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Further observations on sleep abnormalities in Kleine-Levin syndrome: Abnormal breathing pattern during sleep
98
glectroencephalography and Clinical Neurophysiology, 1981, 5 2 : 9 8 - - 1 0 1 Elsevier/North-Holland Scientific Publishers, Ltd.
Clinical note FURTHER OBSERVATIONS ON SLEEP ABNORMALITIES ABNORMAL BREATHING PATTERN DURING SLEEP
IN KLEINE-LEVIN
SYNDROME:
P. LAVIE a,1 E. KLEIN b, N. GADOTH c E. BENTAL d, j. ZOMER a, M. BECHAR c and J. WAJSBORT e
a Sleep Laboratory, Faculty o f Medicine, Technion-Israel Institute o f Technology, Itaifa; b Department o f Psychiatry, R A M B A M University Hospital, Haifa; c Department of Neurology, Beilinson Medical Center, Petach-Tiqva and the Sackler School o f Medicine, Tel-Aviv University, Tel-Aviv; d Department o f Neurology, R A M B A M University Hospital, Haifa; e Linn Clinic, Haifa (Israel) (Accepted for publication: March 24, 1981)
Periodic hypersomnia associated with hyperphagia and abnormal behaviour were termed by Critchley (1962) the Kleine-Levin syndrome (KLS). In this peculiar, not fully understood, syndrome, affecting mainly adolescent males, polygraphic sleep recording revealed alterations in the structure of sleep. A variety of changes have been reported, such as sleep onset REM periods (Wilkus and Chiles 1975; Lavie et al. 1979), decrease in stages 3--4 and in REM sleep (Messimy et al. 1967; Takahashi 1967; Barontini and Zappoli 1968), and frequent interruptions of REM sleep by sleep stage 2 and intrusion of alpha activity (Lavie et al. 1979). In one report only, breathing abnormalities during sleep have been documented (Vardi et al. 1978). In this single case report periodic apnoea with paroxysmal EEG activity was found during somnolent attacks; however, no apnoeic spells were seen during nocturnal sleep. The type of apnoea could not be specified as respiratory monitoring was not performed. We wish to describe abnormal breathing patterns during nocturnal sleep in 4 patients with the KLs. In two boys and two adult males we documented periodic breathing, hypopnoeic episodes and sleep apnoea during hypersomnolent attacks as well as during asymptomatic 'normal' periods.
Case histories
Patient 1 A 16-year-old male had the classical features of KLS since the age of 10 years. Approximately 3 times annually he became gradually sleepy during daytime, showed excessive craving for sweets and bizarre 1 Correspondence and reprints: Dr. Peretz Lavie, Ph.D., Sleep Laboratory, Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
behaviour with hypersexual tendencies. Each attack lasted for 3 weeks, 10 days of which he spent in bed, sleeping. Repeated neurological evaluations during and between attacks, extensive laboratory and endocrine studies, including several EEGs, cerebrospinal fluid analysis and brain scans were all normal. Whole night polygraphic sleep recording, but without respiratory monitoring, was performed twice during one of his attacks and the results were previously reported in detail (Lavie et al. 1979). The abnormal findings included increased amounts of body movement associated with midsleep awakenings. These were present to a lesser extent also durin~ a non-somnolent so-called 'normal' period. The present data were obtained about a year following his last sleep recording, about 8 months after his last somnolent attack ('normal period') and then during his subsequent somnolent attack about a month later. During the 'normal' period his sleepwaking cycle was unremarkable, although some difficulties of waking him up in the morning were reported by his parents.
Patienl 2 A 15-year-old boy had the classical features of KLS since age 12. During this period he suffered from 4 attacks of excessive daytime sleep following febrile illnesses and associated with bizarre behaviour causing two psychiatric hospitalizations. During a third hospitalization, because of a 'psychotic state', hyperphagia and intense hypersexuality preceded by 2 weeks of hypersomnia, the diagnosis of KLS was finally reached. It is to note that he was born after a traumatic labor and was diagnosed as suffering from minimal brain dysfunction at the age of 8 years. Repeated routine blood tests, metabolic screening, EEG recording and neurological evaluations were all unremarkable. Three whole night recordings were made. The first
0013-4649/81/0000--0000/$02.50 © Elsevier/North-Holland Scientific Publishers, Ltd.
BREATHING PATTERN IN KLEINE-LEVIN SYNDROME
99
was done a month following a sleep attack when he was on 200 mg chlorpromazine (CPZ) daily. The second was obtained 2 months later when he received only 50 mg of CPZ daily, and the third recording was obtained a month following discontinuation of CPZ.
Increased appetite was noticed towards the end of some but not all of his hypersomnolent attacks. He was recorded in the laboratory during an asymptomatic period, about a year and a half after the last attack.
Patient
Results
3
A 20-year-old male was healthy until the age of 15. At that time (June 1975) he was involved in a strenuous physical effort for 3 days, followed by excessive daytime sleepiness, and abnormal behaviour lasting for 10 days. In September 1975, following a febrile illness, he had a second attack which lasted for 10 days. Another attack in 1976 was accompanied by hypersexual tendencies and excessive masturbation. In 1979 he had two attacks, each lasting 10 days, and two additional attacks in 1980 during which marked hyperphagia was also present. He was recorded in the laboratory during the second attack in 1980. Patient
4
A 37-year-old male was evaluated for severe diurnal fatigue. He was in perfect health until the age of 10. At that time he was involved in strenuous physical effort for several days followed b~y excessive daytime sleep, abnormal behaviour and poorly defined non-localized headaches. This lasted for a whole week and since then similar 'attacks' recurred yearly until the age of 30. After 5 quiet years he had another somnolent period at the age of 35, lasting for 6 days.
gf$P.
. . . . . . . . . . . .
Common abnormal breathing patterns during sleep were present in the records from all 4 patients. Most prevalent was pronounced periodic breathing during sleep stages 1 and 2, which was not limited to the first non-REM period but appeared throughout the night. Periods of hypopnoea lasting several respiratory cycles alternated with hyperpnoea associated with a brief arousal response. Most arousals were heralded by the appearance of one or several consecutive K complexes, or a burst of large amplitude delta activity followed by a tail of alpha waves (K-alpha complexes) and on many occasions body movements (Figs. I and 2). There were also longer periods of arousal lasting 5--15 rain. Isolated hypopnoeic episodes, containing diminished respiratory drive, terminated by K complexes with a tail of alpha activity and body movements, were found in sleep stage 2 throughout the sleep period. There was no difference in the prevalence of abnormal breathing episodes between the records during the symptomatic and asymptomatic periods obtained from patient 2. The number of microarousals (K-alpha and alpha-delta bursts) exceeded 150 in each of the whole night records.
.
. . .
. ..... . .
FLOW
Fig. 1. A pattern of pronounced periodic breathing associated with K-alpha complexes (indicated by dots) in sleep stage 2 in patient 3. RESP, respiratory belt; FLOW, air flow measured by nostril thermistor.
100
P. LAVIE ET AL• EEG
Discussion Our results add an additional aspect to the sleep abnormality in KLS. It is clearly shown that a breathing disorder during sleep is a characteristic feature in our patients with KLS during both somnolent and non-somnolent periods; one patient was recorded during both, one patient only during a somnolent period and two patients only during non-somnolent periods. Somewhat identical to Vardi et al. (1978) we found pronounced periodic breathing and hypopnoeic episodes in 3 patients and a full blown central sleep apnoea in one patient. There was no difference, however, between the type and severity of breathing disorders in sleep between the records done during the somnolent and non-somnolent periods. This precludes the possibility that the somnolent attack resulted from changes in the severity of the breathing disorders in sleep. Our previous findings (Lavie et al. 1 9 7 9 ) o f an increased number of body movements in sleep and repeated intrusions of alpha activity into sleep stage 2 can be interpreted now as related to the nocturnal abnormal breathing pattern. These findings suggest that nocturnal breathing should be monitored in every patient with KLS. Periodic breathing during the stages of light sleep (1 and 2), which may include brief periods of hypopnoea or apnoea, are common, particularly in persons older than 40--45 years. This type of breathing pattern was attributed to central hypoexcitability associated with changing from the 'awake' to the 'asleep' stages (e.g., Bulow and Ingvar 1961; Lugaresi et al. 1972). We suggest that in KLS there is a general decrement in nervous system excitation which affects both the symptomatic and asymptomatic periods•
RESP
<.
, 72
Fig. 2. Representative sample of K complexes followed by a tail of alpha activity (K-alpha complex) associated with hypopnoeas in patient 3. EEG was recorded from CzP z. Calibration refers to EEG (horizontal bar: 2 sec; vertical bar: 100 pV).
Patient 4, the 37-year-old adult, had in addition 103 central and mixed apnoeic episodes during sleep stage 2 and REM sleep (mean length 30.6 sec, longest episode 74 sec). Each apnoea was terminated by brief arousal and gross body movement (Fig. 3).
EOG
EEG
~
RESP. J
i,~,,f
"~-~,li
: ....,
/ ~ --
_
,, x
~
,
/-~
'~, \.
\. j'
J
',
I
<'
', j
FLOW
L_ Fig. 3. Periodic central apnoea in sleep stale l in p a t i e n t 4. RESP, r e s p i r a t o r y belt; P L O W , air f l o w measured b y nostril t h e r m i s t o r ; s u b m e n t a l E M G ; E E G was r e c o r d e d f r o m CzP z. C a l i b r a t i o n as for Fig. 2.
BREATHING PATTERN IN KLEINE-LEVIN SYNDROME This results in much more pronounced periodic breathing during sleep which is not limited to the wake-sleep transition period but recurs throughout the stages of light sleep. As was evident in the adult patient, the periodic breathing pattern may be developed into a full blown sleep apnoea syndrome. A similar decrease in central excitation could be responsible for modulation of central sleep apnoea observed by us recently in a manic-depressive patient (paper submitted for publication). In this case we observed profound central sleep apnoea with increased daytime somnolence during a depressive stage and only periodic breathing during sleep, associated with bursts of K-alpha and alpha-delta activity during the normal stage. These findings strongly support Bulow and Ingvar's suggestion that disordered breathing would accompany CNS abnormalities that are associated with decreased central arousability. Furthermore, they also suggested that patients with depressed central excitation would show respiratory abnormalities. This suggestion had been supported by the findings of Sieker et al. (1960), who reported depressed respiratory function with retention of carbon dioxide in 8 narcoleptic patients, and of Poole (1960) who reported a close correlation between changes in respiration and episodic EEG abnormalities in two cases of subacute encephalitis.
Summary In two adolescent and two adult patients with Kleine-Levin syndrome, polygraphic sleep recording performed during somnolent and non-somnolent periods revealed various forms of abnormal breathing patterns during sleep. These included periodic breathing and hypopnoeic episodes associated with brief arousals and, in one adult patient, a full blown sleep apnoea syndrome. It is suggested that abnormal breathing in sleep in this syndrome may result from central hypoexcitability.
R~sum~ N o u v e l l e s o b s e r v a t i o n s sur les a n o m a l i e s d u s o m m e i l dans le s y n d r o m e de Kleine-Levin: respiration a n o r m a l e d u r a n t le s o m m e i l
I1 a ~t~ effectu~, chez deux adolescents et deux adultes pr~sentant un syndrome de Kleine-Levin, un enregistrement polygraphique du sommeil durant des ~pisodes de somnolence et de non somnolence. Ceux-
101 ci ont r4v~14 des formes vari~es de patterns respiratoires anormaux pendant le sommeil, telles une respiration p~riodique et des ~pisodes d'hypopn~e associ~s de brefs r4veils, et chez un adulte un syndrome hypnique d'apnde complete. I1 est sugg~r~ que cette respiration anormale pendant le sommeil pourrait dans ce syndrome r~sulter d ' u n e hypoexcitabilit~ centrale.
References Barontini, F. and Zappoli, R. A case of Kleine-Levin syndrome. In: H. Gastaut (Ed.), The Abnormalities of Sleep in Man. Proceedings XVth European Meeting on Electroencephalography, Bologna. 1968: 239--246. Bulow, K. and Ingvar, D.H. Respiration and state of wakefulness in normals studied by spirography, capnography and EEG. Acta physiol, scand., 1961, 51: 230--238. Critchley, M. Periodic hypersomnia and megaphagia in adolescent males. Brain, 1962, 85: 627--656. Lavie, P., Gadoth, N., Gordon, C.R., Goldhammer, G. and Bechar, M. Sleep patterns in Kleine-Levin syndrome. Electroenceph. clin. Neurophysiol., 1979, 47: 369--371. Lugaresi, E., Coccagna, H., Mantovani, M., Cirignotta, F., Ambrosetto, G. and Baturic, P. Hypersomnia with periodic breathing: periodic apneas and alveolar hypoventilation during sleep. Bull. Physiopathol. Resp., 1972, 8: 1103--1107. Messimy, R., Well, B. et Safar, S. Sur un cas d'hypersomnia avec troubles du comportement. Sere. H6p. Paris, 1967, 43: 3100--3105. Poole, E.W. Periodic EEG discharge in subacute encephalitis with reference to respiratory and cardiac cycles. Electroenceph. clin. Neurophysiol., 1960, 12: 759. Sieker, D.O., Heymane, P. and Birchfield, R.I. The effects of natural sleep and hypersomnolent states on respiratory function. Ann. intern. Med., 1960, 52: 500--516. Takahashi, Y. Clinical studies of periodic somnolence: analysis of 28 personal cases. Folia psychiat, neurol. jap., 1967, 67: 853--889. Vardi, J., Fletcher, S., Tupilsky, M., Rabey, J.M., Carasso, R. and Streifler, M. Kleine-Levin syndrome with periodic apnea during hypersomnia stages: EEG study. J. Neural Trans., 1978, 43: 121--132. Wilkus, R.J. and Chiles, J.A. Electrophysiological changes during episodes of the Kleine-Levin syndrome. J. Neurol. Neurosurg. Psychiat., 1975, 38: 1225--1231.
glectroencephalography and Clinical Neurophysiology, 1981, 5 2 : 9 8 - - 1 0 1 Elsevier/North-Holland Scientific Publishers, Ltd.
Clinical note FURTHER OBSERVATIONS ON SLEEP ABNORMALITIES ABNORMAL BREATHING PATTERN DURING SLEEP
IN KLEINE-LEVIN
SYNDROME:
P. LAVIE a,1 E. KLEIN b, N. GADOTH c E. BENTAL d, j. ZOMER a, M. BECHAR c and J. WAJSBORT e
a Sleep Laboratory, Faculty o f Medicine, Technion-Israel Institute o f Technology, Itaifa; b Department o f Psychiatry, R A M B A M University Hospital, Haifa; c Department of Neurology, Beilinson Medical Center, Petach-Tiqva and the Sackler School o f Medicine, Tel-Aviv University, Tel-Aviv; d Department o f Neurology, R A M B A M University Hospital, Haifa; e Linn Clinic, Haifa (Israel) (Accepted for publication: March 24, 1981)
Periodic hypersomnia associated with hyperphagia and abnormal behaviour were termed by Critchley (1962) the Kleine-Levin syndrome (KLS). In this peculiar, not fully understood, syndrome, affecting mainly adolescent males, polygraphic sleep recording revealed alterations in the structure of sleep. A variety of changes have been reported, such as sleep onset REM periods (Wilkus and Chiles 1975; Lavie et al. 1979), decrease in stages 3--4 and in REM sleep (Messimy et al. 1967; Takahashi 1967; Barontini and Zappoli 1968), and frequent interruptions of REM sleep by sleep stage 2 and intrusion of alpha activity (Lavie et al. 1979). In one report only, breathing abnormalities during sleep have been documented (Vardi et al. 1978). In this single case report periodic apnoea with paroxysmal EEG activity was found during somnolent attacks; however, no apnoeic spells were seen during nocturnal sleep. The type of apnoea could not be specified as respiratory monitoring was not performed. We wish to describe abnormal breathing patterns during nocturnal sleep in 4 patients with the KLs. In two boys and two adult males we documented periodic breathing, hypopnoeic episodes and sleep apnoea during hypersomnolent attacks as well as during asymptomatic 'normal' periods.
Case histories
Patient 1 A 16-year-old male had the classical features of KLS since the age of 10 years. Approximately 3 times annually he became gradually sleepy during daytime, showed excessive craving for sweets and bizarre 1 Correspondence and reprints: Dr. Peretz Lavie, Ph.D., Sleep Laboratory, Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
behaviour with hypersexual tendencies. Each attack lasted for 3 weeks, 10 days of which he spent in bed, sleeping. Repeated neurological evaluations during and between attacks, extensive laboratory and endocrine studies, including several EEGs, cerebrospinal fluid analysis and brain scans were all normal. Whole night polygraphic sleep recording, but without respiratory monitoring, was performed twice during one of his attacks and the results were previously reported in detail (Lavie et al. 1979). The abnormal findings included increased amounts of body movement associated with midsleep awakenings. These were present to a lesser extent also durin~ a non-somnolent so-called 'normal' period. The present data were obtained about a year following his last sleep recording, about 8 months after his last somnolent attack ('normal period') and then during his subsequent somnolent attack about a month later. During the 'normal' period his sleepwaking cycle was unremarkable, although some difficulties of waking him up in the morning were reported by his parents.
Patienl 2 A 15-year-old boy had the classical features of KLS since age 12. During this period he suffered from 4 attacks of excessive daytime sleep following febrile illnesses and associated with bizarre behaviour causing two psychiatric hospitalizations. During a third hospitalization, because of a 'psychotic state', hyperphagia and intense hypersexuality preceded by 2 weeks of hypersomnia, the diagnosis of KLS was finally reached. It is to note that he was born after a traumatic labor and was diagnosed as suffering from minimal brain dysfunction at the age of 8 years. Repeated routine blood tests, metabolic screening, EEG recording and neurological evaluations were all unremarkable. Three whole night recordings were made. The first
0013-4649/81/0000--0000/$02.50 © Elsevier/North-Holland Scientific Publishers, Ltd.
BREATHING PATTERN IN KLEINE-LEVIN SYNDROME
99
was done a month following a sleep attack when he was on 200 mg chlorpromazine (CPZ) daily. The second was obtained 2 months later when he received only 50 mg of CPZ daily, and the third recording was obtained a month following discontinuation of CPZ.
Increased appetite was noticed towards the end of some but not all of his hypersomnolent attacks. He was recorded in the laboratory during an asymptomatic period, about a year and a half after the last attack.
Patient
Results
3
A 20-year-old male was healthy until the age of 15. At that time (June 1975) he was involved in a strenuous physical effort for 3 days, followed by excessive daytime sleepiness, and abnormal behaviour lasting for 10 days. In September 1975, following a febrile illness, he had a second attack which lasted for 10 days. Another attack in 1976 was accompanied by hypersexual tendencies and excessive masturbation. In 1979 he had two attacks, each lasting 10 days, and two additional attacks in 1980 during which marked hyperphagia was also present. He was recorded in the laboratory during the second attack in 1980. Patient
4
A 37-year-old male was evaluated for severe diurnal fatigue. He was in perfect health until the age of 10. At that time he was involved in strenuous physical effort for several days followed b~y excessive daytime sleep, abnormal behaviour and poorly defined non-localized headaches. This lasted for a whole week and since then similar 'attacks' recurred yearly until the age of 30. After 5 quiet years he had another somnolent period at the age of 35, lasting for 6 days.
gf$P.
. . . . . . . . . . . .
Common abnormal breathing patterns during sleep were present in the records from all 4 patients. Most prevalent was pronounced periodic breathing during sleep stages 1 and 2, which was not limited to the first non-REM period but appeared throughout the night. Periods of hypopnoea lasting several respiratory cycles alternated with hyperpnoea associated with a brief arousal response. Most arousals were heralded by the appearance of one or several consecutive K complexes, or a burst of large amplitude delta activity followed by a tail of alpha waves (K-alpha complexes) and on many occasions body movements (Figs. I and 2). There were also longer periods of arousal lasting 5--15 rain. Isolated hypopnoeic episodes, containing diminished respiratory drive, terminated by K complexes with a tail of alpha activity and body movements, were found in sleep stage 2 throughout the sleep period. There was no difference in the prevalence of abnormal breathing episodes between the records during the symptomatic and asymptomatic periods obtained from patient 2. The number of microarousals (K-alpha and alpha-delta bursts) exceeded 150 in each of the whole night records.
.
. . .
. ..... . .
FLOW
Fig. 1. A pattern of pronounced periodic breathing associated with K-alpha complexes (indicated by dots) in sleep stage 2 in patient 3. RESP, respiratory belt; FLOW, air flow measured by nostril thermistor.
100
P. LAVIE ET AL• EEG
Discussion Our results add an additional aspect to the sleep abnormality in KLS. It is clearly shown that a breathing disorder during sleep is a characteristic feature in our patients with KLS during both somnolent and non-somnolent periods; one patient was recorded during both, one patient only during a somnolent period and two patients only during non-somnolent periods. Somewhat identical to Vardi et al. (1978) we found pronounced periodic breathing and hypopnoeic episodes in 3 patients and a full blown central sleep apnoea in one patient. There was no difference, however, between the type and severity of breathing disorders in sleep between the records done during the somnolent and non-somnolent periods. This precludes the possibility that the somnolent attack resulted from changes in the severity of the breathing disorders in sleep. Our previous findings (Lavie et al. 1 9 7 9 ) o f an increased number of body movements in sleep and repeated intrusions of alpha activity into sleep stage 2 can be interpreted now as related to the nocturnal abnormal breathing pattern. These findings suggest that nocturnal breathing should be monitored in every patient with KLS. Periodic breathing during the stages of light sleep (1 and 2), which may include brief periods of hypopnoea or apnoea, are common, particularly in persons older than 40--45 years. This type of breathing pattern was attributed to central hypoexcitability associated with changing from the 'awake' to the 'asleep' stages (e.g., Bulow and Ingvar 1961; Lugaresi et al. 1972). We suggest that in KLS there is a general decrement in nervous system excitation which affects both the symptomatic and asymptomatic periods•
RESP
<.
, 72
Fig. 2. Representative sample of K complexes followed by a tail of alpha activity (K-alpha complex) associated with hypopnoeas in patient 3. EEG was recorded from CzP z. Calibration refers to EEG (horizontal bar: 2 sec; vertical bar: 100 pV).
Patient 4, the 37-year-old adult, had in addition 103 central and mixed apnoeic episodes during sleep stage 2 and REM sleep (mean length 30.6 sec, longest episode 74 sec). Each apnoea was terminated by brief arousal and gross body movement (Fig. 3).
EOG
EEG
~
RESP. J
i,~,,f
"~-~,li
: ....,
/ ~ --
_
,, x
~
,
/-~
'~, \.
\. j'
J
',
I
<'
', j
FLOW
L_ Fig. 3. Periodic central apnoea in sleep stale l in p a t i e n t 4. RESP, r e s p i r a t o r y belt; P L O W , air f l o w measured b y nostril t h e r m i s t o r ; s u b m e n t a l E M G ; E E G was r e c o r d e d f r o m CzP z. C a l i b r a t i o n as for Fig. 2.
BREATHING PATTERN IN KLEINE-LEVIN SYNDROME This results in much more pronounced periodic breathing during sleep which is not limited to the wake-sleep transition period but recurs throughout the stages of light sleep. As was evident in the adult patient, the periodic breathing pattern may be developed into a full blown sleep apnoea syndrome. A similar decrease in central excitation could be responsible for modulation of central sleep apnoea observed by us recently in a manic-depressive patient (paper submitted for publication). In this case we observed profound central sleep apnoea with increased daytime somnolence during a depressive stage and only periodic breathing during sleep, associated with bursts of K-alpha and alpha-delta activity during the normal stage. These findings strongly support Bulow and Ingvar's suggestion that disordered breathing would accompany CNS abnormalities that are associated with decreased central arousability. Furthermore, they also suggested that patients with depressed central excitation would show respiratory abnormalities. This suggestion had been supported by the findings of Sieker et al. (1960), who reported depressed respiratory function with retention of carbon dioxide in 8 narcoleptic patients, and of Poole (1960) who reported a close correlation between changes in respiration and episodic EEG abnormalities in two cases of subacute encephalitis.
Summary In two adolescent and two adult patients with Kleine-Levin syndrome, polygraphic sleep recording performed during somnolent and non-somnolent periods revealed various forms of abnormal breathing patterns during sleep. These included periodic breathing and hypopnoeic episodes associated with brief arousals and, in one adult patient, a full blown sleep apnoea syndrome. It is suggested that abnormal breathing in sleep in this syndrome may result from central hypoexcitability.
R~sum~ N o u v e l l e s o b s e r v a t i o n s sur les a n o m a l i e s d u s o m m e i l dans le s y n d r o m e de Kleine-Levin: respiration a n o r m a l e d u r a n t le s o m m e i l
I1 a ~t~ effectu~, chez deux adolescents et deux adultes pr~sentant un syndrome de Kleine-Levin, un enregistrement polygraphique du sommeil durant des ~pisodes de somnolence et de non somnolence. Ceux-
101 ci ont r4v~14 des formes vari~es de patterns respiratoires anormaux pendant le sommeil, telles une respiration p~riodique et des ~pisodes d'hypopn~e associ~s de brefs r4veils, et chez un adulte un syndrome hypnique d'apnde complete. I1 est sugg~r~ que cette respiration anormale pendant le sommeil pourrait dans ce syndrome r~sulter d ' u n e hypoexcitabilit~ centrale.
References Barontini, F. and Zappoli, R. A case of Kleine-Levin syndrome. In: H. Gastaut (Ed.), The Abnormalities of Sleep in Man. Proceedings XVth European Meeting on Electroencephalography, Bologna. 1968: 239--246. Bulow, K. and Ingvar, D.H. Respiration and state of wakefulness in normals studied by spirography, capnography and EEG. Acta physiol, scand., 1961, 51: 230--238. Critchley, M. Periodic hypersomnia and megaphagia in adolescent males. Brain, 1962, 85: 627--656. Lavie, P., Gadoth, N., Gordon, C.R., Goldhammer, G. and Bechar, M. Sleep patterns in Kleine-Levin syndrome. Electroenceph. clin. Neurophysiol., 1979, 47: 369--371. Lugaresi, E., Coccagna, H., Mantovani, M., Cirignotta, F., Ambrosetto, G. and Baturic, P. Hypersomnia with periodic breathing: periodic apneas and alveolar hypoventilation during sleep. Bull. Physiopathol. Resp., 1972, 8: 1103--1107. Messimy, R., Well, B. et Safar, S. Sur un cas d'hypersomnia avec troubles du comportement. Sere. H6p. Paris, 1967, 43: 3100--3105. Poole, E.W. Periodic EEG discharge in subacute encephalitis with reference to respiratory and cardiac cycles. Electroenceph. clin. Neurophysiol., 1960, 12: 759. Sieker, D.O., Heymane, P. and Birchfield, R.I. The effects of natural sleep and hypersomnolent states on respiratory function. Ann. intern. Med., 1960, 52: 500--516. Takahashi, Y. Clinical studies of periodic somnolence: analysis of 28 personal cases. Folia psychiat, neurol. jap., 1967, 67: 853--889. Vardi, J., Fletcher, S., Tupilsky, M., Rabey, J.M., Carasso, R. and Streifler, M. Kleine-Levin syndrome with periodic apnea during hypersomnia stages: EEG study. J. Neural Trans., 1978, 43: 121--132. Wilkus, R.J. and Chiles, J.A. Electrophysiological changes during episodes of the Kleine-Levin syndrome. J. Neurol. Neurosurg. Psychiat., 1975, 38: 1225--1231.