Medication Overuse Headache (MOH)

Not a primary headache but commonly coexists with one — common and under-diagnosed. Prevalence is estimated at 1–2% of the general population, rising to 11–70% among patients attending specialist headache clinics with chronic daily headache; migraine is the underlying primary disorder in around 80% of cases, tension-type or post-traumatic headache in most of the rest. Caused by regular headache medication use for ≥3 months in a patient with a pre-existing headache disorder, with headache present on ≥15 days/month and no better explanation by another diagnosis.

• Patients with migraine or tension-type headache are more susceptible than those with cluster headache.
• Opioids, triptans and ergotamine carry the highest risk (MOH threshold ≥10 days/month). Opioid- and combination-analgesic overuse carries a roughly two-fold higher relative risk of MOH than single-agent overuse.
• Paracetamol and NSAIDs carry lower risk (threshold ≥15 days/month). Risk from combination OTC headache products varies by component (aspirin/NSAID/paracetamol/codeine ± caffeine).
• Worsening headache can follow either continued use or medication reduction.
• Recognised risk factors beyond drug class include anxiety or depression (roughly a 5-fold increase in odds), a family history of MOH or substance misuse, chronic musculoskeletal or GI complaints, smoking, physical inactivity, and high daily caffeine intake — comorbid anxiety/depression is present in up to 40–58% of patients with MOH, though it remains unclear whether these are risk factors for MOH or a consequence of it.

Presentation: headache ≥15 days/month, worse on waking, aggravated by exercise, nausea/GI symptoms, restlessness/anxiety/irritability/poor concentration. The headache usually resembles the patient’s pre-existing primary headache type but is more frequent and intense; examination and neurological assessment are typically normal, and routine neuroimaging is not required unless atypical or focal features are present.

Management

Consider a preventive drug if headaches need treatment >4 days/month. Preventive therapy is usually started concurrently with, or just before, withdrawal of the overused drug rather than deferred until after it — this also helps counter the common patient belief that only the overused medication is effective, since a previously “ineffective” preventive can become effective once overuse stops. Options mirror the underlying primary headache disorder and include topiramate, a TCA, or — for chronic migraine — CGRP-targeted therapy (onabotulinumtoxinA or a CGRP monoclonal antibody; see migraine and headache: diagnostic approach). Gepants (small-molecule CGRP receptor antagonists) are a useful acute option specifically because they do not themselves cause MOH.

Long-term management

• Explain the cause, treatment plan and goals clearly.
• General primary-headache strategies (relaxation, activity, stopping alcohol/caffeine/smoking, diet).
• Stopping the offending drug is the mainstay — via graded reduction or abrupt cessation (abrupt cessation is generally preferred), with or without bridging therapy, guided by the underlying headache disorder. Abrupt discontinuation is preferred for triptans, ergotamine and non-opioid analgesics; opioids, barbiturates and benzodiazepines instead need dose reduction over 2–4 weeks if taken at higher doses (they can still be stopped abruptly at lower doses).
  • In opioid/benzodiazepine withdrawal, timing/setting depends on dose and frequency; some patients need admission for supervised withdrawal. A once-weekly transdermal clonidine patch (0.1–0.2mg/24h) for 1–2 weeks can help manage opioid withdrawal symptoms; for butalbital withdrawal, phenobarbital is used at a rough equivalence of 30mg phenobarbital to 100mg butalbital (maximum ~90mg phenobarbital for 300mg butalbital), to reduce withdrawal-seizure risk.
  • Expect an early (days) withdrawal worsening, then gradual improvement over months — triptan withdrawal is usually complete within 4 days, but withdrawal from standard analgesics is more gradual: it may take 3 months for a two-thirds reduction in headache frequency, and up to 6 months before 6 consecutive headache-free days. Offer regular monitoring and long-term support — relapse risk is significant in the first 12 months.
• Allow sparing use of a different medication (NSAID preferred) during withdrawal, ≤3 days/week.
• Bridging therapy (limited evidence, but reasonable options):
  • NSAID or short prednisolone course while withdrawing an opioid/triptan: naproxen MR 750mg daily for 5 days then 3–4 days/week for 2 weeks then stop; or prednisolone 50mg daily for 3 days, taper over 7–10 days, stop (note: more recent placebo-controlled trials have found prednisolone/ prednisone gives little to no benefit over placebo for withdrawal headache specifically, so it is not a strong substitute for NSAID bridging where one is tolerated).
  • If migraine is the primary disorder: topiramate 25mg daily titrating to 50mg BD, or another migraine preventer.
  • If tension-type headache: a TCA.
  • Any primary headache: long-acting NSAID (naproxen 500mg BD), or short-term antihistamine/antiemetic (metoclopramide, prochlorperazine) PRN; inpatient admission for supervised dihydroergotamine is an option. Intravenous hydration and antiemetics are also useful supportive measures during withdrawal, particularly for patients overusing compound analgesics or ergotamine, who more often develop nausea, vomiting, tachycardia or hypotension during withdrawal.
• After bridging, restart usual acute medication only within stricter maintenance limits than the original overuse thresholds — under 4 days/month for triptans, ergotamine or combination analgesics, and under 6 days/month for NSAIDs — and discourage any return to the specific previously-overused drug.
• If no prophylaxis was started before the first withdrawal attempt, start one and re-attempt withdrawal.
• Refer to neurology if no improvement or relapse. Consider referral earlier for opioid overuse (best managed as an inpatient), multiple-drug overuse, or significant comorbid anxiety/depression.

Relapse

Relapse after successful withdrawal is common — roughly 40% within the first year, and 40–50% by 6 years — so the long-term support above matters as much as the withdrawal itself. Recognised predictors of relapse include a tension-type-headache background (about 3-fold higher relapse risk than a migraine background), a longer duration of overuse before treatment, a high number of acute treatments used, no improvement within 2 months of withdrawal, smoking, alcohol use, and returning to a previously-overused combination analgesic (relapse is less likely after triptan-only overuse). Adding structured behavioural therapy to withdrawal treatment has been shown to substantially cut relapse rates compared with withdrawal alone.