Effects of remote cutaneous pain on trigeminal laser-evoked potentials in migraine patients

A proportion of episodic migraine patients experiences a progressive increase in attack frequency leading to chronic migraine (CM). The most frequent external factor that leads to headache chronification is medication overuse. The neurobiological bases of headache chronification and of the vicious circle of medication overconsumption are not completely elucidated. More recently, the same neurophysiological methods used to study episodic migraine were applied to CM and medication-overuse headache (MOH). Studies of cortical responsivity tend overall to indicate an increase in excitability, in particular of somatosensory and visual cortices, reflected by increased amplitude of evoked responses, decreased activity of inhibitory cortical interneurons reflected in the smaller magnetic suppression of perceptual accuracy, and, at least for visual responses, an increase in habituation. In MOH, overconsumption of triptans or NSAIDs influences cortical excitability differently. Generalized central sensitization is suggested to play an important role in the pathophysiology of headache chronification.

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“…However, LEPs are abnormally modulated by heterotopic conditioning stimuli such as remote capsaicin application [8] and by distraction [9,10].…”

Section: Pain-related Responsesmentioning

confidence: 99%

Cortical Excitability in Chronic Migraine

Coppola

Schoenen

2011

Curr Pain Headache Rep

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“…Understanding the mechanisms involved in CPM is important because it is impaired in several hyperalgesic conditions (see for a review [17]: tension-type headache [18], migraine [19,20], fibromyalgia [21,22], irritable bowel syndrome [23], osteoarthritis [24] and chronic post-surgical pain [25]. …”

Section: Introductionmentioning

confidence: 99%

Cerebral responses and role of the prefrontal cortex in conditioned pain modulation: an fMRI study in healthy subjects

Bogdanov

Viganò

Noirhomme

et al. 2015

Behavioural Brain Research

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The mechanisms underlying conditioned pain modulation (CPM) are multifaceted. We searched for a link between individual differences in prefrontal cortex activity during multi-trial heterotopic noxious cold conditioning and modulation of the cerebral response to phasic heat pain. In 24 healthy female subjects, we conditioned laser heat stimuli to the left hand by applying alternatively ice-cold or lukewarm compresses to the right foot. We compared pain ratings with cerebral fMRI BOLD responses. We also analyzed the relation between CPM and BOLD changes produced by the heterotopic cold conditioning itself, as well as the impact of anxiety and habituation of cold-pain ratings. Specific cerebral activation was identified in precuneus and left posterior insula/SII, respectively, during early and sustained phases of cold application. During cold conditioning, laser pain decreased (n = 7), increased (n = 10) or stayed unchanged (n = 7). At the individual level, the psychophysical effect was directly proportional to the cold-induced modulation of the laser-induced BOLD response in left posterior insula/SII. The latter correlated with the BOLD response recorded 80 s earlier during the initial 10-s phase of cold application in anterior cingulate, orbitofrontal and lateral prefrontal cortices. High anxiety and habituation of cold pain were associated with greater laser heat-induced pain during heterotopic cold stimulation. The habituation was also linked to the early cold-induced orbitofrontal responses. We conclude that individual differences in conditioned pain modulation are related to different levels of prefrontal cortical activation by the early part of the conditioning stimulus, possibly due to different levels in trait anxiety.

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“…Deficient endogenous inhibition has been suggested as a contributing factor in several chronic painful disorders (Peters et al, 1992;Kosek and Hansson, 1997;Lautenbacher and Rollman, 1997;Kosek and Ordeberg, 2000;Staud et al, 2003;Wilder-Smith et al, 2004;Julien et al, 2005;Pielsticker et al, 2005;de Tommaso et al, 2007;King et al, 2009;van Wijk and Veldhuijzen, 2010). It has been suggested that disturbed or restricted sleep may increase pain sensitivity by interfering with one or several pain-inhibitory mechanisms.…”

Section: Introductionmentioning

confidence: 99%