Headache
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US Headache Consortium Guidelines state that persons with migraine with headache-related disability should receive certain acute treatments including migraine-specific and other medications. However, many eligible individuals do not receive these therapies. Individuals with migraine may experience barriers to receiving minimal appropriate care. We aimed to identify barriers to care in a population sample of individuals with episodic migraine. We assessed barriers at 3 levels: medical consultation, diagnosis, and acute pharmacologic therapy use and assessed the contribution of socioeconomic, demographic, and headache-specific variables to these barriers. ⋯ Among persons with migraine in need of medical care (MIDAS Grade II or greater), only one quarter traversed the 3 steps we proposed to be necessary to achieving minimally appropriate care (consulting, diagnosis, and treatment/medication use). Health insurance status was an important predictor of consulting. Among consulters, women were far more likely to be diagnosed than men, suggesting that gender bias in diagnosis may be an important barrier for men. There were economic barriers related to use of appropriate prescription medications. Public health efforts should focus on improving consultation rates, particularly in the uninsured and diagnostic rates particularly in males with migraine.
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The immense burden of headache disorders in America has been very rarely considered during the formal deliberations of Congress. On February 14, 2012, the Committee on Health, Education, Labor, and Pensions of the United States Senate held a public hearing on Pain in America: Exploring Challenges to Relief. During that hearing, Senator Bernard Sanders of Vermont entered into the Congressional Record testimony on the impact of headache disorders on behalf of the Alliance for Headache Disorders Advocacy.
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Allodynia is considered a phenomenon of central sensitization that may lead to migraine transformation, lowering the attack threshold. Migraine triggers are factors that may induce headache attacks in susceptible individuals. We hypothesize that because allodynia decreases the migraine-attack threshold, allodynic migraineurs are more susceptible to triggers than the non-allodynic ones. ⋯ Migraineurs with moderate/severe allodynia had more triggers than those with no/mild allodynia. It is unknown if those with moderate/severe allodynia are more susceptible to triggers, or repetitive stimulation of the trigeminal system by triggers resulted in moderate/severe allodynia.
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The goal of this study was to better understand the cellular mechanisms involved in proton stimulation of calcitonin gene-related peptide (CGRP) secretion from cultured trigeminal neurons by investigating the effects of 2 antimigraine therapies, onabotulinumtoxinA and rizatriptan. Stimulated CGRP release from peripheral and central terminating processes of trigeminal ganglia neurons is implicated in migraine pathology by promoting inflammation and nociception. Based on models of migraine pathology, several inflammatory molecules including protons are thought to facilitate sensitization and activation of trigeminal nociceptive neurons and stimulate CGRP secretion. Despite the reported efficacy of triptans and onabotulinumtoxinA to treat acute and chronic migraine, respectively, a substantial number of migraineurs do not get adequate relief with these therapies. A possible explanation is that triptans and onabotulinumtoxinA are not able to block proton-mediated CGRP secretion. ⋯ Our findings provide evidence that proton regulated release of CGRP from trigeminal neurons utilizes a different mechanism than the calcium and synaptosomal-associated protein 25-dependent pathways that are inhibited by the antimigraine therapies, rizatriptan and onabotulinumtoxinA.
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Orbitofrontal cortex (OFC) dysfunction and poor decision making have been described in patients with chronic migraine and medication overuse. These neurobiological underpinnings might explain dependency-like behaviors often described in this condition, such as loss of control over painkillers, high rates of relapse after detoxification, and compromised social functioning. We investigate whether the OFC impairment was a persistent trait in migraine, independent of clinical and affective features, a dynamic result of the need to cope with the increased pain and disability, or a temporary consequence of medication overuse. ⋯ The present findings suggest the presence of a persistent OFC dysfunction in migraine as a psychobiologic trait that is not influenced by the presence of medication overuse, the clinical severity of the disease, or the patient's affective status. Further studies are needed to elucidate the etiopathological role of OFC in migraine and medication overuse.