more often if people are more depressed, anxious, and demonstrate cognitive biases that direct their attention primarily towards negative things (as mine does from what you all have seen)?
Is there a genetic bases for tinnitus? It can obviously happen to anyone, but why do some get it with hearing loss while others can go deaf without it developing?
What do you guys think?