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Objective: Focal epilepsy is common in low‐ and middle‐income countries. The frequency and nature of possible underlying structural brain abnormalities have, however, not been fully assessed. Methods: We evaluated the possible structural causes of epilepsy in 331 people with epilepsy (240 from Kenya and 91 from South Africa) identified from community surveys of active convulsive epilepsy. Magnetic resonance imaging (MRI) scans were acquired on 1.5‐Tesla scanners to determine the frequency and nature of any underlying lesions. We estimated the prevalence of these abnormalities using Bayesian priors (from an earlier pilot study) and observed data (from this study). We used a mixed‐effect modified Poisson regression approach with the site as a random effect to determine the clinical features associated with neuropathology. Results: MRI abnormalities were found in 140 of 240 (modeled prevalence = 59%, 95% confidence interval [CI]: 53%–64%) of people with epilepsy in Kenya, and in 62 of 91 (modeled prevalence = 65%, 95% CI: 57%–73%) in South Africa, with a pooled modeled prevalence of 61% (95% CI: 56%–66%). Abnormalities were common in those with a history of adverse perinatal events (15/23 [65%, 95% CI: 43%–84%]), exposure to parasitic infections (83/120 [69%, 95% CI: 60%–77%]) and focal electroencephalographic features (97/142 [68%, 95% CI: 60%–76%]), but less frequent in individuals with generalized electroencephalographic features (44/99 [44%, 95% CI: 34%–55%]). Most abnormalities were potentially epileptogenic (167/202, 82%), of which mesial temporal sclerosis (43%) and gliosis (34%) were the most frequent. Abnormalities were associated with co‐occurrence of generalized non‐convulsive seizures (relative risk [RR] = 1.12, 95% CI: 1.04–1.25), lack of family history of seizures (RR = 0.91, 0.86–0.96), convulsive status epilepticus (RR = 1.14, 1.08–1.21), frequent seizures (RR = 1.12, 1.04–1.20), and reported use of anti‐seizure medication (RR = 1.22, 1.18–1.26). Significance: MRI identified pathologies are common in people with epilepsy in Kenya and South Africa. Mesial temporal sclerosis, the most common abnormality, may be amenable to surgical correction. MRI may have a diagnostic value in rural Africa, but future longitudinal studies should examine the prognostic role. [ABSTRACT FROM AUTHOR]

Abstract Background Minimally invasive autopsy by post mortem magnetic resonance (MR) imaging has been suggested as an alternative for conventional autopsy in view of the declining consented autopsy rates. However, large prospective studies rigorously evaluating the accuracy of such an approach are lacking. We intend to compare the accuracy of a minimally invasive autopsy approach using post mortem MR imaging with that of conventional autopsy in fetuses, newborns and children for detection of the major pathological abnormalities and/or determination of the cause of death. Methods/Design We recruited 400 consecutive fetuses, newborns and children referred for conventional autopsy to one of the two participating hospitals over a three-year period. We acquired whole body post mortem MR imaging using a 1.5 T MR scanner (Avanto, Siemens Medical Solutions, Enlargen, Germany) prior to autopsy. The total scan time varied between 90 to 120 minutes. Each MR image was reported by a team of four specialist radiologists (paediatric neuroradiology, paediatric cardiology, paediatric chest & abdominal imaging and musculoskeletal imaging), blinded to the autopsy data. Conventional autopsy was performed according to the guidelines set down by the Royal College of Pathologists (UK) by experienced paediatric or perinatal pathologists, blinded to the MR data. The MR and autopsy data were recorded using predefined categorical variables by an independent person. Discussion Using conventional post mortem as the gold standard comparator, the MR images will be assessed for accuracy of the anatomical morphology, associated lesions, clinical usefulness of information and determination of the cause of death. The sensitivities, specificities and predictive values of post mortem MR alone and MR imaging along with other minimally invasive post mortem investigations will be presented for the final diagnosis, broad diagnostic categories and for specific diagnosis of each system. Clinical Trial Registration NCT01417962 NIHR Portfolio Number: 6794

Objective: Brain proton (1H) magnetic resonance spectroscopy (MRS) lactate/N-acetylaspartate (Lac/NAA) peak area ratio is used for prognostication in neonatal encephalopathy (NE). At 3 Tesla in NE babies, the objectives were to assess: (1) sensitivity and specificity of basal ganglia and thalamus (BGT) 1H MRS Lac/NAA for the prediction of Bayley III outcomes at 2 years using optimised metabolite fitting (Tarquin) with threonine and total NAA; (2) prediction of motor outcome with diffusion-weighted MRI; (3) BGT Lac/NAA correlation with the National Institute of Child Health and Human Development (NICHD) MRI score.Subjects and Methods: 55 (16 inborn, 39 outborn) infants at 39w+5 d (35w+5d-42w+0d) with NE admitted between February 2012 and August 2014 to University College London Hospitals for therapeutic hypothermia underwent MRI and 1H MRS at 3T on day 2-14 (median day 5). MRIs were scored. Bayley III was assessed at 24 (22-26) months.Results: 16 babies died (1 inborn, 15 outborn); 20, 19 and 21 babies had poor motor, cognitive and language outcomes. Using a threshold of 0.39, sensitivity and specificity of BGT Lac/NAA for 2-year motor outcome was 100% and 97%, cognition 90% and 97% and language 81% and 97%, respectively. Sensitivity and specificity for motor outcome of mean diffusivity (threshold 0.001 mm2/s) up to day 9 was 72% and 100% and fractional anisotropy (threshold 0.198) was 39% and 94%, respectively. Lac/NAA correlated with BGT injury on NICHD scores (2A, 2B, 3).Conclusion: BGT Lac/NAA on 1H MRS at 3T within 14 days accurately predicts 2-year motor, cognitive and language outcome and may be a marker directing decisions for therapies after cooling. [ABSTRACT FROM AUTHOR]

Objective: In contrast to adult cohorts, neocortical changes in epileptic children with hippocampal damage are not well characterized. Here, we mapped multimodal neocortical markers of epilepsy‐related structural compromise in a pediatric cohort of temporal lobe epilepsy and explored how they relate to clinical factors. Methods: We measured cortical thickness, gray–white matter intensity contrast and intracortical FLAIR intensity in 22 patients with hippocampal sclerosis (HS) and 30 controls. Surface‐based linear models assessed between‐group differences in morphological and MR signal intensity markers. Structural integrity of the hippocampus was measured by quantifying atrophy and FLAIR patterns. Linear models were used to evaluate the relationships between hippocampal and neocortical MRI markers and clinical factors. Results: In the hippocampus, patients demonstrated ipsilateral atrophy and bilateral FLAIR hyperintensity. In the neocortex, patients showed FLAIR signal hyperintensities and gray–white matter boundary blurring in the ipsilesional mesial and lateral temporal neocortex. In contrast, cortical thinning was minimal and restricted to a small area of the ipsilesional temporal pole. Furthermore, patients with a history of febrile convulsions demonstrated more pronounced FLAIR hyperintensity in the ipsilesional temporal neocortex. Interpretation: Pediatric HS patients do not yet demonstrate the widespread cortical thinning present in adult cohorts, which may reflect consequences of a protracted disease process. However, pronounced temporal neocortical FLAIR hyperintensity and blurring of the gray–white matter boundary are already detectable, suggesting that alterations in MR signal intensities may reflect a different underlying pathophysiology that is detectable earlier in the disease and more pervasive in patients with a history of febrile convulsions. [ABSTRACT FROM AUTHOR]

The article offers information on a research conducted to analyze the epidemiology of multiple sclerosis in childhood population in British Isles. It is mentioned that the study informs on the changes in the childhood nervous system in children with acquired demyelinating syndromes (ADSs). Also, for the study, pediatricians, and ophthalmologists were given a questionnaire on questions related to acute disseminated encephalomyelitis, clinically isolated syndrome, and neuromyelitis optica.

Focal cortical dysplasia is a congenital abnormality of cortical development and the leading cause of surgically remediable drug-resistant epilepsy in children. Post-surgical outcome is improved by presurgical lesion detection on structural MRI. Automated computational techniques have improved detection of focal cortical dysplasias in adults but have not yet been effective when applied to developing brains. There is therefore a need to develop reliable and sensitive methods to address the particular challenges of a paediatric cohort. We developed a classifier using surface-based features to identify focal abnormalities of cortical development in a paediatric cohort. In addition to established measures, such as cortical thickness, grey-white matter blurring, FLAIR signal intensity, sulcal depth and curvature, our novel features included complementary metrics of surface morphology such as local cortical deformation as well as post-processing methods such as the "doughnut" method - which quantifies local variability in cortical morphometry/MRI signal intensity, and per-vertex interhemispheric asymmetry. A neural network classifier was trained using data from 22 patients with focal epilepsy (mean age = 12.1 ± 3.9, 9 females), after intra- and inter-subject normalisation using a population of 28 healthy controls (mean age = 14.6 ± 3.1, 11 females). Leave-one-out cross-validation was used to quantify classifier sensitivity using established features and the combination of established and novel features. Focal cortical dysplasias in our paediatric cohort were correctly identified with a higher sensitivity (73%) when novel features, based on our approach for detecting local cortical changes, were included, when compared to the sensitivity using only established features (59%). These methods may be applicable to aiding identification of subtle lesions in medication-resistant paediatric epilepsy as well as to the structural analysis of both healthy and abnormal cortical development.

Background: Paediatric cerebrovascular CT angiography (CTA) can be challenging to perform due to variable cardiovascular physiology between different age groups and the risk of movement artefact. This analysis aimed to determine what proportion of CTA at our institution was of diagnostic quality and identify technical factors which could be improved., Materials and Methods: a retrospective analysis of 20 cases was performed at a national paediatric neurovascular centre assessing image quality with a subjective scoring system and Hounsfield Unit (HU) measurements. Demographic data, contrast dose, flow rate and triggering times were recorded for each patient., Results: Using a qualitative scoring system, 75% of studies were found to be of diagnostic quality (n=9 'good', n=6 'satisfactory') and 25% (n=5) were 'poor'. Those judged subjectively to be poor had arterial contrast density measured at less than 250 HU. Increased arterial opacification was achieved for cases performed with an increased flow rate (2.5-4 mL/s) and higher intravenous contrast dose (2 mL/kg). Triggering was found to be well timed in nine cases, early in four cases and late in seven cases. Of the scans triggered early, 75% were poor. Of the scans triggered late, less (29%) were poor., Conclusions: High flow rates (>2.5 mL/s) were a key factor for achieving high quality paediatric cerebrovascular CTA imaging. However, appropriate triggering by starting the scan immediately on contrast opacification of the monitoring vessel plays an important role and could maintain image quality when flow rates were lower. Early triggering appeared more detrimental than late.

Objective: Changing trends in multiple sclerosis (MS) epidemiology may first be apparent in the childhood population affected with first onset acquired demyelinating syndromes (ADSs). We aimed to determine the incidence, clinical, investigative and magnetic resonance imaging (MRI) features of childhood central nervous system ADSs in the British Isles for the first time., Methods: We conducted a population active surveillance study. All paediatricians, and ophthalmologists (n = 4095) were sent monthly reporting cards (September 2009-September 2010). International Paediatric MS Study Group 2007 definitions and McDonald 2010 MS imaging criteria were used for acute disseminated encephalomyelitis (ADEM), clinically isolated syndrome (CIS) and neuromyelitis optica (NMO). Clinicians completed a standard questionnaire and provided an MRI copy for review., Results: Card return rates were 90%, with information available for 200/222 positive notifications (90%). After exclusion of cases, 125 remained (age range 1.3-15.9), with CIS in 66.4%, ADEM in 32.0% and NMO in 1.6%. The female-to-male ratio in children older than 10 years (n = 63) was 1.52:1 (p = 0.045). The incidence of first onset ADS in children aged 1-15 years old was 9.83 per million children per year (95% confidence interval [CI] 8.18-11.71). A trend towards higher incidence rates of ADS in children of South Asian and Black ethnicity was observed compared with White children. Importantly, a number of MRI characteristics distinguished ADEM from CIS cases. Of CIS cases with contrast imaging, 26% fulfilled McDonald 2010 MS diagnostic criteria., Conclusions: We report the highest surveillance incidence rates of childhood ADS. Paediatric MS diagnosis at first ADS presentation has implications for clinical practice and clinical trial design.