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Pediatric acquired demyelinating syndromes (PADS) include a heterogeneous group of diagnoses, including acute disseminated encephalomyelitis (ADEM), neuromyelitis optica spectrum disorders (NMOSD), optic neuritis (ON) and transverse myelitis (TM). Myelin oligodendrocyte glycoprotein antibody disease (MOGAD) is often associated with demyelinating conditions, but may also present with encephalopathy without demyelinating lesions. Approximately 30% of patients diagnosed with MOGAD experience a relapse. Neurocognitive outcomes in PADS have reduced performance on tasks related to attention, processing speed, visual motor, and fine motor functioning. Psychosocial problems include anxiety, depression, and fatigue. Neurocognitive and psychosocial impacts of MOGAD events for the pediatric population are sparse. The current study sought to characterize neurocognitive sequelae from MOGAD (MAGAD+) compared to patients diagnosed withPADS without MOGAD (MOGAD-).
Participants and Methods:
Twenty children and adolescents (6–18 years) diagnosed with PADS were recruited using a clinic convenience sample of patients. Study participants completed a neurocognitive battery and parents completed questionnaires of behavioral and emotional functioning. Demographic and medical variables were collected via retrospective chart review. Chi square and t-test analyses were used to compare MOGAD+ and MOGAD- groups. Performance on neuropsychological and behavioral questionnaires were compared to established sex and age norms to assess the degree to which group means deviate from normative expectations.
Results:
MOGAD+ and MOGAD- groups did not significantly differ based on demographic, neurocognitive, or parent reported social and behavioral functioning. Neurocognitive testing documented mean scores that were in the average range between groups. Notable variability in performance was observed within both MOGAD+ and MOGAD- groups. Bilateral fine motor deficits, visual motor, visual perception attention, and executive functioning deficits were notable for the combined PADS group, with 30-50% performing >1.5 SD below the mean. The number of white matter lesions or hospital duration were not significantly associated with performance on neurocognitive measures. However, older age of onset of PADS was significantly correlated with lower performance on visual motor integration and visual perception tasks (r(18) = -.50 p = .026; r(18) = -.53 p = .016). Findings also revealed associations of shorter hospitalization stays with higher behavioral symptoms on a parent measure of social/behavioral functioning (r(18) = -.47 p = .037).
Conclusions:
Consistent with the PADS literature, relative to control norms, lower performance on tasks related to attention, executive functioning, visual motor, and fine motor skills, irrespective of MOGAD status, are observed in the current study. The variability of functioning and heterogeneity observed across PADS diagnoses warrants further study to better understand the impact of clinical course, treatment outcomes, and neuropsychological sequelae over time in this population. Higher behavioral distress with shorter hospital stays may indicate a potential opportunity for patient and family education preparing for return to home/community. The current study was limited by small sample size, variable time since hospitalization, and heterogeneous diagnoses within PADS that make it difficult to generalize findings. Future studies could prospectively follow patients over time to better understand the trajectory of recovery, identify predictors for relapse, and those at greatest risk of neurocognitive and behavioral deficits.
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