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D-dimer level is a useful predictor for mortality in patients with COVID-19: analysis of 483 cases. Diabetes Metab Syndr. 2020;14(6):2245–9.\nStrambo D, De Marchis GM, Bonati LH, Arnold M, Carrera E, Galletta S, et al. Ischemic stroke in COVID-19 patients: mechanisms, treatment, and outcomes in a consecutive swiss stroke registry analysis. Eur J Neurol. 2022;29(3):732–43.\nMao L, Jin H, Wang M, Hu Y, Chen S, He Q, et al. Neurologic manifestations of hospitalized patients with coronavirus disease 2019 in Wuhan, China. JAMA Neurol. 2020;77(6):683–90.\nNtaios G, Michel P, Georgiopoulos G, Guo Y, Li W, Xiong J, et al. Characteristics and outcomes in patients with COVID-19 and acute ischemic stroke: the global COVID-19 stroke registry. Stroke. 2020;51(9):e254–8.\nFure B, Wyller TB, Thommessen B. TOAST criteria applied in acute ischemic stroke. Acta Neurol Scand. 2005;112(4):254–8.\nHuang C, Wang Y, Li X, Ren L, Zhao J, Hu Y, et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet. 2020;395(10223):497–506.\nBelani P, Schefflein J, Kihira S, Rigney B, Delman BN, Mahmoudi K, et al. COVID-19 is an independent risk factor for acute ischemic stroke. Am J Neuroradiol. 2020;41(8):1361–4.\nMartí-Fàbregas J, Guisado-Alonso D, Delgado-Mederos R, Martínez-Domeño A, Prats-Sánchez L, Guasch-Jiménez M, et al. Impact of COVID-19 infection on the outcome of patients with ischemic stroke. Stroke. 2021;52(12):3908–17.\nBhatia R, Pedapati R, Komakula S, Srivastava MVP, Vishnubhatla S, Khurana D. Stroke in coronavirus disease 2019: a systematic review. J Stroke. 2020;22(3):324–35.\nPanigada M, Bottino N, Tagliabue P, Grasselli G, Novembrino C, Chantarangkul V, et al. Hypercoagulability of COVID-19 patients in intensive care unit: a report of thromboelastography findings and other parameters of hemostasis. J Thromb Haemost. 2020;18(7):1738–42.\nGabet A, Grave C, Chatignoux E, Tuppin P, Béjot Y, Olié V. Characteristics, management, and case-fatality of patients hospitalized for stroke with a diagnosis of COVID-19 in France. Neuroepidemiology. 2021;55(4):323–30.\nKihira S, Schefflein J, Mahmoudi K, Rigney B, Delman NB, Mocco J, et al. Association of coronavirus disease (COVID-19) with large vessel occlusion strokes: a case-control study. Am J Roentgenol. 2021;216(1):150–6.\nNannoni S, de Groot R, Bell S, Markus HS. Stroke in COVID-19: a systematic review and meta-analysis. Int J Stroke. 2021;16(2):137–49.\nMehta P, McAuley DF, Brown M, Sanchez E, Tattersall RS, Manson JJ. COVID-19: consider cytokine storm syndromes and immunosuppression. Lancet. 2020;395(10229):1033–4.\nSpence JD, De Freitas GR, Pettigrew LC, Ay H, Liebeskind DS, Kase CS, et al. Mechanisms of stroke in COVID-19. Cerebrovasc Dis. 2020;49(4):451–8.\nBekelis K, Missios S, Ahmad J, Labropoulos N, Schirmer CM, et al. Ischemic stroke occurs less frequently in patients with COVID-19: a multicenter cross-sectional study. Stroke. 2020;51(12):3570–6.\nZhang C, Gu J, Chen Q, Deng N, Li J, Huang L, Zhou X. Clinical and epidemiological characteristics of pediatric SARS-CoV-2 infections in China: a multicenter case series. PLoS Med. 2020;17(6):e1003130–e1003130.\nImam Z, Odish F, Gill I, O’Connor D, Armstrong J, Vanood A, et al. Older age and comorbidity are independent mortality predictors in a large cohort of 1305 COVID-19 patients in Michigan, United States. J Intern Med. 2020;288(4):469–76.\nWu C, Chen X, Cai Y, Zhou X, Xu S, Huang H, et al. Risk factors associated with acute respiratory distress syndrome and death in patients with coronavirus disease 2019 pneumonia in Wuhan. China JAMA Intern Med. 2020;180(7):934–43.\nChen N, Zhou M, Dong X, Qu J, Gong F, Han Y, et al. Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study. Lancet. 2020;395(10223):507–13.\nGrasselli G, Zangrillo A, Zanella A, Antonelli M, Cabrini L, Castelli A, et al. Baseline characteristics and outcomes of 1591 patients infected with SARS-CoV-2 admitted to ICUs of the Lombardy Region. Italy Jama. 2020;323(16):1574–81.\nZhu Z, Cai T, Fan L, Lou K, Hua X, Huang Z, Gao G. Clinical value of immune-inflammatory parameters to assess the severity of coronavirus disease 2019. Int J Infect Dis. 2020;95:332–9.\nPrice-Haywood EG, Burton J, Fort D, Seoane L. Hospitalization and mortality among black patients and white patients with Covid-19. N Engl J Med. 2020;382(26):2534–43.\nChen T, Wu D, Chen H, Yan W, Yang D, Chen G, et al. Clinical characteristics of 113 deceased patients with coronavirus disease 2019: retrospective study. BMJ. 2020;26(368):m1091–m1091.\nHuang S, Wang J, Liu F, Liu J, Cao G, Yang C, et al. COVID-19 patients with hypertension have more severe disease: a multicenter retrospective observational study. Hypertens Res. 2020;43(8):824–31.\nBlanke CD. In response: diabetes is a risk factor for the progression and prognosis of COVID-19. Diabetes Metab Res Rev. 2020;36(7):e3331–e3331.\nWeekly CDC, C. The epidemiological characteristics of an outbreak of 2019 novel coronavirus diseases (COVID-19)—China 2020. China CDC Wkly. 2020;2(8):113–22.\nTan YK, Goh C, Leow AST, Tambyah PA, Ang A, Yap ES, et al. COVID-19 and ischemic stroke: a systematic review and meta-summary of the literature. J Thromb Thrombolysis. 2020;50(3):587–95.\nYu HH, Qin C, Chen M, Wang W, Tian DS. D-dimer level is associated with the severity of COVID-19. Thromb Res. 2020;195:219–25.\nDüz ME, Balcı A, Menekşe E. D-dimer levels and COVID-19 severity: systematic review and meta-analysis. Tuberk Toraks. 2020;68(4):353–60.\nWagner J, Garcia-Rodriguez V, Yu A, Dutra B, DuPont A, Cash B, Farooq A. Elevated D-dimer is associated with multiple clinical outcomes in hospitalized covid-19 patients: a retrospective cohort study. SN Compr Clin Med. 2020;2(12):2561–7.\nCavallieri F, Marti A, Fasano A, Dalla Salda A, Ghirarduzzi A, et al. Prothrombotic state induced by COVID-19 infection as trigger for stroke in young patients: A dangerous association. Eneurologicalsci. 2020;20:100247.",{"EN":162},"",{"EN":164},"Severe acute respiratory syndrome coronavirus 2 (SARS COV 2) infection is associated with multiple neurological complications. Cerebrovascular accidents are considered as one of the common neurological complications associated with corona virus (COVID-19). It may represent the first presentation of the patients of COVID-19 or may occur anytime during the course of the disease. This study included 381 patients after the diagnosis of cerebrovascular accident. The mean age of the participants was 57.1 ± 15 years. 53.5% of the participants were males and 46.5% were females. The participants had COVID-19 infection in past 3 months with mean duration was 35.5 ± 18 days. The mean NIHSS among the participants was 10.5 ± 6.2. Small artery stroke was higher among PCR negative patients and controls, while large artery stroke was higher among PCR positive patients. 26% of patients with stroke and confirmed COVID-19 infection developed stroke immediately after COVID-19 infection (within 1 week). Within 1 month from getting infection with COVID-19, 41.7% of patients developed stroke and 32.3% had developed stroke after 1 month of infection with COVID-19. Female gender, older age of the patients and presence of vascular risk factors were associated with increased severity of infection as evidenced by higher NIHSS and more ICU admission among COVID-19 positive patients. COVID-19 infection has been associated with both venous and arterial stroke, especially in elderly patients. COVID-19 infection was associated with increased stroke severity as evidenced by higher NIHSS and more ICU admission. Small vessel disease was higher among COVID-19 negative patients, while large artery stroke was higher among positive COVID-19 patients.",{"EN":166},"Association between acute stroke and COVID-19 infection among patients with acute stroke",{"VOID":168},"10.1186\u002Fs41983-023-00784-7","PUBLICATION","VERIFIED","Auto Verify","https:\u002F\u002Fejnpn.springeropen.com\u002Farticles\u002F10.1186\u002Fs41983-023-00784-7",[174,192,205,218],{"id":175,"sortIndex":176,"researcher":18,"roles":177,"affiliations":179,"properties":189},"ae66179f-f6fc-43b9-8728-277fdcd066f6",1,[178],"AUTHOR",[180],{"id":18,"sortIndex":19,"affiliation":181,"properties":18},{"id":182,"createTime":183,"updateTime":183,"relativeEntities":184,"slug":185,"properties":186,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"52fb227a-1f92-4ec0-bc64-8244f991001f","2024-04-06T20:09:25.645+00:00",[],"Neurology-Department-Suez-Canal-University-Isamilia-Egypt",{"title":187},{"VI":188},"Neurology Department, Suez Canal University, Isamilia, Egypt",{"title":190},{"VI":191},"M. 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Vitamin D deficiency, N Engl J Med. 2007;357:266.\nLugg ST, Howells PA, Thickett DR. Optimal vitamin D supplementation levels for cardiovascular disease protection. Dis Markers. 2015;2015:1.\nClancy N, Onwuneme C, Carroll A, McCarthy R, McKenna MJ, Murphy N, et al. Vitamin D and neonatal immune function. J Matern Fetal Neonatal Med. 2013;26:639.\nWacker M, Holick MF. Vitamin D effects on skeletal and extraskeletal health and the need for supplementation. Nutrients. 2013;5:111.\nFahmi RM, Lotfy SM, Mohamed WS, Elsaid AF, Murad MH, Abdulmoneem G. Vitamin D levels in patients with multiple sclerosis. Egypt J Neurol Psychiatr Neurosurg. 2014;51:145.\nChaudhuri JR, Mridula KR, Alladi S, Umamahesh M, Balaraju B, Swath A, et al. Serum 25-hydroxyvitamin D deficiency in ischemic stroke and subtypes in Indian patients. J STROKE. 2014;16:44.\nAlfieri DF, Lehmann MF, Oliveira SR, Flauzino T, Delongui F, de Araújo MC, et al. Vitamin D deficiency is associated with acute ischemic stroke, C-reactive protein, and short-term outcome. Metab Brain Dis. 2017;32:493.\nEyles DW, Liu PY, Josh P, Cui X. Intracellular distribution of the vitamin D receptor in the brain: comparison with classic target tissues and redistribution with development. Neuroscience. 2014;268:1.\nCarvalho LS, Sposito AC. Vitamin D for the prevention of cardiovascular disease: are we ready for that? Atherosclerosis. 2015;241:729.\nThapa L, Pokhrel B, Shrestha A, Pradhan M, Bhandari TR, Shrestha S, et al. Status of vitamin D and its association with stroke risk factors in patients with acute ischemic stroke in a tertiary care hospital. J Nepal Med Assoc. 2014;52:935.\nShine P, Shwu W, Tzy W, Lee TK, Tony C. Location and size of infarct on functional outcome of non cardioembolic ischemic stroke. Disabil Rehabil. 2006;28:977.\nBrott T, Adams HP, Olinger CP, Marler JR, Barsan WG, Biller J, et al. Measurements of acute cerebral infarction: a clinical examination scale. Stroke. 1989;20:864.\nNIH Stroke Scale. National Institute of Neurological Disorder website. https:\u002F\u002Fwww. ninds.nih.gov\u002Fsites\u002Fdefault\u002Ffiles\u002FNIH_Stroke_Scale.\nUyttenboogaart M, Stewart RE, Vroomen PC, De Keyser J, Luijckx GJ. Optimizing cutoff scores for the Barthel index and the modified Rankin Scale for defining outcome in acute stroke trials. Stroke. 2005;36:1984.\nMouradian MS, Majumdar SR, Senthilselvan A, Khan K, Shuaib A. How well are hypertension, hyperlipidemia, diabetes, and smoking managed after a stroke or transient ischemic attack? Stroke. 2002;33:1656.\nOrganization WHO. Obesity and overweight. World Health Organization. http:\u002F\u002Fwww.who.int\u002Fmediacentre\u002Ffactsheets\u002Ffs311\u002Fen\u002F.\nCorp IBM. IBM SPSS Statistics for Windows, Version 20. IBM Corp: Armonk, NY; 2010.\nKissela BM, Khoury JC, Alwell K, Moomaw CJ, Woo D, Adeoye O, et al. Age at stroke: temporal trends in stroke incidence in a large, biracial population. Neurology. 2012;79:1781.\nSmajlović D. Strokes in young adults: epidemiology and prevention. Vasc Health Risk Manag. 2015;11:157.\nZhou R, Wang M, Huang H, Li W, Hu Y, Wu T. Lower vitamin D status is associated with an increased risk of ischemic stroke: a systematic review and meta-analysis. Nutrients. 2018;10:277.\nBrondum-Jacobsen P, Nordestgaard BG, Schnohr P, Benn M. 25-hydroxyvitamin D and symptomaticischemic stroke: an original study and meta-analysis. Ann Neurol. 2013;73:38.\nWolf PA, Abbott RD, Kannel WB. Atrial fibrillation as an independent risk factor for stroke: the Framingham Study. Stroke. 1991;22:983.\nAlfieri DF, Lehmann MF, Oliveira SR, Flauzino T, Delongui F, de Araújo MC, et al. Vitamin D deficiency is associated with acute ischemic stroke, C-reactive protein, and short-term outcome. Metab Brain Dis. 2017;32:493.\nChatterjee K, Mandal SK, Chatterjee S. Assessment of vitamin D level in cerebrovascular accident patients in Eastern India. Natl J Med Res. 2014;4:264.\nFahmy E, Sharaf S, Helmy H, Sherif S. Vitamin D status in acute ischemic stroke: relation to initial severity and short-term outcome. Egypt J Neurol Psychiatr Neurosurg. 2019; 55: 18.\nWajda J, Świat M, Owczarek AJ, Brzozowska A, Glinianowicz MO, Chudek J. Severity of vitamin D deficiency predicts mortality in ischemic stroke patients. Dis Markers. 2019;2019:1.\nKannel WB, Wolf PA. Framingham study insights on the hazards of elevated blood pressure. JAMA. 2008;300:2545.\nSantoro D, Caccamo D, Lucisano S, Buemi M, Sebekova K, Teta D, et al. Interplay of vitamin D, erythropoiesis, and the renin-angiotensin system. Bio Med Res Int. 2015;2015:1.\nAfzal S, Bojesen SE, Nordestgaard BG. Low 25-hydroxyvitamin D and risk of type 2 diabetes: a prospective cohort study and metaanalysis. Clin Chem. 2013;59:381.\nSong Y, Wang L, Pittas AG, Del Gobbo LC, Zhang C, Manson JE, et al. Blood 25-hydroxy vitamin D levels and incident type 2 diabetes: a meta-analysis of prospective studies. Diabetes care. 2013;36:1422.\nPonda MP, Huang XX, Odeh MA, Breslow JL, Kaufman HW. Vitamin D may not improve lipid levels: a serial clinical laboratory data study. Circulation. 2012;126:270.\nZittermann AF, Gummert J, Borgermann J. The role of vitamin D in dyslipidemia and cardiovascular disease. Curr Pharm Design. 2011;17:933.\nTu WJ, Zhao SJ, Xu DJ, Chen H. Serum 25-hydroxyvitamin D predicts the short-term outcomes of Chinese patients with acute ischaemic stroke. Clin Sci. 2014;126:339.\nPark KY, Chung PW, Kim YB, Moon HS, Suh BC, Won YS, et al. Serum vitamin D status as a predictor of prognosis in patients with acute ischemic stroke. Cerebrovasc Dis. 2015;40:73.\nMichos ED, Gottesman RF. Vitamin D for the prevention of stroke incidence and disability: promising but too early for prime time. Eur J Neurol. 2013;20:3.\nWitham MD, Dove FJ, Sugden JA, Doney AS, Struthers AD. The effect of vitamin D replacement on markers of vascular health in stroke patients—a randomised controlled trial. Nutr Metab Cardiovas. 2012;22:864.\nEvans MA, Kim HA, Ling YH, Uong S, Vinh A, De Silva TM, et al. Vitamin D3 supplementation reduces subsequent brain injury and inflammation associated with ischemic stroke. Neuromol Med. 2018;20:147.\nMoraes RB, Friedman G, Wawrzeniak C, Marques LS, Nagel FM, Lisboa TC, etal. Vitamin D deficiency is independently associated with mortality among critically ill patients. Clinics (Sao Paulo). 2015; 70: 326.\nVenkatram S, Chilimuri S, Adrish M, Salako A, Patel M, Diaz-Fuentes G. Vitamin D deficiency is associated with mortality in the medical intensive care unit. Crit Care. 2011;15:R292.\nHu W, Liu D, Qin L, Wang L, Tang Q, Wang G. Decreasing serum 25hydroxyvitamin D levels and risk of early neurological deterioration in patients with ischemic stroke. Brain and Behav. 2019;9:1227.",{"EN":272},"Vitamin D deficiency has been proposed as a risk factors of cerebrovascular stroke. The aim of this study was firstly, to assess the serum level of vitamin D in cerebral stroke patients and secondly, to examine if its deficiency was associated with stroke severity and outcome. We utilized a case-control study design and recruited 138 acute stroke patients and 138 age- and sex-matched controls from subjects attending outpatient clinic for other reasons. All participants were subjected to full general and neurological examination. Brain imaging CT and\u002For MRI was performed. Blood samples were collected for measurement of serum level of vitamin D (ng\u002Fml) by ELISA, alkaline phosphatase, serum calcium, and phosphorous. The stroke severity was assessed by the National Institutes of Health Stroke Scale (NIHSS) and stroke outcome was assessed by modified Rankin Scale (mRS). Stroke patients had significant lower levels of vitamin D compared with the control group. Vitamin D deficiency remained significantly associated with the NIHSS stroke severity score and the mRS 3-month stroke outcome after controlling for other significant factors such as age, dyslipidemia, and infarction size using multivariable logistic regression analysis. Our results demonstrated that stroke patients suffer from vitamin D deficiency, which was associated with both stroke severity and poor outcome. Vitamin D supplementation could exert a therapeutic role in the management of cerebral stroke.",{"EN":274},"Serum vitamin D levels in acute stroke patients",{"VOID":276},"10.1186\u002Fs41983-019-0129-0","https:\u002F\u002Fejnpn.springeropen.com\u002Farticles\u002F10.1186\u002Fs41983-019-0129-0",[279,295,311,326,341],{"id":280,"sortIndex":176,"researcher":18,"roles":281,"affiliations":282,"properties":292},"14a8e824-cde0-486f-a78f-9dd4885ace0a",[178],[283],{"id":18,"sortIndex":19,"affiliation":284,"properties":18},{"id":285,"createTime":286,"updateTime":286,"relativeEntities":287,"slug":288,"properties":289,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"3bccab4f-97d6-46d9-a11d-3be4d8b757bf","2024-04-15T05:26:43.070+00:00",[],"Department-of-Neurology-Faculty-of-Medicine-Zagazig-University-Sharkia-Egypt",{"title":290},{"EN":291},"Department of Neurology, Faculty of Medicine, Zagazig University, Sharkia, Egypt",{"title":293},{"VI":294},"Rasha M. Fahmi",{"id":296,"sortIndex":297,"researcher":18,"roles":298,"affiliations":299,"properties":308},"e517b2d4-1b79-4cc3-97d3-63d45e351e5a",4,[178],[300],{"id":18,"sortIndex":19,"affiliation":301,"properties":18},{"id":302,"createTime":303,"updateTime":303,"relativeEntities":304,"slug":18,"properties":305,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"f6238225-d65e-442f-ab8a-929f36ef54a4","2023-12-14T22:49:21.844+00:00",[],{"title":306},{"VI":307},"Department of Public Health and Community Medicine, Zagazig University, Sharkia, Egypt",{"title":309},{"VI":310},"Ahmed F. Elsaid",{"id":312,"sortIndex":194,"researcher":18,"roles":313,"affiliations":314,"properties":323},"271f17b0-510a-470f-8415-c75b4e5c443d",[178],[315],{"id":18,"sortIndex":19,"affiliation":316,"properties":18},{"id":317,"createTime":318,"updateTime":318,"relativeEntities":319,"slug":18,"properties":320,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"9f11d052-5c7f-408c-a4ba-208da380383b","2023-12-14T22:48:58.628+00:00",[],{"title":321},{"VI":322},"Department of Medical Biochemistry, Zagazig University, Sharkia, Egypt",{"title":324},{"VI":325},"Nermin Raafat",{"id":327,"sortIndex":19,"researcher":18,"roles":328,"affiliations":329,"properties":338},"df8841af-af4f-4b8a-9cbe-176c1cf24f0b",[178],[330],{"id":18,"sortIndex":19,"affiliation":331,"properties":18},{"id":332,"createTime":333,"updateTime":333,"relativeEntities":334,"slug":18,"properties":335,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"9e5460a9-7c8f-4076-b66f-07527e149937","2023-12-14T22:49:21.760+00:00",[],{"title":336},{"VI":337},"Department of Internal Medicine, Zagazig University, Sharkia, Egypt",{"title":339},{"VI":340},"Fayrouz O. Selim",{"id":342,"sortIndex":207,"researcher":18,"roles":343,"affiliations":344,"properties":350},"2e3dcdf6-e1c1-4ca3-8194-c939166707ed",[178],[345],{"id":18,"sortIndex":19,"affiliation":346,"properties":18},{"id":332,"createTime":333,"updateTime":333,"relativeEntities":347,"slug":18,"properties":348,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":349},{"VI":337},{"title":351},{"VI":352},"Ayman E. Ali",{"url":277,"publisher":354,"properties":381},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":355,"slug":10,"properties":356,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":359,"manageAffiliations":360,"indexDatabases":361,"url":117,"thumbnailPath":18,"statistic":376,"gsStatistic":18,"type":147,"analyzePriority":18},[],{"issn":357,"title":358},{"VOID":13},{"EN":15},[],[],[362,369],{"id":77,"indexDatabase":363,"url":90,"indexYears":91,"academicFieldIds":368,"indexDatabaseRanking":97},{"id":79,"createTime":80,"updateTime":81,"relativeEntities":364,"label":365,"description":366,"key":87,"publicationTags":367,"standard":18},[],{"EN":84,"VI":84},{"EN":84,"VI":86},[89],[93,94,95,96],{"id":99,"indexDatabase":370,"url":114,"indexYears":18,"academicFieldIds":375,"indexDatabaseRanking":18},{"id":101,"createTime":102,"updateTime":103,"relativeEntities":371,"label":372,"description":373,"key":110,"publicationTags":374,"standard":18},[],{"EN":106,"VI":106},{"VI":108,"EN":109},[112,113],[116],{"impactFactor":19,"impactFactorByYear":377,"i10Index":123,"i10IndexLast5Year":124,"totalPublication":125,"totalPublicationByYear":378,"totalCitation":133,"totalCitationByYear":379,"totalCitationPerPublication":140,"totalCitationPerPublicationByYear":380,"hindexLast5Year":123,"hindex":123},{"2019":120,"2020":121,"2021":122,"2022":122,"2023":121},{"2018":127,"2019":128,"2020":129,"2021":130,"2022":131,"2023":132,"2024":127},{"2018":135,"2019":136,"2020":137,"2021":138,"2022":139},{"2018":142,"2019":143,"2020":144,"2021":145,"2022":146},{"volume":382,"pages":384},{"VOID":383},"55",{"VOID":385},"1-8","2019-12-09",2019,{"id":389,"createTime":390,"updateTime":391,"relativeEntities":392,"slug":393,"properties":394,"entityType":169,"verifyStatus":170,"verifyTime":391,"verifyNote":171,"syncStatus":17,"languages":406,"translateLanguages":18,"viewCount":19,"primaryUrl":408,"fullTextUrl":18,"authors":409,"publicationType":230,"publisherRelationship":442,"citationCount":176,"citationInfo":470,"publishDate":472,"publishYear":473,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":474,"isForceReanalyzing":261},"55a34918-d49d-4077-822c-3ed5559bf6d1","2024-04-14T23:14:04.475+00:00","2024-09-30T23:55:12.848+00:00",[],"Anti-GAD-associated-limbic-encephalitis-an-unusual-clinical-manifestation-from-northwest-of-Ireland",{"mag":395,"keywords":397,"openalex":398,"abstract":400,"title":402,"doi":404},{"VOID":396},"3032095609",{},{"VOID":399},"W3032095609",{"EN":401},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>We report an unusual manifestation of anti-GAD-associated limbic encephalitis in a 59-year-old man following pacemaker insertion for cardiac pauses. Clinically, the association of anti-GAD antibody with limbic encephalitis is rare. He presented with a complex constellation of symptoms, posing a diagnostic and therapeutic challenge.\u003C\u002Fjats:p>",{"EN":403},"Anti-GAD-associated limbic encephalitis: an unusual clinical manifestation from northwest of Ireland",{"VOID":405},"10.1186\u002Fs41983-020-0160-1",[407],"EN","https:\u002F\u002Fejnpn.springeropen.com\u002Farticles\u002F10.1186\u002Fs41983-020-0160-1",[410,428],{"id":411,"sortIndex":19,"researcher":18,"roles":412,"affiliations":413,"properties":423},"cb2a32db-72b1-4cdd-bb18-379a37331751",[],[414],{"id":18,"sortIndex":19,"affiliation":415,"properties":18},{"id":416,"createTime":417,"updateTime":417,"relativeEntities":418,"slug":419,"properties":420,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"6b8f5b93-3a55-4b21-8e4f-ed677ee53063","2024-04-14T23:14:04.484+00:00",[],"Department-of-Neurology-Sligo-University-Hospital-Sligo-Ireland",{"title":421},{"EN":422},"Department of Neurology, Sligo University Hospital, Sligo, Ireland",{"openalex":424,"title":426},{"VOID":425},"A5051589190",{"EN":427},"Salman Mansoor",{"id":429,"sortIndex":176,"researcher":18,"roles":430,"affiliations":431,"properties":437},"7c1a0e86-a2d3-4a98-9f6d-2399f55fb21c",[],[432],{"id":18,"sortIndex":19,"affiliation":433,"properties":18},{"id":416,"createTime":417,"updateTime":417,"relativeEntities":434,"slug":419,"properties":435,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":436},{"EN":422},{"openalex":438,"title":440},{"VOID":439},"A5002713363",{"EN":441},"Kevin Murphy",{"url":18,"publisher":443,"properties":18},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":444,"slug":10,"properties":445,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":448,"manageAffiliations":449,"indexDatabases":450,"url":117,"thumbnailPath":18,"statistic":465,"gsStatistic":18,"type":147,"analyzePriority":18},[],{"issn":446,"title":447},{"VOID":13},{"EN":15},[],[],[451,458],{"id":77,"indexDatabase":452,"url":90,"indexYears":91,"academicFieldIds":457,"indexDatabaseRanking":97},{"id":79,"createTime":80,"updateTime":81,"relativeEntities":453,"label":454,"description":455,"key":87,"publicationTags":456,"standard":18},[],{"EN":84,"VI":84},{"EN":84,"VI":86},[89],[93,94,95,96],{"id":99,"indexDatabase":459,"url":114,"indexYears":18,"academicFieldIds":464,"indexDatabaseRanking":18},{"id":101,"createTime":102,"updateTime":103,"relativeEntities":460,"label":461,"description":462,"key":110,"publicationTags":463,"standard":18},[],{"EN":106,"VI":106},{"VI":108,"EN":109},[112,113],[116],{"impactFactor":19,"impactFactorByYear":466,"i10Index":123,"i10IndexLast5Year":124,"totalPublication":125,"totalPublicationByYear":467,"totalCitation":133,"totalCitationByYear":468,"totalCitationPerPublication":140,"totalCitationPerPublicationByYear":469,"hindexLast5Year":123,"hindex":123},{"2019":120,"2020":121,"2021":122,"2022":122,"2023":121},{"2018":127,"2019":128,"2020":129,"2021":130,"2022":131,"2023":132,"2024":127},{"2018":135,"2019":136,"2020":137,"2021":138,"2022":139},{"2018":142,"2019":143,"2020":144,"2021":145,"2022":146},{"total":176,"publishYear":18,"statisticByYear":471},{"2021":176},"2020-12-01",2020,[475,479,483,487,491,495,499,503,507],{"id":18,"text":476,"url":18,"identifiers":477},"Dalmau J, Rosenfeld MR. Paraneoplastic syndromes of the CNS. Lancet Neurol. 2008;7(4):327–40.",{"doi":478},"10.1016\u002FS1474-4422(08)70060-7",{"id":18,"text":480,"url":18,"identifiers":481},"Lancaster E, Dalmau J. Neuronal autoantigens--pathogenesis, associated disorders and antibody testing. Nat Rev Neurol. 2012;8:380–90.",{"doi":482},"10.1038\u002Fnrneurol.2012.99",{"id":18,"text":484,"url":18,"identifiers":485},"Lernmark A. Glutamic acid decarboxylase--gene to antigen to disease. J Intern Med. 1996;240(5):259–77.",{"doi":486},"10.1046\u002Fj.1365-2796.1996.27859000.x",{"id":18,"text":488,"url":18,"identifiers":489},"Scherbaum WA. Cytoplasmic islet cell antibodies (ICA): towards a molecular understanding of the autoantigens. Clin Endocrinol. 1994;40(1):15–8.",{"doi":490},"10.1111\u002Fj.1365-2265.1994.tb02437.x",{"id":18,"text":492,"url":18,"identifiers":493},"Seissler J, Bieg S, Yassin N, Mauch L, Northemann W, Boehm BO. Association between antibodies to the MR 67,000 isoform of glutamate decarboxylase (GAD) and type 1 (insulin-dependent) diabetes mellitus with coexisting autoimmune polyendocrine syndrome type II. Autoimmunity. 1994;19(4):231–8.",{"doi":494},"10.3109\u002F08916939409071348",{"id":18,"text":496,"url":18,"identifiers":497},"Honnorat J, Saiz A, Giometto B, Vincent A, Brieva L, de Andres C, et al. Cerebellar ataxia with anti-glutamic acid decarboxylase antibodies: study of 14 patients. Arch Neurol. 2001;58(2):225–30.",{"doi":498},"10.1001\u002Farchneur.58.2.225",{"id":18,"text":500,"url":18,"identifiers":501},"Gagnon MM, Savard M. Limbic encephalitis associated with GAD65 antibodies: brief review of the relevant literature. Can J Neurol Sci. 2016 Jul;43(4):486–93.",{"doi":502},"10.1017\u002Fcjn.2016.13",{"id":18,"text":504,"url":18,"identifiers":505},"Ben Achour N, Ben Younes T, Rebai I, Ben Ahmed M, Kraoua I, Ben Y-TI. Severe dysautonomia as a main feature of anti-GAD encephalitis: report of a paediatric case and literature review. Eur J Paediatr Neurol. 2018;22(3):548–51.",{"doi":506},"10.1016\u002Fj.ejpn.2018.01.004",{"id":18,"text":508,"url":18,"identifiers":509},"Malter MP, Helmstaedter C, Urbach H, et al. Antibodies to glutamic acid decarboxylase define a form of limbic encephalitis. Ann Neurol. 2010;67(4):470–8.",{"doi":510},"10.1002\u002Fana.21917",{"id":512,"createTime":513,"updateTime":514,"relativeEntities":515,"slug":516,"properties":517,"entityType":169,"verifyStatus":170,"verifyTime":526,"verifyNote":171,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":527,"fullTextUrl":18,"authors":528,"publicationType":230,"publisherRelationship":617,"citationCount":18,"citationInfo":18,"publishDate":650,"publishYear":651,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":18,"isForceReanalyzing":261},"6c6b852d-9c65-4c48-a21e-e805fc9849cc","2024-01-27T17:55:28.000+00:00","2025-01-25T23:52:03.868+00:00",[],"Safety-and-efficacy-of-sodium-oligomannate-in-patients-with-Alzheimer-s-disease-a-systematic-review-and-meta-analysis",{"references":518,"abstract":520,"title":522,"doi":524},{"VOID":519},"Soria Lopez JA, González HM, Léger GC. Alzheimer’s disease. Handb Clin Neurol. 2019;167:231–55.\nWHO. Dementia cases set to triple by 2050 but still largely ignored: WHO 2012. Available from: https:\u002F\u002Fwww.who.int\u002Fnews\u002Fitem\u002F11-04-2012-dementia-cases-set-to-triple-by-2050-but-still-largely-ignored.\nWong W. Economic burden of Alzheimer disease and managed care considerations. Am J Manag Care. 2020;26(8 Suppl):S177–83.\nLiu S, Li C, Shi Z, Wang X, Zhou Y, Liu S, et al. Caregiver burden and prevalence of depression, anxiety and sleep disturbances in Alzheimer’s disease caregivers in China. J Clin Nurs. 2017;26(9–10):1291–300.\nSerý O, Povová J, Míšek I, Pešák L, Janout V. Molecular mechanisms of neuropathological changes in Alzheimer’s disease: a review. Folia Neuropathol. 2013;51(1):1–9.\nSalloway S, Sperling R, Fox NC, Blennow K, Klunk W, Raskind M, et al. Two phase 3 trials of bapineuzumab in mild-to-moderate Alzheimer’s disease. N Engl J Med. 2014;370(4):322–33.\nCastello MA, Jeppson JD, Soriano S. Moving beyond anti-amyloid therapy for the prevention and treatment of Alzheimer’s disease. BMC Neurol. 2014;14:169.\nPanza F, Solfrizzi V, Imbimbo BP, Logroscino G. Amyloid-directed monoclonal antibodies for the treatment of Alzheimer’s disease: the point of no return? Expert Opin Biol Ther. 2014;14(10):1465–76.\nRogers SL, Farlow MR, Doody RS, Mohs R, Friedhoff LT. A 24-week, double-blind, placebo-controlled trial of donepezil in patients with Alzheimer’s disease. Donepezil Study Group. Neurology. 1998;50(1):136–45.\nRösler M, Anand R, Cicin-Sain A, Gauthier S, Agid Y, Dal-Bianco P, et al. Efficacy and safety of rivastigmine in patients with Alzheimer’s disease: international randomised controlled trial. BMJ. 1999;318(7184):633–8.\nvan Dyck CH, Tariot PN, Meyers B, Malca RE. A 24-week randomized, controlled trial of memantine in patients with moderate-to-severe Alzheimer disease. Alzheimer Dis Assoc Disord. 2007;21(2):136–43.\nWilcock GK, Lilienfeld S, Gaens E. Efficacy and safety of galantamine in patients with mild to moderate Alzheimer’s disease: multicentre randomised controlled trial. Galantamine International-1 Study Group. BMJ. 2000;321(7274):1445–9.\nWang T. New drug research and development for Alzheimer’s pathology: present and prospect. Shanghai Arch Psychiatry. 2017;29(4):237–9.\nKong LN, Geng MY, Mu L, Xin XL, Yang N, Zuo PP. Effects of acidic oligose on differentially expressed genes in the mice model of Alzheimer’s disease by microarray. Yao Xue Xue Bao. 2005;40(12):1105–9.\nFan Y, Hu J, Li J, Yang Z, Xin X, Wang J, et al. Effect of acidic oligosaccharide sugar chain on scopolamine-induced memory impairment in rats and its related mechanisms. Neurosci Lett. 2005;374(3):222–6.\nHu J, Geng M, Li J, Xin X, Wang J, Tang M, et al. Acidic oligosaccharide sugar chain, a marine-derived acidic oligosaccharide, inhibits the cytotoxicity and aggregation of amyloid beta protein. J Pharmacol Sci. 2004;95(2):248–55.\nMoher D, Liberati A, Tetzlaff J, Altman DG. Preferred reporting items for systematic reviews and meta-analyses: the PRISMA statement. Ann Intern Med. 2009;151(4):264–9 (w64).\nHiggins JP, Thomas J, Chandler J, Cumpston M, Li T, Page MJ, et al. Cochrane handbook for systematic reviews of interventions. USA: Wiley; 2019.\nHiggins JP, Altman DG, Gøtzsche PC, Jüni P, Moher D, Oxman AD, et al. The Cochrane Collaboration’s tool for assessing risk of bias in randomised trials. BMJ. 2011;343:5928.\nMustafa RA, Santesso N, Brozek J, Akl EA, Walter SD, Norman G, et al. The GRADE approach is reproducible in assessing the quality of evidence of quantitative evidence syntheses. J Clin Epidemiol. 2013;66(7):736–42 (quiz 42.e1-5).\nZhang LF, Zhang YP, Lin PX, Xue LH. Efficacy and safety of sodium oligomannate in the treatment of Alzheimer’s disease. Pak J Pharm Sci. 2022;35(3):741–5.\nXiao S, Chan P, Wang T, Hong Z, Wang S, Kuang W, et al. A 36-week multicenter, randomized, double-blind, placebo-controlled, parallel-group, phase 3 clinical trial of sodium oligomannate for mild-to-moderate Alzheimer’s dementia. Alzheimers Res Ther. 2021;13(1):62.\nWang T, Kuang W, Chen W, Xu W, Zhang L, Li Y, et al. A phase II randomized trial of sodium oligomannate in Alzheimer’s dementia. Alzheimers Res Ther. 2020;12(1):110.\nWang X, Sun G, Feng T, Zhang J, Huang X, Wang T, et al. Sodium oligomannate therapeutically remodels gut microbiota and suppresses gut bacterial amino acids-shaped neuroinflammation to inhibit Alzheimer’s disease progression. Cell Res. 2019;29(10):787–803.\nKueper JK, Speechley M, Montero-Odasso M. The Alzheimer’s disease assessment scale-cognitive subscale (ADAS-Cog): modifications and responsiveness in pre-dementia populations. A narrative review. J Alzheimers Dis. 2018;63(2):423–44.\nHansen RA, Gartlehner G, Webb AP, Morgan LC, Moore CG, Jonas DE. Efficacy and safety of donepezil, galantamine, and rivastigmine for the treatment of Alzheimer’s disease: a systematic review and meta-analysis. Clin Interv Aging. 2008;3(2):211–25.\nRobert P, Ferris S, Gauthier S, Ihl R, Winblad B, Tennigkeit F. Review of Alzheimer’s disease scales: is there a need for a new multi-domain scale for therapy evaluation in medical practice? Alzheimers Res Ther. 2010;2(4):24.\nLong-term Efficacy and Safety Study of GV-971. https:\u002F\u002FClinicalTrials.gov\u002Fshow\u002FNCT05181475.\nEfficacy and Safety of Donepezil and Sodium Oligomannate in Patients With Mild to Moderate Alzheimer's Disease. https:\u002F\u002FClinicalTrials.gov\u002Fshow\u002FNCT05114499.",{"EN":521},"We aim to evaluate the efficacy and safety of a new marine oligosaccharide drug, sodium oligomannate (GV-971), developed in China to treat Alzheimer’s disease (AD). We researched the following databases: Embase, Web of Science, PubMed, Cochrane library, and Scopus until Sep 2022. We used the Cochrane risk of bias tool to assess the risk of bias and the GRADE scale to assess the quality of the evidence. The meta-analysis was performed using review manager 5.4. We included three randomized controlled trials with 1108 patients. Sodium oligomannate improved the AD assessment scale-cognitive subscale compared to the placebo at 12, 24, and 36 weeks (mean difference (MD) = − 0.69, 95% confidence interval (CI) [− 1.23 to − 0.14], p = 0.01), (MD = − 0.68, 95% CI [− 1.26 to − 0.10], P = 0.02), and (MD = − 3.84, 95% CI [− 6.40 to − 1.27], and P = 0.003), respectively. On the other hand, results showed no significance in terms of adverse events and other assessed scales (Clinician’s Interview-Based Impression of Change with caregiver input, AD Cooperative Study-Activities of Daily Living, and Neuropsychiatric Inventory) (p > 0.05). Sodium oligomannate is a well-tolerated and promising drug for Alzheimer’s patients. However, to better evaluate sodium oligomannate’s efficacy in the clinical setting, we need more randomized controlled trials with larger samples and higher quality.",{"EN":523},"Safety and efficacy of sodium oligomannate in patients with Alzheimer’s disease: a systematic review and meta-analysis",{"VOID":525},"10.1186\u002Fs41983-023-00682-y","2025-01-25T23:52:03.867+00:00","https:\u002F\u002Fejnpn.springeropen.com\u002Farticles\u002F10.1186\u002Fs41983-023-00682-y",[529,546,562,574,586,601],{"id":530,"sortIndex":19,"researcher":18,"roles":531,"affiliations":532,"properties":543},"03b9e46c-2198-4db2-b7b0-9dd3e3e9c546",[178],[533],{"id":18,"sortIndex":19,"affiliation":534,"properties":18},{"id":535,"createTime":536,"updateTime":537,"relativeEntities":538,"slug":539,"properties":540,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"e1a929d1-aebf-4781-846b-8c5430dc3647","2024-04-17T08:32:32.759+00:00","2024-10-16T19:36:32.105+00:00",[],"Faculty-of-Medicine-Al-Azhar-University-Cairo-Egypt-",{"title":541},{"EN":542},"Faculty of Medicine, Al-Azhar University, Cairo, Egypt.",{"title":544},{"VI":545},"Anas Zakarya Nourelden",{"id":547,"sortIndex":548,"researcher":18,"roles":549,"affiliations":550,"properties":559},"b20cb8c9-8367-4809-9fc9-4c07df224cba",5,[178],[551],{"id":18,"sortIndex":19,"affiliation":552,"properties":18},{"id":553,"createTime":554,"updateTime":554,"relativeEntities":555,"slug":18,"properties":556,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"ab99c2bd-9937-448a-9d2f-9faf759de481","2023-12-22T23:00:47.013+00:00",[],{"title":557},{"VI":558},"Faculty of Medicine, Al-Azhar University, Assiut, Egypt",{"title":560},{"VI":561},"Mohamed Sayed Zaazouee",{"id":563,"sortIndex":194,"researcher":18,"roles":564,"affiliations":565,"properties":571},"9556f858-5037-47af-a51f-e6967740aaa3",[178],[566],{"id":18,"sortIndex":19,"affiliation":567,"properties":18},{"id":535,"createTime":536,"updateTime":537,"relativeEntities":568,"slug":539,"properties":569,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":570},{"EN":542},{"title":572},{"VI":573},"Abdulrahman Ibrahim Hagrass",{"id":575,"sortIndex":176,"researcher":18,"roles":576,"affiliations":577,"properties":583},"609f765d-57cc-4c94-81dc-325fe2d57609",[178],[578],{"id":18,"sortIndex":19,"affiliation":579,"properties":18},{"id":535,"createTime":536,"updateTime":537,"relativeEntities":580,"slug":539,"properties":581,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":582},{"EN":542},{"title":584},{"VI":585},"Ibrahim Kamal",{"id":587,"sortIndex":207,"researcher":18,"roles":588,"affiliations":589,"properties":598},"a6938382-32c6-4a88-a72e-dc444eff11b4",[178],[590],{"id":18,"sortIndex":19,"affiliation":591,"properties":18},{"id":592,"createTime":593,"updateTime":593,"relativeEntities":594,"slug":18,"properties":595,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"86fd5203-8a20-44c4-b587-23752a61bbe4","2024-01-30T09:02:44.803+00:00",[],{"title":596},{"VI":597},"Department of Pharmacotherapy, College of Pharmacy, The University of Utah, Salt Lake City, USA",{"title":599},{"VI":600},"Abdelrahman G. Tawfik",{"id":602,"sortIndex":297,"researcher":18,"roles":603,"affiliations":604,"properties":614},"00cd6ab0-84ac-44fc-b041-3392c5f254de",[178],[605],{"id":18,"sortIndex":19,"affiliation":606,"properties":18},{"id":607,"createTime":608,"updateTime":608,"relativeEntities":609,"slug":610,"properties":611,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"c34d918b-36e1-4bbf-86ef-e4e8de83d61f","2024-04-19T23:40:47.839+00:00",[],"Faculty-of-Medicine-Minia-University-Minia-Egypt",{"title":612},{"EN":613},"Faculty of Medicine, Minia University, Minia, Egypt",{"title":615},{"VI":616},"Ahmed Hashem Fathallah",{"url":527,"publisher":618,"properties":645},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":619,"slug":10,"properties":620,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":623,"manageAffiliations":624,"indexDatabases":625,"url":117,"thumbnailPath":18,"statistic":640,"gsStatistic":18,"type":147,"analyzePriority":18},[],{"issn":621,"title":622},{"VOID":13},{"EN":15},[],[],[626,633],{"id":77,"indexDatabase":627,"url":90,"indexYears":91,"academicFieldIds":632,"indexDatabaseRanking":97},{"id":79,"createTime":80,"updateTime":81,"relativeEntities":628,"label":629,"description":630,"key":87,"publicationTags":631,"standard":18},[],{"EN":84,"VI":84},{"EN":84,"VI":86},[89],[93,94,95,96],{"id":99,"indexDatabase":634,"url":114,"indexYears":18,"academicFieldIds":639,"indexDatabaseRanking":18},{"id":101,"createTime":102,"updateTime":103,"relativeEntities":635,"label":636,"description":637,"key":110,"publicationTags":638,"standard":18},[],{"EN":106,"VI":106},{"VI":108,"EN":109},[112,113],[116],{"impactFactor":19,"impactFactorByYear":641,"i10Index":123,"i10IndexLast5Year":124,"totalPublication":125,"totalPublicationByYear":642,"totalCitation":133,"totalCitationByYear":643,"totalCitationPerPublication":140,"totalCitationPerPublicationByYear":644,"hindexLast5Year":123,"hindex":123},{"2019":120,"2020":121,"2021":122,"2022":122,"2023":121},{"2018":127,"2019":128,"2020":129,"2021":130,"2022":131,"2023":132,"2024":127},{"2018":135,"2019":136,"2020":137,"2021":138,"2022":139},{"2018":142,"2019":143,"2020":144,"2021":145,"2022":146},{"volume":646,"pages":648},{"VOID":647},"59",{"VOID":649},"1-10","2023-06-21",2023,{"id":653,"createTime":654,"updateTime":655,"relativeEntities":656,"slug":657,"properties":658,"entityType":169,"verifyStatus":170,"verifyTime":655,"verifyNote":171,"syncStatus":17,"languages":668,"translateLanguages":18,"viewCount":19,"primaryUrl":669,"fullTextUrl":18,"authors":670,"publicationType":230,"publisherRelationship":747,"citationCount":19,"citationInfo":780,"publishDate":18,"publishYear":18,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":782,"isForceReanalyzing":261},"ed787a79-5366-45ed-96ba-f99f43afef75","2024-04-21T02:24:16.393+00:00","2025-01-06T23:51:54.119+00:00",[],"White-matter-lesion-load-and-location-in-relation-to-cognitive-impairment-in-relapsing-remitting-multiple-sclerosis",{"keywords":659,"openalex":660,"abstract":662,"title":664,"doi":666},{},{"VOID":661},"W4394812020",{"EN":663},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:sec>\n                \u003Cjats:title>Background\u003C\u002Fjats:title>\n                \u003Cjats:p>In relapsing–remitting multiple sclerosis (RRMS) the connection between cognitive impairment (CI) and white matter lesion load (WM-LL) and location is still unclear. This study aimed to identify the relationship between CI in RRMS patients and WM-LL and locations using a fully automated platform. CI and WM-LL were evaluated in 90 patients with RRMS using the Brief International Cognitive Assessment for Multiple Sclerosis (BICAMS) and Automated MRI volumetric measures of WM-LL and lesion distribution. Regression analysis of BICAMS as a dependent variable with different clinical and radiological parameters was performed.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Results\u003C\u002Fjats:title>\n                \u003Cjats:p>Data were obtained from 90 patients with RRMS who had a mean age of 32.74 ± 8.43 years and a female-to-male ratio of 3:1. The mean (± SD) cognitive rating scores for the BICAMS subtests were 28.07 ± 11.78 for the Symbol Digit Modalities Test (SDMT), 42.32 ± 12.46 for the California Verbal Learning Test-II (CVLT-II), and 16.13 ± 8.17 for the Brief Visuospatial Memory Test-Revised (BVMT-R). According to the BICAMS criteria, 29 cases (32.2%) had CI. BICAMS scores were significantly correlated with age, education level, relapse frequency, disease duration, and time to start disease-modifying therapies. Whole WM-LL and periventricular lesion load were significantly associated with CI. After controlling for age, sex, and education, logistic regression analysis revealed that total WM-LL was the best predictor for CI together with duration of illness and years of education. The cut-off value of 12.85 cc for total WM-LL predicted CI.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Conclusions\u003C\u002Fjats:title>\n                \u003Cjats:p>Whole WM-LL and periventricular lesion load are the best anatomical predictors for CI probably due to the effect on the anterior commissural fibers while years of education and duration of disease are the best demographic predictors for CI.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>",{"EN":665},"White matter lesion load and location in relation to cognitive impairment in relapsing–remitting multiple sclerosis",{"VOID":667},"10.1186\u002Fs41983-024-00826-8",[407],"https:\u002F\u002Fejnpn.springeropen.com\u002Farticles\u002F10.1186\u002Fs41983-024-00826-8",[671,691,708,725],{"id":672,"sortIndex":194,"researcher":18,"roles":673,"affiliations":674,"properties":684},"36e1325c-558c-4f87-9f84-2b8b6ac92a38",[],[675],{"id":676,"sortIndex":19,"affiliation":677,"properties":18},"2b631f6e-d89f-4305-90a0-d70706c64999",{"id":678,"createTime":679,"updateTime":679,"relativeEntities":680,"slug":18,"properties":681,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"60361e48-4845-4fb5-8e87-c5acc2033747","2023-12-28T19:46:17.200+00:00",[],{"title":682},{"VI":683},"Neuropsychiatry Department, Faculty of Medicine, Assiut University Hospital, Assiut, Egypt",{"openalex":685,"orcid":687,"title":689},{"VOID":686},"A5061495353",{"VOID":688},"https:\u002F\u002Forcid.org\u002F0000-0002-0685-6227",{"EN":690},"Doaa M. Mahmoud",{"id":692,"sortIndex":207,"researcher":18,"roles":693,"affiliations":694,"properties":701},"05d89a55-fcac-4756-a89e-58d4caddba70",[],[695],{"id":696,"sortIndex":19,"affiliation":697,"properties":18},"75ad9e78-a782-49bf-a889-3205e6f8388b",{"id":678,"createTime":679,"updateTime":679,"relativeEntities":698,"slug":18,"properties":699,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":700},{"VI":683},{"openalex":702,"orcid":704,"title":706},{"VOID":703},"A5089262909",{"VOID":705},"https:\u002F\u002Forcid.org\u002F0000-0002-2734-233X",{"EN":707},"Ahmed Nasreldein",{"id":709,"sortIndex":176,"researcher":18,"roles":710,"affiliations":711,"properties":718},"f6ef6c2c-55a1-48e9-97e8-14f36d70ff70",[],[712],{"id":713,"sortIndex":19,"affiliation":714,"properties":18},"4be8ef98-9981-4ecb-ba4d-9ee1266cfc20",{"id":678,"createTime":679,"updateTime":679,"relativeEntities":715,"slug":18,"properties":716,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":717},{"VI":683},{"openalex":719,"orcid":721,"title":723},{"VOID":720},"A5010206884",{"VOID":722},"https:\u002F\u002Forcid.org\u002F0000-0001-5679-9833",{"EN":724},"Eman M. Khedr",{"id":726,"sortIndex":19,"researcher":18,"roles":727,"affiliations":728,"properties":740},"4049055e-666a-459f-aeca-39e06a2ca830",[],[729],{"id":730,"sortIndex":19,"affiliation":731,"properties":18},"aab23672-5124-4584-9f9b-17c25d925567",{"id":732,"createTime":733,"updateTime":734,"relativeEntities":735,"slug":736,"properties":737,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"a09015d9-bc95-4581-a9be-adcd1ed36f6d","2024-04-21T02:24:16.403+00:00","2024-08-27T11:41:54.853+00:00",[],"Neuropsychiatric-Department-Faculty-of-Medicine-South-Valley-University-Qena-University-Hospital-Qena-Egypt",{"title":738},{"EN":739},"Neuropsychiatric Department, Faculty of Medicine, South Valley University, Qena University Hospital, Qena, Egypt",{"openalex":741,"orcid":743,"title":745},{"VOID":742},"A5047466934",{"VOID":744},"https:\u002F\u002Forcid.org\u002F0000-0002-5722-5708",{"EN":746},"Mohammed Y. Ezzeldin",{"url":18,"publisher":748,"properties":775},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":749,"slug":10,"properties":750,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":753,"manageAffiliations":754,"indexDatabases":755,"url":117,"thumbnailPath":18,"statistic":770,"gsStatistic":18,"type":147,"analyzePriority":18},[],{"issn":751,"title":752},{"VOID":13},{"EN":15},[],[],[756,763],{"id":77,"indexDatabase":757,"url":90,"indexYears":91,"academicFieldIds":762,"indexDatabaseRanking":97},{"id":79,"createTime":80,"updateTime":81,"relativeEntities":758,"label":759,"description":760,"key":87,"publicationTags":761,"standard":18},[],{"EN":84,"VI":84},{"EN":84,"VI":86},[89],[93,94,95,96],{"id":99,"indexDatabase":764,"url":114,"indexYears":18,"academicFieldIds":769,"indexDatabaseRanking":18},{"id":101,"createTime":102,"updateTime":103,"relativeEntities":765,"label":766,"description":767,"key":110,"publicationTags":768,"standard":18},[],{"EN":106,"VI":106},{"VI":108,"EN":109},[112,113],[116],{"impactFactor":19,"impactFactorByYear":771,"i10Index":123,"i10IndexLast5Year":124,"totalPublication":125,"totalPublicationByYear":772,"totalCitation":133,"totalCitationByYear":773,"totalCitationPerPublication":140,"totalCitationPerPublicationByYear":774,"hindexLast5Year":123,"hindex":123},{"2019":120,"2020":121,"2021":122,"2022":122,"2023":121},{"2018":127,"2019":128,"2020":129,"2021":130,"2022":131,"2023":132,"2024":127},{"2018":135,"2019":136,"2020":137,"2021":138,"2022":139},{"2018":142,"2019":143,"2020":144,"2021":145,"2022":146},{"volume":776,"issue":778},{"VOID":777},"60",{"VOID":779},"1",{"total":19,"publishYear":18,"statisticByYear":781},{},[783,787,791,795,799,803,807,811,815,819,822,826,830,834,838,842,845,849,853,857,861,864,868,872,876,880,884,887,891,895,899,903,907,911,915,919,923,926,929,933,937,941,945,949,953,957,961,965,969,972,976,980,984,988,991,995],{"id":18,"text":784,"url":18,"identifiers":785},"Vasileiou ES, Fitzgerald KC. Multiple sclerosis pathogenesis and updates in targeted therapeutic approaches. Curr Allergy Asthma Rep. 2023;23(9):481–96.",{"doi":786},"10.1007\u002Fs11882-023-01102-0",{"id":18,"text":788,"url":18,"identifiers":789},"Carotenuto A, Costabile T, Pontillo G, Moccia M, Falco F, Petracca M, et al. Cognitive trajectories in multiple sclerosis: a long-term follow-up study. Neurol Sci. 2022;43(2):1215–22.",{"doi":790},"10.1007\u002Fs10072-021-05356-2",{"id":18,"text":792,"url":18,"identifiers":793},"Portaccio E, Amato MP. Cognitive impairment in multiple sclerosis: an update on assessment and management. NeuroSci. 2022;3(4):667–76.",{"doi":794},"10.3390\u002Fneurosci3040048",{"id":18,"text":796,"url":18,"identifiers":797},"Kavaliunas A, Danylaitė Karrenbauer V, Hillert J. Systematic review of the socioeconomic consequences in patients with multiple sclerosis with different levels of disability and cognitive function. Front Neurol. 2022;12: 737211.",{"doi":798},"10.3389\u002Ffneur.2021.737211",{"id":18,"text":800,"url":18,"identifiers":801},"Henry A, Stefaniak N, Schmid F, Kwiatkowski A, Hautecoeur P, Lenne B. Assessing cognitive changes in multiple sclerosis: criteria for a reliable decision. J Clin Exp Neuropsychol. 2023;45(4):321–44.",{"doi":802},"10.1080\u002F13803395.2023.2232122",{"id":18,"text":804,"url":18,"identifiers":805},"Potticary H, Langdon D. A systematic review and meta-analysis of the brief cognitive assessment for multiple sclerosis (BICAMS) international validations. J Clin Med. 2023;12(2):703.",{"doi":806},"10.3390\u002Fjcm12020703",{"id":18,"text":808,"url":18,"identifiers":809},"Ezegbe C, Zarghami A, van der Mei I, Alty J, Honan C, Taylor B. Instruments measuring change in cognitive function in multiple sclerosis: a systematic review. Brain Behav. 2023;13(6): e3009.",{"doi":810},"10.1002\u002Fbrb3.3009",{"id":18,"text":812,"url":18,"identifiers":813},"Dong X, Xu G, Wang J, Yin N, Meng N. Clinical and MRI predictors of cognitive decline in patients with relapsing-remitting multiple sclerosis: a 2-year longitudinal study. Multiple Sclerosis Relat Disord. 2022;65: 103838.",{"doi":814},"10.1016\u002Fj.msard.2022.103838",{"id":18,"text":816,"url":18,"identifiers":817},"Pike AR, James GA, Drew PD, Archer RL. Neuroimaging predictors of longitudinal disability and cognition outcomes in multiple sclerosis patients: a systematic review and meta-analysis. Multiple Sclerosis Relat Disord. 2022;57: 103452.",{"doi":818},"10.1016\u002Fj.msard.2021.103452",{"id":18,"text":820,"url":18,"identifiers":821},"MRI brain volume loss, lesion burden, and clinical outcome in secondary progressive multiple sclerosis—Marcus W Koch, Jop Mostert, Pavle Repovic, James D Bowen, Eva Strijbis, Bernard Uitdehaag, Gary Cutter, 2022.",{},{"id":18,"text":823,"url":18,"identifiers":824},"Bozsik B, Tóth E, Polyák I, Szabó N, Bencsik K, Klivényi P, et al. Reproducibility of lesion count in various subregions on MRI scans in multiple sclerosis. Front Neurol. 2022;13: 843377.",{"doi":825},"10.3389\u002Ffneur.2022.843377",{"id":18,"text":827,"url":18,"identifiers":828},"Thompson AJ, Banwell BL, Barkhof F, Carroll WM, Coetzee T, Comi G, et al. Diagnosis of multiple sclerosis: 2017 revisions of the McDonald criteria. Lancet Neurol. 2018;17(2):162–73.",{"doi":829},"10.1016\u002FS1474-4422(17)30470-2",{"id":18,"text":831,"url":18,"identifiers":832},"Farghaly M, Langdon DW, Shalaby NM, Shehata HS, Abokrysha NT, Hassan A, et al. Reliability and validity of Arabic version of the brief international cognitive assessment for multiple sclerosis: Egyptian dialect. Egypt J Neurol Psychiatry Neurosurg. 2021;57(1):1–8.",{"doi":833},"10.1186\u002Fs41983-021-00303-6",{"id":18,"text":835,"url":18,"identifiers":836},"Benedict RH, Amato MP, Boringa J, Brochet B, Foley F, Fredrikson S, et al. Brief International Cognitive Assessment for MS (BICAMS): international standards for validation. BMC Neurol. 2012;12:55.",{"doi":837},"10.1186\u002F1471-2377-12-55",{"id":18,"text":839,"url":18,"identifiers":840},"Khedr EM, Desoky T, Gamea A, Ezzeldin MY, Zaki AF. Thalamic atrophy, duration of illness, and years of education are the best predictors of cognitive impairment in multiple sclerosis. Multiple Sclerosis Relat Disord. 2023;80: 105180.",{"doi":841},"10.1016\u002Fj.msard.2023.105180",{"id":18,"text":843,"url":18,"identifiers":844},"Romero J, Coupé P, Tourdias T, Linck P, et al. LesionBrain: an online tool for white matter lesion segmentation. Cham: Springer; 2018.",{},{"id":18,"text":846,"url":18,"identifiers":847},"Manjón JV, Coupé P. volBrain: an online MRI brain volumetry system. Front Neuroinform. 2016;10:30.",{"doi":848},"10.3389\u002Ffninf.2016.00030",{"id":18,"text":850,"url":18,"identifiers":851},"Tran P, Thoprakarn U, Gourieux E, Dos Santos CL, Cavedo E, Guizard N, et al. Automatic segmentation of white matter hyperintensities: validation and comparison with state-of-the-art methods on both multiple sclerosis and elderly subjects. Neuroimage Clin. 2022;33: 102940.",{"doi":852},"10.1016\u002Fj.nicl.2022.102940",{"id":18,"text":854,"url":18,"identifiers":855},"Storelli L, Pagani E, Pantano P, Piervincenzi C, Tedeschi G, Gallo A, et al. Methods for brain atrophy MR quantification in multiple sclerosis: application to the multicenter INNI dataset. J Magn Reson Imaging. 2023;58(4):1221–31.",{"doi":856},"10.1002\u002Fjmri.28616",{"id":18,"text":858,"url":18,"identifiers":859},"Sinnecker T, Schädelin S, Benkert P, Ruberte E, Amann M, Lieb JM, et al. Brain atrophy measurement over a MRI scanner change in multiple sclerosis. NeuroImage Clin. 2022;36:103148.",{"doi":860},"10.1016\u002Fj.nicl.2022.103148",{"id":18,"text":862,"url":18,"identifiers":863},"Nabizadeh F, Balabandian M, Rostami MR, Owji M, Sahraian MA, Bidadian M, et al. Association of cognitive impairment and quality of life in patients with multiple sclerosis: a cross-sectional study. Curr J Neurol. 2022;21(3):144–50.",{},{"id":18,"text":865,"url":18,"identifiers":866},"Elshebawy H, Fahmy EM, Elfayoumy NM, Abdelalim AM, Ismail RS. Clinical predictors to cognitive impairment in multiple sclerosis patients. Egypt J Neurol Psychiatry Neurosurg. 2021;57(1):38.",{"doi":867},"10.1186\u002Fs41983-021-00292-6",{"id":18,"text":869,"url":18,"identifiers":870},"Brochet B, Clavelou P, Defer G, De Seze J, Louapre C, Magnin E, et al. Cognitive impairment in secondary progressive multiple sclerosis: effect of disease duration, age, and progressive phenotype. Brain Sci. 2022;12(2):183.",{"doi":871},"10.3390\u002Fbrainsci12020183",{"id":18,"text":873,"url":18,"identifiers":874},"Graves JS, Krysko KM, Hua LH, Absinta M, Franklin RJM, Segal BM. Ageing and multiple sclerosis. Lancet Neurol. 2023;22(1):66–77.",{"doi":875},"10.1016\u002FS1474-4422(22)00184-3",{"id":18,"text":877,"url":18,"identifiers":878},"Temmerman J, Van Der Veken F, Engelborghs S, Guldolf K, Nagels G, Smeets D, et al. Brain volume loss can occur at the rate of normal aging in patients with multiple sclerosis who are free from disease activity. J Clin Med. 2022;11(3):523.",{"doi":879},"10.3390\u002Fjcm11030523",{"id":18,"text":881,"url":18,"identifiers":882},"Coupé P, Planche V, Mansencal B, Kamroui RA, Koubiyr I, Manjòn JV, et al. Lifespan neurodegeneration of the human brain in multiple sclerosis. Hum Brain Mapp. 2023;44(17):5602–11.",{"doi":883},"10.1002\u002Fhbm.26464",{"id":18,"text":885,"url":18,"identifiers":886},"Multiple sclerosis and aging: the dynamics of demyelination and remyelination—Jorge Correale, Maria Celica Ysrraelit, 2022.",{},{"id":18,"text":888,"url":18,"identifiers":889},"Talebi M, Sadigh-Eteghad S, Talebi M, Naseri A, Zafarani F. Predominant domains and associated demographic and clinical characteristics in multiple sclerosis-related cognitive impairment in mildly disabled patients. Egypt J Neurol Psychiatry Neurosurg. 2022;58(1):48.",{"doi":890},"10.1186\u002Fs41983-022-00485-7",{"id":18,"text":892,"url":18,"identifiers":893},"Hechenberger S, Helmlinger B, Ropele S, Pirpamer L, Bachmaier G, Damulina A, et al. Information processing speed as a prognostic marker of physical impairment and progression in patients with multiple sclerosis. Multiple Sclerosis Relat Disord. 2022;57: 103353.",{"doi":894},"10.1016\u002Fj.msard.2021.103353",{"id":18,"text":896,"url":18,"identifiers":897},"Mistri D, Cacciaguerra L, Storelli L, Meani A, Cordani C, Rocca MA, et al. The association between cognition and motor performance is beyond structural damage in relapsing–remitting multiple sclerosis. J Neurol. 2022;269(8):4213–21.",{"doi":898},"10.1007\u002Fs00415-022-11044-8",{"id":18,"text":900,"url":18,"identifiers":901},"Guerra T, Pipoli A, Viterbo RG, Manghisi N, Paolicelli D, Iaffaldano P, et al. Predictors of unemployment status in people with relapsing multiple sclerosis: a single center experience. Neurol Sci. 2022;43(7):4387–92.",{"doi":902},"10.1007\u002Fs10072-022-06029-4",{"id":18,"text":904,"url":18,"identifiers":905},"Prosperini L, Alcamisi I, Quartuccio ME, Rossi I, Fortuna D, Ruggieri S. Brain and cognitive reserve mitigate balance dysfunction in multiple sclerosis. Neurol Sci. 2023;44(12):4411–20.",{"doi":906},"10.1007\u002Fs10072-023-06951-1",{"id":18,"text":908,"url":18,"identifiers":909},"Benedict RH, Morrow SA, Weinstock Guttman B, Cookfair D, Schretlen DJ. Cognitive reserve moderates decline in information processing speed in multiple sclerosis patients. J Int Neuropsychol Soc. 2010;16(5):829–35.",{"doi":910},"10.1017\u002FS1355617710000688",{"id":18,"text":912,"url":18,"identifiers":913},"Sartori E, Edan G. Assessment of cognitive dysfunction in multiple sclerosis. J Neurol Sci. 2006;245(1–2):169–75.",{"doi":914},"10.1016\u002Fj.jns.2005.07.016",{"id":18,"text":916,"url":18,"identifiers":917},"Russo C, Morabito F, Luise F, Piromalli A, Battaglia L, Vinci A, et al. Hyperhomocysteinemia is associated with cognitive impairment in multiple sclerosis. J Neurol. 2008;255(1):64–9.",{"doi":918},"10.1007\u002Fs00415-007-0668-7",{"id":18,"text":920,"url":18,"identifiers":921},"Patti F, Amato MP, Trojano M, Bastianello S, Tola MR, Goretti B, et al. Cognitive impairment and its relation with disease measures in mildly disabled patients with relapsing–remitting multiple sclerosis: baseline results from the Cognitive Impairment in Multiple Sclerosis (COGIMUS) study. Mult Scler. 2009;15(7):779–88.",{"doi":922},"10.1177\u002F1352458509105544",{"id":18,"text":924,"url":18,"identifiers":925},"Society NM. Cognitive Changes 2023. Available from: https:\u002F\u002Fwww.nationalmssociety.org\u002FSymptoms-Diagnosis\u002FMS-Symptoms\u002FCognitive-Changes.",{},{"id":18,"text":927,"url":18,"identifiers":928},"Fulton JC, Grossman RI, Udupa J, Mannon LJ, Grossman M, Wei L, et al. MR lesion load and cognitive function in patients with relapsing–remitting multiple sclerosis. AJNR Am J Neuroradiol. 1999;20(10):1951–5.",{},{"id":18,"text":930,"url":18,"identifiers":931},"Patti F, De Stefano M, Lavorgna L, Messina S, Chisari CG, Ippolito D, et al. Lesion load may predict long-term cognitive dysfunction in multiple sclerosis patients. PLoS ONE. 2015;10(3): e0120754.",{"doi":932},"10.1371\u002Fjournal.pone.0120754",{"id":18,"text":934,"url":18,"identifiers":935},"Giorgio A, De Stefano N. Cognition in multiple sclerosis: relevance of lesions, brain atrophy and proton MR spectroscopy. Neurol Sci. 2010;31(Suppl 2):S245–8.",{"doi":936},"10.1007\u002Fs10072-010-0370-x",{"id":18,"text":938,"url":18,"identifiers":939},"Nocentini U, Bozzali M, Spanò B, Cercignani M, Serra L, Basile B, et al. Exploration of the relationships between regional grey matter atrophy and cognition in multiple sclerosis. Brain Imaging Behav. 2014;8(3):378–86.",{"doi":940},"10.1007\u002Fs11682-012-9170-7",{"id":18,"text":942,"url":18,"identifiers":943},"Stankiewicz JM, Glanz BI, Healy BC, Arora A, Neema M, Benedict RH, et al. Brain MRI lesion load at 1.5 T and 3T versus clinical status in multiple sclerosis. J Neuroimag. 2011;21(2):e50–6.",{"doi":944},"10.1111\u002Fj.1552-6569.2009.00449.x",{"id":18,"text":946,"url":18,"identifiers":947},"Shaaban SM, Elmongui AE, Razek AAKA, Belal TM. Correlation of cortical lesions of multiple sclerosis at double inversion recovery with cognition screening scores. Egypt J Neurol Psychiatry Neurosurg. 2021;57(1):32.",{"doi":948},"10.1186\u002Fs41983-021-00285-5",{"id":18,"text":950,"url":18,"identifiers":951},"Reuter F, Zaaraoui W, Crespy L, Faivre A, Rico A, Malikova I, et al. Cognitive impairment at the onset of multiple sclerosis: relationship to lesion location. Mult Scler. 2011;17(6):755–8.",{"doi":952},"10.1177\u002F1352458511398265",{"id":18,"text":954,"url":18,"identifiers":955},"Rossi F, Giorgio A, Battaglini M, Stromillo ML, Portaccio E, Goretti B, et al. Relevance of brain lesion location to cognition in relapsing multiple sclerosis. PLoS ONE. 2012;7(11): e44826.",{"doi":956},"10.1371\u002Fjournal.pone.0044826",{"id":18,"text":958,"url":18,"identifiers":959},"Kutzelnigg A, Lucchinetti CF, Stadelmann C, Brück W, Rauschka H, Bergmann M, et al. Cortical demyelination and diffuse white matter injury in multiple sclerosis. Brain. 2005;128(Pt 11):2705–12.",{"doi":960},"10.1093\u002Fbrain\u002Fawh641",{"id":18,"text":962,"url":18,"identifiers":963},"Sumowski JF, Benedict R, Enzinger C, Filippi M, Geurts JJ, Hamalainen P, et al. Cognition in multiple sclerosis: state of the field and priorities for the future. Neurology. 2018;90(6):278–88.",{"doi":964},"10.1212\u002FWNL.0000000000004977",{"id":18,"text":966,"url":18,"identifiers":967},"Kincses ZT, Ropele S, Jenkinson M, Khalil M, Petrovic K, Loitfelder M, et al. Lesion probability mapping to explain clinical deficits and cognitive performance in multiple sclerosis. Mult Scler. 2011;17(6):681–9.",{"doi":968},"10.1177\u002F1352458510391342",{"id":18,"text":970,"url":18,"identifiers":971},"Gaetano L, Magnusson B, Kindalova P, Tomic D, Silva D, Altermatt A, et al. White matter lesion location correlates with disability in relapsing multiple sclerosis. Mult Scler J Exp Transl Clin. 2020;6(1):2055217320906844.",{},{"id":18,"text":973,"url":18,"identifiers":974},"Mesaros S, Rocca MA, Kacar K, Kostic J, Copetti M, Stosic-Opincal T, et al. Diffusion tensor MRI tractography and cognitive impairment in multiple sclerosis. Neurology. 2012;78(13):969–75.",{"doi":975},"10.1212\u002FWNL.0b013e31824d5859",{"id":18,"text":977,"url":18,"identifiers":978},"Papadopoulou A, Müller-Lenke N, Naegelin Y, Kalt G, Bendfeldt K, Kuster P, et al. Contribution of cortical and white matter lesions to cognitive impairment in multiple sclerosis. Mult Scler. 2013;19(10):1290–6.",{"doi":979},"10.1177\u002F1352458513475490",{"id":18,"text":981,"url":18,"identifiers":982},"Calabrese M, Agosta F, Rinaldi F, Mattisi I, Grossi P, Favaretto A, et al. Cortical lesions and atrophy associated with cognitive impairment in relapsing–remitting multiple sclerosis. Arch Neurol. 2009;66(9):1144–50.",{"doi":983},"10.1001\u002Farchneurol.2009.174",{"id":18,"text":985,"url":18,"identifiers":986},"Rinaldi F, Calabrese M, Grossi P, Puthenparampil M, Perini P, Gallo P. Cortical lesions and cognitive impairment in multiple sclerosis. Neurol Sci. 2010;31(Suppl 2):S235–7.",{"doi":987},"10.1007\u002Fs10072-010-0368-4",{"id":18,"text":989,"url":18,"identifiers":990},"Akaishi T, Fujimori J, Nakashima I. Basal ganglia atrophy and impaired cognitive processing speed in multiple sclerosis. Cureus. 2024;16(1): e52603.",{},{"id":18,"text":992,"url":18,"identifiers":993},"Naghavi S, Ashtari F, Adibi I, Shaygannejad V, Ramezani N, Pourmohammadi A, et al. Effect of deep gray matter atrophy on information processing speed in early relapsing–remitting multiple sclerosis. Mult Scler Relat Disord. 2023;71: 104560.",{"doi":994},"10.1016\u002Fj.msard.2023.104560",{"id":18,"text":996,"url":18,"identifiers":997},"Kania K, Pawlak MA, Forycka M, Wiłkość-Dębczyńska M, Michalak S, Łukaszewska A, et al. Predicting clinical progression and cognitive decline in patients with relapsing-remitting multiple sclerosis: a 6-year follow-up study. Neurol Neurochir Pol. 2024.",{"doi":998},"10.5603\u002Fpjnns.97714",{"id":1000,"createTime":1001,"updateTime":1002,"relativeEntities":1003,"slug":1004,"properties":1005,"entityType":169,"verifyStatus":170,"verifyTime":1002,"verifyNote":171,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":1014,"fullTextUrl":18,"authors":1015,"publicationType":230,"publisherRelationship":1083,"citationCount":18,"citationInfo":18,"publishDate":1116,"publishYear":473,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":18,"isForceReanalyzing":261},"f0eb94a7-8d17-4888-abaa-50e169ccb64b","2023-12-02T17:43:33.840+00:00","2025-02-10T23:44:29.786+00:00",[],"Vitamin-D-status-in-idiopathic-Parkinson-s-disease-an-Egyptian-study",{"references":1006,"abstract":1008,"title":1010,"doi":1012},{"VOID":1007},"Rocha EM, De Miranda B, Sanders LH. Alpha-synuclein: pathology, mitochondrial dysfunction and neuroinflammation in Parkinson’s disease. Neurobiol Dis. 2018;109:249–57.\nLv Z, Tang B, Sun Q, Yan X, Guo J. Association study between vitamin d receptor gene polymorphisms and patients with Parkinson disease in Chinese Han population. Int J Neurosci. 2012;123(1):60–4.\nSoliman RH, Oraby MI, Hussein M, El-Shafy SA, Mostafa S. Could vitamin D deficiency have an impact on motor and cognitive function in Parkinson’s disease? The Egyptian Journal of Neurology, Psychiatry and Neurosurgery. 2019;55(1):1–6.\nVinh Quôc Luong K, Thi Hoàng Nguyên L. Vitamin D and Parkinson's disease. J Neurosci Res. 2012;90(12):2227–36.\nSuzuki M, Yoshioka M, Hashimoto M, Murakami M, Kawasaki K, Noya M, et al. 25-hydroxyvitamin D, vitamin D receptor gene polymorphisms and severity of Parkinson's disease. Mov Disord. 2012;27(2):264–71.\nHughes AJ, Daniel SE, Kilford L, Lees AJ. Accuracy of clinical diagnosis of idiopathic Parkinson's disease: a clinico-pathological study of 100 cases. J Neurol Neurosurg Psychiatry. 1992;55(3):181–4.\nPetersen MS, Bech S, Christiansen DH, Schmedes AV, Halling J. The role of vitamin D levels and vitamin D receptor polymorphism on Parkinson's disease in the Faroe Islands. Neurosci Lett. 2014;561:74–9.\nSato Y, Kikuyama M, Oizumi K. High prevalence of vitamin D deficiency and reduced bone mass in Parkinson's disease. Neurology. 1997;49(5):1273–8.\nSato Y, Honda Y, Iwamoto J, Kanoko T, Satoh K. Abnormal bone and calcium metabolism in immobilized Parkinson's disease patients. Mov Disord. 2005;20(12):1598–603.\nEvatt ML, DeLong MR, Khazai N, Rosen A, Triche S, Tangpricha V. Prevalence of vitamin D insufficiency in patients with Parkinson disease and Alzheimer disease. Arch Neurol. 2008;65(10):1348–52.\nAbou-Raya S, Helmii M, Abou-Raya A. Bone and mineral metabolism in older adults with Parkinson's disease. Age Ageing. 2009;38(6):675–80.\nKnekt P, Kilkkinen A, Rissanen H, Marniemi J, Sääksjärvi K, Heliövaara M. Serum vitamin D and the risk of Parkinson disease. Arch Neurol. 2010;67(7):808–11.\nSleeman I, Aspray T, Lawson R, Coleman S, Duncan G, Khoo TK, et al. The role of vitamin D in disease progression in early Parkinson’s disease. J Park Dis. 2017;7(4):669–75.\nBoucher BJ. The problems of vitamin d insufficiency in older people. Aging Dis. 2012;3(4):313.\nPrentice A. Vitamin D deficiency: a global perspective. Nutr Rev. 2008;66(2):153–64.\nJamali AA, Jamali GM, Tanwani BM, Jamali NH, Bhatia MR. Frequency of low vitamin D3 levels in subjects with Parkinson’s disease. Advances in Parkinson’s Disease. 2018;7(1):7.\nChitsaz A, Maracy M, Basiri K, Izadi Boroujeni M, Tanhaei AP, Rahimi M, et al. 25-hydroxyvitamin d and severity of Parkinson’s disease. Int J Endocrinol. 2013;2013.",{"EN":1009},"Vitamin D is suggested to play an important role in neurodegenerative disorders. To examine the association between serum 25 vitamin D3 and Parkinson’s disease (PD). Fifty patients suffering from PD and fifty age- and sex-matched healthy control subjects were included in the study. Patients were subjected to complete clinical assessment, and Unified Parkinson Disease Rating Scale (UPDRS) was done to evaluate severity of PD. Measurement of serum 25 vitamin D3 using enzyme-linked immuno sorbent assay (ELISA) was done for both patients and controls. Serum 25 vitamin D3 was significantly lower in PD patients compared to healthy controls. Twenty-five vitamin D3 serum level was significantly negatively correlated with age and age at onset of disease but not significantly correlated with disease duration and severity of Parkinson’s disease. Multiple regression analysis showed that serum 25 vitamin D3 was not found to be predictor for severity of PD. There is an association between low vitamin D levels and PD. Therefore, vitamin D may have a role in the pathophysiology of PD.",{"EN":1011},"Vitamin D status in idiopathic Parkinson’s disease: an Egyptian study",{"VOID":1013},"10.1186\u002Fs41983-020-00175-2","https:\u002F\u002Fejnpn.springeropen.com\u002Farticles\u002F10.1186\u002Fs41983-020-00175-2",[1016,1032,1044,1056,1068],{"id":1017,"sortIndex":194,"researcher":18,"roles":1018,"affiliations":1019,"properties":1029},"3c395c21-9af6-42c7-a6ff-cae47cbefa2b",[178],[1020],{"id":18,"sortIndex":19,"affiliation":1021,"properties":18},{"id":1022,"createTime":1023,"updateTime":1023,"relativeEntities":1024,"slug":1025,"properties":1026,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"6f26cfbe-f57b-471b-8f5a-b8da84b5a2a4","2024-04-14T02:39:27.270+00:00",[],"Department-of-Neurology-Faculty-of-Medicine-Cairo-University-Giza-Egypt",{"title":1027},{"EN":1028},"Department of Neurology, Faculty of Medicine, Cairo University, Giza, Egypt",{"title":1030},{"VI":1031},"Sarah Heneidy",{"id":1033,"sortIndex":176,"researcher":18,"roles":1034,"affiliations":1035,"properties":1041},"f05fb3ce-86a5-4792-82fa-92336e606ec7",[178],[1036],{"id":18,"sortIndex":19,"affiliation":1037,"properties":18},{"id":1022,"createTime":1023,"updateTime":1023,"relativeEntities":1038,"slug":1025,"properties":1039,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":1040},{"EN":1028},{"title":1042},{"VI":1043},"Mohamed Elsayed 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Sharaf",{"url":1014,"publisher":1084,"properties":1111},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1085,"slug":10,"properties":1086,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":1089,"manageAffiliations":1090,"indexDatabases":1091,"url":117,"thumbnailPath":18,"statistic":1106,"gsStatistic":18,"type":147,"analyzePriority":18},[],{"issn":1087,"title":1088},{"VOID":13},{"EN":15},[],[],[1092,1099],{"id":77,"indexDatabase":1093,"url":90,"indexYears":91,"academicFieldIds":1098,"indexDatabaseRanking":97},{"id":79,"createTime":80,"updateTime":81,"relativeEntities":1094,"label":1095,"description":1096,"key":87,"publicationTags":1097,"standard":18},[],{"EN":84,"VI":84},{"EN":84,"VI":86},[89],[93,94,95,96],{"id":99,"indexDatabase":1100,"url":114,"indexYears":18,"academicFieldIds":1105,"indexDatabaseRanking":18},{"id":101,"createTime":102,"updateTime":103,"relativeEntities":1101,"label":1102,"description":1103,"key":110,"publicationTags":1104,"standard":18},[],{"EN":106,"VI":106},{"VI":108,"EN":109},[112,113],[116],{"impactFactor":19,"impactFactorByYear":1107,"i10Index":123,"i10IndexLast5Year":124,"totalPublication":125,"totalPublicationByYear":1108,"totalCitation":133,"totalCitationByYear":1109,"totalCitationPerPublication":140,"totalCitationPerPublicationByYear":1110,"hindexLast5Year":123,"hindex":123},{"2019":120,"2020":121,"2021":122,"2022":122,"2023":121},{"2018":127,"2019":128,"2020":129,"2021":130,"2022":131,"2023":132,"2024":127},{"2018":135,"2019":136,"2020":137,"2021":138,"2022":139},{"2018":142,"2019":143,"2020":144,"2021":145,"2022":146},{"volume":1112,"pages":1114},{"VOID":1113},"56",{"VOID":1115},"1-4","2020-05-07",{"id":1118,"createTime":1119,"updateTime":1120,"relativeEntities":1121,"slug":1122,"properties":1123,"entityType":169,"verifyStatus":170,"verifyTime":1120,"verifyNote":171,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":1132,"fullTextUrl":18,"authors":1133,"publicationType":230,"publisherRelationship":1176,"citationCount":18,"citationInfo":18,"publishDate":1208,"publishYear":473,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":18,"isForceReanalyzing":261},"186faa53-edc0-4efd-9295-8a2f7fe31aab","2024-01-13T11:49:27.480+00:00","2024-12-30T23:43:10.578+00:00",[],"Somatic-cough-syndrome-a-report-of-two-cases-and-review-of-literature",{"references":1124,"abstract":1126,"title":1128,"doi":1130},{"VOID":1125},"Wei WZY, Li H, Hou J, Lv H, Li C. Detection rate of psychogenic cough in patients with chronic cough in Chinese hospital: a meta analysis. Int J Clin Exp Med. 2016;9(2):504–14.\nHaydour Q, Alahdab F, Farah M, Barrionuevo P, Vertigan AE, Newcombe PA, et al. Management and diagnosis of psychogenic cough, habit cough, and tic cough: a systematic review. Chest. 2014;146(2):355–72.\nMastrovich JD, Greenberger PA. Psychogenic cough in adults: a report of two cases and review of the literature. Allergy Asthma Proc. 2002;23(1):27–33.\nWeinberger M, Lockshin B. When is cough functional, and how should it be treated? Breathe (Sheff). 2017;13(1):22–30.\nIrwin RS, Glomb WB, Chang AB. Habit cough, tic cough, and psychogenic cough in adult and pediatric populations: ACCP evidence-based clinical practice guidelines. Chest. 2006;129(1 Suppl):174S–9S.\nVertigan AE, Murad MH, Pringsheim T, Feinstein A, Chang AB, Newcombe PA, et al. Somatic cough syndrome (previously referred to as psychogenic cough) and tic cough (previously referred to as habit cough) in Adults and Children: CHEST Guideline and Expert Panel Report. Chest. 2015;148(1):24–31.\nVertigan AE. Somatic cough syndrome or psychogenic cough-what is the difference? J Thorac Dis. 2017;9(3):831–8.\nWilkes J. ACCP provides updated recommendations on the management of somatic cough syndrome and tic cough. Am Fam Physician. 2016;93(5):416.\nBernstein L. A respiratory tic: “the barking cough of puberty”. Report of a case treated successfully. Laryngoscope. 1963;73:315–9.\nLindenbaum S, Clark D. Toward an integrative approach to psychotherapy with children. Am J Orthopsychiatry. 1983;53(3):449–59.\nJakati PK, Naskar S, Khanna A. “The barking girl”: a case report of psychogenic cough in a child with a review of literature. Indian J Psychol Med. 2017;39(4):542–5.\nOliveira R, Martins V, Moreira C. Psychogenic cough: a rare cause of chronic cough. Arch Bronconeumol. 2015;51(11):604–5.\nVertigan AE, Theodoros DG, Gibson PG, Winkworth AL. Review series: chronic cough: behaviour modification therapies for chronic cough. Chron Respir Dis. 2007;4(2):89–97.\nFrench CL, Irwin RS, Curley FJ, Krikorian CJ. Impact of chronic cough on quality of life. Arch Intern Med. 1998;158(15):1657–61.\nIrwin RS, Boulet LP, Cloutier MM, Fuller R, Gold PM, Hoffstein V, et al. Managing cough as a defense mechanism and as a symptom. A consensus panel report of the American College of Chest Physicians. Chest. 1998;114(2 Suppl Managing):133S–81S.",{"EN":1127},"Somatic cough syndrome is a somatization disorder that usually presents in children and which is often diagnosed late after an extensive search for organic causes. The condition was redefined by the DSM-5 criteria and grouped with the other conditions under the umbrella of somatoform disorders. Nonetheless, clinical presentation is heterogeneous, and etiology is still not clearly defined. Several management approaches have been proposed, but treatment remains essentially nonpharmacological. We report two cases of somatic cough syndrome that were diagnosed after 4 years and 3 months respectively, and document the successful treatment of both cases using behavioral therapy. Behavioral therapy is the most reportedly successful nonpharmacological treatment in somatic cough syndrome, and it was successful with both our cases. The condition poses a significant burden over the function and quality of life in patients and their caregivers. The heterogeneous nature of this syndrome necessitates a high index of suspicion on part of both the physician and the psychiatrist in order to secure a timely diagnosis and mitigate the impact of this condition.",{"EN":1129},"Somatic cough syndrome: a report of two cases and review of literature",{"VOID":1131},"10.1186\u002Fs41983-020-00215-x","https:\u002F\u002Fejnpn.springeropen.com\u002Farticles\u002F10.1186\u002Fs41983-020-00215-x",[1134,1149,1164],{"id":1135,"sortIndex":207,"researcher":18,"roles":1136,"affiliations":1137,"properties":1146},"7aa8d1d6-697a-4145-9b62-ba682e2848a9",[178],[1138],{"id":18,"sortIndex":19,"affiliation":1139,"properties":18},{"id":1140,"createTime":1141,"updateTime":1141,"relativeEntities":1142,"slug":18,"properties":1143,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"95d5a90f-bc9b-4b29-beef-e32dc1b38f1c","2024-01-13T11:49:27.645+00:00",[],{"title":1144},{"VI":1145},"Neurology Division, Department of Neuroscience, King Abdullah University Hospital (KAUH) of Jordan University of Science and Technology (JUST), Irbid, Jordan",{"title":1147},{"VI":1148},"Belal Aldabbour",{"id":1150,"sortIndex":19,"researcher":18,"roles":1151,"affiliations":1152,"properties":1161},"c518ad9a-ecda-4144-8c02-a955289899ae",[178],[1153],{"id":18,"sortIndex":19,"affiliation":1154,"properties":18},{"id":1155,"createTime":1156,"updateTime":1156,"relativeEntities":1157,"slug":18,"properties":1158,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"742f982f-21d1-4cb4-bd63-e62a62fb8f46","2024-01-13T11:49:27.615+00:00",[],{"title":1159},{"VI":1160},"Psychiatry Division, Department of Neuroscience, King Abdullah University Hospital (KAUH) of Jordan University of Science and Technology (JUST), Irbid, Jordan",{"title":1162},{"VI":1163},"Mahmoud Bashtawi",{"id":1165,"sortIndex":176,"researcher":18,"roles":1166,"affiliations":1167,"properties":1173},"c33f75fc-0cb2-42bc-86a1-8b8ba743bb74",[178],[1168],{"id":18,"sortIndex":19,"affiliation":1169,"properties":18},{"id":1155,"createTime":1156,"updateTime":1156,"relativeEntities":1170,"slug":18,"properties":1171,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":1172},{"VI":1160},{"title":1174},{"VI":1175},"Amal Abuabada",{"url":1132,"publisher":1177,"properties":1204},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1178,"slug":10,"properties":1179,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":1182,"manageAffiliations":1183,"indexDatabases":1184,"url":117,"thumbnailPath":18,"statistic":1199,"gsStatistic":18,"type":147,"analyzePriority":18},[],{"issn":1180,"title":1181},{"VOID":13},{"EN":15},[],[],[1185,1192],{"id":77,"indexDatabase":1186,"url":90,"indexYears":91,"academicFieldIds":1191,"indexDatabaseRanking":97},{"id":79,"createTime":80,"updateTime":81,"relativeEntities":1187,"label":1188,"description":1189,"key":87,"publicationTags":1190,"standard":18},[],{"EN":84,"VI":84},{"EN":84,"VI":86},[89],[93,94,95,96],{"id":99,"indexDatabase":1193,"url":114,"indexYears":18,"academicFieldIds":1198,"indexDatabaseRanking":18},{"id":101,"createTime":102,"updateTime":103,"relativeEntities":1194,"label":1195,"description":1196,"key":110,"publicationTags":1197,"standard":18},[],{"EN":106,"VI":106},{"VI":108,"EN":109},[112,113],[116],{"impactFactor":19,"impactFactorByYear":1200,"i10Index":123,"i10IndexLast5Year":124,"totalPublication":125,"totalPublicationByYear":1201,"totalCitation":133,"totalCitationByYear":1202,"totalCitationPerPublication":140,"totalCitationPerPublicationByYear":1203,"hindexLast5Year":123,"hindex":123},{"2019":120,"2020":121,"2021":122,"2022":122,"2023":121},{"2018":127,"2019":128,"2020":129,"2021":130,"2022":131,"2023":132,"2024":127},{"2018":135,"2019":136,"2020":137,"2021":138,"2022":139},{"2018":142,"2019":143,"2020":144,"2021":145,"2022":146},{"volume":1205,"pages":1206},{"VOID":1113},{"VOID":1207},"1-5","2020-07-31",{"id":1210,"createTime":1211,"updateTime":1212,"relativeEntities":1213,"slug":1214,"properties":1215,"entityType":169,"verifyStatus":170,"verifyTime":1212,"verifyNote":171,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":1224,"fullTextUrl":18,"authors":1225,"publicationType":230,"publisherRelationship":1285,"citationCount":18,"citationInfo":18,"publishDate":1317,"publishYear":1318,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":18,"isForceReanalyzing":261},"11116635-1951-4645-975c-ee481c2333e6","2023-12-05T19:05:31.790+00:00","2025-01-07T23:42:06.189+00:00",[],"Migraine-in-patients-with-rheumatoid-arthritis-and-its-relation-to-disease-activity",{"references":1216,"abstract":1218,"title":1220,"doi":1222},{"VOID":1217},"Collaborators GBDH Global. regional, and national burden of migraine and tension-type headache, 1990–2016: a systematic analysis for the global burden of disease study 2016. Lancet Neurol. 2018;17:954–76.\nWoldeamanuel YW, Cowan RP. Migraine affects 1 in 10 people worldwide featuring recent rise: a systematic review and meta-analysis of community-based studies involving 6 million participants. J Neurol Sci. 2017;372:307–15.\nCavestro C, Ferrero M. Migraine in systemic autoimmune diseases. Endocr Metab Immune Disord Drug Targets. 2018;18(2):124–34.\nAbou Elmaaty AA, Flifel ME, Belal T, Zarad CA. Migraine and tension headache comorbidity with hypothyroidism in Egypt. Egypt J Neurol Psychiatry Neurosurg. 2020;56:78.\nBuse DC, Reed ML, Fanning KM, Bostic R, Dodick DW, Schwedt TJ, et al. Comorbid and co-occurring conditions in migraine and associated risk of increasing headache pain intensity and headache frequency: results of the migraine in America symptoms and treatment (MAST) study. J Headache Pain. 2020;21:23.\nBoer AC, Boonen A, van Mil AHM. Is anti-citrullinated protein antibody-positive rheumatoid arthritis still a more severe disease than anti-citrullinated protein antibody-negative rheumatoid arthritis? A longitudinal cohort study in rheumatoid arthritis patients diagnosed from 2000 onward. Arthritis Care Res. 2018;70(7):987–96.\nGiles JT. Extra-articular manifestations and comorbidity in rheumatoid arthritis: potential impact of pre-rheumatoid arthritis prevention. Clin Ther. 2019;41(7):1246–55.\nLe H, Tfelt-Hansen P, Russell MB, Skytthe A, Kyvik KO, Olesen J. Co-morbidity of migraine with somatic disease in a large population-based study. Cephalalgia. 2011;31:43–64.\nAltamura C, Corbelli I, de Tommaso M, Lorenzo CD, Lorenzo GD, Renzo AD. Pathophysiological bases of comorbidity in migraine. Front Hum Neurosci. 2021. https:\u002F\u002Fdoi.org\u002F10.3389\u002Ffnhum.2021.640574.\nMathieu S, Couderc M, Pereira B, Dubost JJ, Malochet-Guinamand S, Tournadre A, et al. Prevalence of migraine and neuropathic pain in rheumatic diseases. J Clin Med. 2020;9(6):1890.\nKumar N, Abboud H. Iatrogenic CNS demyelination in the era of modern biologics. Mult Scler. 2019;25:1079–85.\nWolfe F. Which HAQ is best? A comparison of the HAQ, MHAQ and RA-HAQ, a difficult 8 item HAQ (DHAQ), and a rescored 20 item`HAQ (HAQ20): analyses in 2,491 rheumatoid arthritis patients following leflunomide initiation. J Rheumatol. 2001;28:982–9.\nPrevoo ML, Vant-Hof MA, Kuper HH, van Leeuwen MA, van de Putte LB, van Riel PL. Modified disease activity score that include twenty-eight-joint counts. Development and validation in a prospective longitudinal study of patients with rheumatoid arthritis. Arthritis Rheum. 1995;38:44–8.\nMourad D, Hajj A, Hallit S, Ghossoub M, Khabbaz LR. Validation of the Arabic version of the migraine disability assessment scale among Lebanese patients with migraine. J Oral Facial Pain Headache. 2019;33(1):47–53.\nHeadache Classification Committee of the International Headache Society(IHS) The International Classification of Headache Disorders, 3rd edn. Cephalalgia. 2018;38(1):1–211.\nOlesen J, Bousser MG, Diener HC, Dodick D, First M, Goadsby PJ, et al. New appendix criteria open for a broader concept of chronic migraine. Cephalalgia. 2006;26:742–6.\nDijkers M. Comparing quantification of pain severity by verbal rating and numeric rating scales. J Spinal Cord Med. 2010;33:232–42.\nTabachnick BG, Fidell LS. Using multivariate statistics. 6th ed. Harlow: Pearson; 2014.\nDaniel WW, Cross CL. Biostatistics: a Foundation for Analysis in the Health Sciences, 10th edn. New York: Wiley. 2013; 6: 161–213.\nWang YC, Huang YP, Wang MT, Wang HI, Pan SL. Increased risk of rheumatoid arthritis in patients with migraine: a population based, propensity score-matched cohort study. Rheumatol Int. 2017;37:273–327.\nZeller J, Weissbarth E, Baruth B, Mielke H, Deicher H. Serotonin content of platelets in inflammatory rheumatic diseases. Arthritis Rheum. 1983;26:532–40.\nCloëz-Tayarani I, Petit-Bertron AF, Venters HD, Cavaillon JM. Differential effect of serotonin on cytokine production in lipopolysaccharide-stimulated human peripheral blood mononuclear cells: involvement of 5-hydroxytryptamine2A receptors. Int Immunol. 2003;15:233–40.\nSacre S, Medghalchi M, Gregory B, Brennan F, Williams R. Fluoxetine and citalopram exhibit potent anti-inflammatory activity in human and murine models of rheumatoid arthritis and inhibit toll-like receptors. Arthritis Rheum. 2010;62:683–93.\nNamas R, Joshi A, Ali Z, Al Saleh J, Abuzakouk M. Demographic and clinical patterns of rheumatoid arthritis in an emirati cohort from United Arab Emirates. Int J Rheumatol. 2019. https:\u002F\u002Fdoi.org\u002F10.1155\u002F2019\u002F3057578.\nYen JH, Chen JR, Tsai WJ, Liu HW. Correlation of tumor necrosis factor alpha levels with disease activity of rheumatoid arthritis. Zhonghua Minguo wei sheng wu ji mian yi xue za zhi Chin J Microbiol Immunol. 1992;25(4):232–43.\nAkdag UZ, Kurt S, Karaer UH. The relationship with restless legs syndrome, fibromyalgia, and depressive symptoms in migraine patients. Neurol Sci. 2018;39(8):1409–14.\nPal B, Gibson C, Passmore J, Griffiths ID, Dick WC. A study of headaches and migraine in Sjögren’s syndrome and other rheumatic disorders. Ann Rheum Dis. 1989;48(4):312–6.\nGökçay F, Öder G, Çelebisoy N, Gökçay A, Sirin H, Kabasakal Y. Headache in primary Sjögren’s syndrome: a prevalence study. Acta Neurol Scand. 2008;118:189–92.\nMorreale M, Marchione P, Giacomini P, Pontecorvo S, Marianetti M, Vento C, et al. Neurological involvement in primary Sjögren syndrome: a focus on central nervous system. PLoS ONE. 2014;9:e84605.\nTjensvoll AB, Harboe E, Gøransson LG, Beyer MK, Greve OJ, Kvaløy JT, et al. Headache in primary Sjøgren’s syndrome: a population-based retrospective cohort study. Eur J Neurol. 2013;20:558–63.\nLe Pira F, Reggio E, Quattrocchi G, Sanfilippo C, Maci T, Cavallaro T, et al. Executive dysfunctions in migraine with and without aura: what is the role of white matter lesions? Headache. 2013;54(1):125–30.\nZhang Q, Datta R, Detre J, Cucchiara B. White matter lesion burden in migraine with aura may be associated with reduced cerebral blood flow. Cephalalgia. 2016;37(6):517–22.\nZeytin A, Tok S, Dogan N. The frequency and localization of white matter lesions in migraine patients with or without aura in Anatolia. Turkey Int J Acad Res. 2014;6(2):37–9.\nLapucci C, Saitta L, Bommarito G, Sormani MP, Pardini M, Bonzano L, et al. How much do periventricular lesions assist in distinguishing migraine with aura from CIS? Neurology. 2019;92:1–6.\nSinnecker T, Clarke MA, Meier D, Enzinger C, Calabrese M, De Stefano N, et al. Evaluation of the central vein sign as a diagnostic imaging biomarker in multiple sclerosis. JAMA Neurol. 2019;76:1446–56.\nRossato G, Adami A, Thijs V, Cerini R, Pozzi-Mucelli R, Mazzucco S, et al. Cerebral distribution of white matter lesions in migraine with aura patients. Cephalalgia. 2010;30(7):855–9.\nNegm M, Housseini AM, Abdelfatah M, Asran A. Relation between migraine pattern and white matter hyperintensities in brain magnetic resonance imaging. Egypt J Neurol Psychiatry Neurosurg. 2018;54:24.\nToghae M, Rahimian E, Abdollahi M, Shoar S, Naderan M. The prevalence of magnetic resonance imaging Hyperintensity in migraine patients and its association with migraine headache characteristics and cardiovascular risk factors. Oman Med J. 2015;30(3):203–7.\nTrauninger A, Leél-Őssy E, Kamson D, Pótó L, Aradi M, Kövér F, et al. Risk factors of migraine related brain white matter hyperintensities: an investigation of 186 patients. J Headache Pain. 2011;12(1):97–103.\nGomez-Beldarrain M, Oroz I, Zapirain B, Ruanova B, Fernandez Y, Cabrera A, et al. Right frontoinsular white matter tracts link cognitive reserve and pain in migraine patients. J Headache Pain. 2016;17(1):4.",{"EN":1219},"The comorbidity between rheumatoid arthritis (RA) and migraine is complex and not completely understood. This study aimed to evaluate migraine frequency in patients with RA and its relation to disease activity. A cross-sectional study was carried out on 210 consecutive RA Egyptian patients fulfilling the 2010 EULAR\u002FACR criteria (joint distribution, serology, symptom duration and acute phase reaction). Prevalence of migraine in RA was 28.2%. Disease activity, fibromyalgia and functional losses were significantly higher in migraine group with RA versus non-migraine group (P \u003C 0.001). Disease Activity Score (DAS-28) was independently significant predictor as increasing DAS-28 score was associated with an increased likelihood of exhibiting migraine (5.5-times higher odds per one-unit increase in DAS-28 score). Prevalence of brain MRI white matter hyper-intensities (WMHs) in RA with migraine was 54.8%. WMHs were significantly higher in migraine patients with aura than migraine patients without aura, especially in older patients, longer migraine duration, longer rheumatoid duration and elevated ESR (p \u003C 0.047, p \u003C 0.034, P \u003C 0.004, P \u003C 0.015 and P \u003C 0.22, respectively). Migraine is highly frequent in RA patients, especially migraine with aura. The presence of rheumatoid activity, fibromyalgia and secondary Sjogren’s syndrome, elevated ESR and CRP are associated with functional losses in RA patients with migraine, especially migraine with aura. MR imaging of brain is a mandatory tool for detection of white matter hyper-intensities in RA patients with migraine, especially migraine with aura.",{"EN":1221},"Migraine in patients with rheumatoid arthritis and its relation to disease activity",{"VOID":1223},"10.1186\u002Fs41983-021-00406-0","https:\u002F\u002Fejnpn.springeropen.com\u002Farticles\u002F10.1186\u002Fs41983-021-00406-0",[1226,1241,1256,1268],{"id":1227,"sortIndex":194,"researcher":18,"roles":1228,"affiliations":1229,"properties":1238},"78802311-ce73-4bb5-bb2f-deea6156d7bf",[178],[1230],{"id":18,"sortIndex":19,"affiliation":1231,"properties":18},{"id":1232,"createTime":1233,"updateTime":1233,"relativeEntities":1234,"slug":18,"properties":1235,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"356b5646-1689-4768-9463-2d795320be24","2024-01-15T02:07:10.130+00:00",[],{"title":1236},{"VI":1237},"Faculty of Medicine, Helwan University, Cairo, Egypt",{"title":1239},{"VI":1240},"Ali Ahmed Abou Elmaaty",{"id":1242,"sortIndex":176,"researcher":18,"roles":1243,"affiliations":1244,"properties":1253},"4c4b78dc-402d-4178-ae15-c6a12388b39d",[178],[1245],{"id":18,"sortIndex":19,"affiliation":1246,"properties":18},{"id":1247,"createTime":1248,"updateTime":1248,"relativeEntities":1249,"slug":18,"properties":1250,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"4236b250-0f9f-4a54-801a-da4ed0cb6fc8","2023-12-05T19:05:31.810+00:00",[],{"title":1251},{"VI":1252},"Port Said University, Port fuad, Egypt",{"title":1254},{"VI":1255},"Carmen Ali Zarad",{"id":1257,"sortIndex":19,"researcher":18,"roles":1258,"affiliations":1259,"properties":1265},"894248d4-ecff-4a3e-8fa1-f074684f0e6b",[178],[1260],{"id":18,"sortIndex":19,"affiliation":1261,"properties":18},{"id":1232,"createTime":1233,"updateTime":1233,"relativeEntities":1262,"slug":18,"properties":1263,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},[],{"title":1264},{"VI":1237},{"title":1266},{"VI":1267},"Hassan Abd-Elaty El-Sonbaty",{"id":1269,"sortIndex":207,"researcher":18,"roles":1270,"affiliations":1271,"properties":1282},"9d291338-174a-4f2b-bd65-7740b6d5a6f6",[178],[1272],{"id":18,"sortIndex":19,"affiliation":1273,"properties":18},{"id":1274,"createTime":1275,"updateTime":1276,"relativeEntities":1277,"slug":1278,"properties":1279,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"0fbec6c6-ea63-4612-a217-b5397b3e4eb2","2024-01-04T18:41:09.751+00:00","2025-01-30T16:42:22.946+00:00",[],"Faculty-of-Medicine-Ain-Shams-University-Cairo-Egypt",{"title":1280},{"VI":1281},"Faculty of Medicine, Ain Shams University, Cairo, Egypt",{"title":1283},{"VI":1284},"Mohamed Rezk Mohamed",{"url":1224,"publisher":1286,"properties":1313},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1287,"slug":10,"properties":1288,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":1291,"manageAffiliations":1292,"indexDatabases":1293,"url":117,"thumbnailPath":18,"statistic":1308,"gsStatistic":18,"type":147,"analyzePriority":18},[],{"issn":1289,"title":1290},{"VOID":13},{"EN":15},[],[],[1294,1301],{"id":77,"indexDatabase":1295,"url":90,"indexYears":91,"academicFieldIds":1300,"indexDatabaseRanking":97},{"id":79,"createTime":80,"updateTime":81,"relativeEntities":1296,"label":1297,"description":1298,"key":87,"publicationTags":1299,"standard":18},[],{"EN":84,"VI":84},{"EN":84,"VI":86},[89],[93,94,95,96],{"id":99,"indexDatabase":1302,"url":114,"indexYears":18,"academicFieldIds":1307,"indexDatabaseRanking":18},{"id":101,"createTime":102,"updateTime":103,"relativeEntities":1303,"label":1304,"description":1305,"key":110,"publicationTags":1306,"standard":18},[],{"EN":106,"VI":106},{"VI":108,"EN":109},[112,113],[116],{"impactFactor":19,"impactFactorByYear":1309,"i10Index":123,"i10IndexLast5Year":124,"totalPublication":125,"totalPublicationByYear":1310,"totalCitation":133,"totalCitationByYear":1311,"totalCitationPerPublication":140,"totalCitationPerPublicationByYear":1312,"hindexLast5Year":123,"hindex":123},{"2019":120,"2020":121,"2021":122,"2022":122,"2023":121},{"2018":127,"2019":128,"2020":129,"2021":130,"2022":131,"2023":132,"2024":127},{"2018":135,"2019":136,"2020":137,"2021":138,"2022":139},{"2018":142,"2019":143,"2020":144,"2021":145,"2022":146},{"volume":1314,"pages":1316},{"VOID":1315},"57",{"VOID":649},"2021-11-04",2021,{"id":1320,"createTime":1321,"updateTime":1322,"relativeEntities":1323,"slug":1324,"properties":1325,"entityType":169,"verifyStatus":170,"verifyTime":1322,"verifyNote":171,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":1334,"fullTextUrl":18,"authors":1335,"publicationType":230,"publisherRelationship":1382,"citationCount":18,"citationInfo":18,"publishDate":1413,"publishYear":473,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":18,"isForceReanalyzing":261},"f061138e-e683-4741-a634-191025938946","2023-12-26T09:34:01.818+00:00","2025-02-01T23:42:04.074+00:00",[],"Relation-between-serum-amylin-level-and-epilepsy",{"references":1326,"abstract":1328,"title":1330,"doi":1332},{"VOID":1327},"Ngugi AK, Bottomley C, Kleinschmidt I, Sander JW, Newton CR. Estimation of the burden of active and life time epilepsy: a meta-analytic approach. Epilepsia. 2010;51(5):883–90.\nFisher RS, Harding G, Erba G, Barkley GL, Wilkins A. Photic- and pattern-induced seizures: a review for the Epilepsy Foundation of America Working Group. Epilepsia. 2005;46(9):1426–41.\nMulley JC, Scheffer IE, Harkin A, Berkovic SF, Dibbens LM. Susceptibility genes for complex epilepsy. Hum Mol Genet. 2005;14 Spec No. 2:R243-R249.\nBrodie M, Covanis T, Gil-Nagel A, Lerche H, Perucca E, Sills G, et al. Antiepileptic drug therapy: does mechanism of action matter? Epilepsy Behav. 2011;21(4):490.\nPerucca E, Tomson T. The pharmacological treatment of epilepsy inadults. Lancet Neurol. 2011;10(5):446–56.\nRossetti AO, Lowenstein DH. Management of refractory status epilepticus in adults: still more questions than answers. Lancet Neurol. 2011;10(10):922–30.\nWilder RM. The effects of ketonemia on the course of epilepsy. Mayo ClinBulletin. 1921;2:307–8.\nFreeman JM, Kossoff EH, Freeman JB, Kelly MT. The ketogenic diet: a treatment for epilepsy in children and others. 4th ed. New York: Demos; 2006.\nElia M, Klepper J, Leiendecker B, Hartmann H. Ketogenic diets in the treatment of epilepsy. Curr Pharm Des. 2017;23(37):5691–701.\nJuhl CB, Pørksen N, Sturis J, Hansen AP, Veldhuis JD, Pincus S, et al. High-frequency oscillations in circulating amylin concentrations in healthy humans. Am J Physiol Endocrinol Metab. 2000;278(3):E484–90.\nHull RL, Westermark GT, Westermark P, Kahn SE. Islet amyloid: a critical entity in the pathogenesis of type 2 diabetes. J Clin Endocrinol Metab. 2004;89(8):3629–43.\nKong MF, Stubbs TA, King P, Macdonald IA, Lambourne JE, Blackshaw PE, et al. The effect of single doses of pramlintide on gastric emptying of two meals in men with IDDM. Diabetologia. 1998;41(5):577–83.\nVella A, Lee JS, Camilleri M, Szarka LA, Burton DD, Zinsmeister AR, et al. Effects of pramlintide, an amylin analogue, on gastric emptying in type 1 and 2 diabetes mellitus. Neurogastroenterol Motil. 2002;14(2):123–31.\nBanks WA, Kastin AJ, Maness LM, Huang W, Jaspan JB. Permeability of the blood-brain barrier to amylin. Life Sci. 1995;57(22):1993–2001.\nvan Rossum D, Ménard DP, Fournier A, St-Pierre S, Quirion R. Autoradiographic distribution and receptor binding profile of [125I]Bolton Hunter-rat amylin binding sites in the rat brain. J Pharmacol Exp Ther. 1994;270(2):779–87.\nSexton PM, Paxinos G, Kenney MA, Wookey PJ, Beaumont K. In vitro autoradiographic localization of amylin binding sites in rat brain. Neuroscience. 1994;62(2):553–67.\nMoon HS, Chamberland JP, Mantzoros CS. Amylin and leptin activate overlapping signalling pathways in an additive manner in mouse GT1-7 hypothalamic, C2C12 muscle and AML12 liver cell lines. Diabetologia. 2012;55(1):215–25.\nMay PC, Boggs LN, Fuson KS. Neurotoxicity of human amylin in rat primary hippocampal cultures: similarity to Alzheimer's disease amyloid-beta neurotoxicity. J Neurochem. 1993;61(6):2330–3.\nWang E, Zhu H, Wang X, Gower AC, Wallack M, Blusztajn JK, et al. Amylin treatment reduces neuroinflammation and ameliorates abnormal patterns of gene expression in the cerebral cortex of an Alzheimer’s disease mouse model. J Alzheimers Dis. 2017;56(1):47–61.\nWestermark P, Andersson A, Westermark GT. Islet amyloid polypeptide, işlet amyloid, and diabetes mellitus. Physiol Rev. 2011;91(3):795–826.\nJanciauskiene S, Ahrén B. Fibrillar islet amyloid polypeptide differentially affects oxidative mechanisms and lipoprotein uptake in correlation with cytotoxicity in two insulin-producing cell lines. Biochem Biophys Res Commun. 2000; 19; 267(2):619-625.\nWendt T, Tanji N, Guo J, Hudson BI, Bierhaus A, Ramasamy R, et al. Glucose, glycation, and RAGE: implications for amplification of cellular dysfunction in diabetic nephropathy. J Am Soc Nephrol. 2003;14(5):1383–95.\nDimsdale JE, Kolterman O, Koda J, Nelesen R. Effect of race and hypertension on plasma amylin concentrations. Hypertension. 1996;27:1273–6.\nValdemarsson S, Leckstrom A, Westermark P, Bergenfelz A. Increased plasma levels of işlet amyloid polypeptide in patients with primary hyperparathyroidism. Eur J Endocrinol. 1996;134:320–5.\nLudvik B, Clodi M, Kautzky-Willer A, Schuller M, Graf H, Hartter E, et al. Increased levels of circulating islet amyloid polypeptide in patients with chronic renal failure have no effect on insulin secretion. J Clin Invest. 1994;94:2045–50.\nDespa S, Margulies KB, Chen L, Knowlton AA, Havel PJ, Taegtmeyer H, et al. Hyperamylinemia contributes to cardiac dysfunction in obesity and diabetes: a study in humans and rats. Circ Res. 2012;110(4):598–608.\nJeong HR, An SS. Causative factors for formation of toxic islet amyloid polypeptide oligomer in type 2 diabetes mellitus. Clin Interv Aging. 2015;10:1873–9.\nAronoff SL, Berkowitz K, APRN K, Shreiner B, Want L. Glucose metabolism and regulation: beyond ınsulin and glucagon. Diabetes Spectrum. 2004;17:183–90.\nMisra M, Bredella MA, Tsai P, Mendes N, Miller KK, Klibanski A. Lower growth hormone and higher cortisol are associated with greater visceral adiposity, intramyocellular lipids, and insulin resistance in overweight girls. Am J Physiol Endocrinol Metab. 2008;295(2):385–92.\nGong W, Liu ZH, Zeng CH, Peng A, Chen HP, Zhou H, et al. Amylin deposition in the kidney of patients with diabetic nephropathy. Kidney Int. 2007;72(2):213–8.\nJackson K, Barisone GA, Diaz E, Jin LW, DeCarli C, Despa F. Amylin deposition in the brain: a second amyloid in Alzheimer disease? Ann Neurol. 2013;74(4):517–26.\nMulder H, Leckström A, Uddman R, Ekblad E, Westermark P, Sundler F. Islet amyloid polypeptide (amylin) is expressed in sensory neurons. J Neurosci. 1995;15(11):7625–32.",{"EN":1329},"Epilepsy is a neurological disorder characterized by convulsions. Identification of biological pathways underlying epilepsy and novel genes may shed light on the pathogenesis of epilepsy as well as new targets for treatment. Amylin is cosecreted with insulin from the pancreatic β-cells in a pulsatile manner as a response to nutrient stimuli. In vitro studies have shown the neurotoxicity potential of amylin. We aimed to investigate serum amylin levels between epilepsy patients and a healthy control group. For this study, 45 patients with epilepsy and 60 healthy controls were enrolled. Routine blood analysis and electroencephalography scan were performed for all participants. Five cc venous blood sample was collected from each participant. Sera were isolated and stored at − 80 °C until the time of amylin analysis with the enzyme-linked immunosorbent assay. Gender distribution of the two groups was as follows: 44.4% males and 55.6% females among epileptic patients and 53.3% males and 46.7% females for control subjects. Body mass index was 23.09 ± 3.99 kg\u002Fm2 for epileptic patients and 26.29 ± 4.83 kg\u002Fm2 for controls, with a statistically significantly higher body mass index in control subjects (p ˂ 0.001). With regard to serum amylin levels, a statistically significant difference was observed between the two groups (p ˂ 0.001). The median serum amylin concentration was 226.62 ng\u002Fml (69.49–6961.19 (min–max)) for epileptic patients and 103.66 ng\u002Fml (37.42–607.11 (min–max)) for controls (p ˂ 0.001). In the present study, a significant difference was observed between patient and control groups in serum amylin concentrations, which were considerably higher in epileptic patients.",{"EN":1331},"Relation between serum amylin level and epilepsy",{"VOID":1333},"10.1186\u002Fs41983-020-00164-5","https:\u002F\u002Fejnpn.springeropen.com\u002Farticles\u002F10.1186\u002Fs41983-020-00164-5",[1336,1351,1366],{"id":1337,"sortIndex":19,"researcher":18,"roles":1338,"affiliations":1339,"properties":1348},"1148d915-ff3d-463a-8bfe-d2f30086223f",[178],[1340],{"id":18,"sortIndex":19,"affiliation":1341,"properties":18},{"id":1342,"createTime":1343,"updateTime":1343,"relativeEntities":1344,"slug":18,"properties":1345,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"868edab8-ff20-4c81-a62b-314a7cdbe648","2023-12-26T09:34:01.879+00:00",[],{"title":1346},{"VI":1347},"Department of Medical Pharmacology, Faculty of Medicine, SANKO University, Gaziantep, Turkey",{"title":1349},{"VI":1350},"Necla Benlier",{"id":1352,"sortIndex":207,"researcher":18,"roles":1353,"affiliations":1354,"properties":1363},"f5e3ffcb-8a00-4ad0-96fb-ad5109e64b10",[178],[1355],{"id":18,"sortIndex":19,"affiliation":1356,"properties":18},{"id":1357,"createTime":1358,"updateTime":1358,"relativeEntities":1359,"slug":18,"properties":1360,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"f2d90a11-ce00-49b7-9992-a2fc8a10f99b","2023-12-26T09:34:01.938+00:00",[],{"title":1361},{"VI":1362},"Medical Park Hospital Department of Biochemistry, Gaziantep, Turkey",{"title":1364},{"VI":1365},"Nuri Orhan",{"id":1367,"sortIndex":176,"researcher":18,"roles":1368,"affiliations":1369,"properties":1379},"ab9fa046-780f-4474-a272-304d9feb80ea",[178],[1370],{"id":18,"sortIndex":19,"affiliation":1371,"properties":18},{"id":1372,"createTime":1373,"updateTime":1373,"relativeEntities":1374,"slug":1375,"properties":1376,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"ea73f0a8-a5fd-4634-983f-7756746da716","2024-04-15T18:36:50.521+00:00",[],"Department-of-Neurology-Faculty-of-Medicine-SANKO-University-Gaziantep-Turkey",{"title":1377},{"EN":1378},"Department of Neurology, Faculty of Medicine, SANKO University, Gaziantep, Turkey",{"title":1380},{"VI":1381},"Gokhan Ozer",{"url":1334,"publisher":1383,"properties":1410},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1384,"slug":10,"properties":1385,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":1388,"manageAffiliations":1389,"indexDatabases":1390,"url":117,"thumbnailPath":18,"statistic":1405,"gsStatistic":18,"type":147,"analyzePriority":18},[],{"issn":1386,"title":1387},{"VOID":13},{"EN":15},[],[],[1391,1398],{"id":77,"indexDatabase":1392,"url":90,"indexYears":91,"academicFieldIds":1397,"indexDatabaseRanking":97},{"id":79,"createTime":80,"updateTime":81,"relativeEntities":1393,"label":1394,"description":1395,"key":87,"publicationTags":1396,"standard":18},[],{"EN":84,"VI":84},{"EN":84,"VI":86},[89],[93,94,95,96],{"id":99,"indexDatabase":1399,"url":114,"indexYears":18,"academicFieldIds":1404,"indexDatabaseRanking":18},{"id":101,"createTime":102,"updateTime":103,"relativeEntities":1400,"label":1401,"description":1402,"key":110,"publicationTags":1403,"standard":18},[],{"EN":106,"VI":106},{"VI":108,"EN":109},[112,113],[116],{"impactFactor":19,"impactFactorByYear":1406,"i10Index":123,"i10IndexLast5Year":124,"totalPublication":125,"totalPublicationByYear":1407,"totalCitation":133,"totalCitationByYear":1408,"totalCitationPerPublication":140,"totalCitationPerPublicationByYear":1409,"hindexLast5Year":123,"hindex":123},{"2019":120,"2020":121,"2021":122,"2022":122,"2023":121},{"2018":127,"2019":128,"2020":129,"2021":130,"2022":131,"2023":132,"2024":127},{"2018":135,"2019":136,"2020":137,"2021":138,"2022":139},{"2018":142,"2019":143,"2020":144,"2021":145,"2022":146},{"volume":1411,"pages":1412},{"VOID":1113},{"VOID":1207},"2020-03-10",{"id":1415,"createTime":1416,"updateTime":1417,"relativeEntities":1418,"slug":1419,"properties":1420,"entityType":169,"verifyStatus":170,"verifyTime":1417,"verifyNote":171,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":1429,"fullTextUrl":18,"authors":1430,"publicationType":230,"publisherRelationship":1485,"citationCount":18,"citationInfo":18,"publishDate":1518,"publishYear":1519,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":18,"openAccess":18,"references":18,"isForceReanalyzing":261},"94010c06-e9e4-4da1-91fb-cb0169210e87","2023-12-21T20:52:53.087+00:00","2024-12-29T23:39:25.603+00:00",[],"Transcranial-Doppler-assessment-of-patients-with-cerebral-small-vessel-disease",{"references":1421,"abstract":1423,"title":1425,"doi":1427},{"VOID":1422},"Abdallah F, Moustafa RR. Burden of stroke in Egypt current status and opportunities. Int J Stroke. 2014;9:52–84.\nAdams HP, Bendixen BH, Kappelle LJ, Biller J, Love BB, Gordon DL, et al. Classification of subtype of acute ischemic stroke (definitions for use in a multicenter clinical trial). Stroke. 1993;24:35–41.\nPantoni L. Definition and classification of small vessel diseases. In: Pantoni L, Gorelick PB, editors. Cerebral small vessel disease first edition 2014, section 1 chapter1; p. 1, 2.\nPantoni L, Poggesi A, Basile AM, Pracucci G, Barkhof F, Chabriat H, et al. Leukoaraiosis predicts hidden global functioning impairment in nondisabled older people; The LADIS (leukoaraiosis and disability in the elderly) study. J Am Geriatr Soc. 2006;54:1095–101.\nPantoni L, Fierini A, Poggesi A, Inzitari D, Fazekas F, Ferro J, et al. Impact of cerebral white matter changes on functionality in older adults; An overview of the LADIS Study results and future directions. Geriatr Gerontol Int J. 2015;15:10–6.\nPantoni L, Garcia JH. Cellular and vascular changes in the cerebral white matter. Annal N Y Acad Sci. 1997;826:92–102.\nGhorbani A, Ahmadi MJ, Shemshaki H. The value of transcranial Doppler derived pulsatility index for diagnosing cerebral small vessel disease. Adv Biomed Res. 2015;4:54.\nKidwell CS, El-Saden S, Livshits Z, Martin NA, Glenn TC, Saver JL. Transcranial Doppler pulsatility indices as a measure of diffuse small vessel disease. J Am Soc Neuroimag. 2001;11:229–35.\nFazekas F, Alavi A, Chawluk JB, Hurtig HI, Zimmerman RA. MR signal abnormalities 1.5 T in Alzheimer dementia and normal aging. Am J Roentgenol. 1987;149:351–6.\nCordonnier C, Potter GM, Jackson CA, Doubal F, Keir S, Sudlowet CLM, et al. Improving interrater agreement about brain microbleeds, development of the Brain Observer MicroBleed Scales (BOMBS). Stroke. 2009;49:94–9.\nPotter GM, Chappell FM, Morris Z, Wardlaw J. Cerebral perivascular spaces visible on magnetic resonance imaging; development of a qualitative rating scale and its observer reliability. Cerebrovasc Dis. 2015;39(4):224–31.\nStaals J, Makin SJ, Doubal FN, Dennis MS, Wardlaw JM. Stroke subtype, vascular risk factors, and total MRI brain small vessel disease burden. Neurol J. 2014;83:1228–34.\nAlwatban M, Edward JT, Abdullah A, Daniel LM, Gregory RB. The breath-hold acceleration index: a new method to evaluate cerebrovascular reactivity using transcranial Doppler. J Neuroimaging. 2018;28(4):429–35.\nAo DH, Zhai FF, Han F, Zhou LX, Ni J, Yao M, et al. Large vessel disease modifies the relationship between kidney injury and cerebral small vessel disease. Front Neurol. 2018;9:498.\nNam KW, Kwon HM, Lim JS, Han MK, Nam H, Lee YS. The presence and severity of cerebral small vessel disease increases the frequency of stroke in a cohort of patients with large artery occlusive disease. PLoS ONE 2017; 12(10).\nDing L, Hong Y, Peng B. Association between large artery atherosclerosis and cerebral microbleeds: a systematic review and meta analysis. Stroke and Vascular Neurology. 2017;2:49.\nArba F, Mair G, Carpenter T, Sakka E, Sandercock PAG, Lindley RI, et al. Cerebral white matter hypoperfusion increases with small vessel disease burden. Data from the third international stroke trial. J Stroke Cerebrovasc Dis. 2017;26(7):1506–13.\nTurk M, Zaletel M, Oblak JP. Characteristics of cerebral hemodynamics in patients with ischemic leukoaraiosis and new ultrasound indices of ischemic leukoaraiosis. J Stroke Cerebrovasc Dis. 2016;25(4):977–84.\nStaszewski J, Skrobowska E, Piusinska-Macoch R, Brodacki B, Stępień A. Cerebral and extracerebral vasoreactivity in patients with different clinical manifestations of cerebral small vessel disease. J Ultrasound Med. 2018;00:1–13.\nGuo ZN, Xing Y, Wang S, Hongyin M, Liu J, Yang Y. Characteristics of dynamic cerebral autoregulation in cerebral small vessel disease: diffuse and sustained. Sci Rep. 2015;5:15269.\nZheng L, Vinters HV, Mack WJ, Zarow C, Ellis WG, Chui HC. Cerebral atherosclerosis is associated with cystic infarcts and microinfarcts but not Alzheimer pathologic changes. Stroke. 2013;44(10):2835–41.\nGeurts LJ, Zwanenburg JJM, Klijn CJM, Luijten PR, Biessels GJ. Higher pulsatility in cerebral perforating arteries in patients with small vessel disease related stroke, a 7T MRI study. Stroke. 2018;50(1):62–8.",{"EN":1424},"Cerebral small vessel disease (SVD) is associated with acute events such as lacunar and hemorrhagic strokes, or chronic events such as cognitive deficit in the form of subcortical dementia, mood deficit in the form of late onset depression, sphincteric affection, and gait apraxia. Under conditions of moderate blood flow deficit, the inability of sclerotic vessels to dilate due to impairment of the cerebral autoregulation, renders the periventricular white matter seriously ischemic. Therefore, it is important to detect the implications of cerebral large artery disease on the severity of SVD, and the ability of transcranial duplex (TCD) to evaluate it in people at risk. Fifty lacunar stroke patients were recruited, and evaluated using MRI brain to assess SVD score, carotid duplex and TCD to assess extracranial and intracranial stenoses, respectively. Both intracranial and extracranial stenoses showed significant relation to the severity of cerebral SVD. Moreover, there were significant relation between intracranial stenosis and presence of lacuna and EPVS. Cerebral large artery disease contributes to the pathogenesis and severity of cerebral SVD. Therefore, TCD may be a useful tool for the prediction of occurrence of cerebral SVD in high-risk individuals, especially hypertensives.",{"EN":1426},"Transcranial Doppler assessment of patients with cerebral small vessel disease",{"VOID":1428},"10.1186\u002Fs41983-022-00591-6","https:\u002F\u002Fejnpn.springeropen.com\u002Farticles\u002F10.1186\u002Fs41983-022-00591-6",[1431,1446,1461,1473],{"id":1432,"sortIndex":176,"researcher":18,"roles":1433,"affiliations":1434,"properties":1443},"83aaac71-ac8d-4caf-9943-084fcda9f715",[178],[1435],{"id":18,"sortIndex":19,"affiliation":1436,"properties":18},{"id":1437,"createTime":1438,"updateTime":1438,"relativeEntities":1439,"slug":18,"properties":1440,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"4823a482-4fa9-4e4d-ac10-b493a9ed4b51","2023-12-21T20:52:53.106+00:00",[],{"title":1441},{"VI":1442},"Specilist of Neuropsychiatry, El-Sahel Teaching Hospitals, Cairo, Egypt",{"title":1444},{"VI":1445},"Alaa Ebrahim",{"id":1447,"sortIndex":19,"researcher":18,"roles":1448,"affiliations":1449,"properties":1458},"480eeb6a-2dce-4012-b644-9e45d50c452d",[178],[1450],{"id":18,"sortIndex":19,"affiliation":1451,"properties":18},{"id":1452,"createTime":1453,"updateTime":1453,"relativeEntities":1454,"slug":18,"properties":1455,"entityType":62,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"syncStatus":17,"languages":18,"translateLanguages":18,"viewCount":19},"b9766487-e1a4-49ab-a06b-585283984b2c","2024-01-16T02:41:44.643+00:00",[],{"title":1456},{"VI":1457},"Department of Neurology, Faculty of Medicine, Ain Shams University, Cairo, Egypt",{"title":1459},{"VI":1460},"Mohamed M. 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