P 169. Is cortical excitability affected by sleep fragmentation?

Abstract

Introduction Sleep plays a critical role in modulating learning processes. Sleep loss and sleep disorders are crucial for sleep dependent plasticity. Sleep fragmentation (SF) is interruption of sleep continuity with frequent and transient arousals. SF and sleep deprivation (SD) are very similar in clinical manifestation, both are associated with increased sleepiness the following day, with impairment of daytime cognitive functions. Transcranial magnetic stimulation (TMS) studies showed that SD may alter neuronal excitability and synaptic communication in neuronal network implicated in cognition, learning, and brain plasticity. Alterations in movement-related cortical plasticity had been demonstrated; also, in Restless legs Syndrome (RLS), clinically characterized by markedly fragmented sleep. Objective By the means of TMS, we evaluated effect of SF on cortical excitability. Material and methods In basal condition (BC), after a full night of spontaneous sleep, and again in fragmented condition (FC), after a fragmented night of sleep, MEP amplitude, motor threshold (MT), silent period (SP), and intracortical inhibition were assessed in healthy subjects. In both conditions each subject performed, also, a bimanual motor task (regular repetitive opening-closing bilateral movements of the index finger onto the thumb). MEPs of the first dorsal interosseus were recorded before exercise (baseline), immediately after each exercise periods of 30, 60, 90 s, and after 15 min of rest. MEP amplitude elicited immediately after each exercise, and then after rest was compared with baseline, to evaluate the presence of post-exercise facilitation and delayed facilitation. Before each experimental session, subjects were asked to report their alertness level (Stanford Sleepiness Scale-SSS). Results MT and SSS were significantly increased in SF. Instead, no significant differences for MEP amplitude or SP or intracortical inhibition were found. In both conditions MEP amplitude was significantly larger than baseline immediately after 30-s and 60-s time periods, indicating the presence of post-exercise facilitation and then again after rest showing delayed facilitation. Comparing the two conditions at each time point we found no significant differences in MEP amplitude. Conclusion SF produces significant disruption of nocturnal sleep, reduces daytime alertness, and increases sleepiness.In accordance with this, we observed a significant increase of SSS and of MT in FC. On the other side, SF was unable to modify both cortical inhibition and cortical plasticity. These results seem in contrast to TMS alterations observed in SD and RLS. A possible explanation of these apparent contradictions is that maybe SD and SF represent different phenomena that can depend on variously networks acting on motor cortex. SF seems to impair the restorative cognitive benefits of sleep via alterations in hippocampal synaptic plasticity, involving mechanisms different from altered in SD. Previously, in RLS patients we demonstrated alterations in movement related cortical plasticity that we did not found in SF. Although RLS involves also problems of partial SD, it is certainly primarily a problem of SF. We speculate that the contradiction between our SF data and our previous results in RLS may not be associated to SF, but related specifically to RLS pathophysiology.