Journal of Psychophysiology,
10 (1990) 181-184
in sleep apnoea presenting episodic phenomena
B. van Sweden ‘, B. Kemp lT2,J.G. van Dijk ’ and H.A.C. Kamphuisen’.2 ’ Department of Clinical Neurophysiologv, and 2 Centre for Sleep Disorders and Chronohiologv, Leiden Umuersiiy Medical Centre (The Netherlands) (Accepted
Key words: REM-dependent
25 June 1990)
Episodic nocturnal phenomena represent a separate cluster of disturbances within the classification of sleep disorders. The reported case history covers paroxysmal signs occurring secondary to a REM-dependent mixed sleep apnoea syndrome. The pathophysiology of similar episodes in elderly (non-)epileptic patients is discussed. Ambulatory monitoring is an appropriate technique for investigation if respiratory and motor activity, and EEG and ECG are recorded simultaneously.
The delineation of nocturnal episodic disturbances in adults and/or the elderly without overt psychopathology mainly includes epilepsy and the parasomnias (Liihdorf et al., 1986; Schenck et al., 1986). As the precise nature of these transient clinical phenomena may be difficult to define, a systematic work-up including long-term EEG-monitoring is usually indicated. We present a case in which sleep apnoea and the associated hemodynamic alterations may have played a major role. A 56-year-old postmenopausal, overweight woman (body-mass index: 44.7), with no history of epilepsy, presented with a nocturnal paroxysmal episode consisting of generalized motor phenomena followed by mental clouding. Neurological, EEG and neuroradiological investigation, including CT-scan, were normal except for bilateral achilles tendon areflexia. The last 2 years the
Partly supported by the Stichting Phoenix, Schiedam, The Netherlands. Correspondence: B. van Sweden, Dept. Clin. Neurophysiology, Leiden University Medical Centre, Rijnsburgerweg 10, 2333 AA Leiden, The Netherlands.
0 1990 Elsevier Science Publishers
patient had developed hypertension (230/140) and diabetes mellitus which was treated with tolbutan-ride. As the patient also had a prominent snoring problem for many years, a sleep apnoea syndrome was suspected, although she had no complaints of excessive daytime sleepiness. For screening purposes we performed an ambulatory 24-h polygraphic cassette recording covering continuous registration of 2 EEG derivations (Fpz-Cz and Pz-Oz), 1 EOG channel (recording horizontal eye-movements) submental muscle tone, and respiration monitored with a nasal/oral airflow thermistor (Kemp, 1987). Sleep visually scored according to Rechtschaffen and Kales criteria, was characterized by a low REM percentage (12%), a shallow non-REM (NREM) pattern, showing almost no deep sleep, spread over 2 long sleep cycles (k 180 min) (Fig. 1A). The 24-h home recording showed some degree of EDS (stage 1 = 40 min), unnoticed by the patient. REM sleep moreover showed a continuous periodic breathing pattern with an interval of 40-50 s (AI-TST = 9, AI REM = 70) absent in NREM sleep (Fig. 2). A more extensive repeat polygraphic sleep recording in the laboratory covered a split
0, saturation was recorded at the fingertip by means of a Nellcor oximeter indicating a mean SaO, every 5 s. The resulting hypnogram showed comparable features with the home-recording, with the exception that as an adaptation effect, sleep onset was delayed in the laboratory (Fig. 1B). Respiratory dysfunction was once again exclusively REM-dependent showing a prominent cyclical breathing pattern (AI-TST = 5.5, AI-REM = 66). Apnoea episodes had initially a central nature but evolved to an obstructive event (Fig. 3). Resumption of respiratory efforts was most often associated with REM clusters. Every mixed apnoea episode ended with a generalized electroencephalographic arousal reaction, not disrupting REM sleep, O2 saturation remaining rather constant throughout NREM sleep ( + 95%). Each REM episode also exhibited a periodic desaturation pattern (*70%) showing a prominent 40-50 s interval (Fig. 1B). O2 desaturation was associated with cardiac brady/ arhythmia and sinus pauses lasting 334 s documenting a cyclical heart variation (Fig. 3). Thus a repetitive periodic pattern regarding respiration, cardiac pacing, 0, desaturation and REM bursting was repeated throughout both REM episodes and the diagnosis of a REM-dependent mixed sleep apnoea syndrome was put forward. As all weight reduction regimens failed. the patient was operated on (uvulopaletopharyngoplasty. U.P.P.) and no further attacks occurred.
30 70 I
* 10 min
Fig. 1. Sleep characteristics in the home (A) versus the laboratory recording (B). Both recordings show only 2 sleep cycles, a comparable REM percentage ( + 12%) and first cycle duration (i 180 min). In the home recording the second cycle is interrupted by nocturia and sleep onset is delayed in the laboratory. 0, saturation in REM sleep shows a periodic pattern exhibiting a 40-50 s interval desaturation.
screen video recording, 4 EEG derivations (FpzGz/ Pz-Oz/ C4-Al/ Pz-03) EMG, EOG and respiratory monitoring with thoracic and abdominal strain gauges and a nasal/oral airflow thermistor.
2 STAGE 2
Fig. 2. This illustrates a 5 min compressed display of respiration, EOG and EEG recorded on cassette-tape. At stage 2, NREM respiratory effects are regular; at stage REM breathing shows a cyclical pattern with a 40-50 s interval. Also note the conjunction of apnoea and REM clusters.
Fig. 3. This figure depicts two consecutive apnoea episodes (50 s/30 s), the periodic heart variation and brady/arrhythmia. episode initially shows a central nature and as respiratory movements resume (associated with REM) the apnoea evolves obstructive hypopnoea, probably related to the obvious REM-state-dependent muscle atonia.
Episodic sleep phenomena are usually presented as a separate cluster of sleep disturbances (Parkes, 1986; ASDA, 1990). Paroxysmal motor/ mental signs are not an essential clinical feature of the sleep apnoea syndrome, although occasionally mentioned in the literature (Houdart et al., 1960, Guilleminault, 1983). The pathophysiology underlying these symptoms often remains unclear. In epileptic patients dyssomnia associated with sleep deprivation is emphasized (Kryger et al., 1974; Wyler and Weymuller, 1981). In spite of the arteriosclerotic stigmatization, including aspecific EEG-alterations present in many apnoeic patients, these signs do not prove ‘vascular’ epilepsy, a controversial entity (Higashitami et al., 1988). In non-epileptic patients, anoxic attacks provoked by severe hypoxia have been documented (Cirignotta et al., 1989). In the reported case clinical symptoms suggest, and polygraphic data document, a REM-dependent mixed sleep apnoea syndrome and our patient most likely suffered an occasional
Each to an
anoxic cerebral seizure induced by the 0, desaturation-dependent, cardiac bradyarrhythmia (Gastaut, 1974). Episodic sleep phenomena may be a secondary sign of other sleep disorders. In the investigation of nocturnal episodic phenomena, cardiac and respiratory parameters are often omitted; neither does the modified respitrace Medilog System used in conventional ambulatory apnoea screening allow EEG/ECG evaluation (Ancoli-Israel, 1989). In clinical practice the REM-dependent occurrence and ECG dysfunction could easily have been missed. In REM-dependent apnoea syndrome, a subtype rarely mentioned (Guilleminault et al., 1977) the remarkable cyclical variation of REM clusters is comparable to the previously reported cyclical heart rate variation (Guilleminault et al., 1984). An association between activity in the respiratory neurons and phasic REM events such as P.G.O. spikes, has been documented in animal experiments (Orem, 1980). Our case report stresses the
need to record respiratory and EEG/EOG/ECG variables simultaneously in elderly patients presenting with episodic nocturnal clinical phenomena.
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