Current pain and headache reports
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The understanding of migraine pathophysiology has evolved from the belief that migraine is a vascular disorder, to evidence that better defines migraine as a neurogenic disorder associated with secondary changes in brain perfusion. There is evidence to suggest that the early phase of migraine pain results from neurogenic inflammation affecting cranial blood vessels and dura. Allodynia, hyperalgesia, and expansion of nociceptive fields occur during most well-established migraine attacks. ⋯ A hypothesis that defines migraine pain as a unique neuropathic pain disorder can imply the potential for neural plasticity and may provide insight into the mechanisms that underlie the transformation of episodic to chronic forms of migraine. The neuropathic pain model of migraine pathophysiology not only paves the way for mechanism-based treatment strategies that can improve the acute and preventive management of migraine attacks, but also opens the door for the discovery of novel therapeutic targets. It also lends momentum to an understanding of clinically intriguing topics such as opiate-induced hyperalgesia and medication-overuse headache (rebound headache), opioid resistance in the treatment of chronic headache, and disease modification in defending against the potential for migraine transformation.
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Curr Pain Headache Rep · Jun 2006
ReviewCurrent views of the risk of stroke for migraine with and migraine without aura.
The association between migraine and stroke is complex and is a continued focus of attention. Several observational studies have identified migraine as an independent risk factor for ischemic stroke. However, a distinction should be made between migraine with and migraine without aura. ⋯ Most studies have not found an association between migraine without aura and ischemic stroke. Although there are several hypotheses about the biologic link between migraine with aura and ischemic stroke, the precise mechanisms remain unclear. However, because the absolute risk of stroke is low in patients with migraine with aura, and migraine without aura is likely not associated with ischemic stroke, most migraine patients will not experience a stroke event.
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The paradigm of early treatment of the migraine attack at mild pain intensity has become one alternative to circumventing the problem of compromised oral absorption of symptomatic drugs due to migraine-induced gastrointestinal dysmotility. Early treatment also has been proposed to be advantageous because most migraineurs could be less responsive to delayed treatment, owing to the development of central sensitization of the trigeminal pain transmission. Ranking the underlying principles, it seems that the improved response to an oral triptan formulation at mild migraine symptom intensity has more to do with less impaired gastrointestinal absorption in the early stage of the attack than decreasing the time and preventing chances for central sensitization and development of cutaneous allodynia. ⋯ Individually tailored use of the available triptan formulations will increase, without any doubt, the within-migraineur consistency of response. It also will reduce the overall proportion of migraine attacks or migraineurs not responding to triptan treatment. Notwithstanding, the recommendation of early treatment during the migraine attack when the pain is mild remains valid.
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Curr Pain Headache Rep · Jun 2006
ReviewInsights from experimental studies into allodynia and its treatment.
Migraine is a common disorder that often is accompanied by cutaneous allodynia. Cutaneous allodynia on the head has been linked to sensitization of neurons in the trigeminal nucleus caudalis in animal models of migraine. In addition, migraine with allodynia is refractory to acute treatment with triptans. ⋯ This paper reviews recent research on the pathogenesis of headache and the generation of allodynia. We discuss the regions of the nervous system that are involved in generating and maintaining headache pain and allodynia. We also discuss recent advances in the treatment of migraine based on translation research.
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Eight measures of neuropathic pain exist that have been designed to discriminate neuropathic from non-neuropathic pain and detect treatment effects. The current paper describes these measures and summarizes the evidence supporting their validity. ⋯ However, given the lack of overlap in measures designed for this purpose, it is likely that the validity of any one measure could be improved by incorporating items from the others. The Neuropathic Pain Scale (NPS) has the most empirical support as a measure of treatment outcome, although a new measure that includes the NPS items (the Pain Quality Assessment Scale) will likely prove to be even more useful, because it includes pain descriptors common to people with neuropathic and other chronic pain conditions not included on the NPS.