Cyclic Alternating Pattern in congenital deaf – quantitative and topographic analysis

Abstract

Introduction Sleep is a reversible behavioral state with attenuation of sensorial modalities and relative preservation of auditory function. Cyclic Alternating Pattern (CAP) is related to sleep instability and arousal. It is formed by CAP (phases A (A1, A2, A3) + B) and NCAP cycles. A1 subtype indicates maintenance of NREM sleep neuronal mechanisms; A2 and A3 are related to sleep instability and onset REM mechanisms. Congenital deaf sleep is a good model of sustained auditory deprivation and an important tool in the study of noise effect in sleep. In this study we aim to 1. Evaluate if the absence of acoustic perturbation in deaf promotes sleep stability; and 2. Evaluate the effect of provoked arousals in congenital deaf and normal-hearing subjects sleep. Materials and methods Eight congenital deaf and eight normal-hearing volunteers were matched according to age and gender. Video-polisonography were made on two consecutive nights, in lab environment, and provoked arousals after every 5 min of stable REM were performed. CAP Rate, Duration, Time Distribution and Topographic Mapping of the frequency bands 0.2–2.5 Hz (FB 1) and 7–12 Hz (FB2) were measured to accomplish aim 1; for aim 2 CAP density (no. events/ sleep time) were obtained for the periods before (PB) and after provoked arousals (AA – 30 min period after the arousal). SPSS 16.0 was used for statistical analysis purposes using p Results Contrary to the expectations, the sleep of the congenital deaf is more unstable as it presents increased A3 rate (p = 0.017) and time variations (p = 0.045) as well as evidence of decreased A1 rate and duration. The deaf subjects have compromised CAP rhythmicity: CAP cycle (p = 0,133) and A1 subtype (p = 0,138) do not vary along the night and there is no clear repetitive and cyclical A2 and A3 pattern in association with REM-on mechanisms. These subjects presented higher spectral power in parieto-occipital regions for A1 (p = 0.049 – BF1) and temporal posterior for A2 (p = 0.015 – FB 1) and B (p = 0.049 – FB 1 e p = 0.033 – FB 2) possibly as a result of cerebral modifications due to deafness. Deaf subjects seem more sensitive to provoked sleep interruption with remarkable decrease of A1 (p = 0/015) in AA periods. Conclusion Deaf subjects have more unstable sleep and higher sensitivity to provoked sleep interruption; compromised CAP rhythmicity as well as cortical and spectral modifications in posterior regions, possibly related to their clinical condition. Acknowledgements Funded by: Fundacao BIAL (No. 107/02 ). Work supported by Helder Bertolo, Joana Pires and Rosa Santos.