Hypersynchronous Slow Delta, Cyclic Alternating Pattern and Sleepwalking

CHRONIC SLEEPWALKING IS AN ABNORMAL BEHAVIOR SEEN PREDOMINANTLY IN CHILDREN AND IN YOUNG ADULTS EFFECTING 2.5% OF THE GENERAL population 15 years and older of the United Kingdom.1 Hypersynchronous slow delta (HSD) has been recognized as present in recordings of sleepwalkers since 1965.2 It significance has been questioned as different authors have reported variable times of incidence preceding sleepwalking events. It was Zucconi et al3 who associated the presence of bursts of delta waves not only in sleepwalking but several parasomnias, including bruxism, with cyclic alternating pattern (CAP) analysis. This analysis of sleep EEG is not necessary well recognized or understood: For example, Pressman4 recently looked at delta bursts in different sleep disorders, and published a clear example of a CAP cycle and never mentioned the term or the possible need to analyze sleep using the CAP atlas when such bursts are seen. Pillon et al. in this issue5 have performed a further-analysis of EEG data obtained from sleepwalkers at baseline and after sleep deprivation. They looked at bursts of high amplitude slow delta (> 150μV HSW) during NREM sleep. These authors concluded that HSD shows a clear fronto-central gradient across all subjects, that is made more evident following sleep deprivation. This is not too surprising considering prior publications on delta wave generation. But this is of interest considering the findings of Ferri et al6 on generation of delta bursts seen with CAP. Pillon et al5 bring up the issue of the relationship of their findings with those observed with CAP scoring, indicating that “HSD events may be viewed by some in relation to the CAP which expresses the organized complexity of arousal-related phasic events in NREM sleep. Specifically, one CAP subtype (A1) could overlap with HSD, as it is characterized by synchronized EEG patterns (e.g., delta bursts), by low delta power and a frontal predominance.” They refer to Ferri et al6 but dismiss the possibility that they essentially scored CAP. There is, however, much evidence today to refute this assertion and to indicate that they were indeed measuring CAP A1 events in sleepwalkers. Some of the rationales these authors used to dismiss the case for CAP are results of studies performed on normals rather than those with pathological sleep as in their own study; and normal and pathological sleep, as seen in sleepwalking, cannot be compared. Also Ferri et al7 using a 19 scalp site EEG recording demonstrated a centro-frontal gradient in CAP as reported in the investigation of HSD. Further analysis using the low resolution brain electromagnetic tomography functional imaging to investigate the source analysis of the frequency components of phase CAP-A, indicates that the generator seems to be localized mostly over the frontal midline cortex for A1 and for the low frequency elements of A2 subtypes. It is difficult to determine where the EEG delta wave generator is located even with sophisticated techniques and more work will be needed combining EEG recording during sleep with imaging studies to confirm it, but the current available data are concordant and the findings of Pillon et al5 are in the same direction independently of the name given to the bursts of delta waves. The lack of recognition that bursts of HSD are part of an abnormal CAP rate has consequences: Similar to Pressman,4 Pillon et al5 deny any informative value to these bursts of HSD, and we disagree on this point. Bursts of HSD during NREM sleep can be a normal phenomenon. As has been well described by Terzano et al,8,9 there is normally during sleep, passage from unstable to stable sleep, associated with progressive recruitment of controlling neurons in the thalamus-forebrain region and development of hypersynchronization of firing that will lead to the appearance of delta waves in the scalp EEG. But these EEG delta bursts are a transient element and normally there is occurrence of a continuous slow frequency (and high amplitude in younger subjects) EEG pattern. Here we see that a bursting pattern is persisting even during stage 3 and 4 NREM sleep as well described with abnormal persistence of CAP. What is abnormal is not the burst of HSD, but the reappearance of the background activity that interrupts the persistence of the slow delta (and this feature is missed in the analysis reported by Pillon et al5). Instead of denying value to these bursts,4,5 one should determine if they are in the range expected for age and gender matched controls, and if they are not, to find out what is interrupting the normal progression of NREM sleep in the studied cycle. Robert et al10 have used such an approach to affirm that they had reached an appropriate nasal CPAP pressure in their sleep apnea patients after eliminating apnea and hypopnea: the EEG patterns used in their approached is based on the disappearance of bursts of delta waves (i.e. CAP). Our study in adults sleepwalkers shows a prominence of CAP during the first 2 sleep cycles and an important decrease during the last cycles.11 Interestingly the Montreal group and ourselves12,13 have shown that despite presence of these bursts of HSD, there is an overall decrease in delta power during the first 2 NREM-REM cycles in chronic sleepwalkers, the difference between Gaudreau et al12 and our13 findings was that we did not reach the same level as normal controls in the last sleep cycle compared to their findHypersynchronous Slow Delta, Cyclic Alternating Pattern and Sleepwalking