Eosinophilic Meningitis: Eleven-Year Experience at Texas Children's Hospital.

Eosinophilic meningitis can be caused by various etiologies and is reported mostly in tropical climates. The diagnosis is rare in the continental US, presenting challenges for management. Following a case of pediatric eosinophilic meningitis, we reviewed our 11-year experience with this diagnosis at a large US children's hospital.

Neurorehabilitation across the Continuum: From the Neurocritical care unit to home.

Children admitted to neurocritical care units often experience new neurodevelopmental disabilities due to both their acquired neurologic injuries and deconditioning from prolonged hospitalizations. Rehabilitation for critically ill children is multifactorial and begins in the intensive care unit itself. The goals of rehabilitation include prevention of complications associated with immobilization and evolving tone, comprehensive evaluation and treatment of functional deficits, and implementation of adaptive strategies with the goal of maximizing recovery. As a child progresses along the medical continuum from the neurocritical care unit to acute care to post-hospitalization settings, their rehabilitative needs and interventions should also evolve. A child in the neurocritical care unit is likely to have sustained an acquired brain injury. Whether resulting from traumatic or non-traumatic causes, all etiologies of pediatric acquired brain injury can result in significant challenges for the child and their family. Post-intensive care syndrome-pediatrics is a clinical construct that that systematically organizes the range of physical, cognitive, psychological, and social symptoms that emerge in both a child and their family members following a critical illness. Ideally, outpatient care for this population evaluates and supports all areas of post-intensive care syndrome-pediatrics through an interdisciplinary clinical care model. Proactive and comprehensive rehabilitation across the continuum provides the opportunity to support the child and their family in all areas affected, thereby minimizing distress, maximizing function, and optimizing outcomes.

Fulminant Anti-Myelin Oligodendrocyte Glycoprotein-Associated Cerebral Cortical Encephalitis: Case Series of a Severe Pediatric Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease Phenotype.

BACKGROUND: We describe a cohort of children with severe myelin oligodendrocyte glycoprotein (MOG)-IgG-associated cerebral cortical encephalitis (CCE), manifesting with bilateral cortical cytotoxic edema and critical neurological illness. METHODS: We retrospectively reviewed our pediatric MOG antibody-associated disease (MOGAD) database and identified patients with specific radiographic pattern of bilateral, multifocal cortical cytotoxic lesions. We collected demographic, clinical, and outcomes data from these patients and compared select variables with radiographically distinct cerebral MOGAD syndromes (case-control analysis). We assessed the correlation of quantitative clinical variables with severity/outcomes measures using simple linear regression. RESULTS: Sixty-five of 88 total MOGAD cases had cerebral disease, and six of 88 met inclusion criteria for fulminant CCE (f-CCE). Age range was 2 to 7 years; five of six were male. Six of six were critically ill with severe encephalopathy and seizures, two of six required barbiturate coma, and two of six required invasive intracranial pressure monitoring. Six of six required treatment escalation beyond steroids. Four of six had favorable outcome; two of six had moderate-severe disability. Compared with other cerebral MOGAD cases (n = 59), children with f-CCE were more likely to have critical illness and poor neurological outcomes scores. Neurofilament light chain and treatment latency positively correlated with intensive care unit length of stay and outcomes scores; cerebrospinal fluid (CSF) white blood cell count and neutrophil-to-lymphocyte ratio did not. CONCLUSIONS: Pediatric CCE with bilateral cytotoxicity is associated with more fulminant disease and worse outcomes than other cerebral MOGAD syndromes.