History, Studies and Specific Uses of Repetitive Transcranial Magnetic Stimulation (rTMS) in Treating Epilepsy

How to Cite This Article: Noohi S, Amirsalari S. History, Studies and Specific Uses of Repetitive Transcranial Magnetic Stimulation (rTMS) in Treating Epilepsy. Iran J Child Neurol. Winter 2016; 10(1):1-8. AbstractObjectiveIn this study, repetitive Transcranial Magnetic Stimulation (rTMS) and its specific use for treating epilepsy were carefully scrutinized. Materials & MethodsTarget researches such as review articles, case reports, books and theses, which had to do with therapeutic method of rTMS were surveyed. It is worth mentioning that until the final stages, the search for records and documents related to rTMS went on and in the end, the collected data underwent a qualitative analysis. ResultsAs the literature review suggests, TMS principally applies electromagnetic induction to generate an electric current inside the brain without physical contact. The therapeutic uses of rTMS are for a wide range of mental disorders, namely epilepsy, chronic pains, motor disorders and so on. ConclusionDespite safety concerns and possible side effects, many researchers subscribe to rTMS and see a bright future for it

Thyroid Function Test Imbalance in Epileptic Children Under Anticonvulsive Therapy

How to Cite this Article: Ravi Torkaman M, Amirsalari S, Saburi A. Thyroid Function Test Imbalance in Epileptic ChildrenUnder Anticonvulsive Therapy. Iranian Journal of Child Neurology 2012;6(1):43-44. Dear Editor,There have been many studies regarding the impact of antiepileptic drugs(AEDs) on thyroid function. There are some challenging scopes which must beconsidered for conducting the study adressing the focused question. “Which oneof the thyroid hormones is related to the AEDs consumption?”. Some studiesdemonstrated that there may be alterations in all thyroid function tests (T3, T4 andTSH) after antiepileptic therapy in children (1). Some studies concluded that longtermprescription of anticonvulsive medications resulted in a decline in serum T4levels, although it had no effect on serum TSH levels. However, changes in serumT3 level was challenging and it must be investigated further (2).There were some confounding factors which may interfere with the conclusion.One of them is the type of the study. There are various study plans for this purposesuch as cross-sectional, case-control, experimental, self-controlled cohort anddouble-blind randomized clinical trial studies. It seems that the proper protocol ofstudy for this propose is a double-blind randomized clinical trial study. By usingother designs, the authors cannot interpret the effect of AEDs on thyroid function;however, they can discuss the prevalence of thyroid hormone imbalance and thecoordination among T3, T4 and TSH.Moreover, one of the confounding factors is the thyroid binding globulin (TBG)effect. It has appeared that some of the AEDs may change the amount of TBGand in this way may affect the amount of thyroid hormones (3). Clonazepamand valproic acid do not have any enzyme inducing effects, but phenobarbital,carbamazepine, phenytoin and primidone may induce the hepatic enzyme (4-6). Therefore, it seems necessary to analyze each group of patients based on thetype of drug which is prescribed and also by using the free amount of thyroidhormones, the researcher will be able to exclude the TBG effect. In addition, ageis an important factor which should be considered. The epileptic patients showextra-thyroid adverse effects such as vitamin D and bone metabolism disordersdue to antiepileptic drugs (7). Other secondary clinical disorders which interactwith the thyroid metabolism should be considered and overruled in the study withthe mentioned proposal, especially in the older population.It appears that the confounding effect of the duration of AED intake mustbe adjusted regarding the children’s age using multivariate analysis such asregression model or partial correlation test. The etiological mechanism of serumconcentrations of thyroid hormone change by AEDs has not been clarified clearlyand besides, patients with a personal or family history of thyroid disorders mayprogress to overt thyroid hormone imbalance secondary to AED consumption (6). Therefore, it is suggested that the pure etiologicalmechanism of thyroid disorders due to AEDs shouldbe studied in such cases. Previous reports suggestedthat return to normal of all parameters was observedafter withdrawal of anticonvulsive therapy and thisreversibility of the thyroid hormone imbalance may bea clue for further investigations in order to study thepatho-physiologic mechanism of this disorder (6).Recently, new pharmaceutical drugs have beensuccessfully used for epileptic patients. It is expectedthat the therapeutic role of these new medications willbecome more prominent in these patients in the futureand future studies should be focused on their adverseeffects.Disclosures: None. References: 1. Talebian A, Eslamian MR, Shiasi K, Moravveji A,Khodayari M, Abedi AR. Changing in thyroid functiontest in children underwent antiepileptic therapy. Iran JChild Neurol 2010;4(1):17-22.2. Mahyar A, Ayazi P, Dalirani R, Hosseini SM, DaneshiKohan MM. Serum thyroid hormone levels in epilepticchildren receiving ant-convulsive drugs. Iran J ChildNeurol 2011;5(4):21-4.3. Eirís-Puñal J, Del Río-Garma M, Del Río-Garma MC,Lojo-Rocamonde S, Novo-Rodríguez I, Castro-GagoM. Long-term treatment of children with epilepsy withvalproate or carbamazepine may cause subclinicalhypothyroidism. Epilepsia 1999;40(12):1761-6.4. Kirimi E, Karasalihoglu S, Boz A. Thyroid functions inchildren under long-term administration of antiepilepticdrugs. Eastern J Med 1999;4(1):23-6.5. Amirsalari S, Kayhanidost ZT, Kavemanesh Z, Torkman M, Beiraghdar F, Teimoori M, et al. Thyroid functionin epileptic children who receive carbamazepine,primidone, phenobarbital and valproic acid. Iranian JChild Neurol 2011;5(2):15-20.6. Verrotti A, Di corcia G, Trotta D, Chiarelli F. Thyroidfunction in children treated with antiepilepticdrugs: effects of treatment withdrawal. Ital J Pediatr 2003;29:242-6.7. Pack AM, Morrell MJ, McMahon DJ, Shane E. Normal vitamin D and low free estradiol levels in women onenzyme-inducing antiepileptic drugs. Epilepsy Behav 2011;21(4):453-8

Computerized cognitive training for improving cochlear-implanted children's working memory and language skills

Abstract Sensory deprivation, including hearing loss, can affect different aspects of a person’s life. Studies on children with hearing impairment have shown that such patients, especially those with cochlear implants (CIs), suffer from cognitive impairments, such as working memory problems and poor language skills. The present study aimed to examine the efficacy of cognitive computer training in improving working memory and language skills in children with a CI.This research was a quasi-experimental study with a pre-test-post-test design and a control group. Fifty-one children with a CI aged 6-12 years were recruited through convenience sampling and randomly assigned to the control and treatment groups. The Wechsler Working Memory Subtest and the Test of Language Development (TOLD) were used to evaluate children’s working memory and language skills pre- and post-treatment. The treatment group attended twenty 50-60-minute cognitive computer training sessions three times a week.Sina-Working Memory Training was used to provide the treatment group with working memory training, whereas no intervention was provided to the control group. Univariate and multivariate analysesof covariance were used to analyze data.The results demonstrated the efficacy of cognitive computer training in improving the performance of cochlear-implanted children’s working memory (auditory and visual-spatial) (P < 0.01). The results also pointed to improved performance in sentence imitation (P < 0.01), word discrimination (P < 0.01), and phonemic analysissubtests (P < 0.01).Overall, the findings indicated that cognitive computer training might improve working memory and language skills for children with CI. Therefore, the development and execution of such programs for children with CIs seem to improve their cognitive functions, such as working memory and language skills

Effectiveness of Neurogenesis in treating Children with Cerebral Palsy

How to Cite this Article: Amirsalary S, Dehghan L, Dalvand H, Haghgoo H. Effectiveness of Neurogenesis in treating children with Cerebral Palsy. Iran J Child Neurol 2012;6(2):1-8. objectiveTissue-specific stem cells divide to generate different cell types for the purpose oftissue repair in the adult. The aim of this study was to detect the significance ofneurogenesis in the central nervous system in patients with cerebral palsy (CP).Materials & MethodsA search was made in Medline, CINAHL, PubMed, ISI Web of Science andGoogle Scholar from 1995 to February 2011. The outcomes measured in thereview were classified to origins, proliferation, and migration of new neurons,and neurogenesis in CP.ResultsAccording to the review of articles, neurogenesis persists in specific brainregions throughout lifetime and can be enhanced from endogenous progenitorcells residing in the subventricular zone by growth factors or neurotrophicfactors and rehabilitation program.ConclusionMost of the studies have been conducted in the laboratory and on animals,more work is required at the basic level of stem cell biology, in the developmentof human models, and finally in well-conceived clinical trials. References1. Buonomano DV, Merzenich MM. Cortical plasticity: from synapses to maps. Annu Rev Neurosci 1998; 21:149-86.2. Haghgoo H. Fundemental of neurosciences. 1st ed. Tehran; USWR Press; 2011.3. Payne BR, Lomber SG. Reconstructing functional systems after lesions of cerebral cortex. Nat Rev Neurosci 2001 Dec;2(12):911-9.4. Bax M, Goldstein M, Rosenbaum P, Leviton A, Paneth N, Dan B, et al. Proposed definition and classification of cerebral palsy. Dev Med Child Neurol 2005 Apr;47(8):571-6.5. Joghataei M, Kazem M. Barresi sathe niazhaie jamee be khadamate behzisti colle keshvar [persian].Tehran: University of. Social Welfare and Rehabilitation Sciences; 1990.6. Johnson A. Prevalence and characteristics of children with cerebral palsy in Europe. Dev Med Child Neurol 2002 Sep;44(9):633-40.7. Yeargin-Allsopp M, Van Naarden Braun K, Doernberg NS, Benedict RE, Kirby RS, Durkin MS. Prevalence of cerebral palsy in 8-year-old children in three areas of the United States in 2002: a multisite collaboration. Pediatrics 2008 Mar;121(3):547-54.8. Uvebrant P. Hemiplegic cerebral palsy. Aetiology and outcome. Acta Paediatr Scand Suppl 1988;345:1-100.9. Marin-Padilla M. Developmental neuropathology and impact of perinatal brain damage. II: white matter lesions of the neocortex. J Neuropathol Exp Neurol 1997 Mar;56(3):219-35.10. Tzarouchi LC, Astrakas LG, Zikou A, Xydis V, Kosta P, Andronikou S, et al. Periventricular leukomalacia in preterm children: assessment of grey and white matter and cerebrospinal fluid changes by MRI. Pediatr Radiol 2009 Dec;39(12):1327-32.11. Dehghan L, Dalvand H. Neuroplasticity after stroke [persian]. Modern rehabilitation 2008;1(4).12. Sanai N, Tramontin AD, Quiñones-Hinojosa A, Barbaro NM, Gupta N, Kunwar S, et al. Unique astrocyte ribbon in adult human brain contains neural stem cells but lacks chain migration. Nature 2004 Feb;427(6976):740-4.13. Doetsch F, Garcia-Verdugo JM, Alvarez-Buylla A. Cellular composition and three-dimensional organization of the subventricular germinal zone in the adult mammalian brain. J Neurosci 1997 Jul 1;17(13):5046-61.14. Laywell ED, Rakic P, Kukekov VG, Holland EC, Steindler DA. Identification of a multipotent astrocytic stem cell in the immature and adult mouse brain. Proc Natl Acad Sci U S A 2000 Dec 5;97(25):13883-8.15. Seri B, Garcia-Verdugo JM, McEwen BS, AlvarezBuylla A. Astrocytes give rise to new neurons in the adult mammalian hippocampus. J Neurosci 2001 Sep 15;21(18):7153-60.16. Seri B, Garcia-Verdugo JM, Collado-Morente L, McEwen BS, Alvarez-Buylla A. Cell types, lineage, and architecture of the germinal zone in the adult dentate gyrus. J Comp Neurol 2004 Oct 25;478(4):359-78.17. Sugiura S, Kitagawa K, Tanaka S, Todo K, OmuraMatsuoka E, Sasaki T, et al. Adenovirus-mediated gene transfer of heparin-binding epidermal growth factor-like growth factor enhances neurogenesis and angiogenesis after focal cerebral ischemia in rats. Stroke 2005 Apr;36(4):859-64.18. Ellsworth JL, Garcia R, Yu J, Kindy MS. Fibroblast growth factor-18 reduced infarct volumes and behavioral deficits after transient occlusion of the middle cerebral artery in rats. Stroke 2003 Jun;34(6):1507-12.19. Wada K, Sugimori H, Bhide PG, Moskowitz MA, Finklestein SP. Effect of basic fibroblast growth factor treatment on brain progenitor cells after permanent focal ischemia in rats. Stroke 2003 Nov;34(11):2722-8.20. Baldauf K, Reymann KG. Influence of EGF/bFGF treatment on proliferation, early neurogenesis and infarct volume after transient focal ischemia. Brain Res 2005 Sep 21;1056(2):158-67.21. Chmielnicki E, Benraiss A, Economides AN, Goldman SA. Adenovirally expressed noggin and brain-derived neurotrophic factor cooperate to induce new medium spiny neurons from resident progenitor cells in the adult striatal ventricular zone. J Neurosci 2004 Mar 3;24(9):2133-42.22. Cho SR, Benraiss A, Chmielnicki E, Samdani A, Economides A, Goldman SA. Induction of neostriatal neurogenesis slows disease progression in a transgenic murine model of Huntington disease. J Clin Invest 2007 Oct;117(10):2889-902.23. Gonzalez-Perez O, Jauregui-Huerta F, GalvezContreras AY. Immune system modulates the function of adult neural stem cells. Curr Immunol Rev 2010 Aug 1;6(3):167-73.24. Doetsch F, Alvarez-Buylla A. Network of tangential pathways for neuronal migration in adult mammalian brain. Proc Natl Acad Sci 1996 Dec 10;93(25):14895-900.25. Weickert CS, Webster MJ, Colvin SM, Herman MM, Hyde TM, Weinberger DR, et al. Localization of epidermal growth factor receptors and putative neuroblasts in human subependymal zone. J Comp Neurol 2000 Jul 31;423(3):359-72.26. Magavi SS, Leavitt BR, Macklis JD. Induction of neurogenesis in the neocortex of adult mice. Nature 2000 Jun 22;405(6789):951-5.27. Lois C, Garcia-Verdugo JM, Alvarez-Buylla A. Chain migration of neuronal precursors. Science. 1996 Feb 16;271(5251):978-81.28. Wichterle H, Garcia-Verdugo JM, Alvarez-Buylla A. Direct evidence for homotypic, glia-independent neuronal migration. Neuron 1997 May;18(5):779-91.29. Lois C, Alvarez-Buylla A. Long-distance neuronal migration in the adult mammalian brain. Science 1994 May 20;264(5162):1145-8.30. Mason HA, Ito S, Corfas G. Extracellular signals that regulate the tangential migration of olfactory bulb neuronal precursors: inducers, inhibitors, and repellents. J Neurosci 2001 Oct 1;21(19):7654-63.31. Lundy-Ekman L. Neuroscience: fundamentals for rehabilitation. 3rd ed. Philadelphia: WB Saunders; 2007.32. Mizuno K, Hida H, Masuda T, Nishino H, Togari H. Pretreatment with low doses of erythropoietin ameliorates brain damage in periventricular leukomalacia by targeting late oligodendrocyte progenitors: a rat model. Neonatology 2008;94(4):255-66.33. Lin S, Fan LW, Pang Y, Rhodes PG, Mitchell HJ, Cai Z. IGF-1 protects oligodendrocyte progenitor cells and improves neurological functions following cerebral hypoxia-ischemia in the neonatal rat. Brain Res 2005 Nov 23;1063(1):15-26.34. Gonzalez FF, Abel R, Almli CR, Mu D, Wendland M, Ferriero DM. Erythropoietin sustains cognitive function and brain volume after neonatal stroke. Dev Neurosci 2009;31(5):403-11.35. Goldman SA. Adult neurogenesis: from canaries to the clinic. J Neurobiol 1998 Aug;36(2):267-86.36. Tureyen K, Vemuganti R, Bowen KK, Sailor KA, Dempsey RJ. EGF and FGF-2 infusion increases post ischemic neural progenitor cell proliferation in the adult rat brain. Neurosurgery 2005 Dec;57(6):1254-63; discussion -63.37. Im SH, Yu JH, Park ES, Lee JE, Kim HO, Park KI, et al. Induction of striatal neurogenesis enhances functional recovery in an adult animal model of neonatal hypoxic-ischemic brain injury. Neuroscience 2010 Aug 11;169(1):259-68.38. Greenough WT, Black JE, Wallace CS. Experience and brain development. Child Dev 1987 Jun;58(3):539-59.39. Daadi MM, Davis AS, Arac A, Li Z, Maag AL, Bhatnagar R, et al. Human neural stem cell grafts modify microglial response and enhance axonal sprouting in neonatal hypoxic-ischemic brain injury. Stroke 2010 Mar;41(3):516-23.40. Lee JA, Kim BI, Jo CH, Choi CW, Kim EK, Kim HS, et al. Mesenchymal stem-cell transplantation for hypoxic-ischemic brain injury in neonatal rat model. Pediatr Res 2010 Jan;67(1):42-6.41. Yasuhara T, Matsukawa N, Yu G, Xu L, Mays RW, Kovach J, et al. Behavioral and histological characterization of intrahippocampal grafts of human bone marrow-derived multipotent progenitor cells in neonatal rats with hypoxic-ischemic injury. Cell Transplant 2006;15(3):231-8.42. van Velthoven CT, Kavelaars A, van Bel F, Heijnen CJ. Repeated mesenchymal stem cell treatment after neonatal hypoxia-ischemia has distinct effects on formation and maturation of new neurons and oligodendrocytes leading to restoration of damage, corticospinal motor tract activity, and sensorimotor function. J Neurosci 2010 Jul 14;30(28):9603-11.43. Chopp M, Li Y, Zhang ZG. Mechanisms underlying improved recovery of neurological function after stroke in the rodent after treatment with neurorestorative cellbased therapies. Stroke 2009 Mar;40(3 Suppl):S143-5.44. Buhnemann C, Scholz A, Bernreuther C, Malik CY, Braun H, Schachner M, et al. Neuronal differentiation of transplanted embryonic stem cell-derived precursors in stroke lesions of adult rats. Brain 2006 Dec;129(Pt 12):3238-48.45. Daadi MM, Lee SH, Arac A, Grueter BA, Bhatnagar R, Maag AL, et al. Functional engraftment of the medial ganglionic eminence cells in experimental stroke model. Cell Transplant 2009;18(7):815-26.46. van Velthoven CT, Kavelaars A, van Bel F, Heijnen CJ. Regeneration of the ischemic brain by engineered stem cells: fuelling endogenous repair processes. Brain Res Rev 2009 Jun;61(1):1-13.47. Qu R, Li Y, Gao Q, Shen L, Zhang J, Liu Z, et al. Neurotrophic and growth factor gene expression profiling of mouse bone marrow stromal cells induced by ischemic brain extracts. Neuropathology 2007 Aug;27(4):355-63.48. Li Y, Chopp M. Marrow stromal cell transplantation in stroke and traumatic brain injury. Neuroscience Letters 2009; 456 (3): 120-123

Neurobrucellosis Presenting with Unilateral Abducens Nerve Palsy

How to Cite This Article: Andisheh M, Amirsalari S, Torkaman M, Sabzechian M, Afsharpaiman Sh. Neurobrucellosis Presenting with Unilateral Abducens Nerve Palsy. Iran J Child Neurol. Spring 2017; 11(2):61-64. AbstractOne of the rare complications of brucellosis is neurobrucellosis. There have been numerous reports showing clinical forms of brucellosis affecting CNS, such as cranial nerve involvement, myelitis, vascular disease, radiculoneuritis, meningitis, meningoencephalitis, and demyelinating disease. In this case report, we introduce a 2.5 yr old girl with unilateral abducens nerve palsy referred to Baghiyatallah Hospital Outpatient Clinic, Tehran, Iran in June 2015. References 1. Pappas G, Akritidis N, Bosilkovski M, Tsianos E. Brucellosis. N Engl J Med 2005; 352:2325–2336.2. Al-Sous MW, Bohlega S, Al-Kawi MZ, Alwatban J, McLean DR. Neurobrucellosis: clinical and neuroimaging correlation. AJNR Am J Neuroradiol 2004; 25:395–4013.Bingöl A, TogayIsikay C. Neurobrucellosis as an exceptional cause of transient ischemic attacks. Eur J Neurol 2006; 13:544–548.4.Adaletli I, Albayram S, Gurses B, et al. Vasculopathic changes in the cerebral arterial system with neurobrucellosis. Am J Neuroradiol 2006; 27:384–386.5.Shakir RA, Al-Din AS, Araj GF, Lulu AR, Mousa AR, Saadah MA. Clinical categories of neurobrucellosis. A report on 19 cases. Brain 1987; 110:213–223.6.Esra Özkavukcu, Zeynep Tuncay, Ferda Selçuk, İlhan Erden: An unusual case of neurobrucellosis presenting with unilateral abducens nerve palsy: clinical and MRI findings; Turkish Society of Radiology 20097. Tena D, Gonzáles-Praetorius A, LópezAlonso A, Peña JL, Pérez-Pomata MT, Bisquert J. Acute meningitis due to Brucella spp. Eur J Pediatr 2006; 165:726–727.8. Rangel Guerra R, Martinez HR, Leon Flores L. Neurobrucellosis. Report of five cases and literature review. Rev Inwest Clin 1982;34:62–8.9. Mugerwa RD, D’Arbela PG. Brucella meningitis; a case report and review of the literature. East African Med J 1976;53:266–9.10. Bashir R, Al-Kawi MZ, Harder EJ, Jinkins J. Nervous system brucellosis: diagnosis and treatment. Neurology 1985; 35:1576–1581.11. Al Deeb SM, Yaqub BA, Sharif HS, Phadge JG. Neurobrucellosis: clinical characteristics, diagnosis, and outcome. Neurology 1989; 39:498–501.12. Lubani MM, Dudin KI, Araj GF, Manandhar DS, Rashid FY. Neurobrucellosis in children. Pediatr Infect Dis J 1989;8:79–82.13. Santini C, Baiocchi P, Berardelli A, Venditti M, Serra P. A case of brain abscess due to Brucella melitensis. Clin Infect Dis 1994;19:977–8.14. Koussa S, Chemaly R. Neurobrucellosis presenting with diffuse cerebral white matter lesions. Eur Neurol 2003; 50:121–123.15. Fincham RW, Sahs AL, Joynt RJ. Protean manifestation of nervous system brucellosis. Case histories and a wide variety of clinical forms. JAMA 1963; 184:269–27516. Marconi G. Su un caso di sclerosis multipla acuta insorta dopo un’infezione da Brucella abortus. Riv Patol Nerv Ment 1966; 87:548–565.17. Bussone G, La Mantia L, Grazzi L, Lamperti E, Salmaggi A, Strada L. Neurobrucellosis mimicking multiple sclerosis: a case report. Eur Neurol 1989; 29:238–240.18. KarakurumGöksel B, Yerdelen D, Karataş M, et al. Abducens nerve palsy and optic neuritis as initial manifestation in brucellosis. Scand J Infect Dis 2006; 38:721–725.19. Yilmaz M, Ozaras R, Mert A, Ozturk R, Tabak F. Abducent nerve palsy during treatment of brucellosis. Clin Neurol Neurosurg 2003; 105:218–220

Risk Factors and Prognosis of Epilepsy in Children with Hemiparetic Cerebral Palsy

ObjectiveEpilepsy is reported in 15-90% of the children with Cerebral Palsy (CP) but its clinical course is not well defined.We conducted a retrospective study on children with hemiparetic CP who were referred to Pediatric Neurology Department of Mofid Hospital. The aim of our study was to evaluate the risk factors and prognosis of epilepsy in children with hemiparetic CP.Materials & MethodsWe evaluated 64 children with hemiparetic CP who were referred to Pediatric Neurology Department of Mofid Hospital between 2006 and 2008.According to our protocol, patients were divided into two groups: 34 children in the case group (hemiparetic patients with epilepsy) and 30 children in the control group (hemiparetic patients without epilepsy).ResultsPrenatal, perinatal and postnatal events, maternal age at the time of delivery, socioeconomic status of the family, familial history of epilepsy, neuroimaging findings, side of the hemiparesia and age at diagnosis of hemiparesis were not considered as risk factors for epilepsy in hemiparetic children, but microcephaly, severity of hemiparetic CP and mental retardation were significantly associated with an increased risk of epilepsy in children with hemiparetic CP.ConclusionOur study showed that microcephaly, severity of hemiparesis and mental retardation were risk factors for developing epilepsy in children with hemiparetic CP; furthermore, they had negative effects on rehabilitation outcome in these patients.

Long term video-EEG monitoring findings in children and adolescents with intractable epilepsy

Introduction:   In spite of appropriate management, seizures are not controlled in10 to 20 percent of epileptic children. If we can find the epileptogenic focus and resect it by surgery, patient may be cured from refractory seizures. Long Term Video-EEG Monitoring (LTM) may give us important information in the preoperative assessment of these patients. We performed this study for the first time in pediatric age group in Iran.Materials and Methods: In this cross-sectional study, 43 children between 4 to 18 years, with intractable epilepsy who were Referred to Shefa Neuroscience Research Center between 1386_1391, were enrolled to study in order to evaluate their long-term video EEG findings.Results: Forty-three children were enrolled to this study with mean age of 10.07 years, that 24(65.9%) were boys and 19(44.1%) were girls.Seven patients with definite epileptogenic zone were advised to perform lesionectomy surgery, in 2 patients there was not any seizure onset focus but corpus callosotomy was advised to control their frequent falling. Eight cases were recommended to perform Electrocorticography or invasive EEG monitoring. Twenty-six cases were recommended to adjust medical treatment. In 3 cases there was not any electrical seizure activity during clinical attacks, so discontinuing anti-epileptic drugs were recommended with diagnosis of conditions that mimic epilepsy.Conclusions:   It is necessary to perform LTM in patients with refractory epilepsy in order to determine their treatment strategy. If there is any doubt about pseudoseizure LTM can help to differentiate epilepsy from conditions that mimic epilepsy

Relationship between Iron Deficiency Anemia and Febrile Seizures

ObjectiveFebrile seizure is the most common convulsive disorder in childhood. The role of iron in metabolism of neurotransmitters and carrying oxygen to the brain suggests the possibility of a relationship between iron deficiency anemia and febrile seizures.The aim of this study was to investigate the relationship between iron deficiency anemia and febrile seizures.Materials & MethodsThis case - control study was performed on 132 cases and 88 controls, aged 9 months to 5 years, from July 2007 to June 2009 in Baqyiatallah Hospital. Patients were selected using simple random sampling. The case group included children with first febrile seizure (core temperature over 38.5˚C during  seizure) without a central nervous system infection or an acute brain insult. The control group included children suffering from a febrile illness without seizure. Iron deficiency anemia was defined with one of these laboratory indexes: 1) Hemoglobin (Hb) <10.5mg/dl 2) Plasma ferritin <12ng/dl 3) Mean corpuscular volume (MCV) <70  fl. The data collected from patients were analyzed with SPSS.13 software.ResultsLow plasma ferritin was found in 35 cases (26.5%) compared to 26 controls (29.5%), low Hb level was found in 4 cases (3%) compared to 6 controls (6.8%) and low MCV was found in 5 cases (3.8%) compared to 6 controls (6.8%).There was no significant difference in plasma ferritin , Hb level and MCV indices between the two group.ConclusionConsidering the above-mentioned results, there is no relationship between iron deficiency anemia and febrile seizures

Prevalence of Epileptiform Discharges in Children with Sensori-Neural Hearing Loss and Behavioral Problems Compared to Their Normal Hearing Peers

How to Cite This Article: Amirsalari S, Radfar Sh, Ajallouyean M, Saburi A, Yousefi J, Noohi S, Tavallaie SA, Hassanalifard M, Ghazavi Y. Prevalence of Epileptiform Discharges in Children with Sensori-Neural Hearing Loss and Behavioral Problems Compared to Their Normal Hearing Peers. Iran J Child Neurol. 2014 Spring 8(2):29-33.ObjectiveOveractivity and behavioral problems are common problems in children with prelingually profound sensorineural hearing loss (SNHL). Data on epileptiform electroencephalography (EEG) discharges in deaf children with psychologicaldisorders are so limited. The primary focus of this study was to determine the prevalence of epileptiform discharges (EDs) in children with SNHL and overactivity or behavioral problems.Materials & MethodsA total of 262 patients with prelingually profound SNHL who were referred to our cochlear implantation center between 2008 and 2010 were enrolled in this study. Children with SNHL who had diagnosis of overactivity and/or behavioralproblems by a pediatric psychiatrist, underwent electroencephalography (EEG).EEG analysis was carried out by a board-certified pediatric neurologist. The control group consisted of 45 cases with overactivity or behavioral problems and normal hearing.ResultsOne hundred thirty-eight children with mean age of 3.5±1.23 year were enrolled in the case group, of whom 88 cases (63.7%) were boy. The control group consisted of 45 cases with mean age of 3.2±1.53 years, of whom 30 (66.6%)cases were male. EDs were detected in 28 (20.02%) children of the case group (with SNHL) in comparison with 4 (8.88%) in the control group (without SNHL), which was statistically significantly different.ConclusionIn this study, we obtained higher frequency of EDs in deaf children with overactivity and/or behavioral problem compared to the children without SNHL. Further studies are required to evaluate the possible association of SNHL withEDs in overactive children.References1. Matsuura M, Okubo Y, Toru M, Kojima T, He Y, Hou Y, et al. A cross-national EEG study of children with emotional and behavioral problems: a WHO collaborative study in the Western Pacific Region. Biol Psychiatry 1993;34(1-2):59-65.2. Hindley P, Kroll L. Theoretical and epidemiological aspects of attention deficit and overactivity in deaf children. J Deaf Stud Deaf Educ 1998;3(1):64-72.3. [No author listed] . Clinical practice guideline: diagnosis and evaluation of the child with attentiondeficit/ hyperactivity disorder. American Academy of Pediatrics. Pediatrics 2000;105(5):1158-70.4. Klinkerfuss GH, Lange PH, Weinberg WA, O’Leary JL. Electroencephalographic abnormalities of children with hyperkinetic behavior. Neurology 1965;15(10):883-91.5. Millichap JJ, Stack CV, Millichap JG. Frequency of epileptiform discharges in the sleep-deprived electroencephalogram in children evaluated for attention-deficit disorders. J Child Neurol 2011;26(1):6-11.6. Fonseca LC, Tedrus GM, Moraes C, Vicente Machado A, Almeida MP, Oliveira DO. Epileptiform abnormalities and quantitative EEG in children with attentiondeficit/ hyperactivity disorder. Arq Neuropsiquiatr 2008;66(3A):462-7.7. Venkatesh C, Ravikumar T, Andal A, Virudhagirinathan BS. Attention - deficit/Hyperactivity Disorder in Children: Clinical Profile and Co-morbidity. Indian J Psychol Med 2012 ;34(1):34-8.8. Monastra VJ, Lubar JF, Linden M. The development of a quantitative electroencephalographic scanning process for attention deficit-hyperactivity disorder: reliability and validity studies. Neuropsychology 2001;15(1):136-44.9. Monastra VJ, Lubar JF, Linden M, VanDeusen P, Green G, Wing W, et al. Assessing attention deficit hyperactivity disorder via quantitative electroencephalography: an initial validation study. Neuropsychology 1999; 13(3):424-33.10. Barry RJ, Johnstone SJ, Clarke AR. A review of electrophysiology in attention-deficit/hyperactivity disorder: II. Event-related potentials. Clin Neurophysiol 2003;114(2):184-98.11. Magee CA, Clarke AR, Barry RJ, McCarthy R, Selikowitz M. Examining the diagnostic utility of EEG power measures in children with attention deficit/hyperactivity disorder. Clin Neurophysiol 2005;116(5):1033-40.12. Loo SK, Barkley RA. Clinical utility of EEG in attention deficit hyperactivity disorder. Appl Neuropsychol 2005;12(2):64-76.13. Venkateswaran S, Shevell M. The case against routine electroencephalography in specific language impairment. Pediatrics 2008;122(4):e911-6.14. Amirsalari S, Ajallouyean M, Saburi A, Haddadi Fard A, Abed M, Ghazavi Y. Cochlear implantation outcomes in children with Waardenburg syndrome. Eur Arch Otorhinolaryngol 2012; 269(10):2179-83.15. Amirsalari S, Yousefi J, Radfar S, Saburi A, Tavallaie SA, Hosseini MJ, et al. Cochlear implant outcomes in children with motor developmental delay. Int J Pediatr Otorhinolaryngol 2012;76(1):100-3.16. Holtmann M, Becker K, Kentner-Figura B, Schmidt MH. Increased frequency of rolandic spikes in ADHD children. Epilepsia 2003;44(9):1241-4.17. Richer LP, Shevell MI, Rosenblatt BR. Epileptiform abnormalities in children with attention-deficithyperactivity disorder. Pediatr Neurol 2002;26(2):125-9.18. Socanski D, Herigstad A, Thomsen PH, Dag A, Larsen TK. Epileptiform abnormalities in children diagnosed with attention deficit/hyperactivity disorder. Epilepsy Behav 2010;19(3):483-6.19. Fonseca LC, Tedrus GM. [Somatosensory evoked spikes and epileptiform activity in “normal” children]. Arq Neuropsiquiatr 2003;61(3B):793-5. [Article in Portuguese]20. Borusiak P, Zilbauer M, Jenke AC. Prevalence of epileptiform discharges in healthy children--new data from a prospective study using digital EEG. Epilepsia 2010;51(7):1185-8.21. Daneshi A, Hassanzadeh S. Cochlear implantation in prelingually deaf persons with additional disability. J Laryngol Otol 2007;121(7):635-8.22. Dye MW, Bavelier D. Attentional enhancements and deficits in deaf populations: an integrative review. Restor Neurol Neurosci 2010;28(2):181-92.

The effect of probiotics on reducing hospitalization duration in infants with hyperbilirubinemia

peer reviewedBackground: Approximately 60% of term and 80% of premature infants are hospitalized for hyperbilirubinemia in the first week of life. Hyperbilirubinemia is the most common cause of infant hospitalization and readmission. Due to the high frequency of hyperbilirubinemia in infants and the high costs of treatment, it is necessary to find a way to decrease hospitalization duration. Objectives: The aim of this study is to assess the adjunctive effect of probiotics on decreasing hospitalization time for infants with hyperbilirubinemia. Methods: In this randomized, controlled clinical trial, 92 term infants with hyperbilirubinemia who met the inclusion criteria were randomly assigned to either the probiotic or control group. Patients in both groups underwent common phototherapy. Once a day, those in the probiotic group were also given half of a capsule of Prokid probiotic, while those in the control group received half of a placebo capsule. The duration of phototherapy and hospitalization, the blood groups of mothers and infants, and each patient’s bilirubin levels before and after phototherapy, direct Coombs test results, and levels of hemoglobin, G6PD, and reticulocytes were recorded. Results: Data from 92 patients with a mean age of 5.25 ± 2.35 days underwent analysis. The control group had 47 (51.1%) patients with a mean age of 5.19 ± 2.51 days and the probiotic group had 45 (48.9%) patients with a mean age of 5.31 ± 2.19 days (P = 0.81). The 92 patients had a mean bilirubin level of 16.70 ± 3.07 mg/dL, with a mean of 16.42 ± 3.53 mg/dL in the control group and 17.00 2.49 mg/dL in the probiotic group (P = 0.37). The duration of hospitalization averaged 3.34 ± 0.70 days overall, with an average of 3.55 ± 0.74 days for the control group and 3.13 ± 0.70 days for the probiotic group. The probiotic group had a significantly lower hospitalization stay in comparison to the control group (P = 0.004). Conclusions: Our findings suggest that probiotics may be beneficial as an adjunct treatment for infants with hyperbilirubinemia by reducing the duration of hospitalization