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

Published online by Cambridge University Press:  01 September 1997

Paolo Marchettini ,
Marco Lacerenza  and
Fabio Formaglio
Paolo Marchettini
Affiliation:
Department of Neurology, Scientific Institute H San Raffaele, 20129 Milan, Italylaceren@hsr.it
Marco Lacerenza
Affiliation:
Department of Neurology, Scientific Institute H San Raffaele, 20129 Milan, Italylaceren@hsr.it
Fabio Formaglio
Affiliation:
Department of Neurology, Scientific Institute H San Raffaele, 20129 Milan, Italylaceren@hsr.it
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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. [blumberg et al.; coderre & katz; dickenson; wiesenfeld-hallin et al.]

Type
Open Peer Commentary
Information
Behavioral and Brain Sciences , Volume 20 , Issue 3 , September 1997 , pp. 458 - 459
Copyright
© 1997 Cambridge University Press

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