Publications
120 results found
Sewani S, Azamian MS, Mendelsohn BA, et al., 2024, Neurodevelopmental and other phenotypes recurrently associated with heterozygous BAZ2B loss-of-function variants., Am J Med Genet A, Vol: 194
The bromodomain adjacent to zinc finger 2B (BAZ2B) gene encodes a chromatin remodeling protein that has been shown to perform a variety of regulatory functions. It has been proposed that loss of BAZ2B function is associated with neurodevelopmental phenotypes, and some recurrent structural birth defects and dysmorphic features have been documented among individuals carrying heterozygous loss-of-function BAZ2B variants. However, additional evidence is needed to confirm that these phenotypes are attributable to BAZ2B deficiency. Here, we report 10 unrelated individuals with heterozygous deletions, stop-gain, frameshift, missense, splice junction, indel, and start-loss variants affecting BAZ2B. These included a paternal intragenic deletion and a maternal frameshift variant that were inherited from mildly affected or asymptomatic parents. The analysis of molecular and clinical data from this cohort, and that of individuals previously reported, suggests that BAZ2B haploinsufficiency causes an autosomal dominant neurodevelopmental syndrome that is incompletely penetrant. The phenotypes most commonly seen in association with loss of BAZ2B function include developmental delay, intellectual disability, autism spectrum disorder, speech delay-with some affected individuals being non-verbal-behavioral abnormalities, seizures, vision-related issues, congenital heart defects, poor fetal growth, and an indistinct pattern of dysmorphic features in which epicanthal folds and small ears are particularly common.
Stafki SA, Turner J, Littel HR, et al., 2023, The Spectrum of MORC2-Related Disorders: A Potential Link to Cockayne Syndrome, PEDIATRIC NEUROLOGY, Vol: 141, Pages: 79-86, ISSN: 0887-8994
Frasca A, Pavlidou E, Bizzotto M, et al., 2022, Not Just Loss-of-Function Variations Identification of a Hypermorphic Variant in a Patient With a CDKL5 Missense Substitution, NEUROLOGY-GENETICS, Vol: 8, ISSN: 2376-7839
Zimmels S, Balfour-Lynn IM, Christodoulou L, et al., 2022, Isolated bulbar palsy and dysphagia in children with respiratory symptoms, DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY, Vol: 64, Pages: 518-522, ISSN: 0012-1622
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- Citations: 1
Fernandez-Garcia MA, Stettner GM, Kinali M, et al., 2021, Genetic neuropathies presenting with CIDP-like features in childhood, NEUROMUSCULAR DISORDERS, Vol: 31, Pages: 113-122, ISSN: 0960-8966
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- Citations: 4
Tang S, Addis L, Smith A, et al., 2020, Phenotypic and genetic spectrum of epilepsy with myoclonic atonic seizures., Epilepsia, Vol: 61, Pages: 995-1007
OBJECTIVE: We aimed to describe the extent of neurodevelopmental impairments and identify the genetic etiologies in a large cohort of patients with epilepsy with myoclonic atonic seizures (MAE). METHODS: We deeply phenotyped MAE patients for epilepsy features, intellectual disability, autism spectrum disorder, and attention-deficit/hyperactivity disorder using standardized neuropsychological instruments. We performed exome analysis (whole exome sequencing) filtered on epilepsy and neuropsychiatric gene sets to identify genetic etiologies. RESULTS: We analyzed 101 patients with MAE (70% male). The median age of seizure onset was 34 months (range = 6-72 months). The main seizure types were myoclonic atonic or atonic in 100%, generalized tonic-clonic in 72%, myoclonic in 69%, absence in 60%, and tonic seizures in 19% of patients. We observed intellectual disability in 62% of patients, with extremely low adaptive behavioral scores in 69%. In addition, 24% exhibited symptoms of autism and 37% exhibited attention-deficit/hyperactivity symptoms. We discovered pathogenic variants in 12 (14%) of 85 patients, including five previously published patients. These were pathogenic genetic variants in SYNGAP1 (n = 3), KIAA2022 (n = 2), and SLC6A1 (n = 2), as well as KCNA2, SCN2A, STX1B, KCNB1, and MECP2 (n = 1 each). We also identified three new candidate genes, ASH1L, CHD4, and SMARCA2 in one patient each. SIGNIFICANCE: MAE is associated with significant neurodevelopmental impairment. MAE is genetically heterogeneous, and we identified a pathogenic genetic etiology in 14% of this cohort by exome analysis. These findings suggest that MAE is a manifestation of several etiologies rather than a discrete syndromic entity.
Yunan Gao Y, Irvine E, Eleftheriadou I, et al., 2020, Gene replacement ameliorates deficits in mouse and human models of cyclin-dependent kinase-like 5 disorder, Brain: a journal of neurology, Vol: 143, Pages: 811-832, ISSN: 0006-8950
Cyclin-dependent kinase-like 5 disorder is a severe neurodevelopmental disorder caused by mutations in the X-linked cyclin-dependent kinase-like 5 (CDKL5) gene. It predominantly affects females who typically present with severe early epileptic encephalopathy, global developmental delay, motor dysfunction, autistic features and sleep disturbances. To develop a gene replacement therapy, we initially characterized the human CDKL5 transcript isoforms expressed in the brain, neuroblastoma cell lines, primary astrocytes and embryonic stem cell-derived cortical interneurons. We found that the isoform 1 and to a lesser extent the isoform 2 were expressed in human brain, and both neuronal and glial cell types. These isoforms were subsequently cloned into recombinant adeno-associated viral (AAV) vector genome and high-titre viral vectors were produced. Intrajugular delivery of green fluorescence protein via AAV vector serotype PHP.B in adult wild-type male mice transduced neurons and astrocytes throughout the brain more efficiently than serotype 9. Cdkl5 knockout male mice treated with isoform 1 via intrajugular injection at age 28–30 days exhibited significant behavioural improvements compared to green fluorescence protein-treated controls (1012 vg per animal, n = 10 per group) with PHP.B vectors. Brain expression of the isoform 1 transgene was more abundant in hindbrain than forebrain and midbrain. Transgene brain expression was sporadic at the cellular level and most prominent in hippocampal neurons and cerebellar Purkinje cells. Correction of postsynaptic density protein 95 cerebellar misexpression, a major fine cerebellar structural abnormality in Cdkl5 knockout mice, was found in regions of high transgene expression within the cerebellum. AAV vector serotype DJ efficiently transduced CDKL5-mutant human induced pluripotent stem cell-derived neural progenitors, which were subsequently differentiated into mature neurons. When treating CDKL5-mutant neuro
Vlachou V, Larsen L, Pavlidou E, et al., 2019, SCN2A mutation in an infant with Ohtahara syndrome and neuroimaging findings: expanding the phenotype of neuronal migration disorders, Journal of Genetics, Vol: 98, ISSN: 0022-1333
Neuronal migration disorders (NMDs) are a heterogeneous group of conditions caused by the abnormal migration of neuroblasts in the developing brain and nervous system, resulting in severe developmental impairment, intractable epilepsy and intellectual disability (Spalice et al. 2009). To date, many genes have been identified as the leading cause of migration defects, i.e. agyria/pachygyria, polymicrogyria, heterotopias, agenesis of the corpus callosum and agenesis of the cranial nerves (Spalice et al. 2009). Here, we present a patient with early infantile epileptic encephalopathy (Ohtahara syndrome) with seizure onset on the first day of life, severe developmental delay and an abnormal brain MRI with excessive folding of small, fused gyri and bilateral perisylvian polymicrogyria, suggestive of neuronal migration disorder. To clarify the unknown aetiology, we conducted whole-exome sequencing, which detected a de novo missense variant (c.5308A>T; p.(Met1770Leu)) in the SCN2A gene. This is a report of SCN2A gene variant identified in a patient with neuronal migration disorder which could further expand the phenotypic spectrum of these genetic disorders.
Benger M, Mankad K, Proukakis C, et al., 2019, The interaction of genetic mutations in PARK2 and FA2H causes a novel phenotype in a case of childhood-onset movement disorder, Frontiers in Neurology, Vol: 10, ISSN: 1664-2295
Mutations in the PARK2 gene have been implicated in the pathogenesis of early-onset Parkinson's disease. We present a case of movement disorder in a 4-year-old child from consanguineous parents and with a family history of Dopamine responsive dystonia, who was diagnosed with early-onset Parkinson's disease based on initial identification of a pathogenic PARK2 mutation. However, the evolution of the child's clinical picture was unusually rapid, with a preponderance of pyramidal rather than extrapyramidal symptoms, leading to re-investigation of the case with further imaging and genetic sequencing. Interestingly, a second homozygous mutation in the FA2H gene, implicated in Hereditary spastic paraplegia, was revealed, appearing to have contributed to the novel phenotype observed, and highlighting a potential interaction between the two mutated genes.
Sri A, Daubeney P, Prasad S, et al., 2019, A case series on cardiac and skeletal involvement in two families with PRKAG2 mutations, Case Reports in Pediatrics, Vol: 2019, ISSN: 2090-6803
Background. PRKAG2 is a rare autosomal dominant syndrome that mainly presents with hypertrophic cardiomyopathy, ventricular preexcitation, and conduction abnormalities. This case report demonstrates that the PRKAG2 mutation presents with various phenotypes already in pediatric patients. Case Summary. We describe the clinical and investigative findings in two families with a PRKAG2 mutation from the different variants in the gene on chromosome 7q36.1, emphasising that the variability of phenotypes and that presentation in childhood is common. Furthermore, we highlight that skeletal myopathy and hypertrophic cardiomyopathy are significant debilitating characteristics of the PRKAG2 mutation. Conclusion. In our report of adult and pediatric patients, early presentation in childhood with hypertrophic cardiomyopathy and skeletal muscle involvement was common, demonstrating the challenges of the clinical management of PRKAG2 mutations.
Addis L, Sproviero W, Thomas SV, et al., 2018, Identification of new risk factors for rolandic epilepsy: CNV at Xp22.31 and alterations at cholinergic synapses., J Med Genet, Vol: 55, Pages: 607-616
BACKGROUND: Rolandic epilepsy (RE) is the most common genetic childhood epilepsy, consisting of focal, nocturnal seizures and frequent neurodevelopmental impairments in speech, language, literacy and attention. A complex genetic aetiology is presumed in most, with monogenic mutations in GRIN2A accounting for >5% of cases. OBJECTIVE: To identify rare, causal CNV in patients with RE. METHODS: We used high-density SNP arrays to analyse the presence of rare CNVs in 186 patients with RE from the UK, the USA, Sardinia, Argentina and Kerala, India. RESULTS: We identified 84 patients with one or more rare CNVs, and, within this group, 14 (7.5%) with recurrent risk factor CNVs and 15 (8.0%) with likely pathogenic CNVs. Nine patients carried recurrent hotspot CNVs including at 16p13.11 and 1p36, with the most striking finding that four individuals (three from Sardinia) carried a duplication, and one a deletion, at Xp22.31. Five patients with RE carried a rare CNV that disrupted genes associated with other epilepsies (KCTD7, ARHGEF15, CACNA2D1, GRIN2A and ARHGEF4), and 17 cases carried CNVs that disrupted genes associated with other neurological conditions or that are involved in neuronal signalling/development. Network analysis of disrupted genes with high brain expression identified significant enrichment in pathways of the cholinergic synapse, guanine-exchange factor activation and the mammalian target of rapamycin. CONCLUSION: Our results provide a CNV profile of an ethnically diverse cohort of patients with RE, uncovering new areas of research focus, and emphasise the importance of studying non-western European populations in oligogenic disorders to uncover a full picture of risk variation.
Vlachou V, Chu V, Pavlidou E, et al., 2018, Benign Infantile Epilepsy Mimicking Reflex Anoxic Seizures in an Infant with <i>PRRT2</i> Gene Mutation, INDIAN JOURNAL OF PEDIATRICS, Vol: 85, Pages: 690-690, ISSN: 0019-5456
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Benger M, Kinali M, Mazarakis N, 2018, Autism spectrum disorder: prospects for treatment using gene therapy, Molecular Autism, Vol: 9, ISSN: 2040-2392
Autism spectrum disorder (ASD) is characterised by the concomitant occurrence of impaired social interaction; restricted, perseverative and stereotypical behaviour; and abnormal communication skills. Recent epidemiological studies have reported a dramatic increase in the prevalence of ASD with as many as 1 in every 59 children being diagnosed with ASD. The fact that ASD appears to be principally genetically driven, and may be reversible postnatally, has raised the exciting possibility of using gene therapy as a disease-modifying treatment. Such therapies have already started to seriously impact on human disease and particularly monogenic disorders (e.g. metachromatic leukodystrophy, SMA type 1). In regard to ASD, technical advances in both our capacity to model the disorder in animals and also our ability to deliver genes to the central nervous system (CNS) have led to the first preclinical studies in monogenic ASD, involving both gene replacement and silencing. Furthermore, our increasing awareness and understanding of common dysregulated pathways in ASD have broadened gene therapy’s potential scope to include various polygenic ASDs. As this review highlights, despite a number of outstanding challenges, gene therapy has excellent potential to address cognitive dysfunction in ASD.
Gao Y, Irvine EE, Eleftheriadou I, et al., 2017, Gene therapy with AAV-CDKL5 vectors in models of CDKL5 disorder, European-Society-of-Gene-and-Cell-Therapy (ESCGT) Congress, Publisher: Mary Ann Liebert, Pages: A6-A7, ISSN: 1043-0342
Larsen LHG, Hao Q, Kako N, et al., 2017, TARGETED NEXT GENERATION SEQUENCING AS A DIAGNOSTIC TOOL IN 644 CHILDHOOD EPILEPSY PATIENTS AND TRANSMISSION OF VARIANTS FROM MOSAIC PARENTS, 32nd International Epilepsy Congress, Publisher: WILEY, Pages: S176-S177, ISSN: 0013-9580
Paleologou E, Ismayilova N, Kinali M, 2017, Use of the Ketogenic Diet to Treat Intractable Epilepsy in Mitochondrial Disorders., J Clin Med, Vol: 6, ISSN: 2077-0383
Mitochondrial disorders are a clinically heterogeneous group of disorders that are caused by defects in the respiratory chain, the metabolic pathway of the adenosine tri-phosphate (ATP) production system. Epilepsy is a common and important feature of these disorders and its management can be challenging. Epileptic seizures in the context of mitochondrial disease are usually treated with conventional anti-epileptic medication, apart from valproic acid. However, in accordance with the treatment of intractable epilepsy where there are limited treatment options, the ketogenic diet (KD) has been considered as an alternative therapy. The use of the KD and its more palatable formulations has shown promising results. It is especially indicated and effective in the treatment of mitochondrial disorders due to complex I deficiency. Further research into the mechanism of action and the neuroprotective properties of the KD will allow more targeted therapeutic strategies and thus optimize the treatment of both epilepsy in the context of mitochondrial disorders but also in other neurodegenerative disorders.
Pavlidou E, Ramachandran V, Govender V, et al., 2017, A novel PLP1 mutation associated with optic nerve enlargement in two siblings with Pelizaeus-Merzbacher disease: A new MRI finding., Brain Dev, Vol: 39, Pages: 271-274
Pelizaeus-Merzbacher disease (PMD) is a rare, X-linked disorder characterized by hypomyelination of the Central Nervous System due to mutations in the PLP1 gene. Certain mutations of the PLP1 gene correlate with specific clinical phenotypes and neuroimaging findings. We herein report a novel mutation of the PLP1 gene in two siblings with PMD associated with a rare and protean neuroimaging finding of optic nerve enlargement. To the best of our knowledge this is the first time that this novel mutation H133P of PLP1 gene is identified and clinically associated with optic nerve enlargement in PMD patients.
Pavlidou E, Pavlou E, Anastasiou A, et al., 2016, Posterior reversible encephalopathy syndrome after intrathecal methotrexate infusion: a case report and literature update., Quant Imaging Med Surg, Vol: 6, Pages: 605-611, ISSN: 2223-4292
Posterior reversible encephalopathy syndrome (PRES) is a rare clinical-radiological entity characterised by seizures, severe headache, mental status instability and visual disturbances. Hypertension is typically present. We report a case of a 13-year old boy with Burkitt lymphoma/leukaemia, who presented with posterior leukoencephalopathy 24 hours after intrathecal methotrexate (MTX) infusion. The child presented with headache, seizures, elevated blood pressure and gradual deterioration of his neurological status. Midazolam, dexamethazone and furosemide were initiated leading to reduction of cerebral oedema and clinical improvement. A thorough literature review is discussed in this report. Pathophysiology of leukoencephalopathy remains unclear. It develops within 5-14 days after intrathecal MTX and resolves within a week usually without permanent neurological sequelae. Broad use of MRI has led to an increasing number of identified cases of PRES. Treatment approach is mainly to manage the underlying cause of PRES. Prognosis is generally benign; however delayed diagnosis and improper management may result in permanent brain insult.
Panjwani N, Wilson MD, Addis L, et al., 2016, A microRNA-328 binding site in PAX6 is associated with centrotemporal spikes of rolandic epilepsy., Ann Clin Transl Neurol, Vol: 3, Pages: 512-522, ISSN: 2328-9503
OBJECTIVE: Rolandic epilepsy is a common genetic focal epilepsy of childhood characterized by centrotemporal sharp waves on electroencephalogram. In previous genome-wide analysis, we had reported linkage of centrotemporal sharp waves to chromosome 11p13, and fine mapping with 44 SNPs identified the ELP4-PAX6 locus in two independent US and Canadian case-control samples. Here, we aimed to find a causative variant for centrotemporal sharp waves using a larger sample and higher resolution genotyping array. METHODS: We fine-mapped the ELP4-PAX6 locus in 186 individuals from rolandic epilepsy families and 1000 population controls of European origin using the Illumina HumanCoreExome-12 v1.0 BeadChip. Controls were matched to cases on ethnicity using principal component analysis. We used generalized estimating equations to assess association, followed up with a bioinformatics survey and literature search to evaluate functional significance. RESULTS: Homozygosity at the T allele of SNP rs662702 in the 3' untranslated region of PAX6 conferred increased risk of CTS: Odds ratio = 12.29 (95% CI: 3.20-47.22), P = 2.6 × 10(-4) and is seen in 3.9% of cases but only 0.3% of controls. INTERPRETATION: The minor T allele of SNP rs662702 disrupts regulation by microRNA-328, which is known to result in increased PAX6 expression in vitro. This study provides, for the first time, evidence of a noncoding genomic variant contributing to the etiology of a common human epilepsy via a posttranscriptional regulatory mechanism.
Pavlidou E, Salpietro V, Phadke R, et al., 2016, Pontocerebellar hypoplasia type 2D and optic nerve atrophy further expand the spectrum associated with selenoprotein biosynthesis deficiency., Eur J Paediatr Neurol, Vol: 20, Pages: 483-488
BACKGROUND: The term Pontocerebellar hypoplasias collectively refers to a group of rare, heterogeneous and progressive disorders, which are frequently inherited in an autosomal recessive manner and usually have a prenatal onset. Mutations in the SEPSECS gene, leading to deficiency in selenoprotein biosynthesis, have been identified in recent times as the molecular etiology of different pre/perinatal onset neurological phenotypes, including cerebello-cerebral atrophy, Pontocerebellar hypoplasia type 2D and progressive encephalopathy with elevated lactate. These disorders share a similar spectrum of central (e.g., brain neurodegeneration with grey and white matter both involved) and peripheral (e.g., spasticity due to axonal neuropathy) nervous system impairment. CASE PRESENTATION: We hereby describe a 9-year-old boy with (i) a typical Pontocerebellar hypoplasia type 2D phenotype (e.g. profound mental retardation, spastic quadriplegia, ponto-cerebellar hypoplasia and progressive cerebral atrophy); (ii) optic nerve atrophy and (iii) mild secondary mitochondrial myopathy detected by muscle biopsy and respiratory chain enzyme analysis. We performed whole exome sequencing which identified a homozygous mutation of the SEPSECS gene (c.1001T > C), confirming the clinical suspect of Pontocerebellar hypoplasia type 2D. CONCLUSION: This report further corroborates the notion of a potential secondary mitochondrial dysfunction in the context of selenoprotein biosynthesis deficiency and also adds optic nerve atrophy as a new potential clinical feature within the SEPSECS-associated clinical spectrum. These findings suggest the presence of a possible shared genetic etiology among similar clinical entities characterized by the combination of progressive cerebello-cerebral and optic nerve atrophy and also stress the biological importance of selenoproteins in the regulation of neuronal and metabolic homeostasis.
Christodoulou L, Pavlidou E, Spyridou C, et al., 2016, Metaphyseal dysplasia associated with chronic facial nerve palsy, Child's Nervous System, Vol: 32, Pages: 1333-1336, ISSN: 1433-0350
IntroductionMetaphyseal dysplasia (Pyle disease) is a rare autosomal recessive disease with impressive and characteristic radiological findings but relatively mild clinical features. It is usually incidentally diagnosed, despite the impressive radiological findings of gross metaphyseal widening and thinning of cortical bone.Case reportHerein, we report an exceptionally unusual case of metaphyseal dysplasia in association with chronic facial nerve palsy.DiscussionChronic facial nerve palsy due to compression of the facial nerve in a patient with Pyle disease represents an unusual novelty. Furthermore, this case delineates the clinical spectrum and phenotype of such a rare clinical entity. To the best of our knowledge, this is the first time that such an association is being described.
Steel D, Salpietro V, Phadke R, et al., 2015, Whole exome sequencing reveals a MLL de novo mutation associated with mild developmental delay and without ‘hairy elbows’: expanding the phenotype of Wiedemann-Steiner syndrome, Journal of Genetics, Vol: 94, Pages: 755-758, ISSN: 0973-7731
Christodoulou L, Krishnaiah A, Spyridou C, et al., 2015, Kenny Caffey syndrome with severe respiratory and gastrointestinal involvement: expanding the clinical phenotype, QUANTITATIVE IMAGING IN MEDICINE AND SURGERY, Vol: 5, Pages: 476-479, ISSN: 2223-4292
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Salpietro V, Phadke R, Saggar A, et al., 2015, Zellweger syndrome and secondary mitochondrial myopathy., Eur J Pediatr, Vol: 174, Pages: 557-563
Defects in peroxisomes such as those associated with Zellweger syndrome (ZS) can influence diverse intracellular metabolic pathways, including mitochondrial functioning. We report on an 8-month-old female infant and a 6-month-old female infant with typical clinical, radiological and laboratory features of Zellweger syndrome; light microscopic and ultrastructural evidence of mitochondrial pathology in their muscle biopsies; and homozygous pathogenic mutations of the PEX16 gene (c.460 + 5G > A) and the PEX 12 gene (c.888_889 del p.Leu297Thrfs*12), respectively. Additionally, mitochondrial respiratory chain enzymology analysis in the first girl showed a mildly low activity in complexes II-III and IV. We also review five children previously reported in the literature with a presumptive diagnosis of ZS and additional mitochondrial findings in their muscle biopsies. In conclusion, this is the first study of patients with a molecularly confirmed peroxisomal disorder with features of a concomitant mitochondrial myopathy and underscores the role of secondary mitochondrial dysfunction in Zellweger syndrome, potentially contributing to the clinical phenotype.
Thomas M, Salpietro V, Canham N, et al., 2015, Mitochondria DNA Depletion Syndrome in a Infant with Multiple Congenital Malformations, Severe Myopathy, and Prolonged Postoperative Paralysis, JOURNAL OF CHILD NEUROLOGY, Vol: 30, Pages: 654-658, ISSN: 0883-0738
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Stuart HM, Roberts NA, Hilton EN, et al., 2015, Urinary Tract Effects of <i>HPSE2</i> Mutations, JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, Vol: 26, Pages: 797-804, ISSN: 1046-6673
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- Citations: 27
Rao V, El-Alem T, Aminu K, et al., 2013, Chitayat-Hall syndrome: extending the clinical phenotype., Clin Dysmorphol, Vol: 22, Pages: 156-160
Cregg R, Laguda B, Werdehausen R, et al., 2013, Novel Mutations Mapping to the Fourth Sodium Channel Domain of Nav1.7 Result in Variable Clinical Manifestations of Primary Erythromelalgia, NEUROMOLECULAR MEDICINE, Vol: 15, Pages: 265-278, ISSN: 1535-1084
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- Citations: 50
Scheffer IE, Grinton BE, Heron SE, et al., 2012, <i>PRRT2</i> phenotypic spectrum includes sporadic and fever-related infantile seizures, NEUROLOGY, Vol: 79, Pages: 2104-2108, ISSN: 0028-3878
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- Citations: 61
Garralda ME, Kinali M, Cirak S, et al., 2011, Emotional impact of a paediatric exon-skipping therapy trial, DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY, Vol: 53, Pages: 1157-1159, ISSN: 0012-1622
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- Citations: 3
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