UPCOMING MISOPHONIA STUDIES:
Currently the Duke Sensory Processing and Emotion Regulation program is collaborating with Dr. Sukhbinder Kumar (Newcastle University) and Mercede Erfanian (University of Maastricht) through the International Misophonia Research Network to better understand misophonic trigger sounds.
“ I have wanted to do this study for 15 years” says Dr. Jennifer Jo Brout of IMRN. “We always look to the sufferers and study what is wrong with them but we never think to deconstruct the sounds to find out why these triggers line up so closely…Why do all of us have aversive reactivity to the so many of the same sounds?”
The researchers all feel that with more knowledge about the sounds the disorder will be better characterized and the potential for treatment will be more easily and more efficiently formulated. Dr. Stephen W. Porges (Indiana University Bloomington) has already done a pilot study in association with IMRN but the research needs to be further expanded to really shed light on this issue. The researchers are currently donating their time to begin this study and hope to find resources, which will allow for more of the misophonia researchers to contribute.
Misophonia Research is ever-evolving. While there are currently only a small number of academic articles published, this is growing rapidly. Misophonia International supports the International Misophonia Research Network (IMRN).
The IMRN was formed to facilitate cross disciplinary research in misophonia and conditions related to auditory over-responsivity. Founded by Jennifer Brout, PsyD, the IMRN aims to connect sufferers and researchers to accurate and current information related to the disorder.
Memory Reconsolidation Study
Research of misophonia is in the very early stages. Therefore, misophonia sufferers and their loved ones are without definitive answers to many essential questions about the underlying mechanisms of the disorder, and possible treatment. However, the small amount of research on misophonia provides evidence that misophonic sounds bring about changes in the autonomic nervous system. Like the accelerator pedal in a car, misophonic trigger sounds quickly rev up the engine of our flight/fight system. One reason for this may be that when an individual with misophonia is exposed to certain sounds, their brain misinterprets these sounds as being dangerous, harmful or toxic. As a result, within milliseconds and without conscious thought, the sympathetic nervous system is thrown into high arousal. In other words, in response to trigger sounds, the body is readied for “fight/flight,” as hormonal and physiological changes take place. While this neurological and physiological response is meant to protect the body from harm, in misophonia it leads to a cascade of negative emotional, cognitive and behavioral responses. The amygdala is a part of the brain that is involved in mediating the flight/flight response.
Research at the LeDoux Lab at NYU has addressed this reactivity in the amygdala in a rodent sample. In this study, rodents taught to associate a repetitive sound with an unpleasant stimulus. Although all the animals were exposed to the exact same stimuli, their reactions to the repetitive unpleasant sound was very different. Depending on the intensity of the reactions, they were separated into three groups: (1) typical responders, (2) under responsive, and (3) over responsive. The last group of animals demonstrated the strongest autonomic nervous system reaction in association with the repetitive auditory stimuli. By presenting the sound multiple times, researchers attempted to extinguish its unpleasant value . Results showed that the over responsive rodents (those who showed higher responses after the initial presentation of the sound together with the unpleasant stimulus) did not extinguish the physiological response (fight/flight) induced by the sound, while this responses were lost in the other two groups. This suggests that the animals showing extreme reactions could not “un-learn” the association they had stored in memory. Similar to the over-responsive rodents, misophonic individuals show strong reactivity to auditory stimuli. Since the brain works in a similar way in rodents and in humans, it is possible that misophonics are resistant to extinguish the emotional responses induced by their triggering sounds.
In the LeDoux lab, scientists have also studied a phenomenon often referred to in people as relapse prevention. Relapse is a significant problem in terms of many behavior therapies that attempt to either extinguish a particular response to particular stimuli, and/or make new and more positive associations between stimuli and nervous system responding. Interested in disorders such as anxiety and Post Traumatic Stress Disorder (PTSD), scientists in the LeDoux lab sought ways to re-associate aversive stimuli and high autonomic nervous system arousal in rodent samples, but without relapse. Through a process called memory re-consolidation, scientists at the LeDoux Lab achieved this in rodents, and we propose to translate this into human research, specific to misophonia.
Memory is consolidated when it is moved from our short-term memory into our long-term memory. Once the memory is encoded it is referred to as a memory trace (or engram). However, contrary to what we may think, recalling memory (or activating a memory trace) is not like watching a recording that replays consistently every time we watch it. Instead, each time we retrieve a memory it alters slightly, as it reconsolidates. In other words, previously consolidated memory are retrieved and then consolidated again. Research on memory reconsolidation has demonstrated that the association between a particular stimuli and high autonomic nervous system arousal can be changed when memory is unstable (at the time of reconsolidation). The result is that while the memory itself is retained, the association between the particular harmful stimulus and the high autonomic arousal is diminished. Using variations of memory reconsolidation-based interventions other researchers have used this for phobias and PTSD.
For misophonia sufferers, this approach may result in the development of new associations between trigger sounds and reduced fight/flight activation in the autonomic nervous system. In order to translate this research into those with misophonia, we propose to conduct a clinical trial at Duke University, in consultation with the LeDoux Lab.
 A memory trace is a way to theoretically describe the physical representation of a memory in the brain
This study is a part of the Duke Misophonia and Emotion Regulation Program
The Sensation and Emotion network by Dr. Jennifer Jo Brout has been at the forefront of sensory advocacy and misophonia research for the past two decades.
Our Programs & Studies
To gain a better understanding of how these averse reactions are controlled by the brain, we are building on our research over the past 30 years. We have shown that the brain region called the amygdala is key to such responses.
One area of the amygdala , the lateral nucleus, is involved in receiving sensory inputs and another, the central nucleus, controls the expression of responses. Over-reactivity to auditory stimuli could be due to a hypersensitive lateral amygdala or an over-reactive central amygdala.
We will study animals that show exaggerated responses to auditory stimuli and will record activity in the lateral or central nucleus to try to determine whether the problem is due to hyper-sensitivity or hyper-reactivity.
Previous studies from this program have examined the effects of meclizine on pre-pulse inhibition (Levin et al., 2014) and the relationship between sensory over-responsivity and emotions in adult psychopathology (Rosenthal et al., 2011; Rosenthal et al., in press).
In addition to research, we are dedicated to developing, evaluating, and establishing best practices for providers working with patients who report having misophonia. The approach we are developing is multi-disciplinary and is done in tandem with patients and their families. The self-help component to this approach is a practical combination of proactive coping skills designed to help individuals identify aversive stimuli, and learn different ways to help calm the physiological and emotional over-arousal associated with that stimuli. The program also seeks to help individuals reevaluate and change ways of thinking about aversive stimuli that may act to acerbate. The program teaches how to help calm the physiological and emotional responses to these aversive stimuli. Updates about this program will be posted periodically.
Sensory Processing and Mental Health Study
Some people respond to sensory cues in their daily environments differently than others. Problem with processing sensory information (e.g., getting angry when hearing certain sounds) can be associated with various behavioral health problems.
This study was funded by the Wallace Research Foundation and is no longer active. The study examines the relationship between self-reported responses to sensory cues (during childhood and adulthood) and various mental health problems.
Generalization of Emotion Regulation
This is a study about the ways in which people cope with emotional distress in their lives. We will be looking at ways to understand how to help people calm down easier after they become emotionally distressed. We are interested in how to do this both inside the clinic and also outside in the real world.
Investigating Antihistamine Treatment to Reduce Sensory Over-responsiveness
Histamine, in addition to being a chemical that controls nasal and stomach acid secretions and itch responses also serves as a transmitter between neurons in the brain. We have found that brain histamine systems play important roles in sensory responsivity. In preclinical studies we have shown that a certain type of antihistamine treatment can help reverse sensory gating impairments. In an initial clinical study with people who have difficulty modulating their sensory responsiveness, antihistamine treatment improved sensory screening without producing sedation. This initial study was in people with general sensory over-responsiveness.Want To Support This Program? Donate Now.
Newcastle University – Sukbinder Kumar
Completed Study The Brain Basis for Misophonia – Dr. Sukhbinder Kumar
Brain imaging data showed greatly exaggerated activation of the anterior insular cortex (AIC) in people with misophonia, but not in controls. In addition, the heightened reactivity in misophonic subjects was specific to trigger sounds. For controls there was no difference between reactions to unpleasant versus trigger sounds.
The AIC detects personally relevant stimuli in the environment and directs attention to that stimulus. Stronger activation of AIC to trigger sounds demonstrates that misophonic subjects assign higher salience to trigger sounds.
In addition, analysis of functional connectivity of AIC showed hyper-connectivity, which was again specific to trigger sounds and to default mode network (DMN) in misophonic subjects. The DMN is active during internally directed thoughts and recall of memories.
Finally, analysis of structural brain data demonstrated that misophonics have greater myelination in the gray matter of ventromedial prefrontal cortex (vmPFC). This structural difference may account for the abnormal functional connectivity of AIC to DMN in misophonics. Overall, Kumar et al. showed abnormal activation and functional connectivity of AIC underlying the symptoms of misophonia.