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Neuropathic Central Pain
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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ABSTRACT
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