Central sensitization theory of migraine: clinical implications.
ABSTRACT The clinical science of migraine headache continues to evolve. Theories of the pathophysiology of migraine have progressed from the early vascular basis of migraine to more complex current theories that emphasize the centrality of neuronal dysfunction. The most recently articulated theory of migraine is the central sensitization hypothesis, which proposes that altered processing of sensory input in the brainstem, principally the trigeminal nucleus caudalis, could account for many of the temporal and symptomatic features of migraine, as well as its poor response to triptan therapy when such treatment is initiated hours after the onset of pain. Both preclinical and clinical data support the central sensitization theory. A critical clinical implication of this theory is that drugs that are capable of either aborting or arresting the process of central sensitization, most prominently dihydroergotamine, may have a unique role in the treatment of migraine. An additional, and highly practical, implication is based upon the finding that cutaneous allodynia-pain arising from innocuous stimulation of the skin, as in hair brushing or the application of cosmetics-is an easily identifiable marker of central sensitization. Thus, the presence or absence of cutaneous allodynia can be integrated into the routine clinical assessment of migraine and utilized as a determinant of treatment. Future basic and clinical research on central sensitization is likely to be of ongoing importance to the field.
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ABSTRACT: To assess the effectiveness of OMT on chronic migraineurs using HIT-6 questionnaire, drug consumption, days of migraine, pain intensity and functional disability. 3-Armed randomized controlled trial setting: all patients admitted in the Department of Neurology of Ancona's United Hospitals, Italy, with a diagnosis of migraine and without chronic illness, were considered eligible for the study. Patients were randomly divided into three groups: (1) OMT+medication therapy, (2) sham+medication therapy and (3) medication therapy only. Patients received 8 treatments in a study period of 6 months. Changing from baseline HIT-6 score. 105 subjects were included. At the end of the study, ANOVA showed that OMT significantly reduced HIT-6 score (mean change scores OMT-conventional care: -8.74; 95% confidence interval (CI) -12.96 to -4.52; p<0.001 and OMT-sham: -6.62; 95% CI -10.85 to -2.41; p<0.001), drug consumption (OMT-sham: RR=0.22, 95% CI 0.11-0.40; OMT-control: RR=0.20, 95% CI 0.10-0.36), days of migraine (OMT-conventional care: M=-21.06; 95% CI -23.19 to -18.92; p<0.001 and OMT-sham: -17.43; 95% CI -19.57 to -15.29; p<0.001), pain intensity (OMT-sham: RR=0.42, 95% CI 0.24-0.69; OMT-control: RR=0.31, 95% CI 0.19-0.49) and functional disability (p<0.001). These findings suggest that OMT may be considered a valid procedure for the management of migraineurs. The present trial was registered on www.ClinicalTrials.gov (identifier: NCT01851148). Copyright © 2015 Elsevier Ltd. All rights reserved.Complementary Therapies in Medicine 01/2015; 23(2). DOI:10.1016/j.ctim.2015.01.011 · 2.22 Impact Factor
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ABSTRACT: Migraine is the most common neurological disorder. Attacks are complex and consist of multiple phases but are most commonly characterized by intense, unilateral, throbbing headache. The pathophysiology contributing to migraine is poorly understood and the disorder is not well managed with currently available therapeutics, often rendering patients disabled during attacks. The mechanisms most likely to contribute to the pain phase of migraine require activation of trigeminal afferent signaling from the cranial meninges and subsequent relay of nociceptive information into the central nervous system in a region of the dorsal brainstem known as the trigeminal nucleus caudalis. Events leading to activation of meningeal afferents are unclear, but nerve endings within this tissue are mechanosensitive and also express a variety of ion channels including acid-sensing ion channels and transient receptor-potential channels. These properties may provide clues into the pathophysiology of migraine by suggesting that decreased extracellular pH and environmental irritant exposure in the meninges contributes to headache. Neuroplasticity is also likely to play a role in migraine given that attacks are triggered by routine events that are typically nonnoxious in healthy patients and clear evidence of sensitization occurs during an attack. Where and how plasticity develops is also not clear but may include events directly on the afferents and/or within the TNC. Among the mediators potentially contributing to plasticity, calcitonin gene-related peptide has received the most attention within the migraine field but other mechanisms may also contribute. Ultimately, greater understanding of the molecules and mechanisms contributing to migraine will undoubtedly lead to better therapeutics and relief for the large number of patients across the globe who suffer from this highly disabling neurological disorder. © 2015 Elsevier Inc. All rights reserved.Progress in molecular biology and translational science 01/2015; 131:537-64. DOI:10.1016/bs.pmbts.2015.01.001 · 3.11 Impact Factor
The Open Pain Journal 05/2010; 3(2):3-13. DOI:10.2174/1876386301003020003