Pediatric Neurology RSS feed: Current Issue. 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.http://www.pedneur.com/?rss=yesElsevier Inc.en © 2010 Elsevier Inc. All rights reserved. Pediatric Neurology0887-8994422February 2010 © 2010 Elsevier Inc. All rights reserved. healthpermissions@elsevier.comhttp://www.pedneur.com/article/PIIS0887899409003452/abstract?rss=yesPostural orthostatic tachycardia syndrome was defined in adult patients as an increase >30 beats per minute in heart rate of a symptomatic patient when moving from supine to upright position. Clinical signs may include postural tachycardia, headache, abdominal discomfort, dizziness/presyncope, nausea, and fatigue. The most common adolescent presentation involves teenagers within 1-3 years of their growth spurt who, after a period of inactivity from illness or injury, cannot return to normal activity levels because of symptoms induced by upright posture. Postural orthostatic tachycardia syndrome is complex and likely has numerous, concurrent pathophysiologic etiologies, presenting along a wide spectrum of potential symptoms. Nonpharmacologic treatment includes (1) increasing aerobic exercise, (2) lower-extremity strengthening, (3) increasing fluid/salt intake, (4) psychophysiologic training for management of pain/anxiety, and (5) family education. Pharmacologic treatment is recommended on a case-by-case basis, and can include β-blocking agents to blunt orthostatic increases in heart rate, α-adrenergic agents to increase peripheral vascular resistance, mineralocorticoid agents to increase blood volume, and serotonin reuptake inhibitors. An interdisciplinary research approach may determine mechanistic root causes of symptoms, and is investigating novel management plans for affected patients.Postural Orthostatic Tachycardia Syndrome: A Clinical ReviewJonathan N. Johnson, Kenneth J. Mack, Nancy L. Kuntz, Chad K. Brands, Coburn J. Porter, Philip R. Fischer10.1016/j.pediatrneurol.2009.07.002Pediatric Neurology 42, 2 (2010)2010-02-01Pediatric Neurology2010-02-01422S0887-8994(09)X0013-5Review Article7785http://www.pedneur.com/article/PIIS0887899409003919/abstract?rss=yesTo investigate the efficacy and safety of levetiracetam adjunctive therapy in childhood intractable epilepsy, data were reviewed for 130 children who had ≥4 seizures per month, whose seizures were intractable to an initial ≥2 antiepileptic drugs, and who could be monitored for at least 6 months after levetiracetam add-on. Reduction in seizure frequency and related variables were investigated. Sixty-two of the 130 patients (48%) showed a seizure reduction of ≥50%, and 28 patients (22%) became seizure-free. A reduction in seizures by ≥50% was observed in 33/64 in children with partial seizures (52%) and in 29/66 children with generalized seizures (44%). Efficacy did not differ significantly among seizure types. Overall efficacy was unaffected by abnormalities evident from magnetic resonance imaging, by mental retardation, or by maintenance dose of levetiracetam. The mean maintenance dose of levetiracetam was 47.0mg/kg per day (S.D. = ± 29.7), and mean follow-up duration was 13.4 months (S.D. =± 8.7). No demographic features differed significantly between patients with seizure freedom and without seizure remission. Levetiracetam was discontinued in 24 children at last visit (retention rate, 82%). The most common complaint was irritability (5%), and none of the adverse events were life threatening. In conclusion, levetiracetam adjunctive therapy is effective and safe for childhood intractable epilepsy.Efficacy and Safety of Adjunctive Levetiracetam Therapy in Pediatric Intractable EpilepsyYun Jin Lee, Hoon-Chul Kang, Heung Dong Kim, Joon Soo Lee10.1016/j.pediatrneurol.2009.08.002Pediatric Neurology 42, 2 (2010)2010-02-01Pediatric Neurology2010-02-01422S0887-8994(09)X0013-5Original Articles8692http://www.pedneur.com/article/PIIS0887899409004019/abstract?rss=yesWe investigated the incidence and 30-day case-fatality of childhood stroke in Estonia, and clinical signs and risk factors of childhood stroke. A retrospective (1995-2003) and prospective study (2004-2006) of childhood stroke (arterial ischemic, hemorrhagic, and sinovenous thrombosis) and transient ischemic attack was conducted. Stroke-incidence calculation was based on the prospective study. Clinical diagnoses of stroke were confirmed by neuroradiology. The incidence rate of childhood stroke in Estonia was 2.73/100,000 person-years for children aged 30 days to 18 years: 1.61/100,000 for arterial ischemic stroke, 0.87/100,000 for hemorrhagic stroke, 0.25/100,000 for sinovenous thrombosis, and 0.37/100,000 for transient ischemic attack. No arterial ischemic stroke patients died within 30 days, but case-fatality for intracerebral hemorrhage was 46%. Focal signs occurred in 100% of arterial ischemic strokes and 64% of intracerebral hemorrhage cases. Risk factors were identified in 35/48 (73%) children with cerebrovascular attacks. Six children with arterial ischemic stroke (6/24, 25%) manifested more than one risk factor. The incidence rate of childhood stroke in Estonia is similar to that in earlier data.Epidemiology of Childhood Stroke in EstoniaRael Laugesaar, Anneli Kolk, Ülle Uustalu, Pilvi Ilves, Tiiu Tomberg, Inga Talvik, Kristel Köbas, Valentin Sander, Tiina Talvik10.1016/j.pediatrneurol.2009.08.009Pediatric Neurology 42, 2 (2010)2010-02-01Pediatric Neurology2010-02-01422S0887-8994(09)X0013-5Original Articles93100http://www.pedneur.com/article/PIIS0887899409003890/abstract?rss=yesNormal-appearing white matter has been shown via diffusion tensor imaging to be affected in tuberous sclerosis complex. Under the hypothesis that some systems might be differentially affected, including the visual pathways and systems of social cognition, diffusion properties of various regions of white matter were compared. For 10 patients and 6 age-matched control subjects, 3 T magnetic resonance imaging was assessed using diffusion tensor imaging obtained in 35 directions. Three-dimensional volumes corresponding to the geniculocalcarine tracts were extracted via tractography, and two-dimensional regions of interest were used to sample other regions. Regression analysis indicated lower fractional anisotropy in the splenium of corpus callosum and geniculocalcarine tracts in tuberous sclerosis complex group, as well as lower axial diffusivity in the internal capsule, superior temporal gyrus, and geniculocalcarine tracts. Mean and radial diffusivity of the splenium of corpus callosum were higher in the tuberous sclerosis complex group. The differences in diffusion properties of white matter between tuberous sclerosis complex patients and control subjects suggest disorganized and structurally compromised axons with poor myelination. The visual and social cognition systems appear to be differentially involved, which might in part explain the behavioral and cognitive characteristics of the tuberous sclerosis complex population.Diffusion Features of White Matter in Tuberous Sclerosis With TractographyMichelle L. Krishnan, Olivier Commowick, Shafali S. Jeste, Neil Weisenfeld, Arne Hans, Matthew C. Gregas, Mustafa Sahin, Simon K. Warfield10.1016/j.pediatrneurol.2009.08.001Pediatric Neurology 42, 2 (2010)2010-02-01Pediatric Neurology2010-02-01422S0887-8994(09)X0013-5Original Articles101106http://www.pedneur.com/article/PIIS0887899409004020/abstract?rss=yesUsing the Child Behavior Checklist, the behavior of 16 children with cryptogenic localization-related epilepsy was assessed at first admission to our epilepsy center, and approximately 2 years later. Behavior improved substantially from t1 (first assessment, when patients were admitted to our center) to t2 (reassessment after approximately 2 years) on almost all subscales of the Child Behavior Checklist. At t2, all subscales scored within normal range. Furthermore, seizure frequency improved considerably in the 2 years between assessments. After a period of approximately 2 years, normalization of behavior in children with cryptogenic localization-related epilepsy occurred.Behavior in Children With Cryptogenic Localization Related Epilepsy: A Follow-Up StudySaskia G.M. van Mil, Rianne P. Reijs, Mariette H.J.A. van Hall, Suzanne M. Snoeijen, Nora M. de la Parra, Albert P. Aldenkamp10.1016/j.pediatrneurol.2009.08.008Pediatric Neurology 42, 2 (2010)2010-02-01Pediatric Neurology2010-02-01422S0887-8994(09)X0013-5Original Articles107110http://www.pedneur.com/article/PIIS0887899409004342/abstract?rss=yesThis study assessed the prevalence rate of epilepsy and its causes in children and adolescents in one area of high deprivation in São Paulo, São Paulo, in Southeast Brazil. Between July 2005 and June 2006, 4947 families from a population of 22,013 inhabitants (including 10,405 children and adolescents between the ages of 0 and 16 years) living in the shantytown of Paraisópolis, were interviewed. In the first phase, a validated questionnaire was administered, to identify the occurrence of seizures. In the second phase, clinical history, neurologic examination, electroencephalography, and structural neuroimaging were performed. The diagnosis of epilepsy, including etiology, seizure types, and epileptic syndrome classification, was according to criteria of the International League Against Epilepsy. The screening phase identified 353 presumptive cases. In the second phase, 101 of these cases (33.8%) received the diagnosis of epilepsy. Crude prevalence of epilepsy was 9.7/1000 and prevalence of active epilepsy was 8.7/1000. Partial seizures were the most frequent seizure type (62/101). Symptomatic focal epilepsy was the most common form, and hypoxic-ischemic encephalopathy the most common etiology, reflecting the socioeconomic conditions of this specific population. Adequate public policies regarding perinatal assistance could help reduce the prevalence of epilepsy.Prevalence of Epilepsy in Children From a Brazilian Area of High DeprivationLetícia P.B. Sampaio, Luis Otávio S.F. Caboclo, Karina Kuramoto, Ângela Reche, Elza Márcia T. Yacubian, Maria Luiza G. Manreza10.1016/j.pediatrneurol.2009.09.002Pediatric Neurology 42, 2 (2010)2010-02-01Pediatric Neurology2010-02-01422S0887-8994(09)X0013-5Original Articles111117http://www.pedneur.com/article/PIIS0887899409004007/abstract?rss=yesMeasures of cognition support diagnostic and treatment decisions in attention deficit hyperactivity disorder. We used an integrative neuroscience framework to assess cognition and associated brain-function correlates in large attention deficit hyperactivity disorder and healthy groups. Matched groups of 175 attention deficit hyperactivity disorder children/adolescents and 175 healthy control subjects were assessed clinically, with the touch screen-based cognitive assessment battery “IntegNeuro” (Brain Resource Ltd., Sydney, Australia) and the “LabNeuro” (Brain Resource Ltd., Sydney, Australia) platform for psychophysiologic recordings of brain function and body arousal. IntegNeuro continuous performance task measures of sustained attention classified 68% of attention deficit hyperactivity disorder patients with 76% specificity, consistent with previous reports. Our additional cognitive measures of impulsivity, intrusive errors, inhibition, and response variability improved sensitivity to 88%, and specificity to 91%. Positive predictive power was 96%, and negative predictive power, 88%. These metrics were stable across attention deficit hyperactivity disorder subtypes and age. Consistent with their brain-based validity, cognitive measures were correlated with corresponding brain-function and body-arousal measures. We propose a combination of candidate cognitive “markers” that define a signature for attention deficit hyperactivity disorder: “sustained attention,” “impulsivity,” “inhibition,” “intrusions,” and “response variability.” These markers offer a frame of reference to support diagnostic and treatment decisions, and an objective benchmark for monitoring outcomes of interventions.Using Brain-Based Cognitive Measures to Support Clinical Decisions in ADHDLeanne M. Williams, Daniel F. Hermens, Thida Thein, C. Richard Clark, Nicholas J. Cooper, Simon D. Clarke, Chris Lamb, Evian Gordon, Michael R. Kohn10.1016/j.pediatrneurol.2009.08.010Pediatric Neurology 42, 2 (2010)2010-02-01Pediatric Neurology2010-02-01422S0887-8994(09)X0013-5Original Articles118126http://www.pedneur.com/article/PIIS0887899409004925/abstract?rss=yesPhilip R. Dodge was born in Beverly, Massachusetts. He received his undergraduate education at the University of New Hampshire and Yale University. He graduated from the University of Rochester's Medical School in 1948. After an internship at Strong Memorial Hospital in Rochester, New York, he pursued training in neurology and neuropathology at Boston City Hospital with Dr. Derek Denny-Brown, and at Massachusetts General Hospital with Dr. Raymond Adams. Dr. Dodge joined the Army during the Korean War, and served for a total of 6 years. His duty stations were in Tokyo, Japan; Fort Campbell, Kentucky; and Honolulu, Hawaii. During his military service, he provided neurosurgical, neurologic, and psychiatric care. These were times he fondly recalled.Philip Rodgers Dodge, MD, 1923-2009Marvin A. Fishman10.1016/j.pediatrneurol.2009.10.008Pediatric Neurology 42, 2 (2010)2010-02-01Pediatric Neurology2010-02-01422S0887-8994(09)X0013-5Tribute127128http://www.pedneur.com/article/PIIS0887899409004871/abstract?rss=yesWe describe two children from a consanguineous family who manifested mega-corpus callosum, polymicrogyria, and psychomotor retardation. These patients also exhibited the brain anomalies of pontine hypoplasia and an abnormal cerebellar vermis. Our report confirms the genetic nature of megalencephaly-polymicrogyria-mega-corpus callosum syndrome, suggests a possible autosomal-recessive inheritance, and expands the spectrum of this rare entity.Mega-Corpus Callosum, Polymicrogyria, and Psychomotor Retardation SyndromeParayil S. Bindu, Arun B. Taly, Sanjib Sinha, Rose D. Bharath10.1016/j.pediatrneurol.2009.09.012Pediatric Neurology 42, 2 (2010)2010-02-01Pediatric Neurology2010-02-01422S0887-8994(09)X0013-5Case Reports129132http://www.pedneur.com/article/PIIS0887899409004883/abstract?rss=yesAcute exacerbations of asthma are common in children, but limb weakness after such exacerbations is very unusual. Hopkins' syndrome, a poliomyelitis-like illness associated with asthma, is seldom reported in the literature. We describe a child with weakness of the lower limbs after an asthmatic attack. The clinical profile, possible pathogenesis, and treatment of Hopkins' syndrome are discussed.Flaccid Paralysis of the Limbs After an Asthmatic AttackSam C.M. Yeung, Gregory Antonio, Kin Sing Ip10.1016/j.pediatrneurol.2009.09.013Pediatric Neurology 42, 2 (2010)2010-02-01Pediatric Neurology2010-02-01422S0887-8994(09)X0013-5Case Reports133136http://www.pedneur.com/article/PIIS0887899409004391/abstract?rss=yesGenetic generalized epilepsy with febrile seizures plus (GEFS+) is an idiopathic generalized epileptic syndrome of heterogeneous phenotype. The cases described here are of two brothers, one with severe myoclonic epilepsy of infancy (Dravet syndrome) and the other myoclonic-astatic epilepsy. Their father experienced one simple febrile seizure in infancy and two generalized tonic-clonic seizures after head trauma in adulthood, and had generalized epileptiform activity in the electroencephalogram. He died in a severe sport accident before genetic testing could be performed. In both siblings, but not in their healthy mother, DNA analysis identified an unreported point mutation (c.3925 C>T) in exon 20 of the SCN1A gene. The missense mutation was therefore assumed to be inherited from the father, who had a very mild clinical picture, with a single febrile seizure and only occasional generalized tonic-clonic seizures. The offspring have GEFS+ phenotypes with opposite severity, an illustration of the broad intrafamilial variability of SCN1A gene mutations.Generalized Epilepsy With Febrile Seizures plus: Novel SCN1A MutationPetia S. Dimova, Iglika Yordanova, Veneta Bojinova, Albena Jordanova, Ivo Kremenski10.1016/j.pediatrneurol.2009.09.007Pediatric Neurology 42, 2 (2010)2010-02-01Pediatric Neurology2010-02-01422S0887-8994(09)X0013-5Case Reports137140http://www.pedneur.com/article/PIIS0887899409004366/abstract?rss=yesIdiopathic intracranial hypertension is the syndrome of elevated intracranial pressure without clinical, laboratory, or imaging evidence of intracranial pathology. The classic symptoms include headache, nausea, and vomiting. It may also be associated with blurry vision, diplopia, stiff neck, increasing head size, photophobia, anorexia, retro-orbital pain, lightheadedness, myalgia, and head tilt. Sixth nerve palsy is documented in 10-40% of patients with pseudotumor cerebri, in most series, but third nerve palsy is very rarely associated with pseudotumor cerebri. Described here is the novel case of a pseudotumor cerebri patient who had bilateral partial oculomotor palsy with sparing of the pupillary fibers.Bilateral Oculomotor Palsy Secondary to Pseudotumor CerebriHüseyin Tan10.1016/j.pediatrneurol.2009.09.004Pediatric Neurology 42, 2 (2010)2010-02-01Pediatric Neurology2010-02-01422S0887-8994(09)X0013-5Case Reports141142http://www.pedneur.com/article/PIIS088789940900486X/abstract?rss=yesHashimoto encephalopathy is a steroid-responsive encephalopathy associated with elevated blood concentrations of antithyroid antibodies. The patients are usually euthyroid or mildly hypothyroid. The clinical picture is pleomorphic, presenting with variable symptoms ranging from behavioral and cognitive changes, myoclonus, seizures, pyramidal tract dysfunction, involuntary movements, and cerebellar signs to psychosis and coma, with relapsing and progressive course. The diagnosis is often overlooked at presentation but is crucial, given that this is a treatable disease. Described here, with a literature review, is the youngest patient reported to date with Hashimoto encephalopathy.Hashimoto Encephalopathy in a Preschool GirlManuel Castro-Gago, Carmen Gómez-Lado, Mercedes Maneiro-Freire, Jesús Eirís-Puñal, Manuel Bravo-Mata10.1016/j.pediatrneurol.2009.09.011Pediatric Neurology 42, 2 (2010)2010-02-01Pediatric Neurology2010-02-01422S0887-8994(09)X0013-5Case Reports143146http://www.pedneur.com/article/PIIS088789940900441X/abstract?rss=yesMiller Fisher syndrome is classically described as an acute inflammatory polyneuropathy clinical variant, associating external ophthalmoplegia, ataxia and loss of tendon reflexes. Despite recent advances in the comprehension of this syndrome, with the description of anti-GQ1b anti-ganglioside antibodies associated with abnormal neuromuscular transmission in the serum of Miller Fisher syndrome patients, there is ongoing debate on the peripheral or central origin of the symptoms. Some authors argue that there is a brainstem and cerebellar involvement. Indeed, since description of the syndrome, numerous cases have been reported with electrophysiologic and imaging evidences of brainstem involvement in the syndrome. Described and discussed here is the case of a 4-year-old child with Miller Fisher syndrome and cerebral lesions evident on magnetic resonance imaging, suggesting a Fisher-Bickerstaff spectrum.A Pediatric Case of Fisher-Bickerstaff SpectrumMichael Tsapis, Vincent Laugel, Meriam Koob, Anne de Saint Martin, Michel Fischbach10.1016/j.pediatrneurol.2009.09.009Pediatric Neurology 42, 2 (2010)2010-02-01Pediatric Neurology2010-02-01422S0887-8994(09)X0013-5Case Reports147150http://www.pedneur.com/article/PIIS088789940900397X/abstract?rss=yesSchmid-Fraccaro syndrome is a rare genetic disease, characterized by modifications of chromosome 22 (partial trisomy or tetrasomy), accompanied by eye abnormality (coloboma) and anal atresia. Clinical and phenotypic features are variable, and neurologic disturbance with delays of mental, psychologic, and motor development may be present. Its definitive diagnosis is based on karyotype. We report on a 17-year-old girl with Schmid-Fraccaro syndrome and severe cognitive deficits and motor deficits, who presented at our healthcare unit for a medical consultation. Her physical examination was remarkable for bilateral coloboma of the iris, hypertelorism, bilateral preauricular tags, scoliosis, and cardiac systolic murmur. After her birth, she was evaluated for anal atresia and congenital cardiac disease, which led to a genetic investigation and a diagnosis of Schmid-Fraccaro syndrome. Life expectancy in Schmid-Fraccaro syndrome depends on the number and variety of malformations, but in most cases the prognosis is favorable.Schmid-Fraccaro Syndrome: Severe Neurologic FeaturesElisa Sfoggia Romagna, Marcelo Campos Appel da Silva, Patrícia Andréia Zanetti Ballardin10.1016/j.pediatrneurol.2009.07.020Pediatric Neurology 42, 2 (2010)2010-02-01Pediatric Neurology2010-02-01422S0887-8994(09)X0013-5Case Reports151153http://www.pedneur.com/article/PIIS0887899409004421/abstract?rss=yesCentral pontine myelinolysis and extrapontine myelinolysis are characterized by symmetric demyelination subsequent to rapid shifts in serum osmolality. Described here is a novel case of transient cortical blindness in association with imaging features of extrapontine myelinolysis, which occurred in a child with carbamoyl phosphate synthetase deficiency after rapid correction of hyperammonemia. Serum sodium levels were within normal limits at presentation and throughout the period of ammonia correction. A potential pathogenic mechanism of osmotic demyelination in the setting of acute treatment for hyperammonemia in a patient with a urea cycle abnormality includes disruption of the blood-brain barrier and re-equilibration of organic osmolytes, particularly glutamine.Extrapontine Myelinolysis Resulting in Transient Cortical BlindnessJennifer E. Langer, William G. Wilson, Prashant Raghavan, Robert S. Rust, Howard P. Goodkin10.1016/j.pediatrneurol.2009.08.012Pediatric Neurology 42, 2 (2010)2010-02-01Pediatric Neurology2010-02-01422S0887-8994(09)X0013-5Case Reports154156http://www.pedneur.com/article/PIIS0887899409004408/abstract?rss=yesSubependymal giant cell astrocytomas are benign tumors that constitute one of the primary features of tuberous sclerosis. Two infants with tuberous sclerosis had very unusual subependymal giant cell astrocytomas, confirmed on biopsy in one of the infants. In both cases, contrast-enhanced cranial magnetic resonance imaging suggested a calcified intra-axial mass with diffuse basal ganglia involvement extending into the lateral ventricle. Computed tomography confirmed calcification in both cases. The first patient had right temporal lobectomy for intractable epilepsy. Biopsy of the basal ganglia lesion in that case suggested subependymal giant cell astrocytoma. In infants, subependymal giant cell astrocytomas can present with unusual morphology and may feature diffuse basal ganglia involvement and severe calcification.Basal Ganglia Location of Subependymal Giant Cell Astrocytomas in Two InfantsUğur Işık, Alp Dinçer, Aydın Sav, Memet M. Özek10.1016/j.pediatrneurol.2009.09.008Pediatric Neurology 42, 2 (2010)2010-02-01Pediatric Neurology2010-02-01422S0887-8994(09)X0013-5Case Reports157159http://www.pedneur.com/article/PIIS0887899409004901/abstract?rss=yesOne of the favorite pursuits of child neurologists involves discussion of the various “spells” that look like epilepsy and are often treated as epilepsy, but that are actually nonepileptic. Perhaps it is the great number and variety of these events that please the neurologist, and cause anguish in anyone else who cares for these children. Dr. DiMario endeavors to entertain the former, and reassure the latter, with an extensive review that emphasizes the diagnostic clues leading to correct diagnoses, plus an epidemiologic overview of the extent of each problem. In considerable detail, he attempts to classify different types of events. He combines the phenomenology and circumstances of events with a child's behavior, age, and movements, to give readers a framework for differential diagnoses. This overview comprises the introductory section. In subsequent chapters, he covers specific entities, grouped as syncope and related events, sleep-related phenomena, conversion or somatoform disorders, factitious disorders, movement disorders, and headache syndromes.Non-Epileptic Childhood Paroxysmal DisordersRobert J. Baumann10.1016/j.pediatrneurol.2009.10.006Pediatric Neurology 42, 2 (2010)2010-02-01Pediatric Neurology2010-02-01422S0887-8994(09)X0013-5Book Review160160http://www.pedneur.com/article/PIIS0887899409005724/abstract?rss=yesCalendar10.1016/S0887-8994(09)00572-4Pediatric Neurology 42, 2 (2010)2010-02-01Pediatric Neurology2010-02-01422S0887-8994(09)X0013-5Calendar161161http://www.pedneur.com/article/PIIS0887899409005566/abstract?rss=yesTable of Contents10.1016/S0887-8994(09)00556-6Pediatric Neurology 42, 2 (2010)2010-02-01Pediatric Neurology2010-02-01422S0887-8994(09)X0013-5FrontmatterA1A2http://www.pedneur.com/article/PIIS0887899409005578/abstract?rss=yesInstructions to Contributors10.1016/S0887-8994(09)00557-8Pediatric Neurology 42, 2 (2010)2010-02-01Pediatric Neurology2010-02-01422S0887-8994(09)X0013-5FrontmatterA7A8