Headache
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The primary aim of our study was to evaluate if a group of medication-overuse headache (MOH) patients present dysfunctions in the mesocorticolimbic dopamine circuit. The secondary aim was to disentangle the role of the medication overuse and of the acute/chronic headache in determining these alterations and to investigate their persistence. ⋯ Our study showed that MOH patients present dysfunctions in the mesocorticolimbic dopamine circuit, in particular in the ventromedial prefrontal cortex and in the substantia nigra/ventral tegmental area complex. The ventromedial prefrontal cortex dysfunctions seem to be reversible and attributable to the acute/chronic headache, whereas the substantia nigra/ventral tegmental area complex dysfunctions are persistent and possibly related to medication overuse. These dysfunctions might be the expression of long-lasting neuroadaptations related to the overuse of medications and/or a pre-existing neurophysiological condition leading to vulnerability to medication overuse. The observed persistent dysfunctions in the midbrain dopamine suggest that MOH may share some neurophysiological features with addiction.
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The possible effects of migraine on executive abilities remain controversial; hence, we studied inter-ictal cognitive performance of individuals with migraine and non migraine headaches (NMH) compared with headache free controls. ⋯ The presence of headaches in late adulthood was related to a worse performance on few measures of executive functioning, suggesting that cognitive impact is not specific to migraine but might be associated to headache.
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High prevalence of headache has been associated with high latitude, thus suggesting a relation with vitamin D. However, there are so far no reports on the association between serum 25-hydroxyvitamin D (25[OH]D) and headache. ⋯ Non-migraine headache was associated with low levels of serum 25(OH)D. Although adjustment were done for possible confounders, this finding may still reflect lifestyle rather than causality, and further studies are needed to investigate this. No association was found between serum 25(OH)D and migraine.
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No single model of migraine explains all of the known features of the disorder. Migraine has recently been characterized as an abnormality in pain-modulating circuits in the brainstem. The periaqueductal gray appears to have a critical role in migraine genesis and has been labeled the "migraine generator." The concept of a "pain matrix," rather than a specific locus of pain, is widely accepted in the pain literature and offers a new dimension to understanding migraine. ⋯ The neurolimbic model expands the model of migraine as a dysfunction of brainstem nuclei. A neurolimbic model may help bridge a gap in understanding the migraine attack, the interictal dysfunctions of episodic migraine, the progression to chronic migraine, and the common comorbidities with other disorders (such as fibromyalgia, irritable bowel syndrome, and mood and anxiety disorders), which may also be considered neurolimbic. A neurolimbic model of migraine may be a useful heuristic that would impact both clinical treatment and research agendas, as well as education of physicians and patients.
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To estimate the prevalence and distribution of chronic migraine (CM) in the US population and compare the age- and sex-specific profiles of headache-related disability in persons with CM and episodic migraine. ⋯ In the US population, the prevalence of CM was nearly 1%. In adjusted models, CM prevalence was highest among females, in mid-life, and in households with the lowest annual income. Severe headache-related disability was more common among persons with CM and most common among females with CM.