Medication overuse headache (MOH) is a very common and largely preventable disorder with considerable impacts on health care costs. In fact, the socioeconomic burden of MOH may be almost double that of chronic migraine.
MOH is comorbid with primary headache disorders, particularly chronic migraine, tension-type headache, and post-traumatic headache, and can result from the overuse of several different agents, including over the counter analgesics such as acetaminophen and NSAIDs, and prescription medications including opioids, barbiturates, and triptans. Chronic daily headache is estimated to have a prevalence of 3 to 4%, and some studies suggest that as many as 70% of patients with frequent headache take these medications on a near daily basis.1
The International Classification of Headache Disorders III (beta) defines MOH as a headache occurring on more than 15 days per month in a patient with a known headache disorder after the regular use of medication for more than 3 months.2 Many patients in this clinical setting will describe a change in pattern of their headache from their baseline, or else describe 2 types of headache: one that they will attribute to their pre-existing disorder and another that they will most typically deem a chronic daily headache. Notably, the chronic daily headache often does not fully meet criteria for their underlying primary headache diagnosis.
MOH can then be further sub-classified depending on the medication to which it can be attributed: ergotamine, triptans, simple analgesics, opiates, or multiple agents,2 however the amount of medication required for diagnosis differs slightly between agents. Opiates, triptans, ergotamine, or combination overuse requires 10 days or more per month, whereas simple analgesic overuse (acetaminophen and NSAIDs) require 15 or more days per month. Additionally, if an individual is not overusing a single class of medication, but rather using multiple medications and the total combined use of all analgesics is greater than 10 days per month, then that also meets criteria for MOH. This denotes the importance of a detailed clinical history with a focus on how patients use non-prescription medications to help establish a proper diagnosis.
The pathophysiology of MOH is complex and incompletely understood. Our current understanding suggests increased neuronal excitability in the cerebral cortex and trigeminal system. The downstream effect is a higher likelihood for cortical spreading depression and central and peripheral sensitization. Dysregulation of serotonergic pathways and altered expression of serotonin receptors, particularly 5-HT2A, have also been implicated. Lower 5-HT levels increase release of CGRP and lead to sensitization of nociceptors in the trigeminal system. The changes outlined above appear to reverse after cessation of the offending agent.3
The clinical phenotype of MOH appears to be quite similar regardless of the offending agent and has characteristics which are similar to the underlying headache disorder. Additionally, MOH appears only to occur in patients with a pre-existing primary headache disorder. For this reason, it is unlikely that the mechanisms of the offending medications are at fault for the clinical presentation of MOH, but rather it is the effect of the medication overuse on the underlying primary headache pathology.3
This article originally appeared on Neurology Advisor