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      Structural and functional footprint of visual snow syndrome

      brief-report

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          Abstract

          Patients with visual snow syndrome suffer from subjective visual and non-visual symptoms, such as tinnitus and concentration problems. Schankin et al. reveal structural and functional changes in extrastriate visual and extra-visual cortex in those affected, emphasizing that the disorder extends beyond the visual system

          Abstract

          Patients with visual snow syndrome suffer from a continuous pan-field visual disturbance, additional visual symptoms, tinnitus, and non-perceptional symptoms. The pathophysiology of visual symptoms might involve dysfunctional visual cortex. So far, the extra-visual system has not been investigated. We aimed at identifying structural and functional correlates for visual and non-visual symptoms in visual snow syndrome. Patients were compared to age- and sex-matched controls using 18F-2-fluoro-2-deoxy- d-glucose PET ( n = 20 per group) and voxel-based morphometry ( n = 17 per group). Guided by the PET results, region of interest analysis was done in voxel-based morphometry to identify structural-functional correspondence. Grey matter volume was assessed globally. Patients had corresponding hypermetabolism and cortical volume increase in the extrastriate visual cortex at the junction of the right lingual and fusiform gyrus. There was hypometabolism in the right superior temporal gyrus and the left inferior parietal lobule. Patients had grey matter volume increases in the temporal and limbic lobes and decrease in the superior temporal gyrus. The corresponding structural and functional alterations emphasize the relevance of the visual association cortex for visual snow syndrome. The broad structural and functional footprint, however, confirms the clinical impression that the disorder extends beyond the visual system.

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          Most cited references24

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          Pathophysiology of Migraine: A Disorder of Sensory Processing.

          Plaguing humans for more than two millennia, manifest on every continent studied, and with more than one billion patients having an attack in any year, migraine stands as the sixth most common cause of disability on the planet. The pathophysiology of migraine has emerged from a historical consideration of the "humors" through mid-20th century distraction of the now defunct Vascular Theory to a clear place as a neurological disorder. It could be said there are three questions: why, how, and when? Why: migraine is largely accepted to be an inherited tendency for the brain to lose control of its inputs. How: the now classical trigeminal durovascular afferent pathway has been explored in laboratory and clinic; interrogated with immunohistochemistry to functional brain imaging to offer a roadmap of the attack. When: migraine attacks emerge due to a disorder of brain sensory processing that itself likely cycles, influenced by genetics and the environment. In the first, premonitory, phase that precedes headache, brain stem and diencephalic systems modulating afferent signals, light-photophobia or sound-phonophobia, begin to dysfunction and eventually to evolve to the pain phase and with time the resolution or postdromal phase. Understanding the biology of migraine through careful bench-based research has led to major classes of therapeutics being identified: triptans, serotonin 5-HT1B/1D receptor agonists; gepants, calcitonin gene-related peptide (CGRP) receptor antagonists; ditans, 5-HT1F receptor agonists, CGRP mechanisms monoclonal antibodies; and glurants, mGlu5 modulators; with the promise of more to come. Investment in understanding migraine has been very successful and leaves us at a new dawn, able to transform its impact on a global scale, as well as understand fundamental aspects of human biology.
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            Selective and divided attention during visual discriminations of shape, color, and speed: functional anatomy by positron emission tomography.

            Positron emission tomography (PET) was used to identify the neural systems involved in discriminating the shape, color, and speed of a visual stimulus under conditions of selective and divided attention. Psychophysical evidence indicated that the sensitivity for discriminating subtle stimulus changes in a same-different matching task was higher when subjects selectively attended to one attribute than when they divided attention among the attributes. PET measurements of brain activity indicated that modulations of extrastriate visual activity were primarily produced by task conditions of selective attention. Attention to speed activated a region in the left inferior parietal lobule. Attention to color activated a region in the collateral sulcus and dorsolateral occipital cortex, while attention to shape activated collateral sulcus (similarly to color), fusiform and parahippocampal gyri, and temporal cortex along the superior temporal sulcus. Outside the visual system, selective and divided attention activated nonoverlapping sets of brain regions. Selective conditions activated globus pallidus, caudate nucleus, lateral orbitofrontal cortex, posterior thalamus/colliculus, and insular-premotor regions, while the divided condition activated the anterior cingulate and dorsolateral prefrontal cortex. The results in the visual system demonstrate that selective attention to different features modulates activity in distinct regions of extrastriate cortex that appear to be specialized for processing the selected feature. The disjoint pattern of activations in extravisual brain regions during selective- and divided-attention conditions also suggests that preceptual judgements involve different neural systems, depending on attentional strategies.
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              Voxel-based morphometry reveals gray matter abnormalities in migraine.

              Migraine is generally considered a functional brain disorder lacking structural abnormalities. Recent magnetic resonance imaging (MRI) studies, however, suggested that migraine may be associated with subtle brain lesions. We evaluated the presence of global or focal gray or white matter alterations in migraine patients using voxel-based morphometry (VBM), a fully automated method of analyzing changes in brain structure. VBM data also were used to evaluate possible differences between episodic and chronic migraine. Twenty-seven migraine right-handed patients and 27 healthy controls were selected for the study. Sixteen patients fulfilled the International Headache Society criteria for episodic migraine and 11 for chronic migraine. MRI scans were analyzed with MATLAB 6.5 and SPM2 software, using VBM method. In comparison with controls, migraineurs presented a significant focal gray matter reduction in the Right Superior Temporal Gyrus, Right Inferior Frontal Gyrus, and Left Precentral Gyrus. Chronic migraine patients, compared to episodic, showed a focal gray matter decrease in the bilateral Anterior Cingulate Cortex, Left Amygdala, Left Parietal Operculum, Left Middle and Inferior Frontal Gyrus, Right Inferior Frontal Gyrus, and bilateral Insula. Considering all the migraine patients, a significant correlation between gray matter reduction in anterior cingulate cortex and frequency of migraine attacks was found. Our study shows that migraine is associated with a significant gray matter reduction in several of the cortical areas involved in pain circuitry. In addition, we found a significant correlation between frequency of migraine attacks and signal alteration in the Anterior Cingulate Cortex. Our data provide new insight into migraine pathophysiology and support the concept that migraine may be a progressive disorder.
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                Author and article information

                Journal
                Brain
                Brain
                brainj
                Brain
                Oxford University Press
                0006-8950
                1460-2156
                April 2020
                24 March 2020
                24 March 2020
                : 143
                : 4
                : 1106-1113
                Affiliations
                [a1 ] Department of Neurology, Inselspital, University Hospital Bern, University of Bern , Bern, Switzerland
                [a2 ] Department of Neurology, University of California , San Francisco, San Francisco, CA, USA
                [a3 ] Department of Neurology, The Royal London Hospital (Barts and the London NHS Trust) , London, UK
                [a4 ] Amgen Inc. , Thousand Oaks, CA USA
                [a5 ] Department of Neurology, Monash Medical Centre, Monash University , Melbourne, Australia
                [a6 ] Department of Neurology, DKD HELIOS Klinik Wiesbaden , Wiesbaden, Germany
                [a7 ] NIHR-Wellcome Trust King’s Clinical Research Facility, SLaM Biomedical Research Center, King’s College London , London, UK
                Author notes
                Correspondence to: Peter J. Goadsby, MD, PhD Wellcome Foundation Building King’s College Hospital London SE5 9PJ, UK E-mail: peter.goadsby@ 123456kcl.ac.uk
                Author information
                http://orcid.org/0000-0003-2797-4676
                http://orcid.org/0000-0003-3260-5904
                Article
                awaa053
                10.1093/brain/awaa053
                7534145
                32211752
                eebe6e17-dfc7-470f-a6d1-c0593c38709e
                © The Author(s) (2020). Published by Oxford University Press on behalf of the Guarantors of Brain.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

                History
                : 24 September 2019
                : 14 January 2020
                : 16 January 2020
                Page count
                Pages: 8
                Funding
                Funded by: Eye on Vision Foundation;
                Funded by: Deutsche Forschungsgemeinschaft, DOI 10.13039/501100001659;
                Award ID: SCHA 1676/1-1
                Categories
                Reports

                Neurosciences
                visual snow,non-visual symptoms,migraine,fdg pet,voxel-based morphometry
                Neurosciences
                visual snow, non-visual symptoms, migraine, fdg pet, voxel-based morphometry

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