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If you need specific help beyond what you’re finding on the internet or GPT with design or prototyping, you can schedule a private meeting with me. https://ryandewitt.as.me/design
If you also wake up with an uncomfortable jaw or a headache, nighttime clenching could be the cause of tinnitus, which can create a feedback loop. I show how to make a switch that vibrates when you clench. I don’t go to sleep without that switch, it’s not a mouthguard, a simple by reliable switch that vibrates. https://www.hacklabdesign.com/products/p/fbs
Try this – ChatGPT Prompt – “Design a Bi-Modal Tinnitus treatment based on Susan Shore’s public Research.” You will need to be logged into GPT to make the schematic.
Link Between Bruxism and Tinnitus:
Bruxism, or teeth grinding and clenching, can be linked to tinnitus, the perception of ringing or buzzing in the ears. This connection is primarily due to the temporomandibular joint (TMJ), located near the ear, and its proximity to the auditory system. When bruxism occurs, it can put pressure on the TMJ, which can then affect the nerves and structures in the ear, leading to tinnitus.
The temporomandibular joint (TMJ), which connects the jaw to the skull, is located near your ear, muscles, and nerves. Pressure and Nerve Irritation: Bruxism, especially when severe or chronic, can cause the jaw muscles to tense and the TMJ to be under pressure. This pressure can affect the nerves and structures in the ear, including the tensor tympani muscle, which is involved in regulating sound. This nerve irritation can lead to the perception of tinnitus, a ringing, buzzing, or other phantom noises in the ear. While not everyone who grinds their teeth will experience tinnitus, studies suggest a higher prevalence of tinnitus in individuals with bruxism and temporomandibular disorders (TMD) compared to the general population.
I mentioned Poor Sleep and Tinnitus (Beta-amyloid and tau proteins). During deep, non-REM sleep, the brain’s glymphatic system is highly active, effectively cleaning out waste products like toxic proteins such as beta-amyloid and tau. These proteins are linked to Alzheimer’s and dementia, and their buildup can impair communication between neurons. Sleep, particularly deep sleep, is crucial for this waste removal process. Beta-amyloid and tau proteins, key players in Alzheimer’s disease (AD), are also associated with age-related hearing loss and tinnitus. Studies suggest that higher levels of these proteins, particularly in the brain, correlate with worsening hearing and increased tinnitus severity.
Glutamate plays a crucial role in transmitting signals between neurons, and its dysregulation is linked to tinnitus. In the auditory system, excessive glutamate release in the synaptic clefts between hair cells and auditory nerve fibers can lead to overstimulation and potentially contribute to the tinnitus sensation. Glutamate, the primary excitatory neurotransmitter in the auditory system, plays a crucial role in normal hearing function, but its dysregulation is also implicated in the generation and persistence of tinnitus.
Excitotoxicity: Excessive release or inadequate removal of glutamate in the auditory pathway can lead to excitotoxicity, a process where neurons are damaged or even die due to overstimulation. This excitotoxic damage can occur at the synapses between inner hair cells and auditory neurons, and can contribute to cochlear damage and potentially result in tinnitus.
NMDA Receptor Overactivation: A specific type of glutamate receptor, the N-methyl-D-aspartate (NMDA) receptor (NMDAR), is widely distributed in the auditory system and plays a role in synaptic plasticity. Overactivation of NMDARs has been observed in animal models of tinnitus and is considered to be a contributing factor to the development of tinnitus.
Altered Auditory Processing: Glutamate dysregulation can contribute to altered neural activity and reorganization within the auditory pathway. This can lead to increased spontaneous firing rates in neurons of the cochlear nucleus and other auditory centers, which is believed to be associated with the perception of tinnitus.
Synaptic Plasticity: NMDARs are involved in long-term potentiation (LTP) and long-term depression (LTD), forms of synaptic plasticity that play a role in maintaining and altering neural connections. In tinnitus, changes in synaptic plasticity, potentially mediated by NMDARs, can lead to increased excitability and aberrant neuronal activity in auditory centers.
Somatosensory Interactions: In some types of tinnitus, interactions between the auditory and somatosensory pathways are involved. Decreased auditory input, potentially due to cochlear damage, can lead to an increase in glutamatergic input from the somatosensory pathway to the dorsal cochlear nucleus, contributing to tinnitus-related changes. NMDARs are thought to play a role in this maladaptive plasticity and are potential targets for therapeutic intervention.
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