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: 1.70

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 1.695
2013 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 1.57
Cited half-life 8.00
Immediacy index 0.24
Eigenfactor 0.01
Article influence 0.49
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
    • Authors pre-print on any website, including arXiv and RePEC
    • Author's post-print on author's personal website immediately
    • Author's post-print on open access repository after an embargo period of between 12 months and 48 months
    • 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
    • Author's post-print may be used to update arXiv and RepEC
    • Publisher's version/PDF cannot be used
    • Must link to publisher version with DOI
    • Author's post-print must be released with a Creative Commons Attribution Non-Commercial No Derivatives License
    • Publisher last reviewed on 03/06/2015
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Objectives: Little is known about the type, frequency, severity, treatment, and outcome of cardiac disease in nemaline myopathy. This review summarizes and discusses findings concerning the type, prevalence, diagnosis, treatment, and outcome of cardiac involvement in nemaline myopathy. Methods: Review of publications about nemaline myopathy and cardiac disease. Results: Altogether, 35 patients with nemaline myopathy with cardiac disease were identified. Age at presentation ranged from 0 to 62 years. In 30 individuals whose gender was described, 22 were male and eight were female. Onset was congenital in 16 patients, infantile in five, and adult in four. Nine patients presented with dilated cardiomyopathy, six with hypertrophic cardiomyopathy, and one with nonspecific cardiomyopathy. Among those with cardiomyopathy, four developed heart failure. One patient experienced sudden cardiac death. A ventricular septal defect was described in two patients. Cardiac treatment included drugs for heart failure (eight patients), implantable cardioverter-defibrillator implantation (one patient), and heart transplant (three patients). Four patients received noninvasive positive-pressure ventilation and two continuous positive-pressure ventilation. The outcome was fatal in 11 patients. Conclusions: Cardiac disease in nemaline myopathy manifests as cardiomyopathy leading to heart failure. If respiratory muscles are affected, the right side of the heart may be secondarily involved. Early detection of cardiac involvement is essential since effective treatment for cardiac disease in nemaline myopathy may be available.
    Pediatric Neurology 10/2015; DOI:10.1016/j.pediatrneurol.2015.08.014

  • Pediatric Neurology 10/2015; DOI:10.1016/j.pediatrneurol.2015.09.007
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    ABSTRACT: Objective: The mechanisms of the ketogenic diet remain unclear, but several predictors of response have been proposed. We aimed is to study the relationship between the etiology of epilepsy, cerebrospinal fluid neurotransmitters, pterins, and amino acids, and response to a ketogenic diet. Methods: We studied 60 patients who began classic ketogenic diet treatment for refractory epilepsy. In 24 of 60 individuals, we analyzed cerebrospinal fluid neurotransmitters, pterins, and amino acids in baseline conditions. Mean age at epilepsy onset was 24 months, 83.3% were focal epilepsies, and in 51.7% the etiology of the epilepsy was unknown. Results: Six months after initiating the ketogenic diet, it was effective (greater than a 50% reduction in seizure frequency) in 31.6% of patients. We did not find a link between rate of efficacy for the ketogenic diet and etiologies of epilepsy, nor did we find a link between the rate of efficacy for the ketogenic diet and cerebrospinal fluid pterins and biogenic amines concentrations. However, we found statistically significant differences for lysine and arginine values in the cerebrospinal fluid between ketogenic diet responders and nonresponders, but not for the other amino acids analyzed. Significance: The values of some amino acids were significantly different in relationship with the ketogenic diet efficacy; however, the epilepsy etiology and the cerebrospinal fluid biogenic amine and pterin values were not.
    Pediatric Neurology 10/2015; 53(5):422-426. DOI:10.1016/j.pediatrneurol.2015.07.013

  • Pediatric Neurology 10/2015; DOI:10.1016/j.pediatrneurol.2015.09.005

  • Pediatric Neurology 10/2015; DOI:10.1016/j.pediatrneurol.2015.08.011

  • Pediatric Neurology 10/2015; DOI:10.1016/j.pediatrneurol.2015.08.017
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    ABSTRACT: Background: Encephalitis lethargica is an encephalitic illness with multiple nervous system symptoms. Lesions only involving substantia nigra on magnetic resonance imaging are uncommon, especially in children. A second encephalitis illness after encephalitis lethargica has never been reported before. Patient description: We describe a 7-year-old boy with humoral immunity deficiency who developed encephalitis lethargica associated with bilateral substantia nigra lesions on magnetic resonance imaging. After a nearly complete recovery, he developed encephalitis once again. He was diagnosed with encephalitis lethargica with somnolence, akinetic mutism, and ophthalmoplegia after intermittent fever. Cerebrospinal fluid pleocytosis and positive oligoclonal bands were documented. Symmetrical substantia nigra lesions on high-intensity magnetic resonance imaging gradually evolved into a liquid signal. He had almost recovered when he developed fatigue and hypersomnia and was diagnosed with encephalitis again, supported by mild pleocytosis in cerebrospinal fluid and subcortical white matter lesions in the frontal lobes. His symptoms resolved following administration of corticosteroids and immunoglobulins. Conclusion: This is the first report of an immune-deficient child to develop encephalitis lethargica with isolated substantia nigra lesions on magnetic resonance imaging and a second encephalitis illness after recovery from encephalitis lethargica.
    Pediatric Neurology 10/2015; DOI:10.1016/j.pediatrneurol.2015.03.030

  • Pediatric Neurology 10/2015; DOI:10.1016/j.pediatrneurol.2015.09.020
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    ABSTRACT: Background: Clinical presentation with motor delay, proximal weakness, and learning difficulties will raise the possibility of a dystrophinopathy, dystroglycanopathy, or myotonic dystrophy. This differential should also include the more recently described choline kinase beta-related muscular dystrophy. This condition is typically characterized by large and abnormally distributed mitochondria on muscle biopsy, which can distinguish this condition from the other muscle conditions in the differential. Methods: We present a case of a boy with choline kinase beta mutations with relatively mild clinical presentation, including proximal weakness, learning difficulties and raised creatine kinase. Investigations included muscle magnetic resonance imaging (MRI) with T1 axial sequences through thigh and calves, and needle muscle biopsy of the left vastus lateralis muscle. Results: MRI showed involvement mainly of the quadriceps femoris, sartorius, and adductor magnus, with selective sparing of the gracilis, hamstrings, and adductor longus and brevis. Muscle biopsy revealed chronic dystrophic features. Oxidative stains demonstrated enlarged mitochondria accentuated peripherally or present diffusely in a few fibres giving a coarsely stippled appearance. A homozygous C.722A>G (p.Asn241Ser) mutation was detected in exon 6 of the CHKB gene. Conclusion: This selective pattern of skeletal muscle involvement might be helpful for identifying other patients with this condition, even in the absence of diagnostic muscle pathology.
    Pediatric Neurology 10/2015; DOI:10.1016/j.pediatrneurol.2015.09.018
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    ABSTRACT: Background: Congenital myasthenic syndromes consist of rare disorders resulting from mutations in genes encoding for presynaptic, synaptic, and postsynaptic proteins that are involved in the signal transmission of the neuromuscular junction. They are characterized by fatigable weakness of the skeletal muscles with symptom onset from birth to early childhood. DOK7 (downstream of tyrosine kinase 7) congenital myasthenic syndrome was previously treated successfully with ephedrine and salbutamol; however, both are unavailable in the United States. Methods: Case report of a child with muscle weakness. Results: This report describes a boy who presented only with progressive limb-girdle muscle weakness since age 2 years. The muscle biopsy with extensive studies revealed no obvious etiologies. His muscle weakness rapidly worsened, requiring a wheelchair for daily activities. Expanded neuromuscular gene panel promptly led to the diagnosis of DOK7 congenital myasthenic syndrome, and his muscle strength dramatically and persistently improved in four weeks with albuterol treatment, allowing him to walk independently. In a brief literature review, 15 patients (five treated between ages 5 and 17 years) from the Mayo Clinic with DOK7 mutations were also successfully treated with albuterol. Conclusion: DOK7 congenital myasthenic syndrome often presents with limb-girdle muscle weakness, which can become progressive without proper treatment. If muscle biopsy reveals no obvious etiology, an expanded neuromuscular gene panel may lead to a specific diagnosis of congenital myasthenic syndrome such as those due to DOK7 mutation. Albuterol is often used to treat bronchial asthma; however, it can also dramatically and persistently improve the muscle strength of DOK7 congenital myasthenic syndrome.
    Pediatric Neurology 10/2015; DOI:10.1016/j.pediatrneurol.2015.09.019
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    ABSTRACT: Background: Mutations of SLC9A6 may cause an X-linked clinical syndrome first described by Christianson in 1999 in which affected males exhibited profound intellectual disability, autism, drug-resistant epilepsy, ophthalmoplegia, mild craniofacial dysmorphism, microcephaly, and ataxia. Methods: We describe a child with an SLC9A6 mutation and an electroencephalographic pattern consistent with electrographic status epilepticus of sleep. Results: Our patient's electrographic status epilepticus of sleep resolved after treatment with felbamate. Following treatment, he remained seizure-free but did not make significant or lasting gains in language. Conclusion: Our report extends the clinical epilepsy phenotype in children with SLC9A6 mutations to include electrographic status epilepticus of sleep. In addition, felbamate was an effective treatment for electrographic status epilepticus of sleep in our patient.
    Pediatric Neurology 09/2015; DOI:10.1016/j.pediatrneurol.2015.07.007
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    ABSTRACT: Objective: We determined the effect of perinatally acquired HIV on neurocognition in Myanmar children treated with antiretroviral therapy by comparison to demographically matched seronegative children. Background: Myanmar has one of the highest HIV-1 prevalence rates in Southeast Asia. Studies from other resource-poor countries have shown that HIV-infected children differ in socioeconomic, nutritional and caregiver status compared to normal controls. Some vertically infected orphans in Myanmar reside separately from HIV-uninfected children in separate orphanages, thus the demographic variables of interest are naturally controlled. This study provides a unique evaluation of the neurocognitive effects of HIV in children, with control over key demographic variables. We hypothesized that HIV-infected orphans would perform significantly worse on cognitive indices compared with HIV-negative orphans. Design/methods: A battery of cognitive tests sensitive to HIV-associated impairments in children was administered to 28 perinatally acquired HIV-positive children and 31 HIV-negative children from two orphanages in Myanmar; 21 children from each cohort underwent testing at baseline and again after 12 months. Results: Baseline comparison of the two groups indicated that the HIV-infected children performed poorly across all tests, with significant group differences in executive function, visuospatial reasoning, fine motor dexterity, and visual motor integration. On subsequent testing, both cohorts of children showed improvements across multiple domains, with no significant effect of age at treatment initiation. Conclusions: Our results demonstrate a strong effect of HIV infection on specific neurocognitive deficits in vertically infected children. Understanding viral and host determinants and timing and choice of antiretroviral therapy on cognition will be critical to preventing cognitive impairment of children with HIV.
    Pediatric Neurology 09/2015; DOI:10.1016/j.pediatrneurol.2015.08.004
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    ABSTRACT: Craniosynostosis is the premature fusion of one or more of the cranial sutures. It may be spontaneous, syndromic, or familial and can present in many different forms. Familiarity with associated head shapes can allow bedside diagnosis and differentiation from positional plagiocephaly. Multiple surgical options for craniosynostosis currently exist, but early referral to a pediatric craniofacial center is needed to allow all options to be explored. This review seeks to familiarize pediatric neurologists with the nuances of craniosynostosis.
    Pediatric Neurology 09/2015; 53(5). DOI:10.1016/j.pediatrneurol.2015.07.006

  • Pediatric Neurology 09/2015; DOI:10.1016/j.pediatrneurol.2015.08.008
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    ABSTRACT: Introduction: Stiff person syndrome is a rare autoimmune, neurological disorder characterized by progressive rigidity and episodic painful spasms, predominantly affecting the proximal limbs and axial muscles, and leading to progressive disability. We report the case of a child who developed symptoms compatible with stiff person syndrome during treatment for pleuropulmonary blastoma. Patient description: A 3-year, 5-month-old girl was admitted for gradually worsening postural tremor, painful spasms, and generalized stiffness. Since the age of 3 years, she had been on adjuvant chemotherapy for pleuropulmonary blastoma before surgical resection. Brain magnetic resonance imaging and electroencephalographic findings were normal. Although serologic tests for autoimmune disease, including paraneoplastic antibodies and antiglutamic acid decarboxylase antibodies, were unremarkable, her findings were attributed to a paraneoplastic syndrome based on her clinical features and medical history. However, following the planned pulmonary lobectomy, her symptoms were paradoxically aggravated, with continuous motor unit potential at rest on electromyography, which occurs in stiff person syndrome. She gradually improved during postadjuvant chemotherapy with simultaneous immunotherapy including intravenous immunoglobulins and methylprednisolone, and she had recovered completely when evaluated at the 22-month follow-up visit after completion of her treatment for pleuropulmonary blastoma. Conclusion: We present the first documented child with stiff person syndrome associated with pleuropulmonary blastoma. The marked clinical improvement following chemotherapy for pleuropulmonary blastoma was yet more proof of the pleuropulmonary blastoma-related stiff person syndrome. In children with a malignancy and stiff person syndrome, a paraneoplastic syndrome should be considered and the treatment for the malignancy must be undertaken.
    Pediatric Neurology 09/2015; 53(5). DOI:10.1016/j.pediatrneurol.2015.06.015

  • Pediatric Neurology 09/2015; 53(5). DOI:10.1016/j.pediatrneurol.2015.08.002
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    ABSTRACT: Objective: We evaluated the temporal course of seizure outcome in children with pathology-confirmed focal cortical dysplasia and explored predictors of sustained seizure freedom. Methods: We performed a single-center retrospective study of children ≤18 years who underwent resective surgery from January 1, 2000 through December 31, 2012 and had pathology-proven focal cortical dysplasia. Surgical outcome was classified as seizure freedom (Engel class I) or seizure recurrence (Engel classes II-IV). Fisher exact and nonparametric Wilcoxon ranksum tests were used, as appropriate. Survival analysis was based on seizure-free outcome. Patients were censored at the time of seizure recurrence or seizure freedom at last follow-up. Results: Thirty-eight patients were identified (median age at surgery, 6.5 years; median duration of epilepsy, 3.3 years). Median time to last follow-up was 13.5 months (interquartile range, 7-41 months). Twenty patients (53%) were seizure free and 26 patients (68%) attained seizure freedom for a minimum of 3 months. Median time to seizure recurrence was 38 months (95% confidence interval, 6-109 months), and the cumulative seizure-free rate was 60% at 12 months (95% confidence interval, 43%-77%). Clinical features associated with seizure freedom at last follow-up included older age at seizure onset (P = .02), older age at surgery (P = .04), absent to mild intellectual disability before surgery (P = .05), and seizure freedom for a minimum of 3 months (P < .001). Conclusion: Favorable clinical features associated with sustained seizure freedom included older age at seizure onset, older age at surgery, absent or mild intellectual disability at baseline, and seizure freedom for a minimum of 3 months.
    Pediatric Neurology 09/2015; DOI:10.1016/j.pediatrneurol.2015.09.004