Abstract
Introduction: Acquired demyelinating syndromes (ADS) disrupt extensive brain networks, especially in paediatrics where disease effects are superimposed upon typical neurodevelopment. It is unclear whether disruptions are functionally relevant to neurodevelopmental outcomes, and whether autoantibodies such as those to myelin oligodendrocyte glycoprotein (MOG-ab) differentially effect network disruption.
Aims: To investigate neurophysiological responses as an indicator of cognitive outcome, using magnetoencephalography (MEG), in paediatric ADS patients with and without MOG-ab.
Methods: To date, n=10 children with ADS have been recruited, of which n=3 had MOG-ab positivity. Neurophysiological responses were assessed using a child-adapted visuomotor MEG task. Participants executed a button press in response to a visual grating. This characterised post-movement beta rebound (PMBR), a motor response following movement cessation, with an observable power increase in beta oscillations (14–30 Hz). Using beamformers, we performed source localisation of greatest difference in beta-band oscillations during the active epochs (500-1000ms relative to button-press) contrasted against baseline (2700-3200ms) and extracted virtual electrode time-series. Time-frequency spectrograms of beta-band oscillatory power at this location, were used to estimate PMBR neurophysiology (e.g. peak power, latency of peak power).
Participants also completed neuropsychological assessment (Wechsler Intelligence Scale for Children (WISC-V)).
Results: In preliminary analyses, no differences were found between participants with and without MOG-ab in behavioural or neurophysiology. However, groups did differ on IQ, with greater scores in the MOG group (t(5.05)= -2.7302, p-value = 0.041). Controlling for age, we found significant negative correlations between latency of the maximum beta power increase and WISC-V IQ (r = -0.90, p=0.006) across all participants.
Conclusions: We echo previous relationships between neurophysiology of PMBR and cognition in MS, and expand these findings to paediatric ADS. This could reflect the role of PMBR in long range integrative processes over distributed brain networks, relying heavily on structural connection integrity, which are more likely to be damaged with increased ADS severity and cognitive difficulties. Further work should establish the feasibility and pathogenic relevance that neurophysiological measures produced using MEG have.
Aims: To investigate neurophysiological responses as an indicator of cognitive outcome, using magnetoencephalography (MEG), in paediatric ADS patients with and without MOG-ab.
Methods: To date, n=10 children with ADS have been recruited, of which n=3 had MOG-ab positivity. Neurophysiological responses were assessed using a child-adapted visuomotor MEG task. Participants executed a button press in response to a visual grating. This characterised post-movement beta rebound (PMBR), a motor response following movement cessation, with an observable power increase in beta oscillations (14–30 Hz). Using beamformers, we performed source localisation of greatest difference in beta-band oscillations during the active epochs (500-1000ms relative to button-press) contrasted against baseline (2700-3200ms) and extracted virtual electrode time-series. Time-frequency spectrograms of beta-band oscillatory power at this location, were used to estimate PMBR neurophysiology (e.g. peak power, latency of peak power).
Participants also completed neuropsychological assessment (Wechsler Intelligence Scale for Children (WISC-V)).
Results: In preliminary analyses, no differences were found between participants with and without MOG-ab in behavioural or neurophysiology. However, groups did differ on IQ, with greater scores in the MOG group (t(5.05)= -2.7302, p-value = 0.041). Controlling for age, we found significant negative correlations between latency of the maximum beta power increase and WISC-V IQ (r = -0.90, p=0.006) across all participants.
Conclusions: We echo previous relationships between neurophysiology of PMBR and cognition in MS, and expand these findings to paediatric ADS. This could reflect the role of PMBR in long range integrative processes over distributed brain networks, relying heavily on structural connection integrity, which are more likely to be damaged with increased ADS severity and cognitive difficulties. Further work should establish the feasibility and pathogenic relevance that neurophysiological measures produced using MEG have.
Original language | English |
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Pages (from-to) | 839 |
Number of pages | 1 |
Journal | Multiple Sclerosis Journal |
Volume | 28 |
Issue number | 3S |
Publication status | Published - 12 Oct 2022 |