Inflammatory response of leptomeninges to a single cortical spreading depolarization.

BACKGROUND: Neurogenic meningeal inflammation is regarded as a key driver of migraine headache. Multiple evidence show importance of inflammatory processes in the dura mater for pain generation but contribution of the leptomeninges is less clear. We assessed effects of cortical spreading depolarization (CSD), the pathophysiological mechanism of migraine aura, on expression of inflammatory mediators in the leptomeninges. METHODS: A single CSD event was produced by a focal unilateral microdamage of the cortex in freely behaving rats. Three hours later intact cortical leptomeninges and parenchyma of ipsi-lesional (invaded by CSD) and sham-treated contra-lesional (unaffected by CSD) hemispheres were collected and mRNA levels of genes associated with inflammation (Il1b, Tnf, Ccl2; Cx3cl1, Zc3h12a) and endocannabinoid CB2 receptors (Cnr2) were measured using qPCR. RESULTS: Three hours after a single unilateral CSD, most inflammatory factors changed their expression levels in the leptomeninges, mainly on the side of CSD. The meninges overlying affected cortex increased mRNA expression of all proinflammatory cytokines (Il1b, Tnf, Ccl2) and anti-inflammatory factors Zc3h12a and Cx3cl1. Upregulation of proinflammatory cytokines was found in both meninges and parenchyma while anti-inflammatory markers increased only meningeal expression. CONCLUSION: A single CSD is sufficient to produce pronounced leptomeningeal inflammation that lasts for at least three hours and involves mostly meninges overlying the cortex affected by CSD. The prolonged post-CSD inflammation of the leptomeninges can contribute to mechanisms of headache generation following aura phase of migraine attack.

Shunt-mediated decompression sickness in a compressed air worker with an atrial septal defect.

We report a compressed air worker who had diffuse cutaneous decompression sickness with pain in his left shoulder and visual disturbance characteristic of migraine aura after only his third hyperbaric exposure. The maximum pressure was 253 kPa gauge with oxygen decompression using the Swanscombe Oxygen Decompression Table. He was found to have a very large right-to-left shunt across a 9 mm atrial septal defect. He had transcatheter closure of the defect but had some residual shunting with release of a Valsalva manoeuvre. Thirty-two other tunnel workers undertook the same pressure profile and activities in the same working conditions during the maintenance of a tunnel boring machine for a total of 233 similar exposures and were unaffected. As far as we are aware this is the first report of shunt-mediated decompression sickness in a hyperbaric tunnel worker in the United Kingdom and the second case reported worldwide. These cases suggest that shunt-mediated decompression sickness should be considered to be an occupational risk in modern compressed air working. A right-to-left shunt in a compressed air worker should be managed in accordance with established clinical guidance for divers.

The Burden of Stroke Mimics Among Hyperacute Stroke Unit Attendees with Special Emphasis on Migraine: A 10-Year Evaluation.

BACKGROUND AND OBJECTIVES: Stroke and migraine are common neurological illnesses that cause tremendous suffering for patients. Certain diseases can mimic the clinical manifestations of an actual stroke. Migraine is one of the most commonly reported stroke mimics. The main goals of this study are to look at the prevalence of stroke mimics on the stroke pathway of Sheffield Teaching Hospitals and how many of them are migraines. MATERIALS AND METHODS: A retrospective service evaluation was conducted at the hyperacute stroke unit (HASU) of the Royal Hallamshire Hospital (RHH) in the United Kingdom. The total admissions from 2013 to 2022 were collected from the Sentinel Stroke National Audit Programme database, and the number of stroke mimics was evaluated each year. The burden of migraine stroke mimics was also evaluated. Then, a one-year sample of stroke mimics was extracted to look for the types of each mimic. RESULTS: From 2013 to 2022, 45.75% (n = 12156) of the stroke pathway patients (n = 26573) were stroke mimics, with an increment of up to 55% in the years 2021 and 2022. During these 10 years, migraine stroke mimics accounted for 10.21% of admissions (n = 1240). The three most common mimics in a one-year sample of stroke pathway patients were migraine (14.70%) (n = 373), functional neurological disorders (FNDs) (7.17%) (n = 182), and Guillain-Barré syndrome (6.66%) (n = 169). Seizures, syncope, and metabolic derangements were reported as mimics in 4.17% (n = 106), 3.14% (n = 80), and 1.77% (n = 45), respectively. CONCLUSIONS: About half of the HASU attendees were stroke mimics rather than actual strokes, and the most common mimics were migraines.

Alice in Wonderland Syndrome (AIWS): prevalence and characteristics in adults with migraine.

OBJECTIVE: Alice in Wonderland Syndrome (AIWS) is a sensory disorder characterized by a distorted somatosensory and/or visual perception. Additionally, distortion of time perception and symptoms of derealization/depersonalization may occur. AIWS is frequently associated with migraine. However, its prevalence, and clinical characteristics remain poorly understood. Here, we investigated the prevalence and features of AIWS in individuals with migraine. We hypothesized AIWS is more frequent in migraine patients with aura than in those without aura. METHODS: This was a prospective cross-sectional cohort study, conducted at a tertiary headache center. Participants with migraine filled out questionnaires, providing details on demographics, headache, AIWS characteristics and the occurrence of transient visual phenomena such as fragmented vision. RESULTS: Of 808 migraine patients, 133 individuals (16.5%, mean age 44.4 ± 13.3 years, 87% women) reported AIWS symptoms throughout their lives. Micro- and/or telopsia (72.9%) were most frequent, followed by micro- and/or macrosomatognosia (49.6%), and macro- and/or pelopsia (38.3%), lasting on average half an hour. AIWS symptoms occurred in association with headache in 65.1% of individuals, and 53.7% had their first AIWS episode at the age of 18 years or earlier. Migraine patients with aura were more likely to report AIWS symptoms than those without aura (19.5% vs. 14.1%, p = 0.04). Participants with AIWS reported a higher incidence of 17 out of the 22 investigated visual phenomena. CONCLUSION: AIWS symptoms appear to be a common lifetime phenomenon in migraine patients. The correlation and clinical parallels between AIWS and migraine aura could indicate shared underlying pathomechanisms.

Persistent aura, visual snow, and other visual symptoms.

In neurology practice, it is common to encounter a variety of visual complaints. Historically, in the absence of known ocular pathology, epilepsy, or insult to the central nervous system, positive symptoms were assumed to be migrainous in origin. This assumption was sometimes made even in the absence of a history of migraine. In the past decade, there has been considerable effort to better delineate and study nonmigrainous visual phenomena, with the most extensive focus on a newly defined syndrome, visual snow syndrome (VSS). The heightened awareness of visual snow as a symptom and syndrome has greatly enhanced the understanding of this visual phenomenon; however, in the last few years, there has been an almost pendulous swing in clinic, with patients now being given the diagnosis of VSS for any dots or flickering they may have in their vision. To avoid clinical misdiagnosis, it is critical that we expand our understanding not just of VSS but also of underlying pathologies that may present similarly. This chapter will review classical migraine aura, persistent migraine aura, visual snow and a number of positive and negative visual complaints that are on the differential when seeing patients with suspected aura or visual snow. This is followed by an in-depth discussion on the current understanding of the presenting symptoms, pathophysiology, evaluation and management of VSS. We also outline secondary causes of visual snow.

Effect of anti-CGRP-targeted therapy on migraine aura: Results of an observational case series study.

INTRODUCTION: Limited clinical evidence is available regarding the potential effectiveness of anti-CGRP monoclonal antibodies for the preventive treatment of migraine with aura. AIM OF THE STUDY: This observational study involved a series of migraine patients affected by either migraine with or without aura, who were investigated for any changes in their frequencies and their migraine aura attack characteristics observed during treatment with anti-CGRP Mabs over a 1-year period. PATIENTS AND METHODS: Twelve migraine patients were included, seven of whom were treated with erenumab, 2 with fremanezumab, and 3 with galcanezumab. Clinical data were collected at baseline, which were defined as 3 months prior to the initiation of treatment, and thereafter at each trimester, over the 1-year treatment period. The parameters included the number of headache and migraine days/month, the frequency of aura episodes, the number of days with acute drug intakes/month, and the scores from the migraine disability status scale (MIDAS), and the Headache Impact Test 6 (HIT-6). RESULTS: Anti-CGRP Mbs antibodies induced significant decreases in mean headache and migraine without aura days per month, the number of days with medication intake, as well as MIDAS and HIT-6 scores (p < 0.0001). In contrast, the anti-CGRP Mab treatment did not appear to impact the frequency of migraine with aura attacks but seemed to reduce both the intensity and the duration of headache phases of migraine aura. Furthermore, some migraine patients referred to having aura attacks without headache over the course of the treatment period. CONCLUSIONS: Based on the above findings, we hypothesize that anti-CGRP Mabs did not influence neuronal and vascular events related to cortical spreading depression (CSD) which is considered the pathophysiological substrate of aura. Conversely, these antibodies are able to counteract, via their peripheral mechanisms of action, the sensitization of the trigemino-vascular pathway which is triggered by CSD. This aforementioned might explain why in our patients, migraine aura attacks remained unchanged in their frequencies, but the headache phases were either reduced or absent.

Characteristics of acute ischemic stroke and unusual aura in patients with migraine with aura.

BACKGROUND: Sometimes migraine aura changes from attack to attack, raising the question of whether the change is heralding an ischemic stroke or an unusual aura. Differentiating unusual migraine aura from the onset of an acute ischemic stroke in patients with migraine with aura (MwA) can be challenging. OBJECTIVE: The aim of this cohort study was to assess clinical characteristics that help distinguish between MwA and minor stroke in patients with a previous history of MwA who presented with suspicion of stroke. METHODS: We interviewed patients with MwA and ischemic stroke (MwA + IS) and patients with MwA and unusual aura, but without ischemic stroke (MwA - IS) from a tertiary hospital using a structured questionnaire. We assessed how symptoms of ischemic stroke or unusual aura differed from usual, that is, the typical aura in each patient. Stroke or exclusion of stroke was verified by multimodal magnetic resonance imaging. RESULTS: Seventeen patients with MwA + IS and twelve patients with MwA - IS were included. New focal neurological symptoms (13/17 [76%] vs. 3/12 [25%]), change of the first symptom (10/17 [59%] vs. 1/12 [8%]), and absence of headache (6/15 [40%] vs. 2/10 [20%]) were more often reported during ischemic stroke. The physical examination was normal in 8/17 (47%) MwA + IS and in 6/12 (50%) MwA - IS patients. In 5/17 (29%) patients with MwA + IS, there were unequivocal physical signs suggestive of stroke such as persistent visual loss, ataxia, or paresis. CONCLUSION: There are clues from the history that might help identify stroke in patients with MwA with changed aura symptoms. These might be particularly useful in patients presenting without physical findings suggestive of stroke.

Grey matter structure within the visual networks in migraine with aura: multivariate and univariate analyses.

BACKGROUND: The visual cortex is involved in the generation of migraine aura. Voxel-based multivariate analyses applied to this region may provide complementary information about aura mechanisms relative to the commonly used mass-univariate analyses. METHODS: Structural images constrained within the functional resting-state visual networks were obtained in migraine patients with (n = 50) and without (n = 50) visual aura and healthy controls (n = 50). The masked images entered a multivariate analysis in which Gaussian process classification was used to generate pairwise models. Generalizability was assessed by five-fold cross-validation and non-parametric permutation tests were used to estimate significance levels. A univariate voxel-based morphometry analysis was also performed. RESULTS: A multivariate pattern of grey matter voxels within the ventral medial visual network contained significant information related to the diagnosis of migraine with visual aura (aura vs. healthy controls: classification accuracy = 78%, p < 0.001; area under the curve = 0.84, p < 0.001; migraine with aura vs. without aura: classification accuracy = 71%, p < 0.001; area under the curve = 0.73, p < 0.003). Furthermore, patients with visual aura exhibited increased grey matter volume in the medial occipital cortex compared to the two other groups. CONCLUSIONS: Migraine with visual aura is characterized by multivariate and univariate patterns of grey matter changes within the medial occipital cortex that have discriminative power and may reflect pathological mechanisms.

A Case of Migraine Aura Status in a Migraine Patient With Typical Aura Without Headache.

Migraine aura status (MAS) is a rare complication of migraine and is listed in the appendix of the International Classification of Headache, Third Edition. MAS occurs in migraine with aura (MwA) patients, with at least three auras occurring over a period of three days. We describe a case of MAS associated with a patient who had a migraine with a typical aura without headache (TAWH). She has experienced only visual auras, including periods of MAS complications, and has not experienced headaches or other auras, including sensory, speech, and motor. The patient is a 45-year-old woman. She had discomfort with visual aura without a headache every two to three months. The visual aura began to gradually darken a portion of the right side of the visual field binocularly, which gradually expanded around it and was surrounded by iridescent flashes running in a zig-zag pattern to the periphery. The area of the visual field abnormality gradually decreased and disappeared after approximately 15 minutes. One day, she had an aura once after dinner, and when she awoke without any trigger after going to bed, the aura appeared and repeated approximately three times. She experienced three to four auras the next day and the day after. In the six-month follow-up period, there was no further recurrence of MAS. Most previous reports of MAS have been associated with typical MwA, and there have been few other reports of MAS associated with TAWH as far as we could investigate.

Pathophysiology of migraine aura.

Migraine aura occurs in about a third of patients with migraine and consists of a group of transient focal neurological symptoms that appear from 5 to 60min and then resolve prior to or in the early phase of a migraine headache attack. Migraine auras may consist of visual, language, unilateral sensory, or motor symptoms. There has been considerable debate as to the origins of the migrainous aura. Investigations during physiologically induced visual auras suggest that the phenomenon of cortical spreading depression or its human equivalent underpins the migraine aura. Single gene defects have been linked to relatively rare forms of the motor subtypes of aura known as familial hemiplegic migraine (FHM). These include CACNA1A (FHM1), ATP1A2 (FHM2), and SCN1A (FHM3). In the familial hemiplegic forms of migraine, the more typical forms of aura are almost always also present. Despite ample epidemiological evidence of increased heritability of migraine with aura compared to migraine without aura, identification of the specific variants driving susceptibility to the more common forms of aura has been problematic thus far. In the first genome-wide association study (GWAS) that focused migraine with aura, a single SNP rs835740 reached genome-wide significance. Unfortunately, the SNP did show statistical significance in a later meta-analysis which included GWAS data from subsequent studies. Here, we review the clinical features, pathophysiological theories, and currently available potential evidence for the genetic basis of migraine aura.

Targeting CGRP pathways and aura: A peripheral site with a central effect.

Targeting CGRP-pathways has substantially expanded our options for treating individuals with migraine. Although the efficacy of these drugs on migraine aura is yet to be fully revealed, it seems from existing studies that CGRP antagonism reduces the number of migraine auras. The present perspective summarizes the evidence linking CGRP to the migraine aura and proposes a model by which targeting the CGRP-pathways and, thus, inhibition the interaction between C- and Aδ-trigeminal fibers might reverse a possible high cortical glutamate level leading to a reduced number of migraine auras.

Migraine Aura-Catch Me If You Can with EEG and MRI-A Narrative Review.

Roughly one-third of migraine patients suffer from migraine with aura, characterized by transient focal neurological symptoms or signs such as visual disturbance, sensory abnormalities, speech problems, or paresis in association with the headache attack. Migraine with aura is associated with an increased risk for stroke, epilepsy, and with anxiety disorder. Diagnosis of migraine with aura sometimes requires exclusion of secondary causes if neurological deficits present for the first time or are atypical. It was the aim of this review to summarize EEG an MRI findings during migraine aura in the context of pathophysiological concepts. This is a narrative review based on a systematic literature search. During visual auras, EEG showed no consistent abnormalities related to aura, although transient focal slowing in occipital regions has been observed in quantitative studies. In contrast, in familial hemiplegic migraine (FHM) and migraine with brain stem aura, significant EEG abnormalities have been described consistently, including slowing over the affected hemisphere or bilaterally or suppression of EEG activity. Epileptiform potentials in FHM are most likely attributable to associated epilepsy. The initial perfusion change during migraine aura is probably a short lasting hyperperfusion. Subsequently, perfusion MRI has consistently demonstrated cerebral hypoperfusion usually not restricted to one vascular territory, sometimes associated with vasoconstriction of peripheral arteries, particularly in pediatric patients, and rebound hyperperfusion in later phases. An emerging potential MRI signature of migraine aura is the appearance of dilated veins in susceptibility-weighted imaging, which may point towards the cortical regions related to aura symptoms ("index vein"). Conclusions: Cortical spreading depression (CSD) cannot be directly visualized but there are probable consequences thereof that can be captured Non-invasive detection of CSD is probably very challenging in migraine. Future perspectives will be elaborated based on the studies summarized.

Clinical Outcomes and Quality of Life after Patent Foramen Ovale (PFO) Closure in Patients with Stroke/Transient Ischemic Attack of Undetermined Cause and Other PFO-Associated Clinical Conditions: A Single-Center Experience.

INTRODUCTION: The aim of this study was to assess clinical outcomes and quality of life after PFO closure in patients with previous stroke/TIA of undetermined cause and in patients with other complex PFO-associated clinical conditions. METHODS: Between July 2009 and December 2019 at our University Cardiology Department, 118 consecutive patients underwent a thorough diagnostic work-up including standardized history taking, clinical evaluation, full neurological examination, screening for thrombophilia, brain magnetic resonance imaging (MRI), ultrasound-Doppler sonography of supra-aortic vessels and 24 h ECG Holter monitoring. Anatomo-morphological evaluation using 2D transthoracic/transesophageal echocardiography (TTE/TEE) color Doppler and functional assessment using contrast TTE (cTTE) in the apical four-chamber view and contrast transcranial Doppler (cTCD) using power M-mode modality were performed to verify the presence, location and amount of right-to-left shunting via PFO or other extracardiac source. Completed questionnaires based on the Quality-of-Life Short Form-36 (QoL SF-36) and Migraine Disability Assessment (MIDAS) were obtained from the patients before PFO closure and after 12 months. Contrast TTE/TEE and cTCD were performed at dismission, 1, 6 and 12 months and yearly thereafter. Brain MRI was performed at 1-year follow-up in 54 patients. RESULTS: Transcatheter PFO closure was performed in 106 selected symptomatic patients (mean age 41.7 ± 10.7 years, range 16-63, 65% women) with the following conditions: ischemic stroke (n = 23), transient ischemic attack (n = 22), peripheral and coronary embolism (n = 2), MRI lesions without cerebrovascular clinical events (n = 53), platypnea-orthodeoxia (n = 1), decompression sickness (n = 1) and refractory migraine without ischemic cerebral lesions (n = 4). The implanted devices were Occlutech Figulla Flex I/II PFO (n = 99), Occlutech UNI (n = 3), Amplatzer PFO (n = 3) and CeraFlex PFO occluders (n = 1). Procedures were performed under local anesthesia and rotational intracardiac monitoring (Ultra ICE) alone. The devices were correctly implanted in all patients. The mean fluoroscopy time was 15 ± 5 min (range = 10-45 min) and the mean procedural time was 55 ± 20 min (range = 35-90 min). The total occlusion rate at follow-up (mean 50 months, range 3-100) was 98.1%. No recurrent neurological events were observed in the long-term follow-up. CONCLUSIONS: The data collected in this study demonstrate that percutaneous PFO closure is a safe and effective procedure, showing long-term prevention of recurrent cerebrovascular events, significant reduction in migraine symptoms and substantial improvement in quality of life.

The Brain's Glymphatic System: Drawing New Perspectives in Neuroscience.

This paper delves into the intricate structure and functionality of the brain's glymphatic system, bringing forth new dimensions in its neuroscientific understanding. This paper commences by exploring the cerebrospinal fluid (CSF)-its localization, production, and pivotal role within the central nervous system, acting as a cushion and vehicle for nutrient distribution and waste elimination. We then transition into an in-depth study of the morphophysiological aspects of the glymphatic system, a recent discovery revolutionizing the perception of waste clearance from the brain, highlighting its lymphatic-like characteristics and remarkable operations. This paper subsequently emphasizes the glymphatic system's potential implications in Alzheimer's disease (AD), discussing the connection between inefficient glymphatic clearance and AD pathogenesis. This review also elucidates the intriguing interplay between the glymphatic system and the circadian rhythm, illustrating the optimal functioning of glymphatic clearance during sleep. Lastly, we underscore the hitherto underappreciated involvement of the glymphatic system in the tumoral microenvironment, potentially impacting tumor growth and progression. This comprehensive paper accentuates the glymphatic system's pivotal role in multiple domains, fostering an understanding of the brain's waste clearance mechanisms and offering avenues for further research into neuropathological conditions.

Near-death experiences are associated with rapid eye movement (REM) sleep intrusions in migraine patients, independent of migraine aura.

BACKGROUND AND PURPOSE: Migraine aura, near-death experiences (NDEs), and rapid eye movement (REM) sleep intrusions might share common mechanisms. Here, we investigated the prevalence of NDEs and REM sleep intrusions in people with migraine. We hypothesized that NDEs and REM sleep intrusions are more prevalent in migraine patients with aura than in those without. METHODS: We conducted a prospective cross-sectional cohort study at a tertiary headache center, based on a prespecified sample size (n = 808). Migraine patients completed a series of questionnaires, including questions about demographic and headache characteristics, the 16-item Greyson NDE scale, four questions about REM sleep intrusions, and the Depression, Anxiety, and Stress Scale 21 (DASS-21). RESULTS: Of 808 migraine patients (mean age 44.4 ± 13.3 years, 87.0% women), 353 (43.7%) had a current or previous history of migraine aura. Prevalence of NDE was 2.7% and not different in patients with and without aura (2.8% vs. 2.6%; p > 0.999). REM sleep intrusions were reported by 5.4% of participants and in a similar proportion of patients with and without aura (6.3% vs. 4.9%; p = 0.43). However, participants with REM sleep intrusions had had an NDE more often than participants without REM sleep intrusions (n = 5/44, 11.4% vs. n = 17/754, 2.2%; p = 0.005). Higher DASS-21 scores were associated with REM sleep intrusions (p < 0.001). CONCLUSIONS: In this tertiary center cohort study, the prevalence of NDE and REM sleep intrusions was not influenced by migraine aura status. However, we identified an association between NDE and REM sleep intrusions, which corroborates the notion that they might share pathophysiological mechanisms.

Migraine with prolonged aphasic aura associated with a CACNA1A mutation: A case report and narrative review.

OBJECTIVE: To demonstrate that a known CACNA1A variant is associated with a phenotype of prolonged aphasic aura without hemiparesis. BACKGROUND: The usual differential diagnosis of prolonged aphasia without hemiparesis includes vascular disease, seizure, metabolic derangements, and migraine. Genetic mutations in the CACNA1A gene can lead to a myriad of phenotypes, including familial hemiplegic migraine (FHM) type 1, an autosomal dominant disorder characterized by an aura of unilateral, sometimes prolonged weakness. Though aphasia is a common feature of migraine aura, with or without hemiparesis, aphasia without hemiparesis has not been reported with CACNA1A mutations. METHODS: We report the case of a 51-year-old male who presented with a history of recurrent episodes of aphasia without hemiparesis lasting days to weeks. His headache was left sided and was heralded by what his family described as "confusion." On examination, he had global aphasia without other focal findings. Family history revealed several relatives with a history of severe headaches with neurologic deficits including aphasia and/or weakness. Imaging revealed T2 hyperintensities in the left parietal/temporal/occipital regions on MRI scan with corresponding hyperperfusion on SPECT. Genetic testing revealed a missense mutation in the CACNA1A gene. CONCLUSIONS: This case expands the phenotypic spectrum of the CACNA1A mutation and FHM to include prolonged aphasic aura without hemiparesis. Our patient's SPECT imaging demonstrated hyperperfusion in areas correlating with aura symptoms which can occur in prolonged aura.

Whole brain surface-based morphometry and tract-based spatial statistics in migraine with aura patients: difference between pure visual and complex auras.

Background: The migrainous aura has different clinical phenotypes. While the various clinical differences are well-described, little is known about their neurophysiological underpinnings. To elucidate the latter, we compared white matter fiber bundles and gray matter cortical thickness between healthy controls (HC), patients with pure visual auras (MA) and patients with complex neurological auras (MA+). Methods: 3T MRI data were collected between attacks from 20 patients with MA and 15 with MA+, and compared with those from 19 HCs. We analyzed white matter fiber bundles using tract-based spatial statistics (TBSS) of diffusion tensor imaging (DTI) and cortical thickness with surface-based morphometry of structural MRI data. Results: Tract-based spatial statistics showed no significant difference in diffusivity maps between the three subject groups. As compared to HCs, both MA and MA+ patients had significant cortical thinning in temporal, frontal, insular, postcentral, primary and associative visual areas. In the MA group, the right high-level visual-information-processing areas, including lingual gyrus, and the Rolandic operculum were thicker than in HCs, while in the MA+ group they were thinner. Discussion: These findings show that migraine with aura is associated with cortical thinning in multiple cortical areas and that the clinical heterogeneity of the aura is reflected by opposite thickness changes in high-level visual-information-processing, sensorimotor and language areas.

Erratum: Migraine aura-like symptoms at onset of stroke and stroke-like symptoms in migraine with aura.

[This corrects the article DOI: 10.3389/fneur.2022.1004058.].

Stroke territory and atherosclerosis in ischemic stroke patients with a history of migraine with aura.

Introduction: The mechanisms subtending the increased stroke risk in migraine with aura (MA) are not fully understood. Our study aims to evaluate if the clinical profile in stroke patients with MA differentiates from those without MA. Methods: We retrieved the prospective registered electronic clinical dossiers of adult patients younger than 60 years with acute ischemic stroke admitted in four hospitals between January 2016 and June 2022. Patients were classified by the history of MA (MA+ and MA-). Results: We identified 851 stroke patients (59 MA+, 6.9%). Compared to MA-, MA+ patients were characterized by younger age (44.0 ± 10.6 vs 50.1 ± 8.2 years), female sex (59.3% vs 29.0%), and affected by cryptogenic (OR 2.594 95% CI 1.483-4.537), and cerebellar stroke (OR 3.218 95% CI 1.657-6.250; p ≤ 0.001 for all comparisons). After adjusting for age and sex, MA+ patients presented less frequently hypertension (OR 0.349 95% CI 0.167-0.470; p=0.005) and dyslipidemia (OR 0.523 95% CI 0.280-0.974; p = 0.041). After adjusting also for risk factors, the MA+ group had less frequently symptomatic large vessel stenosis (OR 0.126 95% CI 0.017-0,924; p = 0.042) and clinical atherosclerosis (OR 0.103 95% CI 0.014-0.761; p = 0.026), while intima-media thickness did not differ (p = 0.395). Discussion: Cryptogenic and cerebellar stroke and fewer vascular risk factors and clinical atherosclerosis seem to characterize stroke patients with MA.

Factors associated with migraine aura mimicking stroke in code stroke.

INTRODUCTION: Migraine with aura (MA) is a frequent stroke simulator that can lead to erroneous diagnosis and subsequent unnecessary acute or secondary prevention treatments. We analyzed clinical and laboratory data of migraine with aura and ischemic stroke patients to detect differences that could help in the diagnosis. METHODS: Retrospective analysis of a consecutive register of code strokes between January 2005 and June 2020. Diagnosis of ischemic stroke or MA was collected. Multivariable logistic regression analyses were performed to test associations between clinical and blood data with ischemic stroke. RESULTS: Of 3140 code strokes, 2424 (77.2%) were ischemic strokes and 34 (1.1%) were MA. Migraine cases were younger, more frequently females and with lower prevalence of vascular risk factors. Initial NIHSS was lower in MA cases, but no differences were seen in fibrinolysis rate (30%). Blood test showed lower levels of glucose, D-dimer, and fibrinogen in MA cases. Multivariable model showed and independent association for ischemic stroke with age [OR, (95%CI): 1.09, (1.07-1.12, p < 0.001], male sex [OR, (95%CI): 4.47, (3.80-5.13), p < 0.001], initial NIHSS [OR, (95%CI): 1.21, (1.07-1.34), p < 0.01], and fibrinogen levels [OR, (95%CI): 1.01, (1.00-1.01), p < 0.05]. A model including sex male OR: 3.55 [2.882; 4.598], p < 0.001, and cutoff points (age > 65, OR: 7.953 [7.256; 8.649], p < 0.001, NIHSS > 6, OR: 3.740 [2.882; 4.598], p < 0.01, and fibrinogen > 400 mg/dL, OR: 2.988 [2.290; 3.686], p < 0.01) showed a good global discrimination capability AUC = 0.89 (95%CI: 0.88-0.94). CONCLUSIONS: In code stroke, a model including age, sex, NIHSS, and fibrinogen showed a good discrimination capability to differentiate between MA and Ischemic stroke. Whether these variables can be implemented in a diagnostic rule should be tested in future studies.