Migraine is a recurrent and commonly disabling primary headache disorder that affects over 17% of women and 5%-8% of men. Migraine susceptibility is multifactorial with genetic, hormonal and ...environmental factors all playing an important role. The physiopathology of migraine is complex and still not fully understood. Many different neuropeptides, neurotransmitters and brain pathways have been implicated. In connection with the myriad mechanisms and pathways implicated in migraine, a variety of multisystemic comorbidities(e.g., cardiovascular, psychiatric and other neurological conditions) have been found to be closely associated with migraine. Recent reports demonstrate an increased frequency of gastrointestinal(GI) disorders in patients with migraine compared with the general population. Helicobacter pylori infection, irritable bowel syndrome, gastroparesis, hepatobiliary disorders, celiac disease and alterations in the microbiota have been linked to the occurrence of migraine. Several mechanisms involving the gut-brain axis, such as a chronic inflammatory response with inflammatory and vasoactive mediators passing to the circulatory system, intestinal microbiota modulation of the enteric immunological milieu and dysfunction of the autonomic and enteric nervous system, have been postulated to explain these associations. However, the precise mechanisms and pathways related to the gut-brain axis in migraine need to be fully elucidated. In this review, we survey the available literature linking migraine with GI disorders. We discuss the possible physiopathological mechanisms, and clinical implications as well as several future areas of interest for research.
Increasing evidence suggests that there is intestinal barrier dysfunction in multiple sclerosis. Camara-Lemarroy et al. address the mechanisms by which an altered intestinal barrier could lead to an ...altered neuroinflammatory response, and discuss the potential of barrier-stabilizing strategies as novel therapeutic avenues in multiple sclerosis.
Abstract
Biological barriers are essential for the maintenance of homeostasis in health and disease. Breakdown of the intestinal barrier is an essential aspect of the pathophysiology of gastrointestinal inflammatory diseases, such as inflammatory bowel disease. A wealth of recent studies has shown that the intestinal microbiome, part of the brain-gut axis, could play a role in the pathophysiology of multiple sclerosis. However, an essential component of this axis, the intestinal barrier, has received much less attention. In this review, we describe the intestinal barrier as the physical and functional zone of interaction between the luminal microbiome and the host. Besides its essential role in the regulation of homeostatic processes, the intestinal barrier contains the gut mucosal immune system, a guardian of the integrity of the intestinal tract and the whole organism. Gastrointestinal disorders with intestinal barrier breakdown show evidence of CNS demyelination, and content of the intestinal microbiome entering into the circulation can impact the functions of CNS microglia. We highlight currently available studies suggesting that there is intestinal barrier dysfunction in multiple sclerosis. Finally, we address the mechanisms by which commonly used disease-modifying drugs in multiple sclerosis could alter the intestinal barrier and the microbiome, and we discuss the potential of barrier-stabilizing strategies, including probiotics and stabilization of tight junctions, as novel therapeutic avenues in multiple sclerosis.
The brain-gut axis serves as the bidirectional connection between the gut microbiome, the intestinal barrier and the immune system that might be relevant for the pathophysiology of inflammatory ...demyelinating diseases. People with multiple sclerosis have been shown to have an altered microbiome, increased intestinal permeability and changes in bile acid metabolism. Experimental evidence suggests that these changes can lead to profound alterations of peripheral and central nervous system immune regulation. Besides being of pathophysiological interest, the brain-gut axis could also open new avenues of therapeutic targets. Modification of the microbiome, the use of probiotics, fecal microbiota transplantation, supplementation with bile acids and intestinal barrier enhancers are all promising candidates. Hopefully, pre-clinical studies and clinical trials will soon yield significant results.
In this topical review, we discuss the history of the area postrema syndrome, with special attention given to early studies aimed at identifying the area postrema and its function, possible early ...cases of the syndrome and its current relevance in neuroimmunology and demyelinating diseases. In 1896, Retzius named a structure in the posterior medulla oblongata as the area postrema. The work of Borison in the middle of the 20th century led to the elucidation of its function as a “vomiting center.” The historical medical literature is filled with excellent examples that could be described as “area postrema syndrome.” While severe and bilateral optic neuritis and transverse myelitis still constitute the classic components of neuromyelitis optica spectrum disorder (NMOSD), intractable vomiting and hiccups due to area postrema involvement is now recognized as essentially pathognomonic, indeed a shiny pearl in neuroimmunology and demyelinating diseases.
Background:
Recent evidence suggests a role for the gut–brain axis in the pathophysiology of multiple sclerosis (MS).
Materials and methods:
We studied biomarkers of intestinal permeability in 126 ...people with MS (57 relapsing-remitting multiple sclerosis (RRMS) and 69 progressive MS) and in a group of healthy controls for comparison. Serum/plasma concentrations of zonulin (a regulator of enterocyte tight junctions), tight junction proteins (ZO-1 and occludin), intestinal fatty acid binding protein (IFABP)/ileal bile acid binding protein (IBABP), D-lactate, and lipopolysaccharide (LPS) binding protein were measured.
Results:
Zonulin concentrations were significantly higher when a concurrent magnetic resonance imaging (MRI) confirmed the presence of blood–brain barrier (BBB) disruption (Gad+ RRMS) and were correlated with tight junction proteins. IBABP and D-lactate were elevated in people with RRMS compared to controls, but did not discriminate between Gad+ and Gad– subgroups. Baseline zonulin concentrations were associated with 1-year disease progression in progressive MS.
Conclusions:
People with MS have altered biomarkers of intestinal barrier integrity. Zonulin concentrations are associated with 1-year disease progression in progressive MS and closely mirror BBB breakdown in RRMS. Zonulin may mediate breakdown of both the intestinal barrier and the BBB in gut dysbiosis through the regulation of tight junctions. This could explain how the gut–brain axis modulates neuroinflammation in MS.
Gastrointestinal complications after ischemic stroke Camara-Lemarroy, Carlos R; Ibarra-Yruegas, Beatriz E; Gongora-Rivera, Fernando
Journal of the neurological sciences,
11/2014, Letnik:
346, Številka:
1
Journal Article
Recenzirano
Abstract Ischemic stroke is an important cause of morbidity and mortality, and currently the leading cause of adult disability in developed countries. Stroke is associated with various ...non-neurological medical complications, including infections and thrombosis. Gastrointestinal complications after stroke are also common, with over half of all stroke patients presenting with dysphagia, constipation, fecal incontinence or gastrointestinal bleeding. These complications are associated with increased hospital length of stay, the development of further complications and even increased mortality. In this article we review the epidemiology, pathophysiology, diagnosis, management and prevention of the most common gastrointestinal complications associated with ischemic stroke.
Furthermore, the diverse signals that regulate lung injury, the complex roles of the immune response in balancing repair versus injury, and the absence of a specific antiviral therapy, all suggest ...that targeting a single molecular pathway may be insufficient in attenuating disease severity. Overall, REIP is able to attenuate pro-inflammatory responses, up-regulate anti-inflammatory signals, reduce oxidative stress, regulate the expression of genes that are conductive to tissue repair, among other effects 3. ...REIPs protective effects in conditions other than ischemic-injury have also been studied. Any study involving REIP in SARS-CoV-2-associated ARDS should therefore carried out in the context of an ethically reviewed clinical trial.Funding/financial support The writing of this manuscript did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.Declaration of competing interest No competing interests to declare.Acknowledgment None.
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•Soluble adhesion markers may represent cognitive biomarkers in multiple sclerosis•Soluble NCAM-1 and VCAM-1 are elevated in primary progressive multiple sclerosis•Cognitive worsening ...in PPMS is associated with higher baseline VCAM-1 levels•Each 100 ng/mL VCAM-1 increase carries a 30% increased odds of cognitive worsening•Lower baseline BDNF is associated with lower baseline cognitive scores in PPMS
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