Multiple Sclerosis in Children

How to Cite This Article: Inaloo S, Haghbin S. Multiple Sclerosis in Children. Iran J Child Neurol. 2013 Spring;7(2):1-10. Multiple sclerosis (MS) is the most important immune-mediated demyelinated disease of human which is typically the disease of young adults. A total of 4% to 5% of MS population are pediatric. Pediatric MS is defined as the appearance of MS before the age of sixteen. About 80% of the pediatric cases and nearly all adolescent onset patients present with attacks typical to adult MS. Approximately 97% to 99% of the affected children have relapsing-remitting MS, while 85% to 95% of the adults experience such condition. MS in children is associated with more frequent and severe relapses. Treatment is the same as adults. We aimed to review the epidemiology, etiology, clinical manifestations, and treatment of MS in children. References1. Lublin F. History of modern multiple sclerosis therapy. J Neurol 2005 Sep;252(Suppl 3):iii3-iii9. Review.2. Murray TJ. Robert Carswell: the first illustrator of MS. Int MS J 2009 Sep;16(3):98-101.3. Kabat EA, Glusman M, Knaub V. Quantitative estimation of the albumin and gamma globulin in normal and pathologic cerebrospinal fluid by immunochemical methods. Am J Med 1948 May;4(5):653-62.4. Kumar DR, Aslinia F, Yale SH, Mazza JJ. Jean-Martin Charcot: the father of neurology. Clin Med Res 2011 Mar;9(1):46-9.5. Dawson JD. The histology of disseminated sclerosis.Trans of the Roy Soc Edinb. 1916;50:517-740.6. Gadoth N. Multiple sclerosis in children. Brain Dev 2003 Jun;25(4):229-32. Review.7. Banwell BL. Pediatric multiple sclerosis. Curr Neurol Neurosci Rep 2004 May;4(3):245-52.8. Renoux C, Vukusic S, Mikaeloff Y, Edan G, Clanet M, Dubois B, et al. Natural history of multiple sclerosis with childhood onset. N Engl J Med 2007 Jun 21;356(25):2603-13.9. Boiko A, Vorobeychicle G, Paty D, Devonshire V, Sondovnick D. Early onset multiple sclerosis: a long longitudinal study. Neurology 2002 Oct 8;59(7):1006-10.10. Yavari MJ, Inaloo S, Saboori S. Multiple sclerosis in children: A review of clinical and paraclinical features in26 cases. Iran J Child Neurol 2008;2(4):41-46.11. Oksenberg JR, Baranzini SE, Sawcer S, Hauser SL. The genetics of multiple sclerosis: SNPs to pathways to pathogenesis. Nat Rev Genet 2008 Jul;9(7):516-26.12. Willer CJ, Dyment DA, Risch NJ, Sadovnick AD, Ebers GC; Canadian Collaborative Study Group. Twin concordance and sibling recurrence rates in multiple sclerosis. Proc Natl Acad Sci USA 2003 Oct 28;100(22):12877-82.13. Ramagopalan SV, Knight JC, Ebers GC. Multiple sclerosis and the major histocompatibility complex. Curr Opin Neurol 2009 Jun;22(3):219-25.14. Banwell B, Krupp L, Kennedy J, Tellier R, Tenembaum S, Ness J, et al. Clinical features and viral serologies in children with multiple sclerosis: a multinational observational study. Lancet Neurol 2007 Sep;6(9):773-81.15. Alotaibi S, Kennedy J, Tellier R, Stephens D, Banwell B. Epstein Barr virus in pediatric multiple sclerosis. JAMA2004;291(15):1875-9.16. Pohl D, Knone B, Rostasy K, Kahler E, Brunner E, Lehnert M, et al. High seroprevalence of Epstein-Barr virus in children with multiple sclerosis. Neurology 2006 Dec12;67(11):2063-5.17. Waubant E, Mowry EM, Krupp L, Chitnis T, Yeh EA, Kuntz N,et al. Antibody response to common viruses and human leukocyte antigen-DRB1 in pediatric multiple sclerosis. Mult Scler. 2012 Dec 11.18. Waubant E, Mowry EM, Krupp L, Chitnis T, Yeh EA, Kuntz N, et al. Common viruses associated with lower pediatric multiple sclerosis risk. Neurology 2011 Jun 7;76(23):1989-95.19. Mikaeloff Y, Caridade G, Rossier M, Suissa S, Tardieu M. Hepatitis B vaccination and the risk of childhoodonsetmultiple sclerosis. Arch Pediatric Adolesc Med 2007;161:1176-82.20. Hammord SR, English DR, Moleod JG. The age-range of risk of developing multiple sclerosis. Brain. 2000 May;123 (Pt 5):968-74.21. Van Amerongen BM, Dijkstra CD, Lips P, Polman CH. Multiple sclerosis and vitamin D: an update. Eur J Clin Nutr 2004 Aug; 58:1095-109. 22. Willer CJ, Dyment DA, Sadovnick AD, Rothwell PM, Murray TJ, Ebers GC, et al. Timing of birth and risk of multiple sclerosis: population based study. BMJ 2005 Jan;330(7):120.23. Mowry EM, Krupp LB, Milazzo M, Chabas D, Strober JB, Bellman AL, et al. Vitamin D status is associated with relapse rate in pediatric-onset multiple sclerosis. Ann Neurol 2010 May;67(5):618-24.24. Banwell B, Bar-Or A, Arnold DL, Sadovnick D, Narayanan S, Mc Gowan M, et al. Clinical, environmental, and genetic determinants of multiple sclerosis in children with acute demyelination: a prospective national cohort study. Lnacet Neurol 2011 May;10(5):436-45.25. Disanto G, Morahan JM, Ramagopalan SV. Multiple sclerosis: risk factors and their interactions. CNS NeurolDisord Drug Targets. 2012 Aug;11(5):545-55. 26. Munger KL, Chitnis T, Ascherio A. Body size and risk of MS in two cohorts of US women. Neuroloty 2009 Nov 10;73(19):1543-50.27. Renoux C, Vukusic S, Mikaeloff Y, Edan G, Clanet M, Dubois B, et al. Natural history of multiple sclerosis withchildhood onset. N Engl J Med 2007 Jun; 356(25):2603-13.28. Gusev E, Boiko A, Bikova O, Maslova O, Guseva M, Boiko S, et al. The natural history of early onset multiple sclerosis: comparison of data from Moscow and Vancouver. Clin Neurol Neurosurg 2002 Jul;104(3):203-7.29. Simone IL, Carrara D, Tortorella C, Liquori M, Lepore V, Pellegrini F, et al. Course and prognosis in early-onsetMS: comparison with adult-onset forms. Neurology 2002 Dec;59(12):1922-8.30. McDonald WI, Compston A, Edan G, Goodkin D, Hartung HP, Lublin FD, et al. Recommended diagnostic criteria for multiple sclerosis: guidelines from the International Panel on the diagnosis of multiple sclerosis. Ann Neurol 2001 Jul; 50(1):121-7.31. Polman CH, Reingold SC, Edan G, Filippi M, Hartung HP, Kappos L, et al. Diagnostic criteria for multiple sclerosis: 2005 revisions to the “McDonald Criteria”. Ann Neurol 2005 Dec;58:840-6.32. Swanton JK, Rovira A, Tintore M, Altmann DR, Barkhof F, et al. MRI criteria for multiple sclerosis in patients presenting with clinically isolated syndromes: a multicentre retrospective study. Lancet Neurol 2007 Aug;6(8):677-86.33. Rovira A, Swanton J, Tintore M, Sastre-Garriga J, Horga A, et al. A single, early magnetic resonance imaging study in the diagnosis of multiple sclerosis. Arch Neurol 2009 May;66(5):587-92.34. Poser CM, Paty DW, Scheinberg L, McDonald WI, Davis FA, Ebers GC, et al. New diagnostic criteria for multiple sclerosis: guidelines for research protocols. Ann Neurol 1983 Mar;13(3):227-31.35. Polman CH, Reingold SC, Banwell B, et al. Diagnostic criteria for multiple sclerosis: 2010 revisions to the McDonald criteria. Ann Neurol 2011 Feb; 69(2):292-302.36. Mikaeloff Y, Adamsbaum C. Husson B, Vallee L, Ponsot G, Confavreux C. et al. MRI prognostic factors for relapse after acute CNS inflammatory demyelination in childhood. Brain 2004 Sep;127(Pt9):1942-7.37. Chabas D, Castillo-Trivino T, Mowry EM, Strober JB, Glenn OA, Woubant E, et al. Vanishing MS T2-bright lesions before puberty: a distinct MRI phenotype? Neurology 2008 Sep;71(14):1090-3.38. Krupp LB, Banwell B, Tenembaum S. Consensus definitions proposed for pediatric multiple sclerosis andrelated disorder. Neurology 2007 Apr;68(16 Suppl 2):S7-S12.39. Yeh EA, Chitnis T, Krupp L, Ness J, Chabas D, Kuntz N, et al. Pediatric multiple sclerosis. Nat Rev Neurol 2009 Nov;5(11):621-31.40. Banwell B, Ghezzi A, Bar-Or A, Mikaeloff Y, Tardien M. Multiple sclerosis in children: clinical diagnosis, therapeutic strategies, and future directions. Lancet Neurol 2007 Oct;6(10):887-902.41. Venkateswaran S, Banwell B. Pediatric multiple sclerosis. Neurologist 2010 Mar;16(2):92-105.42. Waubant E, Chabas D, Okuda DT, Glenn O, Mowry E, Henry RG, et al. Difference in disease burden and activity in pediatric patients on brain magnetic resonance imaging at time of multiple sclerosis onset vs adults. Arch Neurol 2009 Aug; 66(8):967-71.43. Ghassemi R, Antel SB, Narayanan S, Francis J, Bar-or A, Sadovnick AD, et al. Lesion distribution in children with clinically isolated syndromes. Aim Neurol 2008 Mar;63(3);401-5.44. Yeh EA, Weinstock-Guttman B, Ramanathan M, Ramasamy DP, Willis L, Cox JL, et al. Magnetic resonance imaging characteristics of children and adults with paediatric-onset multiple sclerosis. Brain 20 Dec;132:3392-400.45. Mikaeloff Y, Suissa S, Vallee L, Lubetzki C, Ponsot G, Confavreux C, et al. First episode of acute CNS inflammatory demyelination in childhood: prognostic factors for multiple sclerosis and disability. J Pediatr 2004 Feb;144(2):246-52.46. Chabas D, Ness J, Belman A, Yeh EA, Kuntz N, Gorman MP, et al. Younger children with MS have a distinct CSF inflammatory profile at disease onset. Neurology 2010 Feb 2;74(5):399-405.47. Gronseth GS, Ashman U. Practice parameter: the usefulness of evoked potentials in identifying clinicallysilent lesions in patients with suspected multiple sclerosis (an evidence-based review): Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2000 May 9;54(9):11720-5.48. Boutin B, Esquivel E, Mayer M, Chaumet S, Ponsot G, Arthuis M, et al. Multiple sclerosis in children: report of clinical and paraclinical features of 19 cases. Neuropediatrics 1988 Aug;19(3):118-23.49. Waldman AT, Gorman MP, Rensel MR, Austin TE, Hertz NL. Management of pediatric central nervous system demyelinating disorders: consensus of United States neurologists. J Child Neurol 2011 Jun;26(6):675-82.50. Banwell BL. Pediatric multiple sclerosis. Curr Neurol Neurosci Rep 2004 May;4(3):245-52. 51. Yeh EA, Weinstock-Guttman B. The management of pediatric multiple sclerosis. J Child Neurol 2012;27:1384-1393.52. Ghezzi A, Amato MP, Capobianco M, Gallo P, Marrosu G, Matinelli V, et al. Disease-modifying drugs in childhood-juvenile multiple sclerosis: results of an Italian co-operative study. Mult Scler 2005 Aug;11(4):420-4.53. Banwell B, Reder AT, Krupp L, Tenembaum S, Eraksoy M, Alexy B, et al. Safety and tolerability of interferon beta-1 b in pediatric multiple sclerosis. Neurology 2006 Feb;66(4):472-6.54. Tenembaum SN, Segura MJ. Interferon beta-la treatment in childhood and juvenile-onset multiple sclerosis. Neurology 2006 Aug 8;67(3):511-3.55. Pohl D, Waubant E, Banwell B, Chabas D, Chitnis T, Weinstock-Guttman B, et al. Treatment of pediatric multiple sclerosis and variants. Neurology 2007 Apr;68(16 suppl):S54-65.56. Makhani N, Gorman MP, Branson HM, Stazzone L, Banwell BL, Chitnis T, et al. Cyclophosphamide therapy in pediatric multiple sclerosis. Neurology 2009 Jun;72(24):2076-80.57. Goodin DS, Amason BG, Coyle PK, Frohman EM, Paty DW, et al. The use of mitoxantrone (Novantrone) for the treatment of multiple sclerosis: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology 2003 Nov 25;61(10):1332-8.58. Ghezzi A, Pozzilli C, Grimaldi LM, Brescia Morra V, Bartolon F, Capra R, et al. Safety and efficacy of natalizumab in children with multiple sclerosis. Neurology 2010 Sep ;75(10):912-7.59. Mancordi GL, Saccardi R. Autologous heamatopoietic stem cell transplantation in multiple sclerosis. Lancet Neurol 2008 7:626-636.60. Attarian HP, Brown KM, Duntley SP, Carter JD, Cross AH, et al. The relationship of sleep disturbances and fatigue in multiple sclerosis. Arch Neurol 2004 Apr;61(4):525-30.61. Krupp LB, Alvarez LA, LaRocca NG, Scheinberg LC. Fatigue in multiple sclerosis. Arch Neurol 1988 Apr;45(4):435-7.62. MacAllister WS, Belman AL, Milazzo M, Weisbrot DM, Christodoulou C, Scheri WF, et al. Cognitive functioningin children and adolescents with multiple sclerosis. Neurology 2005 Apr;64(8):1422-5

Guillain-Barre Syndrome Presenting With Bilateral Facial Nerve Palsy

How to Cite This Article: Inaloo S, Katibeh P. Guillain-Barre Syndrome Presenting With Bilateral Facial Nerve Palsy. Iran J Child Neurol. 2014 Winter;8(1):69-71.ObjectiveThis case study is about an 11-year-old girl with bilateral facial weakness, abnormal taste sensation, and deep tendon reflexes of both knees and ankles were absent. However, the muscle power of the lower and upper extremities across all muscle groups was normal. After 2 days, she developed paresthesia and numbness in the lower extremities. Other neurologic examinations, such as fundoscopic evaluation of the retina were normal with the muscle power of both upper- and lower-extremities intact. A lumbar puncture revealed albumincytological dissociation. EMG and NCV were in favor of Guillain-Barre syndrome, for which IVIG was prescribed and the abnormal sensations in the lower limbs rapidly improved. Bilateral facial diplegia without weakness and paresthesia is a variant of Guillain-Barre syndrome that mostly presents withacute onset, rapid progression with or without limb weakness, paresthesia, and decreased or absent DTR and albumin-cytological dissociation.References:Barbi F, Ariatti A, Funakoshi K, Meacci M, Odaka M, Galassi G. Parvovirus B19 infection antedating Guillain-Barre’ syndrome variant with prominent facial diplegia. J Neurol 2011 Aug; 258(8):1551-2. doi: 10.1007/s00415-011-5949-5. Epub 2011 Feb 15.Yardimci N, Avci AY, Kayhan E, Benli S. Bilateral facial nerve enhancement demonstrated by magnetic resonance imaging in Guillain-Barré syndrome. Neurol Sci 2009 Oct; 30(5):431-3. doi:10.1007/s10072-009-0120-0.Lim TC, Yeo WS, Loke KY, Quek SC. Bilateral facial nerve palsy in Kawasaki disease. Ann Acad Med Singapore 2009; 38(8):737-8.Quintas E, Silva A, Sarmento A. Bilateral facial palsy in a young patient after meningococcal meningitis, associated to herpetic infection. Arq Neuro-Psiquiatr 2009; 67(3a): 712-14.Jain V, Deshmukh A, Gollomp S. Bilateral facial paralysis: case presentation and discussion of differential diagnosis. J Gen Intern Med 2006; 21(7):C7-10.Kamaratos A, Kokkoris S, Protopsaltis J, Agorgianitis D, Koumpoulis H, Lentzas J et al. Simultaneous Bilateral Facial Palsy in a Diabetic Patient. Diabetes Care 2004; 27 (2): 623-24.Magliocca KR, Leung EM, Desmond JS. Parotid swelling and facial nerve palsy: an uncommon presentation of sarcoidosis. Gen Dent 2009; 57(2):180-2.Atsumi M, Kitaguchi M, Nishikawa S, Susuki K. A variant of Guillain-Barré syndrome with prominent bilateral peripheral facial nerve palsy-facial diplegia and paresthesias. Rinsho Shinkeigaku 2004 Aug; 44(8):549-52.Narayanan RP, James N, Ramachandran K, Jaramillo MJ. Guillain-Barré Syndrome presenting with bilateral facial nerve paralysis: a case report. Cases J 2008 Dec 8;1(1):379.Azarisman SMS, Shahrin TCA, Marzuki AO, Fatnoon NNA, Rathor MY. Bilateral facial nerve palsy secondary to an atypical presentation of Guillain-Barré syndrome. IMJ 2009; 8(1):41-4.Sethi NK, Torgovnick J, Arsura E, Johnston A, Buescher E. Facial diplegia with hyperreflexia--a mild Guillain-Barre Syndrome variant, to treat or not to treat? J Brachial Plex Peripher Nerve Inj 2007; 10(2):9.Burina A, Sinanović O, Smajlović D, Vidovic. Bilateral Oculomotor Nerve Palsy in Guillain-barre Syndrome. Med Arh 2008; 62 (2):119-120.Verma R, Chaudhari TS, Giri P. Unilateral facial palsy in Guillain-Barre syndrome (GBS): a rare occurrence. BMJ Case Rep 2012 Oct 19; 2012. pii: bcr2012007077. doi: 10.1136/bcr-2012-007077.Susuki K, Koga M, Hirata K, Isogai E, Yuki N.A Guillain-Barré syndrome variant with prominent facial diplegia. J Neurol 2009; 256(11): 1899-1905

An epidemiologic study of 389 children with epilepsy in southern Iran

How to Cite this Article: Inaloo S, Katibeh P. An epidemiologic study of 389 children with epilepsy in southern Iran.Iranian Journal of Child Neurology2011;5(4):15-20Objective Approximately 4% of the world's population experience one or more febrile seizures during their lifetime, and 0.5-1% of the population has active epilepsy.Less than one-third of the reported seizures are categorized as epilepsy. The cause of established epilepsy is important in determining the treatment and prognosis.Materials & Methods We studied 389 cases of documented epilepsy in children aged 2 months to 18 years who visited the hospital for neurologic examination during 2005-2010.Chi-square test or Fisher's exact test was performed for categorical variables.Results The most common age for the first seizure was below 2 years, and the most common type of epilepsy was generalized tonic-clonic seizure. Electroencephalography (EEG) showed an epileptic pattern in 60%, 29.8%, and 51% of the patients with idiopathic, symptomatic, and cryptogenic epilepsy, respectively. This pattern was significantly different among these 3 categories of epilepsy.Conclusion The most common type of seizure was cryptogenic; however, in most industrialized countries, idiopathic epilepsies were more frequent. With respect to the age and sex of patients, the prevalence of epilepsy in southern Iran is not so much different from that of patients in other parts of the world. As to generalized or partial epilepsy, there are different reports from different part ofthe world; however, generalized tonic-clonic seizures were more common in our area.References Hauser, Hesdorffer DC. Epilepsy, frequency, causes and consequences. New WA York, NY: Demos Publications;1990.P.1–51.Jallon P. Epilepsy in developing countries. Epilepsia 1997; 38: 1143-51.King M, Newton M, Jackson G, Fitt G, Mitchell L, Silvapulle M, Berkovic S. Epileptology of the first-seizure presentation: a clinical, electroencephalographic, and magnetic resonance imaging study of 300 consecutive patients. The Lancet 1998; 352: 1007-1011.Sridharan S. Epidemiology of epilepsy. Current Science 2002;82:664-70Martin JB, Jacqueline AF. Management of epilepsy in adolescents and adults. Lanset 2000; 356: 323-29.Chang BS, Lowenstein DH. Epilepsy. N Engl J Med 2003; 349: 1257-66.Guerrini R. Epilepsy in children. Lancet 2006; 367:499- 524.Mohammadi MR, Ghanizadeh A, Davidian H, Mohammadi M, Norouzian M. Prevalence of epilepsy and comorbidity of psychiatric disorders in Iran. Seizure 2006;15(7):476-82.Luengo A, Parra J, Colas J, Ramos F, Carreras T, Fernández-Pozos MJ. Prevalence of Epilepsy in Northeast Madrid. J Neurol 2001; 248: 762-767.Sridharan R. Epidemiology of epilepsy.Curr Sci 2002; 82(6):664-70.Najib Kh, Fallahzadeh E, Fallahzadeh MH. Disease spectrum and mortality in hospitalized children of southern Iran. Iran J Pediatr 2007; 17(3):359-363.Commission on Classification and Terminology of the International League against Epilepsy. Proposal for revised clinical and electrographic classification of epileptic seizures. Epilepsia 1981; 22: 489–501.Commission on Classification and Terminology of the International League Against Epilepsy. Proposal for revised classification of epilepsies and epileptic syndromes. Epilepsia 1989;30: 389–99.Kramer U, Nevo Y, Neufeld MY, Fatal A, Leitner Y, Harel S. Epidemiology of epilepsy in childhood: A cohort of 440 consecutive patients. Pediat Neurol 1998; 18 :46-5.Olafsson E, Ludvigsson P, Gudmundsson G, Hesdorffer D, Kjartansson O, Hauser WA. Incidence of unprovoked seizures and epilepsy in Iceland and assessment of the epilepsy syndrome classification: a prospective study. Lancet Neurol 2005;4:627-34.Hauser, W. A. The Prevalence and Incidence of Convulsive Disorders in Children. Epilepsia 1994; 35: S1-S6.Kochen S, Melcon MO. Prognosis of epilepsy in a community based study: 8 years of follow up in an Argentine community. Acta Neurologica Scandinavica 2005; 112: 370-374.Hauser WA, Kurland LT. epidemiology of epilepsy in Rochester, Minnesota 1936 through 1967.Epilepsia 1983;24:502-14. Preux PM, Druet-Cabanac M. Epidemiology and etiology of epilepsy in sub-Saharan Africa. The Lancet Neurol 2005; 4: 21-31.Olafsson E, Hauser W A, Ludvigsson P , Gudmundsson G. Incidence of Epilepsy in Rural Iceland: A Population- Based Study. Epilepsia 1996; 37: 951–955.Joensen P. Prevalence, incidence, and classification of epilepsy in the Faroes. Acta Neurologica Scandinavica1986;74:150–155.Granieri E, Rosati G, Tola R, Pavoni M, Paolino E, Pinna L, Monetti V C. A Descriptive Study of Epilepsy in the District of Copparo, Italy, 1964-1978. Epilepsia 1983; 24:502–514.Nash TE, Del Brutto, Butman JA Corona T, Delgado- Escueta A, Duron RM ,et al. Calcific neurocysticercosis and epileptogenesis. Neurology 2004; 62: 1934-38. Sillanpaa M, Jalava M, Kaleva O, Shinnar S. Long-term prognosis of seizures with onset in childhood. N Engl J Med 1998; 338:1715-22.O’Dell C, Shinnar S. Initiation and discontinuation of antiepileptic drugs. Neurol Clin 2001 ;19(2):289-311.Medina MT, Durón RM, Martínez L, Osorio JR, Estrada AL, Zúniga C, et al. Prevalence, incidence, and etiology of epilepsies in rural Honduras: the SalamáStudy. Epilepsia 2005 Jan;46(1):124-31.Sander JWAS. Some aspects of prognosis in the epilepsies:a review. Epilepsia1993;34:1007-16.Berg AT, Shinnar S, Levy SR, Testa FM, Smith-Rapaport S, Beckerman B. Defining early seizure outcomes inpediatric epilepsy: the good, the bad and the in-between.Epilepsy Res 2001 Jan;43(1):75-84. King M, Newton M, Jackson G, Fitt G, Mitchell L, Silvapulle M, et al. Epileptology of the first-seizure presentation: a clinical, electroencephalographic, and magnetic resonance imaging study of 300 consecutive patients. The Lancet 1998; 352: 1007-1011.Duncan JS. Imaging and Epilepsy. Brain 1997; 120: 339- 77.Lhatoo S D,Sander JWAS. The Epidemiology of Epilepsy and Learning Disability. Epilepsia 2001; 42: 6–9.Aicardi J. Epileptic syndromes in childhood. Epilepsia 1988; 29(suppl 3):551 - 5.Stafstrom CE, Patxot CE, Gilmore HE, et al. Seizures in children with Down’s syndrome: etiology, characteristics and outcome. Dev Med Child Neurol 1991; 33:191 – 200

Cerebral Palsy in 1-12 Year Old Children in Southern Iran

How to Cite This Article: Inaloo S, Katibeh P, Ghasemof M. Cerebral Palsy in 1-12 Year Old Children in Southern Iran. Iran J Child Neurol. Winter 2016; 10(1):35-41.AbstractObjectiveCerebral palsy (CP) is a non-progressive CNS disorder due to an insult to the growing brain, usually occurring in the first two years of life. During the recent years, its etiology has been changed; perinatal and postnatal insults are not considered as its main causes in developed countries any more. The aim of this study was to evaluate the causes of CP in children in southern Iran.Materials & MethodsOverall, 200 children with CP aged 1-12 yr old referring to Pediatric Neurology Clinic affiliated to Shiraz University of Medical Sciences, Shiraz, Iran between 2012 and 2013 were enrolled. In addition, 200 healthy age and sex-matched children were considered as the control group. Exclusion criteria were isolated movement disorders with no other evidence of CP, progressive neurologic disorders, metabolic disorders, and incomplete or uncertain past history. After collecting the data on pregnancy period, prenatal history and past medical problems, they were analyzed with appropriate statistical methods.ResultsMaternal age, medical problems during pregnancy period, route of delivery, head circumference at birth, neonatal admission, neonatal jaundice, and prematurity were the main risk factors for CP.DiscussionThe distribution of risk factors of CP is different from that of developed countries in our region. Pre- and peri-natal etiologies are still among the common causes of CP in Iran

Febrile Seizure in Thalassemic Patients

ObjectiveFebrile seizure is the most common seizure disorder in children. Its pathophysiology is not fully understood yet; however, some risk factors have been cited for it. Iron is one of these influential elements and is involved in the metabolism of some neurotransmitters which are reduced in irondeficiency anemia and also increases the sensitivity of neural cells during a febrile episode. The present study aimed to determine the rate of febrile seizure in thalassemic patients and to compare it with the corresponding rate in the normal population.Materials & MethodsThis descriptive cross-sectional study was conducted on 766 patients with thalassemia major. They were all older than 6 months and were referred to Dastghaib Cooly's Clinic, affiliated to Shiraz University of Medical Sciences, from Oct 2006 to May 2007, and 766 normal and healthy children as the control group. Questionnaires containing demographic data and past history of febrile seizure, age of febrile seizure, number of episodes, hospitalization, and related family history were prepared and filled through interviewing the parents.ResultsFebrile seizure was detected in 7 cases of the patient group (0.9%) versus 18 cases (2.3%) of the control group. The frequency of febrile seizure in the controls was 2.5 times more than that in the thalassemia group, which was statistically significant (P < 0.05).ConclusionThis study showed a lower rate of febrile convulsion in thalassemic patients compared to the control group. Accordingly, it could be suggested that high iron storage is a protective factor against febrile convulsion.

Delayed hypoxic encephalopathy: a rare complication of methadone poisoning in two cases

  Methadone is a kind of opioid that is used to reduce the pain of addicts who decide to withdraw drugs. Sometimes due to a lack of appropriate cautions, this drug will be accessible to children, andpoisoning might occur. Methadone poisoning usually presents with the loss of consciousness and pinpoint pupils. Herein, we present two cases of delayed hypoxic encephalopathy that had been poisoned by methadon

Evaluation of the quality of life in epileptic children of Shiraz, Southern Iran

Introduction: People  suffer chronic disease like epilepsy are highly prone to debilitating changes in factors that affect the quality of life such as physical capacity, self-esteem, relationships with others and fulfillment of their daily life activities.  In this study, we decided to evaluate the quality of life in children with epilepsy in Shiraz, South Iran. Methods: Epileptic patients  referred to epilepsy clinic of Shiraz University of Medical Sciences and had no first time episode of seizures in the previous 6 months and no febrile-seizure were included in the study. Patients were evaluated using the standard KIDSCREEN-27 questionnaire. Data were analyzed using the statistical software SPSS 21, Man Whitney and Chi-square tests and reported in terms of descriptive statistics. The  significance level was considered less than 0.05. Results: In this case-control study, 229 children with epilepsy were compared with a control group of 400 normal individuals. The mean age  was 12.44±3.16 and 12.10±2.69 years. The tonic-clonic seizure had the highest prevalence . Being a boy, older age and having more seizures per year were associated with lower quality of life; in general, epileptic children had significantly lower QOL compared to normal cases. Conclusion: In general, epileptic children had an overall lower QOL while factors such as older age, male gender, and higher number of seizures over the years reduced the quality of life of these patients. 

Acquired CNS Demyelinating Syndrome in Children Referred to Shiraz Pediatric Neurology Ward

How to Cite This Article: Inaloo S, Haghbin S, Moradi M, Dashti H, Safari N. Acquired CNS Demyelinating Syndrome in Children Referred to Shiraz Pediatric Neurology Ward. Iran J Child Neurol. 2014 Spring; 8(2):18-23.ObjectiveIncidence of CNS acquired demyelinating syndrome (ADS), especially multiple sclerosis (MS) in children, appears to be on the rise worldwide. The objective of this study was to determine prevalence, clinical presentation, neuroimagingfeatures, and prognosis of different types of ADS in Iranian children.Materials & MethodsDuring the period 2002-2012, all the patients (aged 1-18 years) with ADS, such as MS, acute disseminated encephalomyelitis (ADEM), optic neurotic (ON), Devic disease, and transverse myelitis (TM), referred to the pediatric neurology ward, Nemazee Hospital, Shiraz University of Medical Sciences, were includedin this study. Demographic data, clinical signs and symptoms, past and family history, preclinical findings, clinical course, and outcome were obtained.ResultsWe identified 88 patients with ADS in our center. The most prevalent disease was MS with 36.5% (n=32), followed by AEDM 26.1% (n=31), ON 17% (n=13), TM 15.9% (n=14), and Devic disease 4.5% (n=4). MS, ON, TM were morecommon among females while ADEM was more common in males. Children with ADEM were significantly younger than those with other types of ADS.Family history was positive in 10% of patients with MS.Previous history of recent infection was considerably seen in cases with ADEM.Clinical presentation and prognosis in this study was in accordance with those in previous studies on children.ConclusionIn this study, the most common type of ADS was MS, which was more common in female and older age cases. ADEM was more common in male and younger children. ADEM and ON had the best and Devic disease had the worst prognosis.References1. Longer-Gould A, Zhaug JL, Chung J, Yeung Y, Wanbant E, Yao J. Incidence of acquired CNS demyelinating syndrome in a multiethnic cohort of children. Neurology 2011;27(12):1143-8.2. Banwell B, Kennedy J, Sandovnick D, Arnold DL, Magalhaes S, Wambera K. Incidence of acquired demyelination of the CNS in Canadian children. Neurology 2009;72(3):232-9.3. Canellas AR, Gols AR, Izquierdo J.R, Subirana MT, Gairin XM. Idiopathic inflammatory demyelinating disease of central nervous system. Neuroradiology 2007;49(5):393-409.4. Renoux C, Vukusic S, Mikaeloff Y. Natural history of multiple sclerosis with childhood onset. N Engl Med 2007;356(25):2603-13.5. Krupp LB, Banwell B, Tenembaum S; International Pediatric MS Study Group. Consensus definition proposed for pediatric multiple sclerosis and related disorders. Neurology 2007;68(16 Suppl 2):S7-12.6. Ebers GC. Environmental factors and multiple sclerosis. Lancet Neurol 2008;77(3):268-77.7. Banwell B, Ghezzi A, Bar-OrA, Mikaeloff Y, Tordieu M. Multiple sclerosis in children, clinical diagnosis, therapeutic strategies and future directions. Lancet Neurol 2007;6(10):887-902.8. Absound M, Lim MJ, Chorg Wk, Goede CGs Foster K, Counny R. Pediatric acquired demyelinating syndromes: incidence, clinical and magnetic resonance imaging features. Mult Scler 2012;19(1):76-86.9. Banwell B, Krupp L, Kennedy J. Clinical features and viral serology in children with multiple sclerosis: a multinational observation study. Lancet Neurology 2007;6(9):773-81.10. Jin Y, Depedro-Cusesta J, Söderströ, M. Stawiarz L, Link H. Seasonal pattern in optic neuritis and multiple sclerosis. A meta-analysis. J Neurol Sci 2000;1(181):56-64.11. Ghobai M, Omrani H, Rosta ئzadeh M. Epidemiology of multiple sclerosis. Tehran Univ Med J 2008;65:74-7.12. Etemadifar M, Hosseini A, Khodabanehlou R, Maghzi AH. Childhood-onset multiple sclerosis: report of 82 patients from Esfahan, Iran. Arch Iranian Med 2007;10(2):152-6.13. Ruggior M, Polizzi A, Pervon L, Grimoldi LM. Multiple sclerosis in children under 6 years of age. Neurology 1999;53(3):478-4.14. Handefield FA. Characteristic of childhood multiple sclerosis. Int MS J 1995;3:91-8.15. Selcen D, Anlar B, Renda Y. Multiple sclerosis in children. Report of 16 cases. Eur Neurol 1996;36(2):79-84.16. Inaloo S, Yavari MJ, Sabori S. Multiple sclerosis in children: A review of clinical and paraclinical features in 26 cases. Iran J Child Neruol 2008;2(4):41-6.17. Hynson JL, Kornberg AJ, Coleman LT, Shield L, Harvey AS, Kean MJ. Clinical and Neuroradiologic feature of acute disseminated encephalomyelitis in children. Neurology 2001;56(13):8-12.18. Murthy KSN, Faden HS, Cohen ME, Bakshi R. Acute disseminated encephalomyelitis in children. Pediatric 2002;110(2):1-8.19. Collard RC, Koehler RP, Mattson DH. Frequency and significance of antinuclear antibodies in multiple sclerosis. Neurology 1997;49(3):857-61.20. Barned S, Goodman AD, Mattson AD. Frequency of antinuclear antibodies in multiple sclerosis. Neurology 1995;45(2):384-5.21. Sri-Udomkajorn S, Pongwatcharaporn K. Clinical feature and outcome of childhood optic neuritis at Queen Sirikit National Institute of Child Health. J Med Assoc Thai 2011;94(Suppl 3):S189-94.22. Absoud M, Cummins C, Desai N, Gika A, McSweeney N, Munot P, et al. Childhood optic neuritis clinical features and outcome. Arch Dis Child 2011;96(9):860-2.23. Thomas T, Branson HM, Verhey LH, Shroff M, Stephens D, Magallhaes S, et al. The demographic, clinical, and magnetic resonance imaging (MRI) features of transverse myelitis in children. J Child Neurol 2012;27(1):11-2

Pediatric Stroke in Southern Iran; Clinical Presentations, Etiologies and Outcomes: A Case-Series and Review of Literature

Background:  Pediatric stroke is defined as rapid developing clinical signs of focal (or global) disturbance of cerebral function without any apparent cause other than of vascular origin lasting for 24 hours or longer in the ages of 1 month to 18 years.  It is relatively rare in children, however, it can lead to significant mortality and morbidity. Objectives:  The present study aimed to identify clinical presentations, etiologies, and outcomes of pediatric stroke in southern Iran. Methods:  This case-series study included all patients that were diagnosed with a pediatric stroke and admitted to the Pediatric Neurology ward at Namazi hospital in Shiraz, Iran, from May 2009 through March 2012. Results:  During the study period, 40 newly diagnosed patients (27 males and 13 females) between the ages of 10 months and 18 years old were identified. The most prevalent referring symptoms were hemiparesis and hemiplagia (65%), seizures (45%), speech difficulties (42.5%), and altered mental status (35%). A known single etiology was identified in 82.5% of patients. The most common single risk factor was cardiac abnormalities with 30% frequency, followed by idiopathic and vascular with 17.5%. The outcome of pediatric patients revealed incomplete recovery with moderate neurological deficits (45%) including residual epilepsy (15%), speech difficulties (15%), and behavioral dysfunction (7%), which indicate their need for help in some of their daily activities. Conclusions: Stroke in southern Iranian pediatric patients demonstrated different patterns of causes and risk factors with similar clinical presentations and outcomes