Department Of Clinical Neurosciences Research Articles

Norman Dott's dome-shaped neurosurgical operating theatres in Edinburgh (1960-2020) - End of an era.

When the new twin operating theatres at the Edinburgh Department of Surgical Neurology opened for the first time on 1 July 1960, they revealed a revolutionary space-pod design. The new department had been designed to firmly establish the specialty in Scotland and the UK, setting the stage for a period of real progress. The most distinctive feature of the two operating theatres was their egg shape, including domed ceilings pierced with operating lights, general lighting, ventilation grilles and viewing ports for visitors. Norman Dott (1897-1973) and his colleagues set the foundation for prosperity and success that lasted decades. However, 60 years after their opening, the DCN theatres at Western General Hospital shut forever, as the department moved to the new Department of Clinical Neurosciences, at the new Royal Infirmary Edinburgh. Echoes of the old theatres will live on in the new; the boldness of the design of the original theatres reflected the close cooperation between clinician-teachers, architects and administrators for the public good. This tradition of tangible confidence and optimism will hopefully carry into a new era, in the new hospital.

Acute and Interventional Treatments.

HomeStrokeVol. 54, No. 2Acute and Interventional Treatments No AccessArticle CommentaryRequest AccessFull TextAboutView Full TextView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toNo AccessArticle CommentaryRequest AccessFull TextAcute and Interventional Treatments Bruce C.V. Campbell, Michael D. Hill, Thanh N. Nguyen and Joseph P. Broderick Bruce C.V. CampbellBruce C.V. Campbell Correspondence to: Bruce C.V. Campbell, MBBS, PhD, Department of Neurology, Royal Melbourne Hospital Victoria, Australia. Email E-mail Address: [email protected] https://orcid.org/0000-0003-3632-9433 Department of Medicine and Neurology, Royal Melbourne Hospital, University of Melbourne, Parkville, Australia (B.C.V.C.). Search for more papers by this author , Michael D. HillMichael D. Hill https://orcid.org/0000-0002-6269-1543 Department of Clinical Neurosciences, University of Calgary, Alberta, Canada (M.D.H.). Search for more papers by this author , Thanh N. NguyenThanh N. Nguyen https://orcid.org/0000-0002-2810-1685 Departments of Neurology and Radiology, Boston Medical Center, MA (T.N.N.). Search for more papers by this author and Joseph P. BroderickJoseph P. Broderick https://orcid.org/0000-0002-7323-7709 Department of Neurology, University of Cincinnati Gardner Neuroscience Institute, OH (J.P.B.). Search for more papers by this author Originally published23 Jan 2023https://doi.org/10.1161/STROKEAHA.122.041254Stroke. 2023;54:591–594FootnotesThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.For Sources of Funding and Disclosures, see page 594.Correspondence to: Bruce C.V. Campbell, MBBS, PhD, Department of Neurology, Royal Melbourne Hospital Victoria, Australia. Email bruce.[email protected]org.au

Commentary: Surgical Management of Peripheral Nerve Pathology in Patients With Neurofibromatosis Type 2.

*Division of Neurosurgery, University Health Network, University of Toronto, Toronto, Ontario, Canada; ‡Department of Clinical Neurosciences, Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada Correspondence: Rajiv Midha, MD, MSc, Foothills Medical Centre, University of Calgary, 1195-1403 29 St NW, Calgary, ABT2N 2T9, Canada. Email: [email protected]

Commentary: The Pennsylvania Postmarket Multicenter Experience With Flow Redirection Endoluminal Device.

*Neurosurgery Division, Department of Clinical Neurosciences, Spectrum Health, Grand Rapids, Michigan, USA; ‡Department of Neurosurgery, College of Human Medicine, Michigan State University, Grand Rapids, Michigan, USA Correspondence: Justin Singer, MD, Division of Neurological Surgery, Department of Clinical Neurosciences, Spectrum Health Medical Group, Michigan State University, 25 Michigan St NE, Suite 6100, Grand Rapids, MI49503, USA. Email: [email protected] Twitter: @JustinSingerMD Andres F. Restrepo, MD, Division of Neurological Surgery, Department of Clinical Neurosciences, Spectrum Health/Michigan State University – College of Human Medicine, 25 Michigan St NE, Suite 6100, Grand Rapids, MI49503, USA. Email: [email protected] Twitter: @AndresRestrepMD

Progressive Vertebrobasilar Vasculopathy and Stroke Secondary to Giant Cell Arteritis.

HomeStrokeVol. 53, No. 9Progressive Vertebrobasilar Vasculopathy and Stroke Secondary to Giant Cell Arteritis No AccessCase ReportRequest AccessFull TextAboutView Full TextView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toNo AccessCase ReportRequest AccessFull TextProgressive Vertebrobasilar Vasculopathy and Stroke Secondary to Giant Cell Arteritis Yasamin Mahjoub, MD, Erica D. McKenzie, MD, Saher Raouf and Mohammed Almekhlafi, MD Yasamin MahjoubYasamin Mahjoub Correspondence to: Yasamin Mahjoub, MD, Foothills Medical Centre, 1403 29 St NW, Calgary, AB T2N 2T9. Email E-mail Address: [email protected] https://orcid.org/0000-0003-0898-3307 Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Alberta, Canada. Search for more papers by this author , Erica D. McKenzieErica D. McKenzie https://orcid.org/0000-0003-4369-413X Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Alberta, Canada. Search for more papers by this author , Saher RaoufSaher Raouf https://orcid.org/0000-0003-3338-7937 Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Alberta, Canada. Search for more papers by this author and Mohammed AlmekhlafiMohammed Almekhlafi https://orcid.org/0000-0001-9550-8197 Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Alberta, Canada. Search for more papers by this author Originally published15 Aug 2022https://doi.org/10.1161/STROKEAHA.122.039503Stroke. 2022;53:e435–e438FootnotesCorrespondence to: Yasamin Mahjoub, MD, Foothills Medical Centre, 1403 29 St NW, Calgary, AB T2N 2T9. Email [email protected]ca

Young Investigator Interview With CSCI Distinguished Scientist Awardee Dr. Michael Hill.

Dr. Michael Hill is President of the Canadian Neurology Federation and Director of the Stroke Unit for the Calgary Stroke Program. He is also a professor at the University of Calgary at the Department of Clinical Neurosciences. Dr. Hill has made outstanding contributions to the field of stroke research, particularly through the ESCAPE and ESCAPE-NA1 trials. Dr. Hill was a recipient of the Canadian Society for Clinical Investigation (CSCI) Distinguished Scientist Award in 2021-recognized as an expert and innovative leader in his research.

202 - PSYCHOSOCIAL INTERVENTIONS FOR PEOPLE WITH DEMENTIA AS STRATEGIES TO MANAGE BEHAVIOURAL AND PSYCHOLOGICAL SYMPTOMS [supported by European Association of Geriatric Psychiatry – EAGP

Symposium ChairsLia Fernandes (Department of Clinical Neurosciences and Mental Health, Faculty of Medicine, University of Porto, Portugal) lfernandes@med.up.ptSujoy Mukherjee (Faculty of Old Age Psychiatry, The Royal College of Psychiatrists, United Kingdom) Sujoy.Mukherjee@westlondon.nhs.ukIntroduction Lia FernandesSymposium OverviewPresentation 1 Sujoy MukherjeeThe treatment of Behavioural and Psychological Symptoms of Dementia: where do we stand?Presentation 2 Ana Rita FerreiraAssessing unmet needs in nursing homes: a promising way to prevent neuropsychiatric symptomsPresentation 3 Slavisa LamounierThe Arts as a medium for improving social inclusion in dementiaPresentation 4 Lídia SousaMusic-based interventions in the acute setting for patients with dementia

The Depiction of ECT in Egyptian Media

Emad Sidhom* Author Affiliations University of Cambridge, Department of Clinical Neurosciences, UK Received: September 17, 2020 | Published: September 29, 2020 Corresponding author: Emad Sidhom, University of Cambridge, Department of Clinical Neurosciences, UK DOI: 10.26717/BJSTR.2020.30.005011

British Society for Gene and Cell Therapy Annual Conference Wednesday 19th June – Friday 21st June 2019 University of Sheffield, Sheffield, UK www.bsgct.org

British Society for Gene and Cell Therapy Annual Conference Wednesday 19th June – Friday 21st June 2019 University of Sheffield, Sheffield, UK www.bsgct.org

How to Review a Clinical Research Paper.

Peer review is an essential component of the scientific process. It is imperfect, to be sure, but there is widespread agreement that it is the best way to ensure that reliable scientific information is published.1–4 Being a reviewer is only 1 component of the process of publication. If you are an author or want to be an author, you have a duty to take part in reviewing your colleagues’ papers, just as your colleagues have reviewed your papers. Reviewing papers is a helpful part of learning the technical art of medical writing because you see and learn by example, both good and bad. Although it is a volunteer duty, there is a skill in providing a useful review and mentorship and experience matter in how you provide your review. Herein, I provide some steps on how to review papers for Stroke , specifically focussing on clinical papers. At many journals, including Stroke , there are a group of associate editors who handle papers through the review and publication process. These people are typically your senior peers and are also volunteers. Your job and duty as a reviewer is that you are advisory to them. The associate editors look at each paper as it comes in, and they may reject a paper outright or provide comments back to the author group for revision even before a paper is sent for peer review. In sending a paper to you as a reviewer, the associate editors seek your advice on quality, content, and context. Comments that you make to the editors directly are confidential and often helpful to them to interpret the context of a given paper. Read the title and abstract of the paper and decide whether you have the relevant expertise and interest to provide a review. If …

11 Cognitive and behavioural effects of chronic alcohol excess

<i>Killian is based at the Robert Fergusson Unit, Scotland’s national neurorehabilitation unit, and runs neuropsychiatry clinics at the Department of Clinical Neurosciences, Western General Hospital. His psychiatry training included an endorsement in substance misuse, and his MD examined the impact of alcohol and cannabis use on brain structure in people at high familial risk of schizophrenia. Clinical interests include the delivery of cognitive and behavioural therapies to cognitively impaired patients and treatment of substance misuse post-brain injury.</i> As anyone who has been designated driver can attest, alcohol intoxication is associated with profound effects on cognition and behaviour. The drinker experiences impairments in judgement, inhibition, motor skills and memory while simultaneously imbued with an inflated sense of their own abilities. While intoxication effects are transient, it is now established that detectable cognitive impairments are the rule rather than the exception in habitual heavy drinkers. These impairments exist on a spectrum, from the relatively modest deficits in memory, executive function and visuospatial abilities commonly seen in alcoholics entering treatment, to the potentially persistent dense amnesia associated with Wernicke-Korsakoff syndrome. In reality, the cognitive deficits present in any individual drinker reflect a complex interaction between individual vulnerabilities, the direct neurotoxic effects of alcohol, the consequences of periods of nutritional deficiency and metabolic disturbance, and other pathologies arising from the adverse health behaviours associated with habitual alcohol use. In recent years alcohol-related brain damage, a usefully catch-all concept which acknowledges that significant cognitive impairment in alcoholics extends far beyond the classic amnestic syndrome, has been increasingly acknowledged as a major public health problem. As the prevalence and importance of cognitive impairment associated with heavy alcohol use has been more fully appreciated, so has its potential reversibility. Central to achieving this is abstinence, or at least drastically reducing intake, and this is an exciting time for advances in therapeutic agents for alcohol dependence. The reality is however that alcohol dependence is associated with considerable co-morbidity, an understanding of which can potentially improve outcomes as well as assist identification of an alcohol problem in the first place. Commonly co-occurring problems include anxiety and mood disturbance, pain, sleep disorders and smoking, all of which can have a complex and potentially bidirectional relationship with alcohol dependence.

Semantic context effects on picture naming in aphasia

Semantic context effects on picture naming in aphasia

Repetitive behaviors in Tourette Syndrome and Obsessive-Compulsive Disorder

Department of Psychiatry, Hospital de Magalhaes Lemos, Porto, Portugal Psychiatry Department, Centro Hospitalar Tâmega e Sousa, Penafiel, Portugal Department of Child and Adolescent Psychiatry, Centro Hospitalar do Porto, Portugal Department of Clinical Neurosciences and Mental Health, Faculty of Medicine University of Porto, Portugal Department of Neurology Hospital Pedro Hispano/ULS Matosinhos, Matosinhos, Portugal Center for Neurosciences, CUF Porto, Porto, Portugal

Hierarchical predictive coding in frontotemporal networks with pacemaker expectancies: evidence from dynamic causal modelling of Magnetoencephalography (MEG)

Event Abstract Back to Event Hierarchical predictive coding in frontotemporal networks with pacemaker expectancies: evidence from dynamic causal modelling of Magnetoencephalography (MEG) Holly Phillips1, 2*, Alejandro Blenkmann3, 4, Laura Hughes2, 5, Tristan Bekinschtein2 and James Rowe2, 5 1 University of Cambridge, Department of Clinical Neurosciences, United Kingdom 2 University of Cambridge, MRC - Cognition and Brain Sciences Unit, UK 3 University of Buenos Aires, Center for Clinical and Experimental Neurosciences, IBCN ‘‘Dr. E. de Robertis’’, School of Medicine, Argentina 4 Ramos Mejía Hospital, Epilepsy Center, Department of Neurology, Argentina 5 University of Cambridge, Department of Clinical Neurosciences, UK Unexpected sensory events engage automatic local and distributed neurophysiological responses, evident in temporal and frontal cortical sources underlying the mismatch negativity (MMN, Näätänen et al. 2007). Dynamic causal modelling (DCM) of the MMN in electroencephalography (EEG, Garrido et al. 2009) and magnetoencephalography (MEG, Hughes et al. 2013) indicate a hierarchy of feedback sensory predictions and feedforward prediction errors, between primary auditory cortex (A1), superior temporal gyrus (STG) and prefrontal cortex (PFC). We posited that where temporal regularities in stimuli exist, an internal pacemaker may provide conditional expectations in PFC that supports high level predictions of auditory events in temporal cortices. Magnetoencephalography (MEG) in healthy adults was recorded during an auditory MMN paradigm (Näätänen et al. 2004), that alternated a standard tone with five deviant tone types (differing by frequency, intensity, location, duration or silent gap). 12 dynamic causal models (SPM8-DCM10) of networks among A1, STG and PFC, were compared using Bayesian model selection to examine first, the net effect of all deviants vs. standard tones, and second, the connectivity associated with the specific deviant types. The models of all deviant types that had greatest evidence included features of (i) bidirectional modulation of frontotemporal connectivity and (ii) a pacemaker signal acting on PFC. In the deviant specific models, those with the greatest evidence of a pacemaker signal, were those of the deviants defined by temporal structure differences (duration and gap), whereas other deviants had greater evidence without it. We confirm the presence of hierarchical frontotemporal networks in agreement with the prediction coding hypothesis, and provide new evidence for an internal pacemaker into PFC, which supports temporally defined predictions of sensory inputs. Keywords: Magnetoencephalography, predictive coding, effective connectivity, mismatch negativity, dynamic casual modelling Conference: XII International Conference on Cognitive Neuroscience (ICON-XII), Brisbane, Queensland, Australia, 27 Jul - 31 Jul, 2014. Presentation Type: Poster Topic: Sensation and Perception Citation: Phillips H, Blenkmann A, Hughes L, Bekinschtein T and Rowe J (2015). Hierarchical predictive coding in frontotemporal networks with pacemaker expectancies: evidence from dynamic causal modelling of Magnetoencephalography (MEG). Conference Abstract: XII International Conference on Cognitive Neuroscience (ICON-XII). doi: 10.3389/conf.fnhum.2015.217.00377 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 19 Feb 2015; Published Online: 24 Apr 2015. * Correspondence: Miss. Holly Phillips, University of Cambridge, Department of Clinical Neurosciences, Cambridge, United Kingdom, holly.phillips@mrc-cbu.cam.ac.uk Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Holly Phillips Alejandro Blenkmann Laura Hughes Tristan Bekinschtein James Rowe Google Holly Phillips Alejandro Blenkmann Laura Hughes Tristan Bekinschtein James Rowe Google Scholar Holly Phillips Alejandro Blenkmann Laura Hughes Tristan Bekinschtein James Rowe PubMed Holly Phillips Alejandro Blenkmann Laura Hughes Tristan Bekinschtein James Rowe Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Systems Training for Emotional Predictability and Problem Solving (STEPPS): Program efficacy and personality features as predictors of drop-out — An Italian study

In this study we present a clinical application of the STEPPS model in an Italian sample of severely affected patients with borderline personality disorder (BPD) or personality disorder (PD) with prominent borderline features in comorbidity with a mood disorder. The aims of this work are: 1) to confirm our preliminary results in a larger sample and at a 12-month follow-up, and 2) to identify predictors of drop-out vs completion of STEPPS in order to understand which characteristics of patients make them suitable or not for this treatment. The sample is composed of 32 subjects recruited from a population of inpatients of the Mood Disorders Center, Department of Clinical Neurosciences, Hospital San Raffaele-Turro, Milan. To confirm STEPPS efficacy at 12-month follow-up, we selected the following outcome criteria: reduction in the number of hospitalizations related to self-harm acts; reduction in the number of suicidal attempts; reduction of perceived emotional intensity levels; changes in cognitive filter scores; changes in the scores on self-report questionnaires. To identify predictors of drop-out vs completion, we analysed the following variables: demographic features (sex, marital status, school level achieved, and job status); Axis-I diagnosis; Axis-II categorical and dimensional diagnosis; and personality features. Seventeen (53%) subjects completed the treatment successfully. The drop-out rate was 47%. Patients who completed the program show a significant decrease in the number of hospitalizations, both at the end of the treatment and at 12-month follow-up. Friedman ANOVA test shows a significant decrease in suicidal attempts during and after STEPPS, and at 12-month follow-up. Analysis of drop-outs showed no significant differences with regard to sex, marital status, school level and job status between the two groups. Axis-I and Axis-II categorical diagnoses did not discriminate between the two groups. Those patients who dropped differ significantly from completers in histrionic personality traits and magical thinking index, given by the interaction between low scores in Self-Directedness and high scores in Self-Transcendence.

The clinical neuroscience of the ageing brain cognitive diseases

Leenaards Memory Centre, Department of Clinical Neurosciences, CHUV, Lausanne, Switzerland Correspondence to Jean-François Démonet, MD, PhD, Leenaards Memory Centre, Department of Clinical Neurosciences, CHUV, Lausanne CH-1011, Switzerland. Tel: +41 (0)21 314 0509; e-mail: [email protected]

Disability, quality of life and well-being in patients undergoing brain surgery

Disability, quality of life and well-being in patients undergoing brain surgery

Methylfolate as Adjunctive Treatment in Major Depression

Back to table of contents Previous article Next article Communications and UpdatesFull AccessMethylfolate as Adjunctive Treatment in Major DepressionEdward H. Reynolds, M.D., F.R.C.Psych.Edward H. ReynoldsSearch for more papers by this author, M.D., F.R.C.Psych.Published Online:1 May 2013https://doi.org/10.1176/appi.ajp.2013.13010084AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: As the principal investigator of the only previous placebo-controlled trial of methylfolate as an adjunctive treatment in major depression 22 years ago (1), I appreciated the new trial by Papakostas et al. (2) in the December 2012 issue confirming the efficacy of the vitamin in some resistant depression.Important differences between the two trials raise interesting questions. Our study was for depressed patients with borderline or definite folate deficiency (red blood cell folate levels <200 pg/mL), but Papakostas et al. did not mention the folate status of their patients. I presume that many would not have been folate deficient. We also used 15 mg of methylfolate, but our trial was for 6 months and demonstrated increasing efficacy at 3 and 6 months in contrast to the 60-day study by Papakostas et al.I first reported in 1967 the beneficial effect of the vitamin on mood and some aspects of cognitive and social function in an open trial of folic acid, 5 mg/day for 1 to 3 years, in folate-deficient patients with epilepsy (3). At the Medical Research Council Neuropsychiatry Research Unit, we then showed not only that folate deficiency was common in depression, as had been reported by Carney (4), but that the deficiency was associated with a poor response to antidepressant therapy (5). I subsequently collaborated with Carney and colleagues in demonstrating that depression was the most common reversible neuropsychiatric manifestation of folate-deficient megaloblastic anemia; in confirming that S-adenosylmethionine had antidepressant properties, thus implying that methylation is a key to understanding mood (6); and in identifying a subgroup of patients with depression, high plasma homocysteine levels, folate deficiency, and impaired neurotransmitter metabolism. This culminated in our positive trial of methylfolate, the transport form of folate into the nervous system, as adjunctive therapy in depression (1).A crucial question for the future is to what extent the antidepressant properties of methylfolate depend on the folate status of the patient. Our own pilot observations suggest that methylfolate may have antidepressant properties as monotherapy, irrespective of folate status, but that responders show a greater rise in red cell folate levels than nonresponders (7). An important clue is the mood-elevating properties of nitrous oxide. This euphoriant effect is probably related to the instantaneous inactivation of methionine synthase, leading to an acute rise in methylfolate in the brain (7). Finally, methylation in the nervous system is a key not just to the biology of mood but to other aspects of cognitive function, including dementia. After 45 years, it is time for academic departments of psychiatry to invest more in this nonpharmaceutical approach to mental illness.From the Department of Clinical Neurosciences, King’s College, University of London.The author reports no financial relationships with commercial interests.References1 Godfrey PSA, Toone BK, Carney MWP, Flynn TG, Bottiglieri T, Laundy M, Chanarin I, Reynolds EH: Enhancement of recovery from psychiatric illness by methylfolate. Lancet 1990; 336:392–395Crossref, Medline, Google Scholar2 Papakostas GI, Shelton RC, Zajecka JM, Etemad B, Rickels K, Clain A, Baer L, Dalton ED, Sacco GR, Schoenfeld D, Pencina M, Meisner A, Bottiglieri T, Nelson E, Mischoulon D, Alpert JE, Barbee JG, Zisook S, Fava M: l-methylfolate as adjunctive therapy for SSRI-resistant major depression: results of two randomized, double-blind, parallel-sequential trials. Am J Psychiatry 2012; 169:1267–1274Link, Google Scholar3 Reynolds EH: Effects of folic acid on the mental state and fit-frequency of drug-treated epileptic patients. Lancet 1967; 1:1086–1088Crossref, Medline, Google Scholar4 Carney MWP: Serum folate values in 423 psychiatric patients. Br Med J 1967; 4:512–516Crossref, Medline, Google Scholar5 Reynolds EH, Preece JM, Bailey J, Coppen A: Folate deficiency in depressive illness. Br J Psychiatry 1970; 117:287–292Crossref, Medline, Google Scholar6 Reynolds EH, Carney MWP, Toone BK: Methylation and mood. Lancet 1984; 2:196–198Crossref, Medline, Google Scholar7 Reynolds EH: Vitamin B12, folic acid, and the nervous system. Lancet Neurol 2006; 5:949–960Crossref, Medline, Google Scholar FiguresReferencesCited byDetailsCited ByFolic Acid, Folinic Acid, 5 Methyl TetraHydroFolate Supplementation for Mutations That Affect Epigenesis through the Folate and One-Carbon Cycles24 January 2022 | Biomolecules, Vol. 12, No. 2Behavioral and neurochemical effects of folic acid in a mouse model of depression induced by TNF-αBehavioural Brain Research, Vol. 414Depressão e distúrbios do sonoFolic acid ameliorates depression-like behaviour in a rat model of chronic unpredictable mild stress15 January 2020 | BMC Neuroscience, Vol. 21, No. 1Perspectives in Psychiatric Care, Vol. 54, No. 2Problemy reproduktsii, Vol. 24, No. 3Fundamental & Clinical Pharmacology, Vol. 29, No. 6 Volume 170Issue 5 May 2013Pages 560-560 Metrics PDF download History Accepted 1 February 2013 Published online 1 May 2013 Published in print 1 May 2013

Editorial introductions

Editorial introductions

Anti-ganglioside antibodies in Pandemrix�-induced narcolepsy

Event Abstract Back to Event Anti-ganglioside antibodies in Pandemrix®-induced narcolepsy Anna-Helena Saariaho1*, Outi Vaarala2, Markku Partinen3, 4 and Seppo Meri1 1 Haartman Institute, University of Helsinki, Finland, Department on Immunology and Bacteriology, Finland 2 National Institute for Health and Welfare, Helsinki, Finland, Department of Vaccines and Immune Protection,, Finland 3 Sleep Clinic, Finnish Narcolepsy Research Centre, Vitalmed Research Centre Helsinki, Finland, Finland 4 University of Helsinki, Helsinki, Finland, Department of Clinical Neurosciences, Finland Narcolepsy with cataplexy (NC) is a chronic, neurological disease with an unknown etiology. It is caused by a selective loss of hypocretin-producing neurons in hypothalamus. This causes the typical symptoms of the disease: various sleep and metabolic disorders, cataplexy and hallucinations. NC is considered as an autoimmune disease, where genetic and environmental risk factors contribute to its development. NC has a strong association with HLA-DQB1*0602 (DQ6), and recent reports from several European countries have confirmed an association between the adjuvanted H1N1 Pandemrix® vaccine and NC in genetically susceptible children and adolescents. However, the triggering role of the vaccine components and the mechanisms behind the disease remain unsolved. We studied the role of humoral immunity in the pathogenesis of Pandemrix-narcolepsy by screening anti-neuronal antibodies from patients’ sera. No antibodies were detected against the neuronal antigens (Hu, Ri, Yo, Tr, MAG, myelin, Ma/Ta, GAD, amphiphysin, aquaporin-4, NMDAR, AMPA-type glutamate receptor, glycine receptor, CASPR2 and LGI1) in patient sera (n=5). However, when sera of Pandemrix-narcolepsy patients (n=20) were screened for 12 anti-ganglioside antibodies (AGA) by line immunoassay a high frequency of (>30%) of AGA (IgG or/and IgM) were found. No AGA were detected in the control sera of healthy unvaccinated children (n=6). The majority of the found AGAs (IgG) were against gangliosides GM4, GM3 and GD3. Our results suggest that humoral immunity is involved in the pathogenesis of Pandemrix-narcolepsy, and that AGA could cause at least part of the neuronal damage of the disease. Keywords: Narcolepsy, H1N1, ganglioside, Neuron, Pandemrix vaccination Conference: 15th International Congress of Immunology (ICI), Milan, Italy, 22 Aug - 27 Aug, 2013. Presentation Type: Abstract Topic: Immune-mediated disease pathogenesis Citation: Saariaho A, Vaarala O, Partinen M and Meri S (2013). Anti-ganglioside antibodies in Pandemrix®-induced narcolepsy. Front. Immunol. Conference Abstract: 15th International Congress of Immunology (ICI). doi: 10.3389/conf.fimmu.2013.02.01075 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 30 Jun 2013; Published Online: 22 Aug 2013. * Correspondence: Dr. Anna-Helena Saariaho, Haartman Institute, University of Helsinki, Finland, Department on Immunology and Bacteriology, Helsinki, Finland, anna-helena.saariaho@helsinki.fi Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Anna-Helena Saariaho Outi Vaarala Markku Partinen Seppo Meri Google Anna-Helena Saariaho Outi Vaarala Markku Partinen Seppo Meri Google Scholar Anna-Helena Saariaho Outi Vaarala Markku Partinen Seppo Meri PubMed Anna-Helena Saariaho Outi Vaarala Markku Partinen Seppo Meri Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.