Medication-overuse headache and opioid-induced hyperalgesia: A review of mechanisms, a neuroimmune hypothesis and a novel approach to treatment
Cephalalgia, ISSN: 0333-1024, Vol: 33, Issue: 1, Page: 52-64
2013
- 41Citations
- 70Captures
- 2Mentions
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Metrics Details
- Citations41
- Citation Indexes41
- CrossRef41
- 41
- Captures70
- Readers70
- 70
- Mentions2
- References2
- Wikipedia2
Review Description
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 mechanismbased 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. © International Headache Society 2012.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84871601949&origin=inward; http://dx.doi.org/10.1177/0333102412467512; http://www.ncbi.nlm.nih.gov/pubmed/23144180; https://journals.sagepub.com/doi/10.1177/0333102412467512; http://cep.sagepub.com/cgi/doi/10.1177/0333102412467512; http://cep.sagepub.com/content/33/1/52
SAGE Publications
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