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Epidemiology, Etiology, and Treatment Options

Robert J. Schwartzman, MD; John Grothusen, PhD; Thomas R. Kiefer, MD; Peter Rohr, MD

Arch Neurol. 2001;58:1547-1550.

Background  Nociceptive 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.

Objective  To review mechanisms underlying the plasticity of dorsal root ganglia and dorsal horn neurons that lead to central pain from a peripheral nerve injury.

Results  Evidence 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.

Conclusions  Central 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.

From the Department of Neurology, Medical College of Pennsylvania, Hahnemann University, Philadelphia, (Drs Schwartzman and Grothusen); Department of Anesthesiology and Intensive Care Medicine, University of Tuebingen, Tuebingen, Germany (Dr Kiefer); and Department of Anesthesiology and Intensive Care and Pain Medicine, University of Saarbruecken, Teaching Hospital of the University of Saarland, Saarbruecken Germany (Dr Rohr).

Corresponding author and reprints: Robert J. Schwartzman, MD, Department of Neurology, Hahnemann University Hospital, Broad and Vine Streets, MS 423, Philadelphia, PA 19102-1192 (e-mail: robert.schwartzman{at}drexel.edu).

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