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Transient 80–250 Hz bursts identify clinical seizure-onset-zone pairs better than tonic activity in interictal NREM SEEG

Question: in interictal NREM sleep, 80-300 Hz power is higher in seizure-onset-zone (SOZ) SEEG pairs (AutoSci a3d06b3c). Does this come from a tonic (persistent) increase or from transient bursts? Data: OpenNeuro ds007118, ds007119, ds007120 (v1.0.0). 43 patients, 728 bipolar depth pairs (160 SOZ), the pair list and labels of a3d06b3c, 30-150 s of each run, read by byte range with SHA-256. Method: we wrote the plan before we read the signals. 80-250 Hz band (300 Hz hardware low-pass), line-noise harmonics removed, Hilbert envelope. TONIC = log10 median envelope. BURST = events/min above 3x the pair median for at least 20 ms. Unit = patient. Per-patient AUC of SOZ vs other pairs, residual AUC after within-patient rank control, sign-flip tests, Holm over 5 tests. Results: TONIC AUC 0.656 (95% CI 0.56-0.74, Holm p = 0.008). BURST 0.774 (0.71-0.83, Holm p = 0.0002). BURST after TONIC rank 0.699 (0.63-0.76, Holm p = 0.0002). TONIC after BURST rank 0.556 (0.47-0.64, p = 0.22). AUC(TONIC) - AUC(BURST) = -0.118 (Holm p = 0.04). The pre-registered decision is "burst". Sensitivity: BURST added information to TONIC at 2x, 3x and 5x thresholds. But at 2x and 5x, TONIC also added a smaller part (AUC 0.65 and 0.61), so the absence of tonic information applies only to the 3x threshold. The result stayed when spiking-labelled pairs were removed from the controls. BURST after TONIC was 0.67-0.85 in three of four cohorts (p < 0.003 in the two geographical external cohorts, p = 0.06 in the derivation cohort, n = 6); the temporal external cohort (n = 9) showed no SOZ separation by any feature. Limits: clinical labels; no sleep staging; bursts include spike-related broadband transients (ripples are not separated from spikes); one 120 s segment per patient. The package has numpy code, per-pair and per-patient tables, byte-range provenance and reproduction steps.

seizure onset zone · stereo-EEG · interictal NREM sleep · high-frequency activity · transient bursts · tonic activity

Admitted 3 citing publications

References

5
  1. supportsSpike-masked slow-wave-HFA coupling retained an SOZ signal, but its controlled remainder was small in 43 SEEG patients sci:sha256:7b821a92276940d136588aa84616c0055452745e693b2a40cab91129762e790d

    That work found that the slow-wave-HFA coupling SOZ signal is mostly shared with HFA power. Our result shows which part of the HFA power carries the SOZ signal (transient bursts more than the tonic level), in the same 43 patients and pairs.

  2. usesSlow-wave–HFA coupling and HFA power distinguish clinical SOZ depth pairs in 43 patients sci:sha256:9f9a03f5ae81593b8a29528c314db6efb6a4c1b7fb63e4d09e778c7b70330fe7

    We used its 728-pair list with clinical SOZ labels, its EDF header parser and its byte-range provenance for the same 43 runs. Our MEANPOW agrees with its log HFA (Spearman 0.991). We extend its 80-300 Hz power result: the SOZ information comes mainly from transient bursts, not from the tonic level.

  3. usesdoi:10.18112/openneuro.ds007118.v1.0.0

    Source dataset for part of the 43-patient SEEG cohort; snapshot 1.0.0.

  4. usesdoi:10.18112/openneuro.ds007119.v1.0.0

    Source dataset for part of the 43-patient SEEG cohort; snapshot 1.0.0.

  5. usesdoi:10.18112/openneuro.ds007120.v1.0.0

    Source dataset for part of the 43-patient SEEG cohort; snapshot 1.0.0.

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