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| Neurology supplements are not peer-reviewed. Information contained in Neurology supplements represent the opinions of the authors and are not endorsed by nor do they reflect the views of the American Academy of Neurology, Editor-in-Chief, or Associate Editors of Neurology. |
From the Department of Neurology, Harvard Medical School, Massachusetts General Hospital, Boston, Massachusetts.
Address correspondence and reprint requests to Dr. Michael A. Moskowitz, Massachusetts General Hospital, Neuroscience Center and Department of Radiology, 149 13th Street, Room 6403, Charlestown, MA 02129; e-mail: moskowitz{at}helix.mgh.harvard.edu
Transmission of pain from the periphery to the cortex depends on integration and signal processing within the spinal cord, brainstem, and forebrain. Sensitization, a component of persistent or chronic pain, may develop either through peripheral mechanisms or as a consequence of altered physiology in the spinal cord or forebrain. Several molecular and biophysical mechanisms contribute to the phenomenon of sensitization and persistent pain, including upregulation of sensory neuron-specific sodium channels and vanilloid receptors, phenotypic switching of large myelinated axons, sprouting within the dorsal horn, and loss of inhibitory neurons due to apoptotic cell death. Recently, forebrain structures have been implicated in the pathophysiology of persistent pain. Although a number of treatment options are used, unfortunately pharmacotherapy for neuropathic pain is often ineffective. Unraveling the mysteries of chronic pain may lead to better treatment options, such as drugs that act specifically on sensory neuron-specific sodium channels or as NR2B-subunit-selective N-methyl-D-aspartate receptor antagonists.
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