Please use this identifier to cite or link to this item:
https://hdl.handle.net/2440/78280
Citations | ||
Scopus | Web of Science® | Altmetric |
---|---|---|
?
|
?
|
Type: | Journal article |
Title: | Medication-overuse headache and opioid-induced hyperalgesia: A review of mechanisms, a neuroimmune hypothesis and a novel approach to treatment |
Author: | Johnson, J. Hutchinson, M. Williams, D. Rolan, P. |
Citation: | Cephalalgia: an international journal of headache, 2013; 33(1):52-64 |
Publisher: | Blackwell Science Ltd |
Issue Date: | 2013 |
ISSN: | 0333-1024 1468-2982 |
Statement of Responsibility: | Jacinta L Johnson, Mark R Hutchinson, Desmond B Williams and Paul Rolan |
Abstract: | INTRODUCTION Patients with chronic headache who consume large amounts of analgesics are often encountered in clinical practice. Excessive intake of analgesics is now considered to be a cause, rather than simply a consequence, of frequent headaches, and as such the diagnosis “medication-overuse headache” (MOH) has been formulated. Despite the prevalence and clinical impact of MOH, the pathophysiology behind this disorder remains unclear and specific mechanism-based treatment options are lacking. DISCUSSION Although most acute headache treatments have been alleged to cause MOH, here we conclude from the literature that opioids are a particularly problematic drug class consistently associated with worsening headache. MOH may not be a single entity, as each class of drug implicated may cause MOH via a different mechanism. Recent evidence indicates that chronic opioid administration may exacerbate pain in the long term by activating toll-like receptor-4 on glial cells, resulting in a pro-inflammatory state that manifests clinically as increased pain. Thus, from the available evidence it seems opioid-overuse headache is a phenomenon similar to opioid-induced hyperalgesia, which derives from a cumulative interaction between central sensitisation, due to repeated activation of nociceptive pathways by recurrent headaches, and pain facilitation due to glial activation. CONCLUSION Treatment strategies directed at inhibiting glial activation may be of benefit alongside medication withdrawal in the management of MOH. |
Keywords: | Medication-overuse headache opioid-induced hyperalgesia codeine glia cytokines ibudilast |
Rights: | © International Headache Society 2012 |
DOI: | 10.1177/0333102412467512 |
Grant ID: | ARC |
Published version: | http://dx.doi.org/10.1177/0333102412467512 |
Appears in Collections: | Aurora harvest Pharmacology publications |
Files in This Item:
File | Description | Size | Format | |
---|---|---|---|---|
hdl_78280.pdf | Accepted version | 722.9 kB | Adobe PDF | View/Open |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.