第848回 千葉医学会例会・第7回 磯野外科例会 60.

<p>Shown are membrane voltages of the cortical pyramidal (top) and the thalamic relay population (bottom). During N3 the model shows ongoing slow oscillatory activity. In contrast to sleep stage N2, SOs cannot be identified as isolated events. Furthermore, there are no isolated spindle oscillations and spindle activity is time-locked to SOs. Parameters are given in <a href="http://www.ploscompbiol.org/article/info:doi/10.1371/journal.pcbi.1005022#pcbi.1005022.t002" target="_blank">Table 2</a>.</p

Changes in EEG spectral power induced by theta-tDCS during REM sleep.

<p>Spectral power for theta-tDCS (black lines) and sham stimulation (gray lines) averaged across all EEG locations (A) and for submental electromyographic (EMG) activity (B). Time course of gamma band activity during the five 1-min stimulation-free periods immediately succeeding the stimulation intervals (S1–S5), averaged across all electrode sites for theta-tDCS (black bars) and sham stimulation (empty bars) (C). ‘Ba’ refers to baseline activity prior to stimulation. **, P<0.01; *, P<0.05; for comparisons between the theta-tDCS and sham stimulation conditions by t-test (n = 16).</p

Sleep during the whole night.

<p>Sleep stage scoring for both NonREM sleep and REM sleep experiments is based on 30-s epochs and mean ± SEM time in the different sleep stages is given as percentage of total sleep time (TST). SO, Sleep onset; SWS, Slow wave sleep. Latency (in min) of sleep onset is calculated with reference to lights off (23.00 h); latencies to SWS and REM sleep are calculated with reference to sleep onset.</p><p>*P<0.05 for longer SWS latency in the theta-tDCS than sham condition.</p

Topographical distribution and temporal pattern of EEG spectral power during NonREM sleep.

<p>(A and C) Topographical distribution of EEG power (± SEM) averaged across the 1-min stimulation-free intervals in the slow oscillation (0.4–1.2 Hz) (A), and slow spindle (8–12 Hz) frequency bands (C) after the five 5-min intervals of theta-tDCS or sham stimulation. (B and D) Time course of EEG spectral power for the five 1-min stimulation-free periods (S1–S5) immediately succeeding stimulation and for 0–30 and 30–60 min after termination of stimulation in the slow oscillation band (B), and slow spindle frequency band at Fz (D). ‘Ba’ refers to baseline activity prior to stimulation. **, P<0.01; *, P<0.05; for comparisons between the theta-tDCS and sham stimulation conditions by t-test (n = 25).</p

Sleep during the five 1-min stimulation-free and the 60 min periods following theta-tDCS during NonREM sleep.

<p>Sleep stage scoring for the five 1-minute stimulation-free periods is based on 10-s with mean ± SEM time in the different sleep stages given in seconds. Sleep stage scoring for the 60 minutes following theta-tDCS is based on 30-s epochs with mean ± SEM time in the different sleep stages given as percentage of 30 min. S1–S4, sleep stages 1–4; SWS, Slow wave sleep; REMS, rapid eye movement sleep.</p>1<p>P<0.001;</p>2<p>P<0.01, for pairwise comparisons between the effects of theta-tDCS and sham stimulation.</p

Time line of the two experiments.

<p>(A) Theta-tDCS during NonREM sleep (NonREM Experiment) and (B) during REM sleep (REM Experiment). Respective upper panels show representative individual sleep profiles (W: wake, REM: REM sleep, S1–S4: NonREM sleep stages 1–4) and periods of stimulation. Lower parts indicate Learning and Retrieval periods for memory testing on declarative and procedural tasks. The horizontal gray bar indicates lights out.</p

Additional file 2: Figure S1. of Predictors of remission with etanercept-methotrexate induction therapy and loss of remission with etanercept maintenance, reduction, or withdrawal in moderately active rheumatoid arthritis: results of the PRESERVE trial

Summary of patient disposition in the open-label and double-blind periods. CDAI Clinical Disease Activity Index, DAS28 Disease Activity Score based on a 28-joint count, ETN etanercept, LDA low disease activity, MTX methotrexate, QW once weekly, SDAI Simplified Disease Activity Index. (EPS 1688 kb

Performance at learning and retention.

<p>Mean ± SEM values are given for performance at learning and retention performance on the declarative word paired-associate task and the two procedural tasks, i.e., finger sequence tapping and mirror tracing. Retention is defined by the difference in performance at retrieval testing (morning after sleep) minus performance at immediate recall at learning (evening before sleep). No significant differences between the theta-tDCS and sham conditions were found for performance at learning.</p><p>**P<0.01 for retention with sham vs. theta-tDCS.</p

Performance on psychometric and cognitive control tests.

<p>Mean ± SEM values for the assessment of mood (by the PANAS), retrieval ability from long-term memory (by the Word fluency test) and working memory (by the Digit Span test in the NonREM Experiment and the REM Experiment. All assessments were conducted at retrieval testing (in the morning after sleep). The PANAS was given additionally at learning (in the evening before sleep).</p><p>*P<0.05 for pairwise comparisons between the effects of theta-tDCS and sham stimulation.</p>†<p>P<0.05 for the interaction Stimulation×Time (learning, retrieval).</p

Transcranial Electrical Stimulation Accelerates Human Sleep Homeostasis

<div><p>The sleeping brain exhibits characteristic slow-wave activity which decays over the course of the night. This decay is thought to result from homeostatic synaptic downscaling. Transcranial electrical stimulation can entrain slow-wave oscillations (SWO) in the human electro-encephalogram (EEG). A computational model of the underlying mechanism predicts that firing rates are predominantly increased during stimulation. Assuming that synaptic homeostasis is driven by average firing rates, we expected an acceleration of synaptic downscaling <em>during</em> stimulation, which is compensated by a reduced drive <em>after</em> stimulation. We show that 25 minutes of transcranial electrical stimulation, as predicted, reduced the decay of SWO in the remainder of the night. Anatomically accurate simulations of the field intensities on human cortex precisely matched the effect size in different EEG electrodes. Together these results suggest a mechanistic link between electrical stimulation and accelerated synaptic homeostasis in human sleep.</p> </div