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Background: Migraine is a highly prevalent and complex neurovascular disease. However, the currently available therapeutic drugs often fall to adequately meet clinical needs due to limited effectiveness and numerous undesirable side effects. This study aims to identify putative novel targets for migraine treatment through proteome-wide Mendelian randomization (MR). Methods: We utilized MR to estimate the causal effects of plasma proteins on migraine and its two subtypes, migraine with aura (MA) and without aura (MO). This analysis integrated plasma protein quantitative trait loci (pQTL) data with genome-wide association studies (GWAS) findings for these migraine phenotypes. Moreover, we conducted a phenome-wide MR assessment, enrichment analysis, protein–protein interaction networks construction, and mediation MR analysis to further validate the pharmaceutical potential of the identified protein targets. Results: We identified 35 protein targets for migraine and its subtypes (p < 8.04 × 10–6), with prioritized targets showing minimal side effects. Phenome-wide MR identified novel protein targets—FCAR, UBE2L6, LATS1, PDCD1LG2, and MMP3—that have no major disease side effects and interacted with current acute migraine medication targets. Additionally, MMP3, PDCD1LG2, and HBQ1 interacted with current preventive migraine medication targets. The causal effects of plasma protein on migraine were partly mediated by plasma metabolites (proportion of mediation from 3.8% to 21.0%). Conclusions: A set of potential protein targets for migraine and its subtypes were identified. These proteins showed rare side effects and were responsible for biological mechanisms involved in migraine pathogenesis, indicating priority for the development of migraine treatments. [ABSTRACT FROM AUTHOR]

Transient receptor potential (TRP) channels, first identified in Drosophila in 1969, are multifunctional ion channels expressed in various cell types. Structurally, TRP channels consist of six membrane segments and are classified into seven subfamilies. Transient receptor potential ankyrin 1 (TRPA1), the first member of the TRPA family, is a calcium ion affinity non-selective cation channel involved in sensory transduction and responds to odors, tastes, and chemicals. It also regulates temperature and responses to stimuli. Recent studies have linked TRPA1 to several disorders, including chronic pain, inflammatory diseases, allergies, and respiratory problems, owing to its activation by environmental toxins. Mutations in TRPA1 can affect the sensory nerves and microvasculature, potentially causing nerve pain and vascular problems. Understanding the function of TRPA1 is important for the development of treatments for these diseases. Recent developments in nanomedicines that target various ion channels, including TRPA1, have had a significant impact on disease treatment, providing innovative alternatives to traditional disease treatments by overcoming various adverse effects. [ABSTRACT FROM AUTHOR]

Aims: Anxiety often coexists with migraine, and both conditions share a commonality in oxidative/nitrosative stress and mitochondrial dysfunction contributing to their pathogenesis. β‐Sitosterol, a plant sterol, has shown promise in mitigating oxidative/nitrosative stress, enhancing mitochondrial function, and exerting neuroprotective effects. In this study, we investigated the impact of β‐sitosterol on migraine‐associated anxiety and whether this effect was associated with alleviation of oxidative/nitrosative stress and improvement in mitochondrial function. Methods: Nitroglycerin was used to induce migraine in adult male Wistar rats. β‐Sitosterol treatment consisted of daily intraperitoneal injections (10 mg/kg) for 10 days following migraine induction. Anxiety levels were evaluated using open‐field test (OFT) and hole‐board test (HBT). Frontal cortex samples were analyzed for malondialdehyde (MDA), glutathione (GSH), reactive oxygen/nitrogen species, nitric oxide (NO) (markers of oxidative/nitrosative stress), and ATP (indicator of mitochondrial function). Results: Migraine induction led to impaired performance in both the OFT and the HBT. Concurrently, it elevated MDA, reactive oxygen/nitrogen species, and NO levels while diminishing GSH levels in the frontal cortex, signifying heightened oxidative/nitrosative stress. Moreover, ATP levels decreased, indicating mitochondrial dysfunction. Treatment with β‐sitosterol significantly restored performance in both behavioral assays and normalized the levels of MDA, GSH, reactive oxygen/nitrogen species, NO, and ATP. Conclusion: β‐Sitosterol exerted anxiolytic effects in migraine, which can be attributed to its ability to ameliorate oxidative/nitrosative stress and enhance mitochondrial function. [ABSTRACT FROM AUTHOR]

Background: Migraine risk factors are associated with migraine susceptibility, yet their mechanisms are unclear. Evidence suggests a role for inflammatory proteins and immune cells in migraine pathogenesis. This study aimed to examine the inflammo-immune association between eight migraine risk factors and the disorder. Methods: This study utilized inverse variance weighted (IVW) method and colocalization analysis to explore potential causal relationships between eight migraine risk factors, migraine, 731 immune cells, and 91 circulating inflammatory proteins. Mediation Mendelian randomization (MR) was further used to confirm the mediating role of circulating inflammatory proteins and immune cells between the eight migraine risk factors and migraine. Results: Migraine risk factors are linked to 276 immune cells and inflammatory proteins, with cigarettes smoked per day strongly co-localized with CD33-HLA DR+ cells. Despite no co-localization, 23 immune cells/inflammatory proteins relate to migraine. Depression, all anxiety disorders, and sleep apnea are correlated with migraine, and all anxiety disorders are supported by strong colocalization evidence. However, the mediating effect of inflammatory proteins and immune cells between eight migraine risk factors and migraine has not been confirmed. Conclusion: We elucidate the potential causal relationships between eight migraine risk factors, migraine, immune cells, and inflammatory proteins, enhancing our understanding of the molecular etiology of migraine pathogenesis from an inflammatory-immune perspective. [ABSTRACT FROM AUTHOR]

Iron is an essential metal ion implicated in several cellular processes. However, the reactive nature of iron renders this metal ion potentially dangerous for cells, and its levels need to be tightly controlled. Alterations in the intracellular concentration of iron are associated with different neuropathological conditions, including neurodegeneration with brain iron accumulation (NBIA). As the name suggests, NBIA encompasses a class of rare and still poorly investigated neurodegenerative disorders characterized by an abnormal accumulation of iron in the brain. NBIA is mostly a genetic pathology, and to date, 10 genes have been linked to familial forms of NBIA. In the present review, after the description of the principal mechanisms implicated in iron homeostasis, we summarize the research data concerning the pathological mechanisms underlying the genetic forms of NBIA and discuss the potential involvement of iron in such processes. The picture that emerges is that, while iron overload can contribute to the pathogenesis of NBIA, it does not seem to be the causal factor in most forms of the pathology. The onset of these pathologies is rather caused by a combination of processes involving the interplay between lipid metabolism, mitochondrial functions, and autophagic activity, eventually leading to iron dyshomeostasis. [ABSTRACT FROM AUTHOR]

Background: Headache is a widespread disorder in children, but little is known about the headache prevalence in northwest Italy, on less frequent migraine equivalents, family history, and treatment habits in children., Method: This is an epidemiologic population-based study of a representative sample of children aged 3 to 11 years, conducted in Alba, Italy. We used a self-administered questionnaire to acquire information on gender, age, headache, possible migraine equivalents, family history for various diseases, and treatment habits., Results: We distributed the questionnaire to 1152 children, and a total of 649 questionnaires were successfully completed. In the preschool age, 10.3% (seven boys and nine girls) of children suffered from headache. In school-age children, the prevalence of headache was 31.4% (75 boys and 80 girls; 27% in 6 year olds and 41% at age 9 years). We found a significant correlation between headache and abdominal pain in the entire sample and with cyclic vomiting syndrome and dizziness in school-age children only. Headache correlated significantly with a family history of headache, thyroid diseases, diabetes, hypertension, and vascular diseases. Headache was treated with drugs, primarily paracetamol, in 60 of the 171 (35%) children who reported headache and in 61% of the children with migraine; no subjects were treated with triptans., Conclusions: Headache is widespread in children, with a high prevalence of associated symptoms and family history for many other headache-related disorders., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Sleep disorders are prevalent neurological conditions linked to neurocognitive impairments. Understanding the neuroplasticity changes in the hippocampus, which plays a central role in regulating neurocognitive function, is crucial in the context of sleep disorders. However, research on neurodegenerative disorders and the influence of sleep disorders on hippocampal neuroplasticity remains largely unclear. Therefore, this review aims to highlight the latest advancements regarding hippocampal neuroplasticity and functional changes during sleep disorders, drawing insights from clinical and preclinical research involving sleep-deprived animal models. These articles were gathered through comprehensive literature searches across databases, including Google Scholar, PubMed, Web of Science, and Scopus. Maternal sleep deprivation has been observed to cause neurocognitive impairment in offspring, along with changes in protein expression levels associated with neuroplasticity. Similarly, sleep deprivation in adult mice has been shown to affect several cognitive functions and fear extinction without influencing the acquisition of fear conditioning. While mechanistic research on neurocognitive dysfunction induced by maternal and adult sleep deprivation is limited, it suggests the involvement of several signaling pathways, including neurotrophic factors, synaptic proteins, and inflammatory molecules, which are triggered by sleep deprivation. Further studies are needed to clarify the mechanistic pathways underlying hippocampal dysfunction and synaptic alterations associated with sleep disturbances. [ABSTRACT FROM AUTHOR]

Sneddon's syndrome is a rare vascular disease affecting mainly skin and brain arterioles leading to their occlusion due to excessive endothelial proliferation. The two main features of this syndrome are livedo reticularis and lacunar subcortical infarcts. Here, we describe the case of a 64-year-old woman presenting with a 4-year history of a throbbing, bilateral, parieto-occipital headache associated with facial pain, but without any other accompanying symptom. The pain, initially misdiagnosed as atypical trigeminal neuralgia, worsened up to chronic daily and such severely disabling headache that she was constrained to bed. She presented with reduced cognitive functions, diffuse and severe livedo reticularis, severe myalgias and mild stiffness. All diagnostic test for different diseases were performed and other diseases excluded except for Sneddon's syndrome. Her symptoms were reduced firstly using acetylsalicylic acid, then ticlopidine 250 mg bid was begun and then Pentoxyphillin, resulting in a significant improvement of symptoms with the disappearance of headache. Her worsening in the first year was characterized by obsessive-compulsive behaviours, body-image misperceptions and panic attacks, improved for a period using olanzapine. Considering this case, we remark the importance of using headache classification to avoid diagnostic errors, secondly, we describe an atypical manifestation of Sneddon's syndrome and therapeutic efficacy of using ticlopidine and pentoxyphillin. [ABSTRACT FROM AUTHOR]

Background: Migraine is a complex biochemical dysfunction attributed to a disorder of the trigeminal and hypothalamic pathways. Impairment of glucose metabolism has been reported in migraine, but data are scanty and inconsistent., Objective: The main aim was to verify whether migraineurs have abnormalities of the glucose and insulin metabolism. We also studied correlations between blood glucose and insulin and between insulin levels and migraine severity., Patients and Methods: Patients with migraine or headache other than migraine, and healthy volunteers were included. All had general blood tests and a standard oral glucose tolerance test after a 12-hour fast, and glucose and insulin were measured., Results: Over a 6-month period, we recruited 84 migraineurs (73 women, 11 men), 25 patients with nonmigraine headache (20 women, 5 men), and 26 healthy controls (24 women, 2 men). Multivariate analysis confirmed a significant difference between groups for glucose levels (P < .0001), but no significant time interaction. The differences were mostly between migraine and healthy controls (P < .0001) and to a lesser extent between other headaches and healthy controls (P < .05). A significant difference between groups was also found for insulin (P < .0001), with a significant time interaction. The difference was confirmed for migraine compared to other headaches (P < .0001) and healthy controls (P < .0001)., Conclusions: Blood glucose levels may be high in headache patients, but do not seem to be specific to migraineurs. Insulin levels were higher in migraineurs, and seemed specific to this group. These findings are in keeping with recent reports on the effects of insulin on brain functions and lend support to the possibility that insulin is involved in the pathogenesis of migraine.

Vertiginous epilepsy (VE) is a rare and underrecognized epilepsy subtype in the pediatric population. Vertiginous symptoms are the sole or predominant feature, arise from the vestibular cortex, and seizures are usually brief. The incidence is estimated to be between six and 15 percent of pediatric patients presenting with dizziness. Diagnosis is often delayed for many years following the onset of symptoms, as there are no widely accepted diagnostic criteria. Diagnostic workup should include a detailed history, physical exam, EEG, and brain imaging with MRI. Vestibular testing is helpful if peripheral vestibulopathy is suspected. Vertiginous epilepsy can have many possible causes, but a large majority are idiopathic or suspected to be genetic. Most patients with vertiginous epilepsy achieve seizure freedom with anti-seizure medications. [ABSTRACT FROM AUTHOR]

Copyright of Osmangazi Journal of Medicine / Osmangazi Tip Dergisi is the property of Eskisehir Osmangazi University and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: The pathogenesis of migraine remains unclear; however, a large body of evidence supports the hypothesis that immunological mechanisms play a key role. Therefore, we aimed to review current studies on altered immunity in individuals with migraine during and outside attacks. Methods: We searched the PubMed database to investigate immunological changes in patients with migraine. We then added other relevant articles on altered immunity in migraine to our search. Results: Database screening identified 1,102 articles, of which 41 were selected. We added another 104 relevant articles. We found studies reporting elevated interictal levels of some proinflammatory cytokines, including IL-6 and TNF-α. Anti-inflammatory cytokines showed various findings, such as increased TGF-β and decreased IL-10. Other changes in humoral immunity included increased levels of chemokines, adhesion molecules, and matrix metalloproteinases; activation of the complement system; and increased IgM and IgA. Changes in cellular immunity included an increase in T helper cells, decreased cytotoxic T cells, decreased regulatory T cells, and an increase in a subset of natural killer cells. A significant comorbidity of autoimmune and allergic diseases with migraine was observed. Conclusions: Our review summarizes the findings regarding altered humoral and cellular immunological findings in human migraine. We highlight the possible involvement of immunological mechanisms in the pathogenesis of migraine. However, further studies are needed to expand our knowledge of the exact role of immunological mechanisms in migraine pathogenesis. [ABSTRACT FROM AUTHOR]

Background and Objectives: From the year 1 anno Domini until 1855, with the third plague, major pandemics occurred on average every 348 years. Since then, they have occurred on average every 33 years, with coronavirus disease 2019 (COVID-19) now underway. Even though current technologies have greatly improved the way of life of human beings, COVID-19, with more than 700,000,000 cases and 6,950,000 deaths worldwide by the end of 2023, reminds us that much remains to be done. This report looks back at 18 months of COVID-19, from March 2020 to August 2021, with the aim of highlighting potential solutions that could help mitigate the impact of future pandemics. Materials and Methods: COVID-19 data, including case and death reports, were extracted daily from the Worldometer platform to build a database for the macroscopic analysis of the spread of the virus around the world. Demographic data were integrated into the COVID-19 database for a better understanding of the spatial spread of the SARS-CoV-2 virus in cities/municipalities. Without loss of generality, only data from the top 30 (out of 200 and above) countries ranked by total number of COVID-19 cases were analyzed. Statistics (regression, t-test (p < 0.05), correlation, mean ± std, etc.) were carried out with Excel software (Microsoft® Excel® 2013 (15.0.5579.1001)). Spectral analysis, using Matlab software (license number: 227725), was also used to try to better understand the temporal spread of COVID-19. Results: This study showed that COVID-19 mainly affects G20 countries and that cities/municipalities with high population density are a powerful activator of the spread of the virus. In addition, spectral analysis highlighted that the very first months of the spread of COVID-19 were the most notable, with a strong expansion of the SARS-CoV-2 virus. On the other hand, the following six months showed a certain level of stability, mainly due to multiple preventive measures such as confinement, the closure of non-essential services, the wearing of masks, distancing of 2 m, etc. Conclusion: Given that densely populated cities and municipal areas have largely favored the spread of the SARS-CoV-2 virus, it is believed that such a demographic context is becoming a societal problem that developed countries must address in a manner that is adequate and urgent. COVID-19 has made us understand that it is time to act both preventatively and curatively. With phenomenological evidence suggesting that the next pandemic could occur in less than 50 years, it may be time to launch new societal projects aimed at relieving congestion in densely populated regions. [ABSTRACT FROM AUTHOR]

Background and aim: White matter hyperintensities (WMHs), presented on T2- weighted or fluid-attenuated inversion recovery magnetic resonance imaging (MRI) sequences, are lesions in the human brain that can be observed in both migraine and multiple sclerosis (MS). Methods: Seventeen migraine patients and 15 patients with relapsing-remitting multiple sclerosis with WMHs, and 17 healthy subjects age-and sex-matched to the migraine group were prospectively enrolled and underwent conventional and advanced MRI studies with diffusion-and perfusion-weighted imaging and single voxel proton magnetic resonance spectroscopy. Results: In both disease groups, elevated T2 relaxation time, apparent diffusion coefficient (ADC) values, and decreased N-acetyl-aspartate levels were found in the intralesional white matter compared to the contralateral normalappearing white matter (NAWM), while there was no difference between the hemispheres of the control subjects. Migraine patients had the lowest intralesional creatine + phosphocreatine and myo-inositol (mI) values among the three groups, while patients with MS showed the highest intralesional T1 and T2 relaxation times, ADC, and mI values. In the contralateral NAWM, the same trend with mI changes was observed in migraineurs and MS patients. No differences in perfusion variables were observed in any groups. Conclusion: Our multimodal study showed that tissue damage is detectable in both diseases. Despite the differences in various advanced MRI measures, with more severe injury detected in MS lesions, we could not clearly differentiate the two white matter lesion types. [ABSTRACT FROM AUTHOR]

Migraine and severe headaches are extremely prevalent neurological disorders that plague humans and society. Prior research has revealed that DII may affect the occurrence of migraines, but there are too few relevant studies and more are required. This study aimed to determine the association between severe headache or migraine and the Dietary Inflammatory Index (DII), with particular attention to age and gender differences. Using data from the National Health and Nutrition Examination Survey (NHANES), we performed a cross-sectional study. In addition, we investigated the association between DII and severe headache or migraine using weighted multivariate logistic regression models, and restricted cubic splines models were plotted to explore their linear correlation. There were a total of 13,439 people participating in the study, and of those, 2745 experienced a severe headache or migraine within the previous three months. The DII was linearly and positively correlated with severe headache or migraine (odds ratio [OR] = 1.05, 95% confidence interval [CI] = 1.01–1.08, p = 0.0051). Stratified analysis showed that this relationship persisted among women and those aged < 60 years, with ORs of 1.08 (95% CI = 1.04–1.13, p = 0.0004) and 1.05 (95% CI = 1.01–1.09, p = 0.0071), respectively. We found that greater levels of DII were significantly related to an increased likelihood of migraine onset, especially among women and young and middle-aged populations. Further research is required to validate and expand upon our results. [ABSTRACT FROM AUTHOR]

Nineteen patients with mild or moderate chronic respiratory insufficiency, mean age, 63.3 y., have been investigated with pulmonary function tests, clinical examination and somatosensory (SEPs), visual (VEPs) and brainstem auditory (BAEPs) evoked potentials. Nineteen age and sex matched subjects acted as controls. None of the subjects had conditions known to affect the central nervous system (CNS). SEP N20 latency was significantly prolonged in 7 out of 19 patients and its mean value in the patients' group was significantly higher (21.02 vs 19.49 msec p < 0.001). VEP P100 latency was prolonged in the patients' group in 16/38 and 15/38 eyes with spatial frequencies of 30' and 15' of arc respectively. The P100 mean value was also significantly prolonged in the patients' group for both eyes and spatial frequencies (108.08 vs 101.87 msec p < 0.001 and 115.82 vs 107.63 msec p < 0.001 for spatial frequencies of 30' and 15' respectively). No significant difference was evident with BAEPs The data seem to support the hypothesis of a subclinical involvement of CNS in these cases, with preferential damage to the newer phylogenetic structures.

Background: With the spread and rise in the number of infections of COVID-19 globally, patients experienced neurologic manifestations such as headache and dizziness, along with other serious medical conditions such as stroke and seizures. Many reported cases highlighted headache to be one of the most common COVID-19-related neurological symptoms. With the evolution of the pandemic, broad studies are needed to better understand the mechanism of headache with COVID-19. The aim of this study is to recognize the epidemiology, characteristic and progression of headache among patients with COVID-19 in Lebanon. Methods: A retrospective cohort study was done to assess 439 patients for headache during the course of COVID-19. The Statistical Package for Social Sciences (SPSS) version 26 was used for descriptive analysis. Results: A confirmed COVID-19 Infection by PCR test was confirmed among 86% of the participants. Tension-like headache was the most common type of headache experienced by participants during COVID-19. Pain was mainly diffuse (48.7%), and compressing in nature (77.0%). Moreover, about 29% required a physician consultation and 7.7% had emergency visits. Partial relief by analgesics was reported in 54.9%, and mainly by paracetamol (64.6%). Those who reported having a history of primary headache before contracting COVID-19 were 46.7%. Among them, 36.7% patients reported a change in the type of headache and about 49.6% reported increased severity. Conclusion: Headache accompanied with COVID-19 is a common symptom during the early stages of illness. COVID-19 related headache was characterized as mainly involving the whole head region, pressuring, and partially relieved by analgesics. Thus, headache should raise early concern for the probability of being infected by COVID-19. [ABSTRACT FROM AUTHOR]

Introduction: Hashimoto's thyroiditis (HT) is nowadays the leading cause of hypothyroidism with high and still growing prevalence in general population, but there are lack of data regarding migraine and HT connection. Methods: The aim of this study was to analyze the prevalence of HT in migraine and to check if the presence of HT influence migraine severity. This retrospective observational cohort study involved consecutive migraine patients consulted at our Headache Center with diagnosis of migraine. Electronic charts of patients were collected, including data on migraine type, presence of cranial autonomic symptoms (CAS), monthly migraine days (MMD), medication overuse headache (MOH), and the presence of comorbidities including HT. Results: We found 928 eligible migraine patients, 88.7% were women. The mean age was 36.09 years. 592 (63.8%) were diagnosed with episodic migraine (EM), the rest with chronic migraine (CM). MOH was additionally diagnosed in 258 (27.8%) patients. The duration of migraine was 15.99 years. 106 (11.4%) was diagnosed with HT, 148 (15.9%) with hypothyroidisms, while 84 (9.05%) had both diagnosis. Migraine patients with HT were significantly older (p < 0.001), were more frequently women (p = 0.0017), had longer duration of migraine (p < 0.001), had CAS more frequently (<0.001), developed CM (p = 0.0169) and depression more frequently (p = 0.0047) and had more MMD (p = 0.0195) as compared with individuals without HT. According to our multivariate logistic model, the presence CM was positively associated with HT (OR 1.76, p = 0.045), MOH and duration of migraine, while negatively associated with aura. Conclusion: HT is very prevalent in migraine patients. This is the first study considering migraine and HT to be comorbid and suggesting that HT may influence the course of migraine causing its chronification. [ABSTRACT FROM AUTHOR]

Migraine is a disabling neurovascular disorder among people of all ages, with the highest prevalence in the fertile years, and in women. Migraine impacts the quality of life of affected individuals tremendously and, in addition, it is associated with highly prevalent metabolic diseases, such as obesity, diabetes mellitus and thyroid dysfunction. Also, the clinical response to drugs might be affected in patients with metabolic disease due to body composition and metabolic change. Therefore, the efficacy of antimigraine drugs could be altered in patients with both migraine and metabolic disease. However, knowledge of the pharmacology and the related clinical effects of antimigraine drugs in patients with metabolic disease are limited. Therefore, and given the clinical relevance, this article provides a comprehensive overview of the current research and hypotheses related to the influence of metabolic state and body composition on the action of antimigraine drugs. In addition, the influence of antimigraine drugs on metabolic functioning and, vice versa, the influence of metabolic diseases and its hormonal modulating medication on migraine activity is outlined. Future exploration on personalizing migraine treatment to individual characteristics is necessary to enhance therapeutic strategies, especially given its increasing significance in recent decades. [ABSTRACT FROM AUTHOR]

Background: Several risk factors are associated with the chronic evolution of migraine. Clinical and preclinical studies have provided data about the role of hypertension (HT) as one of the potential modifiable risk factors of chronic migraine (CM). This review is focused on the biological and clinical evidence supporting common mechanisms underlying HT and migraine and the potential role of HT in the transition from episodic to chronic migraine. Methods: We conducted a narrative review from a literature search covering the available evidence from studies investigating: i) the role of HT in the transition to CM in clinical practice; ii) the biological mechanisms potentially underpinning the association between HT and evolution to CM; iii) the role of antihypertensive medications in migraine prophylaxis. Results: HT proved to be at the base of multiple mechanisms underlying migraine and migraine chronicization. Endothelial dysfunction, blood–brain barrier alterations, calcitonin gene-related peptide signaling, and renin–angiotensin–aldosterone system dysregulation are involved in the worsening effect of HT on migraine frequency, and the role of HT in the transition to CM is supported by clinical observations. Conclusions: The observed evidence supports HT contribution to CM evolution due to shared pathophysiologic mechanisms. While a bidirectional influence appears to be ascertained, data are still lacking about the one-way role of HT as direct risk factor for CM transition. Further research is needed to confirm a causal role of HT in this process. [ABSTRACT FROM AUTHOR]

Migraine is a highly prevalent neurological disorder. Among the risk factors identified, psychiatric comorbidities, such as depression, seem to play an important role in its onset and clinical course. Patients with migraine are 2.5 times more likely to develop a depressive disorder; this risk becomes even higher in patients suffering from chronic migraine or migraine with aura. This relationship is bidirectional, since depression also predicts an earlier/worse onset of migraine, increasing the risk of migraine chronicity and, consequently, requiring a higher healthcare expenditure compared to migraine alone. All these data suggest that migraine and depression may share overlapping biological mechanisms. Herein, this review explores this topic in further detail: firstly, by introducing the common epidemiological and risk factors for this comorbidity; secondly, by focusing on providing the cumulative evidence of common biological aspects, with a particular emphasis on the serotoninergic system, neuropeptides such as calcitonin-gene-related peptide (CGRP), pituitary adenylate cyclase-activating polypeptide (PACAP), substance P, neuropeptide Y and orexins, sexual hormones, and the immune system; lastly, by remarking on the future challenges required to elucidate the etiopathological mechanisms of migraine and depression and providing updated information regarding new key targets for the pharmacological treatment of these clinical entities. [ABSTRACT FROM AUTHOR]

Acute encephalitis syndrome (AES) is a serious disorder characterized by the sudden onset of inflammation in the brain, which may lead to life-threatening clinical situations. This syndrome encompasses a range of neurological disorders, including, but not limited to, viral and bacterial infections, toxins, and metabolic causes. It includes a wide array of spectrum of diseases, and diagnosis is based on clinical symptoms and a wide range of investigations. Treatment is usually symptomatic, and in some instances, definitive treatment is available. Long-term sequelae of AES can include cognitive deficits, behavioral changes, motor impairments, and epilepsy. Rehabilitation and supportive care are often necessary. [ABSTRACT FROM AUTHOR]

Migraine, a neurovascular headache disorder, is a leading cause of disability worldwide. Within the multifaceted pathophysiology of migraine, hormonal fluctuations play an evident triggering and exacerbating role, pointing toward the need for identification and proper usage of both existing and new hormonal targets in migraine treatment. With a threefold higher incidence of migraine in women than in men, the authors delve into sex hormone-related events in migraine patients. A comprehensive overview is given of existing hormonal therapies, including oral contraceptives, intrauterine devices, transdermal and subcutaneous estradiol patches, gnRH-agonists, oral testosterone, and 5α reductase inhibitors. The authors discuss their effectiveness and risks, noting their suitability for different patient profiles. Next, novel evolving hormonal treatments, such as oxytocin and prolactin, are explored. Lastly, the authors cover hormonal conditions associated with migraine, such as polycystic ovary syndrome, endometriosis, and transgender persons receiving gender affirming hormone therapy, aiming to provide more personalized and effective solutions for migraine management. Rigorous research into both existing and new hormonal targets, as well as the underlying pathophysiology, is needed to support a tailored approach in migraine treatment, in an ongoing effort to alleviate the impact of migraine on individuals and society. [ABSTRACT FROM AUTHOR]

Enhancement of vascular remodeling in affected brain tissue is a novel therapy for acute ischemic stroke (AIS). However, conclusions regarding angiogenesis after AIS remain ambiguous. Vascular endothelial growth factor A (VEGFA) and VEGF receptor 2 (VEGFR2) are potent regulators of angiogenesis and vascular permeability. We aimed to investigate the association between VEGFA/VEGFR2 expression in the acute stage of stroke and prognosis of patients with AIS. We enrolled 120 patients with AIS within 24 h of stroke onset and 26 healthy controls. Plasma levels of VEGFA and VEGFR2 were measured by enzyme-linked immunosorbent assay (ELISA). The primary endpoint was an unfavorable outcome defined as a modified Rankin Scale (mRS) score > 2 at 3 months after AIS. Univariate and multivariate logistic regression analyses were used to identify risk factors affecting prognosis. Plasma VEGFA and VEGFR2 were significantly higher in patients with AIS than in health controls, and also significantly higher in patients with unfavorable than those with favorable outcomes. Moreover, both VEGFA and VEGFR2 showed a significantly positive correlation with mRS at 3 months. Univariate and multivariate analyses showed VEGFA and VEGFR2 remained associated with unfavorable outcomes, and adding VEGFA and VEGFR2 to the clinical model significantly improved risk reclassification (continuous net reclassification improvement, 105.71%; integrated discrimination improvement, 23.45%). The new risk model curve exhibited a good fit with an area under the receiver operating characteristic curve (ROC) curve of 0.9166 (0.8658-0.9674). Plasma VEGFA and VEGFR2 are potential markers for predicting prognosis; thus these two plasma biomarkers may improve risk stratification in patients with AIS., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

The reduced pathogenicity of the omicron BA.1 sub-lineage compared to earlier variants is well described, although whether such attenuation is retained for later variants like BA.5 and XBB remains controversial. We show that BA.5 and XBB isolates were significantly more pathogenic in K18-hACE2 mice than a BA.1 isolate, showing increased neurotropic potential, resulting in fulminant brain infection and mortality, similar to that seen for original ancestral isolates. BA.5 also infected human cortical brain organoids to a greater extent than the BA.1 and original ancestral isolates. In the brains of mice, neurons were the main target of infection, and in human organoids neuronal progenitor cells and immature neurons were infected. The results herein suggest that evolving omicron variants may have increasing neurotropic potential. [ABSTRACT FROM AUTHOR]

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Exposure to traffic-related air pollution (TRAP) generates oxidative stress, with downstream effects at the metabolic level. Human studies of traffic density and metabolomic markers, however, are rare. The main objective of this study was to evaluate the cross-sectional association between traffic density in the street of residence with oxidative stress and metabolomic profiles measured in a population-based sample from Spain. We also explored in silico the potential biological implications of the findings. Secondarily, we assessed the contribution of oxidative stress to the association between exposure to traffic density and variation in plasma metabolite levels. Traffic density was defined as the average daily traffic volume over an entire year within a buffer of 50 m around the participants' residence. Plasma metabolomic profiles and urine oxidative stress biomarkers were measured in samples from 1181 Hortega Study participants by nuclear magnetic resonance spectroscopy and high-performance liquid chromatography, respectively. Traffic density was associated with 7 (out of 49) plasma metabolites, including amino acids, fatty acids, products of bacterial and energy metabolism and fluid balance metabolites. Regarding urine oxidative stress biomarkers, traffic associations were positive for GSSG/GSH% and negative for MDA. A total of 12 KEGG pathways were linked to traffic-related metabolites. In a protein network from genes included in over-represented pathways and 63 redox-related candidate genes, we observed relevant proteins from the glutathione cycle. GSSG/GSH% and MDA accounted for 14.6% and 12.2% of changes in isobutyrate and the CH2CH2CO fatty acid moiety, respectively, which is attributable to traffic exposure. At the population level, exposure to traffic density was associated with specific urine oxidative stress and plasma metabolites. Although our results support a role of oxidative stress as a biological intermediary of traffic-related metabolic alterations, with potential implications for the co-bacterial and lipid metabolism, additional mechanistic and prospective studies are needed to confirm our findings. [ABSTRACT FROM AUTHOR]

Background: Systemic infection has always been considered a relative contraindication to neuraxial anesthesia, despite the fact that infectious complications are relatively uncommon. Pregnancy-related physiological changes and coronavirus disease (COVID-19) neurotropic features may facilitate the virus' entry into the central nervous system. The principal aim of this study was to test the safety of spinal anesthesia in "severe acute respiratory syndrome coronavirus 2" (SARS-CoV-2)-positive pregnant women and to examine cerebrospinal fluid (CSF) characteristics. Methods: We conducted a prospective observational single-center study in asymptomatic or paucisymptomatic consecutive pregnant SARS-CoV-2 patients who underwent spinal anesthesia for cesarean section. Women with severe infection were excluded because they underwent general anesthesia. At the time of spinal anesthesia, we collected CSF samples, and then we performed a chemical-physical analysis to look for signs of inflammation and for SARS-CoV-2 genome. Results: We included 26 women. No spinal anesthesia complications were reported in the perioperative period and after 2 months. All CSF samples were crystal clear, and all physical-chemical values were within physiological ranges: the median concentration of CSF/plasma glucose ratio was 0.66, IQR 0.5500 (0.6000–0.7100), and the average CSF protein concentration value was 23.2 mg/dl (SD 4.87). In all samples, genomes of SARS-CoV-2 and other neurotropic viruses were not detected. Conclusions: Spinal anesthesia was safe in SARS-CoV-2 pregnant women with mild disease; no clinical maternal complications were detected, and no CSF changes indicative of inflammatory or infectious diseases that would compromise the safety of the procedure were found. [ABSTRACT FROM AUTHOR]

Background: Polycystic ovary syndrome (PCOS) and migraine headaches are considered to be common health problems that may share some risk factors. This study aimed to discuss the possible association between migraine headache and polycystic ovary syndrome., Methods and Results: In this narrative review, PubMed, Scopus, Web of Science, and Google Scholar were systematically searched for retrieving and summarizing published studies up to January 2021 to explore the possible interplay between migraine headache and PCOS. We discuss the possible pathways that may explain the association between migraine headaches and PCOS signs/symptoms and complications. While genetic factors have profound effects on the pathogenesis of migraine headaches, sex hormones, including estrogen and progesterone may also play an important role in inducing migraine headaches. Some disorders, such as sleep apnea, amenorrhea, and vascular disease that are more likely to occur in women with PCOS, may cause or exacerbate migraine headaches in women with PCOS., Conclusions: Future comprehensive studies are needed to investigate the exact underlining mechanisms related to the association between PCOS and migraine headaches., (© 2021. The Author(s), under exclusive licence to Springer Nature B.V.)

Ferroptosis, a regulated form of cellular death characterized by the iron-mediated accumulation of lipid peroxides, provides a novel avenue for delving into the intersection of cellular metabolism, oxidative stress, and disease pathology. We have witnessed a mounting fascination with ferroptosis, attributed to its pivotal roles across diverse physiological and pathological conditions including developmental processes, metabolic dynamics, oncogenic pathways, neurodegenerative cascades, and traumatic tissue injuries. By unraveling the intricate underpinnings of the molecular machinery, pivotal contributors, intricate signaling conduits, and regulatory networks governing ferroptosis, researchers aim to bridge the gap between the intricacies of this unique mode of cellular death and its multifaceted implications for health and disease. In light of the rapidly advancing landscape of ferroptosis research, we present a comprehensive review aiming at the extensive implications of ferroptosis in the origins and progress of human diseases. This review concludes with a careful analysis of potential treatment approaches carefully designed to either inhibit or promote ferroptosis. Additionally, we have succinctly summarized the potential therapeutic targets and compounds that hold promise in targeting ferroptosis within various diseases. This pivotal facet underscores the burgeoning possibilities for manipulating ferroptosis as a therapeutic strategy. In summary, this review enriched the insights of both investigators and practitioners, while fostering an elevated comprehension of ferroptosis and its latent translational utilities. By revealing the basic processes and investigating treatment possibilities, this review provides a crucial resource for scientists and medical practitioners, aiding in a deep understanding of ferroptosis and its effects in various disease situations. [ABSTRACT FROM AUTHOR]

Iron accumulation in the CNS occurs in many neurological disorders. It can contribute to neuropathology as iron is a redox-active metal that can generate free radicals. The reasons for the iron buildup in these conditions are varied and depend on which aspects of iron influx, efflux, or sequestration that help maintain iron homeostasis are dysregulated. Iron was shown recently to induce cell death and damage via lipid peroxidation under conditions in which there is deficient glutathione-dependent antioxidant defense. This form of cell death is called ferroptosis. Iron chelation has had limited success in the treatment of neurological disease. There is therefore much interest in ferroptosis as it potentially offers new drugs that could be more effective in reducing iron-mediated lipid peroxidation within the lipid-rich environment of the CNS. In this review, we focus on the molecular mechanisms that induce ferroptosis. We also address how iron enters and leaves the CNS, as well as the evidence for ferroptosis in several neurological disorders. Finally, we highlight biomarkers of ferroptosis and potential therapeutic strategies. [ABSTRACT FROM AUTHOR]

Background: Migraine is one of the most common neurological disorders that can severely overshadow people's quality of life, and Helicobacter pylori infection is a health problem in different societies. During the last two decades, many original studies have been conducted on the various aspects of the relationship between these two disorders; however, they have reported different and sometimes contradictory results. Methods: This study was conducted based on the PRISMA protocol. We performed a comprehensive literature search in the online databases up to May 2023, and 22 studies that contained original data on the relationship between H. pylori infection and migraine headaches in adults were included. For performing the meta‐analysis, we calculated the odds ratios (OR) and 95% confidence intervals (CI), using a random‐effects model, and to determine the possible causes of heterogeneity, we conducted a subgroup meta‐analysis. Results: The overall OR for the association of H. pylori infection and migraine headaches through 493,794 evaluated individuals was 2.80 [95% CI = 1.75–4.48; I2 = 89.20, p < 0.01], which reveals a statistically significant association between these disorders. It was found that the studies that were conducted in Asian regions and the recently published ones have clearly shown a higher association between migraine and H. pylori infection. On the other hand, migraine patients who are infected with H. pylori have similar signs and symptoms as H. pylori‐negative migraineurs; meanwhile, the clinical trials conducted in this field strongly emphasize the benefits of eradicating H. pylori infection in migraine patients and have estimated its effectiveness in improving migraine headaches equivalent to current common migraine treatments. Furthermore, it was reported that white matter lesions were 2.5‐fold higher on brain MRI in patients with H. pylori‐positive migraine compared with H. pylori‐negative migraineurs; however, the evidence does not support the role of oxidative stress in patients suffering from H. pylori infection and migraine and refuses the role of Cag‐A‐positive strains of H. pylori in migraine headaches. Conclusion: According to the currently available data, it seem reasonable that patients with a definite diagnosis of migraine who also suffer from gastrointestinal problems, undergo the H. pylori detection tests and if the evaluations are positive, H. pylori eradication treatment can be considered even before any migraine treatment. [ABSTRACT FROM AUTHOR]

The term neurodegeneration with brain iron accumulation (NBIA) brings together a broad set of progressive and disabling neurological genetic disorders in which iron is deposited preferentially in certain areas of the brain. Among NBIA disorders, the most frequent subtype is pantothenate kinase-associated neurodegeneration (PKAN) caused by pathologic variants in the PANK2 gene codifying the enzyme pantothenate kinase 2 (PANK2). To date, there are no effective treatments to stop the progression of these diseases. This review discusses the utility of patient-derived cell models as a valuable tool for the identification of pharmacological or natural compounds for implementing polytarget precision medicine in PKAN. Recently, several studies have described that PKAN patient-derived fibroblasts present the main pathological features associated with the disease including intracellular iron overload. Interestingly, treatment of mutant cell cultures with various supplements such as pantothenate, pantethine, vitamin E, omega 3, α-lipoic acid L-carnitine or thiamine, improved all pathophysiological alterations in PKAN fibroblasts with residual expression of the PANK2 enzyme. The information provided by pharmacological screenings in patient-derived cellular models can help optimize therapeutic strategies in individual PKAN patients. [ABSTRACT FROM AUTHOR]

Background: The most serious respiratory consequences of coronavirus disease (COVID-19) include the common cold, coagulopathy, multiorgan failure, and death. It can also harm essential organs, including the kidney, liver, gastrointestinal tract, lungs, and brain system. Objective: The study's objectives were to investigate the impact of COVID-19 infection on liver damage by analyzing a range of indicators such as alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, C-reactive protein (CRP), and d-dimer protein. Materials and Methods: To achieve the study's goal, blood samples were collected from a group of patients (both males and females), and a series of serological tests were performed, including immunological testing and measurements of CRP, d-dimer, and liver function. Results: In this study of 80 patients (age range between 17 and 70 years), the female-to-male ratio in both groups was 20:20. The difference in CRP level between study groups was statistically significant (P ≤ 0.001). The d-dimer level (ng/mL) in patients with infected COVID was significantly higher (P ≤ 0.001) than in the control group, while there was no statistically significant variation in blood liver enzymes between infected and noninfected COVID groups. According to statistical analysis, there is no discernible gender difference between groups of noninfected people and infected patients. Conclusion: The study findings indicate that there are no significant differences between infected males and females when compared to the comparison group; however, there are distinct variances in CRP and d-dimer levels in the infected group. The results of liver function tests and enzyme measurements revealed no significant changes between the infected and healthy groups. [ABSTRACT FROM AUTHOR]

Objective: To investigate the clinical manifestations, treatment and prognosis of COVID-19-associated central nervous system (CNS) complications. Methods: In this single-centre observation study, we recruited patients with COVID-19-associated CNS complications at the neurology inpatient department of the Eighth Affiliated Hospital, Sun Yat-Sen University (Futian, Shenzhen) from Dec 2022 to Feb 2023. Patients were analysed for demographics, clinical manifestations, cerebrospinal fluid properties, electroencephalographic features, neuroimaging characteristics, and treatment outcome. All patients were followed-up at 1 and 2 months after discharge until Apr 2023. Results: Of the 12 patients with COVID-19-associated CNS complications, the CNS symptoms occur between 0 days and 4 weeks after SARS-CoV-2 infection. The most common CNS symptoms were memory deficits (4/12, 33%), Unresponsiveness (4/12, 33%), mental and behavioural disorders (4/12, 33%). Seven of 12 cases can be categorized as probable SARS-CoV-2 encephalitis, and 5 cases can be described as brainstem encephalitis, acute disseminated encephalomyelitis, optic neuritis, multiple sclerosis or tremor probably associated with SARS-CoV-2 infection. Six patients received antiviral therapy, and 11 patients received glucocorticoid therapy, of which 3 patients received human immunoglobulin synchronously. Nine patients recovered well, two patients had residual neurological dysfunction, and one patient passed away from complications associated with tumor. Conclusion: In this observational study, we found that the inflammatory or immune-related complications were relatively common manifestations of COVID-19-associated CNS complications, including different phenotypes of encephalitis and CNS inflammatory demyelinating diseases. Most patients recovered well, but a few patients had significant neurological dysfunctions remaining. [ABSTRACT FROM AUTHOR]