Etiopathogenetic pathways of vulnerability in chronic pain disorders

• Antragstellerin: Professorin Dr. Kati Thieme
• Fachliche Zuordnung: Persönlichkeitspsychologie, Klinische und Medizinische Psychologie, Methoden
• Förderung: Förderung von 2009 bis 2011
• Projektkennung: Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 119111091

Based on the emerging clinical and experimental evidence for the heterogeneity of psychological and biological signs and symptoms associated with chronic musculoskeletal pain disorders, a set of studies are proposed that seek to systematically examine the psychometric, psychophysiological, endocrine, neural regulatory and genetic variables that underlie the pathways of vulnerability in patients suffering from fibromyalgia (FM) and temporomandibular joint disorder (TMJD). Recent studies have identified psychosocial and psychophysiological subgroups within these two populations of chronic musculoskeletal pain disorders. Own recent studies have identified three major autonomic stress response patterns designated as blood pressure hyperreactive, and hyporeactive, as well as electrodermal response patterns and one minor muscle tension response pattern each of which are associated with variations in pain report, affective and behavioral variables as well as somatic symptoms. These response patterns are likely to be mediated by central nervous regulatory systems and genetic variables that affect autonomic reactivity, mood, and sensory perception. Within this context, three gene-encoding catecholamine-O-methyltransferase (COMT) were identified which are associated with variations in pain variants (haplotypes sensitivity) and the risk of developing TMJD. In addition, associations between haplotypes in the gene that codes for adrenergic receptor beta-(2) (ADRB2) expression, the primary target for epinephrine, with mood and resting arterial blood pressure have been identified. A primary goal of the studies proposed in this application is to further characterize the CNS regulatory and genetic regulatory mechanisms that lead to the expression of multiple clinical phenotypes in FM and TMJD patients. Knowledge gained from the proposed studies will further elucidate the pathophysiological pathways that contribute to FM and TMJD and will further our ability to develop individualized multidisciplinary assessment and treatment strategies.

• DFG-Verfahren: Forschungsstipendien
• Internationaler Bezug: USA
• Gastgeber: Professor Dr. William Maixner