Publications by authors named "Richard E Rosch"

We have investigated the theoretical constraints of the interactions between coupled cortical columns. Each cortical column consists of a set of neural populations where each population is modelled as a neural mass. The existence of semi-stable states within a cortical column is dependent on the type of interaction between the neuronal populations, i.

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Neuronal activity propagates through the network during seizures, engaging brain dynamics at multiple scales. Such propagating events can be described through the avalanches framework, which can relate spatiotemporal activity at the microscale with global network properties. Interestingly, propagating avalanches in healthy networks are indicative of critical dynamics, where the network is organized to a phase transition, which optimizes certain computational properties.

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Neural mass models are used to simulate cortical dynamics and to explain the electrical and magnetic fields measured using electro- and magnetoencephalography. Simulations evince a complex phase-space structure for these kinds of models; including stationary points and limit cycles and the possibility for bifurcations and transitions among different modes of activity. This complexity allows neural mass models to describe the itinerant features of brain dynamics.

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Status epilepticus is a life-threatening neurological emergency that affects both adults and children. Approximately 36% of episodes of status epilepticus do not respond to the current preferred first-line treatment, benzodiazepines. The proportion of episodes that are refractory to benzodiazepines is higher in low-income and middle-income countries (LMICs) than in high-income countries (HICs).

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Network control theory provides a framework by which neurophysiological dynamics of the brain can be modelled as a function of the structural connectome constructed from diffusion MRI. Average controllability describes the ability of a region to drive the brain to easy-to-reach neurophysiological states whilst modal controllability describes the ability of a region to drive the brain to difficult-to-reach states. In this study, we identify increases in mean average and modal controllability in children with drug-resistant epilepsy compared to healthy controls.

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Variants of the gene encoding the neuronal voltage-gated sodium channel Na1.1 cause over 85% of all cases of Dravet syndrome, a severe and often pharmacoresistent epileptic encephalopathy with mostly infantile onset. But with the increased availability of genetic testing for patients with epilepsy, variants in have now also been described in a range of other epilepsy phenotypes.

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Pathogenic variants in the voltage-gated sodium channel gene () are amongst the most common genetic causes of childhood epilepsies. There is considerable heterogeneity in both the types of causative variants and associated phenotypes; a recent expansion of the phenotypic spectrum of associated epilepsies now includes an early onset severe developmental and epileptic encephalopathy with regression and a hyperkinetic movement disorder. Herein, we report a female with a developmental and degenerative epileptic-dyskinetic encephalopathy, distinct and more severe than classic Dravet syndrome.

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Article Synopsis
  • Seizures are a big part of a brain disorder called NMDAR antibody encephalitis, where the body's own antibodies attack important proteins in the brain.
  • Scientists created a rat model to study how these seizures happen and to test new treatments.
  • They discovered that seizures are caused by less excitement in brain signals, and a special treatment called pregnenolone sulphate can help reduce these seizure activities.
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Neurological disorders such as epilepsy arise from disrupted brain networks. Our capacity to treat these disorders is limited by our inability to map these networks at sufficient temporal and spatial scales to target interventions. Current best techniques either sample broad areas at low temporal resolution (e.

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Investigations of the mechanisms generating epileptic seizures have primarily focused on neurons. However, more systemic research of brain circuits has highlighted an important role of non-neuronal cells such as glia in the genesis and spreading of generalized seizures in the brain.

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Epilepsy is a common primary neurological disorder characterized by the chronic tendency of a patient to experience epileptic seizures, which are abnormal body movements or cognitive states that result from excessive, hypersynchronous brain activity. Epilepsy has been found to have numerous etiologies and, although about two-thirds of epilepsies were classically considered idiopathic, the majority of those are now believed to be of genetic origin. Mutations in genes involved in gamma-aminobutyric acid (GABA)-mediated inhibitory neurotransmission have been associated with a broad range of epilepsy syndromes.

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NMDA-receptor antibodies (NMDAR-Abs) cause an autoimmune encephalitis with a diverse range of EEG abnormalities. NMDAR-Abs are believed to disrupt receptor function, but how blocking this excitatory synaptic receptor can lead to paroxysmal EEG abnormalities-or even seizures-is poorly understood. Here we show that NMDAR-Abs change intrinsic cortical connections and neuronal population dynamics to alter the spectral composition of spontaneous EEG activity and predispose brain dynamics to paroxysmal abnormalities.

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Pathophysiological explanations of epilepsy typically focus on either the micro/mesoscale (e.g. excitation-inhibition imbalance), or on the macroscale (e.

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Background: Disturbances in N-methyl-D-aspartate receptors (NMDARs)-as implicated in patients with schizophrenia-can cause regionally specific electrophysiological effects. Both animal models of NMDAR blockade and clinical studies in patients with schizophrenia have suggested that behavioral phenotypes are associated with reduction in inhibition within the frontal cortex.

Methods: Here we investigate event-related potentials to a roving auditory oddball paradigm under ketamine in healthy human volunteers (N= 18; double-blind, placebo-controlled, crossover design).

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Microcephaly is an important sign of neurological malformation and a predictor of future disability. The 2015-16 outbreak of Zika virus and congenital Zika infection brought the world's attention to links between Zika infection and microcephaly. However, Zika virus is only one of the infectious causes of microcephaly and, although the contexts in which they occur vary greatly, all are of concern.

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In this opinion paper, we describe a combined view of functional and effective brain connectivity along with the free-energy principle for investigating persistent disruptions in brain networks of patients with focal epilepsy. These changes are likely reflected in effective connectivity along the cortical hierarchy and construct the basis of increased local functional connectivity in focal epilepsy. We propose a testable framework based on dynamic causal modelling and functional connectivity analysis with the capacity of explaining commonly observed connectivity changes during interictal periods.

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Narcolepsy with cataplexy is a rare, but important differential diagnosis for daytime sleepiness and atonic paroxysms in an adolescent. A recent increase in incidence in the pediatric age group probably linked to the use of the Pandemrix influenza vaccine in 2009, has increased awareness that different environmental factors can "trigger" narcolepsy with cataplexy in a genetically susceptible population. Here, we describe the case of a 13-year-old boy with narcolepsy following yellow fever vaccination.

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Objective: To identify shared genes and pathways between common absence epilepsy (AE) subtypes (childhood absence epilepsy [CAE], juvenile absence epilepsy [JAE], and unclassified absence epilepsy [UAE]) that may indicate common mechanisms for absence seizure generation and potentially a diagnostic continuum.

Methods: We used high-density single-nucleotide polymorphism arrays to analyze genome-wide rare copy number variation (CNV) in a cohort of 144 children with AEs (95 CAE, 26 UAE, and 23 JAE).

Results: We identified CNVs that are known risk factors for AE in 4 patients, including 3x 15q11.

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The pathogenesis of Guillain-Barré syndrome (GBS) is considered to be, at least in part, mediated by autoantibodies directed against neuronal antigens. Antibodies to contactin-associated protein-like 2 (CASPR2), part of the voltage-gated potassium channel complex (VGKC-complex), are associated with neurological disease predominantly affecting the peripheral nervous system but are not known to be associated with GBS. We report two cases of ganglioside antibody-negative paediatric GBS associated with CASPR2 antibodies.

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Historically, most theoretical accounts of hemispheric specialisation have proposed a single underlying factor that leads to left hemisphere language and right hemisphere visuospatial processing in the majority of people. More recently empirical evidence has started to challenge this view, suggesting lateralisation of language and visuospatial attention are independent. However, so far studies did not control for a possible confound, task difficulty.

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Increasing evidence for a cerebellar role in human cognition has accrued with respect to anatomically and functionally distinct lobules. Questions of laterality, however, have been largely overlooked. This study therefore introduced and applied a novel measurement protocol for comparatively bias-free analysis of cerebellar asymmetries.

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