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8 pages, 721 KiB  
Brief Report
Susceptibility Weighted Imaging in Migraines with and Without Aura: A Case–Control Study
by Adrian Scutelnic, Tomas Klail, Diego Moor, Nedelina Slavova, Valentina Petroulia, Simon Jung, Mattia Branca, Urs Fischer, Franz Riederer, Roland Wiest and Christoph J. Schankin
Neurol. Int. 2025, 17(7), 104; https://doi.org/10.3390/neurolint17070104 - 8 Jul 2025
Viewed by 367
Abstract
Background: The asymmetry of cortical veins in susceptibility weighted imaging (SWI) in MRI might be a biomarker for migraine auras and cortical spreading depression (CSD). The aim of this study was to assess in humans if SWI asymmetry can be found in patients [...] Read more.
Background: The asymmetry of cortical veins in susceptibility weighted imaging (SWI) in MRI might be a biomarker for migraine auras and cortical spreading depression (CSD). The aim of this study was to assess in humans if SWI asymmetry can be found in patients who have migraine attacks without auras. Methods: We included patients (n = 100 per group) from the emergency room setting when they (i) presented with an acute neurological deficit or headache; (ii) had a discharge diagnosis of a migraine aura, a migraine without an aura, or neither (controls without stroke or epilepsy); and (iii) had a brain MRI with SWI in the acute setting. Results: In the migraines with auras group, SWI asymmetry was found in 26% (95% CI 18–35) compared to patients with migraines without auras (3%, [95% CI 1–8], p < 0.001) and controls 7% [95% CI 3–14], p < 0.001). There was no difference between patients with migraines without auras and controls (p = 0.19). Conclusions: The distinct SWI changes in migraines with and without auras suggest that CSD might not be involved in the pathophysiology of migraines without auras. Full article
(This article belongs to the Section Pain Research)
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15 pages, 1972 KiB  
Article
Treadmill Exercise Impact on Brain Electrophysiological and Glial Immunoreactivity in Cuprizone-Treated Rats
by Cássia Borges Lima-de-Castro, Noranege Epifânio Accioly, Geórgia de Sousa Ferreira Soares, Catarina Nicácio dos-Santos, Sonia Carolina Guerrero Prieto and Rubem Carlos Araujo Guedes
Brain Sci. 2025, 15(7), 686; https://doi.org/10.3390/brainsci15070686 - 26 Jun 2025
Viewed by 414
Abstract
Background/Objectives: Demyelination occurs to a variable extent in various neurological diseases, such as multiple sclerosis. Physical exercise benefits central neural functions that depend on the brain’s electrophysiological and glial activity. It is unclear whether both factors—i.e., demyelination and exercise—interact in the brain. [...] Read more.
Background/Objectives: Demyelination occurs to a variable extent in various neurological diseases, such as multiple sclerosis. Physical exercise benefits central neural functions that depend on the brain’s electrophysiological and glial activity. It is unclear whether both factors—i.e., demyelination and exercise—interact in the brain. We aimed to investigate if this interaction occurs during brain development. Methods: Developing rats were subjected to a cuprizone-induced demyelination. Part of these rats were treadmill-exercised for five weeks. After this period, some demyelinated animals were allowed to remyelinate by receiving a similar diet, without cuprizone, for six weeks. The exercised groups were compared with the corresponding sedentary groups. All groups were evaluated electrophysiologically (cortical spreading depression features), and their brains were processed for immunohistochemical labeling with four specific glial antibodies (anti-APC, MBP, GFAP, and Iba1). Results: Compared with the corresponding controls, cuprizone demyelination and treadmill exercise accelerated and decelerated CSD propagation. Cuprizone reduced APC, MBP, and GFAP immunolabeling and increased Iba1 immunostaining. Remyelination reverted the cuprizone effects. Exercise counteracted the cuprizone-induced changes in GFAP- and Iba1-containing cells but not in MBP- and APC-containing ones. Conclusions: Our data confirmed the effectiveness of the cuprizone demyelination paradigm. They evidenced the potential neuroprotective effect of regular physical exercise, suggesting that this non-pharmacological intervention could benefit patients with central demyelination-dependent diseases. Full article
(This article belongs to the Section Developmental Neuroscience)
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40 pages, 5811 KiB  
Review
Metabolic Dysfunction and Dietary Interventions in Migraine Management: The Role of Insulin Resistance and Neuroinflammation—A Narrative and Scoping Review
by Cinzia Cavestro
Brain Sci. 2025, 15(5), 474; https://doi.org/10.3390/brainsci15050474 - 29 Apr 2025
Cited by 2 | Viewed by 1769
Abstract
Introduction: Migraine is a prevalent neurological disorder characterized by recurrent headaches with autonomic and neurological symptoms, significantly impacting quality of life globally. Its pathogenesis involves genetic, neurological, inflammatory, and metabolic factors, with insulin resistance and metabolic dysfunction increasingly recognized as important contributors. Historically, [...] Read more.
Introduction: Migraine is a prevalent neurological disorder characterized by recurrent headaches with autonomic and neurological symptoms, significantly impacting quality of life globally. Its pathogenesis involves genetic, neurological, inflammatory, and metabolic factors, with insulin resistance and metabolic dysfunction increasingly recognized as important contributors. Historically, it has been known that certain foods can trigger migraine attacks, which led for many years to the recommendation of elimination diets—now understood to primarily target histamine-rich foods. Over the past two decades, attention has shifted toward underlying metabolic disturbances, leading to the development of dietary approaches specifically aimed at addressing these dysfunctions. Methods: A scoping literature review was conducted using PubMed and Embase to evaluate the relationships among migraine, insulin-related mechanisms, neurogenic inflammation, and dietary interventions. Initial searches focused on “MIGRAINE AND (neurogenic inflammation)” (2019–15 April 2025), followed by expanded searches from 1950 onward using terms such as “MIGRAINE AND (insulin, insulin resistance, hyperinsulinism)”, and “MIGRAINE AND (diet, dietary, nutrition, nutritional)”. A specific search also targeted “(INSULIN OR insulin resistance OR hyperinsulinism) AND (neurogenic inflammation)”. Abstracts were screened, full texts were retrieved, and duplicates or irrelevant publications were excluded. No filters were applied by article type or language. Systematic reviews and meta-analyses were prioritized when available. Results: Migraine pathogenesis involves trigeminovascular system activation, neurogenic inflammation mediated by CGRP and PACAP, immune dysregulation, mast cell activation, and cortical spreading depression (CSD). Emerging evidence highlights significant associations between migraine, insulin resistance, and hyperinsulinism. Hyperinsulinism contributes to migraine through TRPV1 sensitization, increased CGRP release, oxidative stress, mitochondrial dysfunction, and systemic inflammation. Metabolic dysfunction, including obesity and insulin resistance, exacerbates migraine severity and frequency. Dietary interventions, particularly anti-inflammatory, Mediterranean, and ketogenic diets, show promise in reducing migraine frequency and severity through mechanisms involving reduced inflammation, oxidative stress, improved mitochondrial function, and glucose metabolism stabilization. Conclusions: The interplay between insulin resistance, metabolic dysfunction, and neuroinflammation is crucial in migraine pathophysiology. Targeted dietary interventions, including ketogenic and Mediterranean diets, demonstrate significant potential in managing migraines, emphasizing the need for personalized nutritional strategies to optimize therapeutic outcomes. Full article
(This article belongs to the Special Issue Advances in Neuroinflammation and Pain Medicine)
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19 pages, 1040 KiB  
Review
Glutamate as a Therapeutic Substrate in Migraine
by Nazia Karsan, Luiza Bastos Alves and Peter J. Goadsby
Int. J. Mol. Sci. 2025, 26(7), 3023; https://doi.org/10.3390/ijms26073023 - 26 Mar 2025
Cited by 2 | Viewed by 1492
Abstract
Recurrent and intense headache is a well appreciated cardinal feature of migraine, a common and incapacitating neurological disorder. Often, there are associated canonical sensory abnormalities, such as light and sound sensitivity, as well as associated nausea. Given this phenotype of disordered sensory processing [...] Read more.
Recurrent and intense headache is a well appreciated cardinal feature of migraine, a common and incapacitating neurological disorder. Often, there are associated canonical sensory abnormalities, such as light and sound sensitivity, as well as associated nausea. Given this phenotype of disordered sensory processing and, in a third of patients, the phenomenon called aura accompanying migraine attacks, it has been suggested that the pathophysiology of migraine is likely to involve glutamate, the main excitatory neurotransmitter in the central nervous system (CNS). Glutamate plays a role in nociception, central sensitization, and cortical spreading depression (CSD), three processes that are deemed important in migraine biology. With an emphasis on the therapeutic potential of targeting various glutamate receptors in migraine, this review will discuss the currently available literature and emerging findings on the role of targeting glutamatergic pathways for the treatment of migraine. A thorough literature review was carried out on the functions of both metabotropic glutamate receptors (mGluRs), and the ionotropic glutamate receptors (NMDA, AMPA, and kainate) in migraine pathogenesis. The ever-present need for new treatments, the role of glutamate in the migraine aura phenomenon, and the consequences of monogenic migraine mutations on mediating prolonged, complex, or permanent aura are all discussed, culminating in a suggestion that glutamatergic targeting may hold particular promise in the management of migraine aura. There are plausible roles for metabotropic receptors in regulating pain processing in important migraine-related brain structures, like the thalamus and trigeminal nucleus. Similarly, ionotropic receptors contribute to excitatory neurotransmission and neuronal hyperexcitability. Recent studies have shown preclinical and early clinical results for treatments targeting these receptors, but there are still significant issues with treatment response, including drug transport, side effects, and efficacy. With ongoing and emerging discoveries in the field, there is increasing promise of new migraine medications targeting glutamate receptors. For bench to bedside translation in this area, continued study of the molecular basis of migraine, receptor subtypes, and exploration of potential drug delivery methods are needed. Full article
(This article belongs to the Special Issue Molecular and Cellular Neurobiology of Migraine: 2nd Edition)
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26 pages, 2854 KiB  
Review
Magnesium and Migraine
by Ligia J. Dominguez, Nicola Veronese, Shaun Sabico, Nasser M. Al-Daghri and Mario Barbagallo
Nutrients 2025, 17(4), 725; https://doi.org/10.3390/nu17040725 - 18 Feb 2025
Cited by 2 | Viewed by 14713
Abstract
Migraine is a widespread and intricate neurological condition that involves various factors and is marked by recurring headache episodes. Migraine is among the ten neurological conditions accounting for the greatest disability in the whole population, the leading cause of disability for children and [...] Read more.
Migraine is a widespread and intricate neurological condition that involves various factors and is marked by recurring headache episodes. Migraine is among the ten neurological conditions accounting for the greatest disability in the whole population, the leading cause of disability for children and adolescents aged 5–19 years, and the second cause of disability for adults aged 20–59 years. Magnesium deficiency is also a very common condition resulting from diverse reasons, including insufficient dietary consumption or increased loss through the gastrointestinal or renal system. Accumulated evidence from case reports, case–control studies, observational studies, and randomized, placebo-controlled trials has shown the effectiveness of magnesium supplementation in alleviating migraine, both acutely and chronically. Mechanisms that may help explain these results include the potential link between magnesium deficit and spreading cortical depression, vascular changes, oxidative stress, chronic inflammation, nervous excitation, neurotransmitter release, and electrolyte imbalances. This article aims to provide a comprehensive review of the available evidence on the links between magnesium and migraine, considering the role of magnesium in the pathogenesis of migraine and the utility of magnesium in its prevention and treatment. Full article
(This article belongs to the Section Micronutrients and Human Health)
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18 pages, 1856 KiB  
Review
fMRI Insights into Visual Cortex Dysfunction as a Biomarker for Migraine with Aura
by Damian Pikor, Natalia Banaszek-Hurla, Alicja Drelichowska, Mikołaj Hurla, Jolanta Dorszewska, Tomasz Wolak and Wojciech Kozubski
Neurol. Int. 2025, 17(2), 15; https://doi.org/10.3390/neurolint17020015 - 21 Jan 2025
Cited by 1 | Viewed by 2376
Abstract
Migraine with aura (MwA) is a common and severely disabling neurological disorder, characterised by transient yet recurrent visual disturbances, including scintillating scotomas, flickering photopsias, and complex geometric patterns. These episodic visual phenomena significantly compromise daily functioning, productivity, and overall quality of life. Despite [...] Read more.
Migraine with aura (MwA) is a common and severely disabling neurological disorder, characterised by transient yet recurrent visual disturbances, including scintillating scotomas, flickering photopsias, and complex geometric patterns. These episodic visual phenomena significantly compromise daily functioning, productivity, and overall quality of life. Despite extensive research, the underlying pathophysiological mechanisms remain only partially understood. Cortical spreading depression (CSD), a propagating wave of neuronal and glial depolarisation, has been identified as a central process in MwA. This phenomenon is triggered by ion channel dysfunction, leading to elevated intracellular calcium levels and excessive glutamate release, which contribute to widespread cortical hyperexcitability. Genetic studies, particularly involving the CACNA gene family, further implicate dysregulation of calcium channels in the pathogenesis of MwA. Recent advances in neuroimaging, particularly functional magnetic resonance imaging (fMRI), have provided critical insights into the neurophysiology of MwA. These results support the central role of CSD as a basic mechanism behind MwA and imply that cortical dysfunction endures beyond brief episodes, possibly due to chronic neuronal dysregulation or hyperexcitability. The visual cortex of MwA patients exhibits activation patterns in comparison to other neuroimaging studies, supporting the possibility that it is a disease-specific biomarker. Its distinctive sensory and cognitive characteristics are influenced by a complex interplay of cortical, vascular, and genetic factors, demonstrating the multifactorial nature of MwA. We now know much more about the pathophysiology of MwA thanks to the combination of molecular and genetic research with sophisticated neuroimaging techniques like arterial spin labelling (ASL) and fMRI. This review aims to synthesize current knowledge and analyse molecular and neurophysiological targets, providing a foundation for developing targeted therapies to modulate cortical excitability, restore neural network stability, and alleviate the burden of migraine with aura. The most important and impactful research in our field has been the focus of this review, which highlights important developments and their contributions to the knowledge and treatment of migraine with aura. Full article
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10 pages, 975 KiB  
Article
Susceptibility Weighted Imaging as a Biomarker for Cortical Spreading Depression
by Adrian Scutelnic, Isabelle Dominique Stöckli, Antonia Klein, Franz Riederer, Nedelina Slavova and Christoph J. Schankin
Clin. Transl. Neurosci. 2025, 9(1), 3; https://doi.org/10.3390/ctn9010003 - 20 Jan 2025
Viewed by 866
Abstract
Introduction: Cortical spreading depression (CSD) is thought to be the pathophysiologic correlate of migraine aura. In experimental animals, CSD was shown to cause an increase in oxyhemoglobin. Susceptibility weighted imaging (SWI) on magnetic resonance imaging (MRI) depicts cerebral veins according to their concentration [...] Read more.
Introduction: Cortical spreading depression (CSD) is thought to be the pathophysiologic correlate of migraine aura. In experimental animals, CSD was shown to cause an increase in oxyhemoglobin. Susceptibility weighted imaging (SWI) on magnetic resonance imaging (MRI) depicts cerebral veins according to their concentration in oxyhemoglobin. The aim of this study was to assess whether the distribution of SWI changes in people with migraine aura resembles the clinical presentation, with a focus on topology. Methods: In this retrospective single-center study, patients were included if they (i) had acute focal neurological symptoms beginning with visual symptoms, (ii) underwent head MRI including SWI within eight hours of symptom onset, (iii) SWI showed focal dilated veins, and (iv) they had a discharge diagnosis of migraine with aura. Eleven predefined cerebral regions of interest (ROIs) were assessed for prominent focal veins (PFVs) on SWI. We determined whether symptoms correlated with the topography of ROIs with PFVs. Results: We found a posterior to anterior gradient of SWI changes during acute migraine aura when visual symptoms were present. Conclusion: MRI with SWI might be able to detect traces of CSD. The posterior to anterior distribution of areas with SWI changes corresponds anatomically to the canonical succession of symptoms in migraine aura. Full article
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17 pages, 4071 KiB  
Article
Chronic Hyperhomocysteinemia Impairs CSD Propagation and Induces Cortical Damage in a Rat Model of Migraine with Aura
by Elena Gerasimova, Daniel Enikeev, Aleksey Yakovlev, Andrey Zakharov and Guzel Sitdikova
Biomolecules 2024, 14(11), 1379; https://doi.org/10.3390/biom14111379 - 29 Oct 2024
Cited by 2 | Viewed by 1785
Abstract
Hyperhomocysteinemia (hHCY) is a metabolic disorder characterized by elevated levels of homocysteine in plasma. hHCY correlates with a high risk of migraine headaches, especially migraine with aura. Cortical spreading depression (CSD) is a wave of depolarization passing through neurons and glial cells of [...] Read more.
Hyperhomocysteinemia (hHCY) is a metabolic disorder characterized by elevated levels of homocysteine in plasma. hHCY correlates with a high risk of migraine headaches, especially migraine with aura. Cortical spreading depression (CSD) is a wave of depolarization passing through neurons and glial cells of the cortex and is considered an electrophysiological correlate of migraine aura. The aim of the present study was to analyze neuronal activity and CSD in the somatosensory cortex of rats in vivo with prenatal hHCY and to assess cortex viability after 2 h of CSD generation. Female rats were fed a diet high in methionine, and their offspring with high homocysteine levels in plasma were further used in experiments. Recurrent CSD was evoked by local KCl application on the dura surface. Neuronal viability was assessed by measuring the activity of lactate dehydrogenase (LDH) in the brain and 2,3,5-triphenyltetrazolium chloride staining of the somatosensory cortex after two hours of CSD generation. Animals with hHCY exhibited higher neuronal activity, and more CSDs were generated in response to KCl, indicating higher cortical excitability. Propagation of recurrent CSD was impaired in supragranular cortical layers, and the recovery of multiple unit activity and evoked sensory potentials after CSD was delayed in the hHCY group. Finally, in animals with prenatal hHCY, an ischemic focus was identified as a consequence of multiple CSDs, along with elevated levels of LDH activity in brain tissues, suggestive of diminished neuronal viability. These findings imply that prolonged elevated levels of homocysteine may not only predispose to migraine with aura but also potentially elevate the risk of migrainous infarction. Full article
(This article belongs to the Special Issue Homocysteine and H2S in Health and Disease)
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6 pages, 617 KiB  
Case Report
Anti-Calcitonin Gene-Related Peptide Monoclonal Antibody Is Effective for Preventing Migraine Aura Without Headache
by Yasushi Shibata
Neurol. Int. 2024, 16(6), 1279-1284; https://doi.org/10.3390/neurolint16060097 - 29 Oct 2024
Viewed by 1703
Abstract
Background: Anti-calcitonin gene-related peptide monoclonal antibodies (CGRP mAbs) are clinically effective in preventing the migraine attacks, photophobia, and migraine auras associated with headaches. However, no study has yet investigated the effectiveness of CGRP mAbs in preventing migraine aura without headache. Case report: A [...] Read more.
Background: Anti-calcitonin gene-related peptide monoclonal antibodies (CGRP mAbs) are clinically effective in preventing the migraine attacks, photophobia, and migraine auras associated with headaches. However, no study has yet investigated the effectiveness of CGRP mAbs in preventing migraine aura without headache. Case report: A female patient of 49 years old presented with a long history (since age 10) of photosensitivity and typical migraine auras without a headache. The symptoms slightly responded to oral medication, lomerizine chloride, but did not completely resolve. Just one day after the administration of galcanezumab, her photo-hypersensitivity and migraine aura had completely resolved. Consequently, the administration of the oral migraine preventive medication was discontinued. Monthly galcanezumab at a dose of 120 mg was continuously given and she did not re-experience any auras or headaches. Conclusions: The use of CGRP mAbs can be considered as a potential treatment in preventing migraine aura without headache. Currently, CGRP mAb is indicated only for migraines with and without auras. Given our findings and the promising effects of this medication for this migraine subtype, a large clinical trial is required to better assess the effects and potential adverse events of CGRP mAb in patients with migraine aura without headache. Full article
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14 pages, 1420 KiB  
Review
Molecular and Cellular Neurobiology of Spreading Depolarization/Depression and Migraine: A Narrative Review
by Eiji Kitamura and Noboru Imai
Int. J. Mol. Sci. 2024, 25(20), 11163; https://doi.org/10.3390/ijms252011163 - 17 Oct 2024
Cited by 4 | Viewed by 3061
Abstract
Migraine is a prevalent neurological disorder, particularly among individuals aged 20–50 years, with significant social and economic impacts. Despite its high prevalence, the pathogenesis of migraine remains unclear. In this review, we provide a comprehensive overview of cortical spreading depolarization/depression (CSD) and its [...] Read more.
Migraine is a prevalent neurological disorder, particularly among individuals aged 20–50 years, with significant social and economic impacts. Despite its high prevalence, the pathogenesis of migraine remains unclear. In this review, we provide a comprehensive overview of cortical spreading depolarization/depression (CSD) and its close association with migraine aura, focusing on its role in understanding migraine pathogenesis and therapeutic interventions. We discuss historical studies that have demonstrated the role of CSD in the visual phenomenon of migraine aura, along with modern imaging techniques confirming its propagation across the occipital cortex. Animal studies are examined to indicate that CSD is not exclusive to migraines; it also occurs in other neurological conditions. At the cellular level, we review how CSD is characterized by ionic changes and excitotoxicity, leading to neuronal and glial responses. We explore how CSD activates the trigeminal nervous system and upregulates the expression of calcitonin gene-related peptides (CGRP), thereby contributing to migraine pain. Factors such as genetics, obesity, and environmental conditions that influence the CSD threshold are discussed, suggesting potential therapeutic targets. Current treatments for migraine, including prophylactic agents and CGRP-targeting drugs, are evaluated in the context of their expected effects on suppressing CSD activity. Additionally, we highlight emerging therapies such as intranasal insulin-like growth factor 1 and vagus nerve stimulation, which have shown promise in reducing CSD susceptibility and frequency. By elucidating the molecular and cellular mechanisms of CSD, this review aims to enhance the understanding of migraine pathogenesis and support the development of targeted therapeutic strategies. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Treatment of Migraine)
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15 pages, 2122 KiB  
Review
Metabolic Pathophysiology of Cortical Spreading Depression: A Review
by Arren Hill, Alfred B. Amendolara, Christina Small, Steve Cochancela Guzman, Devin Pfister, Kaitlyn McFarland, Marina Settelmayer, Scott Baker, Sean Donnelly, Andrew Payne, David Sant, John Kriak and Kyle B. Bills
Brain Sci. 2024, 14(10), 1026; https://doi.org/10.3390/brainsci14101026 - 16 Oct 2024
Viewed by 3201
Abstract
Cortical spreading depression (CSD) is an electrophysiologic pathological state in which a wave of depolarization in the cerebral cortex is followed by the suppression of spontaneous neuronal activity. This transient spread of neuronal depolarization on the surface of the cortex is the hallmark [...] Read more.
Cortical spreading depression (CSD) is an electrophysiologic pathological state in which a wave of depolarization in the cerebral cortex is followed by the suppression of spontaneous neuronal activity. This transient spread of neuronal depolarization on the surface of the cortex is the hallmark of CSD. Numerous investigations have demonstrated that transmembrane ion transport, astrocytic ion clearing and fatigue, glucose metabolism, the presence of certain genetic markers, point mutations, and the expression of the enzyme responsible for the production of various arachidonic acid derivatives that participate in the inflammatory response, namely, cyclooxygenase (COX), all influence CSD. Here, we explore the associations between CSD occurrence in the cortex and various factors, including how CSD is related to migraines, how the glucose state affects CSD, the effect of TBI and its relationship with CSD and glucose metabolism, how different markers can be measured to determine the severity of CSD, and possible connections to oligemia, orexin, and leptin. Full article
(This article belongs to the Section Neuropharmacology and Neuropathology)
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13 pages, 740 KiB  
Review
Migraine and Stroke: A Scoping Review
by Neal Nathan, Angeline Ngo and Suzan Khoromi
J. Clin. Med. 2024, 13(18), 5380; https://doi.org/10.3390/jcm13185380 - 11 Sep 2024
Cited by 6 | Viewed by 4094
Abstract
An increased risk of ischemic stroke in migraine with aura (MA) has been consistently demonstrated. The pathophysiology of risk factors is not yet well understood. Several mechanisms have been proposed to explain the association between MA and ischemic stroke including decreased focal cerebral [...] Read more.
An increased risk of ischemic stroke in migraine with aura (MA) has been consistently demonstrated. The pathophysiology of risk factors is not yet well understood. Several mechanisms have been proposed to explain the association between MA and ischemic stroke including decreased focal cerebral blood flow and other phenomena linked with cortical spreading depression (CSD) as well as neurovascular pathology, which appear to play a key role in MA. In addition to genetic predisposition, other classic stroke risk factors such as atrial fibrillation, emboli, migraine-associated vasculopathy, endothelial dysfunction, platelet dysfunction, coagulation pathway abnormalities, and inflammatory factors have been examined and investigated. For further clarification, distinctions have been made between features of migrainous infarctions and non-migrainous infarctions among migraineurs. Furthermore, the association is less clear when considering the mixed results studying the risk of ischemic stroke in migraines without aura (MO) and the risk of hemorrhagic stroke in people with all types of migraine. Translational research is investigating the role of biomarkers which can help identify vascular links between stroke and migraine and lead to further treatment developments. We performed a scoping review of the PubMed database to further characterize and update the clinical connections between migraine and stroke. Full article
(This article belongs to the Section Clinical Neurology)
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11 pages, 1145 KiB  
Article
Hypersensitivity of Intrinsically Photosensitive Retinal Ganglion Cells in Migraine Induces Cortical Spreading Depression
by Eiichiro Nagata, Motoharu Takao, Haruki Toriumi, Mari Suzuki, Natsuko Fujii, Saori Kohara, Akio Tsuda, Taira Nakayama, Ayana Kadokura and Manaka Hadano
Int. J. Mol. Sci. 2024, 25(14), 7980; https://doi.org/10.3390/ijms25147980 - 22 Jul 2024
Cited by 2 | Viewed by 2080
Abstract
Migraine is a complex disorder characterized by episodes of moderate-to-severe, often unilateral headaches and generally accompanied by nausea, vomiting, and increased sensitivity to light (photophobia), sound (phonophobia), and smell (hyperosmia). Photophobia is considered the most bothersome symptom of migraine attacks. Although the underlying [...] Read more.
Migraine is a complex disorder characterized by episodes of moderate-to-severe, often unilateral headaches and generally accompanied by nausea, vomiting, and increased sensitivity to light (photophobia), sound (phonophobia), and smell (hyperosmia). Photophobia is considered the most bothersome symptom of migraine attacks. Although the underlying mechanism remains unclear, the intrinsically photosensitive retinal ganglion cells (ipRGCs) are considered to be involved in photophobia associated with migraine. In this study, we investigated the association between the sensitivity of ipRGCs and migraines and cortical spreading depression (CSD), which may trigger migraine attacks. The pupillary responses closely associated with the function of ipRGCs in patients with migraine who were irradiated with lights were evaluated. Blue (486 nm) light irradiation elicited a response from ipRGCs; however, red light (560 nm) had no such effect. Melanopsin, a photosensitive protein, phototransduces in ipRGCs following blue light stimulation. Hypersensitivity of ipRGCs was observed in patients with migraine. CSD was more easily induced with blue light than with incandescent light using a mouse CSD model. Moreover, CSD was suppressed, even in the presence of blue light, after injecting opsinamide, a melanopsin inhibitor. The hypersensitivity of ipRGCs in patients with migraine may induce CSD, resulting in migraine attacks. Full article
(This article belongs to the Special Issue Novel Therapeutic Approaches for Migraine Headaches)
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21 pages, 8607 KiB  
Article
Constructing a Transient Ischemia Attack Model Utilizing Flexible Spatial Targeting Photothrombosis with Real-Time Blood Flow Imaging Feedback
by Xuan Zhu, Zichao Yi, Ruolan Li, Chen Wang, Wenting Zhu, Minghui Ma, Jinling Lu and Pengcheng Li
Int. J. Mol. Sci. 2024, 25(14), 7557; https://doi.org/10.3390/ijms25147557 - 10 Jul 2024
Cited by 2 | Viewed by 1369
Abstract
Transient ischemic attack (TIA) is an early warning sign of stroke and death, necessitating suitable animal models due to the associated clinical diagnostic challenges. In this study, we developed a TIA model using flexible spatially targeted photothrombosis combined with real-time blood flow imaging [...] Read more.
Transient ischemic attack (TIA) is an early warning sign of stroke and death, necessitating suitable animal models due to the associated clinical diagnostic challenges. In this study, we developed a TIA model using flexible spatially targeted photothrombosis combined with real-time blood flow imaging feedback. By modulating the excitation light using wavefront technology, we precisely created a square light spot (50 × 250 µm), targeted at the distal middle cerebral artery (dMCA). The use of laser speckle contrast imaging (LSCI) provided real-time feedback on the ischemia, while the excitation light was ceased upon reaching complete occlusion. Our results demonstrated that the photothrombus formed in the dMCA and spontaneously recanalized within 10 min (416.8 ± 96.4 s), with no sensorimotor deficits or infarction 24 h post-TIA. During the acute phase, ischemic spreading depression occurred in the ipsilateral dorsal cortex, leading to more severe ischemia and collateral circulation establishment synchronized with the onset of dMCA narrowing. Post-reperfusion, the thrombi were primarily in the sensorimotor and visual cortex, disappearing within 24 h. The blood flow changes in the dMCA were more indicative of cortical ischemic conditions than diameter changes. Our method successfully establishes a photochemical TIA model based on the dMCA, allowing for the dynamic observation and control of thrombus formation and recanalization and enabling real-time monitoring of the impacts on cerebral blood flow during the acute phase of TIA. Full article
(This article belongs to the Section Molecular Pathology, Diagnostics, and Therapeutics)
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12 pages, 251 KiB  
Article
Identification of Polymorphisms in EAAT1 Glutamate Transporter Gene SLC1A3 Associated with Reduced Migraine Risk
by Cassie L. Albury, Heidi G. Sutherland, Alexis W. Y. Lam, Ngan K. Tran, Rod A. Lea, Larisa M. Haupt and Lyn R. Griffiths
Genes 2024, 15(6), 797; https://doi.org/10.3390/genes15060797 - 18 Jun 2024
Cited by 1 | Viewed by 1568
Abstract
Dysfunction in ion channels or processes involved in maintaining ionic homeostasis is thought to lower the threshold for cortical spreading depression (CSD), and plays a role in susceptibility to associated neurological disorders, including pathogenesis of a migraine. Rare pathogenic variants in specific ion [...] Read more.
Dysfunction in ion channels or processes involved in maintaining ionic homeostasis is thought to lower the threshold for cortical spreading depression (CSD), and plays a role in susceptibility to associated neurological disorders, including pathogenesis of a migraine. Rare pathogenic variants in specific ion channels have been implicated in monogenic migraine subtypes. In this study, we further examined the channelopathic nature of a migraine through the analysis of common genetic variants in three selected ion channel or transporter genes: SLC4A4, SLC1A3, and CHRNA4. Using the Agena MassARRAY platform, 28 single-nucleotide polymorphisms (SNPs) across the three candidate genes were genotyped in a case–control cohort comprised of 182 migraine cases and 179 matched controls. Initial results identified significant associations between migraine and rs3776578 (p = 0.04) and rs16903247 (p = 0.05) genotypes within the SLC1A3 gene, which encodes the EAAT1 glutamate transporter. These SNPs were subsequently genotyped in an independent cohort of 258 migraine cases and 290 controls using a high-resolution melt assay, and association testing supported the replication of initial findings—rs3776578 (p = 0.0041) and rs16903247 (p = 0.0127). The polymorphisms are in linkage disequilibrium and localise within a putative intronic enhancer region of SLC1A3. The minor alleles of both SNPs show a protective effect on migraine risk, which may be conferred via influencing the expression of SLC1A3. Full article
(This article belongs to the Section Molecular Genetics and Genomics)
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