P300 in sleep state misperception

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1 P300 in sleep state misperception R. J. SCHIMSHEIMER, M.M.R. VERHELST, D. ZEEMAN CENTRE FOR SLEEP AND WAKE DISORDERS, MCH, WESTEINDE HOSPITAL, THE HAGUE Sleep State Misperception is a disorder in which a complaint of insomnia occurs without objective evidence of sleep disturbance. Excessive mentation during sleep has been suggested as a possible explanation for this disorder. A higher mentation during sleep in Sleep State Misperception indicates that there might be a difference in information processing during sleep in these patients. Event related potentials; especially the P300 can be used to study information processing during wake and sleep (1). It may be postulated that P300 amplitude and latency during wake and sleep behave different in patients with Sleep State Misperception. However, in sleep other event related potentials could appear for example SII-P3 that cannot easily be discerned from P300 (1). Therefore we studied the P300 in 3 patients with Sleep State Misperception and 10 controls in 3 conditions: a during wakefulness, at 22:00 hours - W condition b during a forced awakening from the first period of Slow Wave Sleep SWS condition c during a forced awakening from the first period of REM sleep REM condition Methods A simple auditory oddball paradigm was used with 20% rare high tones (40 db 2 khz) and with 80% normal low tones (40 db 1 khz). The stimulus frequency was 0,5 Hz. Patients had to press a button when they heard the rare target tones. During wakefulness two trials of 200 stimuli were offered in one trial by a standard headphone. Rare tones were at random mixed with the frequent tones. After the forced awakenings only 200 stimuli were offered in one trial in order to prevent the patient from falling asleep. Signals were derived from Fz, Cz and Pz with linked ears as reference electrode. Signals were averaged with a band pass of Hz and with an analysis time of 1 s. The EOG was monitored with two electrodes, one supra orbital and one on the outer canthus both of the left eye. Signals contaminated with eye movements were automatically rejected. 143

2 Subjects The control group consisted of 10 healthy persons, 5 males and 5 females, age range years, who had no sleep problems. The patient group consisted of 3 persons, in the age of 16, 36 and 39, who suffered from total Sleep State Misperception (they reported no sleep at all in their sleepdiary in contrast with their normal 2x24 hours polysomnography). Results The results of the latency and amplitude measurements are given in the following tables. Standard deviations were not calculated for the patient group due to the small number of patients. Derived from Fz P300 latency controls 301 ± 34 ms 312 ± 44 ms 320 ± 38 ms P300 latency patients 324 ms 337 ms 367 ms P300 amplitude controls 17 ± 9 µv 15 ± 5 µv 11 ± 6 µv P300 amplitude patients 8 µv 8 µv 4 µv Derived from Cz P300 latency controls 301 ± 36 ms 310 ± 40 ms 322 ± 39 ms P300 latency patients 319 ms 337 ms 379 ms P300 amplitude controls 21 ± 9 µv 16 ± 4 µv 14 ± 6 µv P300 amplitude patients 10 µv 11 µv 3 µv Derived from Pz P300 latency controls 305 ± 38 ms 311 ± 36 ms 325 ± 45 ms P300 latency patients 315 ms 341 ms 379 ms P300 amplitude controls 17 ± 9 µv 15 ± 4 µv 13 ± 6 µv P300 amplitude patients 13 µv 12 µv 8 µv 144

3 Conclusion Although the lower amplitudes and longer latencies in patients compared to controls suggest lower vigilance, the tendency to lower amplitudes in the SWS condition in controls was not seen in patients. This probably indicates higher vigilance/mentation in the patients during the SWS condition. In REM condition this phenomenon did not occur. Although 3 patients are too few to draw definite conclusions, the results suggest that excessive mentation during Slow Wave Sleep may be responsible for Sleep State misperception. 1) H. Bastuji, L. Garcia Larrea. What do studies on P300 tell us about information processing during sleep? J Sleep Res 1998,7; supp. 2: p

4 146

5 The effect of treatment with melatonin for chronic sleep onset insomnia in children with attention deficit hyperactivity disorder: randomized placebo-controlled trial M.G. SMITS*, E.J. NAGTEGAAL**, G.A. KERKHOF***, S. VALENTIJN****, A.L.M. COENEN**** HOSPITAL DE GELDERSE VALLEI, EDE: DEPARTMENT OF NEUROLOGY AND SLEEP- WAKE DISORDERS*, DEPARTMENT OF HOSPITAL PHARMACY RIJNSTAETE HOSPITAL ARNHEM, UNIVERSITY OF LEIDEN, DEPARTMENT OF PHYSIOLOGY***, UNIVERSITY OF NIJMEGEN, NICI****. THE NETHERLANDS. Introduction Generally chronic sleep onset insomnia in children with attention deficit hyperactivity disorder (ADHD) does not respond well to pharmacological and nonpharmacological treatments (1). Melatonin advances sleep onset in adults with chronic sleep onset insomnia and delayed onset of endogenous melatonin (2). Children with delayed sleep onset and bedtime resistance, may also wake up later (3). This suggests that their sleep-wake rhythm is delayed. Early school times or early wake-up times of family members can prevent delayed wake up time. In ADHD children this lack of difficulty to arise in the morning probably is associated with the hyperarousal conditions of this disorder (4). Consequently a delayed sleep-wake rhythm can easily be masked. Endogenous melatonin, a hormone produced by the pineal gland during the dark phase of the day-night cycle, plays a major role in the synchronisation of circadian rhythms (5). As early as the second half of the first year of life melatonin is involved in the evolution of the sleep-wake system (6). The circadian rhythm of melatonin is highly reproducible and generally not easily altered (7). The endogenous 24-h. melatonin profile is a reliable marker for circadian phase position. The time at which melatonin starts to rise in dim light, the Dim Light Melatonin Onset (DLMO), is shown to be particularly convenient, to assess circadian phase position, as it can usually be obtained before sleep (8). In adults with chronic sleep onset insomnia and a delayed sleep-wake rhythm, exogenous administered melatonin, 5 mg, advances both sleep onset and DLMO (9). 147

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