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
Year

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

Elsevier

  • 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, arXiv.org 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: 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; 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.2015.03.010
  • Pediatric Neurology 03/2015; DOI:10.1016/j.pediatrneurol.2015.03.003
  • [Show abstract] [Hide abstract]
    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; 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
  • Pediatric Neurology 03/2015; DOI:10.1016/j.pediatrneurol.2015.02.025
  • Pediatric Neurology 03/2015; 52(6). DOI:10.1016/j.pediatrneurol.2015.02.021
  • [Show abstract] [Hide abstract]
    ABSTRACT: To provide a diagnostic and management approach for narcolepsy in children. Narcolepsy is a chronic disabling disorder characterized by excessive daytime sleepiness, cataplexy, hypnogogic and/or hypnopompic hallucinations, and sleep paralysis. All four features are present in only half of the cases. Excessive daytime sleepiness is the essential feature of narcolepsy at any age and is usually the first symptom to manifest. A combination of excessive daytime sleepiness and definite cataplexy is considered pathognomonic of narcolepsy syndrome. New treatment options have become available over the past few years. Early diagnosis and management can significantly improve the quality of life of patients with narcolepsy with cataplexy. This review summarizes the pathophysiology, clinical features, and management options for children with narcolepsy. Copyright © 2015 Elsevier Inc. All rights reserved.
    Pediatric Neurology 03/2015; 52(6). DOI:10.1016/j.pediatrneurol.2015.02.020
  • Pediatric Neurology 03/2015; 52(6). DOI:10.1016/j.pediatrneurol.2015.02.019
  • [Show abstract] [Hide abstract]
    ABSTRACT: We evaluated the feasibility of using a portable infrared thermal camera to quantify the degree of thermal dysregulation (cold hands/feet) and test for naturally occurring within-patient skin temperature asymmetry in Rett syndrome. Infrared thermal images were acquired passively from 15 patients (mean age = 13.7 years, range 4-47) with clinical diagnoses of Rett. Images were acquired using a FLIR T400 infrared thermal camera (still images recorded at 5 Hz, resolution of 320 × 240 pixels, thermal sensitivity = 0.05°C; capture session lasted approximately 3 minutes). The infrared thermal camera was orthogonal to the body part (hands, feet) and positioned approximately 1 meter from the skin's surface. There were large intraindividual left/right differences in temperature. Seven (47%) and eight (53%) patients had statistically significant (P <0.05) left/right asymmetries between hands (mean difference = 0.87°C, standard deviation = 1.21) and feet (mean difference = 1.73°C, standard deviation = 3.03), respectively. Coders were reliable (intraclass correlations 0.97-0.99) on temperatures and selection of anatomical regions of interest. The degree of thermal asymmetry may reflect prolonged activity of the sympathetic nervous system and individual differences in sympathetic regulation. As clinical trials emerge and endpoints are considered, portable infrared thermal camera may provide one noninvasive means of evaluating changes in sympathetic regulation. Copyright © 2015 Elsevier Inc. All rights reserved.
    Pediatric Neurology 03/2015; DOI:10.1016/j.pediatrneurol.2015.03.018
  • Pediatric Neurology 02/2015; 52(6). DOI:10.1016/j.pediatrneurol.2015.02.022
  • [Show abstract] [Hide abstract]
    ABSTRACT: Diagnosing pediatric encephalitis is challenging because of varied clinical presentation, nonspecific neuroimaging features, and rare confirmation of causality. We reviewed acute neuroimaging of children with clinically suspected encephalitis to identify findings that may correlate with etiology and length of stay. Imaging of 141 children with clinically suspected encephalitis as part of The California Encephalitis Project from 2005 to 2012 at a single institution was reviewed to compare the extent of neuroimaging abnormalities to patient age, gender, length of stay, and unknown, possible, or confirmed pathogen. Scan review was blinded and categorized by extent and distribution of abnormal findings. Abnormal findings were evident on 23% (22/94) of computed tomography and 50% (67/134) of magnetic resonance imaging studies in the acute setting. Twenty children with normal admission computed tomography had abnormal findings on magnetic resonance imaging performed within 2 days. Length of stay was significantly longer among children with abnormal acute magnetic resonance imaging (P < 0.001) and correlated with increased complexity (Spearman rho = 0.4, P < 0.001) categorized as: no imaging abnormality, meningeal enhancement and/or focal nonenhancing lesion, multifocal lesions, confluent lesions, and lesions plus diffusion restriction, hemorrhage, or hydrocephalus. There was no correlation between neuroimaging findings and an identifiable pathogen (P = 0.8). Abnormal magnetic resonance imaging findings are more common than abnormal computed tomography findings in pediatric encephalitis. Increasing complexity of magnetic resonance imaging findings correlated with disease severity as evidenced by longer length of stay, but were not specific for an identifiable pathogen using a standardized diagnostic encephalitis panel. Copyright © 2015 Elsevier Inc. All rights reserved.
    Pediatric Neurology 02/2015; 52(6). DOI:10.1016/j.pediatrneurol.2015.02.024
  • [Show abstract] [Hide abstract]
    ABSTRACT: Spinal muscular atrophy is caused by survival motor neuron gene SMN1 mutations. SMN1 produces a full-length SMN1 protein isoform encoded by exons 1-7, and an axonal-SMN protein isoform encoded by exons 1-3 and intron 3. The axonal-SMN protein is expressed only in the embryonic period and plays a significant role in axonal growth. However, there has been no report on contribution of axonal-SMN to spinal muscular atrophy severity until now. Two Japanese boys with spinal muscular atrophy type 1 in our study presented with generalized muscle weakness and respiratory insufficiency soon after birth and required an artificial ventilator from early infancy. Patient 1 was compound heterozygous for two SMN1 mutations, whole-gene deletion, and an intragenic mutation (c.819_820insT). He retained one copy of SMN1 producing the N-terminal part of SMN1 including axonal-SMN. On the other hand, patient 2 was homozygous for SMN1 deletion. Both of them showed the same copy number of spinal muscular atrophy-modifying genes, NAIP and SMN2. These findings suggested that the C-terminal domain of full-length SMN1 determined the severity, irrespective of presence or absence of axonal-SMN expression. In patient 1, the C-terminal domain of full-length SMN1 determined spinal muscular atrophy severity, rather than the axonal-SMN, one copy of which could be present and intact. The presence or absence of axonal-SMN may not impact disease severity in spinal muscular atrophy type 1 patients. Copyright © 2015 Elsevier Inc. All rights reserved.
    Pediatric Neurology 02/2015; 52(6). DOI:10.1016/j.pediatrneurol.2015.02.023
  • Pediatric Neurology 02/2015; DOI:10.1016/j.pediatrneurol.2015.02.017