• M Zimmermann.
• Arzneimittel Forsch. 1984 Jan 1;34(9A):1053-9.

AbstractPain originating in the peripheral nervous system is based on the excitation of nociceptive afferent fibers, which are contained among A-delta- and C-fibers from skin, viscera, joints and muscles. Often, this excitation originates at the peripheral fiber ending, the nociceptor. Nociceptors are excited by strong stimuli, which may eventually become destructive. Nociceptor excitability is enhanced by endogenous chemical substances as occur, e.g., during inflammation. Some analgesic substances, e.g. acetylsalicylic acid, inhibit the synthesis of prostaglandins and related metabolites, which is thought to be a mechanism of peripheral analgesia. Some forms of chronic pain are due to pathophysiological conditions of peripheral axons. Neuralgic pain may be caused by prolonged compression of a nerve. Here, ectopic impulse generation at the site of compression is considered a mechanism of pain. In a nerve regenerating after trauma the sprouts are sensitive to mechanical and chemical influences and thus may produce abnormal discharges in the neuroma. Sympathetic influences might enhance excitability of sprouts in the neuroma. Excitation of nociceptors by the sympathetic nervous system probably also occurs in other situations of chronic pain, such as Sudeck's syndrome. Here, the chronic pain may be sustained by a positive feedback loop via somato-sympathetic reflexes (sympathetic reflex dystrophy). Similar mechanisms of positive feedback also occur in the skeletomotor system, where chronic pain conditions can be sustained by inappropriate muscle tone. In the central nervous system much of the information from the nociceptive afferent fibers is contained in the discharges of multireceptive neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

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