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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

Bipolar SEEG contacts. A, Bipolar SEEG contacts, color coded by subject, are marked by circles on the medial (left) and lateral (right) surfaces of the brain. Bipolar SEEG contacts are grouped into 1 of 10 anatomical groups, as demarcated by black circles and/or one of the following labels: ac (anterior cingulate and subcallosal); af (anterior prefrontal cortex); pc (posterior cingulate); pf (posterior prefrontal cortex); cs (central sulcus); in (insula); f3op (inferior frontal gyrus; pars opercularis); of (orbitofrontal cortex); tp (temporo-parieto-occipital junction); vt (ventrolateral temporal cortex). B, Example SEEG electrodes for subject 1 (green) and subject 4 (purple) are superimposed on the subjects’ MRIs. The arrows indicate the location of the bipolar contact pair chosen on each electrode. From the MRI, it is possible to see that the two contacts in each pair are spanning the local cortical mantle.
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Figure 1: Bipolar SEEG contacts. A, Bipolar SEEG contacts, color coded by subject, are marked by circles on the medial (left) and lateral (right) surfaces of the brain. Bipolar SEEG contacts are grouped into 1 of 10 anatomical groups, as demarcated by black circles and/or one of the following labels: ac (anterior cingulate and subcallosal); af (anterior prefrontal cortex); pc (posterior cingulate); pf (posterior prefrontal cortex); cs (central sulcus); in (insula); f3op (inferior frontal gyrus; pars opercularis); of (orbitofrontal cortex); tp (temporo-parieto-occipital junction); vt (ventrolateral temporal cortex). B, Example SEEG electrodes for subject 1 (green) and subject 4 (purple) are superimposed on the subjects’ MRIs. The arrows indicate the location of the bipolar contact pair chosen on each electrode. From the MRI, it is possible to see that the two contacts in each pair are spanning the local cortical mantle.

Mentions: To study how KC amplitude and KC occurrence rate may vary across the cortex, bipolar channels were grouped by anatomical locations into 10 groups (Fig. 1). To test KC amplitude, a linear mixed-effects model (Pinheiro et al.,2015) was performed. Location was used as a fixed effect. Placement of electrodes for each patient was chosen to localize the patient’s epilepsy, but electrodes included in this analysis were not shown to be part of each patient’s seizure focus. Therefore, patient and location were considered independent. Interpatient variability was adjusted for by using patient as a random effect. Channel variability due to electrode placement with respect to the surrounding cortex, as well as variable contact spacing, was taken into account by using channel as a random nested effect.


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)

Bipolar SEEG contacts. A, Bipolar SEEG contacts, color coded by subject, are marked by circles on the medial (left) and lateral (right) surfaces of the brain. Bipolar SEEG contacts are grouped into 1 of 10 anatomical groups, as demarcated by black circles and/or one of the following labels: ac (anterior cingulate and subcallosal); af (anterior prefrontal cortex); pc (posterior cingulate); pf (posterior prefrontal cortex); cs (central sulcus); in (insula); f3op (inferior frontal gyrus; pars opercularis); of (orbitofrontal cortex); tp (temporo-parieto-occipital junction); vt (ventrolateral temporal cortex). B, Example SEEG electrodes for subject 1 (green) and subject 4 (purple) are superimposed on the subjects’ MRIs. The arrows indicate the location of the bipolar contact pair chosen on each electrode. From the MRI, it is possible to see that the two contacts in each pair are spanning the local cortical mantle.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 1: Bipolar SEEG contacts. A, Bipolar SEEG contacts, color coded by subject, are marked by circles on the medial (left) and lateral (right) surfaces of the brain. Bipolar SEEG contacts are grouped into 1 of 10 anatomical groups, as demarcated by black circles and/or one of the following labels: ac (anterior cingulate and subcallosal); af (anterior prefrontal cortex); pc (posterior cingulate); pf (posterior prefrontal cortex); cs (central sulcus); in (insula); f3op (inferior frontal gyrus; pars opercularis); of (orbitofrontal cortex); tp (temporo-parieto-occipital junction); vt (ventrolateral temporal cortex). B, Example SEEG electrodes for subject 1 (green) and subject 4 (purple) are superimposed on the subjects’ MRIs. The arrows indicate the location of the bipolar contact pair chosen on each electrode. From the MRI, it is possible to see that the two contacts in each pair are spanning the local cortical mantle.
Mentions: To study how KC amplitude and KC occurrence rate may vary across the cortex, bipolar channels were grouped by anatomical locations into 10 groups (Fig. 1). To test KC amplitude, a linear mixed-effects model (Pinheiro et al.,2015) was performed. Location was used as a fixed effect. Placement of electrodes for each patient was chosen to localize the patient’s epilepsy, but electrodes included in this analysis were not shown to be part of each patient’s seizure focus. Therefore, patient and location were considered independent. Interpatient variability was adjusted for by using patient as a random effect. Channel variability due to electrode placement with respect to the surrounding cortex, as well as variable contact spacing, was taken into account by using channel as a random nested effect.

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