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Shared and disorder-related abnormalities in cortical steady-state responses in ADHD and hypomania at adolescence age

AI Summary
  • Both ADHD and hypomania exhibited reduced prefrontal 40 Hz ASSR amplitude and increased centro-parietal ASSR amplitude versus controls.
  • ADHD showed increased prefrontal and frontal 15 Hz SSVEP amplitude, frontal phase delays and central phase advances.
  • Hypomania displayed enhanced occipital and temporal 15 Hz SSVEP amplitude and ASSR phase advances in central, temporal and occipital regions; SSEPs may aid diagnosis.
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J Affect Disord. 2026 Aug 4:122343. doi: 10.1016/j.jad.2026.122343. Online ahead of print.

ABSTRACT

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.

PMID:42551561 | DOI:10.1016/j.jad.2026.122343

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