Pediatric Neurology (PEDIATR NEUROL)

Publisher: Elsevier

Journal description

Pediatric Neurology publishes timely peer-reviewed clinical and research articles covering all aspects of the developing nervous system.Pediatric Neurology features up-to-the-minute publication of the latest advances in the diagnosis, management, and treatment of pediatric neurologic disorders. The journal's editor, Kenneth F. Swaiman, MD, heads an internationally recognized editorial board, ensuring the most authoritative and extensive coverage of the field. Among the topics covered are: epilepsy, mitochondrial diseases, congenital malformations, chromosomopathies, peripheral neuropathies, perinatal and childhood stroke, cerebral palsy, as well as other diseases affecting the developing nervous system.

Current impact factor: 1.50

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 1.504
2012 Impact Factor 1.416
2011 Impact Factor 1.522
2010 Impact Factor 1.513
2009 Impact Factor 1.497
2008 Impact Factor 1.505
2007 Impact Factor 1.375
2006 Impact Factor 1.542
2005 Impact Factor 1.368
2004 Impact Factor 1.184
2003 Impact Factor 1.243
2002 Impact Factor 1.247
2001 Impact Factor 1.011
2000 Impact Factor 1.007
1999 Impact Factor 1.119
1998 Impact Factor 0.921
1997 Impact Factor 0.918

Impact factor over time

Impact factor

Additional details

5-year impact 1.67
Cited half-life 7.20
Immediacy index 0.32
Eigenfactor 0.01
Article influence 0.56
Website Pediatric Neurology website
Other titles Pediatric neurology
ISSN 1873-5150
OCLC 11930271
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Pre-print allowed on any website or open access repository
    • Voluntary deposit by author of authors post-print allowed on authors' personal website, or institutions open scholarly website including Institutional Repository, without embargo, where there is not a policy or mandate
    • Deposit due to Funding Body, Institutional and Governmental policy or mandate only allowed where separate agreement between repository and the publisher exists.
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months .
    • Set statement to accompany deposit
    • Published source must be acknowledged
    • Must link to journal home page or articles' DOI
    • Publisher's version/PDF cannot be used
    • Articles in some journals can be made Open Access on payment of additional charge
    • NIH Authors articles will be submitted to PubMed Central after 12 months
    • Publisher last contacted on 18/10/2013
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Glucose transporter 1 deficiency syndrome is an autosomal, dominantly inherited neurometabolic disorder caused by mutations in the SLC2A1 gene. Decreased glucose transport into the brain results in seizures and cognitive dysfunction. The ketogenic diet is the treatment of choice, but complicated with compliance problems. Stabilization of blood glucose levels by low glycemic index diet and modified high amylopectin cornstarch would provide steady-state glucose transport into the brain to prevent seizures and cognitive dysfunction in patients with glucose transporter 1 deficiency syndrome as an alternative treatment. We report a new glucose transporter 1 deficiency syndrome patient (c.988C>T; p. Arg330X in the SLC2A1) treated with modified high amylopectin cornstarch (Glycosade) and low glycemic index diet because of compliance problems with the ketogenic diet. She was diagnosed at 11.5 years of age and was treated with the ketogenic diet between ages 12 and 18 years. She was started on modified high amylopectin cornstarch at bedtime and low glycemic index diet with meals and snacks every 3-4 hours. Within the first 6 months of therapy, she improved in her seizures and cognitive functions, but experienced compliance problems afterwards. Neuropsychological assessment was stable at 12 months of therapy. This diet was easy to apply compared with the ketogenic diet and resulted in stable neuropsychological functioning of this glucose transporter 1 deficiency syndrome patient. Modified high amylopectin cornstarch and low glycemic index diet might be an alternative treatment in glucose transporter 1 deficiency syndrome patients with compliance problems to the ketogenic diet treatment, but additional patients should be treated to prove usefulness of this new treatment. Crown Copyright © 2015. Published by Elsevier Inc. All rights reserved.
    Pediatric Neurology 06/2015; DOI:10.1016/j.pediatrneurol.2015.06.018
  • Pediatric Neurology 06/2015; DOI:10.1016/j.pediatrneurol.2015.04.005
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    ABSTRACT: Diffuse white matter abnormalities are identified in up to 80% of very preterm infants on magnetic resonance imaging at 40 weeks' postmenstrual age. Several studies have observed an association between diffuse white matter abnormalities and cognitive deficits. We hypothesized that very preterm infants (gestational age ≤32 weeks) with diffuse white matter abnormalities will exhibit reduced executive control and frontoparietal functional connectivity compared with infants without diffuse white matter abnormalities measured using resting state functional magnetic resonance imaging at term-equivalent age. We quantified diffuse white matter abnormality volume objectively using an automated segmentation approach and defined diffuse white matter abnormality severity as no-mild (volume ≤50th percentile; N = 13) and moderate-severe (N = 14). Resting state networks of interests were identified using probabilistic independent component analysis. Within network functional connectivity was calculated between the different pair of nodes in a given network using partial correlation coefficients. We studied 27 very preterm infants born at a mean (standard deviation) gestational age of 26.9 (2.0) weeks and imaged at 39.6 (1.4) weeks' postmenstrual age. Within-network connectivity was significantly reduced in the moderate-severe diffuse white matter abnormalities group than in the no-mild diffuse white matter abnormalities group for the executive control (P < 0.001) and frontoparietal (P = 0.02) networks. As expected, connectivity in three control resting state networks was similar: visual (P = 0.17), motor (P = 0.89), and somatosensory (P = 0.69) networks. Very preterm infants with moderate or severe diffuse white matter abnormalities exhibited reduced functional connectivity in important cognitive and attention networks. This aberrant connectivity may be the early life antecedent to the cognitive deficits reported at 2 years of age or later in such infants. Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.
    Pediatric Neurology 06/2015; 355. DOI:10.1016/j.pediatrneurol.2015.05.001
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    ABSTRACT: Tuberous sclerosis complex is a heritable multisystem disorder associated with genes involved in the formation of a tumor-suppressor complex acting through the Ras homologue enriched in brain protein to limit activation of the mammalian target of rapamycin complex I. Mutations in these genes result in enhanced mammalian target of rapamycin signaling and may cause neurological manifestations including brain tubers, subependymal nodules, and subependymal giant cell astrocytomas. These astrocytomas are tumors that arise near the foramen of Monro and may lead to obstructive hydrocephalus. Standard therapy has been surgical resection. More recently, mammalian target of rapamycin inhibitor, everolimus, has been approved for treatment after demonstration of efficacy in prospective clinical trials. We report a 15 year-old girl with tuberous sclerosis complex who proceeded to surgical resection of her subependymal giant cell astrocytoma after 3 months of treatment with mammalian target of rapamycin inhibition. We compared her subependymal giant cell astrocytoma tissue specimen with 12 untreated subependymal giant cell astrocytomas accessed from The Hospital for Sick Children in Toronto, Canada. This girl's histopathological findings were consistent with subependymal giant cell astrocytomas with no exposure to mammalian target of rapamycin inhibitors. There were no major differences identified on immunohistochemistry at targets downstream of mammalian target of rapamycin complex 1 or in neighboring signaling pathways. The majority of cells were reactive to glial fibrillary acidic protein, mitogen-activated protein kinase, phospho-S6, caspase 3 (95% positivity), and NP-1. In this one individual, rapamycin therapy did not change the histopathological characteristics of subependymal giant cell astrocytoma. Mammalian target of rapamycin inhibition involves complex signaling pathways inducing subependymal giant cell astrocytoma shrinkage. However, its effect is not easily characterized within tumor tissue. Copyright © 2015 Elsevier Inc. All rights reserved.
    Pediatric Neurology 06/2015; DOI:10.1016/j.pediatrneurol.2015.05.020
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    ABSTRACT: Bupropion is a monocyclic antidepressant in the aminoketone class, structurally related to amphetamines. The Food and Drug Administration withdrew this product from the market in 1986 after seizures were reported in bulimic patients. It was later reintroduced in 1989 when the incidence of seizures was shown to be dose-related in the immediate release preparation. Massive bupropion ingestion has been associated with status epilepticus and cardiogenic shock in adults. Seizures have been reported in children, but not status epilepticus. This report highlights a patient who presented with status epilepticus and developed cardiopulmonary arrest after bupropion ingestion. False-positive amphetamine diagnosis from urine drug screen on presentation was reported. We review the presentation, clinical course, diagnostic studies, and outcome of this patient. We then review the literature regarding bupropion overdose in children. Symptoms of bupropion toxicity and risk for seizures are dose-dependent and fatalities have been reported. Our patient developed status epilepticus and cardiopulmonary arrest and then progressed to have a hypoxic ischemic encephalopathy and refractory symptomatic partial seizures. Our report highlights the need to keep this medication away from children, preventing accidental overdose. Copyright © 2015 Elsevier Inc. All rights reserved.
    Pediatric Neurology 06/2015; DOI:10.1016/j.pediatrneurol.2015.05.018
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    ABSTRACT: Cockayne syndrome (MIM #133540, Cockayne syndrome B; 216400, Cockayne syndrome A) is a rare autosomal recessive inherited disease in which the characteristic symptoms are premature aging, cachectic dwarfism, lack of subcutaneous fat, neurological alterations, light sensitivity, and failure to thrive. The mutated gene responsible for this syndrome has been identified as usually either CSA (CKN1, ERCC8) or CSB (ERCC6). In this study, we describe the case of a 7-year-old Chinese boy with characteristic symptoms of Cockayne syndrome A and the conduction of mutation screening of the CSA gene. The patient was diagnosed with Cockayne syndrome in the pediatrics clinic for growth failure and developmental delay. We collected peripheral blood samples of the patient and his parents and then extracted the genomic DNA. DNA samples from control subjects and the patient were subjected to polymerase chain reaction amplification. All exons and the flanking intron-exon boundaries of CSA were amplified; then, the polymerase chain reaction products were directly sequenced for mutation screening. Two novel heterozygous CSA mutations, c.551-2A>C and c.394_398delTTACA, were identified in the patient. The c.551-2A>C mutation originates from his father and changed the splice acceptor site AG to CG, thus possibly causing alternative splicing. The c.394_398delTTACA from his mother caused a frameshift after the amino acid at position 132, thus introducing a premature stop codon in the gene sequence. These mutations extend the mutation spectrum of Cockayne syndrome in the context of Chinese race and provide possibilities of prenatal diagnosis for future offsprings in this family. Copyright © 2015 Elsevier Inc. All rights reserved.
    Pediatric Neurology 06/2015; DOI:10.1016/j.pediatrneurol.2015.06.006
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    ABSTRACT: Cerebrospinal fluid neurotransmitter collection, analysis, and follow-up are integral to the diagnosis and management of multiple inborn metabolic errors, some of which require prompt identification and intervention to improve outcome. Cerebrospinal fluid pterins and monoamine metabolites are diagnostic in a range of primary neurotransmitter disorders, including disorders of biogenic amine synthesis, metabolism, and transport. Recently described mutations of the human dopamine transporter are associated with an elevated cerebrospinal fluid homovanillic acid:hydroxyindoleacetic acid ratio. Disorders of pyridoxine metabolism are also detectable via cerebrospinal fluid quantification of bioamines, amino acids, and pyridoxal-5-phosphate levels. Cerebrospinal fluid amino acids are diagnostic in disorders of gamma aminobutyric acid, glycine, and serine metabolism. A wide range of acquired and genetic disorders has also been associated with secondary alterations in cerebrospinal fluid levels of monoamine metabolites, glycine, and neopterin. Lumbar puncture is required to detect abnormal cerebrospinal fluid metabolites in a significant proportion of these disorders, including treatable entities such as dopa-responsive deficiencies of guanosine-5'-triphosphate cyclohydrolase I (Segawa disease), sepiapterin reductase, and tyrosine hydroxylase. Copyright © 2015 Elsevier Inc. All rights reserved.
    Pediatric Neurology 06/2015; DOI:10.1016/j.pediatrneurol.2015.04.016
  • Pediatric Neurology 06/2015; DOI:10.1016/j.pediatrneurol.2015.05.005
  • Pediatric Neurology 06/2015; DOI:10.1016/j.pediatrneurol.2015.06.001
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    ABSTRACT: Background Brain radiotherapy plays a central role in certain types of childhood primary central nervous system tumors. However, damage to surrounding normal brain tissue causes different acute and chronic medical and neurological complications. Despite the expected increase in number of childhood primary central nervous system tumor survivors, studies accessing the occurrence of late cerebrovascular complications, such as cavernoma, moyamoya, microbleeds, superficial siderosis, and stroke are sparse. Methods Retrospective consecutive case series review describing the occurrence and characteristics of late cerebrovascular complications in 100 survivors of childhood primary central nervous system tumors treated with radiotherapy. Demographic, clinical, and radiological findings including gradient echo brain magnetic resonance data were retrieved. Results Late cerebrovascular complications were found in 36 (36%) of the patients included in the study. Mean age at radiotherapy was 8.6 years (3-17) and at diagnosis was 23.9 years (3-38). The majority were males (21; 58%). The most common complications were microbleeds (29/36; 80.6%) and cavernomas 19 (52.8%). In seven (19.4%), late cerebrovascular complications were symptomatic: epilepsy (two), motor and language deficit (two), and sensorineural hearing loss and progressive ataxia (three) associated with cavernomas, stroke, and superficial siderosis, respectively. Follow-up length was associated with an increased diagnosis of late cerebrovascular complications (P < 0.0001). Late cerebrovascular complications occurred more commonly in children treated with whole-brain radiation therapy (P = 0.046). Factors such as sex, chemotherapy, and histological type of tumor were not correlated with the occurrence of late cerebrovascular complications. Conclusion Although rarely symptomatic, late cerebrovascular complications are frequent in survivors of childhood primary central nervous system tumors treated with radiotherapy. Prolonged follow-up increases the probability of diagnosis. The impact and prognostic value of these late cerebrovascular complications is yet to be clarified.
    Pediatric Neurology 06/2015; DOI:10.1016/j.pediatrneurol.2015.05.015
  • Pediatric Neurology 04/2015; DOI:10.1016/j.pediatrneurol.2015.01.015
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    ABSTRACT: Paroxysmal nonepileptic events are common in children. Events with a psychological basis, historically referred to as pseudoseizures, are a large subset of paroxysmal nonepileptic events. A review of the relevant pediatric and adult literature was performed. We found that these events have many semioloigc features similar to epileptic events and can be challenging to correctly identify. The use of a detailed history in combination with video encephalography and knowledge of psychogenic paroxysmal nonepileptic events will facilitate making the correct diagnosis. Paroxysmal nonepileptic events are important to identify as comorbid disorders such as depression, anxiety disorder, family discord, and school issues are frequent. In addition, prior sexual, emotional, and/or physical abuse may be present. Pediatric patients with paroxysmal nonepileptic events need to be recognized so as to limit the use of unnecessary antiepileptic drugs and emergency department or hospital visits as well as getting the patients appropriate psychological intervention to address the underlying etiologies. This review will focus on evaluation and identification of paroxysmal nonepileptic events, in addition to reviewing the various comorbidities, effective treatments, and outcomes for pediatric patients. The key differences between pediatric and adult patients with paroxysmal nonepileptic events are addressed. Copyright © 2015 Elsevier Inc. All rights reserved.
    Pediatric Neurology 03/2015; 53(1). DOI:10.1016/j.pediatrneurol.2015.03.017
  • Pediatric Neurology 03/2015; 53(1). DOI:10.1016/j.pediatrneurol.2015.03.014
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    ABSTRACT: Virus encephalitis remains a major cause of acute neurological dysfunction and permanent disability among children worldwide. Although some disorders, such as measles encephalomyelitis, subacute sclerosing panencephalitis, and varicella-zoster virus-associated neurological conditions, have largely disappeared in resource-rich regions because of widespread immunization programs, other disorders, such as herpes simplex virus encephalitis, West Nile virus-associated neuroinvasive disease, and nonpolio enterovirus-induced disorders of the nervous system, cannot be prevented. Moreover, emerging viral disorders pose new, potential threats to the child's nervous system. This review summarizes current information regarding the epidemiology of virus encephalitis, the diagnostic methods available to detect central nervous system infection and identify viral pathogens, and the available treatments. The review also describes immune-mediated disorders, including acute disseminated encephalomyelitis and N-methyl-D-aspartate receptor antibody encephalitis, conditions that mimic virus encephalitis and account for a substantial proportion of childhood encephalitis. Copyright © 2015 Elsevier Inc. All rights reserved.
    Pediatric Neurology 03/2015; DOI:10.1016/j.pediatrneurol.2015.03.013
  • Pediatric Neurology 03/2015; DOI:10.1016/j.pediatrneurol.2015.03.001
  • Pediatric Neurology 03/2015; DOI:10.1016/j.pediatrneurol.2015.03.003
  • Pediatric Neurology 03/2015; DOI:10.1016/j.pediatrneurol.2015.03.010
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    ABSTRACT: Epilepsy with progressive cortical volume loss is described secondary to energy failure such as mitochondrial disorders, infectious, or inflammatory etiologies and associated with temporal lobe epilepsy. Postmortem studies do not support that spontaneous seizures even if present for prolonged periods universally result in cortical volume loss. We describe two children with extratemporal pharmacoresistent epilepsy, slowly progressive gray matter volume loss over several years, and evidence of central nervous system inflammation. Brain magnetic resonance imaging changes and antibody profiles were not typical of a well-defined, antibody-mediated central nervous system syndrome such as N-methyl-D-aspartate receptor encephalitis. These patients illustrate a novel presentation of a subacute inflammatory central nervous system process with epilepsy and progressive cortical volume loss, supporting the role of sequential brain imaging in children with epilepsy. Copyright © 2015 Elsevier Inc. All rights reserved.
    Pediatric Neurology 03/2015; 53(1). DOI:10.1016/j.pediatrneurol.2015.02.009
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    ABSTRACT: The study aims are to evaluate cerebral background patterns using amplitude-integrated electroencephalography in newborns with critical congenital heart disease, determine if amplitude-integrated electroencephalography is predictive of preoperative brain injury, and assess the incidence of preoperative seizures. We hypothesize that amplitude-integrated electroencephalography will show abnormal background patterns in the early preoperative period in infants with congenital heart disease that have preoperative brain injury on magnetic resonance imaging. Twenty-four newborns with congenital heart disease requiring surgery at younger than 30 days of age were prospectively enrolled within the first 3 days of age at a tertiary care pediatric hospital. Infants had amplitude-integrated electroencephalography for 24 hours beginning close to birth and preoperative brain magnetic resonance imaging. The amplitude-integrated electroencephalographies were read to determine if the background pattern was normal, mildly abnormal, or severely abnormal. The presence of seizures and sleep-wake cycling were noted. The preoperative brain magnetic resonance imaging scans were used for brain injury and brain atrophy assessment. Fifteen of 24 infants had abnormal amplitude-integrated electroencephalography at 0.71 (0-2) (mean [range]) days of age. In five infants, the background pattern was severely abnormal. (burst suppression and/or continuous low voltage). Of the 15 infants with abnormal amplitude-integrated electroencephalography, 9 (60%) had brain injury. One infant with brain injury had a seizure on amplitude-integrated electroencephalography. A severely abnormal background pattern on amplitude-integrated electroencephalography was associated with brain atrophy (P = 0.03) and absent sleep-wake cycling (P = 0.022). Background cerebral activity is abnormal on amplitude-integrated electroencephalography following birth in newborns with congenital heart disease that have findings of brain injury and/or brain atrophy on preoperative brain magnetic resonance imaging. Copyright © 2015 Elsevier Inc. All rights reserved.
    Pediatric Neurology 03/2015; 52(6). DOI:10.1016/j.pediatrneurol.2015.02.026