Discussed. S36 Neurophysiology of Headaches Gianluca Coppola G.B. Bietti Foundation-IRCCS, Analysis Unit of Neurophysiology of Vision and Neurophthalmology, Rome, Italy The Journal of Headache and Pain 2017, 18(Suppl 1):S36 Through the final decades, the strategies of neurophysiology proved to become pretty powerful in disclosing subtle functional Maresin 1 In Vivo abnormalities on the brain of patients affected by major headache disorders. These techniques received many refinements during the final years, further improving our understanding of headaches pathophysiology. Abnormal enhanced responsivity was many occasions revealed with virtually each of the sensory modalities of stimulation in migraine amongst attacks, with its normalization during the attacks. Lately, authors observed that the degree of some neurophysiological abnormalities might depends on the distance from the last attack, i.e. on the point exactly where the patient is recorded during the migraine cycle. Thalamicthalamocortical drives were discovered to be much less active interictally, but normallyThe Journal of Headache and Discomfort 2017, 18(Suppl 1):Page 11 ofactive ictally. Somatosensory cortex lateral inhibition, gating, and interhemispheric inhibition had been altered in migraine, and may perhaps contribute to cortical hyperresponsivity and clinical functions. Cluster headache patients are characterized by a deficient habituation of the brainstem blink reflex throughout the bout, outdoors of attacks, around the impacted side. Proof for sensitization of discomfort processing was disclosed by studying temporal summation threshold in the nociceptive withdrawal reflex, which was much less modulated by supraspinal descending inhibitory controls. In conclusion, a lot has been discovered and far more desires to become investigated to improved fully grasp what causes, how it triggers, keeps and runs out recurrent primary headaches. Clarifying some of these mechanisms may help inside the identification of new therapeutic targets. S37 Mechanisms of Photophobia Andrew Russo The Journal of Headache and Discomfort 2017, 18(Suppl 1):S37 In this rejoinder to “Photophobia and Hypothalamus”, I’ll speculate on how the diverse collection of neuropeptides, like CGRP, in the hypothalamus may enhance sensitivity to light. Inside the brain, neuropeptides can modulate the strength of synaptic signaling even at a reasonably huge distance from their web page of release. Given the evidence for CGRP in migraine and prospective roles for other hypothalamic peptides, it seems probably that altered neuropeptide actions could possibly be a common theme underlying the heightened sensory state of migraine. Towards this point, I will briefly talk about our preclinical CGRP and optogenetic research working with light aversive behavior in mouse models as a surrogate for migraine-associated photophobia. I will describe how both the brain as well as the periphery are susceptible to elevated CGRP and how CGRP seems to act by distinct mechanisms in these web sites. In the CNS, we have identified the posterior thalamus as a most likely web-site of CGRP action, which can be in agreement with Burstein’s evidence that this region is really a convergent relay point in the retina and dura. These tips will probably be tied together within a speculative model that integrates peripheral and central CGRP actions in photophobia. S38 Classical trigeminal neuralgia clinical and MRI findings Stine Maarbjerg Department of Neurology, Helse Fonna, Haugesund, Norway The Journal of Headache and Pain 2017, 18(Suppl 1):S38 Background Classical trigeminal neuralgia (TN) can be a uni.
