Iranian Journal of Child Neurology

How to Cite this Article: Mohammadi MR, Salmanian M, Akhondzadeh Sh. Autism Spectrum Disorders in Iran. Iranian Journal of Child Neurology2011;5(4):1-9.ObjectiveAutistic disorder, Asperger syndrome, and PDD-Not Otherwise Specified are subsets of autism spectrum disorders (ASDs), which are characterized by impairments in social communication and stereotyped behavior. This article reviews the prevalence, etiology, diagnosis, and treatment of ASDs in Iran.Materials & MethodsWe searched PubMed, ISI Web of Science, and 4 Iranian databases (IranPsych,IranMedex, Irandoc and Scientific Information Database (SID) to find Iranian studies on  ASDs. The results of 39 investigations, comprising original, review and editorial articles; proceedings; and available dissertations were categorized by prevalence, etiology, diagnosis, and treatment.ConclusionSeveral preliminary investigations have been done to evaluate the prevalence of ASDs, and risk factors and effective variables have been studied with regard to etiology. The diagnostic evaluation of ASDs, especially based on EEG, and several pharmacological and behavioral interventions for ASD have been implemented in Iran. Mental health, stress levels, and personality characteristics were examined in the parents of children with ASDs, which were focused on mothers.References

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How to Cite this Article: Shiva S, Barzegar M, Zokaie N, Shiva Sh. Dose Supplemental Zinc Prevents Recurrence of Febrile Seizures? Iranian Journal ofChild Neurology 2011;5(4):11-14.

Objective

Febrile seizures (FS) are the most common form of seizures in children. Previous studies have suggested that zinc may play a role in the prevention of FS. However, there is limited information on the preventative effects of zinc against FS. This study aimed to determine whether prescribing zinc supplements could prevent FS.

Materials & Methods

In a randomized, placebo-controlled trial, 100 children who had experienced simple FS for the first time were recruited. Children in the case group (50 patients) were orally administered1mg/kg/day zinc sulfate for 1 year, and children in the control group (50 patients) received a placebo. Serum zinc levels in both the control and case groups were measured at the start and at the end of the study,and recurrent cases of FS were recorded.

Results

The case group consisted of 29 boys (58%) and 21 girls (42%) with a mean age of 2.06 ± 0.83, and the control group consisted of 31 boys (62%) and 19 girls (38%) with a mean age of 2.22 ± 1.04 years. An inverse relationship was found between febrile diseases and serum zinc levels. In other words, the occurrence of febrile diseases decreased with an increase in serum zinc levels.Eight children (16%) in the case group and 8 in the control group experienced recurrent FS within a year.

Conclusion

Supplemental doses of zinc (1mg/kg/day) reduced the rate of febrile illnesses,but did not prevent the recurrence of FS.

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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.

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How to Cite this Article: Mahyar A, Ayazi P, Dalirani R, Hosseini SM, Daneshi Kohan MM. Serum Thyroid Hormone Levels in Epileptic Children Receiving AnticonvulsiveDrugs. Iranian Journal of Child Neurology 2011;5(4):21-24.

Objective
The aim of this study was to investigate serum thyroid hormone levels in epileptic children receiving anticonvulsive drugs.
Materials & Methods
In this case- control study, 30 epileptic children who were receiving anticonvulsive drugs (case group) were compared with 30 healthy children (control group). This study was carried out in the Qazvin Children's Hospital (Qazvin, Iran) from October to December 2007. Both groups were matched for age and sex. Thyroid hormone levels were measured using a radioimmunoassay and immunoradiometric assay. Data were analyzed using Chi-square and Student's t-tests.
Results
The mean serum T3 and T4 levels in the case group were 2.36 ± 0.73 nmol/L and 95.96 ± 27.01 nmol/L, respectively, and the corresponding values in the control group were 1.88 ± 0.93 nmol/L and 147.46 ± 35.77 nmol/L, respectively. The mean serum thyroid-stimulating hormone (TSH) levels in the case and control groups were 2.73±0.73 mIU/mL and 2.49 ± 2.17mIU/mL, respectively.
Conclusion
This study revealed that long-term consumption of anticonvulsive drugs resulted in a decline in serum T4 levels and an increase in serum T3 levels, but had no effect on TSH levels.

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10. Schröder-van der Elst J, Van der Heide D, Van der BentC, Kaptein E, Visser T, DiStefano J. Effects of 5, 5 -diphenylhydantoin on the thyroid status in rats. Europeanjournal of endocrinology 1996;134(2):221.

11. Schonberger W, Grimm W, Schonberger G, SinterhaufK, Scheidt E, Ziegler R. [The influence of primidone onthyroid function (author’s transl)]. Dtsch Med Wochenschr1979;104(25):915-7.

12. Tiihonen M, Liewendahl K, Waltimo O, Ojala M,Valimaki M. Thyroid status of patients receiving longtermanticonvulsant therapy assessed by peripheralparameters: a placebo-controlled thyroxine therapy trial.Epilepsia 1995;36(11):1118-25.

13. Benedetti MS, Whomsley R, Baltes E, Tonner F. Alterationof thyroid hormone homeostasis by antiepileptic drugsin humans: involvement of glucuronosyltransferaseinduction. Eur J Clin Pharmacol 2005;61(12):863-72.

How to Cite this Article: Heidari MM, Khatami M, Houshmand M, Mahmoudi E, Nafissi Sh .Increased Prevalence 12308 A > G mutation in MitochondrialtRNALeu (CUN) Gene Associated with earlier Age of Onset in Friedreich Ataxia. Iranian Journal of Child Neurology 2011;5(4):25-31.Objective Friedreich ataxia (FRDA) is an inherited recessive disorder. Mitochondrial DNA is a candidate modifying factor for FRDA.The purpose of this study was to investigate the relationship between the tRNALeu (CUN) 12308 A> G mutation and age of onset in Friedreich ataxia.Materials & Methods The 12308 A> G substitution in mitochondrial tRNALeu (CUN) was examined in DNA samples from 30 Friedreich ataxia patients and 48 control subjects by temporal temperature gradient gel electrophoresis (TTGE) and sequencing. Logistic regression was used to determine of cutoff age of onset.ResultsTwenty-two patients had the 12308 A> G mutation, and we found that its overall prevalence was significantly higher in 20 patients aged 17 years or younger than in 2 patients aged over 17 years (90% versus 10%). The 12308 A> G mutation lies in a region that has been highly conserved between species.Conclusion Our results show that the 12308 A > G mutation is associated with earlier age of onset in Friedreich ataxia. Thus, this mutation might cause the younger age of onset in FRDA.

References

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How to Cite this Article: Asadi-Pooya AA, Emami M. Effects of Antiepileptic Drugs on Electroencephalographic Findings inPatients with Idiopathic Generalized Epilepsy. Iranian Journal of Child Neurology 2011;5(4):33-36.

Objective

Several antiepileptic drugs (AEDs) such as phenobarbital (Pb), carbamazepine (CBZ), and valproate (VPA) may suppress interictal epileptiform activity. We investigated the effects of AEDs on electroencephalography (EEG) data from patients with idiopathic generalized epilepsy (IGE).

Materials & Methods

In this cross-sectional study, all patients electroclinically diagnosed with IGE were recruited in the outpatient epilepsy clinic at Shiraz University of Medical Sciences from September 2008 through August 2010. A routine EEG was requested at the time of referral for all patients. Statistical analyses were performed using Chi square and Fisher’s exact test.

Results

This study comprised of 336 patients. For about 20.8% (70 patients) of them, the initial EEG appeared normal. The first EEG was normal in 14.2% of the patients who had newly diagnosed IGE (19 patients). Normal EEG was also detected for 27.6% of the patients who received VPA monotherapy (16 patients), 31% of the patients who received CBZ monotherapy (9 patients), 29.4% of the patients who received Pb monotherapy (5 patients), and 11.1% of the patients who received lamotrigine (LTG) (1 patient).

Conclusion

This study shows that compared to LTG, VPA suppresses generalized interictal epileptiform activity in patients with IGE more effectively. Theoretically, if a drug can frequently induce normalization of EEG, then it may be a better drug for treating IGEs.

References

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2. Libenson MH, Caravale B. Do antiepileptic drugs differin suppressing interictal epileptiform activity in children? Pediatr Neurol 2001;24(3):214-8.

3. Pro S, Vicenzini E, Pulitano P, Li Voti P, Zarabla A, Randi F, et al. Effects of levetiracetam on generalized discharges monitored with ambulatory EEG in epileptic patients. Seizure 2009;18(2):133-8.

4. Rocamora R, Wagner K, Schulze - Bonhage A. Levetiracetam reduces frequency and duration ofepileptic activity in patients with refractory primarygeneralized epilepsy. Seizure 2006;15(6):428-33.

5. Szaflarski JP. Effects of zonisamide on  the electroencephalogram of a patient with juvenile myoclonic epilepsy. Epilepsy Behav 2004;5(6):1024 -6.

6. Covanis A. Photo sensitivity in idiopathic generalized epilepsies. Epilepsia 2005;46(suppl 9):67-72.

7. Asadi-Pooya AA, Sperling M. Antiepileptic Drugs: AClinician’s Manual. Oxford University Press, USA; 2009.

How to Cite this Article: Ashrafi MR, Nikkhah A, Houshmand M, Aryani O. L-2-Hydroxyglutaric Aciduria is a Diagnostic Indicator of Leukodystrophy: A CaseReport Iranian Journal of Child Neurology 2011;5(4):37-38.

L-2-Hydroxyglutaric aciduria is a rare autosomal recessive inherited neurometabolic disorder.It is characterized by slow progressive neurological dysfunction with cerebellar ataxia, pyramidal and extrapyramidal signs, intellectual decline, and seizures. Herein, we report a case of a 7-year-old boy from Tehran whose symptoms and signs indicated leukoencephalopathy with macrocephaly and motor delay.

References

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3. Haliloglu G, Jobard F, Oguz KK, Anlar B, Akalan N, Coskun T, et al. L-2-hydroxyglutaric aciduria and brain tumors in children with mutations in the L2HGDH gene: neuroimaging findings. Neuropediatrics  2008;39(2):119-22.

4. De Klerk JB, Huijmans JG, Stroink H, Robben SG, Jakobs C, Duran M. L-2-hydroxyglutaric aciduria: clinical heterogeneity versus biochemical homogeneity in a sibship. Neuropediatrics 1997;28(6):314-7.

5. Fenichel GM. Clinical pediatric neurology: a signs and symptoms approach. Saunders:Elsevier, 2009.

6. Diogo L, Fineza I, Canha J, Borges L, Cardoso ML, Vilarinho L. Macrocephaly as the presenting feature of L-2-hydroxyglutaric aciduria in a 5-month-old boy. J Inherit Metab Dis 1996;19(3):369-70.

7. Rzem R, Van Schaftingen E, Veiga-da-Cunha M. The gene mutated in l-2-hydroxyglutaric aciduria encodes l-2-hydroxyglutarate dehydrogenase. Biochimie 2006;88(1):113-6.

8. Shafeghati Y, Vakili G, Entezari A. L-2-hydroxyglutaric aciduria: A report of six cases and Review of the Literature. Arch Iran Med 2006;9(2):165-9.