Risk Factors for Migraine
Obesity has been proposed as a risk factor for the development of chronic daily headaches. Bigal and colleagues predicted that body mass index (BMI) may influence the prevalence, attack frequency, and clinical features of migraine. The study authors assessed the influence of BMI on the prevalence of migraine and its clinical features in a population-based telephone-interview study. They gathered information on headache and medical features, height, and weight, and divided participants into 5 categories that were based on BMI: underweight (< 18.5), normal-weight (18.5-24.9), overweight (25-29.9), obese (30-24.9), and morbidly obese (≥ 35). They assessed migraine prevalence and modeled headache features as a function of BMI, adjusting by covariates. Among 30,215 individuals (65% women; mean age, 38.4), BMI classification was not associated with the prevalence of migraine, but it was associated with the frequency of headache attacks. In the normal-weight group, 4.4% of subjects had 10-15 headache-days per month. In comparison, 5.8% of subjects in the overweight group (odds ratio [OR], 1.3), 13.6% of those in the obese group (OR, 2.9), and 20.7% of those in the morbidly obese (OR, 5.7) group had 10-15 headache-days per month. The proportion of subjects with severe headache pain increased with higher BMI; it was doubled in the morbidly obese group relative to the normal-weight group (OR, 1.9). Similar significant associations were demonstrated with BMI category for disability, photophobia, and phonophobia. In the logistic regression model, after adjusting for covariates (sex, age, use of headache medications, sleep problems, education status, and depression), migraine attack frequency significantly changed as a function of BMI (P < .001). A BMI higher than 30 was also significantly associated with high pain severity (P < .001), high disability (P < .01), and with the proportion of attacks accompanied by photophobia and phonophobia (P < .01). The study authors concluded that although obesity is not a risk factor for having migraine, it is a risk factor for increased attack frequency and severity in those who have migraine.

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Medication Overuse Headache
The new International Classification of Headache Disorders (ICDH-II) distinguishes subtypes of chronic daily headache (CDH), especially chronic migraine (CM) and medication overuse headache (MOH). CM is a new entity defined by migraine headaches on 15 or more days per month for 3 or more months in the absence of medication overuse (MO). If MO is present, the diagnosis of MOH is made, as long as the headache developed or worsened with MO. What is the mechanism of MOH? Opioids paradoxically produce hypersensitivity to evoked nonnoxious stimuli (ie, allodynia) in humans and in rodents. In rats, sustained morphine induces hindlimb allodynia and enhances evoked release of pronociceptive neurotransmitters (eg, calcitonin gene-related peptide [CGRP]) in the spinal cord. King and colleagues[6] hypothesized that morphine treatment would elicit similar actions in trigeminal afferents and in the medullary dorsal horn. These effects might serve as a model to study mechanisms of MOH. King and colleagues[6] therefore conducted experiments designed to determine whether sustained, systemic morphine administration elicits neuroplastic, pronociceptive adaptations in the trigeminal system as a potential model to study mechanisms of morphine overuse headache. Rats received either subcutaneous morphine or saline osmotic minipumps and were tested daily for facial allodynia by measuring the withdrawal threshold to stimulation of the paraocular region of the face with calibrated von Frey filaments. On day 6 of the morphine administration, the animals were evaluated for facial hypersensitivity and then received sumatriptan, ibuprofen, or vehicle, and were retested; touch-evoked Fos expression and capsaicin-evoked CGRP release were assessed within vital capacity. Morphine induced (1) time-dependent expression of facial allodynia that emerged by day 3 and was fully established by day 6, (2) touch-evoked Fos expression, and (3) enhanced capsaicin-evoked CGRP release in the medullary dorsal horn. Sumatriptan and ibuprofen fully reversed established morphine-induced facial allodynia. Migraine pain is often associated with facial allodynia in humans. In rats, sustained morphine produced facial allodynia, increased responsiveness of trigeminal afferent fibers, and increased activation of neurons in the medullary dorsal horn. The increased facial sensitivity was readily reversed by drugs known to be efficacious in human migraine pain, suggesting that the neuroplastic adaptations elicited in the trigeminal system by sustained morphine exposure may serve as a model to study the mechanisms of MOH.