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Although the scientific community has focused on the effects of concussions in contact sports, the role of subconcussive impacts, as it can occur during soccer heading, has recently gained attention, considering that it may represent an additional mechanism of cumulative brain injury. The aim of this study is to investigate the effects of soccer heading on cognitive functioning in active professional soccer players. Male soccer players (

Les syndromes démyélinisants récurrents (SDR) chez les enfants englobent un large éventail d'entités, y compris l'encéphalomyélite aiguë disséminée (ADEM) de la sclérose en plaques (SEP), le trouble du spectre de la neuromyélite optique associé aux anticorps de l'aquaporine-4 (AQP4-NMOSD) et la maladie des anticorps anti-glycoprotéines oligodendrocytaires de la myéline (MOG-AD). En plus de ceux-ci, il existe des syndromes démyélinisants « anticorps-négatifs » qui n'ont pas encore été entièrement caractérisés et définis. La rareté des biomarqueurs spécifiques et le chevauchement des présentations cliniques rendent difficile la distinction entre ces entités de la maladie lors de la présentation initiale et, à ce titre, il existe une forte dépendance aux résultats de l'imagerie par résonance magnétique (IRM) pour satisfaire aux critères d'initiation et d'optimisation du traitement. Un diagnostic erroné n'est pas rare et est généralement lié à l'application inexacte de critères ou à l'incapacité d'identifier des imitations cliniques et radiologiques potentielles. Il est également à noter qu'il existe des cas où les tests d'anticorps AQP4 et MOG peuvent être faussement négatifs lors des premiers épisodes cliniques, ce qui complique encore le problème. Cet article illustre les phénotypes clinico-radiologiques typiques associés au SDR pédiatrique connu lors de la présentation et décrit les imitations neuroimagerie de ceux-ci en utilisant une approche basée sur les motifs dans le cerveau, les nerfs optiques et la moelle épinière. Des conseils pratiques sur les principales caractéristiques distinctives sous la forme de signaux d'alerte cliniques et radiologiques sont incorporés. Une sous-section sur les imitations cliniques avec des modèles d'imagerie caractéristiques qui aident à établir des diagnostics alternatifs est également incluse. Los síndromes desmielinizantes recidivantes (SDR) en niños abarcan un espectro diverso de entidades que incluyen la encefalomielitis diseminada aguda (EM) con esclerosis múltiple (EM), el trastorno del espectro DE neuromielitis óptica asociado a anticuerpos contra la acuaporina-4 (AQP4-NMOSD) y la enfermedad de anticuerpos contra la glicoproteína oligodendrocítica de la mielina (MOG-AD). Además de estos, existen síndromes desmielinizantes "anticuerpos negativos" que aún no se han caracterizado y definido completamente. La escasez de biomarcadores específicos y la superposición en las presentaciones clínicas dificulta la distinción entre estas entidades de la enfermedad en la presentación inicial y, como tal, existe una gran dependencia de los hallazgos de la resonancia magnética (IRM) para satisfacer los criterios de inicio y optimización del tratamiento. El diagnóstico erróneo no es infrecuente y generalmente está relacionado con la aplicación inexacta de criterios o la falta de identificación de posibles imitaciones clínicas y radiológicas. También es notable que hay casos en los que las pruebas de anticuerpos AQP4 y MOG pueden ser falsamente negativas durante los episodios clínicos iniciales, lo que complica aún más el problema. Este artículo ilustra los fenotipos clínicos-radiológicos típicos asociados con el SDR pediátrico conocido en la presentación y describe los imitadores de neuroimagen de estos utilizando un enfoque basado en patrones en el cerebro, los nervios ópticos y la médula espinal. Se incorporan orientaciones prácticas sobre las características distintivas clave en forma de señales de alerta clínicas y radiológicas. También se incluye una subsección sobre imitaciones clínicas con patrones de imágenes característicos que ayudan a establecer diagnósticos alternativos. Relapsing demyelinating syndromes (RDS) in children encompass a diverse spectrum of entities including multiple sclerosis (MS) acute disseminated encephalomyelitis (ADEM), aquaporin-4 antibody associated neuromyelitis optica spectrum disorder (AQP4-NMOSD) and myelin oligodendrocyte glycoprotein antibody disease (MOG-AD). In addition to these, there are "antibody-negative" demyelinating syndromes which are yet to be fully characterized and defined. The paucity of specific biomarkers and overlap in clinical presentations makes the distinction between these disease entities difficult at initial presentation and, as such, there is a heavy reliance on magnetic resonance imaging (MRI) findings to satisfy the criteria for treatment initiation and optimization. Misdiagnosis is not uncommon and is usually related to the inaccurate application of criteria or failure to identify potential clinical and radiological mimics. It is also notable that there are instances where AQP4 and MOG antibody testing may be falsely negative during initial clinical episodes, further complicating the issue. This article illustrates the typical clinico-radiological phenotypes associated with the known pediatric RDS at presentation and describes the neuroimaging mimics of these using a pattern-based approach in the brain, optic nerves, and spinal cord. Practical guidance on key distinguishing features in the form of clinical and radiological red flags are incorporated. A subsection on clinical mimics with characteristic imaging patterns that assist in establishing alternative diagnoses is also included. تشمل المتلازمات الناكسة لإزالة الميالين لدى الأطفال مجموعة متنوعة من الكيانات بما في ذلك التهاب الدماغ والنخاع المنتشر الحاد الناجم عن التصلب المتعدد (ADEM)، واضطراب طيف التهاب الأعصاب والنخاع المرتبط بالأجسام المضادة للأكوابورين-4 (AQP4 - NMOSD) ومرض الأجسام المضادة للبروتين السكري قليل التغصن في المايلين (MOG - AD). بالإضافة إلى ذلك، هناك متلازمات مزيلة للميالين "سلبية الأجسام المضادة" والتي لم يتم تمييزها وتعريفها بالكامل بعد. إن ندرة المؤشرات الحيوية المحددة والتداخل في العروض السريرية يجعل التمييز بين هذه الكيانات المرضية صعبًا عند العرض الأولي، وعلى هذا النحو، هناك اعتماد كبير على نتائج التصوير بالرنين المغناطيسي لتلبية معايير بدء العلاج وتحسينه. التشخيص الخاطئ ليس غير شائع وعادة ما يرتبط بالتطبيق غير الدقيق للمعايير أو الفشل في تحديد المحاكاة السريرية والإشعاعية المحتملة. من الجدير بالذكر أيضًا أن هناك حالات قد يكون فيها اختبار الأجسام المضادة AQP4 و MOG سلبيًا بشكل خاطئ خلال النوبات السريرية الأولية، مما يزيد من تعقيد المشكلة. توضح هذه المقالة الأنماط الظاهرية الإكلينيكية الإشعاعية النموذجية المرتبطة بنظام الكشف الإشعاعي للأطفال المعروف عند العرض وتصف محاكاة التصوير العصبي لهذه الأنماط باستخدام نهج قائم على الأنماط في الدماغ والأعصاب البصرية والحبل الشوكي. يتم دمج إرشادات عملية حول السمات المميزة الرئيسية في شكل أعلام حمراء سريرية وإشعاعية. كما تم تضمين قسم فرعي حول المحاكاة السريرية مع أنماط التصوير المميزة التي تساعد في إنشاء تشخيصات بديلة.

This review focuses on the use of resting-state functional magnetic resonance imaging data to assess functional connectivity in the human brain and its application in intractable epilepsy. This approach has the potential to predict outcomes for a given surgical procedure based on the pre-surgical functional organization of the brain. Functional connectivity can also identify cortical regions that are organized differently in epilepsy patients either as a direct function of the disease or through indirect compensatory responses. Functional connectivity mapping may help identify epileptogenic tissue, whether this is a single focal location or a network of seizure-generating tissues. This review covers the basics of connectivity analysis and discusses particular issues associated with analyzing such data. These issues include how to define nodes, as well as differences between connectivity analyses of individual nodes, groups of nodes, and whole-brain assessment at the voxel level. The need for arbitrary thresholds in some connectivity analyses is discussed and a solution to this problem is reviewed. Overall, functional connectivity analysis is becoming an important tool for assessing functional brain organization in epilepsy.

Survivors of infant traumatic brain injury (TBI) are prone to chronic neurological deficits that impose lifelong individual and societal burdens. Translation of novel interventions to clinical trials is hampered in part by the lack of truly representative preclinical tests of cognition and corresponding biomarkers of functional outcomes. To address this gap, the ability of a high-dose, extended, post-injury regimen of erythropoietin (EPO, 3000U/kg/dose × 6d) to prevent chronic cognitive and imaging deficits was tested in a postnatal day 12 (P12) controlled-cortical impact (CCI) model in rats, using touchscreen operant chambers and regional analysis of diffusion tensor imaging (DTI). Results indicate that EPO prevents functional injury and MRI injury after infant TBI. Specifically, subacute DTI at P30 revealed widespread microstructural damage that is prevented by EPO. Assessment of visual discrimination on a touchscreen operant chamber platform demonstrated that all groups can perform visual discrimination. However, CCI rats treated with vehicle failed to pass reversal learning, and perseverated, in contrast to sham and CCI-EPO rats. Chronic DTI at P90 showed EPO treatment prevented contralateral white matter and ipsilateral lateral prefrontal cortex damage. This DTI improvement correlated with cognitive performance. Taken together, extended EPO treatment restores executive function and prevents microstructural brain abnormalities in adult rats with cognitive deficits in a translational preclinical model of infant TBI. Sophisticated testing with touchscreen operant chambers and regional DTI analyses may expedite translation and effective yield of interventions from preclinical studies to clinical trials. Collectively, these data support the use of EPO in clinical trials for human infants with TBI.

General and central nervous system anatomy and physiology in children is different to that of adults and this is relevant to traumatic brain injury (TBI) and spinal cord injury. The controversies and uncertainties in adult neurotrauma are magnified by these differences, the lack of normative data for children, the scarcity of pediatric studies, and inappropriate generalization from adult studies. Cerebral metabolism develops rapidly in the early years, driven by cortical development, synaptogenesis, and rapid myelination, followed by equally dramatic changes in baseline and stimulated cerebral blood flow. Therefore, adult values for cerebral hemodynamics do not apply to children, and children cannot be easily approached as a homogenous group, especially given the marked changes between birth and age 8. Their cranial and spinal anatomy undergoes many changes, from the presence and disappearance of the fontanels, the presence and closure of cranial sutures, the thickness and pliability of the cranium, anatomy of the vertebra, and the maturity of the cervical ligaments and muscles. Moreover, their systemic anatomy changes over time. The head is relatively large in young children, the airway is easily compromised, the chest is poorly protected, the abdominal organs are large. Physiology changes-blood volume is small by comparison, hypothermia develops easily, intracranial pressure (ICP) is lower, and blood pressure normograms are considerably different at different ages, with potentially important implications for cerebral perfusion pressure (CPP) thresholds. Mechanisms and pathologies also differ-diffuse injuries are common in accidental injury, and growing fractures, non-accidental injury and spinal cord injury without radiographic abnormality are unique to the pediatric population. Despite these clear differences and the vulnerability of children, the amount of pediatric-specific data in TBI is surprisingly weak. There are no robust guidelines for even basics aspects of care in children, such as ICP and CPP management. This is particularly alarming given that TBI is a leading cause of death in children. To address this, there is an urgent need for pediatric-specific clinical research. If this goal is to be achieved, any clinician or researcher interested in pediatric neurotrauma must be familiar with its unique pathophysiological characteristics.

The heterogeneity of stroke prompts the need for predictors of individual treatment response to rehabilitation therapies. We previously studied healthy subjects with EEG and identified a frontoparietal circuit in which activity predicted training-related gains in visuomotor tracking. Here we asked whether activity in this same frontoparietal circuit also predicts training-related gains in visuomotor tracking in patients with chronic hemiparetic stroke. Subjects (