Abstract

Medication overuse headache (MOH) is defined in the latest ICHD-3 criteria as a secondary headache caused by worsening of a pre-existing headache (usually a primary headache) owing to overuse of one or more attack-aborting or pain-relieving medications. MOH can be debilitating and results from biochemical and functional brain changes induced by certain medications taken too frequently. Various risk factors some modifiable, other non-modifiable (Multiple Gene Polymorphisms) have been hypothesised in MOH. Psychiatric co-morbidities in MOH are noticeably (anxiety and depression) found to be co morbid disorders by more than chance. This has to be managed effectively along with treatment strategies for MOH for efficacious response to withdrawal treatment. Ample literature and clinical evidence shown in prospective trials, that withdrawal therapy is the best treatment for MOH. The mainstay of MOH treatment is not only to detoxify the patients and to stop the chronic headache but also, most likely, to improve responsiveness to acute or prophylactic drugs. Studies advocating prophylactic treatment with good response to mainly topiramate and OnabotulinumtoxinA do exist, less prominent for prednisolone, however, not recommended for every patient. Management may be complex and must be done via MDT approach with involvement of specialists when needed along with incorporating adequate treatment of acute withdrawal symptoms, educational and behavioural programs to ensure patient understanding of the condition and compliance. There are arguments on either sides of inpatient and outpatient withdrawal for MOH patients dependent heavily on the individual circumstances i.e. patient’s motivation, the duration of the overuse, the type of overused drugs, possible previous history of detoxification failures and co morbidities. Treatment trials are still required to determine for clinicians the best evidence-based approach for helping these patients break their headache cycle.

Highlights

  • Medication-overuse headache (MOH) is defined by the International Classification of Headache Disorders (ICHD) as a headache in patients with primary headache disorders occurring on ≥15 days per month for >3 months, that is induced by overuse of medications taken as symptomatic treatment for acute headaches

  • In ICHD-3, chronic headache syndromes are described by professional consensus as headache disorders that share traits with pre-existing headache syndromes, happen for a specific duration of time (at least three months in Chronic tensiontype headache (CTTH), Chronic migraine (CM); or at least 12 months in Chronic trigeminal autonomic cephalalgia (TAC)) and have an extra time-rule

  • MOH occurs if the number of days of acute medicine taken for headache per month exceeds a threshold level [1] i.e., 15 or more days for simple painkillers and 10 or more days for triptans, opioids and combination analgesics

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Summary

Introduction

Medication-overuse headache (MOH) is defined by the International Classification of Headache Disorders (ICHD) as a headache in patients with primary headache disorders occurring on ≥15 days per month for >3 months, that is induced by overuse of medications taken as symptomatic treatment for acute headaches. MOH occurs if the number of days of acute medicine taken for headache per month exceeds a threshold level [1] i.e., 15 or more days for simple painkillers and 10 or more days for triptans, opioids and combination analgesics. Overuse of acute and/or symptomatic headache medications for >3 months*C. As ICHD defines MOH as a secondary headache, one must identify the primary headache disorder associated with it for example episodic or chronic migraine. The comprehensive classification of MOH from ICHD-3 is given here: 2.2 International classification of headache disorders third edition (ICHD-3) criteria for medication-overuse headache (MOH)

Non-steroidal anti-inflammatory drug (NSAID)- overuse headache A
Background and pathophysiology
Clinical characteristics
Prevalence and general risk factors
Risk factors
Main risk factors for MOH
Pathophysiology
Angiotensin-converting enzyme polymorphism
Catechol-O-methyltransferase (COMT) polymorphism
10. Pain medications role
11. Activation of trigeminovascular system
12. CO-morbidities
13. Treatment
13.1 Preventive treatment before or following withdrawal
13.2 Abrupt or gradual withdrawal
13.3 Inpatient or outpatient
14. Prophylaxis
15. Bridging therapy
16. Prognosis of withdrawal treatment
Findings
17. Conclusion
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