• Relationship between sleep disturbances (actigraphy, insomnia, seep quality) and inflammation in adults with Temporomandibular Joint Disorder.

    The overall objective of this research is to determine the biopsychological mechanisms underlying case-control differences in inflammatory tone related to experimental pain. The rationale is that preliminary data supports an association between pain-induced inflammatory responses and several outcomes (e.g., a primed immunological state in monocytes, maladaptive psychological appraisals of pain, and poor sleep) in TMJD cases. However, it is unclear if these outcomes are independently associated with the inflammatory response to pain and if it predicts future pain experiences.
  • Do alterations in concurrent structural (cortical grey matter volume) and functional (resting state functional connectivity) brain outcomes are related to clinical measures (migraine frequency) and sleep (self-reported sleep quality)?

  • Endogenous pain modulation is a predictor of cognitive behavioral therapy response in pediatric migraine patients.

  • Sleep, pain modulation, and inflammation adolescents with Juvenile Fibromyalgia

    This research compares effects of an 8-week intervention in adolescents with JFM - cognitive-behavioral therapy (CBT) and graded aerobic exercise (GAE) vs. Fibromyalgia Integrative Training program for Teens (FIT Teens; CBT techniques combined with specialized neuromuscular exercise) on functional disability and clinical pain. Our goal is to understand the biological mechanisms underlying JFM pain and prospectively identify pathways in which modifiable behaviors (sleep) contribute to clinical symptoms and pain-related disability through changes in these mechanisms.  Our objective is to determine if poor sleep and perturbations within the immune system can be observed and if they contribute to clinical symptoms in JFM.  The fidelity of the immune system will be assessed with circulating cytokines, inflammatory gene expression and evoked-release of cytokines by a bacterial endotoxin, lipopolysaccharide (LPS). Flow cytometry will also be used to control for differences in leukocyte subsets (innate immune system).  Our central hypothesis is that poorer sleep leads to peripheral immune perturbations, which in turn will contribute to greater JFM symptoms.