In the classification of complex physical complaints in which the focus is on pain that cannot be adequately explained organically, the diagnosis "multisomatoform disorder" has been introduced, replacing somatoform pain disorder (ICD-10 F 45.4) or chronic pain disorder (DSM-IV 307.89).

It can be assumed that multisomatoform disorder is based on a gene-environment (G-U) interaction in which stressful life events "meet" functionally linked gene variants and thus trigger the clinical picture. It can be assumed that the different phenomenology of multisomatoform disorder depends primarily on the individual gene variants that predominate in each case.

The focus of interest is on genes that are associated with the activity of peripheral afferents (e.g. Na+ channel), CNS activity (e.g. COMT, 5-HTT, MAO-A, dopamine receptor, CB1 receptor), the activity of peripheral (e.g. monocytes) cells (proinflammatory mediators) and the activity of cells (e.g. microglia) in the CNS (proinflammatory mediators).

The aim of this study is to provide as comprehensive a description as possible at both the genetic and phenomenological levels with the aim of identifying interactions between gene variants of different genes as well as G-U interactions in multisomatoform disorder. It is postulated that there are significant differences at all these levels compared to an unaffected control group. In addition, the observation of different phenomenological manifestations in different gene patterns can lead to the classification of subtypes, which can lead to improved and more individualized forms of therapy.

Based on the observation that the course of CRPS can be favorably influenced by TNF-alpha inhibitors (Bernateck M et al., 2007), attempts have been made to visualize TNF-alpha activity using scintigraphy and, in a further step, to monitor the effect of TNF-alpha inhibition using imaging.

The encouraging therapeutic successes in CRPS (Bernateck M et al., 2007), which could be achieved by administering TNF-alpha inhibitors, require clinical placebo-controlled studies. Studies in which TNF-alpha inhibitors are administered as part of an IVRB are particularly suitable for this purpose, as the single dose can be kept low and the intervention consists of a maximum of two to three applications, and there are no clinically relevant delays in the placebo arm before a standard therapy (e.g. systemic glucocorticoids) can be used.

Doctoral thesis Ms. Claudia Götz, cand. med.

How the interaction of simultaneously acting sensitizing signals affects nociceptive neurons has not yet been sufficiently investigated. Both in cultures of primary sensory neurons and in behavioral experiments on rats, the combination of two stimuli surprisingly did not lead to the addition of sensitization. Rather, the neuron sensitized by the first stimulus was reset to its normal starting point by the second stimulus. The two stimuli thus canceled each other out.

A cellular mechanism for this has been worked out and experimentally verified. Since not all cellular experiments can be reproduced in humans, in particular because the majority of pharmacological substances are not admitted for use in humans, only the central basic cellular experiment, the double stimulation of PKC-epsilon by double activation of the beta-2-adrenergic receptor with adrenaline, will be reproduced in humans.

In connection with the effect of acupuncture on the sensation of pain, a number of clinical studies have been and are being carried out, in which the question of control group formation is particularly important.