Hostname: page-component-848d4c4894-ndmmz Total loading time: 0 Render date: 2024-05-10T10:14:12.998Z Has data issue: false hasContentIssue false
  • English
  • Français

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
Get access Rights & Permissions [Opens in a new window]

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

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)