Lab for Clinical &
The Lab for Clinical and Integrative Neuroscience is part of the School of Behavioral and Brain Sciences at the University of Texas at Dallas. Our lab has various locations throughout the Dallas area, including the Callier Center for Communication Disorders, the Center for Brain Health, and on the UT Dallas main campus. Using advanced techniques including brain scanning, electrophysiology, and both invasive and noninvasive neuromodulation, we map how the brain responds to pathological perturbations in an adaptive or maladaptive manner to maintain homeostasis. More specifically, we work to understand the mechanisms of (mal)adaptive plasticity in the brain in different neurological (pain, tinnitus, Parkinson's disease, cognitive impairment) and psychiatric diseases (addiction, OCD, depression).
Our research is based on the idea that the mechanisms of adaptive and maladaptive plasticity fall under a universal construct of hierarchically updating prediction errors in an approximately Bayesian way. This so-called Bayesian brain theory proposes that the brain maintains a predictive internal model and constantly compares it with changing environmental cues.
Whenever there is a mismatch between the two, the brain decides whether and how to adjust its model depending on the novelty or salience of the environmental stimulus. Adaptive plasticity reflects a combination of successful bottom-up compensation and top-down updating of this model. Maladaptive plasticity conversely reflects failure in one or both of these mechanisms, resulting in a constant prediction error.
The reach and extent of the research of the Lab for Clinical and Integrative Neuroscience can only be guaranteed through extensive collaboration with basic neuroscience researchers, engineers, neuroimaging experts and clinicians from non-neurosurgical and neurosurgical fields. We have active collaborations with different labs at UT Dallas as well as several external collaborations. Our external partners include UT Southwestern Medical Center, the Department of Surgical Sciences at the University of Otago in New Zealand, the Department of Otolaryngology at Seoul National University Bundang Hospital in South Korea, as well as various other groups in both Europe and the US.
Permanently affecting one in seven adults, chronic tinnitus lacks both widely effective treatments and adequate understanding of its brain mechanisms. This is largely due to the fact that tinnitus represents a highly heterogeneous condition. Consistent with this idea, our research shows that tinnitus indeed has different subtypes related to the underlying neurogenetic architecture of hearing loss induced tinnitus. We establish, in a human study tightly controlled for hearing loss, that the amount of hearing loss and the COMT Val158Met polymorphism can increase the susceptibility to the clinical manifestation of tinnitus that goes together with not cancelling auditory information, leading to increased tinnitus loudness.
Bayesian models of brain function such as active inference and predictive coding offer a general theoretical framework with which to explain several aspects of normal and disordered brain function. Of particular interest to the present study is the potential for such models to explain the pathology of auditory phantom perception, i.e. tinnitus. To test this framework empirically, we performed an fMRI experiment on a large clinical sample demonstratingthat tinnitus specific stimuli evoke less activity/connectivity in areas related to auditory perception and more activity/connectivity in areas related to the cognitive and emotional aspects of tinnitus, e.g. tinnitus-related distress.
Lab for Clinical & Integrative Neuroscience, School of Behavioral and Brain Sciences, University of Texas at Dallas © 2017