• Marcelo E Bigal, Daniel Serrano, Dawn Buse, Ann Scher, Walter F Stewart, and Richard B Lipton.
• Global Center for Scientific Affairs, Neuroscience, Merck Research Laboratories, Whitehouse Station, NJ, USA.
• Headache. 2008 Sep 1;48(8):1157-68.

BackgroundThough symptomatic medication overuse is believed to play a major role in progression from episodic to chronic or transformed migraine (TM), population-based longitudinal data on these agents are limited.ObjectivesTo assess the role of specific classes of acute medications in the development of TM in episodic migraine (EM) sufferers after adjusting for other risk factors for headache progression.MethodsAs a part of the American Migraine Prevalence and Prevention study (AMPP), we initially surveyed a population sample of 120,000 individuals to identify a sample of migraineurs to be followed annually over 5 years. Using logistic and linear regression, we modeled the probability of transition from EM in 2005 to TM in 2006 in relation to medication use status at baseline. Adjustments were made for gender, headache frequency and severity, and prevention medication use.ResultsOf 8219 individuals with EM in 2005, 209 (2.5%) had developed TM by 2006. Baseline headache frequency was a risk factor for TM. Using acetaminophen user as the reference group, individuals who used medications containing barbiturates (OR = 2.06, 95%CI = 1.3-3.1) or opiates (OR = 1.98, 95%CI = 1.4-2.2) were at increased risk of TM. A dose-response relationship was found for use of barbiturates. Use of triptans (OR = 1.25, 95%CI = 0.9-1.7) at baseline was not associated with prospective risk of TM. Overall, NSAIDs (OR = 0.85, 95%CI = 0.63-1.17) were not associated with TM. Indeed, NSAIDs were protective against transition to TM at low to moderate monthly headache days, but were associated with increased risk of transition to TM at high levels of monthly headache days.ConclusionEM sufferers develop TM at the rate of 2.5% per year. Any use of barbiturates and opiates was associated with increased risk of TM after adjusting for covariates, while triptans were not. NSAIDs were protective or inducers depending on the headache frequency.

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