Aim: To evaluate the effects of systematic rehabilitation on both the neuropsychomotor development, and on the peripheral response from immunological and neuroplastic mediators in children with cerebral palsy.
Methods: This is a prospective cohort study with 90 children with cerebral palsy at 18 months of age. Sixty children received rehabilitation for 6 months, and they were compared to 30 children that were placed in the waiting list. Peripheral biomarkers and neuropsychomotor parameters were compared between the Rehab vs the Nonrehab groups at baseline and at 6 months.
Results: Results showed higher Bayley III scores in the Rehab group, with significant differences in inflammatory and neurotrophic biomarkers between groups. Rehabilitation was associated to decreased levels of IL-12p70, IL-6, IL-1β, CXCL8 IL-8, and CXCL9/MIG and increased levels of BDNF and GDNF. Nonrehab children had stable immune molecule levels but decreased BDNF levels over time.
Conclusion: Rehabilitation improved neurodevelopment parameters and modulated levels of inflammatory (↓) and neurotrophic (↑) biomarkers.
This retrospective chart review examined children with documented Lyme disease serology in New Jersey aged <21 years presenting with facial nerve palsy. The presence of symptoms including tick bite, fever, headache, and arthritis was recorded. Data were categorized based on demographic factors, and multivariate regression was employed. We enrolled 122 children, 54% female (mean age of 11.4 ± 5.1 years); 22.1% had Lyme disease. Fever was a significant predictor of Lyme disease (P = .01), confirmed by multivariate regression (odds ratio [OR] = 16.11, 95% confidence interval [CI] = 2.04, 366.14), as was male gender (P = .01, OR = 3.68, 95% CI = 1.21, 12.89). This association held especially true in Lyme-endemic regions (prevalence ≥ 0.35). The combination of headache with fever was also significantly predictive (P = .01). We found no significant predictive value in the remaining symptoms. These findings suggest that clinical predictors may be useful in diagnosing Lyme disease and initiating early empiric treatment.
Introduction: A number of biomarkers are used to evaluate the duration of the epileptic seizure and the interictal period following neuronal injury. Invasive diagnostic methods are increasingly being replaced by peripheral or minimally invasive biomarkers that give results faster and are more secure.
Purpose: We aimed to evaluate serum glial fibrillary acidic protein (GFAP), S100B, and ubiquitin C-terminal hydrolase (UCHL-1) levels in children with epilepsy.
Methods: Our study included 3 groups: a nonrefractory epilepsy group, a refractory epilepsy group, and a control group. The GFAP, S100B, and UCHL-1 levels in serum samples collected 2-24 hours after the last seizure were analyzed using enzyme-linked immunosorbent assays.
Results: A total of 69 children participated in the study, with 35 participants in the refractory epilepsy group, 18 in the nonrefractory epilepsy group, and 16 in the control group. The GFAP values in the refractory (25.4 ng/mL) and nonrefractory (26.1 ng/mL) epilepsy groups were found to be statistically significantly higher than those in the control group (17.9 ng/mL; P = .001). The S100B values were found to be significantly higher in the refractory epilepsy group (34.13 pg/mL) than in both the control group and the nonrefractory epilepsy group (28.05 pg/mL; P = .028). No significant differences were observed in the UCHL-1 levels between the 3 groups.
Conclusions: We conclude that the observed differences may be due to the increased expression of S100B and GFAP caused by increased and repetitive neuronal damage in refractory epilepsies compared with nonrefractory epilepsies.
Objective: Describe the clinical characteristics, treatment strategies, and outcome data of children with papilledema associated with Lyme disease at a large tertiary care pediatric hospital.
Methods: Retrospective cohort study of children 1-18 years old who received care at our institution between 1995 and 2019 with concurrent diagnoses of papilledema and Lyme disease. Data were abstracted from records and prospective family surveys.
Results: Among 44 children included (median age 9.7 years), 66% (29/44) had additional cranial neuropathies, and 78% (32/41) had cerebrospinal fluid pleocytosis. All children were treated with antibiotics (39% oral, 55% intravenous, 7% both); 61% (27/44) were also treated with oral acetazolamide. Symptoms fully resolved in 86% (30/35) of children with follow-up data. Proportion recovered did not significantly differ by antibiotic administration route or presence/absence of cerebrospinal fluid pleocytosis.
Conclusions: Papilledema in Lyme disease may occur with or without cerebrospinal fluid pleocytosis. Most children recover without residual deficits following treatment, although exceptions exist.
Epilepsy is identified in individuals who experienced 2 or more unprovoked seizures occurring over 24 hours apart, which can have a profound impact on a person's neurobiological, cognitive, psychological, and social well-being. Epilepsy is considerably diverse, with classifications such as genetic epilepsy that result directly from a known or presumed genetic variant with the core symptoms of seizures. The GABAA receptor primarily functions as a heteropentamer, containing 3 of 8 subunit types: α, β, γ, δ, ε, π, θ, and ρ. In the adult brain, the GABAA receptor is the primary inhibitory component in neural networks. The involvement of GABAA receptors in the pathogenesis of epilepsy has been proposed. We extensively reviewed all relevant clinical data of previously published cases of GABAA receptor subunit γ2, δ, β1-3 variants included in PubMed up to February 2024, including the variant types, loci, postulated mechanisms, their relevant regions, first onset ages, and phenotypes. We summarized the postulated mechanisms of epileptic pathogenesis. We also divided the collected 206 cases of epilepsy into 4 epileptic phenotypes: genetic generalized epilepsies, focal epilepsy, developmental and epileptic encephalopathies, and epilepsy with fever sensibility. We showed that there were significant differences in the likelihood of the γ2, β2, and β3 subunit variants causing genetic generalized epilepsies, focal epilepsy, developmental and epileptic encephalopathies, and epilepsy with fever sensibility. Patients with the β3 subunit variant seemed related to an earlier first onset age. Our review supports that GABAA receptor subunit variants are a crucial area of epilepsy research and treatment exploration.
Background: Children diagnosed with subacute sclerosing panencephalitis (SSPE) display a range of neuroimaging abnormalities during different stages of the disease, but their exact clinical significance remains unclear.
Methods: In this retrospective cohort study, our objective was to examine magnetic resonance imaging (MRI) abnormalities in the brains of patients aged 18 years or younger with subacute sclerosing panencephalitis. We aimed to correlate these MRI abnormalities with clinical severity, sociodemographic variables, electroencephalographic (EEG) abnormalities, and cerebrospinal anti-measles antibody titers.
Results: The study included 112 cases of subacute sclerosing panencephalitis (mean age at onset: 8.9 ± 2.6 years). MRI analysis at the time of presentation revealed the following abnormalities: subcortical white matter signal changes (n = 95), periventricular white matter signal changes (n = 76), splenium of corpus callosum involvement (n = 39), diffuse corpus callosum involvement (n = 27), cerebral atrophy (n = 35), basal ganglia involvement (n = 10), and brain stem involvement (n = 2). Notably, subcortical white matter involvement, periventricular white matter involvement, diffuse corpus callosum involvement, and basal ganglia involvement were more prevalent in patients with stage III and IV subacute sclerosing panencephalitis (P < .05 for all). Cerebral atrophy was also significantly more common in patients with stage III compared to those with stage IV subacute sclerosing panencephalitis (P < .0001). However, no substantial positive or negative associations were found between MRI findings and EEG abnormalities, other sociodemographic/clinical variables, and cerebrospinal fluid measles-specific antibody titers (P > .05).
Conclusion: Early in the disease progression of subacute sclerosing panencephalitis, the temporoparietal and parietooccipital regions of the subcortical white matter are affected. Neuroimaging abnormalities exhibit a stronger association with Jabbour's clinical staging, but do not show significant associations with other clinical, sociodemographic, and EEG features.
Background: Postcontrast magnetic resonance imaging (MRI), obtained under anesthesia, is often used to evaluate brain parenchymal and vascular abnormalities in young children, including those with Sturge-Weber syndrome. However, anesthesia and contrast administration may carry risks. We explored the feasibility and potential diagnostic value of a noncontrast, nonsedate MRI acquisition in Sturge-Weber syndrome children and their siblings with a wide range of cognitive and behavioral functioning.
Methods: Twenty children (10 with Sturge-Weber syndrome and 10 healthy siblings; age: 0.7-13.5 years) underwent nonsedate 3-tesla (T) brain MRI acquisition with noncontrast sequences (including susceptibility-weighted imaging) prospectively along with neuropsychology assessment. All images were evaluated for quality, and MRI abnormalities identified in the Sturge-Weber syndrome group were compared to those identified on previous clinical pre- and postcontrast MRI.
Results: Nineteen participants (95%) completed the MRI with good (n = 18) or adequate (n = 1) quality, including all children with Sturge-Weber syndrome and all 5 children ≤5 years of age. The Sturge-Weber syndrome group had lower cognitive functions than the controls, and both groups had several children with behavioral issues, without an apparent effect on the success and quality of the MR images. Susceptibility-weighted imaging detected key venous vascular abnormalities and calcifications and, along with the other noncontrast sequences, provided diagnostic information comparable to previous clinical MRI performed with contrast administration under anesthesia.
Conclusion: This study demonstrates the feasibility and the potential diagnostic value of a nonsedate, noncontrast MRI acquisition protocol in young children including those with cognitive impairment and/or behavioral concerns. This approach can facilitate clinical trials in children where safe serial MRI is warranted.
Aim: To understand the bullying experiences of youth with neuromuscular conditions. Method: Fourteen participants with neuromuscular conditions (10 male; 10-19 years old) participated in semistructured interviews that were analyzed using inductive thematic analysis. Results: Four overarching themes were identified: (1) participants experienced stigma-based bullying; (2) participants exhibited resilience despite bullying victimization; (3) participants identified personally and theoretically helpful and unhelpful supports with regard to bullying; and (4) participants proposed bullying interventions. Interpretation: Individuals with neuromuscular conditions had unique experiences and perspectives on bullying. This qualitative study provides health care professionals with insight into the bullying experiences of patients with neuromuscular conditions. Findings highlight the role for formal and informal education to mitigate stigma-based bullying and increased opportunities for peer support as a protective factor against bullying.
Introduction: Studies suggest disparities in outcomes in minoritized children after severe traumatic brain injury. We aimed to evaluate for disparities in intracranial pressure-directed therapies and outcomes after pediatric severe traumatic brain injury.
Methods: We conducted a secondary analysis of the Approaches and Decisions for Acute Pediatric TBI (ADAPT) Trial, which enrolled pediatric severe traumatic brain injury patients (Glasgow Coma Scale score ≤8) with an intracranial pressure monitor from 2014 to 2018. Patients admitted outside of the United States were excluded. Patients were categorized by race and ethnicity (Hispanic, non-Hispanic Black, non-Hispanic White, and "Other"). We evaluated outcomes by assessing mortality and 3-month Glasgow Outcome Score-Extended for Pediatrics. Our analysis involved parametric and nonparametric testing.
Main results: A total of 671 children were analyzed. Significant associations included older age in non-Hispanic White patients (P < .001), more surgical evacuations in "Other" (P < .001), and differences in discharge location (P = .040). The "other" cohort received hyperventilation less frequently (P = .046), although clinical status during Paco2 measurement was not known. There were no other significant differences in intracranial pressure-directed therapies. Hispanic ethnicity was associated with lower mortality (P = .004) but did not differ in unfavorable outcome (P = .810). Glasgow Outcome Score-Extended for Pediatrics was less likely to be collected for non-Hispanic Black patients (69%; P = .011).
Conclusions: Our analysis suggests a general lack of disparities in intracranial pressure-directed therapies and outcomes in children after severe traumatic brain injury. Lower mortality in Hispanic patients without a concurrent decrease in unfavorable outcomes, and lower availability of Glasgow Outcome Score-Extended for Pediatrics score for non-Hispanic Black patients merit further investigation.
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