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Mohamed O. E. Babiker,
Journal of Pediatric Epilepsy, Volume 06, pp 169-173; https://doi.org/10.1055/s-0037-1606558

Abstract:
This study aims to determine the comprehensiveness of pediatric epilepsy outpatient clinic letters in a tertiary pediatric neurology center with particular focus on the prescribing instructions. A retrospective study was conducted for all pediatric outpatient epilepsy clinic letters between August and October 2016. This study was undertaken in a tertiary pediatric neurology department at the Bristol Royal Hospital for Children, United Kingdom. A total of 160 patients were identified during the time period and included in the study. Letters were evaluated for the following information: patient demographics, inclusion of problem list, and medication details including the clarity of prescribing instructions. The comprehensiveness of letters was scored out of nine based on the nine categories; weight, diagnosis list, medication list, dose in milligrams, dose equivalence in milligrams/kilograms/day, formulation, strength or concentration of medication, if applicable is the volume of medication provided and is the trade name provided. A total of 94% of letters had a diagnosis or problem list provided which was clear. Only 68% letters had a separate medication list provided. The dose of antiepileptic drugs (AEDs) in milligrams was provided in 95% of letters. The formulation of the AED was provided in only 30% of letters. Only 24% of letters where a category 1 AED was prescribed had the trade name provided. This study has demonstrated significant omissions from outpatient pediatric epilepsy letters. The omissions presented in this study may culminate in inefficient communication and increased morbidity. We share practice improving learning points for writing comprehensive letters which we believe can be generalized to other pediatric specialties.
Fumikazu Sano, Tetsuo Ohyama, Kanji Sugita, Masao Aihara, Hideaki Kanemura
Journal of Pediatric Epilepsy, Volume 06, pp 133-140; https://doi.org/10.1055/s-0037-1604354

Abstract:
The relationship between attention deficit/hyperactivity disorder (ADHD) and frontal lobe epilepsy (FLE) in children is not well understood. Patients with FLE between 6 and 15 years of age were studied. Scores on the ADHD rating scale (ADHD-RS) and Wisconsin card sorting test (WCST) were obtained at baseline. Behavioral changes were evaluated using the ADHD-RS scores at 6, 12, and 24 months after seizure onset. Perseverative errors of Nelson (PEN) scales on WCST were also evaluated at same time periods. The relationships between clinical manifestations and neuropsychological disturbances were analyzed. In 34 patients, the ADHD-RS score at 24 months after onset was most strongly associated with the presence of status epilepticus (SE, p = 0.004, β = 0.490) followed by seizure frequency (p = 0.021, β = 0.382). The increase in ADHD-RS score was most strongly associated with seizure frequency (p < 0.001, β = 0.635). The PEN score on WCST at 24 months was most strongly associated with seizure frequency (p = 0.001, β = 0.724). The increase in PEN score on WCST was most strongly associated with seizure frequency (p = 0.001, β = 0.872). The only clinical factor associated with both the ADHD-RS and the PEN scores on the WCST was seizure frequency. Seizure frequency may be correlated with risk for ADHD in children with FLE.
Virupaxi Hattiholi,
Journal of Pediatric Epilepsy, Volume 06, pp 161-163; https://doi.org/10.1055/s-0037-1604293

Abstract:
Nonketotic hyperglycinemia is a fatal disorder of glycine metabolism presenting with intractable epilepsy, hypotonia, and developmental delay in infancy. Diagnostic tests,such as cerebrospinal fluid glycine estimation and genetic diagnostic methods, are not widely available in developing countries and hence many cases are missed or wrongly diagnosed. The magnetic resonance imaging features, such as abnormal signal intensity in the dorsal pons, midbrain, central tegmental tract, cerebral peduncle, and posterior limb of the internal capsule indicate an important clue to the possibility of the disease and help in guiding the treating neonatologist.
Erratum
Raffaele Falsaperla, Robinson Gutierrez, Gabriela Reyes Valenzuela, Piero Pavone, Sebastian Fortini, Juan Pociecha,
Journal of Pediatric Epilepsy, Volume 06; https://doi.org/10.1055/s-0037-1603912

Abstract:
It has been brought to the publisher's attention that the name of author Raffaele Falsaperla was listed incorrectly in the above article in the Journal of Pediatric Epilepsy, published online on May 25, 2017 (DOI: 10.1055/s-0037-1603521). The author's name was originally published as “Raffaelle Falsaperla.” The correct listing of the author's name appears above.
Sean Lew, Christopher Inglese, Wade Mueller,
Journal of Pediatric Epilepsy, Volume 06, pp 125-132; https://doi.org/10.1055/s-0037-1603774

Abstract:
The insula, also known as the fifth lobe of the brain, is a phylogenetically older part of the cortex that forms the floor of the Sylvian fissure. It is densely connected with multiple regions in the brain, reflecting its rich functionality. Epilepsy arising from the insula has been only relatively recently described and characterized in details. Besides having unique features, the insula is believed to be the origin of seizures resembling those of suspected temporal or frontal lobe epilepsy that do not respond to traditional surgical resections. In this review article, we describe the gross and functional anatomy of the insula, clinical and electrophysiological manifestations of insular epilepsy, and surgical evaluation and treatment approaches.
Sarah Marion, Robert Asarnow, Gary Mathern,
Journal of Pediatric Epilepsy, Volume 06, pp 141-148; https://doi.org/10.1055/s-0037-1604000

Abstract:
Hemispherectomy is a routine surgery performed for children with intractable seizures and often in the midst of a life-threatening emergency such as status epilepticus. As the following article will demonstrate, studies of neurocognitive outcome in general, and memory in specific, following hemispherectomy are mixed, although findings tend to indicate stronger lateralization of verbal memory. This is often demonstrated by loss of verbal memory following left hemispherectomy, although there are few studies focusing solely on hemispherectomy and neurocognitive outcome. We examined data from 25 patients who participated in the University of California, Los Angeles (UCLA) Pediatric Epilepsy Surgery Program (right hemisphere = 7; left hemisphere = 18). The California Verbal Learning Test-Children's Version was used as a verbal memory correlate, and the doors visual recall was used as a correlate of nonverbal memory. Based on a review of the literature, we hypothesized that (1) verbal memory would be significantly different between hemispheres with higher scores in the remaining left hemisphere; (2) nonverbal memory would be significantly different between hemispheres with higher scores in the remaining right hemisphere. Exploratory analyses were also undertaken. Implications for lateralization, medical factors, and plasticity are discussed.
Tarek Jallol, Mohammed Chaudhary, Husam Muhaish, Miral Mashhour, Raidah Baradie,
Journal of Pediatric Epilepsy, Volume 06, pp 164-168; https://doi.org/10.1055/s-0037-1603773

Abstract:
Tuberous sclerosis complex (TSC) is a neurocutaneous syndrome with an autosomal dominant pattern of inheritance. It is a multisystem genetic disease caused by mutations in the TSC1 and TSC2 genes. The neuroradiographic findings of TSC include cortical dysplasia (cortical tubers and cerebral white matter radial migration lines), subependymal nodules, and subependymal giant cell astrocytoma. In this article, we describe an interesting case of TSC with an extremely rare radiographic finding of focal right megalencephaly. Molecular genetic testing detected a heterozygous c.3814+2T>G (p.?) variant, not previously described in the literature. As per the 2012 International Tuberous Sclerosis Complex Consensus Group guidelines and the findings of the genetic testing, this mutation most probably should be considered as a pathogenic variant. There are few cases of hemimegalencephaly (HME) reported in the literature, associated with TSC. To our knowledge focal megalencephaly is an extremely rare neuroradiographic finding in patients with TSC and has been previously reported only once by Griffiths et al based on clinical diagnostic criteria. Despite the uncommon association, TSC is the only neurocutaneous syndrome with similar histological appearance to HME. It is recognized that the pathological features in TSC and HME are due to abnormal cell proliferation, migration, and organization which could also be a possible mechanism for the development of focal megalencephaly. The uncommon association of HME and TSC with cytological similarities makes us wonder if there could be similarities in the pathogenesis of these two conditions. The advances in molecular genetic testing, increasing use of next-generation sequencing, and discovery of new pathogenic variants could answer some of these questions.
, Robinson Gutierrez, Gabriela Reyes Valenzuela, , Sebastian Fortini, Juan Pociecha,
Journal of Pediatric Epilepsy, Volume 06, pp 149-155; https://doi.org/10.1055/s-0037-1603521

Abstract:
Objective We evaluated the electroclinical features, etiology, treatment, and outcome of 16 patients with single-epileptic spasms (ESs) with or without hypsarrhythmia (WoH). Methods Nine boys and seven girls had single-ESs. ESs were considered as single epileptic spasm variants when no other spasm occurred for 1 minute before and after each spasm. Age at the onset of ESs was between 2 and 84 months, with a mean age of 11 months. Results We recognized a group of 15 patients with single-ESs as the main type of seizure; 6 patients with WoH and 9 patients with hypsarrhythmia, respectively. Nine of these 15 patients had other types of seizures before the onset of single-ESs, and 12 patients had other types of seizures during the period in which the ESs occurred. Nine of 15 patients had a structural and seven had an unknown etiology. In 10 cases, the ESs were refractory to antiepileptic drugs, while 4 patients responded well to adrenocorticotropic hormone (ACTH), 1 to pyridoxine, and 2 to the ketogenic diet (KD). The remaining patient (patient.16) had single-ESs and electroclinical features of Lennox–Gastaut syndrome (LGS). Conclusion In this article, we present a series of infants who had daily single-ESs with or WoH. Those with single-ESs with hypsarrhythmia evolved to an epileptic encephalopathy. Video-electroencephalogram (EEG) and polygraphic-EEG recordings are crucial to identify the single-ESs.
Anila Babameto-Laku, Serla Grabova, ,
Journal of Pediatric Epilepsy, Volume 06, pp 156-160; https://doi.org/10.1055/s-0037-1603493

Abstract:
Epilepsy is an ever-changing field of research, with genetics and genomics playing a very important role in recent times. Novel technologies detecting chromosomal aberrations are applied widely, and array-based comparative genomic hybridization (array CGH) has become a basic diagnostic tool in a variety of neurologic and neuropsychiatric conditions. The authors describe five Albanian children suffering from epilepsy and screened for genetic problems using array CGH and other methods. A thorough neurological examination and imaging studies were performed for all patients, who in addition to seizures, suffered from diverse medical conditions such as microcephaly, developmental delay, intellectual disability, dysmorphic features, heart anomalies, cryptorchidism, and other clinical stigmata of an aberrant neurodevelopment. It is evident from our case reports that the array CGH as a diagnostic tool in molecular genetics has facilitated the recognition of microdeletions and microduplications as risk factors for both generalized and focal epilepsies. This method, therefore, clearly has a practical and scientific value in the investigation of children with epilepsy and associated intellectual disability and congenital anomalies.
Mostafa Awadh, Mary O'Regan, Timothy R. Martland, Rachel Kneen,
Journal of Pediatric Epilepsy, Volume 06, pp 103-110; https://doi.org/10.1055/s-0037-1599190

Abstract:
The purpose of this study was to collate information on the clinical use of rufinamide in a pediatric population with epilepsy. A standardized proforma was sent to a group of pediatric neurologists and pediatricians in the United Kingdom requesting information about patients who were prescribed rufinamide. A total of 76 patients, with a median (range) age of 10.2 (2.8–19.8) years, were included. The patients had heterogeneous epilepsy syndromes, including 30 (39.5%) with Lennox-Gastaut syndrome (LGS), refractory to a minimum of three previous antiepileptic drugs. The median (range) maintenance dose of rufinamide was 25.4 (6.3–60) mg/kg/d. After 3 months of treatment, two (2.6%) of the 76 patients became seizure free, and 21 (27.6%) had ≥ 50% reduction in seizure frequency. The median (range) duration of treatment was 4.2 (0.5–38.4) months. At the last follow-up, 15 (19.7%) of the 76 patients continued with ≥ 50% reduction in seizure frequency; 2 of whom remained seizure free. Eighteen (23.7%) patients had treatment-emergent unwanted effects contributing to its discontinuation in nine (11.8%). In this study of a heterogeneous group of children and young people with medically refractory epilepsy on rufinamide, there was ≥ 50% seizure reduction in 30% at 3 months and 20% at the last follow-up.
Dallas Armstrong, Jorge Muñoz-Bibiloni, Bridget Redondo, Jason Y. Park,
Journal of Pediatric Epilepsy, Volume 06, pp 119-124; https://doi.org/10.1055/s-0037-1599193

Abstract:
Reflex seizures are evoked by a specific afferent stimulus or activity. The pathophysiology of reflex seizures is thought to be hyperexcitability of cortical or subcortical neuronal areas that respond to a physiologic stimulus in an exaggerated manner. This hyperexcitability could occur due to underlying lesions or genetic abnormalities. We present a 7-year-old Latino boy with epilepsy, autism spectrum disorder, developmental impairment, and reflex seizures triggered by water and bathing. His seizures were refractory to antiseizure medications. After multiple trials of medications, a vagal nerve stimulator was placed and desensitization therapy initiated. An epilepsy gene panel test was obtained, which showed a mutation in the SYN1 gene (c.1264C > T het, p.Arg422*). There is only one other publication of a family with SYN1 gene mutation and reflex bathing seizures. Identification of this correlation may be helpful in recognition and treatment of other patients and families with this rare presentation.
Journal of Pediatric Epilepsy, Volume 06, pp 115-118; https://doi.org/10.1055/s-0037-1599192

Abstract:
Transient oromotor deficits in children with rolandic epilepsy (RE) have been described in literature. It has been reported that thalamic aphasia can be caused by thalamic infarction or hemorrhage; however, it has never been reported that thalamic aphasia can be caused by epileptic disorders. Here, we describe a 6-year-old right-handed boy who showed transient oromotor deficits and speech disturbance with worsening of both epileptic seizure and paroxysmal discharges on electroencephalogram. He had paucity of spontaneous speech, feeble speech, arrest of speech, and anomia, but his repetition skills were intact. A single-photon emission computed tomography (SPECT) scan using technetium-99m hexamethyl propylene amine oxime (99mTc-HMPAO) to measure regional cerebral blood flow showed a reduction in flow in the left thalamus and ipsilateral frontotemporal areas, which appeared concurrently with the speech dysfunction. We suggest that speech disturbance such as thalamic aphasia, which is similar to the symptoms of Landau-Kleffner syndrome, may occur due to epileptic disorders such as RE. It may be possible to miss speech disturbance implicated in the thalamus in cases complicated by oromotor dysfunction. It is important that speech disturbance implicated in the thalamus is not overlooked in patients with RE showing an atypical course.
, , Gian Paolo Ramelli, , Danielle Mercati, Oliver Maier, Christophe Combescure, Maria Isabel Rodriguez, , Eliane Roulet, et al.
Journal of Pediatric Epilepsy, Volume 06, pp 111-114; https://doi.org/10.1055/s-0037-1599191

Abstract:
A significant proportion of children with seizures present with status epilepticus (SE), early in their disease. Our objective was to evaluate whether SCN1A variants predispose children to SE, outside of Dravet's syndrome. SCN1A analyses were performed in children aged 1 month to 16 years with at least one episode of status epilepticus (group A), and in children with short seizures only (group B). Clinical and genetic findings were compared between both groups. Total 99 children were included: 61 in group A, 38 in group B. SCN1A variants were found in 2 (3.3%) of 61 patients with status epilepticus and in 3 (7.9%) of 38 patients with short seizures. The difference between both groups was −4.6% (95% CI −18 to 5.1), and was not statistically significant (p = 0.37, Fisher's exact test). In four of these five children, seizures were observed in a GEFS+ familial context. The last patient had a generalized genetic epilepsy not further determined. SCN1A variants were not significantly more frequent in group A than in group B. Their predicted severity was not higher. Our results indicate that SCN1A variants per se do not determine seizure duration in children not affected by Dravet's syndrome.
Caroline Hadley, , ,
Journal of Pediatric Epilepsy, Volume 06, pp 097-102; https://doi.org/10.1055/s-0037-1599189

Abstract:
Hypothalamic hamartoma (HH) is a congenital intracranial lesion associated with precocious puberty and gelastic epilepsy in children. Surgical management of HH to treat refractory epilepsy is a mainstay of treatment. Our aim was to compare the demographic characteristics and perioperative costs associated with resection by craniotomy and stereotactic laser ablation (SLA) by reviewing our institutional experience with SLA and comparing these data to a national database for craniotomy and resection. Retrospective chart review was conducted for the Texas Children's Hospital cohort of patients who underwent SLA for HH between 2011 and 2013. Information about the craniotomy cohort representing historical cases of craniotomy was obtained from the Kids' Inpatient Database for years 2003, 2006, and 2009. The cohort definition for patients undergoing craniotomy for HH was modified from published adult literature to identify pediatric patients with refractory epilepsy secondary to HH. Our study has shown that children undergoing SLA for HH have a shorter length of stay and lower cost of hospitalization compared with those who underwent craniotomy and resection for the same diagnosis. Together with previous findings from our institution regarding the safety and efficacy of SLA, our findings suggest that SLA may represent an attractive alternative to craniotomy for the treatment of refractory epilepsy secondary to HH.
Nicholas J. Rosculet,
Journal of Pediatric Epilepsy, Volume 06, pp 091-096; https://doi.org/10.1055/s-0037-1599188

Abstract:
For the one-third of patients with epilepsy whose seizures are refractory to medications and who are not surgical or dietary therapy candidates, alternative therapies such as neurostimulation provide a promising alternative. Neurostimulation techniques include vagus nerve stimulation, deep brain stimulation (particularly stimulation of the anterior thalamus), and responsive neurostimulation. Accumulating data support neurostimulation techniques as a safe and effective option for seizure reduction and improved quality of life for drug-refractory patients.
Nancy Nussbaum, Dave Clarke, Cheng Ma,
Journal of Pediatric Epilepsy, Volume 06, pp 081-090; https://doi.org/10.1055/s-0037-1599187

Abstract:
Hot water epilepsy (HWE) refers to a rare form of reflex epilepsy precipitated by the stimulus of pouring hot water over the head or by bathing. Despite being most commonly seen in southern India, isolated HWE cases have surfaced in western countries. HWE classically manifests as simple or complex partial with temporal lobe semiology. About a quarter of patients show interictal EEG abnormalities, which mostly occur over the temporal lobes. HWE has two established variants that are typically benign. We present two cases where HWE preceded spontaneous seizures, which later progressed to pharmacoresistant epilepsy. These cases garner further evidence for a symptomatic variant of HWE. Additionally, clinical features of HWE are discussed and an updated model of pathogenesis incorporating self-inducement phenomenon is proposed.
Journal of Pediatric Epilepsy, Volume 06; https://doi.org/10.1055/s-0037-1599227

Abstract:
Journal of Pediatric Epilepsy wishes to recognize those who contributed as an expert peer reviewer of submitted scientific papers in 2016. Thank you for your contributions to Journal of Pediatric Epilepsy in 2016. Suellen Andrade Amita Atlee Franck Besag Luiz Eduardo Betting Patricia Crumrine Alexandre Datta Cornella Drees Monika Eisermann Edoardo Ferlazzo Orsi Gergo Melissa González Ayşegül Gündüz Boudewijn Gunning Ayako Hattori Gregory Holmes David Hsieh Mary Iype Ritu Kapur Renata R. Kieling Dick Lindhout Jun Mine Romina Moavero Marco Mula Veena Nair Sandra Poliachik Jonathan Roth Estevo Santamarina Dustin Scheinost William Sharp Pawel Sokal Salvatore Striano Gülten Thomas Peter Weber Homer Zeng
Tatyana Gitlevich, , Solomon L. Moshé
Journal of Pediatric Epilepsy, Volume 05, pp 168-175; https://doi.org/10.1055/s-0036-1584914

Abstract:
The Kozhevnikov-Rasmussen syndrome consists of a distinctive constellation of intractable, mainly focal, motor seizures, associated with relentlessly progressive hemiparesis and neuropsychological deterioration with cognitive and linguistic deficits. It dates back to the end of the 19th century and spans two continents. The main seizure type, epilepsia partialis continua, was first described by the Russian neurologist Kozhevnikov in 1894 and shortly after the eponym Kozhevnikov epilepsy was used both in Russian and in Western literature. The description of “focal seizures due to chronic localized encephalitis in children” by Rasmussen and his colleagues took place in 1958 and it was introduced as Rasmussen encephalitis. What began as a clinical observation became a complex syndrome affecting many age groups with a possible neuroimmunological etiology. Here we describe the historical perspectives underlying the establishment of the syndrome.
Dalila Lewis
Journal of Pediatric Epilepsy, Volume 05, pp 199-200; https://doi.org/10.1055/s-0036-1597590

Abstract:
Moder PN, Gupta PK, Sirsi D. Epilepsy Board Review. New York, NY: Demos Medical Publishing; 2017 (200 pp). ISBN 978-1-4939-6772-8 This comprehensive epilepsy review book contains questions that cover a broad range of topics in epilepsy including pediatrics, epidemiology, psychological and socioeconomic issues, neurogenetics, and inpatient/outpatient evaluation and management. I particularly enjoyed the chapter on basic electroencephalography (EEG), and also appreciated the emphasis on genetics and the surgical evaluation and management of epilepsy. The literature references cited in the explanations are appropriately selected and provide a sound basis for further review and learning. One area for improvement would be the quality of the images, as several are difficult to appreciate. For example, the magnetic resonance imaging (MRI) scan in question 6 of Chapter 3 claims to demonstrate increased fluid-attenuated inversion recovery (FLAIR) signal in left parieto-occipital region and right frontal region, supposedly depicting features of tuberous sclerosis; however, neither subependymal nodules nor cortical tubers are easy to discern on this image. Also, question 40 in Chapter 3 shows an MRI scan that purportedly demonstrates increased FLAIR signal in bilateral hippocampi and the left insula, but these findings are challenging to make out. Although many explanations are comprehensive, some lack clarity regarding key learning points or allow for ambiguity in interpretation. For example, question 20 in Chapter 1 concerns West syndrome; the explanation does not focus on the EEG characteristics one would expect in an epilepsy review book and it does not adequately emphasize the appropriate and accepted treatments (i.e., steroids and vigabatrin). Rather, all treatments are lumped together as if each is equally weighted with regard to efficacy; further, there is no mention of the ketogenic diet as a treatment option. Another example is question 22 in Chapter 1, which focuses on early myoclonic encephalopathy (EME). The explanation states, “neuroimaging is normal at onset, but progressive atrophy can be noted.” This statement is not entirely accurate since EME can have multiple etiologies, including brain malformation, in which case the initial MRI would not be normal. However, in general, these discrepancies are infrequent and the occasional lack of clarity is outweighed by repetition of the content in other chapters. As a pediatric neurologist, I was particularly pleased to find that pediatric topics are well represented, spanning the age range from the neonatal period to adolescence. Both familiar and uncommon pediatric epilepsy syndromes are included, such as tuberous sclerosis, infantile spasms, Sturge–Weber syndrome, and Zellweger syndrome. There are some awkwardly worded questions; for example, question 13 of Chapter 1 is about a 19-year-old boy with absence seizures; obviously, the authors meant to say that the boy is 9 years old. Similarly, some questions are oddly placed, for example, a question about the diagnosis of a rare congenital syndrome is placed in the chapter on seizure treatment rather than in the chapter on diagnosis of seizures and epilepsy (question 107 in Chapter 4). In summary, I found this review book to be a very useful and valuable study tool. The questions are sufficiently challenging and the explanations provided are typically succinct yet informative. I will continue to use this book as a platform for learning and certainly recommend it to other epilepsy trainees.
Carl E. Stafstrom
Journal of Pediatric Epilepsy, Volume 05, pp 198-198; https://doi.org/10.1055/s-0036-1597589

Abstract:
Nagarajan L, ed. Neonatal Seizures: Current Management and Future Challenges. London, UK: Mac Keith Press; 2016 (214 pp). ISBN 978–1-909962–67–5 Seizures in the neonatal period reflect dysfunction of the developing brain, with numerous etiologies spanning the spectrum from genetic to acquired. Neonatal seizures differ from seizures in older children and adults in critical ways. This slim volume, part of the International Review of Child Neurology series, provides an up-to-date review of neonatal seizures, covering their definition, pathophysiology, neuroradiological correlates, detection by electrophysiological monitoring, management, and outcome. The remarkable progress in the past decade in understanding the neurobiology of the developing brain, coupled with advances in neurophysiological monitoring (and, to a lesser extent, expanded treatment options) makes this topic a timely one for such a volume. The book provides a comprehensive overview of many important aspects of neonatal seizures. I found the chapter on the clinical approach to the neonate with seizures and the one on treatment options to be particularly valuable, and the chapter on neonatal epilepsy syndromes is notably comprehensive. There is balanced discussion about the various medications used and acknowledgment that we currently lack an ideal, age-specific, rational treatment. Neuroprotective approaches, such as therapeutic hypothermia, receive balanced consideration in several chapters. The chapters on conventional and amplitude-integrated electroencephalography (EEG) are clear and useful, providing well-reasoned indications as to when each modality is most informative. However, the chapter on automated seizure detection will be of marginal usefulness for the practicing physician. Unlike many similar publications, the EEG tracings here are crisp and easy to interpret. Many but not all of the authors are recognized authorities in the field. The book's editor wrote or coauthored 5 of the book's 12 chapters, and these are among the most clearly written. I would have liked to see more coverage of the neurobiology and neurophysiology of the developing brain, with some attempt to correlate seizure outcome with early pathophysiology, that is, how and why do neonatal seizures lead to later epilepsy (potential mechanisms of epileptogenesis). Some of the book's shortcomings warrant mention. There are numerous, avoidable editorial errors including the consistent misspelling of the word dependent in one chapter, the repeated reference to “Sandiper” (supposed to be Sandifer) syndrome, and numerous citations in the text that do not make it to the reference list. Other misspellings are plentiful as well; while these oversights do not diminish the book's impact, they do distract the reader. Overall, I recommend this book strongly to professionals who care for neonates with seizures, including pediatric neurologists, neonatologists, house officers in pediatrics and neurology, and neonatal nurses. It is the most contemporary and comprehensive coverage of neonatal seizures currently available in a single volume, and as such, comprises an important source of clinical information.
M.K. Bakhshandeh Bali, , Seyedeh Mohadeseh Taheri Otaghsara, Mohammad M. Nasehi, Eznollah Azargashb, , Mohammad Ghofrani
Published: 1 January 2013
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Journal of Pediatric Epilepsy, Volume 2, pp 125-129; https://doi.org/10.3233/PEP-13051

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Tiffany Rickertsen, Stephanie Danforth
Published: 1 January 2014
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Journal of Pediatric Epilepsy, Volume 3, pp 25-31; https://doi.org/10.3233/PEP-14070

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Kamer S. Rana, Shuvendu Roy, Daljit Singh
Published: 1 January 2012
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Journal of Pediatric Epilepsy, Volume 1, pp 243-248; https://doi.org/10.3233/PEP-12037

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Lucia Cibils, Juan Cameto, Gabriel Gonzalez
Published: 1 January 2014
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Journal of Pediatric Epilepsy, Volume 3, pp 113-116; https://doi.org/10.3233/PEP-14083

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Emilie Bourel-Ponchel,
Published: 1 January 2013
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Journal of Pediatric Epilepsy, Volume 2, pp 3-18; https://doi.org/10.3233/PEP-13041

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Perumpillichira J. Cherian, Katherine C. Nickels
Published: 1 January 2014
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Journal of Pediatric Epilepsy, Volume 3, pp 67-74; https://doi.org/10.3233/PEP-14074

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Tatiana Munoz, Julian A.J. Raiman
Published: 1 January 2014
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Journal of Pediatric Epilepsy, Volume 3, pp 229-234; https://doi.org/10.3233/PEP-14094

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Syndi A. Seinfeld, Gary W. Tye, Lawrence D. Morton
Published: 1 January 2012
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Journal of Pediatric Epilepsy, Volume 1, pp 125-128; https://doi.org/10.3233/PEP-2012-020

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Imen Abid, Fatma Kamoun, Chokri Boubaker, , Chahnez Triki
Published: 1 January 2014
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Journal of Pediatric Epilepsy, Volume 3, pp 121-125; https://doi.org/10.3233/PEP-14085

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Julia B. Hennermann
Published: 1 January 2014
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Journal of Pediatric Epilepsy, Volume 3, pp 207-215; https://doi.org/10.3233/PEP-14096

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Published: 1 January 2013
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Journal of Pediatric Epilepsy, Volume 2, pp 95-95; https://doi.org/10.3233/PEP-13047

Doerthe Keiner, Michael R. Gaab, Henry W.S. Schroeder, Joerg Baldauf,
Published: 1 January 2012
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Journal of Pediatric Epilepsy, Volume 1, pp 237-242; https://doi.org/10.3233/PEP-12036

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Erin Leyden
Published: 1 January 2013
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Journal of Pediatric Epilepsy, Volume 2, pp 209-214; https://doi.org/10.3233/PEP-13061

Gabriella Di Rosa, Maria Spanò, Patrizia Lenzo, Eleonora Parisi, Emanuela Tripodi, Eva Germanò, Rosamaria Siracusano, Gaetano Tortorella
Published: 1 January 2012
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Journal of Pediatric Epilepsy, Volume 1, pp 113-116; https://doi.org/10.3233/PEP-2012-018

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, Elisa Toffoli, , Ambra Salmaso, Elisabetta Canetta, , Pier A. Battistella,
Published: 1 January 2013
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Journal of Pediatric Epilepsy, Volume 2, pp 229-237; https://doi.org/10.3233/PEP-14063

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Published: 1 January 2013
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Journal of Pediatric Epilepsy, Volume 2, pp 73-85; https://doi.org/10.3233/PEP-13040

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Doris D.M. Lin, Anne Gallagher
Published: 1 January 2013
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Journal of Pediatric Epilepsy, Volume 2, pp 1-2; https://doi.org/10.3233/PEP-13045

Cristel M. Sørensen, Marianne Ifversen, , , Henrik Simonsen
Published: 1 January 2013
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Journal of Pediatric Epilepsy, Volume 2, pp 137-140; https://doi.org/10.3233/PEP-13053

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Vykuntaraju K.N. Gowda, Bharath Reddy, Bhaskar V. Madivala, Premalatha Ramaswamy, Sarala H.S. Gowda
Published: 1 January 2013
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Journal of Pediatric Epilepsy, Volume 2, pp 141-143; https://doi.org/10.3233/PEP-13054

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Eduardo Monese, Ricardo Cersósimo, Nidia Escobal, Adriana Sassone, Roberto Horacio Caraballo
Published: 1 January 2012
by 10.3233
Journal of Pediatric Epilepsy, Volume 1, pp 129-132; https://doi.org/10.3233/PEP-2012-021

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Juan L. Moya-Vilches, Marcelo Devilat
Published: 1 January 2014
by 10.3233
Journal of Pediatric Epilepsy, Volume 3, pp 93-106; https://doi.org/10.3233/PEP-14081

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Richard A. Prayson
Published: 1 January 2012
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Journal of Pediatric Epilepsy, Volume 1, pp 195-201; https://doi.org/10.3233/PEP-12031

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Jennifer Y. Lee, Patricia Bruno, Olivia T. Rabe, Elizabeth A. Thiele,
Published: 1 January 2012
by 10.3233
Journal of Pediatric Epilepsy, Volume 1, pp 97-101; https://doi.org/10.3233/PEP-2012-016

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Mahsa Parviz, Kara Vogel, K. Michael Gibson,
Published: 1 January 2014
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Journal of Pediatric Epilepsy, Volume 3, pp 217-227; https://doi.org/10.3233/PEP-14097

Abstract:
Clinical disorders known to affect inherited gamma-amino butyric acid (GABA) metabolism are autosomal recessively inherited succinic semialdehyde dehydrogenase and GABA-transaminase deficiency. The clinical presentation of succinic semialdehyde dehydrogenase deficiency includes intellectual disability, ataxia, obsessive-compulsive disorder and epilepsy with a nonprogressive course in typical cases, although a progressive form in early childhood as well as deterioration in adulthood with worsening epilepsy are reported. GABA-transaminase deficiency is associated with a severe neonatal-infantile epileptic encephalopathy.
Paul A. Caruso, , Ron Thibert, , Sandra Rincon,
Published: 1 January 2013
by 10.3233
Journal of Pediatric Epilepsy, Volume 2, pp 33-48; https://doi.org/10.3233/PEP-13046

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Taylor J. Abel, Royce W. Woodroffe, Daniel E. Couture, Hiroto Kawasaki
Published: 1 January 2014
by 10.3233
Journal of Pediatric Epilepsy, Volume 3, pp 45-53; https://doi.org/10.3233/PEP-14075

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Sahar A. Abd El-Aziz, Hesham El-Serogy
Published: 1 January 2012
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Journal of Pediatric Epilepsy, Volume 1, pp 229-235; https://doi.org/10.3233/PEP-12035

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Deborah Potvin, Nancy Nussbaum
Published: 1 January 2013
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Journal of Pediatric Epilepsy, Volume 2, pp 215-221; https://doi.org/10.3233/PEP-14067

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Saskia N. van der Crabben, Tom J. de Koning
Published: 1 January 2014
by 10.3233
Journal of Pediatric Epilepsy, Volume 3, pp 241-248; https://doi.org/10.3233/PEP-14098

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