Tinnitus is defined as the perception of sound in the absence of external sound and can manifest itself in variety of ways. The phantom sounds of tinnitus may sound like ringing, clicking or hissing. The disorder is most often caused by damage to the microscopic endings of the hearing nerve in the inner ear, although it can also be attributed to allergies, high or low blood pressure, a tumor, diabetes, thyroid problems, injury to the head or neck, and use of medications such as anti-inflammatories, antibiotics, sedatives, antidepressants, and aspirin.
New research at the University of Michigan Health System suggests over-exposure to noise can actually cause more lasting changes to our auditory circuitry -- changes that may lead to tinnitus, commonly known as ringing in the ears. U-M researchers previously demonstrated that after hearing damage, touch-sensing "somatosensory" nerves in the face and neck can become overactive, seeming to overcompensate for the loss of auditory input in a way the brain interprets -- or "hears" -- as noise that isn't really there. The new study, which appears in the Feb. 1 issue of The Journal of Neuroscience, found that somatosensory neurons maintain a high level of activity following exposure to loud noise, even after hearing itself returns to normal. In normal hearing, a part of the brain called the dorsal cochlear nucleus is the first stop for signals arriving from the ear via the auditory nerve. But it's also a hub where "multitasking" neurons process other sensory signals, such as touch, together with hearing information. During hearing loss, the other sensory signals entering the dorsal cochlear nucleus are amplified, This overcompensation by the somatosensory neurons, which carry information about touch, vibration, skin temperature and pain, is believed to fuel tinnitus in many cases. The involvement of touch sensing (or "somatosensory") nerves in the head and neck explains why many tinnitus sufferers can change the volume and pitch of the sound by clenching their jaw, or moving their head and neck, "This is the first research to show that, in the animals that developed tinnitus after hearing returned to normal, increased excitation from the somatosensory nerves in the head and neck continued.
Prior research has shown that auditory circuits in the brain are more excitable in tinnitus sufferers, but until now it has not been clear whether that is due to hyperactivity of excitatory neural pathways, reduced activity of inhibitory ones, or a bit of both, Thanos Tzounopoulos, Ph.D., assistant professor of otolaryngology and neurobiology, Pitt School of Medicine used a new technique to image auditory circuits using slices of brain tissue in the lab. Dr. Tzounopoulos' team created tinnitus in a mouse model. The scientists then sought to determine what had gone wrong in the balance of excitation and inhibition of the auditory circuits in the affected mice. They established that an imaging technique called flavoprotein autofluorescence (FA) could be used to reveal tinnitus-related hyperactivity in slices of the brain. Experiments were performed in the dorsal cochlear nucleus (DCN), a specialized auditory brain center that is crucial in the triggering of tinnitus. FA imaging showed that the tinnitus group had, as expected, a greater response than the control group to electrical stimulation. Most importantly, despite local stimulation, DCN responses spread farther in the affected mice. Dr. Tzounopoulos' new experimental approach has resolved why tinnitus-affected auditory centers show increased responsiveness. After administering a variety of agents that block specific excitatory and inhibitory receptors and seeing how the brain center responded, his team determined that blocking an inhibitory pathway that produces GABA, an inhibitory neurotransmitter, enhanced the response in the region surrounding the DCN in the control brain slices more so than it did in the tinnitus slices. This means that agents that increase GABA-mediated inhibition might be effective treatments for tinnitus. Dr. Tzounopoulos' team is now trying to identify such drugs.
Because subjective tinnitus is typically localized to the ear with hearing loss, tinnitus was traditionally thought to originate from neural hyperactivity in the damaged ear. However, most studies have found that hearing loss reduces the neural outputs from the damaged cochlea. These negative findings led to the hypothesis that rinnitus arises from aberrant neural activity in the central auditory system. Positron emission tomography imaging studies performed on tinnitus patients that could modulate their tinnitus provide evidence showing that the aberrant neural activity that gives rise to tinnitus resides in the central auditory pathway.
A study conducted at the University of Arkansas for Medical Sciences (UAMS) has shown potential to markedly improve tinnitus. The study aimed at examining the safety and feasibility of using maintenance sessions of low-frequency repetitive transcranial magnetic stimulation (TMS) to reduce tinnitus loudness and prevent its return over time. TMS involved the placement of a coil on the scalp that creates a magnetic field over the brain’s surface. The magnetic field penetrates up to two or three centimeters from the surface of the coil. An electric current is induced by the magnetic field that either activates or inhibits neural activity. The goal of the study was to inhibit excessive neural activity believed to cause tinnitus. They used a PET scan of the patient’s brain to look for excessive neural activity with increased blood flow in the temporal lobe. They then targetted that area with low-frequency TMS to inhibit the neural activity and decrease the tinnitus.
Researchers Dr. Michael Kilgard and Dr. Navzer Engineer from The University of Texas at Dallas and University-affiliated biotechnology firm MicroTransponder report that stimulation of the vagus nerve paired with sounds eliminated tinnitus in rats. The auditory cortex delegates too many neurons to some frequencies. Because there are too many neurons processing the same frequencies, they are firing much stronger than they should be. In addition, the neurons fire in sync with one another and they also fire more frequently when it is quiet. It's these changing brain patterns that produce tinnitus. Brain changes in response to nerve damage or cochlear trauma cause irregular neural activity believed to be responsible for many types of chronic pain and tinnitus. But when they paired tones with brief pulses of vagus nerve stimulation, they eliminated the physiological and behavioral symptoms of tinnitus in noise-exposed rats. The researchers are, in essence, retraining the brain to ignore the nerve signals that simulate ringing. This minimally invasive method of generating neural plasticity is used to precisely manipulate brain circuits, which cannot be achieved with drugs, "Pairing sounds with VNS provides that precision by rewiring damaged circuits and reversing the abnormal activity that generates the phantom sound.
Because subjective tinnitus is typically localized to the ear with hearing loss, tinnitus was traditionally thought to originate from neural hyperactivity in the damaged ear. However, most studies have found that hearing loss reduces the neural outputs from the damaged cochlea. These negative findings led to the hypothesis that rinnitus arises from aberrant neural activity in the central auditory system. Positron emission tomography imaging studies performed on tinnitus patients that could modulate their tinnitus provide evidence showing that the aberrant neural activity that gives rise to tinnitus resides in the central auditory pathway.
A study conducted at the University of Arkansas for Medical Sciences (UAMS) has shown potential to markedly improve tinnitus. The study aimed at examining the safety and feasibility of using maintenance sessions of low-frequency repetitive transcranial magnetic stimulation (TMS) to reduce tinnitus loudness and prevent its return over time. TMS involved the placement of a coil on the scalp that creates a magnetic field over the brain’s surface. The magnetic field penetrates up to two or three centimeters from the surface of the coil. An electric current is induced by the magnetic field that either activates or inhibits neural activity. The goal of the study was to inhibit excessive neural activity believed to cause tinnitus. They used a PET scan of the patient’s brain to look for excessive neural activity with increased blood flow in the temporal lobe. They then targetted that area with low-frequency TMS to inhibit the neural activity and decrease the tinnitus.
Researchers Dr. Michael Kilgard and Dr. Navzer Engineer from The University of Texas at Dallas and University-affiliated biotechnology firm MicroTransponder report that stimulation of the vagus nerve paired with sounds eliminated tinnitus in rats. The auditory cortex delegates too many neurons to some frequencies. Because there are too many neurons processing the same frequencies, they are firing much stronger than they should be. In addition, the neurons fire in sync with one another and they also fire more frequently when it is quiet. It's these changing brain patterns that produce tinnitus. Brain changes in response to nerve damage or cochlear trauma cause irregular neural activity believed to be responsible for many types of chronic pain and tinnitus. But when they paired tones with brief pulses of vagus nerve stimulation, they eliminated the physiological and behavioral symptoms of tinnitus in noise-exposed rats. The researchers are, in essence, retraining the brain to ignore the nerve signals that simulate ringing. This minimally invasive method of generating neural plasticity is used to precisely manipulate brain circuits, which cannot be achieved with drugs, "Pairing sounds with VNS provides that precision by rewiring damaged circuits and reversing the abnormal activity that generates the phantom sound.
Scientific Explanation of VNS Paired Stimulation for Tinnitus and Stroke Rehabilitation
Shaowen Bao's experiments with induced hearing loss in rats explain why the neurons in the auditory cortex generate these phantom perceptions. They showed that neurons that have lost sensory input from the ear become more excitable and fire spontaneously, primarily because these nerves have "homeostatic" mechanisms to keep their overall firing rate constant no matter what. With the loss of hearing, you have phantom sounds. Tinnitus resembles phantom limb pain experienced by many amputees, One treatment strategy, then, is to retrain patients so that these brain cells get new input, which should reduce spontaneous firing. This can be done by enhancing the response to frequencies near the lost frequencies. They changed their (brain training) strategy from one where they completely avoided the tinnitus domain to one where they directly engage it and try to redifferentiate or reactivate it, and it seems to be giving better results. Another treatment strategy was to find or develop drugs that inhibit the spontaneous firing of the idle neurons in the auditory cortex. His experiments showed that tinnitus is correlated with lower levels of the inhibitory neurotransmitter GABA (gamma-aminobutyric acid), but not with changes in the excitatory neurotransmitters. Their findings will guide the kind of research to find drugs that enhance inhibition of auditory corti.
Josef P. Rauschecker, PhD, a neuroscientist, says that the absence of sound caused by hearing loss in certain frequencies, due to normal aging, loud-noise exposure, or to an accident, forces the brain to produce sounds to replace what is now missing. But when the brain's limbic system, which is involved in processing emotions and other functions, fails to stop these sounds from reaching conscious auditory processing, tinnitus results. They believe that a dysregulation of the limbic and auditory networks may be at the heart of chronic tinnitus . "A complete understanding and ultimate cure of tinnitus may depend on a detailed understanding of the nature and basis of this dysregulation. Using functional Magnetic Resonance Imaging (fMRI), the Georgetown researchers found that moderate hyperactivity was present in the primary and posterior auditory cortices of tinnitus patients, but that the nucleus accumbens exhibited the greatest degree of hyperactivity, specifically to sounds that were matched to frequencies lost in patients. Based on their findings, the researchers argue that the key to understanding tinnitus lies in understanding how the auditory and limbic systems interact to influence perception -- be it sound, emotions, pain, etc.
The imaging technique, magnetoencephalography (MEG), can determine the site of perception of tinnitus in the brain, which could in turn allow physicians to target the area with electrical or chemical therapies to lessen symptoms. Since MEG can detect brain activity occurring at each instant in time, it is possible to detect brain activity involved in the network or flow of information across the brain over a 10-minute time interval," Using MEG, the areas in the brain that are generating the patient's tinnitus can actually be visulaized, which then cab be precisely targetted for treating tinnitus. MEG is an effective clinical tool for localizing the probable source of tinnitus in patients' brains. It also has the potential to assist with the development of future interventional strategies to alleviate tinnitus.
Magnetic Source Imaging & Magnetoencephalography
Hilke Bartels of the University Medical Center Groningen, has revealed that a remarkable number of tinnitus patients are depressed and have a negative attitude towards life. They do not dare to share these feelings with others, which means they experience little social support, which in turn leads to withdrawal behaviour. This is also described as the so-called ‘type D personality’. Anxiety and depression appear to strengthen the effect of tinnitus. People with a type D personality in particular should undergo treatment that concentrates on the reduction of anxiety and depression. UMCG started an experimental treatment regime whereby the relevant brain areas were continuously stimulated with the help of a pulse generator, a sort of pacemaker. The patients indicated that the ‘noise’ was reduced to manageable levels.
In the times to come there is a lot of hope for those patients suffering from tinnitus. In the future, those patients who don't respond to sound therapy and counselling might need to go for further investigations like fMRI or Magneto-encephalography. Transcranial magneto therapy or vagus nerve paired stimulation appears to be promising in those cases refractory to conventional treatment modalities.
Source:
- University of Michigan Health System (2012, February 1). Tinnitus: New evidence touch-sensing nerve cells may fuel 'ringing in the ears'.ScienceDaily. Retrieved December 10, 2012, from http://www.sciencedaily.com/releases/2012/02/120201092301.htm
- University of Pittsburgh Schools of the Health Sciences (2011, April 19). Tinnitus caused by too little inhibition of brain auditory circuits, study finds. ScienceDaily. Retrieved December 10, 2012, from http://www.sciencedaily.com/releases/2011/04/110418152322.htm
- Semin Hear 2008 Nov;29(4):333-349.Human Brain Imaging of Tinnitus and Animal Models.Lobarinas E, Sun W, Stolzberg D, Lu J, Salvi R.Source Center for Hearing & Deafness, University at Buffalo, Buffalo, New York.
- University of Arkansas for Medical Sciences (2008, July 11). New Tinnitus Treatment: Potential To Greatly Diminish Ringing In The Ears. ScienceDaily. Retrieved December 10, 2012, from http://www.sciencedaily.com/releases/2008/07/080709125626.htm
- University of Texas at Dallas (2011, January 13). Tinnitus treatment: Rebooting the brain helps stop the ring of tinnitus in rats.ScienceDaily. Retrieved December 10, 2012, from http://www.sciencedaily.com/releases/2011/01/110112132130.htm
- Health Behavior News Service, part of the Center for Advancing Health (2010, December 12). 'White-noise' therapy alone not enough to curb tinnitus. ScienceDaily. Retrieved December 10, 2012, from http://www.sciencedaily.com/releases/2010/12/101210095530.htm
- University of California - Berkeley (2011, September 13). Tinnitus discovery could lead to new ways to stop the ringing: Retraining the brain could reanimate areas that have lost input from the ear. ScienceDaily. Retrieved December 10, 2012, from http://www.sciencedaily.com/releases/2011/09/110912144247.htm?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+sciencedaily%2Fmind_brain%2Ftinnitus+%28ScienceDaily%3A+Mind+%26+Brain+News+--+Tinnitus%29
- Georgetown University Medical Center (2011, January 15). Tinnitus is the result of the brain trying, but failing, to repair itself. ScienceDaily. Retrieved December 10, 2012, from http://www.sciencedaily.com/releases/2011/01/110112122504.htm
- Henry Ford Health System (2009, October 5). Non-invasive Imaging Technique Can Help Diagnose Tinnitus. ScienceDaily. Retrieved December 10, 2012, from http://www.sciencedaily.com/releases/2009/10/091004141223.htm
- University of Groningen (2008, November 24). Tinnitus: Psychological Treatment And Neurostimulation Offer Hope. ScienceDaily. Retrieved December 11, 2012, from http://www.sciencedaily.com/releases/2008/11/081120175851.htm?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+sciencedaily%2Fmind_brain%2Ftinnitus+%28ScienceDaily%3A+Mind+%26+Brain+News+--+Tinnitus%29
Tinnitus is defined as the perception of sound in the absence of external sound and can manifest itself in variety of ways. The phantom sounds of tinnitus may sound like ringing, clicking or hissing. Ringing In Ears
ReplyDeleteWonderful article, thanks for putting this together! This is obviously one great post
ReplyDeleteWork Injury Therapy & Shoulder Pain Specialist CT