Does multimodal pain treatment affect neurotransmitter turnover and functional connectivity in the brain of patients with chronic pain?

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The major aim of this proposal is to investigate short term effects of an interdisciplinary, multimodal pain therapy treatment on alterations of functional brain connectivity and neurotransmitter levels of gluta¬mate and GABA in pain processing regions of the human brain that are related to nonspecific chronic back pain. Patients are recruited via a screening program of the Pain Therapy Section at the University Hospital Jena and are examined before and after treatment with MEGA-PRESS proton MR spectroscopy and resting state functional MR imaging. This patient group will be compared to a second patient group that undergoes the same MR examination including its repetition after four weeks before they start their own therapy. In addition, a healthy control group will undergo the same MR protocol once. Based on these data the following questions are addressed: How do neurochemical and functional alterations manifest themselves in the brain of chronic pain patients? How are they connected among each other and inasmuch does multimodal treatment affect these alterations? Thereby, the hypothesis of central sensitization of cerebral pain processing will be tested. This hypothesis assumes reduced inhibitory neurotransmitter functions as the underlying cause leading to deregulated permanent neuronal excitation. Potential regulation of the latter following multimodal therapy will be also assessed. Further analyses will correlate the extracted MR parameters with clinical scores that characterize the severity of somatic and psychological impairments to investigate whether treatment outcome has improved and whether this is also reflected in metabolic and functional alterations. Besides providing new and deeper insight into the cerebral manifestations of chronic pain, verification of the hypotheses will further open new opportunities for an objective and differentiated analysis of therapy related regularization of pain processing in the brain.