MedElevator
Войти в исследования Journal of affective disorders · 2026
Shared and disorder-related abnormalities in cortical steady-state responses in ADHD and hypomania at adolescence age.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Khaleghi Ali, Mohammadi Mohammad Reza, Baloochi Shahab Alaedin, Zarafshan Hadi
Аннотация
OBJECTIVE: Bipolar disorder (BD) and ADHD share symptomatic overlap during adolescence, yet their distinct neurophysiological underpinnings remain unclear. This study compared cortical steady-state responses to visual (15 Hz SSVEP) and auditory (40 Hz ASSR) stimulation in adolescents with hypomania, ADHD, and healthy controls.
METHODS: EEG was recorded from 105 adolescents (35 per group) during passive exposure to visual and auditory stimuli. SSVEP and ASSR amplitude and phase were analyzed across six cortical regions using repeated-measures MANOVA with FDR correction.
RESULTS: The ADHD group showed increased SSVEP amplitude and phase delays in prefrontal/frontal regions (q (FDR) = 0.019-0.025, d = 0.66-0.73) alongside central phase advances (q (FDR) = 0.006, d = 0.94). Hypomania exhibited enhanced occipital/temporal SSVEP amplitude versus ADHD (q (FDR) = 0.010-0.045, d = 0.55-0.79). For ASSR, both patient groups showed reduced prefrontal amplitude (ADHD: q (FDR) = 0.009, d = 0.89; hypomania: q (FDR) = 0.045, d = 0.48) and increased centro-parietal amplitude (q (FDR) < 0.001, d = 0.88-0.95) versus controls. Hypomania displayed phase advances in central/temporal/occipital regions (q (FDR) = 0.024-0.048, d = 0.45-0.76), while ADHD showed frontal phase delays (q (FDR) = 0.015, d = 0.82).
CONCLUSIONS: ADHD and hypomania share prefrontal auditory deficits but exhibit distinct SSEP patterns. Their neurophysiological signatures are largely dissociable, suggesting that SSEPs warrant further investigation as candidate markers for differential diagnosis. These preliminary findings illustrate how mechanism-level measures can complement symptom-based assessment when diagnostic categories overlap.
METHODS: EEG was recorded from 105 adolescents (35 per group) during passive exposure to visual and auditory stimuli. SSVEP and ASSR amplitude and phase were analyzed across six cortical regions using repeated-measures MANOVA with FDR correction.
RESULTS: The ADHD group showed increased SSVEP amplitude and phase delays in prefrontal/frontal regions (q (FDR) = 0.019-0.025, d = 0.66-0.73) alongside central phase advances (q (FDR) = 0.006, d = 0.94). Hypomania exhibited enhanced occipital/temporal SSVEP amplitude versus ADHD (q (FDR) = 0.010-0.045, d = 0.55-0.79). For ASSR, both patient groups showed reduced prefrontal amplitude (ADHD: q (FDR) = 0.009, d = 0.89; hypomania: q (FDR) = 0.045, d = 0.48) and increased centro-parietal amplitude (q (FDR) < 0.001, d = 0.88-0.95) versus controls. Hypomania displayed phase advances in central/temporal/occipital regions (q (FDR) = 0.024-0.048, d = 0.45-0.76), while ADHD showed frontal phase delays (q (FDR) = 0.015, d = 0.82).
CONCLUSIONS: ADHD and hypomania share prefrontal auditory deficits but exhibit distinct SSEP patterns. Their neurophysiological signatures are largely dissociable, suggesting that SSEPs warrant further investigation as candidate markers for differential diagnosis. These preliminary findings illustrate how mechanism-level measures can complement symptom-based assessment when diagnostic categories overlap.