Cephalalgia : an international journal of headache
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Musculoskeletal disorders are considered the underlying cause of cervicogenic headache, but neck pain is commonly associated with migraine and tension-type headaches. This study tested musculoskeletal function in these headache types. From a group of 196 community-based volunteers with headache, 73 had a single headache classifiable as migraine (n = 22), tension-type (n = 33) or cervicogenic headache (n = 18); 57 subjects acted as controls. ⋯ A discriminant function analysis revealed that collectively, restricted movement, in association with palpable upper cervical joint dysfunction and impairment in the CCFT, had 100% sensitivity and 94% specificity to identify cervicogenic headache. There was no evidence that the cervical musculoskeletal impairments assessed in this study were present in the migraine and tension-type headache groups. Further research is required to validate the predictive capacity of this pattern of impairment to differentially diagnose cervicogenic headache.
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Review
Myofascial trigger points and sensitization: an updated pain model for tension-type headache.
Present pain models for tension-type headache suggest that nociceptive inputs from peripheral tender muscles can lead to central sensitization and chronic tension-type headache (CTTH) conditions. Such models support that possible peripheral mechanisms leading to pericranial tenderness include activation or sensitization of nociceptive nerve endings by liberation of chemical mediators (bradikinin, serotonin, substance P). However, a study has found that non-specific tender points in CTTH subjects were not responsible for liberation of algogenic substances in the periphery. ⋯ Clinical studies have demonstrated that referred pain elicited by head and neck muscles contribute to head pain patterns in CTTH. Based on available data, an updated pain model for CTTH is proposed in which headache can at least partly be explained by referred pain from TrPs in the posterior cervical, head and shoulder muscles. In this updated pain model, TrPs would be the primary hyperalgesic zones responsible for the development of central sensitization in CTTH.
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The aim of this study was to evaluate and define the triggers of the acute migraine attack. Patients rated triggers on a 0-3 scale for the average headache. Demographics, prodrome, aura, headache characteristics, postdrome, medication responsiveness, acute and chronic disability, sleep characteristics and social and personal characteristics were also recorded. ⋯ The trigger frequencies were stress (79.7%), hormones in women (65.1%), not eating (57.3%), weather (53.2%), sleep disturbance (49.8%), perfume or odour (43.7%), neck pain (38.4%), light(s) (38.1%), alcohol (37.8%), smoke (35.7%), sleeping late (32.0%), heat (30.3%), food (26.9%), exercise (22.1%) and sexual activity (5.2%). Triggers were more likely to be associated with a more florid acute migraine attack. Differences were seen between women and men, aura and no aura, episodic and chronic migraine, and between migraine and probable migraine.
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With a recognition that the management of headache remains far from ideal, there may be more immediate potential to reduce the burden of illness from developments in the delivery of headache services. There is a paucity of evidence in this area and a danger that an expanding research agenda will be dominated by inappropriate methodological frameworks that have been so successful in developing medical treatments. The prevailing scientific methods are underpinned by statistical approaches that are aggregative in nature and assume independence of system elements, an approach that may have limited utility in the analysis of complex systems such as headache care delivery. This review calls for a shift in headache research resources to organizational development and briefly outlines alternative methodological considerations.
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A recent population-based prospective study reported that in women, migraine with aura (MA), but not migraine without aura (MoA), was associated with increased risk of coronary heart disease events (CHD). We sought to confirm this association in an Australian population-based cohort of older men and women (n = 2331, aged 49-97 years). We defined MA and MoA from face-to-face interview using International Headache Society criteria. ⋯ In women, a history of MA was associated with a non-significant twofold higher risk of CHD death (age-adjusted relative risk 2.2, 95% confidence interval 0.8, 5.8, P = 0.11), which remained similar after adjustment for cardiovascular risk factors. There were no CHD deaths in men with a history of migraine. Our findings support reports that in women, MA, but not MoA, may be associated with increased risk of CHD.