Article Figures & Data
Figures
- Figure 1.
A, Three schemata illustrating the interaction among stimuli, EEG, and the neural correlates of evoked potentials: I, traditional view of stimuli interacting with neural circuitry independently of EEG; II, phase-resetting view of stimuli interacting with EEG; III, schema suggested by the results of this study whereby neural correlates of stimulation and ongoing EEG modulate each other in a time-dependent manner. B, Schematic of experimental apparatus. C, Example of 10 raw, unstimulated phase-triggered trials from an individual subject. D, Example of experimental protocol for a subject.
- Figure 4.
A, Pooled phase histograms from 20 subjects, indicating the distribution (counts) of Hilbert transform-derived phases at the onset of stimuli for 0, 25, 50, and 75 msec delay phase-triggered stimuli as well as regular and sampled irregular stimuli. For unstimulated (left column) and first tone stimuli (middle column) there is a progressively less restricted set of phases as one progresses from 0 through 25 and 50 msec delays and a nearly uniform distribution of phases at 75 msec delay. Rayleigh statistics parameter R and Bonferroni-corrected p value, p′, are shown for each distribution (significant results with p′ < 0.0001 are denoted by an asterisk). Regular and sampled stimuli phases for first tone and all phase distributions for second tone stimuli are distributed uniformly. B, Averaged evoked potential peak-to-peak amplitudes to first (left column) and second (right column) tones. Mean amplitudes are indicated by heavy horizontal bars. The significant (*) increases in P30 and P50 amplitudes for first tone stimuli at 0 and 50 msec delays, respectively, and the significant decreases in P30 and P50 amplitudes at 50 and 0 msec delays, respectively, are quantified in the text of the figure.
- Figure 3.
Grand average results from 20 subjects. Solid lines represent averages at 0 msec (red), 25 msec (green), 50 msec (blue), and 75 msec (black). Dashed lines indicate bootstrapped confidence intervals (p = 0.025). Insets demonstrate increases and decreases in amplitude of P30 at 0 and 50 msec, respectively, and a comparable decrease and increase in P50 amplitude at 0 and 50 msec, respectively. Inset waveforms are aligned as detailed in Materials and Methods. No significant effects of first stimulus phase are seen in P30 and P50 measured at the second stimulus 500 msec later.
- Figure 2.
A, Example of single epoch of data from one subject. Top panel shows raw EEG signal. Stimuli (S), indicated as vertical solid lines, were delivered at 0 and 500 msec. Horizontal dashed line indicates threshold (T) for extracting phase at π/-π. Bottom panel shows Hilbert transform retrospectively derived phase. B, Averages of the difference between phase-triggered and unstimulated phase control trials from one subject at 0, 25, 50, and 75 msec delay. Latencies for P30 and P50 peaks are indicated with vertical dashed lines; despite changes in amplitude with phase, the latencies are constant. Also shown are averages from regular stimulation intervals and sampled irregular stimulation intervals. C, Origin of phase-triggered evoked potentials from averages of phase-triggered (solid line) and unstimulated phase control trials (dashed line) at 0 msec delay for this subject. P30 and P50 evoked potentials derive from fluctuations in EEG amplitude along similar initial phases of the EEG cycle. Insets show progressive expansion in time scale, with raw difference below and, at bottom, filtered difference (10-50 Hz) customarily used to extract P30 and P50.
