Relationship Between Migraine and Abnormal EEG Findings in Children

How to Cite this Article: Nejad Biglari H, Rezayi A, Nejad Biglari H, Alizadeh M, Ahmadabadi F. Relationship Between Migraine and Abnormal EEG Findings in Children. Iran J Child Neurol 2012; 6(3): 21-24.ObjectiveMigraine is a disabling illness that causes absence from school andaffects the quality of life. It has been stated that headache may representan epileptic event. EEG abnormality is a prominent finding in children with migraine. The aim of this study was to evaluate EEG abnormalities in children with migraine.Materials & MethodsTwo-hundred twenty-eight children were enrolled into the study. Evaluation and following of cases was performed by one physician, paraclinical tests were used to increase the accuracy. The study wasconducted under the supervision of pediatric neurology masters and theselected cases were from different parts of the country.ResultsComparing EEG abnormalities in different types of migraine revealed that there is an association between them. There was also a significant difference between EEG abnormalities in different types of aura. Migraine type was associated with the patient’s age. Sleep disorders were more common in patients with a positive family history of seizure.ConclusionOur study disclosed migraine as a common problem in children with abnormalities present in approximately 20% of the patients. Migraine and abnormal EEG findings are significantly associated.ReferencesOttman, R, Lipton RB, Comorbidity of migraine and epilepsy. Neurology 1994 Nov;44(11):2105-10.Haut SR, Bigal ME, Lipton RB. Chronic disorders with episodic manifestations: focus on epilepsy and migraine.Lancet Neurol 2006 Feb;5(2):148-57.Piccinelli P, Borgatti R, Nicoli F, Calcagno P, Bassi MT,Quadrelli M et al. Relationship between migraine and epilepsy in pediatric age. Headache 2006 Mar;46(3):413-21.Hauser WA, Annegers JF, Anderson VE. Epidemiology and the genetics of epilepsy. Res Publ Assoc Res Nerv Ment Dis 1983;61:267-94.Yankovsky AE, Andermann F, Bernasconi A.Characteristics of headache associated with intractable partial epilepsy. Epilepsia 2005 Aug;46(8):1241-5.The International Classification of Headache Disorders:2nd edition. Cephalalgia 2004; 24 Suppl 1:9-160.Forderreuther S, Henkel A, Noachtar S, Straube A. Headache associated with epileptic seizures:epidemiology and clinical characteristics. Headache 2002 Jul-Aug;42(7):649-55.Lewis DW, Diamond S, Scott D, Jones V. Prophylactic treatment of pediatric migraine. Headache 2004 Mar;44(3):230-7.Holguin J, Fenichel G. Migraine. J Pediatrics 1967 Feb;70(2):290-7.Chu ML, Shinnar S. Headaches in children younger than7 years of age. Arch Neurol 1992 Jan;49(1):79-82.Friedman E, Pampiglione G. Recurrent headache inchildren (a clinical and electroencephalographic study).Arch Neurobiol 1974;37 SUPPL:115-76.Kramer U, Nevo Y, Neufeld MY, Harel S. The valueof EEG in children with chronic headaches. Brain Dev1994 Jul-Aug;16(4):304-8.Schon F, Blau JN. Post-epileptic headache and migraine.J Neurol Neurosurg Psychiatry 1987 Sep;50(9):1148-52

The Clinical Features and Diagnosis of Adrenoleukodystrophy: A Case Series of Iranian Family

How to Cite This Article: Karimzadeh P, Jafari N, Nejad Biglari Hb, Jabbehdari S, Alizadeh M, Alizadeh Gh, Nejad Biglari Hm, Sanii S. The Clinical Features and Diagnosis of Adrenoleukodystrophy: A Case Series of Iranian Family. Iran J Child Neurol. Winter 2016; 10(1):61-64.AbstractObjectiveAdrenoleukodystrophy disorder is one of the x-linked genetic disorders caused by the myelin sheath breakdown in the brain. In this study, we present 4 yr experience on this disorder.Materials & MethodsThe patients diagnosed as adrenoleukodystrophy in the Neurology Department of Mofid Children’s Hospital in Tehran, Iran from 2010 to 2014 were enrolled into the study. The disorder was confirmed by neuroimaging and clinical findings along with genetic and neurometabolic assessment at Reference Laboratory in Germany. We assessed age, gender, past medical history, developmental status, clinical manifestations, and neuroimaging findings of populous family with adrenoleukodystrophy.ResultsAll of the patients were one populous family with high rate of consanguineous marriages. This disorder was confirmed by genetic assessment, VLCFA and brain MRI.c.253_254insC, p.R85Pfs112* was found in heterozygote state and the VLCFA assessment showed the typical pattern for adrenoleukodystrophy/ adrenomyeloneuropathy. This diagnosis was in agreement with the family history and the clinical history of the patient. Since there have been a number of cases in patient’s family in the past, so intensive follow-up on the family especially detection the female members of the family of childbearing age was recommended. The amount of C-26, C24/C22 and C26/C22 was elevated. All patients with the same genotype had wide ranges of clinical presentation.ConclusionEarly diagnose of this disease might help us for early intervention and prenatal diagnosis for the disease in next siblings

Migraine Types and Triggering Factors in Children

How to Cite this Article: Nejad Biglari H, Karimzadeh P, Mohammadi Kord-kheyli M, Hashemi SM. Migraine Types and Triggering Factors in Children. Iran J  Child Neurol 2012;6(2):33-38.Objective Migraine is a common problem in children and the mean prevalence of migraine in Europe among 170,000 adults was 14.7% (8% in men and 17.6% in women) and in children and youth (36,000 participants), the prevalences were (9.2% for all, 5.2% in boys and 9.1% in girls) and the lifetime prevalences were (16, 11 and 20%, respectively). To determine the epidemiology of migraine and evaluate migraine triggering factors in children. Materials & Methods Two-hundred twenty-eight children with a maximum age of 12 years who fulfilled the ICHD-II criteria for pediatric migraine were enrolled into the study. Results This study shows that migraine is slightly more common in boys and its peak incidence is between ages 8 and 12 and most patients have three to five headache attacks per month. The pain has a tightening, stabbing or vague quality in about 70% of children with migraine and bilateral headache is slightly more common. The common triggering factors in children migraine were stress, noise, sleeplessness, hunger and light and the common relieving factors were sleep, analgesics, silence, darkness and eating. Conclusion Migraine is a common problem in children with an equal incidence in boys and girls before adolescence and more common in girls after adolescence. ReferencesPowers SW, Andrasik F. Biobehavioral treatment, disability, and psychological effects of pediatric headache. Pediatr Ann 2005;34(6):461-5. Rosenblum RK, Fisher PG. A guide to children with acute and chronic headaches. J Pediatr Health Care 2001;15(5):229-35. Fallahzadeh H, Alihaydari M. Prevalence of migraine and tension-type headache among school children in Yazd, Iran. J Pediatr Neurosci 2011;6(2):106-9. Ayatollahi SM, Khosravi A. Prevalence of migraine and tension-type headache in primaryschool children in Shiraz. East Mediterr Health J 2006;12(6):809-17. Stovner LJ, Andree C. Prevalence of headache in Europe: a review for the Eurolight project. J Headache Pain 2010;11(4):289-99. Bille B. A 40-year follow-up of school children with migraine. Cephalalgia 1997;17(4):488-91; discussion 487. Bille B. Migraine and tension-type headache in children and adolescents. Cephalalgia 1996;16(2):78. Bille B. Migraine in childhood and its prognosis. Cephalalgia 1981;1(2):71-5. Lewis DW, Ashwal S, Dahl G, Dorbad D, Hirtz D, Prensky A, et al. Practice parameter: evaluation of children and adolescents with recurrent headaches: report of the Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society. Neurology 2002;59(4):490-8. Shah UH, Kalra V. Pediatric migraine. Int J Pediatr 2009;2009:424192. Fukui PT, Gonçalves TR, Strabelli CG, Lucchino NM, Matos FC, Santos JP, et al. Trigger factors in migraine patients. Arq Neuropsiquiatr 2008;66(3A):494-9. Neut D, Fily A, Cuvellier JC, Vallée L. The prevalence of triggers in paediatric migraine: a questionnaire study in 102 children and adolescents. J Headache Pain 2012;13(1):61-5. Lewis DW, Diamond S, Scott D, Jones V. Prophylactic treatment of pediatric migraine. Headache 2004;44(3):230-7. Barabas G, Matthews WS, Ferrari M. Childhood migraine and motion sickness. Pediatrics 1983;72(2):188-90. Holguin J, Fenichel G. Migraine. J Pediatr 1967;70(2):290-7. The International Classification of Headache Disorders: 2nd edition. Cephalalgia 2004;24 (Suppl 1):9-160

Evaluating the Correlation between Brain Ultra Sonographic, Brain MRI, and Electroencephalography Findings and the Severity of Asphyxia and Neurodevelopment in Infants with Hypoxic-ischemic Injury

ObjectiveHypoxia-ischemia-induced brain injury is a major cause of acute mortality and chronic neurological disability in infants and children.Imaging plays a vital role in diagnosing and treating hypoxicischemic encephalopathy (HIE) and as an adjunct to acute conditions and provides valuable information on long-term prognosis.Materials & MethodsOur study was prospective with 50 neonates aged 34 weeks and older with HIE. Cerebral ultrasound and MRI were performed on the infants, and the pattern of lesions was recorded. A pediatric neurologist examined the infants, and their developmental status was assessed and recorded with electroencephalography (EEG) findings.The data were analyzed. ResultsThe sonography pattern was normal in 26 (76.5%) term neonates, and also, the PVL pattern was observed in 10 term neonates. The incidence of observing an edema pattern (17.6%) was significantly different between the term and pre-term infants (P-value = 0.001).MRI findings were normal in 20 (58.8%) term neonates and 11 premature neonates. However, the PVL pattern was observed in MRI performed in six term neonates (6.6%). The watershed pattern (17%) showed that these differences were significant between the term and pre-term infants (P-value = 0/001). ConclusionNormal sonography was significantly higher in neonates with normal neurodevelopment than in patients with normal MRI and EEG findings but with poor neurodevelopment. Also, the probability of having normal MRI results was lower in neonates with moderate to severe asphyxia compared to ultrasound and EEG. &nbsp

The clinical features and diagnosis of Metachromatic leukodystrophy: A case series of Iranian Pediatric patients

How to Cite This Article: Jabbehdari S, Rahimian E, Jafari N, Sanii S, Khayatzadeh Kakhki S, Nejad Biglari H. The Clinical Features and Diagnosis of Metachromatic Leukodystrophy: A Case Series of Iranian Pediatric Patients. Iran J Child Neurol. Summer 2015;9(3):57-61.AbstractObjectiveMetachromatic leukodystrophy disorder (MLD) is one of the rare neurometabolicdiseases caused due to lack of saposin B and arylsulfatase A enzyme deficiency.Materials & MethodsEighteen patients diagnosed as metachromatic leukodystrophy in the NeurologyDepartment of Mofid Children’s Hospital in Tehran, Iran between 2010 and2014 were included in our study. The disorder was confirmed by clinical,EMG-NCV, arylsulfatase A enzyme checking and neuroimaging findings alongwith neurometabolic and genetic assessment from reference laboratory in Iran.We assessed age, gender, past medical history, developmental status, clinicalmanifestations, and neuroimaging findings of 18 patients with metachromaticleukodystrophy.ResultsFrom 18 patients, 80% were offspring from consanguineous marriages. A familyhistory of metachromatic leukodystrophy disease was positive for four patients.Twelve patients had late infantile form of this disorder and six patients had juvenile form. A history of tonic type seizure was positive in 20% of the patients and tonic spasm was confirmed with clinical information. Electromyographgraphy (EMG) in 96% of patients was abnormal with demyelinating sensorimotor neuropathy pattern. MRI in all patients showed the leukodystrophic pattern as arcuate fibers sparing and subcortical rim in white matter and periventricular involvement. Our diagnosis was confirmed by EMG-NCV findings with sensorimotor neuropathy pattern and the assessment of arylsulfatase A enzyme function. ConclusionMLD is an inheritance metabolic disorder, which was confirmed by theassessment of arylsulfatase A enzyme function, peripheral blood leukocyte thatassessed in a referral laboratory in Iran

The Clinical Features and Diagnosis of Canavan’s Disease: A Case Series of Iranian Patients

How to Cite This Article: Karimzadeh P, Jafari N, Nejad Biglari H, Rahimian E, Ahmadabadi F, Nemati H, Nasehi MM, Ghofrani M, Mollamohammadi M. The Clinical Features and Diagnosis of Canavan’s Disease: A Case Series of Iranian Patients. Iran J Child Neurol. 2014 Autumn;8(3): 66-71.AbstractObjectiveCanavan’s disease is a lethal illness caused by a single gene mutation that is inherited as an autosomal recessive pattern. It has many different clinical features especially in the non-Ashkenazi Jewish population.Material & Methods45 patients were referred to the Pediatric Neurology Department of Mofid Children’s Hospital in Tehran-Iran from 2010–2014 with a chief complaint of neuro developmental delays, seizures, and neuroimaging findings of leukodystrophy were included in this study. Magnetic Resonance Spectrometry (MRS) and neuro metabolic assessment from a referral laboratory in Germany confirmed that 17 patients had Canavan’s disease.ResultsVisual impairment, seizure, hypotonia, neuro developmental arrest, and macrocephaly were the most consistent findings in the patients in this study. Assessments of neuro developmental status revealed that 13 (76%) patients had neuro developmental delays and 4 (24%) patients had normal neuro development until 18 months of age and then their neuro developmental milestones regressed.  In this study, 100% of cases had macrocephalia and 76% of these patients had visual impairment. A history of seizures was positive in 8 (47%) patients and began around 3 months of age with the most common type of seizure was tonic spasm. EEGs were abnormal in all epileptic patients. In ten of the infantile group, we did not detect elevated level of N-acetylaspartic acid (NAA) in serum and urine. However, the MRS showed typical findings for Canavan’s disease (peaks of N-acetylaspartic acid).ConclusionWe suggest using MRS to detect N-acetylaspartic acid as an acceptable method for the diagnosis of Canavan’s disease in infants even with normal serum and urine N-acetylaspartic acid levels. ReferencesAdornato BT, O’Brien JS, Lampert PW, Roe TF, Neustein HB. Cerebral spongy degeneration of infancy. A biochemical and ultrastructural study of affected twins. Neurology 1972;22(2):202-10.Banker BQ, Robertson JT, Victor M. Spongy Degeneration of the Central Nervous System in Infancy. Neurology 1964; 14:981-1001.Chou SM, Waisman HA. Spongy Degeneration of the Central Nervous System: Case of Homocystinuria. Arch Pathol 1965; 79:357-63.Divry P, Vianey-Liaud C, Gay C, Macabeo V, Rapin F, Echenne B. N-acetylaspartic aciduria: report of three new cases in children with a neurological syndrome associating macrocephaly and leukodystrophy. J Inherit Metab Dis 1988; 11(3):307-8.Feigenbaum A, Moore R, Clarke J, Hewson S, Chitayat D, Ray PN, et al. Canavan disease: carrier-frequency determination in the Ashkenazi Jewish population and development of a novel molecular diagnostic assay. Am J Med Genet A 2004;124a(2):142-7.Hagenfeldt L, Bollgren I, Venizelos N. N-acetylaspartic aciduria due to aspartoacylase deficiency--a new aetiology of childhood leukodystrophy. J Inherit Metab Dis 1987; 10(2):135-41.Ishiyama G, Lopez I, Baloh RW, Ishiyama A. Canavan’s leukodystrophy is associated with defects in cochlear neurodevelopment and deafness. Neurology 2003; 60(10):1702-4.Janson CG, Kolodny EH, Zeng BJ, Raghavan S, Pastores G, Torres P, et al. Mild-onset presentation of Canavan’s disease associated with novel G212A point mutation in aspartoacylase gene. Ann Neurol 2006; 59(2):428-31.Kaul R, Gao GP, Aloya M, Balamurugan K, Petrosky A, Michals K, et al. Canavan disease: mutations among Jewish and non-Jewish patients. Am J Hum Genet 1994; 55(1):34-41.Kaul R, Gao GP, Balamurugan K, Matalon R. Cloning of the human aspartoacylase cDNA and a common missense mutation in Canavan disease. Nat Genet 1993; 5(2):118-23.Kvittingen EA, Guldal G, Borsting S, Skalpe IO, Stokke O, Jellum E. N-acetylaspartic aciduria in a child with a progressive cerebral atrophy. Clin Chim Acta 1986;158(3):217-27.Mahloudji M, Daneshbod K, Karjoo M. Familial spongy degeneration of the brain. Arch Neurol 1970; 22(4):294-8.Matalon R, Kaul R, Casanova J, Michals K, Johnson A, Rapin I, et al. SSIEM Award. Aspartoacylase deficiency: the enzyme defect in Canavan disease. J Inherit Metab Dis 1989; 12(Suppl 2):329-31.Matalon R, Michals K, Sebesta D, Deanching M, Gashkoff P, Casanova J. Aspartoacylase deficiency and N-acetylaspartic aciduria in patients with Canavan disease. Am J Med Genet 1988; 29(2):463-71.Morcaldi L, Salvati G, Giordano GG, Guazzi GC. Congenital familial spongy idiocy (van Bogaert-Bertrand syndrome) in a non-Jewish family (study of a 2d Italian family)]. Acta Genet Med Gemellol (Roma) 1969; 18(2):142-57.Ozand PT, Gascon GG, Dhalla M. Aspartoacylase deficiency, and Canavan disease in Saudi Arabia. Am J Med Genet 1990; 35(2):266-8.Schmidt H, Rott HD, Neuhauser G, Neumann W. [Spongious cerebral dystrophy at an infant age (Canavan-Bogaert-Bertrand types) in three siblings of a non-Jewish family in upper Franconia (author’s transl)]. KlinPadiatr 1978; 190(6):580-5.Shaag A, Anikster Y, Christensen E, Glustein JZ, Fois A, Michelakakis H, et al. The molecular basis of Canavan (aspartoacylase deficiency) disease in European non-Jewish patients. Am J Hum Genet 1995; 57(3):572-80.Sistermans EA, de Coo RF, van Beerendonk HM, Poll-The BT, Kleijer WJ, van Oost BA. Mutation detection in the aspartoacylase gene in 17 patients with Canavan disease: four new mutations in the non-Jewish population. Eur J Hum Genet 2000; 8(7):557-60.Toft PB, Geiss-Holtorff R, Rolland MO, Pryds O, Muller-Forell W, Christensen E, et al. Magnetic resonance imaging in juvenile Canavan disease. Eur J Pediatr 1993; 152(9):750-3.Michals K, Matalon R. Canavan’s disease. In: Raymond GV, Eichler F, Fatemi A, Naidu S, eds. Leukodystrophies. London: Mac Keith Press.2011.P.156-69.Breitbach-Faller N, Schrader K, Rating D, Wunsch R. Ultrasound findings in follow-up investigations in a case of aspartoacylase deficiency (Canavan disease). Neuropediatrics 2003; 34:96–9.Matalon RM, Michals-Matalon K. Spongy degeneration of the brain, Canavan disease: biochemical and molecular findings. Front Biosci 2000; 5:D307–11.Matalon R, Michals K, Kaul R. Canavan disease: from spongy degeneration to molecular analysis. J Pediatr 1995; 127:511–7

Epidemiology of Guillain-BarréSyndrome in Iranian Children Aged 0-15 Years (2008-2013)

Abstract Objective: Guillain-Barre Syndrome (GBS) is an acute inflammatory polyneuropathy characterized by a rapid progressive symmetric weakness. This is the most common cause of Acute Flaccid Paralysis (AFP) in most parts of the world. This study was carried out to investigate the epidemiological features of GBS in Iranian children. Materials & Methods: Data were extracted using the AFP surveillance system: a National screening program to detect all cases of AFP aged 0-15 years, around the country. National Population Statistics data and AFP demographic data during 2008-2013 intervals was obtained from the relevant authorities in ministry of health. GBS cases were then extracted from this data base. Chi-square and Fisher's exact test were used for statistical analysis. Results: 1884 cases of GBS were identified in years of study and average annual incidence rate was 1.72 per 100,000 populations. The highest incidence rate was in the range of 0-5 years. There was no statistically significant relation between the incidence of GBS and the season in the whole country. Conclusion: High costs of GBS treatment, morbidity and occasional mortality and the number of new cases which is estimated to be about 300 people per year, need particular attention of health system

An unusual case of a toddler with Canavan disease with frequent intractable seizures: A case report and review of the literature

Canavan disease is a rare fetal inherited leukodystrophy, caused by accumulation of N-acetyl-aspartate in the brain. Here, we report a child presented with frequent intractable seizures and visual impairment. A 14-month-old female infant with a complaint of the absence of neck holding and generalized tonic-clonic seizures was referred to our hospital. Macrocephaly, setting sun eyes, tremor, and hypotonia were observed. Funduscopy showed optic atrophy. Our patient’s flash visual evoked potential showed blindness. Her brain magnetic resonance imaging showed diffuse white matter in subcortical, basal ganglia, and dorsal pons. Electroencephalography showed diffuse slow and sharp waves. The genetic study detected a hemizygous mutation in the aspartoacylase gene. Our patient was diagnosed with Canavan disease and began anticonvulsant treatment. However, seizures were not under control. Then, her medications were discontinued, and clobazam and primidone were administered. In conclusion, starting clobazam and primidone may help prevent frequently intractable seizures in Canavan disease patients

Electroencephalography, Magnetic Resonance Imaging and Response to Treatment in Children with Focal Seizures A Prospective Cohort Study: Nejad Biglari et al., Focal-onset Seizures

ObjectivesThis study aimed to evaluate patients with focal seizures, their clinical manifestations, and their response to treatment, then compared the accuracy of electroencephalography and Magnetic Resonance Imaging (MRI) to assess the cost-effectiveness of the latter.Materials & MethodsAfter selecting the appropriate individuals, the authors obtained the data by clinically evaluating the cases and interviewing them or their caretaker(s) on admission and the six-month follow-up visit. The researchers then analyzed the obtained data.ResultsMost cases (88.4%) had idiopathic seizures. A positive family history of seizures was observed in eight cases (5.4%). Respectively, theoccipital, frontal, and temporal lobes showed the highest frequencyo normalities on electroencephalography, while periventricular leukomalacia was the highest abnormal MRI finding (4.1%).However, in 87.8% of cases, this modality’s results were normal. No recurrence of seizures was observed in 116 cases (78.9%) on the sixmonth follow-up visit, pointing towards an appropriate response to treatment.ConclusionWhile this study revealed that most had normal MRI, reporting an abnormality in electroencephalography was a more prevalent occurrence. This finding undermines the cost-effectiveness of the former modality, even though its importance in diagnosing the underlying abnormalities necessitates further studies regarding thesubject at hand. Furthermore, the study of age groups showed that treatment response is less desirable in children under two years of age, suggesting more intense workups

sj-docx-1-icr-10.1177_11795476231188061 – Supplemental material for Adolescence Onset Primary Coenzyme Q10 Deficiency With Rare CoQ8A Gene Mutation: A Case Report and Review of Literature

Supplemental material, sj-docx-1-icr-10.1177_11795476231188061 for Adolescence Onset Primary Coenzyme Q10 Deficiency With Rare CoQ8A Gene Mutation: A Case Report and Review of Literature by Mahsa Hojabri, Abolfazl Gilani, Rana Irilouzadian, Habibe Nejad biglari and Roham Sarmadian in Clinical Medicine Insights: Case Reports</p