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1. JAMA Pediatr. 2018 Nov 30. doi: 10.1001/jamapediatrics.2018.4890. [Epub ahead of print]Clinical Subpopulations in a Sample of North American Children Diagnosed WithAcute Flaccid Myelitis, 2012-2016.Elrick MJ(1), Gordon-Lipkin E(2), Crawford TO(1), Van Haren K(3), Messacar K(4), Thornton N(5), Dee E(5), Voskertchian A(6), Nance JR(1), Mu?oz LS(1), GormanMP(7), Benson LA(7), Thomas DL(8), Pardo CA(1), Milstone AM(5)(6), Duggal P(5).Author information: (1)Department of Neurology, Johns Hopkins University School of Medicine,Baltimore, Maryland.(2)Kennedy Krieger Institute, Baltimore, Maryland.(3)Department of Neurology and Neurological Sciences, Stanford University,Stanford, California.(4)Department of Pediatrics, Children's Hospital Colorado, the University ofColorado, Aurora.(5)Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health,Baltimore, Maryland.(6)Division of Infectious Disease, Department of Pediatrics, Johns Hopkins Schoolof Medicine, Baltimore, Maryland.(7)Department of Neurology, Boston Children's Hospital, Boston, Massachusetts.(8)Division of Infectious Disease, Department of Medicine, Johns HopkinsUniversity School of Medicine, Baltimore, Maryland.Importance: Acute flaccid myelitis (AFM) is an emerging poliolike illness ofchildren whose clinical spectrum and associated pathogens are only partiallydescribed. The case definition is intentionally encompassing for epidemiologicsurveillance to capture all potential AFM cases. Defining a restrictive,homogenous subpopulation may aid our understanding of this emerging disease.Objective: To evaluate the extent to which the US Centers for Disease Control andPrevention (CDC) case definition of AFM incorporates possible alternativediagnoses and to assess the plausibility of a case definition that enriches thebiological homogeneity of AFM for inclusion in research studies.Design, Setting, and Participants: Retrospective case analysis of childrenyounger than 18 years diagnosed as having AFM between 2012 and 2016 using the CDCcase definition. Group 1 included patients recruited from the United States andCanada based on the CDC case definition of AFM. Group 2 included patientsreferred to the Johns Hopkins Transverse Myelitis Center for evaluation ofsuspected AFM. Patients' records and imaging data were critically reviewed by 3neurologists to identify those cases with definable alternative diagnoses, andthe remaining patients were categorized as having restrictively defined AFM(rAFM). Clinical characteristics were compared between patients with rAFM (cases)and those with alternative diagnoses, and a case description distinguishing theseAFM groups was identified. Interrater reliability of this description wasconfirmed for a subset of cases by a fourth neurologist. Data were analyzedbetween May 2017 and November 2018.Main Outcomes and Measures: Proportion of patients with possible alternativediagnosis.Results: Of the 45 patients who met the CDC AFM case definition and wereincluded, the mean age was 6.1 years; 27 were boys (60%); and 37 were white(82%), 3 were Asian (7%), 1 was Hispanic (2%), and 4 were mixed race/ethnicity(9%). Of the included patients, 34 were classified as having rAFM, and 11 hadalternate diagnoses (including transverse myelitis, other demyelinatingsyndromes, spinal cord stroke, Guillain-Barre syndrome, Chiari I myelopathy, and meningitis). Factors differing between groups were primarily asymmetry ofweakness, lower motor neuron signs, preceding viral syndrome, symptoms evolvingover hours to days, absence of sensory deficits, and magnetic resonance imagingfindings. A case description was able to reliably define the rAFM group.Conclusions and Relevance: We present an approach for defining a homogeneousresearch population that may more accurately reflect the pathogenesis of theprototypical poliomyelitis-like subgroup of AFM. The definition of rAFM forms ablueprint for inclusion criteria in future research efforts, but more work isrequired for refinement and external validation.DOI: 10.1001/jamapediatrics.2018.4890 PMID: 30500056 2. J Neurol Sci. 2018 Dec 15;395:47-53. doi: 10.1016/j.jns.2018.09.028. Epub 2018Sep 26.Concurrent Guillain-Barré syndrome, transverse myelitis and encephalitispost-Zika: A case report and review of the pathogenic role of multiple arboviral immunity.Mancera-Páez O(1), Román GC(2), Pardo-Turriago R(3), Rodríguez Y(4), Anaya JM(5).Author information: (1)Universidad Nacional de Colombia, Hospital Universitario Nacional, Faculty of Medicine, Department of Neurology, Bogotá, Colombia.; David Cabello InternationalAlzheimer Disease Scholarship Fund, Houston Methodist Hospital, Houston, TX,USA.. Electronic address: ogmancerap@unal.edu.co.(2)Department of Neurology, Methodist Neurological Institute and the Institutefor Academic Medicine Houston Methodist Research Institute, Houston MethodistHospital, Houston, TX, USA; Weill Cornell Medical College, Department ofNeurology, Cornell University, NY, New York, USA. Electronic address:GCRoman@.(3)Universidad Nacional de Colombia, Hospital Universitario Nacional, Faculty of Medicine, Department of Neurology, Bogotá, Colombia.. Electronic address:rpardot@unal.edu.co.(4)Center for Autoimmune Diseases Research (CREA), School of Medicine and Health Sciences, Universidad del Rosario, Bogotá, Colombia. Electronic address:johanintel@.(5)Center for Autoimmune Diseases Research (CREA), School of Medicine and Health Sciences, Universidad del Rosario, Bogotá, Colombia. Electronic address:juan.anaya@urosario.edu.co.Erratum in J Neurol Sci. 2018 Dec 15;395:207-209.We review post-infectious and post-vaccination neurological syndromes involvingperipheral and central nervous system (CNS) and report an illustrative case ofsimultaneous occurrence of Guillain-Barré syndrome (GBS), confirmed by nerveconduction velocities, plus MRI-demonstrated transverse myelitis (TM) and acuteencephalitis [acute disseminated encephalomyelitis] (ADEM+GBS) affecting a24-year-old woman from Cúcuta, Colombia, who developed acute Zika virus (ZIKV)infection confirmed by serum reverse transcriptase-polymerase chain reaction(RT-PCR) and convalescent ZIKV IgG antibodies. With intensive care treatment,respiratory support, steroids, and intravenous immunoglobulin (IVIg), patientsurvived with residual flaccid paraparesis. She had preexisting immunity against Chikungunya virus (CHIKV) and Dengue virus (DENV) acquired before the arrival of ZIKV in Colombia. From reports in the Caribbean, Central and South America wereview 19 cases of ZIKV-associated TM, encephalitis and ADEM occurring after amean latent period of 10.5?days (range 1-96) post-infection. Although GBS andADEM are usually considered post-infectious and associated with development ofantibodies against peripheral nerve and CNS epitopes, we postulate that our case of ADEM+GBS is para-infectious, induced by acute ZIKV neurotropism boosted byactive immunity against other arboviruses. Animal models of ZIKV demonstratedstrong viral neurotropism enhanced by passive immunity with antibodies againstarboviruses such as West Nile virus, CHIKV, or DENV. These considerations arerelevant to prevent potential ZIKV vaccine-induced reactions involving centraland peripheral nervous system.Copyright ? 2018 The Authors. Published by Elsevier B.V. All rights reserved.DOI: 10.1016/j.jns.2018.09.028 PMID: 30292020 3. Continuum (Minneap Minn). 2018 Apr;24(2, Spinal Cord Disorders):441-473. doi:10.1212/CON.0000000000000597.Infectious Myelopathies.Grill MF.PURPOSE OF REVIEW: This article reviews bacterial, viral, fungal, and parasiticpathogens associated with myelopathy. Infectious myelopathies may be due todirect infection or parainfectious autoimmune-mediated mechanisms; this articlefocuses primarily on the former.RECENT FINDINGS: Some microorganisms exhibit neurotropism for the spinal cord(eg, enteroviruses such as poliovirus and flaviviruses such as West Nile virus), while others are more protean in neurologic manifestations (eg, herpesvirusessuch as varicella-zoster virus), and others are only rarely reported to causemyelopathy (eg, certain fungal and parasitic infections). Individuals who areimmunocompromised are at increased risk of disseminated infection to the central nervous system. Within the last few years, an enterovirus D68 outbreak has beenassociated with cases of acute flaccid paralysis in children, and emerging Zikavirus infection has been concurrent with cases of acute flaccid paralysis due to Guillain-Barré syndrome, although cases of myelitis have also been reported.Associated pathogens differ by geographic distribution, with myelopathies relatedto Borrelia burgdorferi (Lyme disease) and West Nile virus more commonly seen in the United States and parasitic infections encountered more often in LatinAmerica, Southeast Asia, and Africa. Characteristic CSF and MRI patterns havebeen identified with many of these infections.SUMMARY: A myriad of pathogens are associated with infectious myelopathies. Host factors, geographic distribution, clinical features, CSF profiles, and MRIfindings can assist in formulating the differential diagnosis and ultimatelyguide management.DOI: 10.1212/CON.0000000000000597 PMID: 29613895 4. Clin Infect Dis. 2018 Feb 10;66(5):653-664. doi: 10.1093/cid/cix860.Clinical Features of Acute Flaccid Myelitis Temporally Associated With anEnterovirus D68 Outbreak: Results of a Nationwide Survey of Acute FlaccidParalysis in Japan, August-December 2015.Chong PF(1), Kira R(1), Mori H(2), Okumura A(3), Torisu H(4), Yasumoto S(5),Shimizu H(6), Fujimoto T(7), Hanaoka N(7), Kusunoki S(8), Takahashi T(9), OishiK(7), Tanaka-Taya K(7); Acute Flaccid Myelitis Collaborative Study Investigators.Collaborators: Toyofuku E, Fukuyama T, Sato T, Takahashi Y, Kanazawa A, Hiyane M,Fukushima T, Toki T, Hayashi R, Kubota S, Ishii W, Akasaka M, Miyazawa H,Motobayashi M, Asaoka M, Shiihara T, Miyoshi Y, Tsuru T, Ikeda K, Matsukura M,Nakamura R, Moriyama K, Sugawara Y, Takami Y, Fujita T, Yano T, Kasai M, UchidaT, Fujita M, Uematsu M, Hata A, Ogata H, Miyamoto T, Sumi K, Ishida Y, Takeshita E, Kawazoe T, Kawabata T, Miyatake C, Yakuwa A, Kakimoto Y, Terashima H, KubotaM, Abe Y, Nagura M, Yamanouchi H, Mori S, Konishi Y, Ikegami M, Tomonaga Y,Takashima Y, Ichikawa K, Moriyama N, Oba C, Kashiwagi M, Yoshikawa S, Tanaka K,Ohta G, Hattori A, Ieda D, Ono S, Tanimura T, Ban K, Sugiyama N, Kouzan N, YamadaY, Inoue M, Sakajiri K, Ohyama K, Yamamuro M, Ishigaki H, Seino A, Igarashi S,Nakamoto T, Sugimoto K, Ochi M, Hamanaka E, Ohi K, Kawasaki H, Nishitani M, UnoH, Inoue M, Okuyama M, Yamamoto A, Sato R, Azuma N, Mabuchi S, Shida Y, HashimotoY, Yoshimura M, Matsuhisa Y, Nakano K, Yamashita Y, Kikuchi E, Yamamoto A,Igarashi N, Yoshida N, Nishiki S, Yasutomi D, Kusano N, Wakahara R, Furuyama M,Mikami H, Taniguchi H, Yoshii Y, Narabayashi A, Takahashi T, Nakamura T, KaburagiY, Nagasao A, Kuwahara M.Author information: (1)Department of Pediatric Neurology, Fukuoka Children's Hospital.(2)Department of Radiology, Graduate School and Faculty of Medicine, Universityof Tokyo.(3)Department of Pediatrics, Aichi Medical University, Nagakute.(4)Department of Pediatrics, Fukuoka Dental College Medical and Dental Hospital.(5)Medical Education Center, Fukuoka University School of Medicine.(6)Department of Virology II, Tokyo.(7)Infectious Disease Surveillance Center, National Institute of InfectiousDiseases, Tokyo.(8)Department of Neurology, Kindai University Faculty of Medicine, Osaka-Sayama.(9)Department of Neurology, Tohoku University Graduate School of Medicine,Sendai, Japan.Background: Acute flaccid myelitis (AFM) is an acute flaccid paralysis syndromewith spinal motor neuron involvement of unknown etiology. We investigated thecharacteristics and prognostic factors of AFM clusters coincident with anenterovirus D68 (EV-D68) outbreak in Japan during autumn 2015.Methods: An AFM case series study was conducted following a nationwide surveyfrom August to December 2015. Radiographic and neurophysiologic data weresubjected to centralized review, and virology studies were conducted foravailable specimens.Results: Fifty-nine AFM cases (58 definite, 1 probable) were identified,including 55 children and 4 adults (median age, 4.4 years). The AFM epidemiccurve showed strong temporal correlation with EV-D68 detection from pathogensurveillance, but not with other pathogens. EV-D68 was detected in 9 patients: 5 in nasopharyngeal, 2 in stool, 1 in cerebrospinal fluid (adult case), and 1 intracheal aspiration, nasopharyngeal, and serum samples (a pediatric case withpreceding steroid usage). Cases exhibited heterogeneous paralysis patterns from1- to 4-limb involvement, but all definite cases had longitudinal spinal graymatter lesions on magnetic resonance imaging (median, 20 spinal segments).Cerebrospinal fluid pleocytosis was observed in 50 of 59 cases (85%), and 8 of 29(28%) were positive for antiganglioside antibodies, as frequently observed inGuillain-Barré syndrome. Fifty-two patients showed variable residual weakness at follow-up. Good prognostic factors included a pretreatment manual muscle strengthtest unit score >3, normal F-wave persistence, and EV-D68-negative status.Conclusions: EV-D68 may be one of the causative agents for AFM, while hostsusceptibility factors such as immune response could contribute to AFMdevelopment.? The Author 2017. Published by Oxford University Press for the InfectiousDiseases Society of America.DOI: 10.1093/cid/cix860 PMCID: PMC5850449PMID: 29028962 5. Eur J Neurol. 2017 Nov;24(11):e81-e82. doi: 10.1111/ene.ment on 'Acute flaccid myelitis in childhood: a retrospective cohort study'.Ben Achour N(1)(2), Jeridi C(1), Rebai I(1)(2), Nagi S(2)(3), Kraoua I(1)(2), BenYoussef-Turki I(1)(2).Author information: (1)Research unit UR12 SP24 and Department of Child and Adolescent Neurology,National Institute Mongi Ben Hmida of Neurology, Tunis, Tunisia.(2)Faculté de Médecine de Tunis, Université de Tunis El Manar, Tunis, Tunisia.(3)Department of Neuroradiology, National Institute Mongi Ben Hmida of Neurology,Tunis, ment on Eur J Neurol. 2017 Aug;24(8):1077-1083.DOI: 10.1111/ene.13402 PMID: 29024358 [Indexed for MEDLINE]6. Ned Tijdschr Geneeskd. 2017;161:D1566.[Acute flaccid myelitis after a respiratory tract infection; first Dutch caserelated to enterovirus type D68 infection].[Article in Dutch]Helfferich J(1), Kingma EM, Meiners LC, Sch?lvinck EH, Mulder HD, Brouwer OF.Author information: (1)Rijksuniversiteit Groningen-UMCG, Groningen.BACKGROUND: Acute flaccid myelitis (AFM) is a relatively rare disorder affecting the anterior horn of the spinal cord and brain stem. It is characterised by rapidprogressive weakness of the limbs and respiratory muscles, often combined withcranial nerve dysfunction. This used to be seen in infections with the poliovirus, but in recent years, AFM has been mainly associated with enterovirus D68infection.CASE DESCRIPTION: A boy of nearly 4 years-old developed rapidly progressiveweakness and respiratory failure after an upper airway infection. Initially,Guillain-Barré syndrome was suspected, but after further investigationsenterovirus D68 was detected in the nasopharyngeal aspirate and the diagnosis of AFM was made.CONCLUSION: Progressive weakness after a respiratory tract infection should raisethe suspicion of enterovirus-associated AFM. This syndrome can be distinguishedfrom Guillain-Barré syndrome by its more rapid progression, asymmetrical weaknessand greater involvement of the upper limbs. The diagnosis can be confirmed bytypical findings on MRI and electromyography of the spinal cord and brain stem,combined with the detection of enterovirus D68 in nasopharyngeal specimens.PMID: 28832294 [Indexed for MEDLINE]7. J Pediatr (Rio J). 2017 Nov - Dec;93 Suppl 1:26-35. doi:10.1016/j.jped.2017.06.003. Epub 2017 Jul 27.Assessment of acute motor deficit in the pediatric emergency room.Vasconcelos MM(1), Vasconcelos LGA(2), Brito AR(3).Author information: (1)Universidade Federal Fluminense (UFF), Hospital Universitário Ant?nio Pedro,Departamento Materno Infantil, Niterói, RJ, Brazil. Electronic address:mmdvascon@.(2)Associa??o Brasileira Beneficente de Reabilita??o (ABBR), Divis?o dePediatria, Rio de Janeiro, RJ, Brazil.(3)Universidade Federal Fluminense (UFF), Hospital Universitário Ant?nio Pedro,Departamento Materno Infantil, Niterói, RJ, Brazil.OBJECTIVES: This review article aimed to present a clinical approach, emphasizingthe diagnostic investigation, to children and adolescents who present in theemergency room with acute-onset muscle weakness.SOURCES: A systematic search was performed in PubMed database during April andMay 2017, using the following search terms in various combinations: "acute,""weakness," "motor deficit," "flaccid paralysis," "child," "pediatric," and"emergency". The articles chosen for this review were published over the past tenyears, from 1997 through 2017. This study assessed the pediatric age range, from 0 to 18 years.SUMMARY OF THE DATA: Acute motor deficit is a fairly common presentation in thepediatric emergency room. Patients may be categorized as having localized ordiffuse motor impairment, and a precise description of clinical features isessential in order to allow a complete differential diagnosis. The two mostcommon causes of acute flaccid paralysis in the pediatric emergency room areGuillain-Barré syndrome and transverse myelitis; notwithstanding, otheretiologies should be considered, such as acute disseminated encephalomyelitis,infectious myelitis, myasthenia gravis, stroke, alternating hemiplegia ofchildhood, periodic paralyses, brainstem encephalitis, and functional muscleweakness. Algorithms for acute localized or diffuse weakness investigation in theemergency setting are also presented.CONCLUSIONS: The clinical skills to obtain a complete history and to perform adetailed physical examination are emphasized. An organized, logical, and stepwisediagnostic and therapeutic management is essential to eventually restorepatient's well-being and full health.Published by Elsevier Editora Ltda.DOI: 10.1016/j.jped.2017.06.003 PMID: 28756061 [Indexed for MEDLINE]8. Isr Med Assoc J. 2016 Oct;18(10):590-593.Causality Assessment of Serious Neurologic Adverse Events Following bOPV NationalVaccination Campaign in Israel.Tasher D(1)(2)(3), Kopel E(4)(5)(6), Anis E(4)(5)(6)(3), Grossman Z(7)(8), SomekhE(9)(2)(3).Author information: (1)Pediatric Infectious Diseases Unit, Wolfson Medical Center, Holon, Israel.(2)Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.(3)Israeli National Polio Accreditation Committee, Ministry of Health, Jerusalem,Israel.(4)Division of Epidemiology, Public Health Services, Ministry of Health,Jerusalem, Israel.(5)Public Health Services, Ministry of Health, Jerusalem, Israel.(6)Hebrew University-Hadassah Braun School of Public Health and CommunityMedicine, Jerusalem, Israel.(7)Israel Pediatric Association, Wolfson Medical Center, Holon, Israel.(8)Maccabi Health Services, Tel Aviv, Israel.(9)Pediatric Infectious Diseases Unit, and Israel Pediatric Association WolfsonMedical Center, Holon, Israel.BACKGROUND: During 2013-2014 Israel experienced a continuous circulation of wild poliovirus type 1 (WPV1) but with no clinical cases. WPV1 circulation wasgradually terminated following a national vaccination campaign of bivalent oralpoliovirus vaccine (bOPV) for 943,587 children < 10 years. Four cases of childrenwith neurological manifestations that appeared following bOPV vaccinations werereported during the campaign: three of Guillain-Barré syndrome (GBS) and one ofacute disseminated encephalomyelitis (ADEM).OBJECTIVES: To present an analysis of these cases, the rapid response and thetransparent publication of the results of this analysis.METHODS: The clinical, laboratory and epidemiological data of these four patientswere available during the analysis. In addition, data regarding the incidence of GBS and ADEM during previous years, and reported cases of acute flaccid paralysis(AFP) and the incidence of Campylobacter jejuni enteritis were collected from theEpidemiology Department of the Israel Ministry of Health.RESULTS: The incidence of GBS among bOPV-vaccinated children was not higher than among bOPV-unvaccinated children. For all the cases reviewed the "incubationperiod" from vaccination to the event was longer than expected and other moreplausible causes for the neurologic manifestations were found. There is noevidence in the literature of a causal relationship between bOPV and ADEM.CONCLUSIONS: There was no association between the bOPV vaccine and the reportedneurological manifestations. We believe that our experience may assist otherpublic health professionals when confronting a similar problem of alleged sideeffects during a mass medical intervention.PMID: 28471617 [Indexed for MEDLINE]9. Spinal Cord Ser Cases. 2016 Jan 7;2:15032. doi: 10.1038/scsandc.2015.32.eCollection 2016.Rehabilitation of a patient with overlap of acute transverse myelitis andBickerstaff's brainstem encephalitis: a case report.Solinsky R(1), Bunnell AE(1).Author information: (1)Department of Rehabilitation Medicine, University of Washington , Seattle, WA,USA.We report on one patient with Bickerstaff's brainstem encephalitis (BBE) andassociated flaccid weakness. Counter to previous studies with BBE which indicate weakness due to Guillain-Barre syndrome, our patient's presentation of paraplegiafollowing BBE is consistent with concomitant acute transverse myelitis. Herfindings of BBE largely resolved, although she remained with T6 American SpinalInjury Association (ASIA) A paraplegia. Motor functional impairment measurescores improved from 20 at admission to 66 before discharge home with assistance.This case presents the first potential overlapping case of acute transversemyelitis with BBE and describes how acute inpatient rehabilitation can beeffective in facilitating transition back to independence following tetraplegiawith BBE.DOI: 10.1038/scsandc.2015.32 PMCID: PMC5129443PMID: 28053734 10. Indian J Pediatr. 2017 Apr;84(4):315-321. doi: 10.1007/s12098-016-2276-y. Epub2016 Dec 21.Uncommon Disorders Masquerading as Acute Flaccid Paralysis in Children.Garg M(1), Kulkarni SD(2), Patil V(2), Sayed R(2), Hegde AU(2).Author information: (1)Department of Pediatric Neurosciences, Bai Jerbai Wadia Hospital for Children,Parel, Mumbai, Maharashtra, 400012, India. docmeenal@.(2)Department of Pediatric Neurosciences, Bai Jerbai Wadia Hospital for Children,Parel, Mumbai, Maharashtra, 400012, India.The syndrome of acute flaccid paralysis (AFP) is a common medical emergency inchildren. In the era of poliomyelitis eradication, the common causes of AFPinclude Guillain-Barré syndrome (GBS), transverse myelitis and traumaticneuritis. However, many common diseases can uncommonly present as AFP and someuncommon diseases may also masquerade like it. Uncommon causes of AFP seen at atertiary care pediatric hospital are discussed along with relevant points indiagnosis and management. Also, common pitfalls in diagnosis of pediatric AFP andan approach to investigations are discussed.DOI: 10.1007/s12098-016-2276-y PMID: 28000111 [Indexed for MEDLINE]11. J Ayub Med Coll Abbottabad. 2015 Jul-Sep;27(3):673-6.ACUTE FLACCID PARALYSIS SURVEILLANCE: A 5 YEARS STUDY OF BANNU, PAKISTAN.Faheem MU, Haroon MZ, Khan AA, Shaukat M, Anwar SA.BACKGROUND: Acute flaccid paralysis (AFP) is clinical presentation marked byacute onset of weakness and reduced tone. Aetiologies of AFP are diverseincluding infectious agents, trauma or autoimmune reaction. Currently only three countries in the world that are Nigeria, Pakistan and Afghanistan have endemicpoliomyelitis. Pakistan's polio crisis represents one of the last hurdles in a23-year campaign run by the World Health Organization. Bannu due to itsgeographical location stands out to be one of highest risk areas forPoliomyelitis. The objective of this study was to determine frequency of AFP and their aetiologies in District of Bannu during time period of four years from 2007to 2011.METHODS: It was a cross-sectional descriptive study. Data was collected from EDO office District Bannu and analysed using Microsoft Excel 2007. Results: Duringthis period there were 180 cases of AFP in district Bannu. 15% of cases werediagnosed as Guillian Barre Syndrome, making it the leading aetiology. Only 3(1.66%) cases were diagnosed with Poliomyelitis. Out of 180 AFP cases 104 caseswere male and 76 cases were female.CONCLUSION: Bannu needs enthusiastic educational and vaccination campaigns toeradicate Polio from the area and henceforth from the Pakistan.PMID: 26721037 [Indexed for MEDLINE]12. Pediatr Neurol. 2016 Feb;55:17-21. doi: 10.1016/j.pediatrneurol.2015.10.007. Epub2015 Oct 20.Recognition and Management of Acute Flaccid Myelitis in Children.Nelson GR(1), Bonkowsky JL(2), Doll E(2), Green M(3), Hedlund GL(4), Moore KR(4),Bale JF Jr(2).Author information: (1)Division of Pediatric Neurology, Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah. Electronic address:gary.nelson@hsc.utah.edu.(2)Division of Pediatric Neurology, Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah.(3)Physical Medicine and Rehabilitation, University of Utah School of Medicine,Salt Lake City, Utah.(4)Department of Medical Imaging, Primary Children's Hospital, Salt Lake City,Utah; Department of Radiology, University of Utah School of Medicine, Salt LakeCity, Utah.BACKGROUND: In 2014-2015, several regions of the United States experienced anoutbreak of acute flaccid myelitis in pediatric patients. A common, uniquefeature was disease localization to the gray matter of the spinal cord.METHODS: We report 11 children, ages 13 months to 14 years (median 9 years), inthe Intermountain West who presented with extremity weakness (n = 10) or cranial neuropathy (n = 1) of varying severity without an apparent etiology.RESULTS: All children experienced acute paralysis, and 10 had symptoms or signsthat localized to the spinal cord. Maximum paralysis occurred within 4 days ofonset in all patients. All had spinal gray matter lesions consistent with acutemyelitis detected by magnetic resonance imaging; no single infectious cause wasidentified. Despite therapy with intravenous immunoglobulin, corticosteroids, or plasma exchange, nine of 10 (90%) children had motor deficits at follow-up.CONCLUSIONS: Recognition of this disorder enables clinicians to obtainappropriate imaging and laboratory testing, initiate treatment, and providefamilies with accurate prognostic information. In contrast to other causes ofacute flaccid paralysis in childhood, most children with acute flaccid myelitishave residual neurological deficits.Copyright ? 2016 Elsevier Inc. All rights reserved.DOI: 10.1016/j.pediatrneurol.2015.10.007 PMID: 26621554 [Indexed for MEDLINE]13. Iran J Pediatr. 2014 Apr;24(2):131-9.Acute flaccid paralysis and its differential diagnosis in in kurdistan province, Western iran; an 11-year surveillance.Soltani J Md(1), Esmailnasab N Md(2), Roshani D PhD(2), Karimi M Mhs(3), AmjadiMJ Mhs(3).Author information: (1)Department of Pediatrics.(2)Department of Epidemiology & Biostatistics, Faculty of Medicine.(3)Center for Disease Control and Prevention, Kurdistan University of MedicalSciences , Sanandaj, Iran.OBJECTIVE: The surveillance of acute flaccid paralysis (AFP) is a key strategyfor monitoring the progress of poliomyelitis eradication and is a sensitivemeasure for detecting potential cases of poliomyelitis and poliovirus infection. This study was conducted to describe the characteristics of patients reportedwith AFP, and to evaluate the performance of the surveillance system in Kurdistanprovince, western Iran, using indicators recommended by the World HealthOrganization (WHO).METHODS: This observational study was conducted from January 2000 to December2010 at the Kurdistan Center for Disease Control and the Department ofPediatrics. All children who fulfilled the WHO definition for AFP were includedin our study. The stool samples of all the children were sent for poliovirusisolation. All the patients were evaluated for 60 days after the onset ofsymptoms to identify the signs of residual weakness.FINDINGS: One-hundred thirty nine children aged <15 years were reported to theCenter for Diseases Control with AFP. In 138 (99%) stool samples no polioviruswas isolated. None of the patients was diagnosed as having acute poliomyelitis orpolio-compatible paralysis. Guillain-Barré syndrome was the most frequent finaldiagnosis (79 cases) followed by Transverse Myelitis (7 cases) and Encephalitis(6 cases). By detecting 1.3 to 3.6 (mean 3.2) AFP cases per 100 000 population inKurdistan during the study period, we achieved the WHO target for AFPsurveillance. All performance indicators but one consistently met the WHOrequirements and therefore demonstrated the effectiveness of the AFP surveillanceprogram in Kurdistan.CONCLUSION: The effective surveillance system in Kurdistan and its evaluation mayserve as a model for the surveillance of other infectious diseases.PMCID: PMC4268831PMID: 25535530 14. Hum Vaccin Immunother. 2015;11(1):277-81. doi: 10.4161/hv.36164. Epub 2014 Nov 1.Surveillance of acute flaccid paralysis (AFP) in Lombardy, Northern Italy, from1997 to 2011 in the context of the national AFP surveillance system.Pellegrinelli L(1), Primache V, Fiore L, Amato C, Fiore S, Bubba L, Pariani E,Amendola A, Barbi M, Binda S.Author information: (1)a Department of Biomedical Sciences for Health; University of Milan; Milan,Italy.Erratum in Hum Vaccin Immunother. 2015;11(7):1880.An Acute Flaccid Paralysis (AFP) surveillance system was set up in Lombardy(Northern Italy) in 1997 in the framework of the national AFP surveillancesystem, as part of the polio eradication initiative by the World HealthOrganization (WHO). This surveillance system can now be used to detect Poliovirus(PV) reintroductions from endemic countries. This study aimed at describing theresults of the AFP surveillance in Lombardy, from 1997 to 2011. ? Overall, 131AFP cases in Lombardy were reported with a mean annual incidence rate of0.7/100?000 children &lt;15 years of age (range: 0.3/100?000-1.1/100?000). Thesensitivity of the surveillance system was optimal from 2001-2003. The monthlydistribution of AFP cases was typical with peaks in November, in January, and in March. The major clinical diagnoses associated with AFP were Guillain-BarréSyndrome (GBS, 40%) and encephalomyelitis/myelitis (13%). According to thevirological results, no poliomyelitis cases were caused by wild PV infections,but two Vaccine-Associated Paralytic Paralysis (VAPP) cases were reported in 1997when the Sabin oral polio vaccine (OPV) was still being administered in Italy.Since a surveillance system is deemed sensitive if at least one case of AFP per100,000 children &lt;15 years of age is detected each year, our surveillancesystem needs some improvement and must be maintained until global polioviruseradication will be declared.DOI: 10.4161/hv.36164 PMCID: PMC4514231PMID: 25483546 [Indexed for MEDLINE]15. BMC Infect Dis. 2014 Aug 20;14:448. doi: 10.1186/1471-2334-14-448.An epidemiological analysis of acute flaccid paralysis and its surveillancesystem in Iraq, 1997-2011.Jasem JA(1), Marof K, Nawar A, Khalaf Y, Al-Hamdani F, Ali S, Kalil AC, Islam KM.Author information: (1)School of Medicine, Faculty of Medical Sciences, University of Duhok, Duhok,Kurdistan Region, Iraq. jagar.jasem@osumc.edu.BACKGROUND: Acute flaccid paralysis surveillance (AFP) is an essential strategyof the WHO's Polio Eradication Initiative. This is the first study conducted toestimate the incidence, etiology, distribution, and surveillance performance ofAFP in Iraq.METHODS: Surveillance data about the AFP cases under the age of 15?years reportedfrom Iraq during January 1997 to December 2011 were depended in the currentstudy.RESULTS: A total of 4974 cases of AFP were reported from Iraq during the studyperiod, with an annual incidence of 2.5/100,000 population. Guillain-Barrésyndrome represented more than half of the reported cases (N?=?2611, 52.5%),followed by traumatic neuritis (N?=?715, 14.4%), and other CNS infections(N?=?292, 5.9%). Poliomyelitis accounted for 166 (3.3%) of cases, the lastreported case being in January 2000. Surveillance performance showed that all,but two, indicators were below the required WHO recommended levels.CONCLUSIONS: AFP surveillance remains the gold standard method for poliomyelitis detection. It witnessed dramatic changes over the last two decades. This hasraised people's and clinicians' awareness to the importance of promptness innotifying suspected cases and timely transportation of stool specimens to theNational Poliovirus Laboratory in Baghdad, or alternatively having more than one laboratory for poliovirus detection in the country, all of which are very useful measures to increase the surveillance performance in the country.DOI: 10.1186/1471-2334-14-448 PMCID: PMC4159501PMID: 25141887 [Indexed for MEDLINE]16. J Paediatr Child Health. 2014 Jul;50(7):545-52. doi: 10.1111/jpc.12492. Epub 2014Feb 17.Fifteen years of acute flaccid paralysis surveillance in Hong Kong: findings from1997 to 2011.National Committee for the Certification of Wild Poliovirus Eradication in HongKong.AIM: Acute flaccid paralysis (AFP) surveillance system was set up in Hong Kong in1997 for World Health Organization's (WHO) certification of poliomyelitiseradication. This paper describes and reviews the demographic, clinical andvirological characteristics of AFP cases reported to the system in its first 15years.METHODS: All patients aged under 15 years presented with acute onset of paralysisof any limbs reported to the Department of Health from January 1997 to December2011 were reviewed. Data on demographic characteristics, vaccination history,clinical presentation and virological investigation on stool specimens collected during investigation were analysed with descriptive statistics.RESULTS: Of the 247 cases reported, about 45% were aged under five. All caseswere classified as non-polio AFP according to WHO classification. About 60% were identified with neurological disorders, with Guillain-Barré syndrome (25.9%) and myelitis (13.4%) being the most common. Viruses were detected in 14.0% of the AFPcases, with non-polio enteroviruses (NPEV) (60.0%) and adenoviruses (31.4%)accounted for most of the positive detections. Most performance indicators set bythe WHO were fulfilled.CONCLUSIONS: The AFP surveillance facilitated the clinical, virological andepidemiological examination of paediatric AFP cases. From 1997 to 2011,Guillain-Barré syndrome and myelitis were the most common among paediatric AFPcases in Hong Kong. NPEV and adenoviruses accounted for most of the positiveviral detections. No wild poliovirus was detected, and all cases were classified as non-polio AFP.? 2014 The Author. Journal of Paediatrics and Child Health ? 2014 Paediatrics andChild Health Division (Royal Australasian College of Physicians).DOI: 10.1111/jpc.12492 PMID: 24528511 [Indexed for MEDLINE]17. BMC Infect Dis. 2013 Aug 21;13:384. doi: 10.1186/1471-2334-13-384.Potential for the Australian and New Zealand paediatric intensive care registryto enhance acute flaccid paralysis surveillance in Australia: a data-linkagestudy.Hobday LK, Thorley BR, Alexander J, Aitken T, Massey PD, Cretikos M, Slater A,Durrheim DN.BACKGROUND: Australia uses acute flaccid paralysis (AFP) surveillance to monitor its polio-free status. The World Health Organization criterion for a sensitiveAFP surveillance system is the annual detection of at least one non-polio AFPcase per 100,000 children aged less than 15?years, a target Australia has notconsistently achieved. Children exhibiting AFP are likely to be hospitalised and may be admitted to an intensive care unit. This provides a potential opportunity for active AFP surveillance.METHODS: A data-linkage study for the period from 1 January 2005 to 31 December2008 compared 165 non-polio AFP cases classified by the Polio Expert Panel with880 acute neurological presentations potentially compatible with AFP documentedin the Australian and New Zealand Paediatric Intensive Care (ANZPIC) Registry.RESULTS: Forty-two (25%) AFP cases classified by the Polio Expert Panel werematched to case records in the ANZPIC Registry. Of these, nineteen (45%) caseswere classified as Guillain-Barré syndrome on both registries. Ten additionalGuillain-Barré syndrome cases recorded in the ANZPIC Registry were not notifiedto the national AFP surveillance system.CONCLUSIONS: The identification of a further ten AFP cases supports inclusion of intensive care units in national AFP surveillance, particularly specialistpaediatric intensive care units, to identify AFP cases that may not otherwise be reported to the national surveillance system.DOI: 10.1186/1471-2334-13-384 PMCID: PMC3765192PMID: 23964831 [Indexed for MEDLINE]18. J Nat Sci Biol Med. 2012 Jan;3(1):81-3. doi: 10.4103/0976-9668.95976.Hypokalemic quadriparesis: An unusual manifestation of dengue fever.Gutch M(1), Agarwal A, Amar A.Author information: (1)Department of Internal Medicine, CSMMU, Lucknow, Uttar Pradesh, India.Dengue is the most important mosquito-borne, arboviral infection found intropical and sub-tropical climates. Clinical presentation varies from a severeflu-like illness to a potentially lethal dengue hemorrhagic fever. Dengue hasbeen regarded as a nonneurotropic virus. However, there are reports describingneurological involvements in dengue virus infection. The neurological involvementin dengue virus infection includes encephalitis, acute disseminatedencephalomyelitis, transverse myelitis, and Guillain-Barre syndrome. Theneurological spectrum of dengue patients has been limited because of small numberof case reports, paucity of imaging, and neurophysiologic studies. There are onlya few isolated case reports and case series documenting acute pure motorquadriparesis in dengue fever. We report acute pure motor reversiblequadriparesis due to hypokalemia. Clinicians in the endemic area should be aware of such association of acute pure motor reversible quadriparesis with denguefever.DOI: 10.4103/0976-9668.95976 PMCID: PMC3361784PMID: 22690057 19. Medicina (B Aires). 2009;69(1 Pt 1):84-91.[Guillain Barré syndrome in pediatrics].[Article in Spanish]Erazo Torricelli R(1).Author information: (1)Hospital Luis Calvo Mackenna, Santiago, Chile. ricardoerazo@This paper reviews the current knowledge about Guillain-Barré syndrome (GBS). GBSis defined as an acute, areflexic, flaccid paralysis, which is classified into 4 subgroups: acute inflammatory demyelinating polyneuropathy (AIDP), acutemotor-sensory axonal neuropathy (AMSAN), acute motor axonal neuropathy (AMAN) andMiller-Fisher syndrome (MFS). AIDP is associated in 30-50% of cases with cranial nerve involvement, which is not observed in AMAN. MFS is characterized by ataxia,ophthalmoplegia and areflexia, but it may also present cranial nerve dysfunction.Recent data on the pathology and pathophysiology of GBS emphasize the importantrole of Campylobacter jejuni infection in generating anti-ganglioside antibodies (GM1 in AIDP, GQ1b in MFS and GD1a in AMAN), which damage myelin in AIDP and MFS and axons in AMAN. The differential diagnosis must rule out other disorders ofthe central nervous system (encephalitis, encephalomyelitis, myelitis),myasthenic syndromes, toxic neuropathies induced by heavy meals, drugs, chemical substances or animal toxins, and myopathic conditions, especially acute benigninfectious myositis and neuromyopathy of the intensive care unit patient. It isimportant the treatment with immune globulin, at a total dose of 2 grams perkilogram administered over 48 hours. Plasmapheresis can be equally effective. GBShas a good prognosis in children with a total recovery in 85% of cases.Rehabilitation is crucial to attain a more rapid and global improvement.PMID: 19240005 [Indexed for MEDLINE]20. BMC Infect Dis. 2008 Oct 9;8:135. doi: 10.1186/1471-2334-8-135.Surveillance of acute flaccid paralysis in the Marches region (Italy): 1997-2007.D'Errico MM(1), Barbadoro P, Bacelli S, Esposto E, Moroni V, Scaccia F, Tantucci L, Prospero E; AFP Study Group.Collaborators: AngeAirini B, De Bellis I, Magni B, Mancini C, Saracino C, VaccaroA, Pertosa ME, Bernacchia R, Carducci E, Felici L, D'Errico A, Moscillo A,Pallottelli C, Panariello A, Angeletti C, Mariani, Ranieri L, Ripanti G,Fracassini F, Moretti U, Petrelli E, Carboni P, Cioppi A, Belardinelli N,Balduccim M, Stoppini L, Pieretti C, Pierini G, Fronzoni M, Bianchini LM,Giuliani S, Belardinelli, Marangoni, Corbelli, Dhamo, Filomeni N, Genga R,Carboni D, Guidi A, Sabatini E, Manzoni, Franchi G, Casciati AM, Barocci G,Ranieri L, Ricci T, Quintini, Francini L, Migliozzi L, Basili G, Radicioni P,Rizzo V, Bruni L, Del Pesce M, Cianvrignoni E, Massi G, Pettinari R, Ricolfi A,Francolini P, Dellantonio R, Vignoni, Bonucci, Carotti G, Gaetti MT, Ricci S,Vianell P, Agostinelli P, Piretti B, Burattini M, Cerotti A, Giaccaglini E,Ciarmatori M, Alesi C, Sconocchini C, Bellocci P, Rosati, Bolzonetti P, Lombardi M, Grassi R, Maddaloni D, Franceschetti L, Coppa V, Gabrielli O, Rocchi E,Burattini I, Fabrizi B, Bruni S, Caramia G, Bruschi B, CordialI, Osimani P,Ruffini E, Cardinali C, Porfiri L, Zamponi N, Tavoni MA, Ficcadenti, Capriotti,Scalise G, Drenaggi D, Ancarani F, Fiorentini, Dini M, Burzachini F, PiersimoneF, Mataloni A, Cingolani M, Simeone M, Del Gobbo R, Provinciali L, Angeleri F,Paladini D, Grifoni SC, Catani S, Luconi, Taffi, Scarpino O, Pelliccioni G, DelGobbo M, Zoppi A, Leone L, Coltroneo P, Bonifazi V, Ruffini A, Mariani, Nori P,Bartolotta E, Mariani, Bonazza, Guazzarotti L, Lampacrescia M, Pecora R, PerriPF, Piatti M, Principi M, Mercuri A, Staffolani M, Ercoli L, GelsominI S, BettiF, Bocosi D, Castelli R, Urbani C, Beccierica E, Piccinini, Rosini A, Tubaldi L, Guerrini D, Mancini AL, Coppola MC, Castellini, Gobbi C, Caucci AM, Tacchetti P, Taccari LM, Fabbrizi E, Paoloni, Padovani, Amadio G, Mecozzi F, Sequini FM,Traini E, Fedeli A, Signorino M, Speranzini A, Angeloni R, fortuna, Gismondi,Rogantini F, Ripani P, Guastaferro N, De Angelis F, Galanti E, Infriccioli G,Curatola L, Carboni T, Gobbato R, Sanguigni S, Carlucci A, Di Stefano P,Candelotti P, Lucani L, Pace F, Amadio C, Pasquini, Tucci, Gobbi M, Petroni S,Vittucci P, Bamonti E, Corbelli G, Altilia F, Ragno M, Sirocchi G, Scarcella S,Cacchio G, Manente G, Tasca R, Bianchi, Brunelli B, Mainardi G, Cinque M,Lombardi Mistura E, Amadio C.Author information: (1)Institute of Infectious Diseases and Public Health, Università Politecnicadelle Marche, Italy. derrico@univpm.itBACKGROUND: The last case of poliomyelitis due to transmission of indigenous wildpoliovirus occurred in Italy in 1982, however, it is important to guarantee ahigh quality surveillance as there is a risk of importation of cases from areaswhere polio is endemic. Stopping poliovirus transmission is pursued through acombination of high infant immunization coverage and surveillance for wildpoliovirus through reporting and laboratory testing of all cases of acute flaccidparalysis (AFP) among children under fifteen years of age. The aim of this study was to describe and to evaluate 11 years of active surveillance in the Marches(Italy) in terms of: incidence, aetiology and clinical manifestation of AFPcases.METHODS: The active Acute Flaccid Paralysis surveillance has been carried out in the Marches region since February 1997 by the Chair of Hygiene which established a regional hospital network. Active surveillance involves 15 hospital centres.RESULTS: In the considered period, 0-15 years population varied between 187,051in 1997 to 201,625 in 2007, so the number of AFP expected cases is 2 per year.From February 1997 to October 2007, 27 cases were found with rates of 1.0/100,000in 1997; 2.0/100,000 in 1998; 1.0/100,000 in 1999; 0.5/100,000 in 2000;2.5/100,000 in 2001; 1.0/100,000 in 2002; 0 in 2003; 0.5/100,000 in 2004;1.5/100,000 in 2005; 2.0/100,000 in 2006; 1.5/100,000 in 2007. In 29.6% of cases two stool samples were collected in 14 days from the symptoms onset. The 60-days follow-up is available for 23 out of 27 cases reported. In 44.5% of cases thedefinite diagnosis was Guillain Barrè syndrome.CONCLUSION: In general, the surveillance activity is satisfactory even if inpresence of some criticalities in biological samples collection. The continuationof surveillance, in addition to the maintenance of current levels of performance,will tend to a further and more detailed sensitization of all workers involved,in order to obtain spontaneous and prompt reporting, and to achieve the optimalstandards recommended by the WHO both in the collection of biological samples andthe availability of 60 days follow-up, with the goal of eradicating polio fromall countries.DOI: 10.1186/1471-2334-8-135 PMCID: PMC2576306PMID: 18844987 [Indexed for MEDLINE]21. Zh Mikrobiol Epidemiol Immunobiol. 2007 Mar-Apr;(2):24-31.[Surveillance of acute flaccid paralysis in Belarus].[Article in Russian]Samo?lovich EO, Ermolovich MA, Kotova IF, Svirchevskaia EIu, Shimanovich VP,Kozhemiakin AK, Protas II, Fel'dman EV.The ten-years experience of acute flaccid paralysis (AFP) surveillance in Belarushas been summarized. Among 456 AFP cases reported from 1996 to 2005, 11 wereclassified as vaccine-associated paralytic poliomyelitis (VAPP), 445--asnon-polio AFP. The risk of VAPP for the period 1996-2001 was 1 case per 745,000used doses of oral poliovaccine (OPV). For the recipients of OPV the risk was 1case per 911,700 doses and for the first-dose recipients--1 case per 96,000doses. The high incidence of VAPP was a reason for implementation of sequentialpolio vaccination schedule in 2000. Guillain-Barre syndrome dominated amongnon-polio AFP (39.3% of cases); more rare were traumatic neuritis (27.9% ofcases), transient monoparalysis (12.1%), myelitis (7.6%). Non-polio AFP differed from VAPP by following epidemiological and virological characteristics:predominance of previously repeatedly vaccinated against poliomyelitis;development of paralysis in long-term period after vaccination; isolation ofnon-polio viruses belonged to three serotypes of Coxsackie B viruses (B1, B4, B6)and six serotypes of Echo viruses (6, 7, 11, 14, 24, 25) in 8.1% of cases;absence of typical for polio residual paralyses in patients who excreted vaccine polioviruses.PMID: 17523475 [Indexed for MEDLINE]22. Indian Pediatr. 2005 Oct;42(10):1049-50.Acute flaccid paralysis: Guillain-Barre syndrome with enterovirus infection.Madhukar M, Menon A.PMID: 16269848 [Indexed for MEDLINE]23. Hong Kong Med J. 2005 Jun;11(3):164-73.Surveillance of acute flaccid paralysis in Hong Kong: 1997 to 2002.Lam RM(1), Tsang TH, Chan KY, Lau YL, Lim WL, Lam TH, Leung NK; NationalCommittee for the Certification of Wild Poliovirus Eradication.Author information: (1)Centre for Health Protection, Department of Health, Hong Kong.OBJECTIVES: To describe the characteristics of patients reported with acuteflaccid paralysis between 1997 and 2002, and to evaluate the performance of theacute flaccid paralysis surveillance system using indicators recommended by theWorld Health Organization.DESIGN: Retrospective study.SETTING: Department of Health, Hong Kong.PARTICIPANTS: Children aged younger than 15 years who were reported to theDepartment of Health between 1997 and 2002 with acute flaccid paralysis.RESULTS: Of 120 children with acute flaccid paralysis reported between 1997 and2002, 42% were younger than 5 years of age. None of the cases were acutepoliomyelitis or polio-compatible. A neurological cause was identified in 67.5%of cases, of which the most common was Guillain-Barre syndrome (42%), followed bytransverse myelitis (15%). All except one of the performance indicatorsconsistently met World Health Organization requirements and thus demonstrated theeffectiveness of the acute flaccid paralysis surveillance programme. The acuteflaccid paralysis notification rate consistently exceeded 1.0 per 100 000population below 15 years of age. The requirement for adequate stoolinvestigation was the single indicator that did not satisfy World HealthOrganization requirements. This highlighted the importance of maintainingphysicians' awareness of acute flaccid paralysis surveillance.CONCLUSION: Hong Kong should remain vigilant for acute flaccid paralysis. Theeffective surveillance system and its evaluation may serve as a model forsurveillance of other infectious diseases.PMID: 15951581 [Indexed for MEDLINE]24. Neurology. 2004 Jul 27;63(2):206-7.West Nile virus and "poliomyelitis".Sejvar JJ(1).Author information: (1)Division of Viral and Rickettsial Diseases, National Center for InfectiousDiseases, Centers for Disease Control and Prevention, 1600 Clifton Road, MS A-39,Atlanta, GA 30333, USA. zea3@West Nile virus (WNV) has recently been associated with a syndrome of acuteflaccid paralysis. Most cases of WNV-associated weakness have clinical,histopathologic, and electrophysiologic characteristics indistinguishable fromthose of poliomyelitis caused by infection with poliovirus. There is debate aboutthe nomenclature of this manifestation of WNV infection. An historicalperspective of the term "poliomyelitis" suggests that the term "WNVpoliomyelitis" seems appropriate, but members of the neurologic and infectiousdisease communities should engage in discussion regarding the terminology of thissyndrome.PMID: 15277609 [Indexed for MEDLINE]25. J Paediatr Child Health. 2004 Mar;40(3):127-30.Five-year surveillance of acute flaccid paralysis in Malaysia.Hussain IH(1), Ali S, Sinniah M, Kurup D, Khoo TB, Thomas TG, Apandi M, Taha AM.Author information: (1)Expert Poliomyelitis Eradication Review Committee, Kuala Lumpur, Malaysia.drhussain@.myOBJECTIVE: The nation-wide surveillance for acute flaccid paralysis (AFP) wasimplemented in Malaysia in 1995 and further intensified in 1996 as part of theWorld Health Organization's (WHO) certification process for polio eradication in the Western Pacific Region. Clinical data on AFP cases during a 5-yearsurveillance period from 1997 to 2001 were compiled and analysed.RESULTS: Based on 517 cases of AFP reported during this 5-year period, theoverall rate of AFP was 1.2 per 100 000 children below 15 years old. The majorclinical diagnosis associated with AFP were Guillain-Barre syndrome (30.2%),central nervous system infection (16.2%), transverse myelitis (10.6%) non-polioenterovirus infection (6.2%), and hypokalaemic paralysis (5.2%). This unusualpattern with an excess of CNS infection and non-polio enterovirus infection wasattributed to the outbreak of enterovirus 71 infection nation-wide in 1997.According to the WHO virological classification, there was no case ofpoliomyelitis due to wild poliovirus. Three cases were 'polio compatible', there were no cases of vaccine-associated paralytic polio (VAPP), while 62 cases(12.0%) were merely classified as 'non-polio AFP'.CONCLUSION: Overall, these data suggest the absence of circulation of wildpoliovirus in Malaysia from 1997 to 2001. The pattern of AFP in this study isdifferent from other published reports.PMID: 15009577 [Indexed for MEDLINE]26. Cent Eur J Public Health. 2003 Dec;11(4):213-8.Vaccine-associated paralytic poliomyelitis and other diseases with acute flaccid paralysis syndrome in Belarus.Samoilovich EO(1), Feldman EV, Yermalovich MA, Protas II, Titov LP.Author information: (1)Research Institute for Epidemiology and Microbiology, Ministry of Health,Minsk, Republic of Belarus. esamoil@briem.ac.byAccording to the WHO global polio eradication initiative acute flaccid paralysis (AFP) surveillance has been conducted in Belarus since 1996. For the period1996-2002, 295AFP cases were reported. The main indices ofAFP surveillance inBelarus met the WHO criteria. A11 AFP cases, with the exception of one, werevirologically examined. Polioviruses (PV) were isolated from 28 (9.5%) of them.Results of intratypic differentiation (a neutralization test with type-specificmonoclonal antibodies and a restriction fragment length polymorphism assay)proved vaccine origin of all isolated PV. According to the final classification, 11 AFP cases were classified as vaccine-associated paralytic poliomyelitis(VAPP). Nine VAPP cases were recipient [six of them developed after the first,two--after the third and one--after the fourth oral poliovirus vaccine (OPV)dose] and two cases in non-vaccinated children were classified as contact VAPPcases. PV of all three serotypes were isolated with an equal frequency from therecipient cases and only PV2--from contact ones. Immunological investigations of children with VAPP showed that the majority of them had disorders in B-cellimmunity. A risk of one VAPP case per 96,000 first OPV doses and per 745,000distributed ones was estimated. The other 284 AFP cases were classified as AFP ofnon-polio etiology (non-polio AFP). Among them Guillain-Barré syndrome (118cases, 41.5% of all non-polio AFP cases), traumatic neuritis (63 cases, 22.2%),transient monoparesis of limb (35 cases, 12.3%), myelitis (26 cases, 9.2%) wereregistered most frequently. Vaccine PV were isolated from 19 (6.7%) children withnon-polio AFP, 28 (9.9%) children excreted non-polio enteric viruses. In contrastto VAPP, other AFP with PV isolation had no clinical picture typical ofpoliomyelitis, and had no any residual paralysis 60 days after the onset ofparalysis. PV isolation from them seemed to be not related to the etiology of thedisease, but was a mere coincidence of paralysis with the recent vaccination.Results of AFP surveillance supported the previous data on the absence ofclassical poliomyelitis cases caused by wild PV in Belarus for more than 35years.PMID: 14768785 [Indexed for MEDLINE]27. Curr Opin Infect Dis. 2003 Oct;16(5):375-81.Infectious causes of acute flaccid paralysis.Solomon T(1), Willison H.Author information: (1)Department of Neurological Science, and Medical Microbiology, University ofLiverpool, Walton Centre for Neurology and Neurosurgery, Liverpool, UK.tsolomon@liv.ac.ukPURPOSE OF REVIEW: Although acute flaccid paralysis (AFP) is more frequently seenin the tropics than in temperate regions, recent outbreaks of West Nile virus(WNV) in North America have drawn attention to this important presentation.Starting with anatomical and neurophysiological considerations, this articleexamines data on AFP caused by WNV, and considers recent data on paralysis causedby enteroviruses, and Guillain-Barré syndrome (GBS).RECENT FINDINGS: Neurophysiological, radiological and pathological studiessuggest WNV causes AFP by damaging anterior horn cells in the spinal cord. Theclinical presentation is probably best described as a 'poliomyelitis-likeillness', and the disease as 'WNV myelitis'. Other findings during the recentoutbreaks include increasing recognition of a Parkinson's-disease likepresentation, and descriptions of virus transmission in blood transfusions andtransplanted organs. GBS is now recognized as several disorders characterized by immune-mediated attack on peripheral nerves: in acute inflammatory demyelinating polyneuropathy the myelin sheath and Schwann cell of sensory and motor nerves aretargeted; acute motor axonal and acute motor and sensory axonal neuropathy often follow Campylobacter jejuni enteritis and are associated with antibodies against the ganglioside component of the nerve axolemmal membrane. In Asia-Pacific,enterovirus 71 has caused outbreaks of neurological diseases with AFP andencephalitis, but no single genogroup of virus appears responsible for severedisease.SUMMARY: Despite the near eradication of poliomyelitis, AFP caused by virusesremains an important clinical presentation. Distinguishing direct viral causesfrom GBS is important for public health reasons, and to avoid inappropriatetherapies.DOI: 10.1097/01.qco.0000092807.64370.1e PMID: 14501988 [Indexed for MEDLINE]28. Neurology. 2003 Jul 8;61(1):55-9.West Nile virus infection: a new acute paralytic illness.Jeha LE(1), Sila CA, Lederman RJ, Prayson RA, Isada CM, Gordon SM.Author information: (1)Department of Neurology, The Cleveland Clinic Foundation, OH 44195, USA.jehal@OBJECTIVE: To determine the clinical, laboratory, electrodiagnostic, radiologic, and pathologic characteristics that define the spectrum of CNS disease caused by West Nile virus (WNV) infection.METHODS: The records of all patients hospitalized at the Cleveland Clinic fromAugust 2002 to September 2002 with WNV infection were reviewed.RESULTS: Of 23 cases, the median age was 74 years old, and 74% were men. Symptomsincluded fever (100%), altered mental status (74%), gastrointestinal complaints(43%), back pain (35%), and rash (26%). In half, meningitis or encephalitisoverlapped with flaccid weakness that progressed over 3 to 8 days, with atendency to be proximal and asymmetric. Laboratory abnormalities includedhyponatremia (30%) and initial CSF neutrophilic pleocytosis. Electrodiagnosticstudies in two patients showed reduced motor amplitudes with normal conductionvelocities and active denervation. In two other patients, reduced sensoryamplitudes were also seen. MRI changes included cauda equina enhancement andparenchymal spinal cord signal abnormalities and parenchymal or leptomeningealsignal changes in the brain. Autopsy in three cases showed chronic perivascularinflammation in the brain and inflammatory changes with anterior horn cell lossin the spinal cord.CONCLUSION: An overlapping spectrum of meningitis, encephalitis, andmyeloradiculitis occurs in CNS WNV infection. Fever, rash, abdominal and backpain, preceding a proximal, asymmetric flaccid weakness, with CSF pleocytosishelp distinguish the motor syndrome from Guillain-Barré syndrome. Pathologicchanges in the CNS resembled poliomyelitis.PMID: 12847156 [Indexed for MEDLINE]29. J Paediatr Child Health. 2003 Jan-Feb;39(1):22-6.Acute flaccid paralysis in Australian children.Morris AM(1), Elliott EJ, D'Souza RM, Antony J, Kennett M, Longbottom H.Author information: (1)Australian Paediatric Surveillance Unit, The Children's Hospital at Westmead, Westmead, Australia.OBJECTIVES: To describe the epidemiology and causes of acute flaccid paralysis(AFP) in Australian children, and the clinical features of the two most commoncauses of AFP, Guillain-Barré syndrome and transverse myelitis.METHODS: Monthly active surveillance for AFP was carried out through theAustralian Paediatric Surveillance Unit, with AFP defined as 'acute onset offlaccid paralysis in one or more limbs or of bulbar paralysis in any child lessthan 15 years of age'.RESULTS: Between March 1995 and December 1999, 143 cases of AFP were reported(approximately 0.8 per 100000 children < 15 years of age per annum). The agerange was 2 months-14 years and 59% were boys. Out of these children, 137 (96%)were hospitalized and 47 required intensive care. No case of wild orvaccine-associated poliomyelitis was identified. The most common causes of AFPwere Guillain-Barré syndrome in 67 (47%) and transverse myelitis in 27 (19%).Other diagnoses included acute disseminated encephalomyelitis, trauma, tick-bite paralysis and infantile botulism.CONCLUSION: The participation of paediatricians in AFP surveillance contributedto the accreditation of Australia (along with the other 36 countries of thewestern Pacific region) as 'polio free' by the World Health Organization inOctober 2000. The surveillance also provided data on the frequency of AFP andidentified Guillain-Barré syndrome and transverse myelitis as the most commondiagnoses. In this large national series, many other conditions that may present as non-polio AFP were identified.PMID: 12542807 [Indexed for MEDLINE]30. Bull World Health Organ. 2002;80(11):846-51. Epub 2002 Dec 3.Using the two-source capture-recapture method to estimate the incidence of acute flaccid paralysis in Victoria, Australia.Whitfield K(1), Kelly H.Author information: (1)Department of Human Services, Victorian Public Health Training Scheme,Melbourne, ment in Bull World Health Organ. 2002;80(11):845.OBJECTIVE: To estimate the incidence and the completeness of ascertainment ofacute flaccid paralysis (AFP) in Victoria, Australia, in 1998-2000 and todetermine its common causes among children aged under 15 years.METHODS: : The two-source capture-recapture method was used to estimate theincidence of cases of AFP and to evaluate case ascertainment in the routinesurveillance system. The primary and secondary data sources were notificationsfrom this system and inpatient hospital records, respectively.FINDINGS: The routine surveillance system indicated that there were 14 cases and the hospital record review identified 19 additional cases. According to thetwo-source capture-recapture method, there would have been 40 cases during thisperiod (95% confidence interval (CI) = 29-51), representing an average annualincidence of 1.4 per 100000 children aged under 15 years (95% CI = 1.1- 1.7).Thus case ascertainment based on routine surveillance was estimated to be 35%complete. Guillain-Barré syndrome was the commonest single cause of AFP.CONCLUSIONS: Routine surveillance for AFP in Victoria was insensitive. Aliterature review indicated that the capture-recapture estimates obtained in thisstudy were plausible. The present results help to define a target notificationrate for surveillance in settings where poliomyelitis is not endemic.PMCID: PMC2567677PMID: 12481205 [Indexed for MEDLINE]31. MMWR Morb Mortal Wkly Rep. 2002 Sep 20;51(37):825-8.Acute flaccid paralysis syndrome associated with West Nile virusinfection--Mississippi and Louisiana, July-August 2002.Centers for Disease Control and Prevention (CDC).West Nile virus (WNV) infection can cause severe, potentially fatal neurologicillnesses including encephalitis and meningitis. Acute WNV infection also hasbeen associated with acute flaccid paralysis (AFP) attributed to a peripheraldemyelinating process (Guillain-Barré Syndrome [GBS]), or to an anteriormyelitis. However, the exact etiology of AFP has not been assessed thoroughlywith electrophysiologic, laboratory, and neuroimaging data. This report describessix cases of WNV-associated AFP in which clinical and electrophysiologic findingssuggest a pathologic process involving anterior horn cells and motor axonssimilar to that seen in acute poliomyelitis. Clinicians should evaluate patients with AFP for evidence of WNV infection and conduct tests to differentiate GBSfrom other causes of AFP.PMID: 12353741 [Indexed for MEDLINE]32. Arq Neuropsiquiatr. 2002 Jun;60(2-B):367-73.Guillain Barré syndrome in a population less than 15 years old in Brazil.Dias-Tosta E(1), Kückelhaus CS.Author information: (1)Neurology Unit, Hospital de Base do Distrito Federal, Brasilia, DF, Brazil.To know the impact of the Guillain Barré syndrome (GBS) in the population lessthan 15 years old, after the eradication of poliomyelitis. Data bank from theprogram of epidemiological surveillance of acute flaccid palsies (AFP) from theFunda??o Nacional de Saúde were analyzed between 1990-1996. From 3619notifications of AFP there were 1678 GBS. GBS yearly incidence rates is 0.39-0.63cases/100,000. No consistent seasonal variation existed or relationship tovaccines. Weakness at inclusion were, moderate 52.1%, severe in 47.9%, sixty daysafter 57.1% normal, 7.4% mild, 15.7% moderate, 10.4% with severe deficits, death in 5.4%. 67 (4.0%) cases unknown. Death rates varies from 2.8% in southeast to7.9% in the northeast. GBS was the most frequent cause of AFP. In spite of theseverity of this disease being similar in the different regions, the outcomevaries according to origin of the cases, possibly reflecting the economicalconditions in those places.PMID: 12131933 [Indexed for MEDLINE]33. Neuropediatrics. 2002 Apr;33(2):93-6.Polyradiculoneuritis with myelitis: a rare differential diagnosis ofGuillain-Barré syndrome.Martens-Le Bouar H(1), Korinthenberg R.Author information: (1)Department of Neuropaediatrics and Muscular Disorders, Paediatric UniversityHospital, Freiburg, Germany.AIM: To describe the symptoms, signs, findings and prognosis in childrensuffering simultaneously from polyradiculoneuritis and myelitis.METHODS: Retrospective review of eight patients aged 2 to 13 years out of 210patients with polyradiculoneuritis reported from 70 hospitals. Diagnosticcriteria for polyradiculoneuritis were: flaccid paresis with loss of tendonreflexes, increased CSF protein and slowing of nerve conduction velocity.Criteria for myelitis were: severe and persistent bladder dysfunction, a sharply defined sensory level and/or evolving spastic paresis, with or without myeliticchanges in spinal MRI.RESULTS: In the disease's earliest stage it was difficult to differentiatepolyradiculoneuritis with myelitis from classical GBS. However, onset was oftenunusually rapid compared to GBS. Five patients developed a sensory level andseven suffered from severe bladder dysfunction. Four of the six children studied showed focal myelitic changes in MRI. All seven children with sufficientfollow-up remained with residual paresis and significant long-term motordeficits.CONCLUSION: Due to its severe long-term prognosis, polyradiculoneuritis withmyelitis must be differentiated from classical GBS. In the disease's early stage,the detection of a sensory level, severe bladder dysfunction and an unusuallyrapid onset can be helpful. The effect of high-dose corticosteroids is not yetclear. After the acute phase, most children require extended rehabilitation.DOI: 10.1055/s-2002-32369 PMID: 12075491 [Indexed for MEDLINE]34. Aust N Z J Public Health. 2002 Feb;26(1):45-9.Retrospective hospital-based searches for cases of acute flaccid paralysis.D'souza RM(1).Author information: (1)National Centre for Epidemiology and Population Health, Australian NationalUniversity, Canberra, Australian Capital Territory. rennie.dsouza@anu.edu.auComment in Aust N Z J Public Health. 2002;26(3):281-2.OBJECTIVE: Australia had to demonstrate adequate acute flaccid paralysis (AFP)surveillance by achieving a rate of one per 100,000 in children under the age of 15 to fulfil one of the requirements of the Regional Commission for theCertification of Poliomyelitis Eradication to be declared polio free. To increasethe ascertainment rate of AFP cases, a hospital search was conducted to identify cases not reported to the active AFP surveillance.METHODS: A computerised search of hospital admissions in New South Wales (NSW)and Western Australia (WA) on ICD-9 codes of Guillain Barré Syndrome (GBS),unspecified encephalitis, poliomyelitis, vaccine-associated paralytic polio(VAPP) and flaccid paralysis was conducted for the period 1995-98. Medicalrecords of cases that were not reported to the active surveillance were reviewed in three hospitals of NSW and two hospitals in WA.RESULTS: Twenty additional cases recorded as GBS and five as transverse myelitis (TM) were identified through the searches, which increased the average four-year AFP rate from 1.0 to 1.4 per 100,000 in children under the age of 15 years inthese two states and the overall AFP rate in Australia increased from 0.78 to1.14. There were no cases of polio or VAPP found. Nine cases of GBS and five ofTM reported to the active AFP surveillance were not found in the hospitalsearches.CONCLUSION: A combination of active surveillance and hospital-based searchesincreased the investigated AFP rate, which fulfilled one of the certificationrequirements for Australia to be certified polio free.IMPLICATIONS: Until global certification is achieved, AFP surveillance needs tobe improved to identify cases of importation of wild poliovirus.PMID: 11895024 [Indexed for MEDLINE]35. Neurol Neurochir Pol. 2001;35(4 Suppl):97-109.[Acquired inflammatory neuropathies in children and their therapy].[Article in Polish]Kaciński M(1).Author information: (1)Klinika Neurologii Dzieciecej Wydzia?u Lekarskiego Collegium MedicumUniwersytetu Jagiellońskiego w Krakowie. neupedkr@.plNeuropathies where there is an association with acquired peripheral nervesdysfunction and inflammation include inflammatory neuropathies (IN), as well assequelae of vaccinations involving peripheral nerves. In a small portion of thesediseases central nervous system is involved. In the years 1996-2000, among 22children with acute flaccid paresis who were hospitalized in the KrakówDepartment of Paediatric Neurology, there were 16 patients with IN, including 13 with Guillain-Barré syndrome, single cases of Miller-Fisher syndrome, chronicinflammatory demyelinating polyneuropathy involving central nervous system andneuroborreliosis. Additionally, four children were hospitalized for opticneuritis. The author presents data on aetiology, electrophysiology and follow-up of these patients, as well as describes the management and outcome. Apart fromtheir cognitive and practical value, these data significantly correspond with thecurrently implemented program of poliomyelitis eradication.PMID: 11873621 [Indexed for MEDLINE]36. Acta Neurol Scand. 2001 Oct;104(4):239-42.Acute transverse myelitis and Guillain-Barré overlap syndrome with serologicalevidence for mumps viraemia.Bajaj NP(1), Rose P, Clifford-Jones R, Hughes PJ.Author information: (1)Department of Neurology, Hurstwood Park Neurology Centre, Hurstwood Lane, WestSussex, United Kingdom. spgtnpb@iop.kcl.ac.ukBoth acute transverse myelitis (ATM) and Guillain-Barré syndrome (GBS) occur asrare associations with mumps viraemia but to our knowledge, concurrent ATM andGBS related to mumps has only been reported once previously. We describe the caseof a young woman presenting with confusion and collapse 2 weeks after a flu-like illness. An initial diagnosis of transverse myelitis was made on the basis of theclinical findings and radiological evidence of a swollen spinal cord with uniformhigh signal change on T2 weighted MRI. The patient was treated with intravenousmethylprednisolone without significant recovery. The diagnosis was later revised to include GBS on the basis of worsening facial diplegia in the setting of aflaccid tetraparesis, and neurophysiological evidence of a sensorimotor axonalpolyradiculoneuropathy. Acute mumps viraemia was confirmed on serologicalgrounds. The patient made an improvement in ventilatory capacity with intravenousimmunoglobulin treatment.PMID: 11589654 [Indexed for MEDLINE]37. Semin Pediatr Neurol. 2000 Jun;7(2):91-102.Guillain-Barré syndrome: perspectives with infants and children.Jones HR Jr(1).Author information: (1)Department of Neurology, Lahey Clinic, Burlington, MA 01805, USA.An acute flaccid paraparesis or ascending quadriparesis in an infant or childconstitutes a very important pediatric neurology emergency. The Guillain-Barrésyndrome (GBS) is the most frequent cause. This is primarily an autoimmune,post-infectious, demyelinating, peripheral nervous system process. A smallpercentage of children develop a primary axonal process not unlike thatidentified more commonly in China. Because of the potential for acute respiratorycompromise, any child suspected of having GBS needs immediate hospitalization.The major considerations in differential diagnosis include transverse myelitis,toxic neuropathies, tick paralysis, infantile botulism, myasthenia gravis, anddermatomyositis. On occasion, some younger children present with an acute severe pain syndrome that may mask as a pseudo-encephalopathy. Another clinical variant is the Miller-Fisher syndrome characterized by ataxia, ophthalmoparesis, andareflexia. This is associated with a high frequency of the anti-GQ-1-bantibodies. Although most children with GBS have a relatively benign clinicalcourse, some become very ill and require intubation with intensive caremonitoring. Immunomodulating treatment should be used for any child who loses theability to walk. To date, no well-controlled study has been completed analyzingthe relative merits of the two most commonly used therapies, namelyplasmapheresis or intravenously administered immunoglobulin.PMID: 10914410 [Indexed for MEDLINE]38. Bull World Health Organ. 2000;78(3):298-304.Surveillance of patients with acute flaccid paralysis in Finland: report of apilot study.Hovi T(1), Stenvik M.Author information: (1)Department of Virology, National Public Health Institute, Helsinki, Finland.tapani.hovi@ktl.fiWHO recommends that surveillance of patients with acute flaccid paralysis (AFP)be used to demonstrate the eradication of wild poliovirus. In this article wereport the results of a study to assess the frequency of AFP patients referred toFinnish hospitals and whether virological diagnostic coverage could be improvedby repeated reminders and active feedback. For this purpose, we sent monthlyquestionnaires to all neurological and paediatric neurological units in Finland, requesting retrospective reporting on investigated paralytic patients withdefined clinically relevant diagnoses, rather than AFP. Reminder letters includeda pre-paid return envelope. Virological investigations were offered cost free. Ofthe 492 reporting forms sent, 415 (84%) were returned, evenly covering both thepopulation and the study period (July 1997 to June 1998). Of the 90 patientsreported, 83 were evaluable. The apparent incidences of the diagnoses coveredwere 1.6 per 100,000 at any age, and 1.0 per 100,000 for under--15-year-olds.Guillain-Barré syndrome was the most common diagnosis (0.80 per 100,000). The twofaecal specimens required were virologically investigated in nine out of the 10patients under 15 years of age, but in only 46% of all patients. Four adenovirus strains, but no polioviruses or other enteroviruses, were isolated. We concludethat a satisfactory monthly reporting system was readily established and that asufficient number of patients with diagnoses resembling AFP are being referred toFinnish hospitals. Active feedback did not increase the proportion ofvirologically investigated patients to an acceptable level in all age groups. It is clear that other approaches must be used to quantify the circulation ofpoliovirus in Finland.PMCID: PMC2560699PMID: 10812725 [Indexed for MEDLINE]39. Ann Trop Paediatr. 1999 Dec;19(4):317-20.Asian paralysis syndrome.Phadke MA(1), Gambhir PS, Deshpande AS, Kurlekar SU, Godbole KG.Author information: (1)Department of Pediatrics, B.J. Medical College, Pune, India. bjmcpune@We report 20 children admitted to the paediatric ward of a public generalhospital for acute flaccid paralysis, which was bilaterally symmetrical in allcases and was associated with bulbar involvement in eight of them. Recovery waspartial. Nerve conduction studies showed motor axonal neuropathy. This newdisease, variously termed as non-inflammatory neuropathy/Chinese paralysissyndrome must be differentiated from Guillain-Barré syndrome (GBS) andpoliomyelitis. Both GBS and Asian paralysis syndrome have bilaterally symmetricalflaccid paralysis but GBS tends to have sensory involvement, full recovery occursin 90% of cases and nerve conduction shows demyelinating neuropathy. Asianparalysis syndrome and poliomyelitis are pure motor lesions without sensorychanges and partial recovery, but poliomyelitis differs in that paralysis isasymmetrical and unequal, muscle spasm is always present in the initial stage andthere are prodromal symptoms. Nerve conduction studies show anterior horn celldisease. This new entity, common in Asian populations, assumes public healthimportance when it mimics poliomyelitis in a country that has tried to eliminate poliomyelitis by universal immunization. To the best of our knowledge, this isthe first report of Asian paralysis syndrome in children in our area.PMID: 10716023 [Indexed for MEDLINE]40. J Paediatr Child Health. 1999 Dec;35(6):536-40.Surveillance of acute flaccid paralysis in Australia, 1995-97. AustralianPaediatric Surveillance Unit.D'Souza RM(1), Kennett M, Antony J, Herceg A, Harvey B, Longbottom H, Elliott E.Author information: (1)Surveillance and Management Section, National Centre for Disease Control,Department of Health and Aged Care, Canberra, Australian Capital Territory,Australia. Rennie.D'Souza@.auOBJECTIVE: Acute flaccid paralysis (AFP) surveillance in Australia as part of theWorld Health Organization (WHO) certification process for polio eradication inthe Western Pacific region.METHODS: Active monthly AFP surveillance through the Australian PaediatricSurveillance Unit, from March 1995 to December 1997.RESULTS: Based on 80 cases, the reported overall rate of AFP was 0.73 per 10(5)children < 15 years (below the expected 1 per 10(5)). The major causes of AFPwere Guillain-Barré syndrome (51%) and transverse myelitis (19%). According tothe WHO virological classification, there was no case of poliomyelitis, 37.5%were 'non-polio' and 62.5% cases were 'polio compatible' due to inadequate stool testing and follow-up. However, case review by an expert panel enabled 95% to be classified as 'non-polio'.CONCLUSION: Australia must improve AFP surveillance to confirm absence of wildpoliovirus. Paediatricians can help Australia meet its certification requirementsand contribute to the global eradication effort by reporting and investigatingall cases of AFP.PMID: 10634978 [Indexed for MEDLINE]41. Trans R Soc Trop Med Hyg. 1998 Jan-Feb;92(1):25-8.Enterovirus 71 infection and acute neurological disease among children in Brazil (1988-1990).Takimoto S(1), Waldman EA, Moreira RC, Kok F, Pinheiro Fde P, Saes SG, Hatch M,de Souza DF, Carmona Rde C, Shout D, de Moraes JC, Costa AM.Author information: (1)Department of Virology, Instituto Adolfo Lutz, S?o Paulo, Brazil.Surveillance for Enterovirus 71 (EV-71) infection in children up to 15 years ofage was carried out in Brazil, from 1988 to 1990. Patients with acuteneurological diseases (AND) such as flaccid paralysis, Bell's palsy, acutecerebellar ataxia and Guillain-Barré syndrome were included in the study. EV-71infection was detected in 24 of 426 children (5.6%) with AND. EV-71 infection wasconfirmed only by virus isolation in 13 children, by virus isolation andseroconversion in 4, and by seroconversion alone in 7. EV-71 was also isolatedfrom 15 of the 427 household contacts (3.5%) of 165 AND patients. There was some evidence of high infectivity of EV-71: household clusters were detected in thecase of 7 of 24 children (29.1%) infected with EV-71 and manifesting AND; EV-71was isolated from 11/40 household contacts (27.5%) of the infected patients butfrom only 4/387 household contacts (1.0%) of children in whom it was not possibleto demonstrate EV-71 infection. Seven of the 24 children infected with EV-71exhibited residual motor deficiency when examined 6 months after the diseaseonset. The relevance of these results for the Plan for Global Eradication of WildPoliovirus is discussed, as well as the need to increase knowledge about thebehaviour of this virus and its possible association with AND.PMID: 9692141 [Indexed for MEDLINE]42. Lancet. 1998 Apr 11;351(9109):1094-7.Poliomyelitis-like illness due to Japanese encephalitis virus.Solomon T(1), Kneen R, Dung NM, Khanh VC, Thuy TT, Ha DQ, Day NP, Nisalak A,Vaughn DW, White NJ.Author information: (1)Wellcome Trust Clinical Research Unit, Cho Quan Hospital, Ho Chi Minh City,ment in Lancet. 1998 Jun 27;351(9120):1964.BACKGROUND: Acute flaccid paralysis remains common among Vietnamese childrendespite a pronounced fall in the incidence of poliomyelitis.METHODS: During 1995, all 22 children presenting with acute flaccid paralysis to a referral centre in Ho Chi Minh City, Vietnam, had virological cultures andantibody measurements done on serum, cerebrospinal fluid, and faeces. A yearlater the children were reassessed and electrophysiological studies were done.FINDINGS: Wild poliovirus type 1 was isolated from the faeces of only onepatient, and non-polio enteroviruses from three patients. 12 (55%) of the 22children with acute flaccid paralysis had evidence of acute Japanese encephalitisvirus (JEV) infection, compared with only one (1%) of 88 age-matched hospitalcontrols (children with diphtheria; p<0.0001). Compared with JEV-negativepatients, weakness in JEV-infected children was more rapid in onset, tended to beasymmetrical, but was less likely to involve the arms. All 12 children with JEVinfection were febrile at the onset of weakness, seven had acute retention ofurine, and ten had CSF pleiocytosis. Seven of eight JEV-negative patients met thecase-definition of Guillain-Barré syndrome, compared with only one of 12JEV-positive children. At follow-up, patients with JEV infection had greaterdisability and were more likely to have muscle wasting than were JEV-negativechildren. Nerve conduction and electromyographic studies indicated damage to the anterior horn cells.INTERPRETATION: JEV causes an acute flaccid paralysis in children that hassimilar clinical and pathological features to poliomyelitis. In endemic areas,children with acute flaccid paralysis should be investigated for evidence of JEV infection.DOI: 10.1016/S0140-6736(97)07509-0 PMID: 9660579 [Indexed for MEDLINE]43. Neurology. 1997 Dec;49(6):1723-5.A prospective clinical and electrophysiologic survey of acute flaccid paralysisin Chinese children.Wu HS(1), Liu TC, Lü ZL, Zou LP, Zhang WC, Zhaori G, Zhang J.Author information: (1)Department of Neurology, Beijing Children's Hospital, Beijing, P.R.C.We studied 29 children admitted to Beijing Children's Hospital (BCH) with acuteflaccid paralysis between June 1991 and June 1993. Twenty-seven patients hadGuillain-Barré syndrome--7 with acute inflammatory demyelinating polyneuropathyand 20 with acute motor axonal neuropathy (AMAN). Two had poliomyelitis. The mostcommon cause of acute flaccid paralysis at BCH is the AMAN pattern of GBS.PMID: 9409379 [Indexed for MEDLINE]44. J Child Neurol. 1996 Jan;11(1):4-12.Childhood Guillain-Barré syndrome: clinical presentation, diagnosis, and therapy.Jones HR(1).Author information: (1)Department of Neurology, Children's Hospital and Harvard Medical School, BostA rapidly progressive, generally symmetric, ascending flaccid paraparesis orquadriparesis that develops in an infant or child constitutes an uncommon butimportant pediatric neurologic emergency that requires immediate evaluation andtreatment. The differential diagnosis primarily includes acute neuropathies, mostcommonly the childhood Guillain-Barré syndrome and, rarely, acute transversemyelitis or infantile poliomyelitis. A clinical distinction may be difficult inthe younger child in whom detailed sensory examination is not possible. Although most children with Guillain-Barré syndrome usually have a benign and relativelylimited clinical illness, some become severely ill, requiring intubation andcareful intensive monitoring. To date, no well-controlled multi-institutionalstudies of treatment with either plasmapheresis or intravenously administeredimmunoglobulin have been developed in children despite the success of thesemodalities in adults. A review of the data available using these therapies isincluded in this study.DOI: 10.1177/088307389601100102 PMID: 8745378 [Indexed for MEDLINE]45. S Afr Med J. 1994 Oct;84(10):664-8.Eradication of poliomyelitis in South Africa.Blecher MS(1), Hussey G, Keen GA, Eggers R, Girdler-Brown B.Author information: (1)Department of Community Health, University of Cape Town.An international campaign under the leadership of the World Health Organisationis underway to eradicate polio from the world by the year 2000. South Africa may already be free of polio. However, to ensure eradication we need to move from apolio control programme to a polio eradication programme. This necessitates theinstitution of a surveillance programme for acute flaccid paralysis (AFP) andimprovement of the delivery of polio vaccine. All children with AFP (includingthose with suspected Guillain-Barré syndrome) should be investigated with stoolculture to exclude polio. Primary care services need strengthening so that oralpolio vaccine coverage greater than 90% is achieved in all regions by allauthorities. Outbreak response activities need to be developed. Considerationneeds to be given to national immunisation days and mopping-up activities.PMID: 7839253 [Indexed for MEDLINE]46. Bull World Health Organ. 1994;72(6):915-20.Poliomyelitis surveillance in Shandong Province, China, 1990-92.Chiba Y(1), Xu A, Li L, Lei T, Takezaki T, Hagiwara A, Yoneyama T, Fujiwara T,Hara M, Yamamoto T.Author information: (1)Department of EPI, Shandong Provincial Epidemic Prevention Station, Jinan,China.In Shandong Province, China, programmes were initiated in 1991 for massimmunization against poliomyelitis and for the immediate reporting of acuteflaccid paralysis (AFP). The incidence of non-poliomyelitis AFP was found to be0.46-0.61 cases per 100,000 children per annum. It appeared that illnessresembling the Guillain-Barré syndrome was underreported. The incidence of suchillness peaked among children aged 2-3 years. Although laboratory investigations have improved, in 1992 they were still inadequate in nearly a third of confirmed poliomyelitis cases. As the prevalence of wild poliovirus declines in China,reliable laboratory support needs to be established and adequately sensitive and specific AFP surveillance be developed if poliomyelitis is to be eradicated.PMCID: PMC2486721PMID: 7867137 [Indexed for MEDLINE]47. Bull World Health Organ. 1994;72(6):907-14.Poliomyelitis in Oman: acute flaccid paralysis surveillance leading to earlydetection and rapid response to a type 3 outbreak.Robertson SE(1), Suleiman AJ, Mehta FR, al-Dhahry SH, el-Bualy MS.Author information: (1)Global Programme for Vaccines and Immunization, World Health Organization,Geneva, Switzerland.Countries are increasingly requesting guidance on carrying out acute flaccidparalysis (AFP) surveillance, aimed at detecting and confirming all cases ofacute paralytic poliomyelitis. The experience of Oman provides many lessons inthis respect. AFP surveillance in Oman was established systematically. First, an epidemiologist was assigned to coordinate surveillance, and a laboratory forperforming polio-virus isolation was identified. Next, operational guidelines forAFP surveillance were developed and widely promoted among health staff. Thequality of the system has been monitored for more than 3 years with selectedperformance indicators. From January 1990 to April 1993, 49 AFP cases werereported, corresponding to an average annual rate of 2.1 AFP cases per 100,000children aged less than 15 years. A total of 98% of the AFP cases wereinvestigated within 48 hours of being reported; two stool samples were obtainedfrom 94% of the cases. Following complete investigation, nearly a third of thereported AFP cases were classified as being clinically compatible withGuillain-Barré syndrome. Four AFP cases, all reported in 1991, were confirmed to be due to wild type 3 poliovirus. Because AFP surveillance detected these casesrapidly, Oman was able to carry out outbreak control measures promptly and morethan 350,000 extra doses of oral poliovirus vaccine were delivered to childrenunder 6 years of age.PMCID: PMC2486735PMID: 7867136 [Indexed for MEDLINE]48. Bol Med Hosp Infant Mex. 1993 Feb;50(2):136-44.[The differential diagnosis of poliomyelitis and other acute flaccid paralyses].[Article in Spanish]Alcalá H(1).Author information: (1)Departamento de Neurología, Hospital Infantil de México Federico Gómez, D.F.Between June 1988 to January 1991 a total of 246 children with acute flaccidparalysis (AFP) were seen at Hospital Infantil de México, Federico Gómez whichwas the center of study for AFP for the Poliomyelitis Eradication Program ofMexico. Of the 246 children, 42 has poliomyelitis (17%); 156 has Guillain-Barrésyndrome (GBS) (63.4%); 16 had traumatic neuritis of the sciatic nerve secondary to IM injections (TNC) (6.5%); five had transverse myelitis (2%); the rest (27)had other diseases misdiagnosed as polio (10.9%). The basic clinicalcharacteristics for the diagnosis of poliomyelitis are: myalgias and fever at theonset AFP, paralysis is asymmetrical, of distal predominance and causes severemuscular atrophy and skeletal deformities; the GBS presents as an ascending,symmetrical, areflexic paralysis of distal predominance. It does not causesatrophy or deformities. TNC presents several days after IM injections with painand hypothermia in the affected limbs; TM is a flaccid, symmetrical paraparesiswith neurogenic bladder and a sensory level. CSF and neurophysiological studies(EMG and NCV) are very useful for diagnosis. Other entities misdiagnosed aspoliomyelitis were: osteoarticular trauma, myopathies and dystrophies, viralmyositis, acute cerebellitis, retroperitoneal tumors and upper motor neuronsyndromes. Viral studies in stool specimens are essential for the diagnosis ofpoliomyelitis.PMID: 8442872 [Indexed for MEDLINE]49. Brain. 1976 Dec;99(4):771-90.Radiculomyelitis following acute haemorrhagic conjunctivitis.Hung TP, Sung SM, Liang HC, Landsborough D, Green IJ.The clinical manifestations and natural history of radiculomyelitis following anewly reported disease--acute haemorrhagic conjunctivitis (AHC)--have beenstudied in 33 patients in Taiwan, and the following observations made: All thepatients in this series were adults at ages ranging from 21 to 55 years; thesalient initial neurological manifestations were radicular pains and acuteflaccid paralysis which developed from five to thirty-seven days after the onset of AHC. In some patients, signs and symptoms indicating involvement of themeninges, cranial nerves and the white matter of the cord were observed; motorparalysis was the most striking feature during the whole clinical course; itconsisted of flaccid asymmetrical weakness in one or more limbs, usually beingmore severe in the lower limbs than in the upper, and often more proximal thandistal. Atrophy in the severely affected muscles usually became apparent in thesecond or third week of the weakness; the prognosis regarding the return offunction in the affected muscles was dependent on the severity of theinvolvement. Permanent incapacitation due to paralysis and muscular atrophy inthe affected proximal muscles of lower limbs was the main sequel in severe cases.The pattern and prognosis of flaccid motor paralysis were reminiscent of acutepoliomyelitis in which the anterior horn cells of the spinal cord are mainlyinvolved. Pleocytosis ranging from 11 to 270 per mm3 was noted in the majority ofthe patients when the cerebrospinal fluid was examined within the first threeweeks from the onset of neurological symptoms; the total protein level was raisedinvariably from the second week onwards in all specimens, and remained sothroughout the subsequent course as long as the seventh week or later. Tissueculture neutralization tests were performed on the sera from 9 patients;significant rises in the antibody titres (greater than or equal to 1:16) to AHCvirus antigens were found in 8 cases, and in 2 of them a fourfold rise in thepaired sera was noted. The differentiation of this syndrome from poliomyelitisand from Guillain-Barré syndrome, the relative freedom of children fromneurological complications of AHC and the aetiological relationship of AHC virus to the syndrome have been discussed. It is concluded that this unusualneurological syndrome is caused by the neurovirulent properties of the AHC virus.PMID: 1030657 [Indexed for MEDLINE] ................
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