• R J Schwartzman, J Grothusen, T R Kiefer, and P Rohr.
• Department of Neurology, Medical College of Pennsylvania, Hahnemann University, Philadelphia, USA. robert.schwartzman@drexel.edu
• Arch Neurol Chicago. 2001 Oct 1; 58 (10): 1547-50.

BackgroundNociceptive pain is a major problem in clinical neurology. Peripheral nerve injury may change the physiology of the dorsal horn so that pain becomes progressively centralized.ObjectiveTo review mechanisms underlying the plasticity of dorsal root ganglia and dorsal horn neurons that lead to central pain from a peripheral nerve injury.ResultsEvidence is reviewed that points to molecular changes in nociceptive terminals, ectopic firing of afferent pain fibers at the level of the dorsal root ganglia, and physiologic changes of the N-methyl-D-aspartate receptor that cause chronic nociceptive pain.ConclusionsCentral sensitization is the physiologic manifestation of many severe peripherally induced pain states. It is maintained by nociceptive input and a physiologic change in the N-methyl-D-aspartate receptor. It consists of: (1) hypersensitivity at the site of injury; (2) mechanoallodynia; (3) thermal hyperalgesia; (4) hyperpathia; (5) extraterritoriality in the case of complex regional pain syndrome/reflex sympathetic dystrophy; and (6) associated neurogenic inflammation, autonomic dysregulation, and motor phenomena.

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