Migraine affects up to 20 percent of the global population and ranks as the second leading cause of disability worldwide. In parallel, ischemic stroke stands as the second leading cause of mortality and the third leading cause of disability worldwide. This review aims to elucidate the intricate relationship between migraine and stroke, highlighting the role of genetic, vascular, and hormonal factors. Epidemiological evidence shows a positive association between migraine, particularly with aura, and ischemic stroke (IS), though the link to hemorrhagic stroke (HS) remains inconclusive. The shared pathophysiology between migraine and stroke includes cortical spreading depression, endothelial dysfunction, and genetic predispositions, such as mutations linked to conditions like CADASIL and MELAS. Genetic studies indicate that common loci may predispose individuals to both migraine and stroke, while biomarkers such as endothelial microparticles and inflammatory cytokines offer insights into the underlying mechanisms. Additionally, hormonal influences, particularly fluctuations in estrogen levels, significantly impact migraine pathogenesis and stroke risk, highlighting the need for tailored interventions for women. The presence of a patent foramen ovale (PFO) in migraineurs further complicates their risk profile, with device closure showing promise in reducing stroke occurrence. Furthermore, white matter lesions (WMLs) are frequently observed in migraine patients, suggesting potential cognitive and stroke risks. This review hopes to summarize the links between migraine and its associated conditions and ischemic stroke, recognizing the profound implications for clinical management strategies for both disorders. Understanding the complex relationship between migraine and ischemic stroke holds the key to navigating treatment options and preventive interventions to enhance overall patient outcomes.

Physical activity can worsen migraine, leading to reduced activity levels in adults with chronic migraine. This study investigated the change in average steps per day, as a surrogate marker of physical activity, in adults with chronic migraine successfully treated with monoclonal antibodies against calcitonin gene-related peptide or its receptor. Data were obtained from adults with chronic migraine, who were classified as responders to preventive treatment with monoclonal antibodies. The primary endpoint was the difference in a mean number of steps per day between the 3 months prior to treatment initiation and the first 3 months after treatment initiation. The secondary endpoint was the correlation between the change in steps per day and the change in monthly migraine days. Twenty-two (20 females) participants with a median age of 48.5 years were enrolled. The median number of steps per day increased from 4421 at baseline to 5241 after treatment (P = 0.039). We found a positive correlation between the increase in steps per day and the treatment response (P = 0.013). In conclusion, an increase in physical activity, based on steps per day, positively correlated with treatment response to monoclonal antibodies. Automatically registered daily step count data might be used to monitor physical activity as a response to preventive treatment in adults with chronic migraine.

Patent foramen ovale (PFO) is a prevalent congenital cardiac anomaly associated with a persistent opening between the atrial septum, allowing communication between the left and right atria. Despite often being asymptomatic, PFO can lead to various clinical presentations, including cryptogenic stroke and other embolic events. Transient visual disturbances, alterations in the visual field, migraine with aura, impaired eye movement and endogenous eye infections may prompt patients to seek ophthalmological consultation. Understanding these diverse clinical scenarios is crucial for early detection, appropriate management and mitigating the morbidity burden associated with PFO. This narrative review aims at examining the spectrum of clinical presentations of ocular pictures associated with PFO. The pathophysiology, diagnosis and treatment methods for PFO will be described, emphasizing the importance of a multidisciplinary approach involving ophthalmologists, cardiologists, neurologists and imaging specialists. In the future, prospective studies and clinical trials are warranted to provide further insights into the preventive role and optimal therapeutic strategies for managing PFO-related ocular complications, ultimately guiding clinical decision making and optimizing patient care.

Migraine, classified as a neurovascular disease, has been identified as a potential risk factor for ocular vascular complications. Our study aimed to compare retinal vessel density and perfusion density between subjects with migraine and healthy subjects using optical coherence tomography angiography (OCTA). In this cross-sectional case-control study, we enrolled 30 migraine subjects with aura (MWA), 30 migraine subjects without aura (MWOA) and 30 age and gender-matched healthy controls (HC). The foveal avascular zone (FAZ) in superficial capillary plexus (SCP), Vessel density (VD) and perfusion density (PD) in SCP and deep capillary plexus (DCP) were assessed in a 3 × 3 mm scan of the macula with the swept source OCT. Results indicated that the FAZ of MWA and MWOA subjects was significantly larger from HC. Also, FAZ of MWA was larger from MWOA. VD and PD in both SCP and DCP were significantly reduced in both MWA and MWOA groups compared to HC. However, VD and PD did not show significant differences among MWA and MWOA. Additionally, the duration of disease was the main determinant of the FAZ. In conclusion, the FAZ in the SCP, VD and PD in the SCP and DCP of the macula were affected in both MWA and MWOA. FAZ, specifically, was increased with the evolution of the disease. These findings might contribute to an increased risk of ocular vascular complications among subjects with migraine and could potentially use OCTA as a biomarker for this population.

UNASSIGNED: A growing body of evidence underscores a significant association between neurological disorders, particularly migraines, and the gut microbiota. However, a research gap persists in understanding the cause-and-effect dynamics between these elements. Therefore, we employed robust methodologies aimed at thoroughly exploring the causal relationship between the gut microbiome and migraines.
UNASSIGNED: Employing bidirectional Two Sample Mendelian Randomization (TSMR) analysis, we investigated the causal association between the composition of the gut microbiota and migraines. Data summarizing the relationship between gut microbiota and migraines were extracted from one or more genome-wide association studies. The TSMR analysis employed five methods to assess the correlation between the gut microbiota and migraines, with the inverse variance-weighted method serving as the primary approach for analyzing causal links. Sensitivity analyses were applied to address horizontal pleiotropy and heterogeneity. Simultaneously, a meta-analysis was performed to strengthen the robustness of the findings. Additionally, a reverse TSMR was carried out to explore potential occurrences of reverse causal relationships.
UNASSIGNED: The ongoing TSMR analysis identified a collection of 14 bacterial taxa connected to migraines. Among these, 8 taxa exhibited a protective effect, while 5 taxa had a detrimental impact, and 1 taxon maintained a neutral relationship. The reverse Mendelian randomization analysis highlighted stable outcomes for only one bacterial taxonomic group.
UNASSIGNED: The study confirms a causal relationship between the gut microbiota and migraines, offering a new perspective for migraine research. Strategically targeting specific bacterial taxa with dysregulation may be effective in both preventing and treating migraines, thus opening new avenues for therapeutic strategies.

Recently, interest in sarcopenia has been increasing in patients with various neurological diseases. Thus, we investigated the presence of sarcopenia in patients with episodic migraine (EM) based on temporal muscle thickness (TMT). This was a retrospectively observational study following STROBE guidelines. We enrolled patients with EM and healthy controls. Both groups underwent brain magnetic resonance imaging, including three-dimensional T1-weighted imaging. We calculated the TMT using T1-weighted imaging, which is a marker for sarcopenia. We compared TMT between patients with EM and healthy controls, and analyzed it according to presence of migraine aura. We retrospectively enrolled 82 patients with EM and 53 healthy controls. TMT was not different between patients with EM and healthy controls (10.804 ± 2.045 mm in patients with EM vs 10.721 ± 1.547 mm in healthy controls, P = .801). Furthermore, TMT was not different according to presence of migraine aura in patients with EM (10.994 ± 2.016 mm in patients with migraine aura vs 10.716 ± 2.071 mm in those without, P = .569). There were no correlations between TMT and clinical characteristics in patients with EM, including age, age of onset, duration of migraine, headache intensity, and headache frequency. This study found no statistical difference in TMT between patients with EM and healthy controls or between patients with EM with and without aura. These findings suggest that there is no evidence of sarcopenia in patients with EM.

BACKGROUND:  Migraine is associated with several genetic or acquired comorbidities. Studies conducted in recent years emphasize that the frequency of thrombophilia is high in migraine, especially migraine with aura (MA). Similarly, the presence of white matter lesions (WMLs) on brain magnetic resonance imaging (MRI) scans has been associated with migraine for many years.
OBJECTIVE:  Based on the knowledge that both WMLs and thrombophilia variants are frequently observed in MA, we aimed to investigate whether there is a relationship between genetic thrombophilia and the presence of WMLs in these patients.
METHODS:  The levels of proteins S and C, antithrombin III activities, activated protein C (APC) resistance, antiphospholipid immunoglobulin G/immunoglobulin M (IgG/IgM) and anticardiolipin IgG/IgM antibodies were investigated in 66 MA patients between the ages of 18 and 49 years who presented no cardiovascular risk factors. The presence of WMLs and the Fazekas grade was determined from the brain magnetic resonance imaging (MRI) scans\' T2-weighted and fluid-attenuated inversion recovery (FLAIR) sequence taken from the patients. The rates of WMLs were compared in patients with and without thrombophilia.
RESULTS:  Thrombophilia was detected in 34.8% of the patients, and 27.3% were determined to have WMLs in brain MRI scans. The WMLs were detected in 23.3% of the patients without thrombophilia, in 34.8% of those with thrombophilia, and in 50% of the subjects with multiple thrombophilia disorders. Among the thrombophilia disorders, only APC resistance was significantly more common in patients with WMLs.
CONCLUSIONS:  The results of the present study showed that thrombophilia may be a mechanism that should be investigated in the etiology of increased WMLs in MA.
BACKGROUND:  La migraña se asocia con una serie de comorbilidades genéticas o adquiridas. Los estudios realizados en los últimos años destacan que la frecuencia de trombofilia es elevada en la migraña, especialmente en la migraña con aura (MA). De manera similar, la presencia de lesiones de la sustancia blanca (LSB) en las imágenes por resonancia magnética (RM) del cerebro se ha asociado con la migraña hace muchos años.
OBJECTIVE:  Con base en la información de que se suelen observar tanto LSB como variantes de la trombofilia en MA, nuestro objetivo fue investigar si existe una relación entre la trombofilia genética y la presencia de LSB en estos pacientes. MéTODOS:  Se investigaron los niveles de proteína S y de proteína C, actividades de antitrombina III, resistencia a la proteína C activada (PCA), anticuerpos antifosfolípidos inmunoglobulina G/inmunoglobulina M (IgG/IgM) y anticuerpos anticardiolipina IgG/IgM en 66 pacientes con MA entre 18 y 49 años que no presentaban factores de riesgo cardiovascular. Se determinaron la presencia de LSB y el grado de Fazekas a partir de imágenes por RM del cerebro en la secuencia ponderada en T2 y recuperación de la inversión atenuada de fluido (fluid-attenuated inversion recovery, FLAIR, en inglés) obtenidas de los pacientes. Se compararon las tasas de LSB en pacientes con y sin trombofilia.
RESULTS:  Se detectó trombofilia en el 34,8% de los pacientes y LSB en el 27,3%. Las LSB estuvieron presentes en el 23,3% de los pacientes sin trombofilia, en el 34,8% de los que tenían trombofilia, y en el 50% de los que tenían múltiples trastornos trombofílicos. La resistencia a la PCA fue significativamente más común en aquellos pacientes con LSB. CONCLUSIóN:  Los resultados del presente estudio mostraron que la trombofilia puede ser un mecanismo que debe investigarse en la etiología del aumento de LSB en MA.

A 19-year-old male suffered from sporadic hemiplegic migraine (SHM) for several years and experienced significant pain and disability with sensory and motor disturbances during the migraine headaches. Weakness, abnormal vision, abnormal sensation, one-sided disabling motor weakness, and other signs of SHM were diagnosed. The patient had received previous physical therapy, chiropractic and over-the-counter medications, as well as migraine-specific prescriptions without lasting improvements. Chiropractic BioPhysics® (CBP®) spinal structural rehabilitation protocols were used to increase cervical lordosis and improve cervical muscular strength, mobility, and posture. These protocols include spine-specific prescriptions for Mirror Image® postural exercises, traction, and spinal manipulative therapy. After 24 treatments over eight weeks, all subjective and objective outcomes improved dramatically with a near resolution of all initial symptoms of SHM. There were a significant increase in cervical lordosis and a reduction in forward head posture. The neck disability index improved from 26% to 6%, and all pain scores for all regions improved following treatment. A 10-month follow-up exam showed the outcomes were maintained. SHM is rare and debilitating, is part of the global burden of disease, and is a major cause of disability in the world. Reports of successful conservative and non-conservative long-term treatments for SHM are rare, and there are no clinical trials showing successful treatments for SHM. This successful case demonstrates preliminary evidence that CBP spinal structural rehabilitation may serve as a treatment option for SHM. Future studies are needed to replicate the findings from this case.

Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) is a hereditary small vessel disease of the brain characterized by progressive white matter lesions, subcortical infarcts, and cognitive decline. This autosomal dominant disorder is caused by mutations in the NOTCH3 gene located on chromosome 19, resulting in the accumulation of granular osmiophilic material within the walls of small arteries and arterioles. Clinically, CADASIL typically manifests in mid-adulthood with recurrent ischemic events, migraine with aura, mood disturbances, and cognitive impairment. Neuroimaging plays a crucial role in the diagnosis of CADASIL, with characteristic findings including white matter hyperintensities particularly in the anterior temporal lobe and external capsule.

A 56-year-old right-handed man was referred to our hospital for evaluation of sudden-onset transient quadrantanopia, which was followed by throbbing headache consistent with migraine with aura (MA). Magnetic resonance imaging (MRI) of the right parieto-occipital cortex on admission showed a hyperintense region on diffusion-weighted imaging, which disappeared 7 days later. A small cortical infarct in the parieto-occipital cortex can cause MA-like headache, and the present infarct lesion was only detectable on MRI during the acute phase. Performing MRI for patients with suspected acute MA might help identify the cause of MA-like headache and ensure appropriate management of patients.