Dynamics of neuromagnetic power in the default mode network throughout the whole-course of childhood absence epilepsy_Journal of Epilepsy

Authors：

ZHU Yinjie , LI Minghao , JIANG Peilin ,  WANG Xiaoshan

Department of Neurology, The Affiliated Brain Hospital of Nanjing Medical University, Nanjing 210000, China;

Corresponding author：

WANG Xiaoshan, Email: lidou2005@126.com

Keywords：

Childhood absence epilepsy; Default Mode Network; Magnetoencephalography; Spectral power; Characteristics analysis

DOI：

10.7507/2096-0247.202411003

Video：

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Objective To investigate biological markers that differentiate states during various seizure periods of childhood absence epilepsy (CAE) by examining the spatiotemporal dynamics of magnetoencephalographic (MEG) signals from Default Mode Network (DMN) nodes, revealing the neurophysiological mechanisms underlying changes in consciousness during CAE seizures. Methods Thirty-six drug-native children diagnosed with CAE were recruited. The interictal data, ictal data of CAE children were collected using a CTF-225 channel MEG system. Conduct temporal homogeneity partitioning for all seizure period data, co-registering 14 distinct seizure states. Identify 12 brain regions associated with the default mode network (DMN) as regions of interest (ROI); employ minimum norm estimation in conjunction with the Welch method to compute the power spectral density (PSD) of the ROI; conduct differential analysis on the relative PSD values; and use a random forest model to identify significant PSD features that differentiate between states of epilepsy. Results Power changes in DMN-related brain regions across various frequency bands show significant synchrony. During a seizure, the power in the δ band rapidly increases at the onset and quickly decreases at the end. Meanwhile, the power in the θ-γ2 bands decreases at the beginning and gradually recovers after the seizure. During the O+2 phase following seizure onset, the power in the β band peaks briefly before rapidly declining. The medial frontal cortex has lower power in the δ frequency band during seizures compared to other DMN brain regions, but higher power in the α frequency band. The random forest model's feature importance analysis reveals that the precuneus, lateral temporal lobe and medial temporal lobe play important roles in identifying seizure states. Power changes in the precuneus in the α and δ frequency bands improve the model's classification accuracy. Conclusions This study investigated the dynamic spatiotemporal characteristics of the DMN during CAE seizures, revealing the typical manifestations of power changes in specific brain regions and frequency bands at the onset, maintenance, and termination of seizures. It was discovered that power of the precuneus can act as an important feature to distinguish between different stages of CAE seizures. These findings shed new light on the pathophysiological mechanisms underlying changes in consciousness states in CAE.

1.	Smallwood J, Bernhardt BC, Leech R, et al. The default mode network in cognition: a topographical perspective. Nat Rev Neurosci, 2021, 22(8): 503-513.
2.	Menon V. 20 years of the default mode network: a review and synthesis. Neuron, 2023, 111(16): 2469-2487.
3.	Mcgill ML, Devinsky O, Kelly C, et al. Default mode network abnormalities in idiopathic generalized epilepsy. Epilepsy Behav, 2012, 23(3): 353-359.
4.	Whitfield-Gabrieli S, Ford JM. Default mode network activity and connectivity in psychopathology. Annu Rev Clin Psychol, 2012, 8: 49-76.
5.	Siniatchkin M, Capovilla G. Functional neuroimaging in epileptic encephalopathies. Epilepsia, 2013, 54(Suppl 8): 27-33.
6.	Hirsch E, French J, Scheffer IE, et al. ILAE definition of the idiopathic generalized epilepsy syndromes: position statement by the ILAE Task Force on Nosology and Definitions. Epilepsia, 2022, 63(6): 1475-1499.
7.	Devinsky O, Elder C, Sivathamboo S, et al. Idiopathic generalized epilepsy. Neurology, 2024, 102(3): 1156-1168.
8.	Kessler SK, Shinnar S, Cnaan A, et al. Pretreatment seizure semiology in childhood absence epilepsy. Neurology, 2017, 89(7): 673-679.
9.	Elmali AD, Auvin S, Bast T, et al. How to diagnose and classify idiopathic (genetic) generalized epilepsies. Epileptic Disorders, 2020, 22(4): 399-420.
10.	Sadleir LG, Farrell K, Smith S, et al. Electroclinical features of absence seizures in childhood absence epilepsy. Neurology, 2006, 67(3): 413-418.
11.	Crunelli V, Lőrincz ML, Mccafferty C, et al. Clinical and experimental insight into pathophysiology, comorbidity and therapy of absence seizures. Brain, 2020, 143(8): 2341-2368.
12.	Parsons N, Bowden SC, Vogrin S, et al. Default mode network dysfunction in idiopathic generalised epilepsy. Epilepsy Research, 2020, 159: 106254.
13.	Luo C, Li Q, Lai Y, et al. Altered functional connectivity in default mode network in absence epilepsy: a resting‐state fMRI study. Hum Brain Mapp, 2011, 32(3): 438-449.
14.	Tangwiriyasakul C, Perani S, Centeno M, et al. Dynamic brain network states in human generalized spike-wave discharges. Brain, 2018, 141(10): 2981-2994.
15.	Guo JN, Kim R, Chen Y, et al. Impaired consciousness in patients with absence seizures investigated by functional MRI, EEG, and behavioural measures: a cross-sectional study. The Lancet Neurology, 2016, 15(13): 1336-1345.
16.	Carney PW, Masterton RaJ, Harvey AS, et al. The core network in absence epilepsy. Neurology, 2010, 75(10): 904-911.
17.	Killory BD, Bai X, Negishi M, et al. Impaired attention and network connectivity in childhood absence epilepsy. NeuroImage, 2011, 56(4): 2209-2217.
18.	Yang T, Luo C, Li Q, et al. Altered resting‐state connectivity during interictal generalized spike‐wave discharges in drug‐naïve childhood absence epilepsy. Hum Brain Mapp, 2012, 34(8): 1761-1767.
19.	Ward RJ, Zucca FA, Duyn JH, et al. The role of iron in brain ageing and neurodegenerative disorders. The Lancet Neurology, 2014, 13(10): 1045-1060.
20.	Englot DJ, Hinkley LB, Kort NS, et al. Global and regional functional connectivity maps of neural oscillations in focal epilepsy. Brain, 2015, 138(8): 2249-2262.
21.	Hillebrand A, Nissen IA, Ris-Hilgersom I, et al. Detecting epileptiform activity from deeper brain regions in spatially filtered MEG data. Clin Neurophysiol, 2016, 127(8): 2766-2769.
22.	Sun F, Wang S, Wang Y, et al. Differences in generation and maintenance between ictal and interictal generalized spike-and-wave discharges in childhood absence epilepsy: A magnetoencephalography study. Epilepsy Behav, 2023, 148: 109440.
23.	Gupta D, Ossenblok P, Van Luijtelaar G. Space–time network connectivity and cortical activations preceding spike wave discharges in human absence epilepsy: a MEG study. Med Biol Eng Comput, 2011, 49(5): 555-565.
24.	Wu C, Xiang J, Sun J, et al. Quantify neuromagnetic network changes from pre-ictal to ictal activities in absence seizures. Neuroscience, 2017, 357: 134-144.
25.	Scheffer IE, Berkovic S, Capovilla G, et al. ILAE classification of the epilepsies: Position paper of the ILAE Commission for Classification and Terminology. Epilepsia, 2017, 58(4): 512-521.
26.	Cheng C-H, Wang P-N, Mao H-F, et al. Subjective cognitive decline detected by the oscillatory connectivity in the default mode network: a magnetoencephalographic study. Aging, 2020, 12(4): 3911-3925.
27.	Wang S, Wang Y, Li Y, et al. Alternations of neuromagnetic activity across neurocognitive core networks among benign childhood epilepsy with centrotemporal spikes: A multi-frequency MEG study. Front Neurosci, 2023, 17: 11568.
28.	Sun J, Gao Y, Miao A, et al. Multifrequency dynamics of cortical neuromagnetic activity underlying seizure termination in absence epilepsy. Front Hum Neurosci, 2020, 14.
29.	Hong H, Xiaoling G, Hua Y. Variable selection using mean decrease accuracy and mean decrease gini based on random forest; proceedings of the 2016 7th IEEE International Conference on Software Engineering and Service Science (ICSESS), F 26-28 Aug, 2016.
30.	Meeren HKM, Pijn JPM, Van Luijtelaar ELJM, et al. Cortical focus drives widespread corticothalamic networks during spontaneous absence seizures in rats. The Journal of Neuroscience, 2002, 22(4): 1480-1495.
31.	Gotman J, Grova C, Bagshaw A, et al. Generalized epileptic discharges show thalamocortical activation and suspension of the default state of the brain. PNAS, 2005, 102(42): 15236-15240.
32.	Holmes MD, Brown M, Tucker DM. Are "generalized" seizures truly generalized? Evidence of localized mesial frontal and frontopolar discharges in absence. Epilepsia, 2004, 45(12): 1568-1579.
33.	Avoli M. A brief history on the oscillating roles of thalamus and cortex in absence seizures: thalamus and cortex roles in absence seizures. Epilepsia, 2012, 53(5): 779-789.
34.	Paz JT, Huguenard JR. Microcircuits and their interactions in epilepsy: is the focus out of focus?. Nat Neurosci, 2015, 18(3): 351-359.
35.	Shepherd GMG, Yamawaki N. Untangling the cortico-thalamo-cortical loop: cellular pieces of a knotty circuit puzzle. Nature Reviews Neuroscience, 2021, 22(7): 389-406.
36.	Harmony T. The functional significance of delta oscillations in cognitive processing. Front Integr Neurosci, 2013, 7: 83.
37.	Unterberger I, Trinka E, Kaplan PW, et al. Generalized nonmotor (absence) seizures-what do absence, generalized, and nonmotor mean?. Epilepsia, 2018, 59(3): 523-529.
38.	Steriade M, Dossi RC, Paré D, et al. Fast oscillations (20-40 Hz) in thalamocortical systems and their potentiation by mesopontine cholinergic nuclei in the cat. PNAS, 1991, 88(10): 4396-4400.
39.	Steriade M, Contreras D, Amzica F, et al. Synchronization of fast (30-40 Hz) spontaneous oscillations in intrathalamic and thalamocortical networks. The Journal of Neuroscience, 1996, 16(8): 2788-2808.
40.	Li H, Kraus A, Wu J, et al. Selective changes in thalamic and cortical GABAA receptor subunits in a model of acquired absence epilepsy in the rat. Neuropharmacology, 2006, 51(1): 121-128.
41.	Russo E, Citraro R, Constanti A, et al. Upholding WAG/Rij rats as a model of absence epileptogenesis: hidden mechanisms and a new theory on seizure development. Neurosci Biobehav Rev, 2016, 71: 388-408.
42.	Sorokin JM, Jeanne TP, Huguenard JR. Absence seizure susceptibility correlates with pre-ictal β oscillations. J Physiol-Paris, 2016, 110(4): 372-381.
43.	Baillet S. Magnetoencephalography for brain electrophysiology and imaging. Nat Neurosci, 2017, 20(3): 327-339.
44.	Rosburg T. Alpha oscillations and consciousness in completely locked-in state. Clin Neurophysiol, 2019, 130(9): 1652-1654.
45.	Purdon PL, Pierce ET, Mukamel EA, et al. Electroencephalogram signatures of loss and recovery of consciousness from propofol. PNAS, 2013, 110(12): E1142-E1151.
46.	Meyer J, Maheshwari A, Noebels J, et al. Asynchronous suppression of visual cortex during absence seizures in stargazer mice. Nat Commun, 2018, 9(1): 1938.
47.	Vijayan S, Ching S, Purdon PL, et al. Thalamocortical mechanisms for the anteriorization of α rhythms during propofol-induced unconsciousness. The Journal of Neuroscience, 2013, 33(27): 11070-11075.
48.	Mashour GA, Pal D, Brown EN. Prefrontal cortex as a key node in arousal circuitry. Trends Neurosci, 2022, 45(10): 722-732.
49.	Szaflarski JP, Difrancesco M, Hirschauer T, et al. Cortical and subcortical contributions to absence seizure onset examined with EEG/fMRI. Epilepsy Behav, 2010, 18(4): 404-413.
50.	Carney PW, Masterton RaJ, Flanagan D, et al. The frontal lobe in absence epilepsy. Neurology, 2012, 78(15): 1157-1165.
51.	Miao A, Xiang J, Tang L, et al. Using ictal high-frequency oscillations (80-500Hz) to localize seizure onset zones in childhood absence epilepsy: a MEG study. Neurosci Lett, 2014, 566: 21-26.
52.	Cavanna AE, Trimble MR. The precuneus: a review of its functional anatomy and behavioural correlates. Brain, 2006, 129(Pt 3): 564-583.
53.	Utevsky AV, Smith DV, Huettel SA. Precuneus is a functional core of the default-mode network. The Journal of Neuroscience, 2014, 34(3): 932-940.
54.	Moeller F, Levan P, Gotman J. Independent component analysis (ICA) of generalized spike wave discharges in fMRI: comparison with general linear model-based EEG-fMRI. Hum Brain Mapp, 2011, 32(2): 209-217.
55.	Bai X, Vestal M, Berman R, et al. Dynamic time course of typical childhood absence seizures: EEG, behavior, and functional magnetic resonance imaging. The Journal of Neuroscience, 2010, 30(17): 5884-5893.
56.	Benuzzi F, Mirandola L, Pugnaghi M, et al. Increased cortical BOLD signal anticipates generalized spike and wave discharges in adolescents and adults with idiopathic generalized epilepsies. Epilepsia, 2012, 53(4): 622-630.
57.	Kumar A, Lyzhko E, Hamid L, et al. Neuronal networks underlying ictal and subclinical discharges in childhood absence epilepsy. J Neurol, 2023, 270(3): 1402-1415.

1. Smallwood J, Bernhardt BC, Leech R, et al. The default mode network in cognition: a topographical perspective. Nat Rev Neurosci, 2021, 22(8): 503-513.
2. Menon V. 20 years of the default mode network: a review and synthesis. Neuron, 2023, 111(16): 2469-2487.
3. Mcgill ML, Devinsky O, Kelly C, et al. Default mode network abnormalities in idiopathic generalized epilepsy. Epilepsy Behav, 2012, 23(3): 353-359.
4. Whitfield-Gabrieli S, Ford JM. Default mode network activity and connectivity in psychopathology. Annu Rev Clin Psychol, 2012, 8: 49-76.
5. Siniatchkin M, Capovilla G. Functional neuroimaging in epileptic encephalopathies. Epilepsia, 2013, 54(Suppl 8): 27-33.
6. Hirsch E, French J, Scheffer IE, et al. ILAE definition of the idiopathic generalized epilepsy syndromes: position statement by the ILAE Task Force on Nosology and Definitions. Epilepsia, 2022, 63(6): 1475-1499.
7. Devinsky O, Elder C, Sivathamboo S, et al. Idiopathic generalized epilepsy. Neurology, 2024, 102(3): 1156-1168.
8. Kessler SK, Shinnar S, Cnaan A, et al. Pretreatment seizure semiology in childhood absence epilepsy. Neurology, 2017, 89(7): 673-679.
9. Elmali AD, Auvin S, Bast T, et al. How to diagnose and classify idiopathic (genetic) generalized epilepsies. Epileptic Disorders, 2020, 22(4): 399-420.
10. Sadleir LG, Farrell K, Smith S, et al. Electroclinical features of absence seizures in childhood absence epilepsy. Neurology, 2006, 67(3): 413-418.
11. Crunelli V, Lőrincz ML, Mccafferty C, et al. Clinical and experimental insight into pathophysiology, comorbidity and therapy of absence seizures. Brain, 2020, 143(8): 2341-2368.
12. Parsons N, Bowden SC, Vogrin S, et al. Default mode network dysfunction in idiopathic generalised epilepsy. Epilepsy Research, 2020, 159: 106254.
13. Luo C, Li Q, Lai Y, et al. Altered functional connectivity in default mode network in absence epilepsy: a resting‐state fMRI study. Hum Brain Mapp, 2011, 32(3): 438-449.
14. Tangwiriyasakul C, Perani S, Centeno M, et al. Dynamic brain network states in human generalized spike-wave discharges. Brain, 2018, 141(10): 2981-2994.
15. Guo JN, Kim R, Chen Y, et al. Impaired consciousness in patients with absence seizures investigated by functional MRI, EEG, and behavioural measures: a cross-sectional study. The Lancet Neurology, 2016, 15(13): 1336-1345.
16. Carney PW, Masterton RaJ, Harvey AS, et al. The core network in absence epilepsy. Neurology, 2010, 75(10): 904-911.
17. Killory BD, Bai X, Negishi M, et al. Impaired attention and network connectivity in childhood absence epilepsy. NeuroImage, 2011, 56(4): 2209-2217.
18. Yang T, Luo C, Li Q, et al. Altered resting‐state connectivity during interictal generalized spike‐wave discharges in drug‐naïve childhood absence epilepsy. Hum Brain Mapp, 2012, 34(8): 1761-1767.
19. Ward RJ, Zucca FA, Duyn JH, et al. The role of iron in brain ageing and neurodegenerative disorders. The Lancet Neurology, 2014, 13(10): 1045-1060.
20. Englot DJ, Hinkley LB, Kort NS, et al. Global and regional functional connectivity maps of neural oscillations in focal epilepsy. Brain, 2015, 138(8): 2249-2262.
21. Hillebrand A, Nissen IA, Ris-Hilgersom I, et al. Detecting epileptiform activity from deeper brain regions in spatially filtered MEG data. Clin Neurophysiol, 2016, 127(8): 2766-2769.
22. Sun F, Wang S, Wang Y, et al. Differences in generation and maintenance between ictal and interictal generalized spike-and-wave discharges in childhood absence epilepsy: A magnetoencephalography study. Epilepsy Behav, 2023, 148: 109440.
23. Gupta D, Ossenblok P, Van Luijtelaar G. Space–time network connectivity and cortical activations preceding spike wave discharges in human absence epilepsy: a MEG study. Med Biol Eng Comput, 2011, 49(5): 555-565.
24. Wu C, Xiang J, Sun J, et al. Quantify neuromagnetic network changes from pre-ictal to ictal activities in absence seizures. Neuroscience, 2017, 357: 134-144.
25. Scheffer IE, Berkovic S, Capovilla G, et al. ILAE classification of the epilepsies: Position paper of the ILAE Commission for Classification and Terminology. Epilepsia, 2017, 58(4): 512-521.
26. Cheng C-H, Wang P-N, Mao H-F, et al. Subjective cognitive decline detected by the oscillatory connectivity in the default mode network: a magnetoencephalographic study. Aging, 2020, 12(4): 3911-3925.
27. Wang S, Wang Y, Li Y, et al. Alternations of neuromagnetic activity across neurocognitive core networks among benign childhood epilepsy with centrotemporal spikes: A multi-frequency MEG study. Front Neurosci, 2023, 17: 11568.
28. Sun J, Gao Y, Miao A, et al. Multifrequency dynamics of cortical neuromagnetic activity underlying seizure termination in absence epilepsy. Front Hum Neurosci, 2020, 14.
29. Hong H, Xiaoling G, Hua Y. Variable selection using mean decrease accuracy and mean decrease gini based on random forest; proceedings of the 2016 7th IEEE International Conference on Software Engineering and Service Science (ICSESS), F 26-28 Aug, 2016.
30. Meeren HKM, Pijn JPM, Van Luijtelaar ELJM, et al. Cortical focus drives widespread corticothalamic networks during spontaneous absence seizures in rats. The Journal of Neuroscience, 2002, 22(4): 1480-1495.
31. Gotman J, Grova C, Bagshaw A, et al. Generalized epileptic discharges show thalamocortical activation and suspension of the default state of the brain. PNAS, 2005, 102(42): 15236-15240.
32. Holmes MD, Brown M, Tucker DM. Are "generalized" seizures truly generalized? Evidence of localized mesial frontal and frontopolar discharges in absence. Epilepsia, 2004, 45(12): 1568-1579.
33. Avoli M. A brief history on the oscillating roles of thalamus and cortex in absence seizures: thalamus and cortex roles in absence seizures. Epilepsia, 2012, 53(5): 779-789.
34. Paz JT, Huguenard JR. Microcircuits and their interactions in epilepsy: is the focus out of focus?. Nat Neurosci, 2015, 18(3): 351-359.
35. Shepherd GMG, Yamawaki N. Untangling the cortico-thalamo-cortical loop: cellular pieces of a knotty circuit puzzle. Nature Reviews Neuroscience, 2021, 22(7): 389-406.
36. Harmony T. The functional significance of delta oscillations in cognitive processing. Front Integr Neurosci, 2013, 7: 83.
37. Unterberger I, Trinka E, Kaplan PW, et al. Generalized nonmotor (absence) seizures-what do absence, generalized, and nonmotor mean?. Epilepsia, 2018, 59(3): 523-529.
38. Steriade M, Dossi RC, Paré D, et al. Fast oscillations (20-40 Hz) in thalamocortical systems and their potentiation by mesopontine cholinergic nuclei in the cat. PNAS, 1991, 88(10): 4396-4400.
39. Steriade M, Contreras D, Amzica F, et al. Synchronization of fast (30-40 Hz) spontaneous oscillations in intrathalamic and thalamocortical networks. The Journal of Neuroscience, 1996, 16(8): 2788-2808.
40. Li H, Kraus A, Wu J, et al. Selective changes in thalamic and cortical GABAA receptor subunits in a model of acquired absence epilepsy in the rat. Neuropharmacology, 2006, 51(1): 121-128.
41. Russo E, Citraro R, Constanti A, et al. Upholding WAG/Rij rats as a model of absence epileptogenesis: hidden mechanisms and a new theory on seizure development. Neurosci Biobehav Rev, 2016, 71: 388-408.
42. Sorokin JM, Jeanne TP, Huguenard JR. Absence seizure susceptibility correlates with pre-ictal β oscillations. J Physiol-Paris, 2016, 110(4): 372-381.
43. Baillet S. Magnetoencephalography for brain electrophysiology and imaging. Nat Neurosci, 2017, 20(3): 327-339.
44. Rosburg T. Alpha oscillations and consciousness in completely locked-in state. Clin Neurophysiol, 2019, 130(9): 1652-1654.
45. Purdon PL, Pierce ET, Mukamel EA, et al. Electroencephalogram signatures of loss and recovery of consciousness from propofol. PNAS, 2013, 110(12): E1142-E1151.
46. Meyer J, Maheshwari A, Noebels J, et al. Asynchronous suppression of visual cortex during absence seizures in stargazer mice. Nat Commun, 2018, 9(1): 1938.
47. Vijayan S, Ching S, Purdon PL, et al. Thalamocortical mechanisms for the anteriorization of α rhythms during propofol-induced unconsciousness. The Journal of Neuroscience, 2013, 33(27): 11070-11075.
48. Mashour GA, Pal D, Brown EN. Prefrontal cortex as a key node in arousal circuitry. Trends Neurosci, 2022, 45(10): 722-732.
49. Szaflarski JP, Difrancesco M, Hirschauer T, et al. Cortical and subcortical contributions to absence seizure onset examined with EEG/fMRI. Epilepsy Behav, 2010, 18(4): 404-413.
50. Carney PW, Masterton RaJ, Flanagan D, et al. The frontal lobe in absence epilepsy. Neurology, 2012, 78(15): 1157-1165.
51. Miao A, Xiang J, Tang L, et al. Using ictal high-frequency oscillations (80-500Hz) to localize seizure onset zones in childhood absence epilepsy: a MEG study. Neurosci Lett, 2014, 566: 21-26.
52. Cavanna AE, Trimble MR. The precuneus: a review of its functional anatomy and behavioural correlates. Brain, 2006, 129(Pt 3): 564-583.
53. Utevsky AV, Smith DV, Huettel SA. Precuneus is a functional core of the default-mode network. The Journal of Neuroscience, 2014, 34(3): 932-940.
54. Moeller F, Levan P, Gotman J. Independent component analysis (ICA) of generalized spike wave discharges in fMRI: comparison with general linear model-based EEG-fMRI. Hum Brain Mapp, 2011, 32(2): 209-217.
55. Bai X, Vestal M, Berman R, et al. Dynamic time course of typical childhood absence seizures: EEG, behavior, and functional magnetic resonance imaging. The Journal of Neuroscience, 2010, 30(17): 5884-5893.
56. Benuzzi F, Mirandola L, Pugnaghi M, et al. Increased cortical BOLD signal anticipates generalized spike and wave discharges in adolescents and adults with idiopathic generalized epilepsies. Epilepsia, 2012, 53(4): 622-630.
57. Kumar A, Lyzhko E, Hamid L, et al. Neuronal networks underlying ictal and subclinical discharges in childhood absence epilepsy. J Neurol, 2023, 270(3): 1402-1415.

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Latest ArticlesDynamics of neuromagnetic power in the default mode network throughout the whole-course of childhood absence epilepsy

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