SS-12-01

Classification of neuropathic pain

D. P. Hendriksson. Sweden

SS-12-02

Epidemiology of fibromyalgia

F. Blotman, E. Thomas. Rheumatology department Lapeyronie Hospital, Montpellier cedex 5, France

Fibromyalgia,characterised by diffuse aching and pain or stiffness in the muscles or joints is usually defined by the ACR criteria including the presence of widespread pain in combination with tenderness of 11 or more specific tender points sites. Its existence is still controversial, as well as its relationships to chronic pain disease. The exact meaning of tender points is also hypothetic. The usefulness of ACR criteria is also questioned. The epidemiology is also confused by so -called secondary fibromyalgias (sicca syndrome, rheumatoid arthritis, lupus…). The mean age at fibromyalgia onset is about 30 years. Fibromyalgia is rarely diagnosed in chidren and is uncommon in elderly. Associated conditions and risk factors are various ; the most common are irritable bowel syndrome, chronic fatigue, thyroid diseases. Depression is also very often discovered. We will review the most important studies on epidemiology of fibromyalgia. The prevalence is approximatively 2 %, 3.4 % in women and 0, 5 % in men (Wolfe et al 1995), with range from 0.7 to 4,8 % in the litterature. Some recent datas (Myon et al 2004) suggest this prevalence is underestimated and the estimated prevalence seems to be as high as 7.4 % in France and 10.45 % in Portugal.

SS-12-03

The pathophysiology of pain

W. Zieglgänsberger. Max-Planck-Institut für für Psychiatrie, München, Germany

Under physiological circumstances noxious stimuli activate nociceptors, the peripheral endings of high-threshold primary sensory neurons. In contrast to nociceptive pain, neuropathic pain results from damage to the peripheral or central nervous system. Action potentials generated in nociceptors, as well as injured nerve fibers release excitatory neurotransmitters at their synaptic terminals such as L-glutamate and substance P, and trigger cellular events in the central nervous system that extend over different time frames. Short-term alterations of neuronal excitability, reflected e.g. in rapid changes of neuronal discharge activity, are sensitive to conventional analgesics and do not commonly involve alterations in activity- dependent gene expression. Novel compounds and new regimes for drug treatment to influence activity-dependent long-term changes (memory of pain) in pain transducing and suppressive systems (pain matrix) are emerging. Acquisition and storage of aversive social and somatic memories is one of the basic principles of nervous systems. In the absence of reinforcement, the behavioral response will gradually diminish to be finally extinct. Besides in somatosensory areas in the thalamus and the neocortex, activity-dependent gene expression also induces longterm alterations in the excitability of neurons in limbic structures, such as the prefrontal cortex, anterior cingulate cortex, amygdala and hippocampus, structures considered as gateways to emotions. It is to be expected that conventional analgesics often show only limited therapeutic value in the treatment of this multitude of dynamic changes that operate to produce the symptoms. We still lack the diagnostic tools to more effectively select the optimal treatment for the various chronic pain states.

SS-12-04

Is there a common genetic basis for depression and the fibromyalgia syndrome?

A. Bondy. Psychiatric Hospital, Munich, Germany

Objective: Several features of the fibromyalgia syndrome (FMS) including depression or sleep disturbances as well as the fact that FM runs within families suggests that FMS might be a “depressive spectrum disorder”. Concerning the aetiology of both disorders an involvement of the serotonergic mechanism, substance P and a genetic contribution in vulnerability were proposed.

Methods: Genomic DNA of 275 FMS patients and 300 controls was genotyped for various variants in genes of the serotonergic pathway, as the 5-HT-transporter (5-HTTLPR), the 5-HT2A receptor, the MOA and both isoofrms of the tryptophan hydroxylase (TPH1 and TPH2).

Results: We have found a higher frequency of the 5-HTLPR SS genotype in FMS patients and higher levels of depression and psychological distress among them. We further observed increased frequency of the 5-HT2A CC genotype and a relation between TT genotype and pain perception. Further, the recently identified association between the 19918 A/G SNP of the TPH2 gene and depression was also observed in FMS patients and further related to several parameters of the SCL-R-90

Conclusion: The available data implicate the importance of polymorphic variants in several genes genes coding for the serotonergic pathway in fibromyalgia. The role played by these various polymorphisms remains to be determined, as to whether they are indicative for common pathophysiological mechanisms, or identifying a subgroup of patients with somatic disorders, that are more closely related to psychiatric symptoms.

SS-12-05

Current trend in treatments of neuropathic pain

M. Ackenheil. LMU Munich Psychiatry Hospital, München, Genrtany

Neuropathic pain and fibromyalgia are prevalent diseases which have major consequences on healthcare resources and the individual. From the clinical point of view neuropathic pains represent a heterogeneous group of aetiologically different diseases ranging from cancer to diabetes. Patients with fibromyalgia syndrome also display clinical features common in neuropathic pain suggesting that there might be some overlap. The mechanisms responsible for symptoms and signs in both diseases are still unknown. During the last years there have been numerous reports of various pharmacological treatments of neuropathic pain and FM with disappointing results. Most of the studies were of short duration, had high attrition rates and displayed other methodological problems. In addition some compounds had high rates of adverse side effect which makes it often difficult for the patients to tolerate the treatment, especially in the long-term use. Future research will have to apply new approaches, e.g. using a mechanism based classification of neuropathic pain and callying out studies in populations with the same symptom but not necessarily the same disease, in order to find effective treatments for these common and often debilitating diseases.