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<jats:p> We examined the association between the severity of acute concussion symptoms and time to return to school and to sports in adolescent student athletes. We hypothesized that there would be an association between the severity of acute symptoms experienced in the first 72 hours and functional recovery such that adolescents with the lowest burden of acute symptoms would have the fastest return to school and sports and those with the highest burden of symptoms would have the slowest return to school and sports. This injury surveillance cohort included 375 adolescent student athletes aged 14-19 years who sustained a sport-related concussion between 2014 and 2020. Athletic trainers documented time to return to school and to sports. A greater proportion of adolescents with the highest acute symptoms remained out of school at 3 (odds ratio [OR] = 2.5, 95% confidence interval [CI] 1.5-4.4), 5 (OR = 2.4, 95% CI 1.4-4.0), 7 (OR = 2.6, 95% CI 1.5-4.3), and 10 days (OR = 2.3, 95% CI 1.3-3.9) compared to those with the lowest acute symptoms. Similarly, a greater proportion of athletes with the highest acute symptoms remained out of sports at 7 (OR = 3.5, 95% CI 1.5-8.1), 10 (OR = 3.1, 95% CI 1.8-5.6), 14 (OR = 1.8, 95% CI 1.1-3.0), and 21 days (OR = 1.9, 95% CI 1.0-3.6) compared to those with the lowest acute symptoms. This study underscores the adverse effect of high acute symptom burden following concussion on return to school and to sports among adolescent student athletes. Conversely, student athletes with a low burden of acute symptoms have a faster return to school and to sports. </jats:p>

<jats:p> Identifying the etiology of childhood arterial ischemic stroke helps prevent stroke recurrence. In addition, stroke may herald a serious underlying condition requiring treatment, such as acquired heart disease, malignancy, or autoimmune disorder. Evidence-based guidelines exist for adults to identify and treat common risk factors for primary and secondary stroke, including hypertension, diabetes, elevated lipids, atrial fibrillation, and sleep apnea, which are rarely relevant in children. However, guidelines do not exist in pediatrics. Identifying the cause of childhood stroke may be straightforward or may require extensive clinical and neuroimaging expertise, serial evaluations, and reassessment based on the evolving clinical picture. Risk factors may be present but not necessarily causative, or not causative until a triggering event such as infection or anemia occurs. Herein, we describe strategies to determine stroke etiology, including challenges and potential pitfalls. </jats:p>

<jats:sec><jats:title>Background</jats:title><jats:p> Continuous spike wave in sleep (CSWS) is an electroencephalogram (EEG) pattern associated with developmental and epileptic encephalopathy with spike-and-wave activation in sleep (DEE-SWAS). This etiologically heterogeneous syndrome may occur because of genetic factors and congenital or acquired brain lesions. We studied the pattern of clinical presentation and underlying etiologies in patients with DEE-SWAS that respond to resective surgery. </jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p> We reviewed our clinical and research databases for patients who had resolution of CSWS following surgical resection of a focal lesion. </jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p> We identified 5 patients meeting inclusion criteria. In 3 of 5, an epileptogenic structural abnormality was not apparent on brain magnetic resonance imaging (MRI). In all 3 patients, focal cortical dysplasia was identified through intracranial EEG monitoring. </jats:p></jats:sec><jats:sec><jats:title>Significance</jats:title><jats:p> DEE-SWAS may be a secondary bilateral network epilepsy syndrome, which can be treated with resection of the inciting focal lesion. In patients with drug-resistant CSWS, clinicians should consider a complete epilepsy presurgical workup, including intracranial EEG monitoring. </jats:p></jats:sec>

<jats:sec><jats:title>Background</jats:title><jats:p> Children with self-limited epilepsy with centrotemporal spikes often face language impairments and central auditory processing difficulties. The correlations between these issues, seizure timing, and neuropsychiatric challenges are not fully understood. This study delves into the connections between language impairments and central auditory processing difficulties in cases with self-limited epilepsy with centrotemporal spikes, examining their links with seizure occurrence and neuropsychiatric function. </jats:p></jats:sec><jats:sec><jats:title>Materials and Methods</jats:title><jats:p> Patients with self-limited epilepsy with centrotemporal spikes were categorized based on seizure timing: group 1 experienced seizures postbedtime, and group 2 prewaking. Both, alongside controls, underwent the Turkish Expressive and Receptive Language Test (TIFALDI) for language skills, and the Frequency Pattern and Duration Pattern tests for central auditory processing difficulties. Neuropsychiatric assessments involved the Wechsler Intelligence Scale for Children–Revised, the Strengths and Difficulties Questionnaire, the Conners Parent Rating Scale–Revised Short, and the Barratt Impulsiveness Scale–11. </jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p> The study comprised 56 patients with self-limited epilepsy with centrotemporal spikes (ages 6-13) and 32 healthy controls. Both groups significantly lagged behind controls on the Frequency Pattern and Duration Pattern tests ( P &lt; .001). In the TIFALDI, the expressive language scores varied between group 1 and controls ( P = .04) but not the receptive language scores or the test’s expressive and receptive language results between group 2 and controls ( P &gt; .05). In the Strengths and Difficulties Questionnaire, group 1 diverged from controls in behavioral and kind and helpful behavior scores ( P = .016 and P = .012). Group 1's Barratt Impulsiveness Scale–11 values surpassed controls’ ( P = .038). </jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p> Children with self-limited epilepsy with centrotemporal spikes have a high central auditory processing difficulties prevalence, regardless of seizure timing. Those with postsleep seizures tend to confront expressive language difficulties, alongside issues in prosocial behavior and impulsivity. </jats:p></jats:sec>

<jats:sec><jats:title>Background and Objectives</jats:title><jats:p> Myelin-oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a recently defined demyelinating disorder with an age-related phenotypic spectrum. At disease onset, there is considerable clinical overlap between MOGAD and other demyelinating conditions, and it remains difficult to identify MOGAD radiographically. This study aims to further describe neuroimaging findings in the brain and the spine at presentation and throughout relapses in children with MOGAD. </jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p> We present a retrospective cohort study including all children presenting to a single center between 2010 and 2020 with acute demyelination who were positive for serum MOG-IgG antibodies and negative for serum aquaporin-4 antibodies. For each patient, magnetic resonance imaging (MRI) scans of the brain and spine at presentation and on each relapse were reviewed and categorized in a blinded fashion by 2 pediatric neuroradiologists. </jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p> Sixteen patients met the inclusion criteria. Four had diffuse and bilateral fluid-attenuated inversion recovery signal in the white matter, but only on initial presentation. The area postrema was never affected. All 5 patients with optic neuritis had pre-chiasmatic (but not chiasmatic) involvement on presentation. The brachium pontis was involved in 3 patients on initial presentation, and in 8 patients at any time. Eleven patients demonstrated spinal cord involvement, and the cervical, thoracic, and lumbar regions were involved at similar frequencies. </jats:p></jats:sec><jats:sec><jats:title>Discussion</jats:title><jats:p> The radiographic features of MOGAD in children appear to reflect their presenting demyelinating syndromes. However, certain features, such as diffuse fluid-attenuated inversion recovery hyperintensities and expansile fluid-attenuated inversion recovery signal in the brachium pontis, may be more frequent in MOGAD compared with other demyelinating disorders. </jats:p></jats:sec>

<jats:p> Paroxysmal dyskinesias, marked by sudden involuntary movements, poses diagnostic challenges because of its heterogeneous nature and overlap with other movement disorders. Genetic factors, especially variants in the <jats:italic>ATP1A3</jats:italic> gene, have been linked to various neurologic conditions, including paroxysmal dystonia. We report a 5-year-old patient with a rare <jats:italic>ATP1A3</jats:italic> gene variant (c.2309T&gt;G, p.(Leu770Arg)), previously documented in only 1 other patient. Unlike the earlier report, the patient presented distinct clinical features, with a focus on dystonia rather than hemiplegia and no intellectual impairment. This phenotypic variability highlights the challenges in diagnosis and treatment. We discuss differential diagnoses, including Alternating Hemiplegia of Childhood, and emphasize the need for comprehensive genetic testing and multidisciplinary care. Our study advocates for further research to better understand the spectrum of <jats:italic>ATP1A3</jats:italic> -related disorders and enhance diagnostic accuracy and patient management in paroxysmal dystonia. </jats:p>

<jats:p>To provide the best possible care, neurologists must have a thorough understanding of the social and historical context of disability. Knowledge of the biology of neurologic conditions alone is insufficient. Currently, there is a scarcity of explicit education and training on disability beyond the traditional medical lens. Additionally, neurologists may be unfamiliar with the neurodiversity movement and its principles. This lack of awareness may inadvertently perpetuate ableist perspectives and practices, resulting in harm for our patients. In this article, we provide an overview of ableism and language-use considerations. We also discuss the history and current context of the neurodiversity movement and review neurodiversity-affirming core principles and clinical practices. This article offers perspective on an important shift in paradigms of the brain, as well as tools that can be used for a career-long commitment to excellent and equitable neurologic care.</jats:p>