Objective: The authors estimated the prevalence and severity of cutaneous allodynia (CA) in individuals with primary headaches from the general population. Methods: We mailed questionnaires to a random sample of 24,000 headache sufferers previously identified from the population. The questionnaire included the validated Allodynia Symptom Checklist (ASC) as well as measures of headache features, disability, and comorbidities. We modeled allodynia as an outcome using headache diagnosis, frequency and severity of headaches, and disability as predictor variables in logistic regression. Covariates included demographic variables, comorbidities, use of preventive medication, and use of opioids. Results: Complete surveys were returned by 16,573 individuals. The prevalence of CA of any severity (ASC score ≥3) varied with headache type. Prevalence was significantly higher in transformed migraine (TM, 68.3%) than in episodic migraine (63.2%, p < 0.01) and significantly elevated in both of these groups compared with probable migraine (42.6%), other chronic daily headaches (36.8%), and severe episodic tension-type headache (36.7%). The prevalence of severe CA (ASC score ≥9) was also highest in TM (28.5%) followed by migraine (20.4%), probable migraine (12.3%), other chronic daily headaches (6.2%), and severe episodic tension-type headache (5.1%). In the migraine and TM groups, prevalence of CA was higher in women and increased with disability score. Among migraineurs, CA increased with headache frequency and body mass index. In all groups, ASC scores were higher in individuals with major depression. Conclusions: Cutaneous allodynia (CA) is more common and more severe in transformed migraine and migraine than in other primary headaches. Among migraineurs, CA is associated with female sex, headache frequency, increased body mass index, disability, and depression.

We assessed the prevalence of neck pain in the population in relation to headache. In a cross-sectional study, a total of 797 individuals completed a headache interview and provided self-reported data on neck pain. We identified migraine, TTH or both migraine and TTH (M+TTH) groups. Pericranial tenderness was recorded in 496 individuals. A total tenderness score (TTS) was calculated as the sum of local scores with a maximum score of 48. The one-year prevalence of neck pain was 68.4% and higher in those with vs. without primary headache (85.7% vs. 56.7%; adjusted OR 3.0, 95% CI 2.0–4.4, p < 0.001). Adjusting for age, gender, education and poor self-rated health, in comparison with those without headaches, the prevalence of neck pain (56.7%) was significantly higher in those with M+TTH (89.3%), pure TTH (88.4%) and pure migraine (76.2%) (p < 0.05 for all three group comparisons). Individuals with neck pain had higher TTS than individuals without neck pain (15.1 ± 10.5 vs. 8.4 ± 8.0, p < 0.001). Neck pain is highly prevalent in the general population and even more prevalent in individuals with primary headaches. Prevalence is highest in coexistent M+TTH, followed by pure TTH and migraine. Myofascial tenderness is significantly increased in individuals with neck pain.

Objective: To evaluate the association between migraine without aura (MO) and migraine with aura (MA) and 3 types of structural brain abnormalities detected by MRI: white matter abnormalities (WMAs), infarct-like lesions (ILLs), and volumetric changes in gray and white matter (GM, WM) regions. Methods: PubMed as well as the reference lists of identified studies and reviews were used to identify potentially eligible studies through January 2013. Candidate studies were reviewed and eligible studies were abstracted. Pooled odds ratios (OR) and 95% confidence intervals (CI) were calculated for WMAs and ILLs. Results: Six population-based and 13 clinic-based studies were identified. The studies suggested that structural brain changes, including WMAs, silent ILLs, and volumetric changes in GM and WM regions, were more common in migraineurs than in control groups. The results were strongest for MA. The meta-analysis of WMAs showed an association for MA (OR 1.68; 95% CI 1.07–2.65; p = 0.03) but not for MO (OR 1.34; 95% CI 0.96–1.87; p = 0.08). The association of ILLs was greater for MA (OR 1.44; 95% CI 1.02–2.03; p = 0.04) than for MO, but no association was found for MA (p = 0.52) and MO (p = 0.08) compared to controls. Conclusion: These data suggest that migraine may be a risk factor for structural changes in the brain. Additional longitudinal studies are needed to determine the differential influence of migraine without and with aura, to better characterize the effects of attack frequency, and to assess longitudinal changes in brain structure and function.

The aim of this study was to assess the role of depression as a predictor of new onset of chronic migraine (CM) among persons with episodic migraine (EM). The American Migraine Prevalence and Prevention (AMPP) study followed 24,000 persons with severe headache identified in 2004. Using random-effects logistic regression, we modeled the probability that persons with EM in 2005 or 2006 would develop CM in the subsequent year. Depression was assessed in two ways, using a validated questionnaire (PHQ-9 score ≥15) and based on self-reported medical diagnosis. Analyses were adjusted for multiple covariates including sociodemographics, body mass index, headache pain intensity, headache frequency, migraine symptom severity, cutaneous allodynia, acute medication overuse, anti-depressant use and anxiety. Of 6,657 participants with EM in 2005, 160 (2.4 %) developed CM in 2006. Of 6,852 participants with EM in 2006, 144 (2.2 %) developed CM in 2007. In fully adjusted models, PHQ-9 defined depression was a significant predictor of CM onset [odds ratio (OR) = 1.65, 95 % CI 1.12–2.45]. There was a depression-dose effect; relative to participants with no depression or mild depression, those with moderate (OR = 1.77, 95 % CI 1.25–2.52), moderately severe (OR = 2.35, 95 % CI 1.53–3.62), and severe depression (OR = 2.53, 95 % CI 1.52–4.21) were at increased risk for the onset of CM. Among persons with EM, depression was associated with an increased risk of CM after adjusting for sociodemographic variables and headache characteristics. Depression preceded the onset of CM and risk increased with depression severity suggesting a potentially causal role though reverse causality cannot be excluded.