![]() ![]() This particular form of altered excitability has been found interictally ( 12), although it typically fluctuates through the migraine cycle and can revert with disease chronification ( 13). ![]() This uncovered important pathophysiological mechanisms now known to be typical of the migrainous brain, such as lack of habituation ( 10, 11). Recent evidence has led to better insight on the link between light inputs and pain, through the discovery of a pathway where photic signals from the retina converge on thalamic trigeminovascular neurons ( 7).įinally, the notion that visual function is abnormal in migraineurs even in between attacks has lead researchers in the past to carry out extensive neurophysiological investigation of the visual network in migraine ( 8, 9). The most obvious explanation is certainly linked to the intriguing phenomenon of aura, a fully reversible neurological dysfunction which occurs in about a third of migraine cases and is represented chiefly by positive or negative visual symptoms ( 3, 4).Īnother reason for the rising interest in studying visual function has been photophobia, a clinical hallmark of migraine both during attacks and in the interictal phase ( 5, 6). The visual network has been one of the most studied systems in the migraine brain for several reasons. One of the main aspects that has emerged from these studies is the confirmation, previously shown through animal models, that migraine does not represent a primary vascular disorder, rather a complex brain dysfunction involving several cortical and subcortical networks ( 1, 2). In the field of primary headaches, and migraine in particular, a growing body of neuroimaging work has served the purpose of dissecting important structural and functional alterations that characterize the disorder. Several conventional and more advanced neuroimaging techniques have been implemented over the years and have proven to be important tools in the understanding of normal and pathological brain biology. In the last decades, imaging has gained considerable interest in the field of neuroscience and has allowed researchers to begin to unravel important mechanisms in the biology of complex neurological disorders. We also present possible hypotheses on the underlying pathophysiology of visual snow, for which very little is currently known. We do this by taking into account the broader spectrum of migrainous biology, thus analyzing migraine both with and without aura, focusing on light sensitivity as the most relevant visual symptom in migraine, and finally analyzing the visual snow syndrome. Here, we review the most relevant neuroimaging literature to date, considering studies that have either attempted to investigate the visual network or have indirectly shown visual processing dysfunctions in migraine. Finally, visual snow, a recently recognized neurological disorder characterized by a continuous visual disturbance, is highly comorbid with migraine and possibly shares with it some common pathophysiological mechanisms. Further, the study of photophobia, a hallmark migraine symptom, has allowed unraveling of distinct connections that link retinal pathways to the trigeminovascular system. Not only is the aura phenomenon linked to cortical alterations primarily localized in the visual cortex but also migraine without aura has shown distinct dysfunction of visual processing in several studies in the past. ![]() The involvement of the visual network in migraine pathophysiology has been well-known for more than a century.
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