Article Figures & Data
Figures
- Figure 1.
EEG analysis pipeline. A, Unfiltered intracerebral EEG signals are bandpass filtered to extract spectral frequencies in theta ( θ), low gamma
- Figure 2.
High gamma event coupling in the SOZ and different brain regions. A, Examples of connectivity matrices of high gamma event coupling (HGEC) for patient 13 who was seizure-free (SF) and patient 19 who was not seizure-free (not-SF). The matrices are organized with respect to SOZ. If both electrode contacts are in SOZ, then the connectivity value is part of the SOZ, if both contacts are outside SOZ, then it is part of the NSOZ (complement), otherwise it is between the SOZ and NSOZ. The lower row illustrates HGEC organized by brain region (M: mesial temporal, L: lateral temporal, E: extratemporal). B, Violin plot and box plot (inside) shows the distribution, median and interquartile range of HGEC values for patients 13 and 19 with respect to SOZ (top rows) f and brain regions (bottom rows). In most cases, HGEC is stronger in patient 13 than patient 19. Check Extended Data Figure 2-1 for GEC matrices of all patients.
- Figure 3.
Connectivity strength in relation to seizure outcome and SOZ interaction. A–C, Violin plots that show HGEC, LGEC, and TEC in relation to SOZ and seizure outcome (SF upper row, NSF lower row). The significant differences (p < 0.05) are marked by asterisks (*). Results for level 1 interactions between connectivity and either zones or outcome are depicted in Extended Data Figure 3-1.
- Figure 4.
Connectivity strength in relation to seizure outcome, brain Regions and SOZ. A, Violin plots show HGEC values in relation to SOZ and brain region (columns; abbreviations same as Fig. 2) for all patients. B, Violin plots show LGEC values in relation to SOZ (upper row), NSOZ (lower row), and brain regions (columns) for all patients. C, Violin plots show ThEC values in relation to NSOZ and brain regions (columns) for all patients. Seizure-free patients were shaded white and not seizure-free outcome were shaded black. The significant differences (p < 0.05) are marked by asterisks (*).
- Figure 5.
Correlation between HGEC and interictal spike rate and electrode distance. A, B, Scatter plots illustrating HGEC in relation to spike rate (A) and electrode contact distance (B). Values are represented as normalize z scores. C, Specific examples of high (top) and low (bottom) correlation between spike rate and HGEC. The vertical bar to the right shows the percentage correlation coefficients for all patients. High r > 0.5 (shaded green), medium 0.25 < r < 0.5 (red), and low correlation r < 0.25 (blue). In most patients, the correlation between spike rate and HGEC was low. D, Same as panel C but correlation with electrode distance. In most patients, there was a high correlation between electrode distance and HGEC, i.e., as electrode distance decreases, HGEC increases. All correlations shown had a p < 0.0001.
- Figure 6.
Comparing event connectivity in three frequency bands. A, Violin plots show median Euclidean distance between pairs of contacts in relation to SOZ (abbreviation same as Fig. 2) and seizure outcome for all patients (abbreviation and shading same as Fig. 4). B, Violin and box plots of correlation coefficient between electrode distance and strength of functional coupling in high gamma
- Figure 7.
Average high gamma event connectivity (HGEC) as a function of (A) epilepsy duration, (B) seizure frequency, (C) patients age, (D) type of surgery, and (E) presence of an MRI lesion. Extended Data Figure 7-1 gives examples of different types of MRI abnormalities.
- Figure 8.
Relating connectivity to neuronal circuits mechanisms. A, A schematic illustrating brain regions involved in generating seizures (red dots) or those not involved (green dots). Clinically-defined seizure onset zone (SOZ; shaded orange) and not seizure onset zone (NSOZ; shaded blue). In an ideal seizure outcome, i.e., seizure free, all regions involved in generating a seizure are in the SOZ. The synchrony between brain regions is illustrated as connections (black lines), and a greater number of lines indicates greater synchrony. In not seizure-free patients, the SOZ is incompletely identified and a portion of the NSOZ contains regions involved in generating seizures. B, Prediction of the differences in the event connectivity when the strength of connectivity corresponds with increased synchronous inhibitory activity (blue dots and black lines) that is proportional to increased synchronous excitatory activity (red triangles and green lines). An assumption is greater synchrony associated with brain regions involved in generating seizures, which leads to the following predictions: (1) in seizure-free (SF) patients, stronger connectivity in SOZ than NSOZ; (2) in not seizure-free (NSF) patients, little or no difference in connectivity between SOZ and NSOZ; and (3) stronger connectivity in the NSOZ of NSF than SF patients. Results from our analysis are presented as three squares for each frequency band (theta = θ, low gamma = LG, high gamma = HG), which are colored red and white for actual results that are consistent or inconsistent, respectively, with the aforementioned predictions.
Tables
Temporal
lobeFrontal
lobeCingulate
cortexParietal
lobeOccipital
lobePatient A EC MH AH PH PHG STG TP PT FG OF SMA FP FO F SS AC MC PC IP AP PTB SG OT O 1 RL RL RL RL 2 RL R R RL R R R 3 RL L L R L L R 4 RL RL RL RL RL 5 RL R RL RL RL 6 RL RL RL RL 7 RL R RL R RL R R 8 RL RL RL RL RL RL 9 L L RL L L RL L 10 RL R RL R RL R 11 RL RL RL RL RL RL 12 RL RL RL RL RL RL 13 RL RL RL RL RL 14 R RL RL RL 15 RL RL RL RL RL L 16 RL RL RL RL RL 17 R RL RL R RL 18 RL RL RL RL 19 R R R R R RL 20 RL RL RL RL RL 21 RL RL RL RL RL 22 L RL R L RL 23 RL RL R L RL RL 24 R RL RL RL RL R R 25 RL L RL L RL L RL 26 R RL R L R RL R 27 RL RL R R RL 28 RL RL RL RL L L L 26 R RL L RL R RL 27 RL RL RL RL R R 31 R RL R R R R R 28 L RL L R RL L R 29 RL RL RL RL RL 30 L RL R L L L L L 31 RL RL RL L L L 36 L L RL R RL RL 32 RL RL RL RL RL 38 RL RL R RL RL RL 34 RL RL L R L R R 40 L RL RL L 41 L RL R R R 42 R RL R R R R R 43 RL RL RL R RL RL TP = temporal pole, FP = frontal pole, A = amygdala, OF = orbitofrontal, EC = entorhinal cortex, F = frontal lobe, AH = anterior hippocampus, FO = frontal operculum, MH = middle hippocampus, AC = anterior cingulate, PH = posterior hippocampus, MC = middle cingulate, PHG = parahippocampal gyrus, PC = posterior cingulate, FG = fusiform gyrus, SMA = supplementary motor area, PT = posterior temporal, SS = supra-sylvian, STG = superior temporal gyrus, AP = anterior parietal lobe, IP = inferior parietal lobe, SG = supramarginal gyrus, PTB = parietal-temporal border, O = occipital lobe, OT = occipital-temporal border, R: Right, L: Left.
Patient Spiking sites Detector highest 5% electrodes Percentage 1 RAH1-3, RA1-3, REC1-3, RPHG1-3, LA1-3 RAH1, RAH 2, REC 1 100% 4 RA1-3, REC1-3, RAH1-3, RPHG1-3, LA1-3, LEC1-3, LAH1-3, LPHG1-3 RA1, RA2, LAH2, LAH3, LAH1 100% 5 RAH1-3, RA1-3, RPH1-3, LAH1-3, REC1-3 RPH3, RAH3, RA2, ROF3 75% 7 RA5-6, REC5-6, RAH1-6, RPHG3-6, RSTGP2-3, RMC1-4, LAH1-2 RA2, RAH1, RAH2, RPHG6, RPSTG2,
REC2, RAH570% 8 LA3-4, LAH1-2, LEC1-4, RA1-2, RAH1-2 RAH1, LEC1, REC1, REC2, RAH2 60% 11 LAH1-3, LA1-3, LEC1-3, RAH1-3, RA1 3, REC1-3 RA7, REC3, LEC 1, REC1, LAH3 80% 14 LEC1-3, LMH1-3 LEC1, LEC2, LMH1, LA1 75% 15 REC4-5, RMH1-2, LEC1-2, LMH1-2 REC5, LEC3, RMH1 66% 16 RA1-7, RAH1-4, REC1-7, RPHG4-7, ROF3-7, LA1-7, LEC1-7,
LAH1-7, LPHG1-7REC1, REC2, LA2 100% 17 RSTA2-3, RSTP3-4 RSTA3, RMH1, RSTP3, RIPP8, LST5 40% 18 REC1-4, RMH1-3, LA1-2, LEC1-2, LMH1-2 REC1, REC2, RMH2, RA2 75% 19 REC4-7, RMH4-7, RPH4-7, RSTG1-7 RA2, RMH5, RA1, RMH4 50% 20 RA1-2, REC1-2, RMH1-2, RPHG1-2, LA1-2, LEC1-2, LMH1-2,
LPHG1-2,REC1, RMH3, LMH1, LEC2 80% 21 RA1-2, RMH1-2, LEC1-3, LMH1-2, LA1-2 RA4, RMH5, LEC1, LA1 50% 22 LEC1-3, LA1-3, LEC4-7, LA4-7 LEC,1, LA1, RA1, RAH1 50% 23 RA1-3, REC1-3, RMH1-3, LA1-3, LEC1-3, LMH1-3 LEC1, REC4, LMH4, RMH7 25% 24 REC1-4, RMH1-2, RA1-3 RA1, RA2, LAH1, LA1, LAH2 40% 25 RTO5-7, RMH1-3, LA6-7, LPH5-6 RMH2, LPH4, LPH5, LPH6 75% 26 LAH1-3, LEC1-2, RMH1-2, RPHG1-3, REC1-3 LAH1, LAH2, LAH3 100% 27 REC1-3, RMH1-2, RPHG1-2, LMH1-2 RMH2, RMH4, RPHG2, LMH1 75% 28 LMH4-7, LEC4-7, LA4-7, LPSM4-7, LOF4-7, LAC4-7, REC4-7,
RMH4-7, RA4-7LMH4, LMH6, LPSM5, LMH5 100% 29 RAH1-3, RA1-3, REC1-3, RPHG1-3 LEC7, LEC6, REC3, REC2, REC1 60% 30 RA1-2, REC1-2, RMH1-2, RPHG1-2, LA1-2, LEC1-2, LMH1-2,
LPHG1-2RA1, LMH1, RA2, REC1 100% 31 RA1-7, REC1-7, RAH1-7, RPHG1-7, ROF1-3, RAF1-3, RAC5-7 RAH1, REC1, REC2, RPHG1, RAH2 100% 32 LEC1-3, LMH1-2, RAH1-7, REC1-7, RPHG1-7 LEC1, LEC3, REC7, RPHG7 100% 33 REC1-3, RAH1-3, RPHG1-3, LAH1-2, LPHGA1-2, RPHG7-8,
LPHGA7-8REC1, REC2, RAH1, RPHG3 100% 34 LPH1-2, LEC1-2, LA1-2 LEC1, LPHG7, LEC2, LPH1 75% 35 LAH1-2, LEC 1-2, LA 1-4, LPHG1-3 LA3, RA3, LA2 66% 36 LMH1-2, LPHG1-3, LA1-2, ROF4-5 LPHG1, LPHG2, LA1 100% 37 LEC1-2, LAH1-2, REC1-2, RAH1-2 LA1, LA2, LAH1, LA7 25% 38 RSTG1-4, RPT 7-8, LPT1-2, LSTG5-7, LEC5-7, LAH5-7, LMTG3-7,
REC3-7LAH6, LAH5, RAH6, RPHG6 50% 39 REC1-3, RMH1-3, RMNH3-7, RPNH2-6, RINH4-6, LPC 5-8 RMH1, LPC7, RMH3, RMNH5 100% 40 LEC1-4, LA1-4, LA5-7, LAH1-4, LPNH6-8, LSTG1-5 LEC1, LEC2, LA1, LEC3 100% 41 RSTGA1-4, RSTG1-4, LSTG1-4 LSTG2, RPST4, LSTG1, LSTG3 75% 42 REC1-7, RSTA1-7, RSTG1-7, RMH1-7, RIF1-7, RSO3-7, RIO3-7,
RAIP3-7RIO1, RSTG4, RAIP7, RMH6, RSTG3 80% 43 LEC1-3, LA1-3, RA1-3, REC1-3, LOF3-7, ROF3-7 LA5, LOF3, RA3, RA2, LEC1 80% Twelve patients showed 100% correspondence in the top 5% of channels with the highest spike rates between the automated spike detector and those manually identified channels containing interictal discharges. Twenty patients showed at least 50%, 11 of which with >70% correspondence. Only four patients <40% correspondence.
R: right, L: left, TP = temporal pole, FP = frontal pole, A = amygdala, OF = orbitofrontal, EC = entorhinal cortex, F = frontal lobe, AH = anterior hippocampus, FO = frontal operculum, MH = middle hippocampus, AC = anterior cingulate, PH = posterior hippocampus, MC = middle cingulate, PHG = parahippocampal gyrus, PC = posterior cingulate, FG = fusiform gyrus, SMA = supplementary motor area, PT = posterior temporal, STG = superior temporal gyrus, AP = anterior parietal lobe, O = occipital lobe, OT = occipital-temporal border.
Patients Sex/age Epilepsyduration Seizurefrequency(/month) Site(s) of SOZ MRI Resected area Surgicaloutcome/follow-up Pathology IIS sites 1 F/38 36 6 RA, RAH, REC, RPHG R/L HA R AMTL IIIB/73 HS, gliosis RAH, RA, REC, RPHG, LA 2 F/17 8 90 RIP, RAP, RMH Normal R parietotemporal neocortex IIC/126 Subcortical WM ectopic neurons NA 3 F/42 30 20 LA, LEC, LAH L HA L AMTL IB/51 FCD Ia NA 4 F/39 32 5 RAH, RPHG, RA, REC R/L HA R AMTL IA/43 Gliosis RA, REC, RAH, RPHG, LA, LEC, LAH, LPHG 5 F/28 20 2 RA, RAH, REC, RPHG Normal R AMTL, temporal neocortical IVB/72 Subcortical WM ectopic neurons RAH, RA, RPH, LAH, REC 6 F/30 29 28 LA, LAH L HA VNS IA/12 NA NA 7 M/21 9 4 REC, RAH, RPHG R FCD, PNH R AMTL, temporooccipital IIIA/84 FCD Ic, IIa RA, REC, RAH, RPHG, RSTP, RMC, LAH 8 F/25 20 27 RAH, RA, REC R/L HA R AMTL IB/60 None LA, LAH, LEC, RA, RAH 9 M/42 22 16 LEC, LPHG, LA, LAH, RAH R/L hippocampal hyperintensity L AMTL II/36 None NA 10 F/48 32 9 RAH, RA Normal R AMTL IIIC/42 HS NA 11 M/40 5 1 LA, LEC, LAH L caudate nucleus atrophy L AMTL IA/24 None LAH, LA, LEC, RAH, RA, REC 12 F/20 9 12 LA, LEC Normal L AMTL IIB/51 FCD IIa NA 13 F/46 46 6 LA, LEC, LAH L HA L AMTL IB/9 HS NA 14 F/53 51 12 LEC, LMH, LA L hippocampal hyperintensity L AMTL IA/86 None LEC, LMH 15 M/45 5 8 LEC, LMH L HA L AMTL IA/58 None REC, RMH, LEC, LMH 16 M/29 8 13 RA, REC, RAH, RPHG, ROFLA, LAH Normal RNS anterior hippocampus IVB/25 NA RA, RAH, REC, RPHG, ROF, LA, LEC, LAH, LPHG, 17 F/50 24 2 RSTA, RSTP R perisylvian polymicrogyria R temporoparietal neocortex, STG IB/2 Gliosis RSTA, RSTP 18 F/49 19 3 RA, REC, RMH, LA, LEC, LMH Normal R AMTL IIA/61 FCD Ic REC, RMH, LA, LEC, LMH 19 F/41 12 30 REC, RMH, RPHG, RSTG Normal R AMTL, R lateral TL IIA/17 HS, gliosis REC, RMH, RPH, RSTG 20 M/49 31 20 RA, REC, RMH, RPHG Normal R AMTL IA/1.5 FCD Ic, gliosis RA, REC, RMH, RPHG, LA, LEC, LMH, LPHG 21 F/35 30 110 LEC, LA, RA L HA VNS IA/10 NA RA, RMH, LEC, LMH, LA 22 M/56 20 2 LA, LEC L posterior comm. artery infarct L AMTL IIB/27 Subcortical WM ectopic neurons LEC, LA 23 F/40 12 4 RA, REC, RMH, RPHG R FCD temporal pole R AMTL IB/45 FCD IIb, gliosis RA, REC, RMH, LA, LEC, LMH 24 F/34 22 8 REC, RMH Normal R AMTL IVC/48 Gliosis REC, RMH, RA 25 F/27 13 8 LEC, LTO, LPH, REC, RMH PVH, polymicrogyria DBS IVB/9 NA RTO, RMH, LA, LPHG 26 M/35 16 170 REC, RMH, RPHG Normal Entorhinal cortex
replace RNSIIIA/29 NA LAH, LEC, RMH, RPHG, REC 27 F/27 7 4 REC, RMH, RPHG, RA Normal RNS MTLE IIIA/74 NA REC, RMH, RPHG, LMH 28 M/26 18 4 LEC, LA, LMH, LOF, LAC, RA, REC, RMH, ROF Encephalomalacia L lateral superior TL TL ATL sparing mesial structures, RNS L hippocampal-LOF IIB/20 Gliosis, heterotopia WM LMH, LEC, LA, LPSM, LOF, LAC, REC, RMH, RA 29 F/34 20 8 RAH, RA, REC R/L PNH RNS RAH and REC IVB/45 NA RAH, RA, REC, RPHG 30 M/27 9 1 RA, REC, RPHG, LA, LEC, LMH, LPHG R HA RNS L/R EC IIIA/38 NA RA, REC, RMH, RPHG, LA, LEC, LMH, LPHG 31 F/30 15 15 RA, RPHG ROF atrophy R lesionectomy IA/34 Gliosis RA, REC, RAH, RPHG, ROF, RAF, RAC 32 F/21 4 2 LEC, LA, LMH, LPHG L temporal pole encephalocele L AMTL IB/35 HS, gliosis LEC, LMH, RAH, REC, RPHG 33 M/51 23 4 LEC, LAH, LPHG, REC, RPHG R HA, L FCD RNS L/R medial TL IB/24 NA REC, RAH, RPHG, LAH, LPHG 34 M/58 8 1 LPH, LEC, LA, RAH, REC L HA L AMTL IIIA/63 HS, gliosis LPH, LEC, LA 35 F/49 13 3 LA, LAH, LEC, LPHG L hippocampal hyperintensity RNS L medial TL and L EC IIB/28 NA LAH, LEC, LA, LPHG 36 F/43 27 3 LOF, LMH, LPHG FCD RT pole R AMTL, RNS L MTL–R Middle OF IID/36 HS LMH, LPHG, LA, ROF 37 M/69 5 0.5 LEC, LAH L HA L amygdalo-hippocampectomy w/Visualase IIIA/55 NA LEC, LAH, REC, RAH 38 M/50 38 90 LEC, LMH, LMTG, LAH, RSTG, RTP, RPT, LPT, LAH, REC Hyperintensity L post-TL VNS IVB/31 NA RSTG, RPT, LPT, LSTG, LEC, LAH, LMTG, REC 39 F/44 9 120 REC, RMH R/L PNH R AMTL IIIA/59 None REC, RMH, RMNH, RPNH, RINH, LPC 40 F/34 8 5 LEC, LA, LAH, LSTG, LPNH, LMNH, LANH L PVH, hypothalamic hamartoma RNS LEC-LPNH IIB/38 NA LEC, LA, LAH, LPNH, LSTG 41 M/35 25 0 RASTG, RPSTG, LSTG Hyperintensity RT pole, PVH R AMTL, TL R superior, middle, inferior temporal extended IV/33 Gliosis RSTGA, RSTG, LSTG 42 M/25 15 8 RMH, RSTG, RSTA, RA, REC Atrophy R hemisphere
Vascular new infarct R post-TLR ML TL/TL R TPO, RNS RSTG, RO IVC/12 Gliosis, CD REC, RSTA, RSTG, RMH, RIF, RSO, RIO, RAIP 43 M/28 25 60 LA, LEC, LMH, RA, REC, RMH L MTS hyperintensity amygdala R>L, L ant TL RNS L entorhinal, L anterior insula IIIA/33 NA LEC, LA, RA, REC, LOF, ROF R = right, L = left, A = amygdala, AH = anterior hippocampus, MH = middle hippocampus, PH = posterior hippocampus, EC = entorhinal cortex, PHG = parahippocampal gyrus, OF = orbitofrontal cortex, FA = anterior frontal, STG/A/P = superior temporal gyrus/anterior/posterior, AMTL = anteromesial temporal lobectomy, RNS = responsive neurostimulation, NA = not available, FCD = focal cortical dysplasia, HA = hippocampal atrophy, HS = hippocampal sclerosis, PNH = periventricular nodular heterotopia, TS = tuberous sclerosis. See Extended Data Table 3-1 that shows examples for resection or RNS therapy in the SOZ.
Hypothesis p-value F value Nb samples Zone significant predictor of HGEC 0.000497 7.60 52,203 Zone significant predictor of LGEC 0.130 2.041 52,203 Zone significant predictor of ThEC 0.057 2.860 52,203 Regions significant predictor of HGEC 2.14e–191 180 52,203 Regions significant predictor of LGEC 4.85–25 241 52,203 Regions significant predictor of ThEC 4.31e–105 99.7 52,203 SF patients significantly different from NSF in HGEC 0.206 1.65 52,203 SF patients significantly different from NSF in LGEC 0.910 0.013 52,203 SF patients significantly different from NSF in ThEC 0.205 1.66 52,203 Seizure outcome significant predictor of HGEC 0.162 2.02 52,203 Seizure outcome significant predictor of LGEC 0.539 0.384 52,203 Seizure outcome significant predictor of ThEC 0.520 0.421 52,203 SOZ HGEC > NSOZ HGEC in SF patients 1.10e–9 18.8 ( 401 SOZ LGEC > NSOZ LGEC in SF patients 0.0217 8.23 ( 401 SOZ ThEC < NSOZ ThEC in SF patients 1.12e–6 12.1 ( 2785 SOZ ThEC < NSOZ ThEC in NSF patients 0.00855 14.9 ( 2785 In SOZ, M-L, HGEC SF > HGEC NSF 0.00114 11.8 ( 996 In SOZ, M-L, LGEC SF > LGEC NSF 0.00205 9.94 ( 996 In NSOZ, E-E, LGEC SF < LGEC NSF 0.0089 7.46 ( 5069 In NSOZ, L-L, ThEC SF < ThEC NSF 0.0111 7.03 ( 6106 Spikes significant predictor of HGEC 1.22e–100 455 ( β = 0.00410) 52,203 Spikes significant predictor of LGEC 7.71e–106 479 ( β = 0.00279) 52,203 Spikes significant predictor of ThEC 1.54e–50 233 ( β = 0.00165) 52,203 Distance significant predictor of HGEC 7.32e–110 5504 ( β = 0.900) 52,203 Distance significant predictor of LGEC 1.40e–121 6401 ( β = 0.868) 52,203 Distance significant predictor of ThEC 2.12e–87 3804 ( β = 0.717) 52,203 Significant values are shown in bold.
Extended Data Figure 1-1
Effect of low sampling and up-sampling on HGEC. A, Ratio of low γ events to numbers of high γ events is box-plotted for patients with 2-kHz sampling (N = 15) and those with 200-Hz sampling rate (N = 28). B, Same as A but for ratio of powers instead of ratio of number of events. We calculated those measures on five channels randomly selected from each patient on a randomly selected 30-s window and repeated the procedure 10 times. In total, we had
Extended Data Figure 1-2
HGEC in NSOZ ipsilateral versus contralateral. Comparison between HGEC connectivity values in channels located outside the SOZ but in same hemisphere (ipsilateral) and those in the opposite hemisphere (contralateral). A, Connectivity matrix where the NSOZ is organized by connectivity within the ipsilateral hemisphere (I), contralateral hemisphere (C), and between ipsilateral and contralateral hemispheres (I-C). B, Boxplots illustrate the connectivity values of ipsilateral NSOZ channels and contralateral NSOZ channels. No significant difference was obtained (effect size
Extended Data Figure 2-1
High γ events connectivity (HGEC) matrices for all seizure-free patients (green) and not seizure-free patients (red) are presented. The matrices are organized by connectivity within the seizure onset zone (SOZ; upper triangle), within the seizure onset zone complement (NSOZ; lower triangle) and between the SOZ and NSOZ (rectangle) networks. Download Figure 2-1, TIF file.
Extended Data Figure 3-1
Connectivity strength in relation to seizure outcome or SOZ. A, Violin plots that show HGEC, LGEC, and ThEC in relation to seizure outcome where SF patients are shaded in white and NSF are shaded in black. B, Violin plots that show HGEC, LGEC, and ThEC in relation to SOZ. Download Figure 3-1, TIF file.
Extended Data Figure 6-1
The exponential relationship between HEC and Euclidian distance is plotted slow decaying HGEC (A, patient 3) and fast decaying HGEC (B, patient 24). Download Figure 6-1, TIF file.
Extended Data Figure 7-1
Representative MRI from three patients in this study illustrating the different types of MRI pathology found in these cases that required invasive EEG. Download Figure 7-1, TIF file.
Extended Data Figure T3-1
Resection or RNS therapy in the SOZ. A, Resection of tissue corresponding to SOZ in patient 24. Postimplant CT (left, axial) registered with postsurgical MRI in coronal (middle) and axial planes (right). Red dots denote contacts of depth electrode with distal contacts positioned in right entorhinal cortex. Area outlined in white indicates the margins of resection in the plane of view. B, Same as panel A, but patient 39 and yellow dots denote contacts of depth electrode positioned to sample right middle hippocampus. C, RNS therapy of the left mesial temporal lobe SOZ, including entorhinal cortex, in patient 35. Full-head model illustrates trajectories of two RNS probes (magenta lines) with one entry (E) from occipital cortex with contacts (magenta dots) positioned in left amygdala, hippocampus, and parahippocampal gyrus, and the other E from lateral aspect of temporal cortex with contacts in and adjacent to entorhinal cortex. Yellow dots denote depth electrode contacts of the left SOZ involving amygdala, entorhinal cortex, middle hippocampus, and parahippocampal gyrus. Sagittal view (top), clockwise-rotated posterolateral view (middle), and axial view (bottom). A = anterior, P = posterior, D = dorsal, V = ventral, L = left, and R = right. Download Figure T3-1, TIF file.
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