Medication Overuse Headache: When the Cure is the Cause of the Pain

Pain Management, August 2012, Volume 5, Issue 5

Also known as rebound headache, medication overuse headache is a fairly common condition that can be missed by non-specialists who are unfamiliar with its presentation and clinical signs. This article reviews the causes and types of medication overuse headache and discusses the current thinking on treatment.

Brett Dees, MD

Also known as rebound headache, medication overuse headache is a fairly common condition that can be missed by non-specialists who are unfamiliar with its presentation and clinical signs. This article reviews the causes and types of medication overuse headache and discusses the current thinking on treatment.

Medication overuse headache (MOH) is the phenomenon by which frequent use of abortive or symptomatic medications (SM)‑‑triptans, barbiturates, opioids and other analgesics—for the treatment of primary headaches such as migraine or tension-type headache causes worsening of the pre-existing condition. It has been described throughout the world1 and is a major contributor to the syndrome of chronic daily headache (CDH).1,2 MOH is estimated to be present in 1-2% of the general population, and constitutes up to 70% of patients seen in specialty headache clinics.1-4

The typical pattern for MOH is one of insidious onset with the patient initially taking an SM for relief of headache.1,5 In some subjects the headache becomes more frequent for various reasons, leading to increased use of the SM. When they get to the point where they are using SM 10-15 days each month, the patient may note the frequency and severity of their headaches are accelerating, despite the fact they are taking more and more medication. The paradox is that the patient usually gets progressively less relief from each dose in terms of amount and duration of headache, but continues to increase usage. The problem develops from self-treatment of headaches and from physicians’ instructions to use the SM early to achieve the best response.

This is an appropriate strategy for patients who have two or fewer headaches per week. However, at greater headache frequency, early treatment of headaches that may never become severe can lead to acceleration of SM usage. Very often, patients as well as health care providers do not equate the increasing headache problem with their increasing medication usage, as the increase in SM utilization may develop over weeks to months. They simply renew the prescriptions for SM without taking into account the amount of medication being taken by the patient, leading to gradually increasing use of SM and eventually, MOH.


CDH itself is a major problem throughout the world, occurring in 2-4.5% of various populations studied, and is the usual precursor to MOH. In industrialized nations MOH occurs in approximately 20% of CDH subjects.1 As CDH develops, a pattern of “big” and “little” headaches is often seen.5 The “big” headaches usually exhibit features of migraine, while the “little” headaches are more like tension-type headaches. When SM is overused, the “big” headaches become more frequent; when the SM is not taken or is delayed in usage, the “little” headaches often evolve into “big” headaches. This element of CDH is indicative of MOH. CDH impairs quality of life and the ability to work gainfully; MOH exacerbates the problem.6

Although diagnostic criteria are available,7 MOH is commonly missed in the primary care setting. Whether MOH is an extension of CDH or a separate syndrome is not clear. The International Headache Society has set forth diagnostic criteria for MOH in the second edition of The International Classification of Headache Disorders (ICHD-II).7 These are presented in table 1.

Certain risk factors are associated with a greater incidence of MOH, namely high headache frequency, musculoskeletal complaints, and anxiety and/or depression. Increasing age, daily smoking, physical inactivity, normal systolic BP, sick leave of >2 weeks, and in particular, regular use of tranquilizers are also associated.4,8 These should be noted and evaluated when the diagnosis of MOH is considered, and appropriate treatment instituted if possible.

James R. Couch, MD, PhD

Different medications show different propensities for producing MOH. Triptans, ergotamines, opioids, and combination analgesics containing butalbital or opioids appear to be the worst, and among the most common, offenders.1,3 Combination medications with aspirin and acetaminophen such as Excedrin® can also induce MOH. This is reflected by ICHD-II diagnostic criteria for specific substances such as ergotamine, triptans, opioids, simple analgesics, and compound analgesics (simple analgesics combined with opioids, butalbital, and/or caffeine). The criteria for most of these medications require intake on at least 10 days per month on a regular basis for more than three months, while the criteria for simple analgesics require use on at least 15 days per month on a regular basis for more than three months for diagnosis.7 Whether use of a single, simple analgesic such as aspirin, acetaminophen, ibuprofen, or naproxen can induce MOH is still unproven. Dihydroergotamine (DHE) appears unlikely to produce this phenomenon.

Treatment methods

There is an ongoing debate on the best method for MOH treatment. The longstanding belief among headache experts has been that complete withdrawal of the offending medication is crucial to break the MOH cycle, as preventive medications usually will not work in the face of the overuse of the MOH-producing agents. In the authors’ experience, this is the usual case. However, one recent study suggested that some patients who are taking chronic opioids for reasons other than headache may find that their headaches improve if they use topiramate as a prophylactic antimigraine agent without withdrawing from the MOH agent.9 In this study, however, only a small percentage of subjects achieved complete relief from headache.

Overall, withdrawal of the overused medication and use of preventative antimigraine medications has been the most successful strategy for treating MOH. For severe cases of MOH, this approach has usually been accomplished on an inpatient basis because discontinuation of the acute medication can result in severe withdrawal problems, including headache, nausea, vomiting, and sleep disturbances, and, in the case of butalbital, seizures.5 For less severe cases, outpatient strategies based on gradual withdrawal of the MOH agent can be successful if patients are educated on the problem and the use of SM is monitored closely.

Another hotly debated issue has been whether to start a prophylactic medication during withdrawal, or after two months as needed.9 We have been very successful with an inpatient treatment program that initiates prophylactic medications and discontinues the MOH agent as soon as the patient is admitted.5 Amitriptyline, doxepin, topiramate, and/or valproate have been the most effective prophylactic medications in this program. The treatment can be combined with intravenous dihydroergotamine for acute symptomatic relief. The same prophylactic antimigraine agents can be employed for an outpatient withdrawal program, again using a preventive medication from day one and gradual withdrawal of the MOH agent over several weeks. Severe or long-standing MOH often requires inpatient treatment, especially those that have been on long-term narcotics or barbiturates.

Tables. Medication Overuse Headache

As noted, several recent studies have demonstrated the efficacy of the migraine prophylactic medication, topiramate, in reducing MOH without withdrawal of the offending medication. 9 This has led to a change in treatment paradigm on the part of some experts, who now seriously question the need for complete withdrawal. However, there is still an emphasis on decreasing the MOH agent. It is likely that both inpatient and outpatient stratagems have a place in clinical practice. In our experience, continued exposure to the MOH agent usually results in continuation of the headache problem.

Another issue of concern in formulating a treatment plan is the duration of MOH. In the authors’ experience, MOH that is present for more than six months is much harder to manage than MOH that has been present for less than six months. In treating patients with frequent headaches, the physician should vigilantly monitor for MOH and scrutinize usage of SM carefully. If there is rapid acceleration of SM utilization, the patient should be evaluated for and educated about MOH, and appropriate therapy should be initiated, including cessation of the MOH agent if possible.

Regardless of the optimal treatment method, one concept remains clear: MOH is best avoided. Recognition of the risk factors, including medications, that may cause MOH, early recognition of the syndrome, and patient education provide a sound basis for avoiding the situation altogether.

Brett Dees, MD, is an assistant professor of neurology in the Department of Neurology at the University of Oklahoma Health Sciences Center. James R. Couch, MD, PhD, is a professor of neurology in the Department of Neurology at the University of Oklahoma Health Sciences Center, Oklahoma City, OK.


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