European Society of Sleep Technologists

Newsletter 2002

Contents:

Letter from the Past President
Cinzia Castrono
Page: 2
Message from the President
Maud Verhelst
Page: 3

How to measure flow during sleep studies
Josep Montserrat

Page: 4
Recording respiration: different technics for airflow assesment
Jacob Zomer
Page: 5

How to assess ventilatory effort
Einar Orn Einarsson

Page: 6
Alpha sleep and fatigue
Melissa Vandeputte
Page: 7
Vigilance measuring systems: MSLT, MWT and the OSLER-test
Jo Tiete
Page: 8
Diagnostic criteria for PLM and RLS syndrome: coring rules and controversy
Emilia Sforza
Page: 9
CAP: the Cyclic Alternating Pattern
Liborio Parrino
Page: 10
Spectral Analysis of the REM sleep: technical approach
Francesco Lullo
Page: 11
Polysomnography in children
Marie Jo Challamel
Page: 12
Sleep disorders breathing in children: recording techniques
Cinzia Castronovo
Page: 13
Insomnia in children
Oliviero Bruni
Page: 14
Parasomnia in children
Marco Zucconi
Page: 15
Sleep recording; The significance of in between napping in the MSLTest ambulatory vs. Clinical recordings
Maud Verhelst
Page: 16
Diagnosis and treatment of sleep related breathing disorders in Iceland
Bryndis Haldorsdottir
Page: 17
Sleep service provision in the UK
Simone De Lacy
Page: 18
CPAP attribution in different countries
Ann Ryckx
Page: 19
   
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Page 2

Letter from the Past President

Dear members and friends of ESST,
Ten years had passed since the foundation of ESST (European Society of Sleep Technologists) held in Helsinky, Finland in June 1992. During this long time I dedicated work and time as well as a lot of efforts to the development and growth of the Society. Now it is for me time to leave for dedicating to other activities still in the field of sleep medicine and research that remain fascinating for me.Thank to your offer of becoming Honorary President I will always be present and available to help and collaborate with the new elected Board hoping to see a continuous growing of our Society towards the trend of a united Europe.
I am sure the new elected Board where almost all the elected members have been with us in the last years will keep with the same aims that we had at the beginning.
I wish to all of you a successful work and again I would like to thank everybody for the collaboration of these past productive years.
A special thank to Ann Ryckx that really assisted and helped me a lot in the last years.

Thinking a little about the past I remember the meeting in Helsinki in 1992, then Florence in 1994, then Bruxelles in 1996, then Madrid in 1998, then  Istanbul in 2000 and the at last the recent meeting in Reykjavik last June. I have to say that all our meetings combined with the ESRS Congress have been a real success both in terms of scientific program and of participation: and every year it has been better. Scientific programs always have been more interesting by covering new aspects in the methodological field of sleep medicine and research together with stimulating physician lectures covering different clinical  and research aspects in our field.
All this have been possible thank to the close collaboration between our Board, the ESRS Board and the different local organising committes to whom goes my special thank.

Another  special thank goes to Professor Michel Billiard that closely collaborated with us and helped us in being part of the activities of ESRS: thank to him we are part of the education and clinical committee that are working on the creation of quality standards in sleep medicine for both personnel and sleep laboratories. We can say that we have the honor of being able to contribute to the creation of guidelines for sleep medicine and education. We would all like to give our best thank for his efforts and dedication also to our society; he has been a fundamental link and promoter in these past years for our place in the ESRS.
I really hope this close collaboration would be kept by the new Board.

And at last but not least a very grateful thank goes to our sponsors: companies that  with their support made possible our life and gave us the opportunity to be updated on the latest technological innovation in our field.
I really hope that all of you would put all the efforts needed to keep what we have built in these past years.

Good luck to all of you and my best wishes for a long life of our Society.
With my best regards,

Cinzia Castronovo
Honorary President

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Page 3

Message from the (New) President

ESRS Congress in Reykjavik, June 2002.

The 16th ESRS Congress in Reykjavik was a success. The day before the congress we had a successful 6th meeting of the ESST.
My appreciation goes to the entire team of Local Organizers who have made this meeting possible.
A word of welcome was given by Dr. Thorarinn Gislason.
A special thanks goes to Professor Irene Tobler for her excellent, inspirational talk on ‘Why we sleep’ in relation to phylogenesis.
In this newsletter you will find the abstracts of all the lectures held that day. 

At the end of the day elections for the new board and delegates were held. You can find the names and addresses here.
As you can see, we succeeded to expand the number of delegates to 10.

On behalf of the previous board I’d like to thank Cinzia Castronovo for all her efforts done for our society. We’re happy that she is willing to give advise in the future as Honorary President. Her past work will inspire me and the rest of the board to unite technologists all over Europe.

During our first board meeting we decided for a new approach. In the past the membership of the ESST was quite expensive. From now on it will be free of charge. In this way we can make a bigger network in Europe. Our second aim is to work exclusively through the Internet. Our website will be updated and before the end of the year we will make a newsgroup. Members will be able to log in and discuss all things concerning sleep, especially from the technologist’s point of view. On this website, our sponsors will be able to advertise and have links to their own Internet sites.

Please join our Society and send your application form (again) to our secretary, Melissa Vandeputte. If you have ideas, have names of new members or you want to represent your country as a national delegate, please let us know.

Hoping to meet you or to hear from you in the near future as an ESST member. 

Maud Verhelst

August 2002

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Page 4

How to measure flow during sleep studies.

Josep Montserrat (Barcelona)


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Page 5

Recording respiration : different technics for airflow assessment.

Jacob Zomer (Haifa, Israel)

In order to optimally diagnose ,determine the syndrome severity and treat patients with breathing disorders during sleep we need to choose the best way to assess respiration functions.

Recording respiration can be done by each of many channels of physical changes that are created by the subject ( of course recording more channels may improve the decision making ).
We can chose direct or semi-direct recordings of : Air-Flow, Air Temperature changes (via thermistor or thermocouple ), Pressure at the nostrils, exhaled Air -CO2 changes, Air Humidity changes and Respiratory Sounds, or non direct recordings like : Internal Pressure (Esophageal Balloon), chest or abdominal expansion (Belts) and phase relations between them (Respitrace),  Sternal Notch deflection (optiflex), EMG (diaphragmatic or intercostals ) changes, oximetry , Ecg changes ( amplitude and rate variations ) , snoring noise (Db metering) and others. Since each of the methods has its cons and pros, its a good idea to simultaneously record several signals (of different entities) to add non overlapping data and improve the quality of the decision making, but we have to keep in mind that we are dealing with a sleeping patient and his undisturbed sleep is crucial to the test outcome .

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Page 6

How to assess ventilatory effort

Einar Orn Einarsson (Gardabaer, Iceland)

Various methods have been devised to measure different aspects of ventilatory effort during sleep. These methods include esophageal pressure, diaphragm electromyography (EMG), Respiratory Inductance Plethysmography (RIP), Piezo sensors and Strain Gauge. The measurement of nocturnal esophageal pressure (Pes) by means of esophageal catheter is the reference standard for measuring ventilatory effort and differentiates between obstructive sleep apnea-hypopnea (OSAH)and central sleep apnea-hypopnea (CSAH). Pes with nocturnal Polysomnography (NPSG) is also the reference standard for measuring respiratory effort related arousals (RERA). Calibrated RIP measures changes in lung volume and can, with standard NPSG, detect respiratory effort-related arousals. Maintaining the calibration can be difficult because of artifacts during changes in body positions. Uncalibrated RIP still gives semi-quantitative measurements of ventilation and allows differentiation between OSAH and CSAH. Properly calibrated Strain Gauges can quantitatively measure dynamic volume changes but are highly sensitive to displacement. Uncalibrated Strain Gauge and Piezo belts only give qualitative information on changes in ventilation and cannot contrast OSAH from CSAH. Diaphragm EMG is an indirect, qualitative  measurement of ventilatory effort. It is not widely used and can be difficult to record reliably throughout all-night studies. In conclusion, esophageal pressure is still the reference standard for measuring respiratory effort although less invasive method such as RIP seem promising.

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Page 7

Alpha sleep and fatigue

Melissa Vandeputte, B. Kemp and A. W. de Weerd (The Netherlands)

Alpha-activity (frequency 7.5-13 Hz) can be part of the normal sleep EEG but is also often found during sleep in disorders such as psychophysiological insomnia, inadequate sleep- and wake hygiene, fibromyalgia (1), rheumatoid arthritis, chronic fatigue syndrome and after sleep deprivation (2). The presence of alpha-activity in sleep, “alpha-sleep”, is not limited to one specific sleep-stage or one particular part of the night. Patients with alpha-sleep do not perform worse on tests that measure attention, concentration, memory, and reaction time.  Alpha-sleepers overestimate their sleep length and underestimate the intermittent waking periods during sleep (3). There is no relationship between alpha-sleep, number of awakenings and sleep efficiency (4). The clinical significance of alpha-sleep is not clear.      The results of our previous pilot-study (5) showed that 15 out of 21 patients having a clear alpha-peak during NREM-sleep felt tired and not rested. Because of the shortcomings of that pilot-study (retrospective character) we performed a prospective study on a larger population and increased the amount of questionnaires to encompass the patients’ fatigue.
Patients
We included  100 consecutive insomnia patients from our outpatient sleepclinic (38 male and 62 female, age between 15 and 69) that underwent two 24-hour polysomnography tests (PSG’s) at home. Exclusion criteria were an abnormal PSG macro-structure (for example not enough REM or delta sleep), Periodic Limb Movement Disorder (Periodic Limb Movement Index > 15) and or Obstructive Sleep Apnea Syndrome (Apnea Index > 10).
Method

Fpz-Cz EEG was Fourier analyzed during the first 20 minutes of continuous NREM sleep in both nights (stages 2, 3 and/or 4). Our sleeplab uses Fpz-Cz and Pz-Oz derivations to measure sleep (6). We opted for FPz-Cz because alpha activity during sleep occurs predominantly in frontal derivations (7).  The peak frequency in the alpha-band was determined from the resulting amplitude spectrum. The normalized alpha amplitude was obtained by dividing the amplitude at the peak by the amplitude of the background (5). Quantification of fatigue was based on the following questionnaires:the Groningen Sleep Quality scale (8) at the mornings following each PSG nightthe Multidimensional Fatigue Inventory (MVI-20) (9) was assessed once, preceding the first PSG nightthe Profile of Mood scale (POMS) (10) at the evenings before and the mornings after both PSG nights The Groningen Sleep Quality scale includes two questions related to fatigue:“this morning, when I got up, I felt tired” (yes: score 1, no: score 0)“this morning, when I got up, I was not rested” (yes: score 1, no: score 0)The MVI-20 includes 1 score each of general fatigue, physical fatigue, mental fatigue, reduction in daily activity and reduction of motivation (score range 4-20). The POMS scale provides a total score  (score range 5-20) and one question each on tiredness (question 6), anxiety (question 1) and depressive mood (question 2) both in the morning and evening (score range 1-5).These items sum up to a total of 15 parameters on fatigue during daytime for each PSG night per person.In order to compare the 15 characteristics between subjects with alpha sleep and those without we performed a linear regression analysis as well as correlation analysis between normalized alpha amplitude and the fatigue parameters. This was done separately for both nights and also on the summed (over both nights) normalized alpha amplitude and fatigue parameters.10 fatigue parameters (those from the Groningen Sleep Quality scale and those from the POMS) were obtained on both nights. In order to assess any correlation between normalized alpha amplitude and those characteristics, we computed the inter-night difference of normalized alpha amplitude and these 10 characteristics. Linear regression analysis as well as correlation analysis was performed with difference between night 1 and night 2 of the normalized alpha amplitude and the difference in the fatigue parameters over both nights.
Results
The difference between the two PSG nights in normalized alpha amplitude never exceeded 1.3. The amount of alpha sleep was similar in both nights.

alpha night 1

alpha night 2

Alpha night 1 + 2

Significance

VAF

0.030

0.047

0.028

0.048

0.024

0.051

Tabel 1: regression analysis and correlation analysis on the normalized alpha amplitude and reduction in activity. VAF: variation accounted for.Of the 15 analyzed intersubject relationships, only normalized alpha amplitude and reduction in activity were significantly (negatively) correlated in both nights as well as in the combined nights: p<0.030, p<0.028 and p<0.024, respectively (tabel 1).None of the 10 analyzed inter-night differences were significant.Discussion
Despite the large number of subjects, this study does not confirm the suspected relationship between alpha-sleep and fatigue.  The same is true for reduction in motivation, anxiety and depressive mood. Patients with alpha sleep are not more fatigued during the day than patients without alpha sleep.  The only parameter that scored was the feeling of diminished daily activity. This factor was more pronounced in patients with less alpha-sleep. Since this was found independently in both nights, this probably indicates a real relationship. Why patients without alpha-sleep feel less active than those with alpha-sleep is not clear.

References

1.      Moldofsky H.; Lue F. The relationship of alpha and delta EEG frequencies to pain and mood in fibrositis patients treated with chlorpromazine and L-tryptophane. Elecectroencephalogr Clin Neurophysiol. 1980; 50: 71-80.
2.      Kryger M.H.; Roth T.; Dement W.C. Principles and Practice of Sleep Medicine, second edition. W.B. Saunders Company. 1994: 530-531.
3.      Schneider-Helmert D. Alpha-sleep variations with sleepless patients. (Abstract), Brussels: 13th congress of the European Sleep Research Society. 1996: 4-6.
4.      Moldofsky H.; Lue F.; Mously C.; Roth-Schechter B.; Reynolds W.J. The effect of Zolpidem in patients with fibromyalgia: a dose ranging, double blind, placebo controlled, modifed crossover study. J Rheumatol. 1996; 23: 529-533.
5.      Vandeputte M; Kemp B; de Weerd A.W. Alphasleep and fatigue. Sleep-Wake Research in the Netherlands. Volume 11 2000: 127-129.
6.      Van Sweden B., Kemp B., Kamphuisen H. A. C., Van der Velde E. A. Alternative electrode placement in (automatic) sleep scoring  (Fpz-Cz/Pz-Oz versus C4-A1). Sleep. 1990; 13: 279-283.
7.      Horne J.A.; Shackell B.S. Alpha-like EEG activity in non REM sleep and the fibromyalgia (fibrositis) syndrome. Electroencephalogr Clin Neurophysiol. 1991; 79: 271-276.
8.      Mulder-Hajonides van der Meulen W.R.E.H.; Van der Hoofdakker R.H. The Groningen Sleep Quality Scale. Book of Abstracts, 14th CINP Congress. 1984.
9.      Smets E.M.A.; Garssen B.; Bonke B.  The Multidimensional Fatigue Inventory (MVI-20). Academisch Medisch Centrum. Universiteit van Amsterdam. 1995.
10.  Mc. Nair D.M.; Lorr M.; Droppleman L.F.; (1981). Edits Manual for        the Profile of Mood States. San Diego, CA: Educational and Industrial Testing Service (original work published 1971).

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Page 8

Multiple Sleep Latency Test, Maintenance of Wakefulness Test and the OSLER-test: technics, value and latest findings.

Jo Tiete (Luxembourg)

MSLT and MWT are considered as helpfull diagnostic tests, for disorders of excessive somnolence like narcolepsy and sleep apnea syndrome. They are used as a clinical tool to evaluate excessive daytime sleepiness (EDS) of a subject. MSLT and/or MWT are used for evaluating professional drivers and (dangerous) machine handlers.
The methodology: International guidelines for performing these tests, the difference or utility between MSLT and MWT. The preparation of the subject, the procedure and the interpretation of the results.What about the value, sensitivity of these tests, are they really usefull in clinic and/or research?A brief overview of studies around MSLT and MWT. MSLT & MWT are on the other hand not very sensitive for detection of microsleep. A simplified behavior MWT like the OSLER-test (Oxford Sleep Resistance Test) is mainly designed to detect microsleep and could objectively measure this symptom and be more accurate for EDS. The test require also less technician workload.

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Page 9

Diagnostic criteria for PLM and RLS syndrome: scoring rules and controversy

E. Sforza, Sleep laboratory, Department of Psychiatry, University of Geneva, Switzerland.

Periodic leg movements (PLM) are a laboratory finding present in 86% of patients with restless legs syndrome (RLS) or an associate finding in other sleep disorders such as narcolepsy and obstructive sleep apnea syndrome. Specific criteria have been proposed  to record and to detect PLM according to Coleman description (Coleman 1982) and to ASDA criteria (ASDA 1993).

Three points are cardinal in the scoring of the PLM: the event detection, the event classification and the event analysis. Considering the PLM detection two criteria are commonly used: the duration, i.e. 0.5- to 5 s, and the amplitude, i.e. an increase of at least 25% of the EMG envelope recorded during calibration. For the PLM analysis the most important criterion is the definition of a PLM sequence that is a sequence of 4 or more leg movements separated by at least 5 s and no more than 90 s. The PLM sequence analysis allows the scorer to define the leg movement period, the leg movements periodicity and the number of leg movements occurring as a part of the PLM sequence. Considering the PLM classification two points need to be considered: the relationship with indices of sleep fragmentation and the relationship with respiratory disorders. These points are interesting to evaluate the impact on sleep continuity and the etiology of the PLM.

Although these criteria allow the scorer to identify the PLM and its effect on sleep, some controversial data are present in the literature for detection and analysis. The most interesting points of discussion are the definition of the movement amplitude, the pattern of muscle activation and the detection of PLM during wakefulness. Since in clinical practice only the tibialis anterior muscles are recorded, the amplitude criteria may underestimate the number of leg movements occurring in other muscles. The pattern of expression of EMG activity may induce an underestimation of the PLM when phasic and shorter EMG activation occurred just before the onset of a leg movement. The most controversial point is the detection of leg movements during wakefulness for which no standardized criteria are present. The only criteria reported in the literature consider a duration from 0.5 to 10 s, a periodicity from 5 to 120 s, and an analysis of the bursts of EMG activity occurring in association with a tonic EMG activity to detect a PLM during wakefulness.

In any case nocturnal video-polygraphic recording is the gold standard to improve the detection of a PLM and to differentiate these movements from other motor disorders arising from sleep.

References.

1) Coleman RM. Periodic leg movements in sleep (nocturnal myoclonus) and restless legs syndrome. In: C. Guilleminault (Ed.) Sleeping and waking disorders. Addison-Wesley, Menlo Park, CA, 1982, 265-295.

2) ASDA Report. Atlas and Scoring rules. Recording and scoring leg movement. Sleep 1993, 16:748-759

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Page 10

CAP : the Cyclic Alternating Pattern

Liborio Parrino and Mario Giovanni Terzano (Italy)

Periodic EEG activities. Periodic EEG activities are electrocortical events recurring at regular intervals in the range of seconds. These EEG features are clearly distinguishable from the background rhythm as abrupt frequency shifts or amplitude changes.

Periodic activities can be characterized with 3 parameters: 

  1. The repetitive element (phase A of the period), represented by the recurring EEG feature.
  2. The intervening background (phase B of the period), identified by the interval that separates the repetitive elements.
  3. The period or cycle (the sum of phase A and phase B duration), characterizing the recurrence rate.

Definition of cyclic alternating pattern. The cyclic alternating pattern (CAP) is a periodic EEG activity of non-REM sleep in which both phase A and phase B can range between 2 and 60 s. A phase A (A) and the following phase B (B) compose a cycle (C).  CAP appears in sequences throughout sleep stages 1, 2, 3, 4. Phase A of CAP is identified by transient events typically observed in non-REM sleep, which clearly stand out from the background rhythm, usually differing in frequency and/or amplitude. Compared to phase Bs,  phase As can be composed of slower, higher-voltage rhythms, faster lower-voltage rhythms, or by mixed patterns including both. The identification of CAP should be preceded by the definition of sleep stages according to the conventional criteria.

Onset and termination of a CAP sequence. A CAP sequence is composed of a succession of CAP cycles. A CAP cycle is composed of a phase A and the following phase B. All CAP sequences begin with a phase A and end with a phase B. Each phase of CAP is 2-60 s in duration.

Non-CAP. The absence of CAP for > 60 s is scored as non-CAP. An isolated phase A, (that is, preceded or followed by another phase A but separated by more than 60 s), is classified as non-CAP. The phase A that terminates a CAP sequence is counted as non-CAP.

Minimal criteria for the detection of a CAP sequence. CAP sequences have no upper limits on overall duration and on the number of CAP cycles. However, at least two consecutive CAP cycles are required to define a CAP sequence. Consequently,  three or more consecutive phase As must be identified with each of the first two phase As followed by a phase B (interval < 60 s) and the third phase A followed by a non-CAP interval ( > 60 s).

REM sleep. CAP sequences commonly precede the transition from non-REM to REM sleep and end just before REM sleep onset. REM sleep is characterized by the lack of EEG synchronization; thus phase A features in REM sleep consist mainly of desynchronized patterns (fast low-amplitude rhythms), which are separated by a mean interval of 3-4 min. Consequently, under normal circumstances, CAP does not occur in REM sleep. However, pathophysiologies characterized by repetitive phase As recurring at intervals < 60 s (for example, periodic REM-related sleep apnea events), can produce CAP sequences in REM sleep.

EEG montages. CAP is a global EEG phenomenon involving extensive cortical areas. Therefore, phase As should be visible on all EEG leads. Bipolar derivations such as Fp1-F3, F3-C3, C3-P3, P3-O1 or Fp2-F4 , F4-C4, C4-P4, P4-O2 guarantee a favorable detection of the phenomenon. A calibration of 50 mV / 7 mm. with a time constant of 0.1 s and a high frequency filter in the 30 Hz range is recommended for the EEG channels. Monopolar EEG derivations (C3-A2 or  C4-A1 and O1-A2 or O2-A1), eye movement channels and submentalis EMG, currently used for the conventional sleep staging and arousal scoring, are also essential for scoring CAP. For clinical studies, airflow and respiratory effort, cardiac rhythm, oxygen saturation, and leg movements should be included as part of standard polysomnographic technique.

Amplitude limits. Changes in EEG amplitude are crucial for scoring CAP. Phasic activities initiating a phase A must be 1/3 higher than the background voltage (calculated during the 2 s before onset and  2 s after offset of a phase A). However, in some cases, a phase A can present ambiguous limits due to inconsistent voltage changes. Onset and termination of a phase A are established on the basis of an amplitude/frequency concordance in the majority of EEG leads. The monopolar derivation is mostly indicated when scoring is carried out on a single derivation. All EEG events which do not meet clearly the phase A characteristics cannot be scored as part of phase A.

Temporal limits. The minimal duration of a phase A or a phase B is 2 s. If two consecutive phase As are separated by an interval < 2 s, they are  combined as a single phase A. If they are separated by a ³ 2 s interval,  they are scored as independent events.

Subtype classification. Phase A activities can be classified into three subtypes. Subtype classification is based on the reciprocal proportion of high-voltage slow waves (EEG synchrony) and low-amplitude fast rhythms (EEG desynchrony) throughout the entire phase A duration. The three phase A subtypes are described below.

  • Subtype A1. EEG synchrony is the predominant activity. If present, EEG desynchrony occupies < 20% of the entire phase A duration. Subtype A1 specimens include delta bursts, K-complex sequences, vertex sharp transients, polyphasic bursts with < 20% of EEG desynchrony.
  • Subtype A2. The EEG activity is a mixture of slow and fast rhythms with 20%-50% of phase A occupied by EEG desynchrony. Subtype A2 specimens include polyphasic bursts with more than 20% but less than 50% of EEG desynchrony.
  • Subtype A3. The EEG activity is predominantly  rapid low-voltage rhythms with > 50% of  phase A occupied by EEG desynchrony. Subtype A3 specimens  include K-alpha, EEG arousals, and polyphasic bursts with > 50% of EEG desynchrony. A movement artifact within a CAP sequence is also classified as subtype A3.

Slow rhythms represent the main features of subtypes A1. Within subtypes A2 and A3, slow rhythms mostly prevail in the initial part of phase A. Different phase A subtypes can occur within the same CAP sequence. Subtype A1 is most common as sleep EEG synchrony increases (from light to deep non-REM sleep) and when synchrony predominates (stages 3 and 4) . Subtypes A2 and A3 are mostly concentrated as sleep-related brain activity progresses from synchrony to greater desynchrony (for example, in stage 2 preceding the onset of REM sleep).

The significance of CAP. The cyclic alternating pattern (CAP) is an EEG activity that may signify sleep instability, sleep disturbance, or both. CAP can appear spontaneously in non-REM sleep, but it can occur also in association with identifiable sleep pathophysiologies (e.g., sleep-disordered breathing and periodic leg movement activity). Individual variants of CAP have been recognized and are well described, albeit known by other names (for example, periodic K-alpha). The CAP sequence, originally conceptualized as an arousal phenomenon, has evolved theoretically to encompass both the process of sleep maintenance and sleep fragmentation. With respect to CAP as an arousal process, its subtype classification extends the current American Sleep Disorders Association definitions to include a periodicity dimension and a possible marker of pre-arousal activation. High-amplitude EEG bursts, be they delta-like or K-complexes, have long been thought to reflect a possible arousal process. However, evidence connecting such phenomena to clinical correlates typical of sleep disturbance was lacking. An alternative view is that these phenomena are associated with sleep instability (possibly an external or internal challenge to the sleep process) and that this type of slow wave activity (subtypes A1 of CAP) marks the brain’s attempt to preserve sleep. However, if sleep becomes too unstable or the preservation attempt fails, then a frank EEG arousal will accompany or replace the high-amplitude, slow activity. Thus, subtypes A2 and A3 of CAP constitute a central nervous system arousal.

The CAP Atlas and Standardized Manual. In 2001, an atlas and standardized manual were published by the International CAP workgroup to facilitate utility of CAP recording and scoring and to provide a consensus terminology [1]. The availability of agreed rules common will certainly be useful and will help stimulate investigation in this area of sleep research. For example, cyclic autonomic activations’ potential linkage with the sleep process, the role of increasing and decreasing synchronization, and the failure to maintain sleep continuity in some pathological conditions can be explored using CAP analysis. Factors that alter CAP periodicity may provide a clue to the overall sleep process.  In addition, a periodicity dimension to the concept of sleep stability and arousal will provide a new and valuable perspective to appreciate underlying physiological sleep mechanisms. CAP analysis is not meant to replace sleep stage scoring or arousal scoring, but rather to extend quantitative sleep analysis and provide a new tool to use in our quest to understand human sleep.

Terzano MG, Parrino L, Smerieri A, Chervin R, Chokroverty S, Guilleminault C, Hirshkowitz M, Mahowald M, Moldofsky H, Rosa A, Thomas R, Walters A. Atlas, rules and recording techniques for the scoring of cyclic alternating pattern (CAP) in human sleep. Sleep Med 2001 ; 2 : 537-553.

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Page 11

Spectral Analysis of the REM sleep: technical approach.

Francesco Lullo , G.Russo1, G.Paone1,  C.Luongo2, S.Vescia2 (Italy)

REM sleep is distinguishable from NREM sleep by changes in physiological states, including its characteristic rapid eye movements. In normal sleep, heart rate and respiration speed up and become erratic, while the face, fingers, and legs may twitch. Breathing, heart rate and brain wave activities quicken. Paradoxical sleep (PS), in which periods with (phasic) and without (tonic) rapid eye movements are intermingled. This study focuses on differentiation between phasic and tonic. Based on all-night sleep polysomnogram  was recorded using derivations  (Fp2, Fp1, C4, C3, O2, O1) two transversal EOG , one EMG (mentalis) one EKG (V4 lead)and one PNG (breath at thorax). Using high and low filtering (band pass) EEG (0.3-70 Hz), EOG and EKG (0.3 -30 Hz), the EMG (5- off Hz), the signals were digitized at a 256 sampling rate with 16-bit resolution. The R.E.M phases ware identified and converted in ASCII file, including the PSD (Power Spectral Density). The off-line analysis was performed using a software developed by the authors from commercial software (National Instruments  LabView 5.1).

The off-line analysis is divided in four steps:

  1. PSD (0.5-64 Hz) of R.E.M. performed on a six seconds epochs length.
  2. Each epoch was divided in phasic and tonic.
  3. For same epoch ware calculated  the hearth rate and the breath frequency.
  4. Statistical analysis.

The method of analysis used in our laboratory, is presented. Further data are still in phase of acquisition.

 

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Page 12

Polysomnograpyh in children
M J Challamel (France)
Introduction
Polysomnography is the term used to describe a procedure of objective, simultaneous recording of many different physiological parameters during sleep. Polygraphic recordings give information on each parameter recorded and on the interaction between different parameters. Only complete nocturnal (or 24-H) sleep polygraphic recordings provide accurate information regarding : sleep architecture, characterization of cardiorespiratory function (including airflow, respiratory efforts, blood gases,  cardiac rate and rhythm) ; characterization of arousals and body movements.

Methods:
The most important aspect in obtaining a high quality polygraphic recording in children is methodological and careful preparation. Transducers should be adapted to children. (Table 1).
Parents and children must be prepared in advance: doctors should discuss with the child and his parents the reason for the recording and the procedures that will be used. Parents of young children should be required to stay overnight in the laboratory with their children. In our laboratory we ask parents to arrive at least 3 hours prior to the preparation of the children for the recording.
Polygraphic parameters :
In any cases, recording for sleep studies should include information on at least 5 polygraphic parameters: electroencephalogram (EEG), electrooculogram (EOG), chin electromyogram (chin EMG), heart rate (HR) or electrocardiogram (EKG) and respiration in addition to behavioral observation (visual or video).
Montages :
Montage selection should be determined by the need of the diagnostic study.
EEG : either bipolar or unipolar. As in adults Ag/Agcl electrode positions are defined according to the international 10-20 system. The positions more frequently used are Fp1, Fp2, C3, C4, T3, T4, 01, O2. A minimum of 3 EEG leads with frontal, parietal and occipital positions are necessary to stage and quantify sleep. More channels of EEG may be necessary when the EEG is the major focus of investigation ( for example in children with parasomnias or with nocturnal epilepsy). In the younger children usual gain is 10 mm for 50 µV.
EOG : Standard EOG activity is monitored using two electrodes placed lateral to the outer canthus of each eye. Two channels referenced to one mastoid are generally recommended. In preterm infants, because of the immaturity of the retino-corneal dipole,  the use of piezo-electric crystal transducers is the most reliable.
EMG activity : Standard chin muscle should be used as one criterion for sleep-state identification.  When exploring respiration during sleep proper placement of the electrodes can also provide information regarding activity of glosso-pharyngeus muscles.
Limb movements, respiratory efforts can also be monitored by EMG activities recorded at limb, abdominal and intercostal levels
EKG, HR: Bipolar chest lead. When SaO2 is measured by pulse oximetry the measurement of the pulse wave form amplitude is a mean to control the validity of a desaturation event.
RESPIRATION: Both thoracic and abdominal movements, nasal and oral airflow  must be recorded, to allow the classification of apnea in their different types: central, obstructive or mixed.
Recording of respiratory effort: Chest efforts and abdominal efforts should be recorded on separate recording channels with either strain gauges, piezo electric crystal or respiratory inductive plethysmography (RIP). They should be calibrated in phase when the child is awake since the presence of out of phase movements during sleep, referred as paradoxical respiration, is an important criteria for suspecting partial or complete airway obstruction during sleep. Oesophageal pressure recording, which is commonly measured in adults, is rarely used in children. Pulse transit time is an indirect mean to evaluate respiratory efforts ; it has not been validated in children.
Airflow is recorded at nasal and oral level by  nasal transducer canulae and/or end tidal CO2.Thermistors are less sensitive although an oral thermistor is recommended when using a nasal pressure canulae.
Blood gases: blood gases are non invasively estimated with PACO2, SAO2 (by pulse oximetry) or transcutaneous techniques (tcp O2 or CO2 are used in infants). Because of the importance in children of prolonged partial airway obstruction and obstructive hypoventilation, PACO2 measurement of end tidal or alveolar CO2 which requires placing a small sampling catheter within the nostrils, is considered essential for assessment of obstructive sleep apnea syndrome in children.

Sleep scoring, arousal scoring

Four sources for scoring polygraphic recording are available in children: in premature infants the manual from Curzi and Mirmiran is a very useful tool ; after one year polygraphic recordings are scored, as in adult, according to Rechtschaffen and Kales criteria ; Anders’ manual is used in full- term children less than 6 weeks, from 6 weeks to one year modifications proposed by Guilleminault and Souquet are recommended.
In adults arousal is defined using standard criteria laid out by theAmerican Disorders Association (ASDA 1992). In children a modification of  adult’s criteria has been proposed by Mograss et al..
The problem of norms (References, Table 2, 3)
They are very few, the structure of sleep and normal values for respiration change with age.

References

Norms for sleep architecture

- Carskadon MA, Keenan SH, Dement WC. Nighttime sleep and daytime sleep tendency in preadolescents. In C Guilleminault ed. Sleep and its disorders in children. Raven press, New York, 1987 pp 43-52
- Carskadon MA, Dement WC. Sleepiness in normal adolescent. In C Guilleminault ed. Sleep and its disorders in children. Raven press, New York, 1987 pp 53-66.
- Challamel MJ, Debilly G, Leszczynski MC, Revol M. Sleep state development in Near-Miss Sudden Death infants. In Sudden Infant Death Syndrome: Risk factors and basic mechanisms. Eds RM Harper, JF Hoffman, PMA Publishing Corp 1984, 423-434.
-Coble PA, Kupfer DJ, Taska LS, Kane J. EEG sleep in normal healthy children; part 1: Findings using standard measurement methods ; scoring rules and examples. Sleep 1992, 2: 174-183.
- Curzi-Dascalova l, Challamel MJ. Neurophysiological basis of sleep development. In sleep and breathing in children : a developmental approach. Loughlin GM, Carrol JL, Marcus CL(eds) ; Marcel Dekker, New-York 2000  ;  chap 1 : 3-38
- Feinberg I, Korso RL, Heller N. EEG sleep patterns as a function of normal and pathological  aging in man; J Psychiat Rev 1967 5: 107-144.
- Goetz et al. EEG sleep of adolescents with major depression and normal controls Arch Gen Psychiatry 1987, 44: 61-68.
- Greenhill L et al. Sleep architecture and REM sleep measures in prepubertal children with Attention Deficit Disorder with hyperactivity. Sleep  1983, 6: 91-101.
-  Kahn A, Fisher C, Edwards A, Davis M. 24 h sleep patterns. A comparison between 2 to 3 year old and 4 to 6 year old children. Arch Gen Psychiatry 1973, 29: 380-385.
- Kohyama J, Shiiki T, Shimohira M, Hasegawa T. Asynchronous breathing during sleep. Arch Dis Child 2001 ; 84 : 174-177.
- Kotagal S, Goulding PM. The laboratory assessment of daytime sleepiness in childhood . J Clin Neurophysiol 1996, 13: 208-218.
-  Louis J, Cannard C, Bastuji H, Challamel MJ. Sleep ontogenesis revisited: A longitudinal 24-H home polygraphic study on 15 normal infants during the first two years of life. Sleep, 1997, 20: 223-233.
- Mograss MA, Ducharme FM, Brouillette RT. Movement/arousals. Description, classification, and relationship to sleep apnea in children. Am J Respir Crit Care Med 1994 ; 150 : 1690-1696.
- Navelet Y, d’Allest AM. Organisation du sommeil au cours de la croissance. In Pathologie respiratoire du sommeil du nourrisson et de l’enfant. Ed. C Gaultier. Ed Vigot 1989, pp 23-32.
- Palm l, Persson E, Elmquist D, Blennow G. Sleep and wakefulness in normal preadolescent children. Sleep, 1989, 12: 299-308.
- Palm L, Elmquist D, Blennow G; Automatic versus EEG sleep staging in preadolescent children. Sleep 1989, 12: 150-156.
- Ross JJ, Agnew HW, Williams RL, Webb WB. Sleep pattern in preadolescent children: An EEG-EOG study. Pediatrics, 1968, 42: 324_335.
- Scholle S, Zwacka G. Arousals and obstructive sleep apnea syndrome in children. Clin Neurophysiol 2001 ; 112 : 984-991.
- Serebrisky D, Cordero R, Mandeli J, Kattan M, Lamm C. Assessment of inspiratory flow limitation in children with sleep-disordered breathing by nasal cannula pressure transducer system. Pediatr Pulmonol 2002 ; 33 : 380-387.

Sleep scoring

- Anders T, Emde R et al. A manual of Standardized  Terminology: Techniques and criteria for scoring states of sleep and wakefulness in Newborn Infants; UCLA Brain Information Service/brain research Institute, Los Angeles, 1971.
- Carskadon MA, Dement WC, Mitler MM et al. Guidlines for the Multiple Sleep Latency Test (MSLT). A standard measure of sleepiness. Sleep 1986, 9 : 519-524.
- Curzi-Dascalova L, Mirmiran M. Manual of methods of recording and analysing sleep-wakefulness states in pre-term and full-term infants . INSERM ed, 1996, 162 pp.
- Guilleminault C, Souquet M. Sleep states and related pathology In R Korobkin and C Guilleminault Eds. Advance in perinatal neurology. New York, SP Medical and Scientific Books 1979, 2: 225-247.
- Lamblin MD, d’Allest M, André M, Challamel MJ, Curzi-Dascalova L de Giovanni E et al.  Monography on EEG in premature and full-term infants : developmental features and glossary. Neurophysiol Clin 1999 ; 29 : 123-219.
- Rechtschaffen A, Kales A, eds. A manual of standardized terminology, techniques, and scoring systems for sleep stages of human  subjects. Los Angeles: UCLA Brain Information Service/Brain Research Institute, 1968.

Respiration techniques and norms.

- Brouillette RT. Assessing cardiorespiratory function during sleep in infants and children. RC Beckerman, RT Brouillette, CE Hunt, Eds. Williams & Wilkins. Baltimore 1992, 125-141.
- Carroll JL, Loughlin GM. Diagnostic criteria for Obstructive sleep apnea syndromes in children. Pediatr Pulmonol 1992, 14: 71-74.
- Carroll JL, Loughlin GM. Obstructive Sleep apnea syndrome in infants and children: Diagnosis and management . In principles and practice of sleep medicine in the child; Eds R Ferber, M Kryger, WB Saunder, Philadelphia, 1995: 193-216.
- Lafontaine VM, Ducharme TM, Brouillette RT. Pulse oximetry : accuracy of methods of interpreting graphic summaries. Pediatric pulmonology 1996, 21 :121-131.
- Gaultier C, Praud JL, Canet E. Paradoxical rib cage motion during rapid-eye- movement sleep in infants and young children. J Dev Physiol 1987, 9: 391-397.
- Marcus CL, Omlin KJ, Basinski DJ, Bailey SL, Rachal AB, Von Pechmann WS, Keens TG, Davidson-Ward SL. Normal polysomnographic values for children and adolescents . Am Rev Respir Dis 1992, 146: 1235-1239.
- Standards and indications for cardiopulmonary sleep studies in children. American Thoracic Society. Am J Respir Crit Care Med 1996, 153: 866-878

Table 1 : calibration

PARAMETERS

DERIVATIONS

SENS/50 µVolt

TIME CST (LFF)

HFF

EEG

System 10-20

5-10 mm

0.3 sec. (0.5)

60-75 Hz

EMG

Chin

Intercostal, Abd.

Limbs

15-20 mm

Adaptable

Adaptable

0.05 sec. (5)

0.03 sec. (0.5)

0.03 sec.(0.5)

120 Hz

120 Hz

120 Hz

EOG

ROC/A1, A2

LOC/A1, A2

7,5-10 mm

0.3 sec. (0.5)

30-70 Hz

EKG

Bipolar, D1

Adaptable

0,1 sec.(1,5)

30 Hz

RESPIRATION

Naso-oral

Thorax, Abdomen

Thermistor,

End tidal CO2

Nasal Pressure

Strain gauges, Piezo, RIP.

Adaptable

Calibration

Adaptable

Adaptable

Adaptable

1 sec. (0.15)

DC

1 sec. (0.15)

1 sec. (0.15)

15 Hz

-

15 Hz

15 Hz

15 Hz

SaO2

Pulse oximetry

Calibration

DC

-

Table 2: Main steps in sleep wake maturation

Sleep wake cycle

·        Ultradian rhythm (3-4 hrs) during the fetal period and first days of  life.
·        Emergence of circadian rhythmicity during the first weeks of life
·        (free running cycle or irregular rhythms).
·        Entrainment to a 24 H cycle after 4 weeks.
·        Consolidation of nocturnal sleep from 6 months of age.
·        Disappearance of naps between 3 and 6 years of life.

Sleep structure

·        Emergence of AS/QS at 27w GA.
·        AS increases, IS decreases; cycle duration increases (40-45 to 55-60 min) at 34-35 w GA.
·        Emergence of sleep spindles  between 1.5 and 3 months.
·        Significant decrease in REMS with concomitant increase in NREMS; emergence of stages 1, 2 and 3-4 between 2 and 3 months.
·        Disappearance of REM sleep onset from 9 months.
·        Nycthemeral organization of SWS and REMS between 9 and 12 months.
·        Lengthening of the sleep cycle to adult level between 2 and 6 years.

Table 3 : Respiration, normal values

·         Obstructive Apnea Index > 3or 5 sec. <1.1/h TST
·         Max Pa CO2 <55 mmHg
·         Percentage of TST spent with PETCO2 >50 mmHg <10%
·         Percentage of TST spent with PETCO2 >45 mmHg <60%
·         Minimum SaO2 > 90%
·         Max delta SaO2 <8%
·         No Obstructive Apnea > 10 sec in children > 3 months
·         No Obstructive Apnea >15 sec in children < 3 months

(C Gaultier 1987, CL Marcus et al 1992)

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Page 13

Sleep disordered breathing in children: Recording techniques

Cinzia Castronovo (Italy)

Obstructive sleep apnea syndrome (OSAS) in childhood is a disorder of breathing during sleep characterized by prolonged partial upper airway obstruction and/or intermittent complete obstruction that disrupts normal ventilation during sleep and normal sleep patterns. A spectrum of severity related to the degree of upper airway resistance, to the duration of the disease, to the presence or absence of hypoxemia episodes, and to certain clinical features can be described. Symptomatic children may not fit the criteria for diagnostic establishment for OSAS in adults; age-specific standards are needed. Both anatomical factors that increase upper airway resistance (e.g. adenotonsillar hypertrophy, and functional processes that decrease upper airway tone (e.g. REM sleep) contribute to the pathogenesis of pediatric OSAS. Sequelae of OSAS in children include neurobehavioral abnormalities, problems of growth, and cor pulmonale. Both the history and physical examination should target the sleeping child; parents often report loud snoring, difficulty breathing, and obstructive apneas. The gold standard investigation to establish the diagnosis and to quantitative assess disease severity is overnight polysomnography. Home cardiopulmonary sleep studies have been shown to be an accurate and practical alternative to overnight laboratory polysomnography for routine evaluation of non-complex children with adenotonsillar hypertrophy. Children with documented severe OSAS are at increased post-operative risk for airway compromise and should be observed and monitored carefully. Adenotonsillectomy is the most common therapy for OSAS in children; as a second-line treatment, the use of nasal CPAP in children with OSAS has been very successful in experienced hands.Different methodologies for recording sleep disordered breathing in children can be used:1.      Asking the parents to obtain an audio or audio-visual tape of the child sleeping may prove to be an efficient means of observing the child asleep. Whether such recordings are representative or worst case data should be ascertained.2.      Portable devices (MesamIV, Polymesam)  and overnight oximetry3.      Diurnal PSG with at least 2.5 hours of sleep that have to include at least one REM period. 4.      For children with a history and/or physical examination suggestive of obstructive sleep apnea, the gold standard investigation for confirmation of both diagnosis and disease severity is overnight polysomnography (PSG). Studying children in this manner presents unique challenges. Skilled and experienced technicians are essential in order to win the cooperation and trust of young children. The laboratory settings must be soothing and non-threatening. A typical hospital sleep laboratory setting may frighten a child, thus preventing the technicians from obtaining even the most elementary set-up. Removing all non-essential hospital equipment from the immediate area, the display of colorful and interesting posters, diversion with favorite video shows and a relaxed, non-threatening approach to lead application all help to gain the cooperation of the child. Parents should be encouraged to bring favorite toys or items from home that may help to create normal bed-time routines in the sleep laboratory. We strongly recommend that a parent be required to stay with the child in the laboratory. The American Thoracic Society recently established standards and criteria far cardio­pulmonary sleep studies in children. These include measurements of respiratory movements, airflow, ventilation and oxygenation, sleep staging, electrocardiogram, electromyogram and audiovisual recording. Supervision by a trained technician is required throughout the study with additional record keeping of unusual event or behaviours during the night. Additional information regarding sleep positioning, snoring, and arousal frequency is easily obtained by adding videotaping during PSG. Unfortunately, few scientific data examining the correlation between PSG abnormalities, clinical symptoms, and sequelae of OSAS in children are currently available.The American Thoracic Society reccomended further investigation of abbreviated testing such as unattended home monitoring of oxygen saturation and respiratory pattern. In some countries as our (Italy) home cardiopulmonary sleep studies were shown to be an accurate and practical alternative to overnight laboratory polysomnography for routine evaluation of non-complex children with adenotonsillar hypertrophy that helps the diagnosis where only few labs perform laboratory PSG.

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Page 14

Insomnia in children: behavioral correlates and predicitive factors

Oliviero Bruni (Italy)

Maturational processes are involved in the consolidation of sleep and in the adaptation of the sleep-wake rhythms of the infants to the 24 hours cycle. These processes take place during the first months of life and are based on the interactions of several factors such as neurophysiological development, individual characteristics of the child, environmental influences. In the majority of children this process evolves smoothly, without crisis or abrupt steps. The children adapt their rhythms to the parental desired habits. However, in about 20-30% of children this process is longer, difficult and the child’s own rhythm tend to persist fighting with the parents’ attempts to regulate on appropriate schedule.The main manifestation of this unsuccessful adaptation is a disorders of initiating and maintaning sleep (DIMS) mainly represented by betdtime difficulties and/or recurring night wakings in a more or less cyclic manner. These disorders represent the most frequent request for consultation in pediatric sleep clinics, with a prevalence of 30% in the general population during the first three years of life:awakenings are reported in about 30% of 1-3 years old children, and both awakenings and bedtime resistance accounted for 23% of 2-3 year- old children (Ottaviano et al., 1996). Several reports showed that poor sleepers’ preschool children had a very high rate of behavior problems (55% estimated from Richman, 1982). However, the correlation between sleep disturbances and behavior is still not well clarified and the influence of parenting style on sleep behavior is not yet established. In a group of 114 males (59%) and 80 females (41%) with a mean age 27 months (range 22-38 months, we evaluated the relationships between night awakenings, bedtime resistance and/or sleep problems with daytime behavior disturbances (evaluated by Child Behavior Checklist 2/3 – CBCL 2/3; Achenbach, 1992) and parenting style, since the parental behavior has been concerned as a predisposing factor in developing early sleep problems. We analyzed the differences in daytime behavior between nightwakers without bedtime problems (40 s..= 20.62%) and bedtime resistance children without awakenings (36 ch.= 18.56%) and a group of children without sleep problems (118 ch.=60.82%). Nightwakers showed significant differences vs. controls on the following CBCL scales: Somatization (54.70 vs. 52.16; p < 0.01); Externalizing (52.43 vs. 48.98; p < 0.05) and Total (52.33 vs. 48.71; p < 0.01). Bedtime resistance children showed differences on Withdrawal (52.97 vs. 51.30; p < 0.05) and Somatization (54.31 vs. 52.16; p < 0.05). Bedtime resistance children showed a higher value of negative parental self-esteem (16.03 vs. 13.36; p < 0.01) while no differences have been found in nightwakers.These findings demonstrated that these two sleep disturbances, although often associated, if isolated, form two distinct entities either as sleep disturbances or as behavioral style. Bedtime resistance is often a matter of mother-infant relationship and the parenting style (higher negative parental self-esteem in this group of children) could influence the transition between wake and sleep; the parenting style could lead to the development of a behavior in the internalizing direction (more anxiety and withdrawal).On the other hand, awakenings, seemed to be more “genetically determined” and the resulting sleep fragmentation could lead to serious behavioral disturbances, in the direction of externalization. However, if we considered the two disorders together, as in the group of poor sleepers, we found an association with overall behavior problems and not with a specific behavior disorder, confirming data reported by Richman (1982).The observations that children with early sleep disturbances presented multiple sleep disorders at later ages (Salzarulo and Chevalier, 1983) and that sleep disorders persisted after 3 years in 84% of cases (Kataria et al., 1987) and in 75% after 5 years (Richman, 1982) support the hypothesis of a primary effect of sleep disorders on behavior. In a study on predictive value of behaviors at 3 years, Abe et al. (1982) found that sleep disturbances were of the most persistent group. These relationships between early waking-sleeping rhythm disturbances and later sleep problems indicated a continuity of the sleep-disturbed behavior. Several studies attempted to evaluate the predictors of sleep disorders in school age children; a wide range of possible causes of sleep disturbance have been reported by Pollock (1994) that showed that a large number of factors were significantly associated with disturbed sleep: maternal age at child's birth, West Indian and African origin, method of delivery, writing problems, and previous attendance at child guidance services. Most research identified predisposing factors for sleep disorders in infancy and children, leading often to contradictory results: no association with socio-economic status has been found in several studies (Zuckerman et al., 1988; Bernal, 1973; Moore and Ucko, 1957) while a British study found a difference in terms of ethnic origin (Rona et al., 1998). Breast-feeding has been reported by some Authors as contributing factor to sleep disorders (Carey, 1975) but not confirmed by others (Weissbluth et al., 1984). Most studies have failed to find a relationship between gender and sleeping pattern (Anders and Keener, 1985). Perinatal factors have been found to be more prevalent in sleep-disordered children by Bernal (1983) and Moore and Ucko (1957), not confimed by Anders and Keener (1985). The role of parents in determining or in enforcing the disorders of initiating and maintaining sleep has not been yet established; different family dynamics as well as different kind of mother-child relationship and quality of attachment could be involved in nocturnal awakenings and in bedtime difficulties. (Kahn et al., 1989). The absence of specific somatic or mental disorders in children with both early and later sleep disturbances (Salzarulo and Chevalier, 1983) suggested that probably other variables (i.e. genetic, neurobiological substrate) could affect sleep behavior and disturbances. In a recent study we evaluated the influence of biological and historical and clinical factors on the different aspect of sleep behavior and disturbances evaluated through the Sleep Disturbance Scale for Children (SDSC) (Bruni et al., 1996) in school-age children (Bruni et al., 2000).We found that the presence of early sleep-wake rhythm disorders and of familiarity for sleep disorders was the most significant factors influencing the persistence and/or the appearance of sleep disorders in school age children indicating that a continuity of sleep disorders exists and emphasizing the importance of the genetic substrate. The problem of genetic predisposition has been raised from other studies in which preadolescents had similar prevalence of sleep disturbances as their parents and had had problems in initiating and maintaining sleep since infancy  (Kahn et al., 1989). Regarding the specific aspect of insomnia (analyzing the DIMS-SDSC subscale), our results futher supported the importance of the genetic substrate showing that, early sleep disorders and parents’ sleep disorders had significant main effects on disorders of initiating and maintaining sleep.Sleep disorders tend to persist because, although nighttime behavior disorders are the most common reported problem in children, only 2% of parents expressed a lot of concern about these (Stallard, 1993), with the consequence that they are not recognized and treated. It should be therefore emphasized that the accurate evaluation and early treatment are important in order to prevent the development of behavioral problems that could affect the quality of life of the children and of their parents.

References

Abe K; Ohta M; Amatomi M; Oda N. Persistence and predictive value of behaviours of 3-year-olds. A follow-up study at 8 years. Acta Paedopsychiatr, 1982, 48:185-191
Anders TF, Keener MA. Developmental courses of night-time sleep-wake patterns in full-term and premature infants during the first year of life I. Sleep 1985; 8:173-192
Bernal F. Night waking in infancy during the first 14 months. Dev Med Child Neurol 1973, 15:760-769
Bruni O, Ottaviano S, Guidetti V, Romoli M, Innocenzi M. The sleep disturbance Scale for children. Construction and validation of an instrument to evaluate sleep disturbances in childhood and adolescence. J Sleep Res 1996; 5:251-261
Bruni O, Verrillo E, Miano S and Ottaviano S. Clinical and historical predictors of sleep disturbances in school-age children. Sleep and Hypnosis, 4:147-151, 2000
Carey W. Sleep and breast feeding. J Pediatr, 1975; 87:327
Kahn A, Van de Merckt C, Rebuffat E, Mozin MJ, Sottiaux M, Blum D, Hennart P. Sleep problems in healthy preadolescents. Pediatrics, 1989; 84:542-546
Kataria S, Swanson M S, Trevanthan G E: Persistence of sleep disturbances in preschool children. J Dev Behav Pediatr, 1987, 8: 642-646
Moore T and Ucko LE. Night waking in early infancy. Arch. Dis Child, 1957; 32:333-342
Ottaviano S, Giannotti F, Cortesi F, Bruni O, Ottaviano C. Sleep characteristics in healthy children from birth to 6 years of age in the urban area of Rome. Sleep 19 (1):1-3, 1996
Pollock JI. Night-waking at five years of age:predictors and prognosis. J Child Psychol Psychiat, 1994; 35:699-708,
Richman N, Stevenson J, Graham P. Preschool to school: a behavioral study. London Academic, 1982
Rona RJ, Li L, Gulliford MC, Chinn S. Disturbed sleep: effects of sociocultural factors and illness. Arch Dis Child, 1998; 78:20-25
Salzarulo P, Chevalier A: Sleep problem in children and their relation ship with early disturbance of the waking-sleeping rhitms. Sleep, 1983, 6: 47-51,.
Stallard P. The behaviour of 3-year-old children: prevalence and parental perception of problem behaviour: a research note. J Child Psychol Psychiatry, 1993, 34: 413-421
Weissbluth M, Davis AT, Poncher J. Night waking in 4- to 8-month old infants. J Pediatr, 1984; 104:477-480
Zuckermann B, Stevenson J, and Bailey V. Sleep probloems in early childhood: continuities and predictive factors and behavioral correlates. Pediatrics 1988; 80:664-671

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Page 15

Parasomnias in children

Marco Zucconi (Italy)

Parasomnias emerging from NREM sleep such as sleep walking, sleep terrors and confusional arousals are considered arousal disorders. Nocturnal video-polysomnography is the gold standard to diagnose and differentiate parasomnias from other arousals with atypical motor behaviors such as nocturnal frontal lobe epilepsy (NFLE), a recent form of nocturnal seizures with prominent dystonic-dyskinetic components, in some cases genetic, identified by means of detailed video-analysis of movements during sleep.

Clinical picture of parasomnias (onset in early childhood, rare episodes of long duration, absence of stereotypy, general disappearance after puberty) is different from NFLE (start in the second decade, frequent complex and repetitive behaviors, short duration excluding rare prolonged seizures, nocturnal agitation, sometimes daytime complaints such as fatigue or sleepiness, persistence into adulthood).

Classical sleep parameters are similar to controls whilst microstructure analysis shows sleep instability and arousals fluctuation in parasomnias and NFLE.

Also in children, at least in our experience, the differential diagnosis between the two disorders is difficult and require one or more nocturnal complete video-polygraphic recording. In any case the diagnosis of NFLE should be considered in children with nocturnal motor episodes or nocturnal motor agitation, when the attacks persist; this diagnosis is probably more frequent than expected.

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Page 16

Sleep recording; THE SIGNIFICANCE OF IN BETWEEN NAPPING IN THE MULTIPLE SLEEP LATENCY TEST

Ambulatory vs. Clinical recordings

MMR Verhelst (The Netherlands)

The Netherlands – Belgium – Italy : differences in methods

Introduction.

The diagnosis of hypersomnolence- and excessive daytime sleepiness is difficult. The Multiple Sleep Latency Test (MSLtest) is often considered to be the ‘golden standard’ for this matter. However the MSLtest has some considerable limitations. For example: no information about napping in between the test periods is available. Up to now no research was done to evaluate the influence of  ‘internapping’ on the Msltest results. In our sleep laboratory all patients with excessive somnolence complaints (not only narcoleptics)  undergo both a MSLtest and an Ambulatory PolySomnoGraphy in order to capture naps in between the test periods. In this retrospective study we determined the importance of ‘internapping’.

Materials and Methods.

The records of 34 patients (20 men, 14 women, age 18-69 yrs., mean age 39 yrs.), were screened.For the MSLtest patients were instructed to attempt to sleep at 4 fixed times a day: at 9:00, 11:00, 13:00 and 15:00 hours. Between the test periods patients stayed at the neurology department and were told not to sleep.

Results.

The MSLtest was positive (MSL+), mean sleep latency less or equal 5 minutes, in 13 patients and negative (MSL-), mean sleep latency more than 5 minutes, in 21 patients. 4 of the 13 MSL+ patients slept between the test periods (30%) versus 4 of the 21 MSL- patients (19 %) (table 1). The number of naps is depicted in table 1. Remarkably most of the naps occurred between 12:00 and 14:30 hours. Only 2 patients showed a nap outside this time frame. The mean sleep time of the naps was 15 minutes, ranging from 5–40 minutes. Only 1 nap had REM sleep, found by a MSL+ patient without Sleep Onset REM Periods. No clear relation could be found between REM periods in the MSLtest and in the naps between.

Table 1

  

Discussion and conclusions.

The results show that only a minority of the patients, 30% in the MSLtest+ group versus 19% in the MSLtest- group, napped between the test periods. The time of occurrence of the ‘internapping’ probably reflects a natural siesta tendency in combination with high sleep pressure or may even be independent from this sleep pressure. In this review, the influence of ‘internapping’ is difficult to estimate but is certainly not negligible. Additional Ambulant PolySomnoGraphy during the test periods in is recommended to get a complete picture of sleep propensity and to avoid false negative MSLtest results.

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Page 17

Diagnosis and treatment of sleep related breathing disorders in Iceland

Bryndís S. Halldórsdóttir, RN, Bsc., Thorbjörg Sóley Ingadóttir, RN, Bsc.



Diagnosis and treatment of sleep related breathing disorders in Iceland began in 1987 at the Pulmonary Department of Vifilsstadir Hospital. It started with one bed and only rudimentary equipment. Because of increasing demand for diagnosis and treatment in recent years, and limited resources to meet those demands, special emphasis has been on ambulatory studies.
Most patients using home ventilators are diagnosed through ambulatory studies and auto-titrated ambulatory. Treatment-control studies can also be done ambulatory. All patients who undergo an ambulatory study are thoroughly trained by skilled personnel. Currently the pulmonary department has capacity for 3 fully attended Polysomnography (PSG) studies, 1 ambulatory PSG, 4 portable [sleep apnea] diagnostic systems (PDS) and 15 auto-titrating ventilators. In addition other organizations own 6 PDS. As of May 1st, 1158 CPAP and BiPAP patients are being treated by the Pulmonary Department and around 12 patients start CPAP treatment every week.

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Page 18

Sleep service provision in the UK

Simone de Lacy (St. Thomas’ Hospital, London)

Introduction

The number of sleep centres in the UK would appear to be increasing but there are, as yet, no guidelines or recommendations as to what they can and should offer. On behalf of the British Sleep Society, a survey was designed and mailed to all establishments that were thought to provide sleep disorder investigation of some description in the UK.

The aim of this survey was to:

  • Identify the nature and location of the UK’s Sleep Centres
    From this, work could then begin on:
  • Improving networking between centres
  • Identifying training and education needs
  • Developing a united/structured approach to service delivery
  • Directing referrals to appropriate centres

Method

The survey requested information on the following:

  • Affiliation
  • Clinical features
  • Clinical services
  • Speciality
  • Referrals
  • Treatments offered
  • Staffing

281 surveys were sent out, and approximately 65% returned, some explaining that did not or no longer have a sleep centre (~10%)

Results


             Clinical or Research?                                      Specialty Affiliation?:

 

Results Continued…

NHS or Private?:                                        No. Dedicated Sleep Beds/Centre?:

Sleep Services Offered:

Sleep Disorders Investigated:

% Total Workload % Total Workload

No. Units

Adult

Paediatric

Snoring

113

34.9

4.3

OSA

113

38

5.0

Hypersomnia

68

3.7

0.4

Insomnia

35

3.5

1.3

Parasomnia

48

3.1

0.4

Seizure

32

3.0

0.8

Others

40

4.2

2.1

Referral Source:

Results Continued…

Categories of Sleep Centre in the UK

Conclusions

  • There are now >130 Sleep Service Providers in the UK
  • The Range of Facilities, Equipment, Sleep Disorders Investigated that Currently Constitute a “Sleep Service” is highly variable
  • The Majority of UK Sleep Centres are Affiliated to Respiratory Medicine

The future:

  • Maintain & up-date Sleep Survey Database
  • Establish ‘Working Groups’ to Draw-up Protocols for United Approach to Sleep Disorder Management
  • Support Staff Education and Training Programmes
  • Notify Referral Sources of nearest, Appropriate Sleep Service Provider

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Page 19

CPAP attribution in different countries

Ann Ryckx (Montana, Switzerland)

The methods used to prescribe CPAP for patients with obstructive sleep apnoea syndrome have been compared, using the replies to a questionnaire sent to sleep-technicians and distributors of CPAP equipment in 17 (16) countries. Austria, Germany, Switzerland, Netherlands, Belgium, Luxemburg, Italy, France, United Kingdom, Finland, Greece, Turkey, Poland, Israel, Japan, China, (Hongkong).  The results have to be read with caution, particularly as in one country, contradicting  replies were given.For the diagnosis of sleepapnea syndrome, the UK only seldom performs a full polysomnography, six countries (CH, Ne, It, Fr, Fin, Gr) also allow diagnosis by polygraphy, three by oximetry (CH, UK, Fin), and three by reference only to the patient’s history and the Epworth Sleepiness Scale (UK, Fin, Pol).  The technique of AutoCPAP to decide the therapeutic CPAP-pressure is performed in ten countries.  In five countries CPAP pressure is only decided after manual titration under full polysomnographic control (Au, Ge, Lu, Chi, Is).  In five countries pressure titration can also be performed at the patient’s home (CH, Ne, Fr, Gr, Pol).In seven countries CPAP is given to patients with an AHI > 15/h (1:30/h), while in four, the limit is fixed by AHI > 10/h.  In eight countries CPAP is allowed for symptomatic patients with lower AHI.In only three countries does a private insurer decide on the type of CPAP machine.  One has the impression that public health authorities  do not prescribe strict limitations for CPAP treatment.  In some countries CPAP is state funded (UK, Finland & Japan).The management of CPAP treatment is mostly in the hands of the existing sleep laboratories which can lead to an important accumulation of the number of patients  (new + control) and, regrettably, less CPAP-compliance control.   In only a few countries compliance controls are organised.  Eight countries perform check-ups  after 3 months, two after 6 months, four only after 1 year, while in one country, compliance control is only carried out occasionally.  In fifteen out of seventeen countries, full polysomnography can be performed to control the efficacy of treatment.The UK adopts a very pragmatic approach to OSAS and CPAP treatment with diagnosis being based on patient history, clinical examination and the Epworth Sleepiness Scale and pressure titration being performed with oximetry control;  therapy evaluation is used as appropriate to each patient’s needs (from history and ESS to full polysomnography with MSLT).From China, the reply to the questionnaire was quite impressive; social security does not consider CPAP therapy for OSAS.  Out of ten patients, only one to two are treated by CPAP (financed by the patient) and six to eight are treated with surgery (UPPP or radio-frequency, even performed by pulmonologists), despite high AHI levels (>40/h).  Further research on the Web gave me the practices for  CPAP management in the USA, Australia and Germany and.  In the USA, the national coverage policy for CPAP, as set out in 1986 stipulated that OSAS can be diagnosed after a recorded history of at least 30 episodes of apnoea, each lasting a minimum of 10 seconds, during 6 to 7 hours of recorded sleep.  However following a proposal from the AASM (American Association of Sleep Medicine) in 2000, the Health Care Financing Administration decided on a new coverage policy, which was published recently, on the 5th November 2001. In summary:The gist of the new policy is that CPAP will be covered under the Medicare Programme in adult patients with OSA if either of the following criteria is met:1.      AHI> 152.      AHI> 5 and < 14 with documented symptoms of excessive daytime sleepiness, impaired cognition, mood disorders or insomnia, or documented hypertension, ischemic heart disease or history of stroke The AHI is equal to the average number of episodes of apnoea and hypopnea per hour and must be based on a minimum of 2 hours sleep recorded by polysomnography. Apnoea is defined as a cessation of airflow for at least 10 seconds.  Hypopnea is defined as an abnormal respiratory event lasting at least 10 seconds with at least 30% reduction in thoracoabdominal movement or airflow as compared to baseline, and with at least a 4% oxygen desaturation.The latest (found on the Web) policy for Australia (1993) concluded that CPAP therapy is an efficacious technique for preventing or greatly reducing the number of obstructive apnoeas and alleviating the symptoms of OSAS; and is the treatment of choice for OSAS, with only minor side effects; and there is need of a follow-up to optimise patient compliance.  The AHTAC (Australian Health Technology Advisory Committee) found CPAP should be readily available to patients with severe OSAS, but did not see any justification for provision of CPAP treatment in milder cases.On the Australian lungnet Website I found that nowadays in some states there may be a subsidy for CPAP treatment, and some health insurance companies may assist with the cost of a machine.An interesting German publication of a cost/benefit study concluded that CPAP treatment is an efficacious technique.  Obstructive sleepapnoea  syndrome must be based on sleep recording by full polysomnographic study, CPAP pressure is to be decided after manual titration under polysomnographic control; Diagnosis and treatment adjustment take several days in stationary conditions.

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