(A) Three examples in three different patients of depth EEG along with corresponding spectrograms in the spindle frequency range (10–16 Hz) during 15 s of NREM sleep. Note that, regardless of slow waves, local spindles often occur without spindle activity in other regions, including homotopic regions across hemispheres and regions with equivalent SNR showing the same global slow waves. (B) Quantitative analysis of spindle occurrence across pairs of channels. Top row (concordant events, 34% of cases) shows spectrograms for events in which a spindle was detected in the “seed” channel but not in the “target” channel (N = 13,750 events in 156 pairs of regions in 12 individuals). Bottom row (nonconcordant events, 66% of cases) shows spectrograms for events in which a spindle was detected in the seed channel but not detected in the target channel (N = 26,874 events in 156 pairs of regions in 12 individuals). Note that spindle power in nonconcordant target channels is at near-chance levels, indicating that our detection can reliably separate between presence and absence of spindle activity. (C) Distribution of involvement (percentage of monitored brain structures expressing each spindle) is shown across 22,914 spindles in 50 electrodes of 12 individuals. Note that the distribution is skewed to the left, indicating that most spindles are local. (D) Scatter plot of spindle amplitudes as a function of involvement (percentage of brain structures expressing each spindle) shows that global spindles have some tendency to be of higher amplitude (r = 0.63; p
(A) Slow waves become more local in late sleep. Slow wave involvement (percentage of monitored brain structures expressing each wave) in early NREM sleep versus late NREM sleep in five individuals exhibiting a clear homeostatic decline of SWA during sleep (Figure S1). Error bars denote SEM (n = 1436 and 1698 events in early and late sleep). Asterisk denotes statistically significant difference (p −10, unequal variance t test). (B) Kcomplexes are more global and similarinearly and latesleep. Same sleep segments and analysisas (A). Error barsdenote SEM (n = 148 and 181 eventsinearly and late sleep; p = 0.98, unequal variance t test). (C) Spindles become more global in late sleep. Same sleep segments and analysis as (A). Error bars denote SEM (n = 1272 and 2554 events in early and late sleep, p
Figure 7. Sleep Slow Waves Propagate Across…
Figure 7. Sleep Slow Waves Propagate Across Typical Paths
(A) Left: Average depth EEG slow…
Figure 7. Sleep Slow Waves Propagate Across Typical Paths (A) Left: Average depth EEG slow waves in different brain structures of one individual illustrate propagation from frontal cortex (yellow) to MTL (red). All slow waves are triggered by scalp EEG negativity. Black, scalp mean waveform. Right: Distributions of time lags for individual waves in supplementary motor area (SM, yellow) and hippocampus (HC, red) relative to scalp. (B) Mean position in sequences of propagating waves in all 129 electrodes across 13 individuals. Each circle denotes one depth electrode according to its precise anatomical location. Yellow-red colors denote waves observed sooner in frontal cortex compared with MTL (see legend). (C) Quantitative analysis: mean position in propagation sequences as a function of brain region. Abbreviations: SM, supplementary motor area; PC, posterior cingulate; OF, orbitofrontal cortex; AC, anterior cingulate; ST, superior temporal gyrus; EC, entorhinal cortex; Am, amygdala; HC, hippocampus; PH, parahippocampal gyrus. (D) An example of individual slow waves propagating from frontal cortex to MTL. Rows (top to bottom) depict activity in scalp EEG (Cz, red), supplementary motor area (SM), entorhinal cortex (EC), hippocampus (HC), and amygdala (Am). Colors denote the following: blue, depth EEG; green, MUA; and black lines, spikes of isolated units. Red dots mark center of OFF periods in each brain region based on the middle of silent intervals as defined by last and first spikes across the local population. Diagonal green lines are fitted to OFF period times via linear regression and illustrate propagation trend. (E) Left: The average unit activity in frontal cortex (top, n = 76) and MTL (bottom, n = 155), triggered by the same scalp slow waves reveals a robust time delay (illustrated by vertical red arrow). Right: Distribution of time delays in individual frontal (top) and MTL (bottom) units reveals a time delay of 187 ms. Red vertical arrows denote mean time offset relative to scalp EEG. (F) Left: The average unit activity in parahippocampal gyrus (PH, n = 32), entorhinal cortex (EC, n = 49) and hippocampus (HC, n = 35), triggered by the same depth EEG slow waves reveals a cortico-hippocampal gradient of slow wave occurrence (illustrated by vertical red arrows). Right: Distribution of time delays in individual PH, EC, and HC units reveals a time delay of 121 ms between PH and HC. Red vertical arrows denote mean time offset relative to depth EEG.
Figure 8. Afferent Information Predicts Occurrence and…
Figure 8. Afferent Information Predicts Occurrence and Timing of Activity Onsets in Individual Slow Waves
Figure 8. Afferent Information Predicts Occurrence and Timing of Activity Onsets in Individual Slow Waves (A) Predicting occurrence of individual amygdala slow waves with information about slow waves in other limbic regions. Each subpanel shows prediction accuracies for one patient using either ipsilateral (red) or contralateral (blue) information, as a function of the number of regions made available to the classifier. Green horizontal line shows chance prediction at 50%. Error bars denote SEM across 100 classifier iterations in which training and testing datasets (individual waves) as well as the identity of available neighbors were shuffled. Black and gray asterisks denote significant differences in prediction accuracy (p−39 in all nine individuals, paired t test, n = 100 classifier iterations). (B) Same as above when predicting the timing of individual amygdala slow waves (before or after slow waves in parietal scalp electrode Pz). Timing prediction was likewise more accurate based on ipsilateral information (p −7 in eight individuals and p = 0.02 in ninth individual, paired t test, n = 100 classifier iterations).