In this article the role of neurobiological, psychological and social factors in pathogenesis of chronic pain is analyzed. The chronic pain is considered not as a symptom of damage of tissue and as independent illness due to non-adequate neuroplasticity of systems involved into regulation of pain sensitivity. The major role in development and maintenance of chronic pain is devoted to the primary genetically determined and/or secondary disturbance of interaction between nociceptive and antinociceptive systems at various levels - from peripheral neuron to central structures – that provides pain perception and painful behaviour development.

The effect of antiserotonin antibodies on basal electrocorticogram was studied in electrophysiological experiments on rats. Intracortical injection of 10 microg antiserotonin antibodies into the sensorimotor cortex induced epileptiform activity in this area. It is assumed that antiserotonin antibodies modulate activity of cortical neurons due to both binding serotonin molecules and interaction with serotonin receptors.

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