Role of Team Work in The Management Of Mitochondrial Disease In Children (Case Report)

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Approach to NPC Disease

How to Cite This Article: Tonekaboni SH. Approach to NPC Disease. Iran J Child Neurol. 2015 Autumn;9:4(Suppl.1): 7.Pls see Pdf

Neurodegeneration with Brain Iron Accumulation: An Overview

How to Cite This Article: Tonekaboni SH, Mollamohammadi M. Neurodegeneration with Brain Iron Accumulation: An Overview. Iran J Child Neurol. 2014 Autumn;8(4): 1-8.AbstractObjectiveNeurodegeneration with brain iron accumulation (NBIA) is a group of neurodegenerative disorder with deposition of iron in the brain (mainly Basal Ganglia) leading to a progressive Parkinsonism, spasticity, dystonia, retinal degeneration, optic atrophy often accompanied by psychiatric manifestations and cognitive decline. 8 of the 10 genetically defined NBIA types are inherited as autosomal recessive and the remaining two by autosomal dominant and X-linked dominant manner. Brain MRI findings are almost specific and show abnormal brain iron deposition in basal ganglia some other related anatomicallocations. In some types of NBIA cerebellar atrophy is the major finding in MRI.ReferencesShevel M. Racial hygiene, activeeuthanasia, and Julius Hallervorden. Neurology 1992;42:2214-2219.HayflickSJ. Neurodegeneration with brain Iron accumulation: from genes to pathogenesis.Semin Pediatr Neurol 2006;13:182-185.Zhou B, Westawy SK, Levinson B, et al. A novel pantothenate kinase gene(PANK2) is defective in Hallervorden-Spatzsyndrome. Nat Genet 2001;28:345- 349.www.ncbi.nlm.nihgov/NBK111Y/university of Washington, seattle. Allison Gregory and Susan Hayflick.Paisan-Ruiz C, Li A, Schneider SA, et al. Widesread Levy body and tau accumulation in childhood and adult onset dystonia-parkinsonism cases with PLA2G6 mutations. Neurobiol Aging 2012;33:814-823.Dick KJ, Eckhardt M, Paison-Ruiz C, et al. Mutation of FA2H underlies a complicated form of hereditary spastic paraplegia(SPG 35). Hum Mutat 31: E1251-E1260.Edvardson S, Hama H, Shaag A, et al. Mutation in the fatty acid 2-Hydroxylase gene are associated with leukodystrophy with spastic paraparesis and dystonia. Am I Hum Genet 2008;83:647-648.Schneider SA, Aggarwal A, Bhatt m, et al. Severe tongue protrusion dystonia: clinical syndromes and possible treatment. Neurology 2006;67: 940-943.Egan RA, Weleber RG, Hogarth P. et al. Neuroopthamologic and electroreinographic finding in pantothenate kinase associated neurodegeneration. Am J ophtalmol 2005;140:167-274.Kruer MC, Boddaert N. Adiadnostic Algorithm. Semin Pediatrn Neurol  2012;19: 67-74.Dezfouli MA, Alavi A, Rohani M, Rezvani M, Nekuie T, Klotzle B, Tonekaboni SH, Shahidi GA, Elahi E. PANK2 and C19orf12 mutations are common causes of neurodegeneration with brain iron accumulation. Mov Disord 2013 Feb;28(2):228-32. doi: 10.1002/mds.25271.Epub 2012 Nov 19.Hartig MB, Hortnagel K, Garavaglia B, et al. Genotype and phenotypic spectrum of PANK2 mutations in patients with neurodegeneration with brain iron accumulation Ann Neurol 2006;59: 248-256.Kotzbauer PT, Truax AC, Trojanowsli JQ, et al. Altered neuronal mitochondrial coenzyme A synthesis in neurodegeneration with brain iron accumulation cause by abnormal processing of mutant pantothenase Kinase2. J Neurosci 2005;25:689-698.Poli M, Deosas M, Lusciete S, et al. Pantothenate Kinase2 silencing causes cell growth reduction and iron  deregulation Neurobiol Dis 2010;39: 204-210.Wakabayashi K, Fukushima T, Koide R, et al. Juvenile-nset generalized neuroaxonal dystrophy with  diffuse neurofibrillary and Lewy body pathology. ActaNeuropathonal 2000;99: 331-336.Galvin JE, Giasson B, Hurting HI, et al. Neurodegeneration with brain iron accumulation, type1 is characterized by alpha, beta and gamma-synuclein neuropathology, Am T Pathol 2000;157: 361-368.Li A, Paudel R, Johnson R, et al. Pantothenate Kinaseassocated neurodegeneration is not a  synucleinopathyneuropathol Appl Neurobiol(in press).Gregory A, Polster BJ, Hayflick SJ: Clinical and genetic delineation of neurodegeneration with brain iron accumulation. J Med Genet 2009;46:73-80.Gregory A, Westaway SK, Holm IE, et al. Neurodegeneration associated with genetic defects in phospholipase A2. Neurology 2008;71:1402-1409.Harting MB, Lsao A, Haa KT, et al. Absence of an orphan mitochondrial protein, c19orf12 with brain iron accumulation, Am J Hum Genet 2011;89: 543-550.Najim al-Din AS, Wriekat A, Mubaidin A, et al. Pallidopyramidal degeneration, supraneuclearupgaze paresis and dementia: Kufor- Rakeb syndrome. Acta Neurol Scand 2011;89: 347-352.Tobias B Hoak, Penelope Hogarth, Micheal C Kruer et al. Am J Hum Genet 2012 Dec 7; 91 (6): 1144-49.Chummery PF, Crompton DE, Bircholl D, et al. Clinical features and matural history of Neuroferritinopathy caused by the FTL1 gene mutation. Brain 2007;130:110-119.Mc Neil A, Bircholl D, Hayflich SJ, et al. T2 and FSE MRI distinguishes L subtypes of NBIA, Neurology 2008;70: 1614- 1619. McNeil A , Pandolfo M, Kuhn J,et al.The Neurological presentation of ceruloplasmin gene  mutations. Eur Neurol 2008;60:200-205.Dusi S, Valletta L, Hoach TB, et al. Exone sequencing reveals mutations in Co A synthtas as a cause of neurodegeneration with brain iron accumulation: Am J Hum Genetic Jan2, 2014. Aras M Alazim, Amir Alsaif, Abdulaziz Al-Semari, et al. mutation in C2 orf 37, cause hypogonadism, diabetes Melitus, Mental retardation and extrapyramidal syndrome: Am J Hum Genetic. 2008 Dec 12; 83(6): 684-691

Proton MR Spectroscopy in The Diagnostic Evaluation of Suspected Mitochondrial Disease in Iran

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Pregabalin in childhood epilepsy: a clinical trial study

How to Cite This Article: Mollamohammadi M, Tonekaboni SH, Pirzadeh Z, Vahedian M . Pregabalin in Childhood Epilepsy: A Clinical TrialIran J Child Neurol. 2014 Autumn;8(4): 62-65.AbstractObjectiveThe prevalence of active epilepsy is about 0.5–1%, and approximately 70% of patients are cured with first anti-epileptic drugs and the remaining patients need multiple drugs. Pregabalin as an add-on therapy has a postive effect on refractory seizures in adults. To the best of our knowledge, there is no research with this drug in childhood epilepsy. We use pregabalin in children with refractory seizures as an add-on therapy. The objective of this study is to evaluate the effects of pregabalin in the reduction of seizures for refractory epilepsy.Material & MethodsForty patients with refractory seizures who were referred to Mofid Children’s Hospital and Hazrat Masoumeh Hospital were selected. A questionnaire based on patient record forms, demographic data (age, gender,…), type of seizure, clinical signs, EEG record, imaging report, drugs that had been used, drugs currently being used, and the number of seizures before and after Pregabalin treatment was completed. We checked the number of seizures after one and four months.ResultsAfter one month, 26.8% of patients had more than a 50% reduction in seizures and 14.6% of these patients were seizure-free; 12.2% had a 25–50% reduction; and approximately 61% had less than a 25% reduction or no change in seizures.After the fourth month, 34.1% of patients had more than a 50% reduction in seizures and 24.4% of these patients were seizure-free. Additionally, 65.9% of patients had less than 50% reduction in seizures (9.8% between 25–50% and 56.1% less than 25% or without improvement).ConclusionWe recommend Pregabalin as an add-on therapy for refractory seizures (except for myoclonic seizures) for children.ReferencesKwan P., Brodie MJ. Early identification of refractory epilepsy. N Engl J Med 2000;342(5):314-9.Mikati MA. Seizures in childhood. In: Kliegmann RM, Behrman RE, Jenson HB, Stanton BF, editors. Nelson Textbook of Pediatrics. 19th ed. Philadelphia, Pa:Saunders Elsevier. 2011.P.2013-2039.Camfield PR, Camfield CS. Pediatric Epilepsy. In: Swaiman KF, editors. Swaiman`s pediatric neurology: Principles and Practice.7th ed. Edinburgh: Elsevier Saunders; 2012.P 703-710.Piña-Garza EJ. Fenichel’s clinical pediatric neurology. Altered States of Consciousness. 7th ed. Elsevier Saunder. 2013.P.47-75.Austin JK, Smith S, Risinger MW, McNehs AM. Childhood epilepsy and asthma comparison of quality of life. Epilepsia 1994:35(3):608-15.Farvwell JR, Dodrill CB, Batzel LW. Neuropsychological abilities of children with epilepsy. Epilepsia 1985;26(5):395-400.Kotagal P, Rothner AD, Erenberg G, Cruse RP, Wyllie E. Complex partial seizures of childhood onset. Arch Neurol 1987:44(11):1177-80.Miller R, Frame B, Corrigan B, Burger P, Backbrader H, Garofalo EA, et al. Exposure- response analysis of pregabalin add- on treatment of patients with refractory partial seizures. Clin Pharmacol Ther 2003;73(6):491-505.Fink K, Dooley DJ, Meder WP, Suman-Chauhan N, Duffy S, Clusmann H, et al. Inhibition of neuronal ca(2+) influx by gabapentin and pregabalin in the human neocortex. Neuropharmacology 2002;42(2):229-36.Topol A. Pregabalin for epilepsy. New medicines profile 2004 November; (04/12):1-3.Arroyo S, Anhut H, Kugler AR, Lee CM, Knapp LE, Garofalo EA, et al. Pregabalin add-on treatment: a randomized, double-blind, placebo-controlled, doseresponse study in adults with partial seizures. Epilepsia 2004; 45(1):2-7.Beydoun A, Uthman BM, Kugler AR, Greiner MJ, Knapp LE, Garoflo EA. Safely and efficacy of two pregabalin regimens for add-on treatment of partial epilepsy. Neurology 2005;64(3):475-80.French JA, Kugler AR, Robbins JL, Knapp LE, Garoflo EA. Dose-response trial of pregabalin adjunctive therapy in patients with partial seizures. Neurology 2003;60(10):1631-7.Carreno M, Maestro I, Molins A, Donaire A, Falip M, Becerra JL, et al. Pregabalin as add-on therapy for refractory seizures in every day clinical practice. Seizure 2007;16(8):709-12.Jan MM, Zuberi SA, Alsaihati BA. Pregabalin: Preliminary experience in intractable childhood epilepsy. Pediatr Neurol 2008;40(5):347-50.Chisanga E, Manford M. Pregabalin drug information. NHS foundation trust. March 2013.Gil-Nagel A. Zaccara G. Baldinetti F. Leon T. Add-on treatment with pregabalin for partial seizures with or without generalization: pooled data analysis of four randomized placebo-controlled trials. Seizure 2009;18(3):184-92

Efficacy of The Ketogenic Diet as A Therapy for Intractable Epilepsy in Children

ObjectiveTo determine the role of ketogenic diet in the treatment of intractable epilepsy in children.Materials & MethodsSixty six consecutive children (1-16 years old) with intractable epilepsy whose seizure were not neurodegenerative nor febrile in origin were recruited. They received the ketogenic diet and we evaluated its effect on seizure frequency for 3 months. All these children had more than five seizures per week despite adequate therapy with at least 3-4 anticonvulsant medications. Carbohydrates were initially limited to 10 gr/day and fats constituted 75% of the total energy requirement. Response to the diet was categorized as free of seizure, 99%-75%, 50%-75%, 25%-49% and lower than 25% reduction (resistant to therapy).ResultsFifty five patients (84%) out of 66 children initiating the diet continued it after 1 week. After 3 months, 80% of the patients kept the diet. After one week, one month and 3 months, there was a more than 50% decrease in the frequency of the seizures in 40 (60%), 50 (75%) and 39 (59%) of the patients, respectively. Three patients (4.5%) were seizure-free after 1 week, 12 (18%) were seizure-free after one month and 12 (18%) were seizure-free after three months and a significant relationship was found between seizure reduction and the type of epilepsy (p<0.017).ConclusionThe ketogenic diet should be considered as an alternative therapy for children with intractable seizures. It is more effective than many of the new anticonvulsant medications and is well tolerated by children andtheir families

Exploring the Psychometric Properties of the Farsi Version of Quality of Life Kindl Questionnaire for 4-7 Year-Old Children in Iran

How to Cite This Article: Rojhani Shirazi M, Tonekaboni SH, Azargashb E, Derakhshannia M, Aghdasta E. Exploring the Psychometric Properties of The Farsi Version of Quality of Life Kindl Questionnaire for 4-7 Year-Old Children in Iran. Iran J Child Neurol. Spring 2016; 10(2):42-52.AbstractObjectiveThe aim of this study was to translate and validate the psychometric properties of the Quality of Life Kindl questionnaire.Materials & MethodsParents of 4-7 yr-old healthy and ill children referred to Mofid Children Hospital in Tehran in 2013, Iran were sampled randomly in two groups each of which 130 people. After translation, the questionnaie’s validity and reliability was evaluated and was confirmed for face and content validity. Questionnaire was also completed by two (one healthy and one ill) groups for which inclusion criteria included consent of the parents, age of the children being beween 4 and 7 yr, and presence of the child in a nursery school, kindergarten, school or any class at least for one month. Exclusion criteria were inability of the parents in answering the questions accurately. Inclusion criterion for the ill group was having chronic cardiac, neurologic, hematologic, or respiratory diseases, lasting longer than 3 months for which they were followed up in outpatient clinic in the hospital. The reliability of questionnaire was measured by the Cronbach’s alpha.Data were analyzed using factor analysis, Spearman’s correlation coefficient, Mann-Whitney and Chi-square test.ResultsThe reliability was 0.85 and 0.81 in healthy and ill groups, respectively. The results of factor analysis showed that each of eight subscales of questionnaire had acceptable construct validity. Only two of 52 questions of the questionnaire did not have proper correlation coefficient.ConclusionQuality of Life Kindl Questionnaire is a valid and reliable test for assessing healthy and ill children in Iran. References1. The WHOQOL Group. The World Health Organization Quality of Life Assessment (WHOQOL). Development and psychometric properties. Soc Sci Med 1998; 46:1569-1585.2. Gandek B, Sinclair SJ, Kosinski M, Ware JE Jr. Psychometric evaluation of the SF-36 health survey in Medicare managed care. Health Care Financ Rev 2004; 25(4):5-25.3. DeSalvo KB, Bloser N, Reynolds K, He J, Muntner P. J. Mortality prediction with a single general self-rated health question. A meta-analysis. Gen Intern Med 2006; 21(3):267-75.4. Conolly MA, & Johnson JA. Measuring quality of life in paediatric patients. Pharmacoeconomics 1999; 16,605–25.5. Eiser C, Morse R. The measurement of quality of life in children: past and future perspectives. J Dev Behav Pediatr 2001; 22,248 –56.6. Ravens-Sieberer U, Bullinger M. Manual KINDL-R 2000; Hamburg, Germany. 7. Ravens-Sieberer U. Quality of Life Kindl Questionnaire. Available at: http://kindl.org/cms/information. 8. Spilker B. Quality of Life and Pharmacoeconomics in Clinical Trials. Philadelphia, Lippincott-Raven; 1996.9. Lovas K, Kalo Z, McKenna SP, Whalley D, Péntek M, Genti G. Establishing a standard for patient-completed instrument adaptations in Eastern Europe: Experience with the Nottingham Health Profile in Hungary. Health Policy 2003; 63(1):49–61.10. Bullinger M, von Mackensen S, Kirchberger I. KINDL –Ein Fragebogen zur Erfassung der gesundheitsbezogenen Lebensqualität von Kindern. Sonderdruck Zeitschrift für Gesundheitspsychologie 1994; 1:64-77.11. Asano M, Sugiura T, Miura K, Torii S, Ishiguro A. Reliability and validity of the self-report Quality of Life Questionnaire for Japanese School-age Children with Asthma (JSCA-QOL v.3). Allergy Int 2006; 55(1):59-65.12. Yaghmaei, F. Designing and measuring the psychometric properties of “Quality of Life scale for the Children suffering from Asthma”. Journal of Shahid Beheshti School of Nursing & Midwifery 2009; 20(68):32-36. 13. El Miedany, YM, Youssef SS, El Gaafary M. Cross cultural adaptation and validation of the Arabic version of the Childhood Health Assessment Questionnaire for measuring functional status in children with juvenile idiopathic arthritis. Clin Exp Rheumatol 2003; 21(3):387–393

The Ketogenic and Atkins Diets Effect on Intractable Epilepsy: A Comparison

How to Cite This Article: Ghazavi A, Tonekaboni SH, Karimzadeh P, Nikibakhsh AA, Khajeh A, Fayyazi A. The Ketogenic and Atkins Diets Effect on Intractable Epilepsy: A Comparison. Iran J Child Neurol. 2014 Summer;8(3): 12-17.AbstractObjectiveIntractable epilepsy is a major difficulty in child neurology, because the numbers of drugs that are available for treatment are limited and new treatments such as diets must be tried. Now there are some diets available for treating patients with intractable epilepsy. The oldest diet is the classic ketogenic diet and one of thenewest diets is the modified Atkins diet. Patients have a harder time accepting the classic ketogenic diet than the Atkins diet, which is easier to accept because the food tastes better. This study compares the efficacy of the ketogenic diet and the Atkins diet for intractable epilepsy in children.Materials & MethodsThis study is a clinical trial survey with sample size of 40 children with refractory epilepsy who were patients at Mofid hospital in Tehran, Iran. Initially, from Jan 2005–Oct 2007, 20 children were treated with the Atkins diet, and then from Oct 2007–March 2010, the other group was treated with the classic ketogenic diet and the results were compared. ResultsIn this study, response to treatment was greater than a 50% reduction in seizures and at the end of first, second, and third months for the ketogenic diet were 55%, 30%, and 70% and for the Atkins diet were 50%, 65%, and 70%, respectively.ConclusionThe results of this study show that there is no significant difference between the classic Ketogenic diet and the Atkins diet at the end of first, second, and third months and both had similar responses to the treatments.References Camfield CS, Canfield PR, Gordon K, Wirrell E, Dooley JM. Incidence of epilepsy in childhood and adolescents in Nova Scotia. Epilepsia, 1996 Jan;37(1):19-23.Gessner U, Sagmeister M, Horisberger B. The cost of Epilepsy in Switzerland. Int J Health Sci 1993;4:121-8.Aicardi J. Epilepsy in children. Philadelphia: Lippincott Williams & Wilkins; 2004. p. 38.4. Kossof EH. More fat and fewer seizures: dietary therapy ofepilepsy. Lancet Neurol 2004 Jul;3()7):415-20.Hassan AM, Keene DL, Whiting SE, Jacob PJ, Champagne JR, Humphreys P. Ketogenic diet in the treatment of refractory epilepsy in childhood. Pediatr. Neurol. 1999; 21: 548-552.Vining EP, Freeman JM, Ballaban-Gil K, Camfield CS, Camfield PR, Holmes GL et al. A multicenter study of the efficacy of the ketogenic diet. Arch Neurol 1998 Nov;55(11):1433-7.Nordli DR, Kuroda MM. Experience with the ketogen diet in infants. Pediatrics 2001 Jun; 108(1):129-33.Tonekaboni SH, Mostaghimi P, Mirmiran P, Abbaskhanian A, Abdollah GF, Ghofrani M, et al. Efficacy of Atkins diet as therapy for intractable epilepsy in children. Arch Iran Med 2010 Nov;13(6):492-7.Kossoff EH, Dorward JL. The modified Atkins diet. Epilepsia 2008 Nov;49 Suppl 8:37-41.Mirjavadi SAR, Tonekaboni SH, Ghazavi MR, Azarghashb E, Abdollah GF, Ghofrani M. Efficacy of ketogenic diet as a therapy for intractable epilepsy in children. Iran J Child Neurol 2010 Sep;4(2):27-36.Karimzadeh P, Tabarestani S, Mahvelati F, Tonekaboni SH, Ghofrani M. Intractable seizure disorfes; efficacy of the classic ketogenic diet. Iran J Child Neurol 2009 Jan; 3(1):15-20.Barzegar M, Ostad Rahimi AR, Eslampour Sh, Shabazi Sh. The Ketogenic diet for refractory epilepsy. Med J Tabriz Uni Med Sci Health Serv 2009;31:15-20.Lefevre F, Aronson N. Ketogenic diet for the treatment of refractory epilepsy in children: A systematic review of efficacy. Pediatrics 2000 Apr;105(4):105-9.Keene DL. A systematic review of the use of the ketogenic diet in childhood epilepsy. Pediatr Neurol 2006 Jul;35(1):1-5.Porta N, Vallee L, Boutry E, Fontaine M, Dessein AF, Joriot S, et al. Comparsion of seizure reduction and serum fatty acid levels after receiving the ketogenic and modified Atkins diet. Seizure 2009 Jun 18(5):359-64

Use of Complementary and Alternative Medicine for Epileptic Children in Tehran: A Cross-Sectional Study (2009-2011)

How to Cite This Article: Tonekaboni Sh, Jafari Naeini S, Khajeh A, Yaghini O, Ghazavi A, Abdollah Gorji F. Use of Complementary and Alternative Medicine for Epileptic Children in Tehran: A Cross-Sectional Study (2009-2011). Iran J Child Neurol. 2014 Winter; 8(1):26-31.ObjectiveAlthough the use of Complementary and Alternative Medicine (CAM) has been evaluated globally, there are few studies in our country on this subject. The purpose of this study was to determine the prevalence, pattern of use, parental sources of information, and benefits of CAM in epileptic children in Tehran.Materials & MethodsOne hundred thirty-three parents or relatives of epileptic children who were referred to outpatient clinics or admitted in neurologic ward of four major hospitals in Tehran, were interviewed by our researcher based on a structured questionnaire; from 2009 to 2010. The information obtained comprised the demographic data of patients and their parents, frequency and morphology of convulsions, the type and sources of CAM and finally, the benefits and adverseeffects of this practice.ResultsForty-four percent of the respondents had used CAM methods either alone or in combination with other methods. The most frequently used CAM was written prayers followed by oral herbs and special diets. CAM was mainly introduced to them by relatives. Only 16.7% of these parents had discussed this matter with their children’s physicians. No efficacy to control seizure was observed for most of these methods.ConclusionThis study showed that use of CAM in our study group is relatively common and may have a potentially hazardous role in the treatment process. So, it is necessary for physicians to have enough information about CAM practice in their patients. References:National Institutes of health. More than one third of US adults use complementary and alternative medicine, according to new government survey. [Serial online] 2004 (cited 2004 May 27). Available from: http://nccam. nih.gov/news/2004/052704.htm.Traditional Medicine: The Fifty-Sixth World Health Assembly WHO, 2003. World Health Organization, 2011. Available from: http://apps.who.int/gb/archive/ pdf_files/WHA56/ea56r31.pdfMichi CA. The use of herbal remedies in Jamaica. Ann Trop Paediatr 1992;12(1):31-6.Ricotti V, Delanty N. Use of complementary and alternative medicine in epilepsy. Curr Neurol Neurosci Rep 2006;6(4):347-53.Aburahma SK, Khader YS, Alzoubi k, Sawalha N. Complemetary and alternative medicine use in a pediatric neurology clinic. Complement Ther Chin Pract 2010;16(3):117-20.Eisenberg DM, Davis RB, Ettner SL, Appel S, Wilkey S, Van Rompay M, et al. Trends in alternative medicine use in United States, 1990-1997: results of a follow-up national survey. JAMA 1998;280(18):1569-75.Khonsari A, Gorji K, Abdollahpur F, Dehestani S, Mousavi A, Delfan B et al. Study of international approaches on treatment of common diseases using different methods of complementary medicine. J Ilam Uni Med Sci 2009;4:37-45. (Full text in Persian)Kwan P, Brodie MJ. Early identification of refractory epilepsy. N Engl J Med 20003;342(5):314-9.Oshikoya KA, Senbanjo IO, Njokanma OF, Soipe A. Use of complementary and alternative medicine for children with chronic health conditions in Lagos, Nigeria. BMC Complement Altern Med 2008;8:66.Liow K, Ablah E, Nguyen JC, Sadler T, Wolfe D, Tran KD et al. Pattern and frequency of use of complementary and alternative medicine among patients with epilepsy in the mid western United States. Epilepsy Behav 2007;10(4):576-82.Tehrani Banihashemi SA, Asgharifard H, Haghdoost AA, Barghamdi M, Mohammadhosseini N. The use of complementary/ Alternative medicine among the general population in Tehran /Iran. Payesh 2008;7(4):355-62.(Full text in Persian)Ekici B, That B, Abah S, Aydinli N, Ozmen M. Application of complementary and alternative medicine in epileptic children at a tertiary pediatric neurology center in Turkey. Eur J Integr Med 2011;4:e71-5.Soo I, Mah JK, Barlow K, Hamiwka L, Wirrell E. Use of complementary and alternative medical therapies in pediatric neurology clinic. Can J Neurol Sci 2005;32(4):524-28.Cuzzolin L, Zaffani S, Murgia V, Gangemi M, Meneghelli G, Chiamenti G, et al. Patterns and perceptions of complementary/alternative medicine among paediatricians and patients’ mothers: a review of the literature. Eur J Pediatr 2003;162(12):820-7

Neuroimaging Findings in First Unprovoked Seizures: A Multicentric Study in Tehran

How to Cite This Article: Molla Mohammadi M, Tonekaboni SH, Khatami AR, Azargashb E, Tavasoli A, Javadzadeh M, Zamani GR. Neuroimaging Findings in First Unprovoked Seizures: A Multicentric Study in Tehran. Iran J Child Neurol. 2013 Autumn; 7(4):24-31.ObjectiveSeizure is an emergency in pediatrics. It really matters to the parents of the involved child to have information about the causes, management and prognosis.First unprovoked seizures (FUS) are seizures that occur in patients without fever, trauma or infection. Due to the rapid improvement in diagnostic techniques in the last few decades, the etiology will be revealed and this term will no longer exist. This Study was designed to evaluate brain imaging findings in FUS patients. Materials & MethodsNinety-six children with FUS, who were admitted in three major children’s hospitals in Tehran, underwent brain imaging and were enrolled into the study.The decision about the type of imaging (CT or MRI) was based on the patient’s medical and financial conditions. An expert radiologist in the field of pediatric neuroimaging interpreted the images. ResultsAltogether, 27.1% had abnormal findings of which 29.2% were in the brain MRI group and 14.3% were in the brain CT scan group.Abnormal results were gliosis (10.4%), hemorrhage (4.2%), dysgenesis (2.1%), dysmyelination (7.3%), encephalomalacy (1%), atrophy (5.2%) and infarction (2.1%). In some patients, the lesions were in 2 or 3 sites and some had more than one type of lesion.There was no association between the duration, age and type of seizure and imaging abnormlities. However, we found an association between the location of the lesion and the type of seizure. ConclusionWe recommend brain imaging in all patients with FUS and apart from some exceptions, brain MRI is superior to CT. ReferencesJohnston MV. Siezure in childhood. In: Kliegman RM, Behrman RE, editors. Nelson text book of pediatrics. 18th ed. Philadelphia: Saunders; 2010. p. 2457-70.Bluestein JS, Moshe SL. First unprovoked seizure. In: Maria BL, editor. Currents in management in child neurology. 3rd ed. Hamilton: BC Decker; 2005. p. 89-92.Khodapanahandeh F, Hadizadeh H. Neuroimaging in children with first afebrile seizures: to order or not to order? Arch Iran Med 2006 Apr;9(2):156-8.Alawaneh H, Bataineh HA. Urgent neuroimaging in children with first nonfebrile seizures. Middle East JFam Med 2008 Feb;6(1):24-6.Shinnar S, O’Dell C, Mitnick R, Berg AT, Moshe SL. Neuroimaging abnormalities in children with an apparent first unprovoked seizure. Epilepsy Res 2001 Mar;43(3):261-9.Kalnin AJ, Fastenau PS, deGrauw TJ, Musick BS, Perkins SM, Johnson CS, et al. Magnetic resonance imaging findings in children with a first recognized seizure. Pediatr Neurol 2008 Dec;39(6):404-14.King MA, Newton MR, Jackson GD, Fitt GJ, Mitchell LA, Silvapulle MJ et al. Epileptology of the first-seizure presentation: a clinical, electroencephalographic, and magnetic resonance imaging study of 300 consecutive patients. Lancet 1998 Sep 26;352(9133):1007-11.Pohlmann-Eden B, Beghi E, CarnfieldC, Carnfield P. The first seizure and its management in adults and children. BMJ 2006 Feb;332(11):339-34.Raman S, Susan K, Joyce W. Paroxysmal disorders.In: Menkes J, editor. Child neurology. 7th ed. Philadelphia: Lipincott; 2006. p. 857-942.Wical B. The first unprovoked seizure.Gillette Children’sSpecialty Healthcare. A PediatricPerspective 1999 Mar;8(3).Bano S, Yadav SN.Neuroimaging in epilepsy.Medi-Focus2010 Apr-Sep;9(3&4):2-4.Rauch DA,Carr E, Harrington J.Inpatient brain MRI for new-onset seizures: utility and cost effectiveness.Clin Pediatr (Phila) 2008 Jun;47(5):457-60.Gaillard WD, Chiron C, Cross JH, Harvey AS, Kuzniecky R, Hertz-Pannier L et al. Guidelines for imaging infants and children with recent-onset epilepsy. Epilepsia 2009 Sep;50(9):2147-53.Barkovich AJ. Techniques and methods in pediatric neuroimaging. 4thed. Philadelphia: Lippincott Williams &Wilkins; 2005. p. 4-7.Doescher JS, deGrauw TJ, Musick BS, Dunn DW, Kalnin AJ, Egelhoff JC et al. Magnetic resonance imaging and electroencephalic findings in a cohort of normal children with newly dignosed seizures. J Child Neurol 2006 Jun; 21(6):490-5.