• M Zimmermann.
• Swiss Med Wkly. 1981 Dec 12; 111 (50): 1927-36.

AbstractUsually, pain is caused by the excitation of nociceptors or of nociceptive afferent fibers. The responsiveness of the nociceptors can be modulated by endogenously released algesic substances or local hormones. Lesioned and regenerating nerve fibers show enhanced excitability and spontaneous activity. Motor and sympathetic reflexes sometimes have an excitatory action on nociceptors, a positive feedback which often is essential in chronic pain states such as the sympathetic reflex dystrophies. Proper diagnosis of these influences on nociceptor excitation is crucial if therapeutic interference is to be rendered possible at the peripheral site of encoding of pain stimuli. No pain center exists in the central nervous system. The cognitive, affective, motor and vegetative dimensions of pain perception and pain behaviour are based on a complex interaction of several brain systems. An important feature of brain function in relation to pain is the fact that nervous information related to pain can be modulated in the central nervous system. Various inhibitory modulations have recently been described which may be used for pain therapy. Inhibition of spinal neurons, and analgesia, can be produced by stimulation of brain stem structures. Pharmacologically, pain inhibitory systems may involve serotonin and endogenous opioids as transmitter or modulator substances. For pain therapy, pain inhibitory systems may be activated e.g. by morphine and ther analgesic drugs, focal brain stimulation, various means of somatosensory afferent stimulation and by psychological influences such as stress.

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