Quirine van Engen’s research while affiliated with University of California, San Diego and other places

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Publications (4)


Dissociating Contributions of Theta and Alpha Oscillations from Aperiodic Neural Activity in Human Visual Working Memory
  • Preprint

December 2024

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29 Reads

Quirine van Engen

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Geeling Chau

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Aaron Smith

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[...]

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While visual working memory (WM) is strongly associated with reductions in occipitoparietal 8-12 Hz alpha power, the role of 4-7 Hz frontal midline theta power is less clear, with both increases and decreases widely reported. Here, we test the hypothesis that this theta paradox can be explained by non-oscillatory, aperiodic neural activity dynamics. Because traditional time-frequency analyses of electroencephalopgraphy (EEG) data conflate oscillations and aperiodic activity, event-related changes in aperiodic activity can manifest as task-related changes in apparent oscillations, even when none are present. Reanalyzing EEG data from two visual WM experiments (n = 74), and leveraging spectral parameterization, we found systematic changes in aperiodic activity with WM load, and we replicated classic alpha, but not theta, oscillatory effects after controlling for aperiodic changes. Aperiodic activity decreased during WM retention, and further flattened over the occipitoparietal cortex with an increase in WM load. After controlling for these dynamics, aperiodic-adjusted alpha power decreased with increasing WM load. In contrast, aperiodic-adjusted theta power increased during WM retention, but because aperiodic activity reduces more, it falsely appears as though theta “oscillatory” power (e.g., bandpower) is reduced. Furthermore, only a minority of participants (31/74) had a detectable degree of theta oscillations. These results offer a potential resolution to the theta paradox where studies show contrasting power changes. We identify novel aperiodic dynamics during human visual WM that mask the potential role that neural oscillations play in cognition and behavior. Significance statement Working Memory (WM) is our ability to hold information in mind without it being present in our external environment. Years of research focused on oscillatory brain dynamics to discover the mechanisms of WM. Here, we specifically look at oscillatory and non-oscillatory, aperiodic activity as measured with scalp EEG to test their significance in supporting WM. We challenge earlier findings regarding theta oscillations with our analysis approach, while replicating alpha oscillation findings. Furthermore, aperiodic activity is found to be involved in WM, over frontal regions in a task-general manner, and over anterior regions this activity is reduced with an increase the number of items that are remembered. Thus, we have identified novel aperiodic dynamics during human visual WM.



Overview of ECT and MST
This describes important details of both treatment types, electroconvulsive therapy (ECT), and magnetic seizure therapy (MST). Both treatments are typically only used on patients with treatment-resistant depression and involve inducing a seizure, either with an electrical current or a magnetic field. The main difference is that ECT has a more global spread to subcortical structures and hippocampus, whereas MST affects more local cortical structures. However, both treatment types significantly reduce depression ratings, with MST having a comparable but more modest therapeutic effect than ECT. We can see this clinical improvement in the datasets analyzed here, as measured by the HAMD-17 for ECT (pre median(IQR) = 23.0 (22, 24.5), post median(IQR) = 10 (8.5, 19), W(18) = 6, δCliff = 0.89, p = 5.3 ×10⁻⁵) and the HAMD-24 for MST (pre-MST = 26.5 (24, 29), post-MST = 20 (19, 26), W(13) = 7, δCliff = 0.55, p = 2.3 × 10⁻³).
Using spectral parameterization to disambiguate periodic and aperiodic contributions to delta band power
A Simulated power spectrum illustrating parameterized spectra. Unlike traditional band power measures that conflate periodic and aperiodic activity, spectral parameterization defines oscillation power as relative power above the aperiodic component (pink dashed line). B Increases in the aperiodic exponent can cause apparent increases in total (T) band power, while power relative (R) to the aperiodic component remains unchanged. We see this here in a simulated power spectrum depicting an increase in exponent with no delta oscillation changes after treatment. C True increases in oscillation power show increases in both total power and relative power. We see this here in a simulated power spectrum depicting an increase in delta oscillation power after treatment with no change in exponent. D Delta in the EEG trace vs. aperiodic activity. EEG with delta oscillations (where a delta peak is present in the spectra) is visibly different from EEG with only aperiodic activity in the delta band.
EEG results -aperiodic vs. delta band power slowing
Spectral differences in aperiodic exponent and delta oscillations in ECT (top) and MST (bottom). A Raw power spectra averaged across channels for each patient pre- and post-ECT. Bolded spectra represent average across patients. B Increase in aperiodic exponent post-ECT (pre = 0.88 ± 0.21 µV²Hz⁻¹, post = 1.25 ± 0.33 µV²Hz⁻¹, t(21) = −9.07, dz = 2.00, ɑadj = 6.25 x 10⁻³, p = 1.05 x 10⁻⁸), inset shows scalp topography of median exponent change, with significant electrodes (p < 0.05) marked in white. C Increase in total power in the delta band post-ECT (pre = −11.88 ± 0.27 µV²Hz⁻¹, post = −11.69 ± 0.51 µV²Hz⁻¹, t(21) = −2.23, dz = 0.45, ɑadj = 1.25 x 10⁻², p = 0.036), inset shows scalp topography of median delta band power change, with significant electrodes (p < 0.05) marked in white. D Increase in aperiodic-adjusted oscillation power in the delta band – only 12 out of 22 patients exhibited a delta oscillation peak both pre- and post-ECT (pre = 0.16 (0.08, 0.66) µV², post = 0.46 (0.23, 0.76) µV², W(11) = 10, δCliff = −0.26, ɑadj = 5.00 x 10⁻², p = 0.02). Many patients exhibited an emergence of delta peaks post-ECT, hence the increased number of data points in post-ECT. No scalp topography is depicted because delta oscillation presence was not consistent across electrodes and patients. E Increase in the abundance of delta oscillations post-ECT (pre = 0.023 (0, 0.15), post = 0.36 (0.07, 0.67), W(21) = 20.5, δCliff = −0.67, ɑadj = 1.00 x 10⁻², p = 1.77 x 10⁻⁴). F Raw power spectra averaged across channels for each patient pre- and post-MST. Bolded spectra represent average across patients. G Increase in aperiodic exponent post-MST (pre = 0.98 ± 0.18 µV²Hz⁻¹, post = 1.14 ± 0.21 µV²Hz⁻¹, t(21) = −3.06, dz = 0.80, ɑadj = 7.14 x 10⁻³, p = 6.0 x 10⁻³), inset shows scalp topography of median exponent change, with significant electrodes (p > 0.05) marked in white. H No significant change in total power in the delta band post-MST (pre = −11.88 ± 0.27 µV²Hz⁻¹, post = −11.69 ± 0.51 µV²Hz⁻¹, t(21) = −2.23, dz = 0.45, ɑadj = 1.25 x 10⁻², p = 0.036), inset shows scalp topography of median delta band power change, with significant electrodes (p > 0.05) marked in white. I No significant change in aperiodic-adjusted oscillation power in the delta band–only 10 out of 22 patients exhibited a delta oscillation peak both pre- and post-MST (pre = 0.16 ± 0.14 µV², post = 0.35 ± 0.21 µV², t(9) = −3.26, dz = 1.14, ɑadj = 8.33 × 10⁻³, p = 9.8 x 10⁻³), with a few patients exhibiting emerging delta peaks post-MST, hence the increased number of data points post-MST. J No significant change in the abundance of delta oscillations post-MST (pre = 0.02 (0, 0.07), post = 0.03 (0, 0.05), W(21) = 62.5, δCliff = −0.15, ɑadj = 5.00 x 10⁻², p = 0.80).
EEG results–changes in theta and alpha oscillations
Changes in theta (4–7 Hz) and alpha (7–12 Hz) oscillations in ECT (top) and MST (bottom). A Observed increase in theta oscillation power post-ECT (pre = 0.30 ± 0.15 µV², post = 0.70 ± 0.32 µV², t(19) = −5.65, dz = 1.55, ɑadj = 8.33 x 10⁻³, p = 1.90 x 10⁻⁵), inset shows scalp topography of median theta oscillation change. B Increase in theta abundance post-ECT (pre = 0.23 (0.03, 0.63), post = 0.69 (0.34, 0.91), W(21) = 35, δCliff = −0.45, ɑadj = 1.67 x 10⁻², p = 5.40 x 10⁻³). C Power spectra from electrode F8 in a patient who received ECT showing the emergence of a theta oscillation and a decrease in alpha oscillation power post-ECT. D Decrease in alpha oscillation power post-ECT (pre = 1.32 ± 0.49 µV², post = 0.99 ± 0.39 µV², t(21) = 3.33, dz = 0.78, ɑadj = 1.25 × 10⁻², p = 3.20 x 10⁻³), inset shows scalp topography of median alpha oscillation power change. E Decrease in alpha abundance post-ECT (pre = 1.0 (1, 1), post = 1.0 (0.94, 1), W(21) = 42 δCliff = 0.35, ɑadj = 2.50 x 10⁻², p = 0.020). F Increase in theta oscillation power post-MST (pre = 0.35 (0.14, 0.42) µV², post = 0.53 (0.44, 0.82) µV², W(17) = 3.0, δCliff = −0.97, ɑadj = 6.25 x 10⁻³, p = 3.80 x 10⁻⁵), inset shows scalp topography of median theta oscillation power change. G No significant change in theta abundance (pre = 0.39(0.07, 0.98), post = 0.68(0.21, 0.95), W(21) = 47, δCliff = −0.34, ɑadj = 1.00 × 10⁻², p = 0.02). H Power spectra from electrode F8 in a patient who received MST showing the emergence of a theta oscillation and a decrease in alpha oscillation power post-MST. I There is no significant change in alpha oscillation power post-MST (pre = 1.19 ± 0.44 µV², post = 1.13 ± 0.37 µV², t(21) = 0.88, dz = 0.15, ɑadj = 2.50 x 10⁻², p = 0.39), inset shows scalp topography of median change in alpha oscillation power. J No significant change in alpha abundance post-MST (pre = 1.0 (1.0, 1.0), post = 1.0 (1.0, 1.0), W(21) = 2.0, δCliff = 0.18, ɑadj = 1.67 ×10⁻², p = 0.18).
Partial regression analysis – baseline exponent and treatment outcome
Partial regression of combined ECT and MST datasets showing a positive trending relationship between patients’ aperiodic exponent at baseline and clinical outcome, as measured by normalized HAM-D (β = 0.30, p = 0.091, 95% CI[−0.05, 0.657]). Here, patients whose baseline aperiodic exponent is lower, visible in a flatter pre-treatment power spectrum, show lower post-treatment symptom severity.
Magnetic seizure therapy and electroconvulsive therapy increase aperiodic activity
  • Article
  • Full-text available

November 2023

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221 Reads

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6 Citations

Translational Psychiatry

Major depressive disorder (MDD) is a leading cause of disability worldwide. One of the most efficacious treatments for treatment-resistant MDD is electroconvulsive therapy (ECT). Recently, magnetic seizure therapy (MST) was developed as an alternative to ECT due to its more favorable side effect profile. While these approaches have been very successful clinically, the neural mechanisms underlying their therapeutic effects are unknown. For example, clinical “slowing” of the electroencephalogram beginning in the postictal state and extending days to weeks post-treatment has been observed in both treatment modalities. However, a recent longitudinal study of a small cohort of ECT patients revealed that, rather than delta oscillations, clinical slowing was better explained by increases in aperiodic activity, an emerging EEG signal linked to neural inhibition. Here we investigate the role of aperiodic activity in a cohort of patients who received ECT and a cohort of patients who received MST treatment. We find that aperiodic neural activity increases significantly in patients receiving either ECT or MST. Although not directly related to clinical efficacy in this dataset, increased aperiodic activity is linked to greater amounts of neural inhibition, which is suggestive of a potential shared neural mechanism of action across ECT and MST.

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Fig. 1| ECT vs. MST. This figure highlights the most important similarities and differences between electroconvulsive therapy (ECT), and magnetic seizure therapy (MST). Both treatments are typically only used on patients with treatment-resistant depression and involve inducing a seizure, either with an electrical current or a magnetic field. The main difference is that ECT has a more global spread to subcortical structures and hippocampus, whereas MST affects more local cortical structures. However, both treatment types significantly reduce depression ratings, as measured by the HAMD-17 for ECT (pre = 24.26, post = 13.21, t(18) = 5.94, d z = 2.07, p = 1.3 x 10 -5 ) and the HAMD-24 for MST (pre = 28.13, post = 21.40, t(14) = 4.14, d z = 0.93, p = 9.97 x 10 -4 ).
Fig. 3| EEG results -Aperiodic vs. delta band power slowing Spectral differences in aperiodic exponent and delta oscillations in ECT (top) and MST (bottom). (A) Raw power spectra averaged across channels for each patient pre-and post-ECT. Bolded spectra represent average across patients. (B) Comparison of aperiodic exponent pre-and post-treatment (pre = 0.89 µV 2 Hz -1 , post = 1.56 µV 2 Hz -1 , t(21) = -8.12, d z = 1.85, p = 6.15 x 10 -8 ), (C) total power in the delta band (pre = -11.91 µV 2 Hz -1 , post = -10.97 µV 2 Hz -1 , t(21) = -8.03, d z = 1.96, p = 7.69 x 10 -8 ), (D) aperiodic-adjusted oscillatory power in the delta band (pre = 0.16 µV 2 Hz -1 , post = 0.61 µV 2 Hz -1 ), and (E) abundance of delta oscillations (pre = 0.03, post = 0.26, t(21) = -3.16, d z = 0.79, p = 4.75 x 10 -3 ). (F) Raw power spectra averaged across channels for each patient pre-and post-MST. Bolded spectra represent average across patients. (G) Comparison of aperiodic exponent pre-and post-treatment (pre = 0.97 µV 2 Hz -1 , post = 1.16 µV 2 Hz -1 , t(22) = -3.17, d z = 0.80, p = 4.42 x 10 -3 ), (H) total power in the delta band (pre = -11.87 µV 2 Hz -1 , post = -11.64 µV 2 Hz -1 , t(22) = -2.39, d z = 0.58, p = 0.03), (I) aperiodic-adjusted oscillatory power in the delta band (pre = 0.63 µV 2 Hz -1 , post = 0.54 µV 2 Hz -1 ), and (J) abundance of delta oscillations (pre = 0.01, post = 0.03, t(22) = -2.05, d z = 0.23, p = 0.18).
ECT and MST dataset details for patients included in this paper ECT dataset details were from REF #16 and further correspondence. MST dataset details were from REF #9 and further correspondence.
Magnetic seizure therapy and electroconvulsive therapy increase frontal aperiodic activity

January 2023

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237 Reads

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2 Citations

Major depressive disorder (MDD) is a leading cause of disability worldwide. One of the most efficacious treatments for treatment-resistant MDD is electroconvulsive therapy (ECT). Recently, magnetic seizure therapy (MST) was developed as an alternative to ECT due to its more favorable side effect profile. While these approaches have been very successful clinically, the neural mechanisms underlying their therapeutic effects are unknown. For example, clinical slowing of the electroencephalogram has been observed in both treatment modalities. A recent longitudinal study of a small cohort of ECT patients revealed that observed clinical slowing was better explained by increases in frontal aperiodic activity, an emerging EEG signal linked to neural inhibition. Here we investigate the role of aperiodic activity in a cohort of patients who received ECT and a cohort of patients who received MST treatment. We find that across treatments, frontal aperiodic activity better explains increases in delta band power associated with clinical slowing, compared to delta oscillations. Increased aperiodic activity is also linked to therapeutic efficacy, which is suggestive of a potential shared neural mechanism of action across ECT and MST: an increase in frontal inhibitory activity.

Citations (2)


... The emerging evidence from neuroimaging studies also suggests that the therapeutic effects of MST are possibly due to changes produced by MST in regional cerebral blood flow, neurotransmitter levels, and functional neural connectivity patterns [14][15][16]. Functional neuroimaging imaging-based studies have revealed changes in regional brain activity and connectivity patterns following MST, with alterations observed in areas implicated in emotion regulation, reward processing, and cognitive control. MST has been shown to enhance connectivity within the default mode network and favorably modulate activity in the anterior cingulate cortex and dorsolateral prefrontal cortex, and other regions thought to play a critical role in mood regulation and executive functioning. ...

Reference:

Magnetic Seizure Therapy in Management of Depression: A Narrative Review
Magnetic seizure therapy and electroconvulsive therapy increase aperiodic activity

Translational Psychiatry

... The rotations along the other two axes were chosen to ensure symmetric placement of the coil above both sides of the head.  Distance and E-field optimization of the MagVenture MST-Twin coil: Clinical applications aim to place the two coil halves above the F3/F4 electrode positions, respectively [17,18]. ...

Magnetic seizure therapy and electroconvulsive therapy increase frontal aperiodic activity