Treating Rebound or Chronic Daily Headaches
Question: What is better for treating rebound headaches—long-acting or short-acting NSAIDs?
Answer: Chronic daily headache (CDH) is surprisingly common in the United States, with 4% to 5% of the population suffering from some form of CDH, and an estimated 60% to 80% of patients using analgesics on a daily basis to relieve their headache.1 Patients often are counseled not to use these acute therapies more than 2 days a week because analgesic overuse (as well as overuse of ergotamines and triptans) can result in rebound headaches.2 Despite this education, patients continue to suffer from rebound headaches associated with the medications taken to relieve their headaches. This paradoxical effect is a common barrier to relief of chronic headaches and is known as medication overuse headache (MOH).2 Medication overuse is defined as the use of acute abortive therapy at least 15 days a month for 3 consecutive months.2
Often the most important steps in prevention of MOH is to educate the patient on any medication that is associated with possible rebound. If medication overuse is suspected, then discontinuation of the agent for a period is recommended. During this discontinuation period, the patient may require a bridge therapy if rebound headache occurs. Bridge therapy with a long-acting analgesic or other agent is preferable. However, bridge therapy is controversial with reputable sources claiming that no withdrawal treatment is recommended.3
Therapies previously studied for MOH that are associated with the greatest efficacy and safety are naproxen (Aleve, Naprosyn, others), tizanidine (Zanaflex, others), and glucocorticoids (a brief course) for oral outpatient therapy, and dihydroergotamine (DHE 45, others) and valproate sodium (Depacon, others) for intravenous inpatient therapy.3,4 The most common outpatient non-steroidal anti-inflammatory agent (NSAID) is naproxen (500 mg twice daily).5-6 Another option for patients with CDH is onabotulinumtoxin A (Botox), which is FDA-approved for chronic migraines.
It is important to realize that there is very little evidence supporting the use of any pharmacological therapy in the treatment of MOH. Long-acting NSAIDs such as naproxen are theorized to be less likely to cause MOH than short-acting NSAIDs or NSAIDs with caffeine. Exact guidance for prophylaxis is difficult due to patient variability. Therefore, health care professionals should use their clinical judgment to determine which long-acting agent is best, and whether MOH is a potential problem for their patients.3
—Mallory Reuter, PharmD and McKenzie G. Ferguson, PharmD
Answer: Much has been written about MOH and medication overuse that seems straightforward on the surface, but when you examine the literature more closely, this issue is seen to be more complex. Until recently, all NSAIDs were lumped under the umbrella of “MOH-causing medications,” which makes no sense pathophysiologically or clinically. The mantra among neurologists and headache physicians was that “every abortive medications is bad,” “NSAIDs cause rebound headache,” “triptans cause MOH,” and “most patients with chronic migraine have MOH.” These statements were shown to be largely untrue , and these views, for the most part, have been discounted.
We do know that, for some patients, opioids, butalbital-acetaminophen-caffeine (Fioricet, others), and ergots may cause MOH. A small minority of people experience MOH from use of NSAIDs and/or triptans. Analgesics with a high caffeine content (eg, Excedrin) also may contribute to MOH. However, there is great variance among patients—some will have MOH from small amounts of an abortive, while others do not suffer MOH even when consuming vast quantities of analgesics. The pathophysiology of MOH is complex, and there certainly is a genetic predisposition toward MOH as well. If someone has a migraine 30 days in the month, is it deemed “medication overuse” when the patient takes abortive medications 15 of those days? The definition of medication overuse and MOH is very arbitrary.
In several studies involving 1,400 patients, I have found that over the long-term (>1 year), only 46% of CDH patients obtain consistent relief from any daily preventive therapy. Some daily preventive options include onabotulinumtoxin A, beta blockers, tricyclic antidepressants, topiramate (Topamax, others), and many others.3 If one agent or class does not provide the relief a patient needs, adding another agent or switching agents should be the next step. In this manner, patients are more likely to be controlled chronically and do not have to turn to short-acting analgesics or abortive therapy as often.
But what are the other 54% of patients who do not respond to prophylactic medication to do? Everyone says “don’t take this, don’t take that,” and the poor suffering patient says, “fine, but what DO I take, or should I just lay in bed?” In my experience NSAIDs usually do not cause MOH. Occasionally, patients will have MOH from the short-acting NSAIDs, particularly ibuprofen (Advil, Motrin, others). However, we do not want them to go from the frying pan to the fire—that is, stopping ibuprofen and using stronger analgesics, often with large amounts of caffeine (that may be more likely to be associated with MOH.
So, the medication overuse and MOH arena is filled with arbitrary statements that lack science behind them. Certainly we want to minimize the use of abortive agents, and withdraw patients from daily analgesics, but many refractory patients have no other recourse. We need more studies delineating who suffers from MOH, identifying which drugs are involved and outlining what patients should do to treat their headaches.
—Lawrence Robbins, MD