Experimental pain models and clinical chronic pain: Is plasticity enough to link them?

Author(s): Lacerenza, M., Formaglio, F.

Journal/Book: Behav Brain Sci. 1997; 20: 40 West 20TH Street, New York, NY 10011-4211. Cambridge Univ Press. 458.

Abstract: The central hyperexcitability observed in animal models supports a pathophysiological explanation for chronic human pain. Novel information on cholecystokinin (CCK) upregulation offers a rationale for reduced opioid response in neuropathic pain. However, the basic information provided by scientists should not lead clinicians to equate experimental models to chronic human conditions. Clinicians should provide careful reports and attempt to classify pathophysiologically clinical conditions that have so far been grouped generically.

Note: Editorial Marchettini P, San Raffaele Sci Inst, Dept Neurol, I-20129 Milan, ITALY

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