First night effect in children and adolescents undergoing polysomnography for sleep-disordered breathing

Clinical Neurophysiology 114 (2003) 2138–2145 www.elsevier.com/locate/clinph

First night effect in children and adolescents undergoing polysomnography for sleep-disordered breathing S. Schollea,*, H.-Ch. Scholleb, A. Kempera, S. Glasera, B. Riegera, G. Kempera, G. Zwackaa a

Centre of Sleep Medicine and Children’s Hospital, Robert-Koch-Hospital Apolda, Jenaer Straße 66, Apolda D-99510, Germany b Institute of Pathophysiology, Friedrich-Schiller-University Jena, D-07740 Jena, Germany Accepted 5 June 2003 Dedicated to Professor Dr Marianne E. Schla¨fke on the occasion of her 65th birthday.

Abstract Objective: To establish whether there is a first night effect (FNE) in children and adolescents with suspected obstructive sleep apnoea undergoing polysomnography (PSG) and whether this affects sleep and breathing, furthermore, to determine the extent to which age may influence the sleep and cardiorespiratory parameters. Methods: One hundred and thirty-one children and adolescents (age classes—A: 2 –6 years n ¼ 37; B: 7 – 12 years n ¼ 60; C: 13 – 17 years n ¼ 34) underwent PSG on 2 consecutive nights (I and II) under identical conditions for suspected sleep-related respiratory disorders. One hundred and five patients including 3 patients with obstructive sleep apnoea syndrome (OSAS) treated by adenotonsillectomy and 18 OSAS patients receiving nCPAP-therapy had no PSG-abnormalities (Group 1—A: n ¼ 28; B: n ¼ 53; C: n ¼ 24). A further 26 patients (Group 2) had clinically and polysomnographically confirmed untreated OSAS (A: n ¼ 9; B: n ¼ 12; C: n ¼ 5). Results: There were no statistically significant differences between children with no PSG-abnormalities (Group 1) and those with OSAS (Group 2) in terms of sleep parameters (arousal indices excluded), oxygen saturation (SaO2) and heart rate (HR), and these parameters have, therefore, been pooled for the entire group (n ¼ 131) in the 3 age classes A, B and C. In the second and third age classes, sleep efficiency on the first night was reduced. In all age classes, there was significantly more wakefulness during the first night. In the second and third age ranges, the proportion of NREM 1 in the first night was significantly higher, with a correspondingly reduced proportion of NREM 4 in the third age group. In all age classes, REM sleep was significantly less during the first night, but REM latency was comparable on both nights. On the first night, the mean HR was higher. There were significant differences in apnoea/hypopnoea-index (AHI), electroencephalogram (EEG)-arousal-index (AI) and motoric arousal index (jerk index, JI) between Groups 1 and 2. In neither group, were there any significant differences in AHI, mean SaO2 or number of EEG-arousals between nights 1 and 2. Only in the age class A, in Group 2 (n ¼ 9) was the number of motoric arousals significantly higher on the first night. Comparison of the age classes A, B, and C revealed that most polysomnographic parameters were age-dependent. Increasing age was found to correlate with a higher proportion of NREM 1, especially on the first night. Also, there was an age-dependent increase in NREM 2 on both nights, a decrease in NREM 3 on the first night, and a decrease in NREM 4 on both nights. In older children, we also found a lower proportion of REM sleep on the first night and a lower HR on both nights. In Group 1, we found a lowered AHI, AI and JI (for JI significant only on the first night) in older patients. No such age dependence of AHI, AI and JI was seen in OSAS patients (Group 2). Conclusions: In children and adolescents, there is an FNE comparable with that described in adults. In OSAS children and also in children with no PSG-abnormalities, there is night-to-night-variability in sleep parameters, but not in respiratory parameters. An adaptation night is, therefore, necessary when sleep architecture is to be studied, but not when only the nocturnal respiratory pattern is investigated. Sleep parameters, HR and arousal indices are all age-dependent. q 2003 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved. Keywords: First night effect; Childhood; Obstructive sleep apnoea syndrome; Sleep structure; Arousal

1. Introduction * Corresponding author. Tel.: þ 49-3644-571711; fax: þ 49-3644571601. E-mail address: [email protected] (S. Scholle).

Sleep studies in children and adolescents are still scant, and there is a lack of uniformity regarding data acquisition

1388-2457/03/$30.00 q 2003 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved. doi:10.1016/S1388-2457(03)00209-8

S. Scholle et al. / Clinical Neurophysiology 114 (2003) 2138–2145

and interpretation. Methodological differences among studies may result in different findings. Although the diagnostic evaluation of a sleep problem on the basis of a single-night polysomnography (PSG) is common (Acebo et al., 1996), doubt is often voiced that the first night is not representative when sleep organization and architecture need to be addressed. The first night effect (FNE) in adults, described by Agnew et al. (1966), is also observable in children in the form of diminished sleep quality, but few data on this effect in children have so far become available (Palm et al., 1989; American Thoracic Society, 1996; Emslie et al., 2001; Katz et al., 2002). In this study, we aimed to identify the parameters (sleep architecture, cardiac parameters, and respiratory parameters) that reflect sleep disturbances caused by the unfamiliar environment of a pediatric sleep laboratory in a first night polysomnographic study. The aim of the study was to show that sleep organization and architecture differ between the first and second nights. The question whether an adaptation night is necessary in polysomnographic studies in children and adolescents remains unanswered, and must also be seen in relation to changes in sleep behavior during development. Since data on the magnitude and nature of the FNE on respiratory patterns in children are limited, we also wished to determine the influence of the first night on respiratory parameters, and establish whether a single overnight PSG suffices to identify the presence and severity of sleep-related respiratory disturbances in this age category. Finally, we aimed to present normative polysomnographic data on sleep, breathing and heart rate (HR) in children and adolescents investigated for suspected sleepdisordered breathing, as a function of age.

2. Methods 2.1. Patient population The patients were referred to our laboratory for evaluation of suspected sleep-disordered breathing, and were examined on two consecutive nights (I and II) under identical conditions. In 105 children (Group 1) (age classes—A: 2 –6 years n ¼ 28; B: 7– 13 years n ¼ 53; C: 14 –17 years n ¼ 24), no PSG-abnormalities were found. This group included 3 post-adenotonsillectomy patients and 18 patients on nCPAP-therapy. No statistical differences were seen between obstructive sleep apnoea syndromepatients (OSAS) after/under treatment and children/ adolescents with no PSG-abnormalities. In addition, we investigated 26 patients (Group 2) with clinically and polysomnographically confirmed untreated obstructive sleep apnoea (A: n ¼ 9; B: n ¼ 12; C: n ¼ 5). Patients with a history of psychiatric or neurologic disorders were excluded.

2139

Written informed consent was obtained from all parents. No sedation or sleep deprivation was applied. 2.2. Polysomnography During nocturnal PSG (sleep period time (SPT) median 8.3 h, quartile range (qur) 1.1 h), the following parameters were recorded: referential electroencephalograms (EEG) F4A1, F3A2, submental surface electromyogram (EMG), referential electrooculograms (‘ROC/A1 and LOC/A2’), surface EMG from the right and left tibialis anterior muscle, electrocardiogram (ECG), HR from ECG (R– R interval triggered), nasal airflow (thermistor), thoracic and abdominal effort (strain gauge), oxygen saturation (SaO2) (pulse oximetry, Oxycon, Sensormedics, interval for calculations: beat to beat), and snoring (microphone). The examinations were conducted in accordance with the guidelines in the ‘Standards and indications for cardiopulmonary sleep studies in children’ (American Thoracic Society, 1996). The Somnostar 4100 PSG system (Sensormedics) was used. Behavior was observed and recorded directly by a technician. 2.3. Analysis of polygraphic recordings The following parameters were analyzed: sleep macrostructure (sleep efficiency (SE), NREM 1– 4, REM, REM latency (RL)) and sleep microstructure (EEG- and motoric arousals/jerks). The computer-aided evaluation (Somnostar 4100, Sensormedics) of all parameters was checked manually (30 s epochs for sleep staging, 2 min epochs for respiratory parameters). Sleep was staged in accordance with Rechtschaffen and Kales (1968) guidelines adapted for age (Scholle and Scha¨ fer, 1999). To exclude interindividual differences, the staging was done by a single person. With regard to EEG-arousals, the definition applied to adult PSG (ASDA, 1992) was modified, with EEG frequency shifts . 1 s being considered (Scholle and Zwacka, 2001). Motoric arousals were scored whenever activation of the tibialis anterior muscle (jerks) occurred together with activation of any other polygraphic parameter, for example, HR or EEG. Sleep efficiency was defined as total sleep time (TST) divided by time in bed (TIB). RL was defined as the period from sleep onset to first REM. The following respiratory parameters were evaluated: obstructive, mixed and central apnoeas and hypopnoeas lasting longer than two breaths (Marcus, 1997) were applied to calculate the apnoea/hypopnoea-index (AHI) per hour of TST. In addition, mean HR and mean SaO2 were calculated. HR and SaO2 artifacts were eliminated manually before HR and SaO2 were analyzed automatically (Somnostar 4100, Sensormedics).

2140

S. Scholle et al. / Clinical Neurophysiology 114 (2003) 2138–2145

2.4. Statistics Descriptive data are presented as the median and quartile range. Differences between children/adolescents with no PSGabnormalities (n ¼ 84), OSAS patients under/after therapy (n ¼ 21) and OSAS patients not receiving treatment (n ¼ 26) were investigated for the different age classes by the Mann and Whitney U-test. The two nights were compared using Wilcoxon’s rank sum test. Differences between the age classes were detected by the Kruskal – Wallis test. A probability value ( p) of less than 0.05 was considered significant. The computer statistical program Statview was used.

3. Results There were no significant differences between children/ adolescents with no PSG-abnormalities and OSAS patients under/after therapy (nCPAP/adenotonsillectomy) and OSAS patients in terms of sleep parameters (excluding arousal indices), SaO2 and HR. Sleep parameters (excluding arousal indices), SaO2 and HR have, therefore, been pooled and representative values (medians, qur, minima and maxima) for the age classes A, B and C presented in Table 1a (n ¼ 131). Significant differences in AHI, EEG-arousal index (AI) and motoric arousal index were found between patients with no PSG-abnormalities (Group 1: n ¼ 105) (Table 2a) and OSAS patients (Group 2: n ¼ 26) (Table 2b). In the age class A (n ¼ 37), in all children (Table 1a) significantly more wakefulness was seen on the first than on the second night (W—I: 3.40% SPT, qur 5.80; II: 1.50% SPT, qur 2.47). Time spent in NREM 1 –4 did not differ significantly between the two nights. There was significantly less REM sleep on the first night (I: 16.0% SPT, qur 10.00; II: 18% SPT, qur 8.00), but the RL was comparable on both nights. On the first night, the mean HR was higher (I: 72.00/min, qur 10.75; II: 72.00/min, qur 12.25). In the age range B (n ¼ 60), significantly more wakefulness was seen on the first than on the second night (W—I: 5.15% SPT, qur 10.10; II: 1.05% SPT, qur 3.20) (Table 1) reflecting a significantly lower sleep efficiency (SE—I: 89.00%, qur 13.50; II: 96.00%, qur 8.00). The percentage of NREM 1 was higher on the first night (NREM 1—I: 7.05% SPT, qur 8.80; II: 5.30% SPT, qur 8.20), and there was significantly less REM sleep (REM—I: 17.00% SPT, qur 5.50; II: 18.50% SPT, qur 7.50), whereas the RL was comparable on both nights. On the first night, the mean HR was higher (I: 65.50/min, qur 14.00; II: 63.50/min, qur 14.00). In the age range C (n ¼ 34), the differences between the two nights reflecting the FNE were similar. First night sleep

efficiency (SE—I: 94.00%, qur 9.00; II: 96.00%, qur 5.00) was lower, the proportion of wakefulness (W—I: 4.85% SPT, qur 7.40, II: 2.40% SPT, qur 3.40) was higher, and NREM 1 longer (NREM 1—I: 9.30% SPT, qur 9.20; II: 6.00% SPT, qur 10.40). Furthermore, on the adaptation night, the NREM 4 was shorter (NREM 4—I: 14.00% SPT, qur 6.30; II: 16.00% SPT, qur 8.00) and the percentage of REM sleep smaller (REM—I: 12.00% SPT, qur 8.10; II: 18.00% SPT, qur 5.00). Comparison of the two nights in Groups 1 and 2 (Table 2a, b), patients revealed no significant differences in AHI, mean SaO2 and number of EEG-arousals. On the first night, the number of motoric arousals was significantly enhanced only in age class A in the group of OSAS patients (n ¼ 9) (I: 14.28/h TST, qur 6.81; II: 12.65/h TST, qur 3.75). As exemplified in Fig. 1, sleep continuity in the first night was usually disturbed. Comparison of the age classes A, B and C showed an age dependence of the sleep and cardiorespiratory parameters (Table 1a, b). With increasing age, a higher proportion of NREM 1 was found, especially on the first night. Also, NREM 2 was increased on both nights, NREM 3 was decreased on the first night and NREM 4 on both nights. A lower proportion of REM sleep was found in older children on the first night. With increasing age, the mean HR decreased. In Group 1, lower AHI values, lower AI and lower motoric arousal indices (significant only on the first night) were found in older patients (Table 2a, c). This age dependence was not found in OSAS patients (Group 2) (Table 2b, c).

4. Discussion In specialized centres, PSG is routinely performed to evaluate children with sleep disturbances, for example sleep-disordered breathing. Individual sleep patterns, development-related changes and technical aspects of sleep recording have a considerable influence on the results of PSG in children. Methodological aspects of sleep evaluation in particular have, however, not yet been adequately defined. Our study presents polysomnographic data obtained from children and adolescents; in comparison with PSG in adults, there are some differences in data collection and evaluation. Rechtschaffen and Kales (1968) recommended the use of central EEG leads for sleep staging. As shown by Kubicki et al. (1982), however, frontal leads have advantages over central leads. The so-called vertex sharp waves characteristic for the end of stage NREM 1 and the beginning of stage NREM 2, represent the only pattern undetectable in frontal leads. Sleep spindles, K complexes and delta waves are adequately recorded in frontal leads. Furthermore, in childhood, arousal patterns are more readily recognizable

S. Scholle et al. / Clinical Neurophysiology 114 (2003) 2138–2145

2141

Table 1 (a) Sleep parameters, oxygen saturation (SaO2) and heart rate (HR) and (b) statistical significance of age-dependency of sleep parameters, oxygen saturation (SaO2) and heart rate (HR) in 131 patients evaluated for suspected obstructive sleep apnoea on two consecutive nights ( p: Kruskal–Wallis-test) First night Median

Second night Quartile range

Min

Max

Median

Quartile range

Min

Max

p Wilcoxon

(a) Age group A n ¼ 37 Age [years] SPT [min] SE [%] W [%SPT] NREM 1 [%SPT] NREM 2 [%SPT] NREM 3 [%SPT] NREM 4 [%SPT] REM [%SPT] REM latency [min] SaO2 [%] HR [/min]

5.92 526.00 94.00 3.40 4.70 38.00 10.00 19.00 16.00 139.00 95.00 72.00

1.76 63.50 8.25 5.80 7.15 10.25 5.15 6.00 10.00 73.25 1.25 10.75

2.4 303.00 74.00 0.00 0.00 22.00 6.20 11.00 5.80 46.00 93.00 52.00

6.99 610.00 100.00 24.00 32.00 63.00 27.00 29.00 27.00 369.00 98.00 88.00

527.00 94.00 1.50 4.50 41.00 11.00 21.00 18.00 134.00 95.00 72.00

61.00 9.00 2.47 9.55 7.50 5.72 6.25 8.00 68.00 2.00 12.25

445.00 81.00 0.00 0.30 23.00 5.30 6.40 12.00 26.00 92.00 56.00

598.00 100.00 12.00 27.00 51.00 21.00 30.00 31.00 263.00 98.00 92.00

0.6893 0.5259 0.0026 0.5144 0.9087 0.4276 0.2959 0.0009 0.2105 0.5401 0.0355

Age group B n ¼ 60 Age [years] SPT [min] SE [%] W [%SPT] NREM 1 [%SPT] NREM 2 [%SPT] NREM 3 [%SPT] NREM 4 [%SPT] REM [%SPT] REM latency [min] SaO2 [%] HR [/min]

9.86 495.50 89.00 5.15 7.05 39.00 8.45 20.00 17.00 157.00 95.00 65.50

2.22 65.00 13.50 10,10 8.80 7.50 4.10 7.50 5,50 86.00 1.50 14.00

7.04 428.00 61.00 0.20 0.90 20.00 3.40 4.30 4.00 48.00 93.00 47.00

12.98 633.00 100.00 39.00 20.00 63.00 18.00 28.00 27.00 445.00 99.00 93.00

498.00 96.00 1.05 5.30 42.00 9.30 19.00 18.50 144.50 95.00 63.50

47.50 8.00 3.20 8.20 6.00 3.85 6.00 7.50 84.50 1.00 14.00

408.00 78.00 0.00 0.00 8.00 4.40 8.40 4.40 57.00 94.00 48.00

575.00 100.00 17.00 27.00 53.00 43.00 29.00 32.00 412.00 98.00 82.00

0.2158 ,0.0001 ,0.0001 0.0449 0.1234 0.0558 0.1283 0.0004 0.4504 0.5132 ,0.0001

14.73 465.50 94.00 4.85 9.30 47.50 8.55 14.00 12.00 145.50 95.00 58.00

1.77 53.00 9.00 7.40 9.20 9.00 4.00 6.30 8.10 98.00 1.00 9.00

13.12 380.00 62.60 0.00 0.00 28.00 2.50 0.00 2.10 54.00 92.00 38.00

17.64 534.00 100.00 28.00 29.00 62.00 15.00 24.00 27.00 396.00 97.00 77.00

461.50 96.00 2.40 6.00 45.00 10.00 16.00 18.00 101.00 95.00 57.00

72.00 5.00 3.40 10.40 8.00 4.60 8.00 5.00 68.00 1.00 11.00

392.00 83.00 0.00 0.20 35.00 3.10 6.60 3.80 54.00 92.00 39.00

594.00 100.00 15.00 17.00 60.00 17.00 26.00 26.00 219.00 97.00 73.00

0.2892 0.0010 0.0022 0.0006 0.2098 0.1323 0.0020 0.0004 0.0529 0.8241 0.1631

Age group C n ¼ 34 Age [years] SPT [min] SE [%] W [%SPT] NREM 1 [%SPT] NREM 2 [%SPT] NREM 3 [%SPT] NREM 4 [%SPT] REM [%SPT] REM latency [min] SaO2 [%] HR [/min] (b)

SE [%] W [%SPT] NREM 1 [%SPT] NREM 2 [%SPT] NREM 3 [%SPT] NREM 4 [%SPT] REM [%SPT] REM latency [min] SaO2 [%] HR [/min]

First night p 0.2240 0.1636 0.0210 ,0.0001 0.0001 ,0.0001 0.0028 0.3492 0.7932 ,0.0001

Second night p 0.2560 0.1195 0.6589 0.0003 0.1740 0.0008 0.1492 0.0341 0.3866 ,0.0001

(a) The two nights were compared using Wilcoxon’s rank sum test. Age classes A: 2–6 years, B: 7– 12 years and C: 13–17 years.

2142

S. Scholle et al. / Clinical Neurophysiology 114 (2003) 2138–2145

Table 2 (a) Apnoea/hypopnoea-index (AHI), EEG-arousal index (AI) and motoric arousal index (JI) on two consecutive nights in patients with no PSG-abnormalities including treated OSAS patients (Group 1), (b) in untreated OSAS patients (Group 2) and (c) the statistical significance of age-dependency of apnoea/hypopnoea-index (AHI), EEG-arousal index (AI) and motoric arousal index (JI) in patients with no PSG-abnormalities including treated OSAS patients (Group 1: n ¼ 105) and untreated OSAS patients (Group 2: n ¼ 26) on two consecutive nights ( p: Kruskal–Wallis-test) First night Median

Second night Quartile range

Min

Max

Median

Quartile range

Min

Max

p Wilcoxon

(a) Age group A n ¼ 28 AHI [/h TST] AI [/h TST] JI [/h TST]

3.25 11.05 10.82

2.05 5.10 3.85

0.40 5.10 3.97

4.90 20.60 16.05

2.80 9.14 9.59

1.65 5.54 6.05

0.00 3.10 3.80

6.20 25.10 25.40

0.8554 0.4860 0.9330

Age group B n ¼ 53 AHI [/h TST] AI [/h TST] JI [/h TST]

1.70 7.76 8.54

1.95 3.99 4.42

0.00 3.10 2.30

5.80 28.90 19.20

2.00 7.43 7.86

1.80 4.11 4.96

0.10 2.99 2.74

4.50 24.97 22.28

0.3356 0.4152 0.3122

1.60 8.00 8.20

1.85 4.38 5.87

0.10 3.13 1.85

4.00 36.97 16.74

1.60 7.44 8.67

1.77 3.36 5.49

0.20 2.30 2.17

4.70 23.92 17.65

0.5963 0.5163 0.6987

Age group A n ¼ 9 AHI [/h TST] AI [/h TST] JI [/h TST]

11.90 12.90 14.28

5.22 2.78 6.81

5.00 9.40 9.40

27.40 25.87 28.75

8.10 12.20 12.65

4.05 4.41 3.75

5.20 7.14 7.70

12.80 21.46 21.65

0.0858 0.1386 0.0109

Age group B n ¼ 12 AHI [/h TST] AI [/h TST] JI [/h TST]

9.55 10.65 12.30

5.55 8.46 5.29

6.00 6.30 5.90

40.20 26.97 21.10

6.10 10.14 10.88

5.65 5.77 6.44

2.70 5.79 5.80

31.00 25.80 19.10

0.1579 0.6379 0.3332

Age group C n ¼ 5 AHI [/h TST] AI [/h TST] JI [/h TST]

10.30 10.88 13.83

21.73 1.60 9.17

5.40 10.24 8.47

66.20 14.09 13.83

8.80 10.35 8.79

18.47 4.42 3.42

5.20 5.80 4.52

70.40 14.60 11.95

0.6858 0.3452 0.2249

Age group C n ¼ 24 AHI [/h TST] AI [/h TST] JI [/h TST] (b)

(c) Group 1

AHI [/h TST] AI [/h TST] JI [/h TST]

First night p 0.0014 0.0187 0.0157

Group 2 Second night p 0.0021 0.0470 0.0637

First night p 0.7711 0.2358 0.5933

Second night p 0.5094 0.3868 0.1039

(a) The two nights were compared using Wilcoxon’s rank sum test. Age classes A: 2– 6 years, B: 7–12 years and C: 13–17 years. (b) The two nights were compared using Wilcoxon’s rank sum test. Age classes A: 2–6 years, B: 7–12 years and C: 13 –17 years.

in frontal than in central or occipital leads (Scholle and Scha¨fer, 1999). The evaluation of sleep architecture in childhood is complicated by the changes in EEG patterns during development (American Thoracic Society, 1996; Scholle and Scha¨fer, 1999). For example, the posterior basic rhythm changes from 2– 4 Hz at 2 – 4 months to 6 –7 Hz at 12 months and 6 –8 Hz at 3– 5 years, and attains the typical alpha rhythm at 12– 20 years (Niedermeyer and Lopes da Silva, 1992). This gradual change from the theta to the alpha frequency band complicates the scoring of brief intrasleep wake and arousal periods. For this reason, an additional occipital referential EEG lead as proposed for arousal

scoring in adults (ASDA, 1992) is not helpful in childhood. Nevertheless, in childhood, brief wake periods are very easy to classify since, in addition to EEG changes, typical HR acceleration, changes in respiratory pattern and often a motoric activation occur (Scholle and Scha¨fer, 1999). As a modification of the definition of arousal in adult PSG (ASDA, 1992), EEG frequency shifts greater than 1 s were applied (Scholle and Zwacka, 2001). As Mograss et al. (1994) showed, most EEG frequency shifts in childhood are shorter than 3 s—the minimal duration of an arousal in adults (ASDA, 1992). The pattern of breathing during sleep changes with age. Because children have a higher respiratory rate and

S. Scholle et al. / Clinical Neurophysiology 114 (2003) 2138–2145

2143

Fig. 1. First night effect in an 8-year-old boy. Sleep continuity on the first night is disturbed (many brief awakenings and arousals). First night: sleep efficiency, SE 80%; sleep latency, SL 70 min; W 8.6% SPT; NREM 1 4.2% SPT; NREM 2 32% SPT; NREM 3 14% SPT; NREM 4 25% SPT; REM 16% SPT. EEGarousals 11.7/h TST, motoric arousals (jerks) 10.8/h TST. Second night: SE 93%; SL 15 min; W 4.4% SPT; NREM 1 2.7% SPT; NREM 2 46% SPT; NREM 3 8.7% SPT; NREM 4 22% SPT; REM 16% SPT. EEG-arousals 6.7/h TST, motoric arousals (jerks) 5.5/h TST. TST, total amount of NREM 1–4 and REM; SPT, time in bed minus wake before sleep minus wake after sleep.

a lower functional residual capacity than adults, we score as apnoea cessation of breathing lasting for $ 2 breaths (in adults . 10 s), as proposed by Davidson et al. (1996) and Marcus (1997). Although diagnosing a sleep problem on the basis of a single-night recording is common practice (Acebo et al., 1996), some clinicians caution that more than 1 night of recording may be necessary, to enable the patient to acclimatize to the unfamiliar environment and sleep more naturally (Meyer et al., 1993; Le Bon et al., 2000, 2001; Rains, 2001). PSG itself represents an external stimulus inducing a sleep disturbance, especially on the first night. Sleep is typically of reduced quality compared with that in the subject’s usual sleep environment with no bothersome electrodes and leads. Subjects usually habituate to the laboratory by the second night. This FNE described by Agnew et al. (1966) in adults is also observable in children. Toussaint et al. (1995) reported a varyingly marked FNE in different groups, e.g. normal subjects, insomniacs or depressed patients. In our study, we investigated children

and adolescents for sleep-disordered breathing. No patients with a history of psychiatric or neurologic disorders were included. FNE in adults is characterized by a reduction in TST and REM sleep, lower sleep efficiency, increased intrasleep wake time and longer RL (Rechtschaffen and Verdone, 1964; Agnew et al., 1966; Hartmann, 1968; Rains, 2001; Le Bon et al., 2001). No clear pattern has been identified for NREM sleep. Toussaint et al. (1997, 2000) described changes in EEG power density during sleep laboratory familiarisation. Increased delta, theta and beta 1 power densities accompanied by a decrease in mean frequency were seen in REM sleep on the second night. Delta and theta power density values in the first NREM episode were lower on the first night than on the second night. In children/adolescents without sleep-disordered breathing, treated OSAS patients and OSAS patients not receiving therapy, we found no significant difference in sleep structure (excluding arousal indices), SaO2 and HR for the age ranges 2 –6, 7 –12 and 13– 17 years. We, therefore, pooled these groups in Table 1a to obtain normative values for these

2144

S. Scholle et al. / Clinical Neurophysiology 114 (2003) 2138–2145

parameters on the first and second nights of PSG. In children aged 7 –12 years and adolescents aged 13– 17 years, we observed lower sleep efficiency in the first night due to a greater percentage of wakefulness during the TIB. As shown in Fig. 1, sleep latency is usually longer. FNE is further characterized by disturbed sleep continuity, i.e. there are numerous brief awakenings. Despite prolongation of NREM 1 on the first night in the age classes 7– 12 and 13– 17 years and NREM 4 prolongation on the second night in the 13– 17-year-olds (Table 1a), NREM duration was not significantly influenced by the habituation phenomenon—as was also described by Le Bon et al. (2001) for adults. In children, the first deep sleep period in particular, is not disturbed by FNE. On the first night, a significantly lower percentage of REM sleep was found in all 3 age classes. This may be caused by slower adaptation of REM sleep—as described for adults—reflecting a more protracted and progressive habituation process as compared with NREM sleep (Endo et al., 1998). In contrast to adults, first night REM sleep latency is not statistically significantly longer. In most children, however, the initial sleep cycle is incomplete, with no REM phase (Roffwarg et al., 1964; Feinberg and Floyd, 1979; Palm et al., 1989; Kahn et al., 1996). Thus, in all 3 age groups, the time between sleep onset and the first epoch of REM is long, but with considerable variability so that shortening of REM sleep latency, while demonstrable, is not statistically significant (Table 1a). The characterization of the microstructure of sleep in terms of the EEG-arousals or motoric arousals (Fig. 1) appears to be an important marker for sleep disturbances in children (Scholle and Zwacka, 2001). But we failed to find any statistically significant differences in the number of arousals between first and second nights in any of the 3 age classes. This was true of both Groups 1 and 2, with the exception of age class A in Group 2 which had significantly more motoric arousals on the fist night (Table 2a, b). As we show here, the FNE in children is also characterized by an elevated mean HR. This statistical difference may be accounted for by the higher proportion of wakefulness with associated higher HR. The effect of the first night of PSG on the next night may be compared to partial sleep deprivation (Le Bon et al., 2001). Toussaint et al. (1997) summarized that the second night might be affected by REM sleep deprivation on the first night. We are, therefore, of the opinion that FNE can be observed only on immediately consecutive nights and not in nocturnal polysomnograms performed 7– 27 nights apart, as described by Katz et al. (2002). This would explain why they failed to find night-to-night variability of sleep efficiency, arousal index, percent REM, or percent of slow wave sleep in children, leading them to reject a FNE in this age group. We believe that the interval between the first and second examinations in their study was too long to identify a FNE.

Katz et al. (2002) also failed to find any night-to-night variability of respiratory parameters. In a group of 26 children with OSAS (Group 2), we, too, saw no statistically significant differences in AHI and mean arterial SaO2 between the first and second nights, indicating that a single polysomnographic night might suffice to demonstrate respiratory disturbances. Mendelson (1994) also failed to find any differences in AHI, mean minimal arterial oxygen desaturation or absolute minimum desaturation between the two nights in adults. This is in contrast to the results of Le Bon et al. (2000) and Meyer et al. (1993) showing underdiagnosis of respiratory events in adults when only the first night is considered. Children show considerable interindividual differences in sleep quality. If first night sleep quality is poor, we repeat PSG on a second night, even when investigating for obstructive sleep apnoea. A repeat study is also mandatory when parents report a typical night’s sleep that is at variance with our first night findings (American Thoracic Society, 1996). Webb and Campbell (1979) reported a more pronounced FNE in older subjects. This prompted us to determine the extent to which age may influence the FNE. We found the FNE to be more pronounced in the older children and adolescents. In age ranges B and C, differences in sleep parameters became progressively more statistically significant—as Table 1 shows. Currently, few polysomnographic reference values are available for the pediatric age group (Acebo et al., 1996; Davidson et al., 1996; Kahn et al., 1996; Stores et al., 1998; Katz et al., 2002). In Tables 1a and 2a, b, we present normative data on sleep, breathing, oximetry and HR in children and adolescents evaluated for sleepdisordered breathing. We found age-dependency for most of these parameters. In common with Kahn et al. (1996), we identified a prolongation of NREM 1, an increase in the proportion of NREM 2, and a decrease in NREM 3 and NREM 4. Furthermore, there was a decrease in REM sleep in older children/adolescents (Table 1a, b). With increasing age, there are fewer apnoeas/hypopnoeas and fewer EEG- and motoric arousals (Table 2a –c). This agedependency was affected by the FNE and sleep-disordered breathing (OSAS). The FNE, which represents the sleep-altering effect of the monitoring process itself, is demonstrable in both adults and childhood. In some cases, the FNE may obscure the clinical diagnosis (Rains, 2001). When interpreting polysomnographic results, therefore, account must be taken of the FNE, as also of the age-dependency of most of the physiologic parameters. References Acebo C, Millman RP, Rosenberg C, Cavallo A, Caskardon MA. Sleep, breathing and cephalometrics in older children and young adults. Part I—Normative values. Chest 1996;109:664–72.

S. Scholle et al. / Clinical Neurophysiology 114 (2003) 2138–2145 Agnew HW, Wilse B, Webb B, Williams RL. The first night effect: an EEG study of sleep. Psychophysiologie 1966;2:263–6. American Sleep Disorders Association. Arousals: scoring rules and examples. A preliminary report from the sleep disorders atlas task force of the American Sleep Disorders Association. Sleep 1992;15: 173–84. American Thoracic Society: standards and indications for cardiopulmonary sleep studies in children. Am J Respir Crit Care Med 1996;153: 866–78. Davidson W, Sally L, Marcus CL. Obstructive apnoea in infants and young children. J Clin Neurophysiol 1996;13:198–207. Emslie GJ, Armitage R, Weinberg WA, Rush AJ, Mayes TL, Hoffmann RF. Sleep polysomnography as a predictor of recurrence in children and adolescents with major depressive disorder. Int J Neuropsychopharmacol 2001;4:159–68. Endo T, Roth C, Landolt HP, Werth E, Aeschbach D, Achermann P, et al. Selective REM sleep deprivation in humans: effects on sleep and sleep EEG. Am J Physiol 1998;274:R1186–94. Feinberg I, Floyd TC. Systematic trends across the night in human sleep cycles. Psychophysiology 1979;16:283–91. Hartmann E. Adaption to the sleep laboratory and placebo effect. Psychophysiology 1968;4:389. Kahn A, Dan B, Groswasser J, Franco P, Sottiaux M. Normal sleep architecture in infants and children. J Clin Neurophysiol 1996;13: 184–97. Katz ES, Greene MG, Carson KA, Galster P, Loughlin GM, Caroll J, et al. Night-to-night variability of polysomnography in children with suspected obstructive sleep apnoea. J Pediatr 2002;140:589–94. Kubicki S, Phermann WM, Scheuler W. Kritische Bemerkungen zu den Regeln von Rechtschaffen und Kales u¨ber die visuelle Auswertung von EEG-Schlafableitungen. Z EEG EMG 1982;13:51 –60. Le Bon O, Hoffmann G, Tecco J, Staner L, Noseda A, Pelc I, et al. Mild to moderate sleep respiratory events: one negative night may not be enough. Chest 2000;118:353–9. Le Bon O, Staner L, Hoffmann G, Dramaix M, San Sebastian I, Murphy JR, et al. The first-night effect may last more than one night. Psychiatry Res 2001;35:165 –72. Marcus CL. Clinical and pathophysiological aspects of obstructive sleep apnoea in children. Pediatr Pulmonol 1997;(Suppl 16):123–4. Mendelson WB. Use of the sleep laboratory in suspected sleep apnoea syndrome: is one night enough? Cleve Clin J Med 1994;61:299 –303.

2145

Meyer TJ, Eveloff SE, Kline LR, Millman RP. One negative polysomnogram does not exclude obstructive sleep apnoea. Chest 1993;103: 756– 60. Niedermeyer E, Lopes da Silva F. Electroencephalography—basic principles, clinical application, and related fields, 3rd ed. Baltimore/ Philadelphia/Hong Kong/London/Munich/Sydney/Tokyo: Williams & Wilkins; 1992. p. 178. Palm L, Person E, Elquist D, Blenno WG. Sleep and wakefulness in normal preadolescent children. Sleep 1989;12:299–308. Rains JC. Polysomnography necessitates experimental control of the ‘First night effect’. Headache 2001;41:917–8. Rechtschaffen A, Verdone P. Amount of dreaming: effect of incentive, adaption to laboratory, and individual differences. Percept Mot Skills 1964;19:947–58. Rechtschaffen A, Kales A. In: Berger RJ, Dement WC, Jacobson A, Johnson LC, Jouvet M, Monroe LJ, Oswald I, Roffwarg HP, Roth B, Walter RD, editors. A manual of standardized terminology, techniques and scoring system for sleep stages of human subjects. Washington, DC: Public Health Service, US Government Printing Office; 1968. Roffwarg HP, Dement WC, Fisher C. Preliminary observations of the sleep–dream pattern in neonates, infants, children and adults. In: Harms E, editor. Problems of sleep and dreams in children. Monographs on child psychiatry, vol. 2. New York: Pergamon Press; 1964. p. 60– 72. Stores NG, Crawford C, Selman J, Wiggs L. Home polysomnographic norms for children. Technol Health Care 1998;6:231–6. Scholle S, Scha¨fer T. Atlas of states of sleep and wakefulness in infants and children. Somnologie 1999;3:163 –241. Scholle S, Zwacka G. Arousals and obstructive sleep apnoea syndrome in children. Clin Neurophysiol 2001;112:984–91. Toussaint M, Luthringer R, Schaltenbrand N, Carelli G, Lainey E, Jacqmin A, et al. First-night effect in normal subjects and psychiatric inpatients. Sleep 1995;18:463 –9. Toussaint M, Luthringer R, Schaltenbrand N, Nicolas A, Jacqmin A, Carelli G, et al. Changes in EEG power density during sleep laboratory adaption. Sleep 1997;20:1201 –7. Toussaint M, Luthringer R, Staner L, Muzet A, Macher J. Changes in EEG power density during sleep laboratory adaption in depressed inpatients. Biol Psychiatry 2000;47:626– 33. Webb WB, Campbell SS. The first night effect revisited with age as a variable. Waking Sleeping 1979;3:319–24.