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Distribution, Amplitude, Incidence, Co-Occurrence, and Propagation of Human K-Complexes in Focal Transcortical Recordings(1,2,3).

Mak-McCully RA, Rosen BQ, Rolland M, Régis J, Bartolomei F, Rey M, Chauvel P, Cash SS, Halgren E - eNeuro (2015)

Bottom Line: KCs were marked manually on each channel, and local generation was confirmed with decreased gamma power.Locally generated KCs were found in all sampled areas, including cingulate, ventral temporal, and occipital cortices.These results open a novel view where KCs overall are universal cortical phenomena, but each KC may variably involve small or large cortical regions and spread in variable directions, allowing flexible and heterogeneous contributions to sleep homeostasis and memory consolidation.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Neurosciences, University of California, San Diego , San Diego, California 92093.

ABSTRACT
K-complexes (KCs) are thought to play a key role in sleep homeostasis and memory consolidation; however, their generation and propagation remain unclear. The commonly held view from scalp EEG findings is that KCs are primarily generated in medial frontal cortex and propagate parietally, whereas an electrocorticography (ECOG) study suggested dorsolateral prefrontal generators and an absence of KCs in many areas. In order to resolve these differing views, we used unambiguously focal bipolar depth electrode recordings in patients with intractable epilepsy to investigate spatiotemporal relationships of human KCs. KCs were marked manually on each channel, and local generation was confirmed with decreased gamma power. In most cases (76%), KCs occurred in a single location, and rarely (1%) in all locations. However, if automatically detected KC-like phenomena were included, only 15% occurred in a single location, and 27% occurred in all recorded locations. Locally generated KCs were found in all sampled areas, including cingulate, ventral temporal, and occipital cortices. Surprisingly, KCs were smallest and occurred least frequently in anterior prefrontal channels. When KCs occur on two channels, their peak order is consistent in only 13% of cases, usually from prefrontal to lateral temporal. Overall, the anterior-posterior separation of electrode pairs explained only 2% of the variance in their latencies. KCs in stages 2 and 3 had similar characteristics. These results open a novel view where KCs overall are universal cortical phenomena, but each KC may variably involve small or large cortical regions and spread in variable directions, allowing flexible and heterogeneous contributions to sleep homeostasis and memory consolidation.

No MeSH data available.


Related in: MedlinePlus

Example KC localizations, waveforms, and down state confirmations. KCs are plotted from representative sites across the cortical areas sampled. Individual KCs for each bipolar location are plotted in black with the average KC overlaid in red. The number of individual KCs plotted is listed above the waveforms. Below the KC waveforms, time frequency plots from 5 to 120 Hz with a −1.5 to −0.5 s baseline relative to the most negative peak of the KC at time zero indicate a significant drop (p < 0.01, uncorrected) in high gamma power at the time of the KC. Arrows indicate the bipolar locations where the plotted waveforms and time–frequency plots were recorded. Circles indicate the subject color-coded bipolar channel locations, as in Figure 1. The four additional red squares indicate sites where KCs were located, but not included for additional analysis because they were part of an epileptic region or potentially in entorhinal cortex.
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Figure 2: Example KC localizations, waveforms, and down state confirmations. KCs are plotted from representative sites across the cortical areas sampled. Individual KCs for each bipolar location are plotted in black with the average KC overlaid in red. The number of individual KCs plotted is listed above the waveforms. Below the KC waveforms, time frequency plots from 5 to 120 Hz with a −1.5 to −0.5 s baseline relative to the most negative peak of the KC at time zero indicate a significant drop (p < 0.01, uncorrected) in high gamma power at the time of the KC. Arrows indicate the bipolar locations where the plotted waveforms and time–frequency plots were recorded. Circles indicate the subject color-coded bipolar channel locations, as in Figure 1. The four additional red squares indicate sites where KCs were located, but not included for additional analysis because they were part of an epileptic region or potentially in entorhinal cortex.

Mentions: KCs were manually marked, independently on each bipolar channel. A total of 13,821 KCs were manually marked over all channels for all subjects. For each channel, KCs were verified as down states by a significant drop in high gamma power at the time of the KC (Fig. 2). Locally generated KCs were demonstrated in all sampled regions, including subcallosal, orbital, cingulate (anterior and posterior), frontal (superior, middle and inferior, pars opercularis, triangularis, and orbitalis), supramarginal, angular, annectant, temporal (inferior and middle) gyri, the insula and frontal operculum, and the central and anterior occipital sulci (Fig. 2).


Distribution, Amplitude, Incidence, Co-Occurrence, and Propagation of Human K-Complexes in Focal Transcortical Recordings(1,2,3).

Mak-McCully RA, Rosen BQ, Rolland M, Régis J, Bartolomei F, Rey M, Chauvel P, Cash SS, Halgren E - eNeuro (2015)

Example KC localizations, waveforms, and down state confirmations. KCs are plotted from representative sites across the cortical areas sampled. Individual KCs for each bipolar location are plotted in black with the average KC overlaid in red. The number of individual KCs plotted is listed above the waveforms. Below the KC waveforms, time frequency plots from 5 to 120 Hz with a −1.5 to −0.5 s baseline relative to the most negative peak of the KC at time zero indicate a significant drop (p < 0.01, uncorrected) in high gamma power at the time of the KC. Arrows indicate the bipolar locations where the plotted waveforms and time–frequency plots were recorded. Circles indicate the subject color-coded bipolar channel locations, as in Figure 1. The four additional red squares indicate sites where KCs were located, but not included for additional analysis because they were part of an epileptic region or potentially in entorhinal cortex.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4596022&req=5

Figure 2: Example KC localizations, waveforms, and down state confirmations. KCs are plotted from representative sites across the cortical areas sampled. Individual KCs for each bipolar location are plotted in black with the average KC overlaid in red. The number of individual KCs plotted is listed above the waveforms. Below the KC waveforms, time frequency plots from 5 to 120 Hz with a −1.5 to −0.5 s baseline relative to the most negative peak of the KC at time zero indicate a significant drop (p < 0.01, uncorrected) in high gamma power at the time of the KC. Arrows indicate the bipolar locations where the plotted waveforms and time–frequency plots were recorded. Circles indicate the subject color-coded bipolar channel locations, as in Figure 1. The four additional red squares indicate sites where KCs were located, but not included for additional analysis because they were part of an epileptic region or potentially in entorhinal cortex.
Mentions: KCs were manually marked, independently on each bipolar channel. A total of 13,821 KCs were manually marked over all channels for all subjects. For each channel, KCs were verified as down states by a significant drop in high gamma power at the time of the KC (Fig. 2). Locally generated KCs were demonstrated in all sampled regions, including subcallosal, orbital, cingulate (anterior and posterior), frontal (superior, middle and inferior, pars opercularis, triangularis, and orbitalis), supramarginal, angular, annectant, temporal (inferior and middle) gyri, the insula and frontal operculum, and the central and anterior occipital sulci (Fig. 2).

Bottom Line: KCs were marked manually on each channel, and local generation was confirmed with decreased gamma power.Locally generated KCs were found in all sampled areas, including cingulate, ventral temporal, and occipital cortices.These results open a novel view where KCs overall are universal cortical phenomena, but each KC may variably involve small or large cortical regions and spread in variable directions, allowing flexible and heterogeneous contributions to sleep homeostasis and memory consolidation.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Neurosciences, University of California, San Diego , San Diego, California 92093.

ABSTRACT
K-complexes (KCs) are thought to play a key role in sleep homeostasis and memory consolidation; however, their generation and propagation remain unclear. The commonly held view from scalp EEG findings is that KCs are primarily generated in medial frontal cortex and propagate parietally, whereas an electrocorticography (ECOG) study suggested dorsolateral prefrontal generators and an absence of KCs in many areas. In order to resolve these differing views, we used unambiguously focal bipolar depth electrode recordings in patients with intractable epilepsy to investigate spatiotemporal relationships of human KCs. KCs were marked manually on each channel, and local generation was confirmed with decreased gamma power. In most cases (76%), KCs occurred in a single location, and rarely (1%) in all locations. However, if automatically detected KC-like phenomena were included, only 15% occurred in a single location, and 27% occurred in all recorded locations. Locally generated KCs were found in all sampled areas, including cingulate, ventral temporal, and occipital cortices. Surprisingly, KCs were smallest and occurred least frequently in anterior prefrontal channels. When KCs occur on two channels, their peak order is consistent in only 13% of cases, usually from prefrontal to lateral temporal. Overall, the anterior-posterior separation of electrode pairs explained only 2% of the variance in their latencies. KCs in stages 2 and 3 had similar characteristics. These results open a novel view where KCs overall are universal cortical phenomena, but each KC may variably involve small or large cortical regions and spread in variable directions, allowing flexible and heterogeneous contributions to sleep homeostasis and memory consolidation.

No MeSH data available.


Related in: MedlinePlus