Epilepsiu, 33( 3799-804, 1YY2 Raven Press, Ltd., New York 0 International League Against Epilepsy
Sleep Microstructure and EEG Epileptiform Activity in Patients with Juvenile Myoclonic Epilepsy “PG. L. Gigli, *E. Calia, *M. G. Marciani, $S. Mazza, $G. Mennuni, *M. Diomedi, 8M. G. Terzano, and ]ID. Janz *Clinicu Neurologica, Universita di Roma “Tor Vergutu”; tI.R.C.C.S., Clinicu S . Luciu; Slstituto di Neurologia, Universitu Cuttolica del Sucro Cuore, Rome; 9Clinica Neurologica, Universita di Purmu, Italy; und liNeuro1ogische Ahteilung, Frei Universitaet, Berlin, Germuny
Summary: Clinical and EEG manifestations of juvenile myoclonic epilepsy (JME) occur in a strict relationship to the sleepwake cycle, particularly to transition phases (awakening, falling asleep, afternoon relaxation after work). JME manifestations are deactivated during sleep. Because arousal fluctuations during NREM sleep may be controlled by the same neurophysiologic mechanisms regulating awakening, we studied the relationship between the cyclic alternating pattern (CAP) and JME manifestations. All-night polysomnographic recordings of 10 JME patients were analyzed for variations of epileptiform EEG abnormalities in relation to sleep stages and to different microstructural variables (NCAP, CAP, phases A and B). CAP rates (ratio between total CAP duration and total NREM sleep duration) were also calculated. Average CAP rate was 46.70%, significantly higher than that (23%) of an age-matched control group. Macrostructural analysis showed only a trend toward a slight predomi-
nance of EEG epileptiform activity during slow wave sleep but no significant correlation between spiking rates and sleep stages. Microstructural analysis confirmed the CAP modulation of EEG epileptiform activity, with maximum appearance of epileptiform abnormalities during phase A CAP (normalized spiking rate = 4.00 ? 0.98) and strong inhibition during phase B (0.06 +- 00.6). Intermediate values were noted during NCAP (0.54 ? 0.27). N o correlation was noted between spiking rates during NREM sleep and CAP rates, possibly indicating that in JME patients the increased CAP rate may be partially independent of epileptiform EEG activity. Our data suggest that in JME patients CAP may be a neurophysiologic oscillator organizing expression of the epileptiform discharges independent of the tendency of the individual patient to produce epileptiform EEG discharges. Key Words: Juvenile myoclonic epilepsy-Sleep-Electroencephalography-Sleep stages-REM sleep.
The distribution of epileptic seizures and EEG epileptiform activity during wakefulness and sleep stages in different epileptic syndromes, as well as modifications of sleep organization resulting from interictal and ictal activity have been studied (Baldy-Moulinier et al. , 1984; Broughton, 1984). Because of inclusion of nonhomogeneous cases and probably because of limits intrinsic to study methods, results have been contradictory and not very significant. The relationships between sleep and epilepsy have been studied (Dahl and Dam, 1985; Montplaisir et al., 1985; Billiard et al., 1987) by the classic scoring criteria of wakefulness and sleep stages de-
fined by Rechtschaffen and Kales (1968). This scoring system considers only average sleep depth in a time unit (epoch) and does not take into consideration modifications in each epoch; e.g., if
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Epilepsia, Vol. 33, N o . 5 , 1992
SLEEP AND EPILEPTIFORM ACTIVITY IN JME probably results from different recording methods and use of nonhomogeneous case descriptions including presence and type of seizures, and type of therapy. The discordance between subjective altered sleep symptoms and objective polygraphic findings also could result from the inadequacy of the macrostructural analysis to “photograph” very short variations in sleep stability, whereas CAP can do this faithfully. The slight variation in CAP rates in individual patients rules out the possibility that the increased CAP rate of epileptic patients results merely from the presence of EEG epileptiform abnormalities. The lack of a positive correlation between spiking rates during NREM sleep and CAP rates (Y = 0.3901) suggests the possibility that an increase in the CAP rate in JME could occur, at least in part, independently of EEG epileptiform abnormalities; the increase in CAP rates could also be the result of exogenous or endogenous factors able to disturb sleep. Even if the relationship between cyclic activity and epileptiform discharges remains unclear, the two phenomena may coexist and potentiate each other (Terzano et al., 1992). The observation of individual phase A periods in which the epileptiform discharges are located at the beginning or, alternatively, in the middle of the phase, appears to validate this hypothesis (Fig. 1). The sharp activation of epileptiform discharges during phase A and inhibition during phase B of CAP appears to indicate that CAP acts as a neurophysiologic oscillator, with epileptiform activity appearing at the two extremes of oscillation. CAP phase A could be viewed as a window through which the epileptiform activity could pass more easily. Our findings support the hypothesis of Halasz (1981,1984), who postulated that bidirectional fluctuations of arousal play an important role in appearance of generalized EEG epileptiform discharges. Halasz interpreted K-complexes and arousal delta as phenomena protective of sleep that is disturbed by arousal stimuli. Similarly, CAP phase A could be considered the organism’s response to protect sleep continuity from arousal stimuli. Using this theory, the separation between awakening and sleep in JME would be artificial only. The observation that JME epileptiform discharges occurring during sleep appear mainly during the “dynamic” periods (i.e., during conditions of transition and instability) is not incompatible with the high degree of activation that occurs after nocturnal and final morning awakenings when a tendency to new sleep onset still exists.
803
Animal studies contribute to our theory. Feline epilepsy induced by systemic penicillin administration has a similar temporal relationship with the sleep-wake cycle and neurophysiologic mechanisms similar to those of JME (Gloor and Testa, 1974; Testa and Gloor, 1974; Gloor et al., 1977; Avoli and Gloor, 1982; Shouse, 1987). In the feline model, distribution of EEG ictal and interictal abnormalities is temporally related to variations of cortical excitability, as measured by somatosensory evoked potentials (Shouse, 1987). The amplitude of these potentials, considered an index of cortical excitability, is usually greatest during somnolence that accompanies wakefulness, during slow wave sleep, and during somnolence that accompanies awakenings following slow wave sleep (Shouse, 1987). All these are conditions that maximally favor epileptic manifestations, both in JME and in the systemic penicillin model. The situation is very different when awakening follows a REM period and epileptiform activity is at minimal levels, as has been shown both in experimental model (Shouse, 1987) and clinical studies (Gigli et al., 1991). Acknowledgment: W e t h a n k Dr. U. R o e d e r - W a n n e r for assistance in selecting patients.
REFERENCES Avoli M, Gloor P. Role of thalamus in generalized penicillin epilepsy: observations on decorticate cats. Exp Neurol 1982; 17:3 8 6 4 2 . Baldy-Moulinier M, Touchon J, Besset A, Billiard M, Cadilhac J, Passouant P. Sleep architecture and epileptic seizures. In: Degen R, Niedermeyer E, eds. Epilepsy, sleep and sleep deprivation. Amsterdam: Elsevier, 1984: 109-18. Besset A. Influence of generalized seizures on sleep organization. In: Sterman MB, Schouse MN, Passouant P, eds. Sleep and epilepsy. New York: Academic Press, 1982:339-46. Billiard M, Besset A, Zachariev Z, Touchon J, Baldy-Moulinier M, Cadilhac J. Relation of seizure discharges to sleep stages. In: Wolf P, Dam M, Janz D, Dreifuss FE, eds. Advances in epileptology, XVIth Epilepsy International Symposium. New York: Raven Press, 1987:665-70. Brougthon RJ. Epilepsy and sleep: a synopsis and prospectus. In: Degen R, Niedermeyer E, eds. Epilepsy, sleep and sleep deprivation. Amsterdam: Elsevier, 1984:317-56. Cadhillac J. Complex partial seizures and REM sleep. In: Sterman MB, Schouse MN, Passouant P, eds. Sleep and epilepsy. New York: Academic Press, 1982:315-24. Dahl M, Dam M. Sleep and epilepsy. Ann Clin R e s 1985;17:23542. Gigli GL, Calia E , Luciani L, et al. Eye-closure sensitivity without photosensitivity in juvenile myoclonic epilepsy: polysomnographic study of EEG epileptiform discharge rates. Epilepsia 1991;32:677-83. Gloor P, Quesney LF, Zumstein H. Pathophysiology of generalized penicillin epilepsy in the cat: the role of cortical and subcortical structures. 11. Topical application of penicillin to the cerebral cortex and to subcortical structures. Electroencephalogr Clin Neurophysiol 1977;43:19-94. Epilepsia, Vol. 33, N o . 5 . 1992
804
G . L . GIGLI ET AL.
Gloor P, Testa GF. Generalized penicillin epilepsy in the cat: effects of intracarotid and intravertebral pentyletetrazol and amobarbital injections. Electroencephalogr Clin Neurophysiol 1974;36:499-5 IS. Halasz P. Generalized epilepsy with spike-wave paroxysms as an epileptic disorder of the function of sleep promotion. A c t a Physiol Acad Sci Hung 1981;57:51-86. Halasz P. Sleep, arousal and electroclinical manifestations of generalized epilepsy with spike wave pattern. In: Degen R, Niedermeyer E, eds. Epilepsy, sleep and sleep deprivation. Amsterdam: Elsevier, 1984:97-107. Janz D. The grand ma1 epilepsies and the sleep-waking cycle. Epilepsia 1962;3:69-109. Janz D. Die Epilepsien. Stuttgart, Thieme, 1969:135-63. Janz D. Epilepsy and the sleep-waking cycle. In: Vinken W, Bruyn GW, eds. Handbook of clinical neurology: Volume 15: the epilepsies. Amsterdam: Elsevier, 1974:457-90. Janz D. Epilepsy with impulsive-petit ma1 (juvenile myoclonic epilepsy). A c t a Neurol Scund 1985;72:449-59. Janz D. Juvenile myoclonic epilepsy. Cleve Clin J M e d 1989;56: S23-33. Montplaisir J, Laverdiere M, Saint-Hilaire JM. Sleep and epilepsy. In: Gotman J, Ives JR, Gloor P, eds. Long-term monitoring and computer analysis of the EEG in epilepsy. Amsterdam: Elsevier, 1985:215-39. Niedermeyer E. Sleep electroencephalograms in petit mal. Arch Neurol 1965;12:625-30. Niedermeyer E. Petit mal, primary generalized epilepsy and sleep. In: Sterman MB, Schouse MN, Passouant P, eds. Sleep and epilepsy. New York: Academic Press, 1982:191207. Niedermeyer E . Awakening epilepsy (“ Aufwach-Epilepsie”) revisited 30 years later. In: Degen R, Niedermeyer E, eds. Epilepsy, sleep and sleep deprivation. Amsterdam: Elsevier, 1984:85-96. Rechtschaffen A, Kales A. A manual of standardized terminolo g y , techniques and scoring system f o r sleep stages of human subjects. Los Angeles: BlSlBRI UCLA Los Angeles, 1968. Shouse MN. Thalamocortical mechanisms of state-dependent seizures during amygdala kindling and systemic penicillin epilepsy in cats. Brain R e s 1987;425:198-203. Stevens JR, Lonsbury BL, Goel SL. Seizure occurrence and interspike interval. Arch Neurol 1972;26:409-19. Terzano MG, Mancia D, Salati MR, Costani G , Decembrino A, Parrino L. The cyclic alternating pattern as a physiologic component of normal NREM sleep. Sleep 1985;8: 137-45. Terzano MG, Parrino L, Spaggiari MC. The cyclic alternating pattern in the dynamic organization of sleep. Electroencephalogr Clin Neurophysiol 1988a;69:437-47. Terzano MG, Parrino L, Piroli A, Spaggiari MC, Anelli S, Arcelloni T. Comparison of cyclic alternating pattern (CAP) parameters in normal sleep of young and aged adults. In: Koella WP, Obal H, Schulz H, Visser P, eds. Sleep ’86. StUttgdrt: Gustav Fischer Verlag, 19886:290-2. Terzano MG, Parrino L, Anelli S, Halasz P. Modulation of generalized spike-and-wave discharges during sleep by cyclic alternating pattern. Epilepsia 1989;30:772-81.
Epilepsia, Vol. 33, No. 5 , 1992
Terzano MG, Parrino L, Spaggiari MC, Barusi K, Simeoni S. Discriminatory effect of cyclic alternating pattern in focal lesional and benign rolandic interictal spikes during sleep. Epilepsia 1991;32:616-28. Terzano MG, Parrino L, Anelli S, Boselli M, Clemens B. Effects of generalized interictal EEG discharges on sleep stability: assessment by means of cyclic alternating pattern. Epilepsia 1992;33:3 17-26. Testa GF, Gloor P. Generalized penicillin epilepsy in the cat: effect of midbrain cooling. Electroencephalogr Clin Neurophysiol I974;36:5 17-24. Touchon J. Effect of awakening on epileptic activity in primary generalized myoclonic epilepsy. In: Sterman MB, Shouse MN, Passouant P, eds. Sleep and epilepsy. New York: Academic Press, 1982:23948.
RESUME Les manifestations cliniques et EEG de l’epilepsie myoclonique juvenile (EMJ) surviennent en stricte relation avec le cycle veille-sommeil, particulitrement avec les phases transitionnelles (reveil, endormissement, relaxation en fin d’apres-midi a p e s le travail, etc . . .). Les manifestations de I’EMJ sont dtsactivees pendant le sommeil. Comme les fluctuations de la vigilance pendant le sommeil lent sont vraisemblablement contrblees par les m&mes mkcanismes neurophysiologiques qui regulent la veille, les auteurs ont etudie la relation entre les patterns cycliques alternants (CAP) (et les manifestations de I’EMJ). Des enregistrements polysomnographiques de nuit pratiques chez 10 patients presentant une EMJ ont 6te analyses pour Ctudier les variations des anomalies EEG paroxystiques en relation avec les stades de sommeil et les diffkrentes variables de la microstructure du sommeil (NCAP, CAP, phase A et B). Les taux de CAP (rapport entre la durCe totale des CAP et la duree totale du sommeil lent) ont Cgalement Cte calcults. Le taux moyen de CAP a ete de 46.7% et il est significativement plus ClevC que dans un groupe contrble (23%). L’analyse macrostructurelle n’a pas montre de c o d a t i o n significative entre le taux des anomalies paroxystiques et les stades de sommeil, avec cependant une tendance vers une discrete predominance des anomalies paroxystiques EEG pendant le sommeil A ondes lentes. L’analyse microstructurelle a confirme la modulation de I’activite EEG paroxystique, avec apparition maximale des anomalies pendant la phase A des CAP (taux normalisC: 4.00 2 0.98) et inhibition importante pendant la phase B (0.06 0.06). Des valeurs intermtdiaires ont CtC trouvCes en pkriode NCAP (0.54 0.27). Les auteurs n’ont pas constate de correlation entre le taux d’anomalies paroxystiques pendant le sommeil lent et le taux de CAP, ce qui indique peut-Ctre que, chez les patients presentant une EMJ, I’augmentation du taux de CAP peut Ctre partiellement independant de I’activitC EEG paroxystique. Ces donnCes suggerent que, chez les patients avec EMJ, les CAP peuvent &treun instigateur neurophysiologique qui organise I’expression des decharges paroxystiques, independamment de la tendance individuelle du patient A produire ce type de dkcharge.
*
*
(P. Genton, Marseille)
Sleep Microstructure and EEG Epileptiform Activity in Patients with Juvenile Myoclonic Epilepsy “PG. L. Gigli, *E. Calia, *M. G. Marciani, $S. Mazza, $G. Mennuni, *M. Diomedi, 8M. G. Terzano, and ]ID. Janz *Clinicu Neurologica, Universita di Roma “Tor Vergutu”; tI.R.C.C.S., Clinicu S . Luciu; Slstituto di Neurologia, Universitu Cuttolica del Sucro Cuore, Rome; 9Clinica Neurologica, Universita di Purmu, Italy; und liNeuro1ogische Ahteilung, Frei Universitaet, Berlin, Germuny
Summary: Clinical and EEG manifestations of juvenile myoclonic epilepsy (JME) occur in a strict relationship to the sleepwake cycle, particularly to transition phases (awakening, falling asleep, afternoon relaxation after work). JME manifestations are deactivated during sleep. Because arousal fluctuations during NREM sleep may be controlled by the same neurophysiologic mechanisms regulating awakening, we studied the relationship between the cyclic alternating pattern (CAP) and JME manifestations. All-night polysomnographic recordings of 10 JME patients were analyzed for variations of epileptiform EEG abnormalities in relation to sleep stages and to different microstructural variables (NCAP, CAP, phases A and B). CAP rates (ratio between total CAP duration and total NREM sleep duration) were also calculated. Average CAP rate was 46.70%, significantly higher than that (23%) of an age-matched control group. Macrostructural analysis showed only a trend toward a slight predomi-
nance of EEG epileptiform activity during slow wave sleep but no significant correlation between spiking rates and sleep stages. Microstructural analysis confirmed the CAP modulation of EEG epileptiform activity, with maximum appearance of epileptiform abnormalities during phase A CAP (normalized spiking rate = 4.00 ? 0.98) and strong inhibition during phase B (0.06 +- 00.6). Intermediate values were noted during NCAP (0.54 ? 0.27). N o correlation was noted between spiking rates during NREM sleep and CAP rates, possibly indicating that in JME patients the increased CAP rate may be partially independent of epileptiform EEG activity. Our data suggest that in JME patients CAP may be a neurophysiologic oscillator organizing expression of the epileptiform discharges independent of the tendency of the individual patient to produce epileptiform EEG discharges. Key Words: Juvenile myoclonic epilepsy-Sleep-Electroencephalography-Sleep stages-REM sleep.
The distribution of epileptic seizures and EEG epileptiform activity during wakefulness and sleep stages in different epileptic syndromes, as well as modifications of sleep organization resulting from interictal and ictal activity have been studied (Baldy-Moulinier et al. , 1984; Broughton, 1984). Because of inclusion of nonhomogeneous cases and probably because of limits intrinsic to study methods, results have been contradictory and not very significant. The relationships between sleep and epilepsy have been studied (Dahl and Dam, 1985; Montplaisir et al., 1985; Billiard et al., 1987) by the classic scoring criteria of wakefulness and sleep stages de-
fined by Rechtschaffen and Kales (1968). This scoring system considers only average sleep depth in a time unit (epoch) and does not take into consideration modifications in each epoch; e.g., if
5
-6 C
R1
L
a
Epilepsia, Vol. 33, N o . 5 , 1992
SLEEP AND EPILEPTIFORM ACTIVITY IN JME probably results from different recording methods and use of nonhomogeneous case descriptions including presence and type of seizures, and type of therapy. The discordance between subjective altered sleep symptoms and objective polygraphic findings also could result from the inadequacy of the macrostructural analysis to “photograph” very short variations in sleep stability, whereas CAP can do this faithfully. The slight variation in CAP rates in individual patients rules out the possibility that the increased CAP rate of epileptic patients results merely from the presence of EEG epileptiform abnormalities. The lack of a positive correlation between spiking rates during NREM sleep and CAP rates (Y = 0.3901) suggests the possibility that an increase in the CAP rate in JME could occur, at least in part, independently of EEG epileptiform abnormalities; the increase in CAP rates could also be the result of exogenous or endogenous factors able to disturb sleep. Even if the relationship between cyclic activity and epileptiform discharges remains unclear, the two phenomena may coexist and potentiate each other (Terzano et al., 1992). The observation of individual phase A periods in which the epileptiform discharges are located at the beginning or, alternatively, in the middle of the phase, appears to validate this hypothesis (Fig. 1). The sharp activation of epileptiform discharges during phase A and inhibition during phase B of CAP appears to indicate that CAP acts as a neurophysiologic oscillator, with epileptiform activity appearing at the two extremes of oscillation. CAP phase A could be viewed as a window through which the epileptiform activity could pass more easily. Our findings support the hypothesis of Halasz (1981,1984), who postulated that bidirectional fluctuations of arousal play an important role in appearance of generalized EEG epileptiform discharges. Halasz interpreted K-complexes and arousal delta as phenomena protective of sleep that is disturbed by arousal stimuli. Similarly, CAP phase A could be considered the organism’s response to protect sleep continuity from arousal stimuli. Using this theory, the separation between awakening and sleep in JME would be artificial only. The observation that JME epileptiform discharges occurring during sleep appear mainly during the “dynamic” periods (i.e., during conditions of transition and instability) is not incompatible with the high degree of activation that occurs after nocturnal and final morning awakenings when a tendency to new sleep onset still exists.
803
Animal studies contribute to our theory. Feline epilepsy induced by systemic penicillin administration has a similar temporal relationship with the sleep-wake cycle and neurophysiologic mechanisms similar to those of JME (Gloor and Testa, 1974; Testa and Gloor, 1974; Gloor et al., 1977; Avoli and Gloor, 1982; Shouse, 1987). In the feline model, distribution of EEG ictal and interictal abnormalities is temporally related to variations of cortical excitability, as measured by somatosensory evoked potentials (Shouse, 1987). The amplitude of these potentials, considered an index of cortical excitability, is usually greatest during somnolence that accompanies wakefulness, during slow wave sleep, and during somnolence that accompanies awakenings following slow wave sleep (Shouse, 1987). All these are conditions that maximally favor epileptic manifestations, both in JME and in the systemic penicillin model. The situation is very different when awakening follows a REM period and epileptiform activity is at minimal levels, as has been shown both in experimental model (Shouse, 1987) and clinical studies (Gigli et al., 1991). Acknowledgment: W e t h a n k Dr. U. R o e d e r - W a n n e r for assistance in selecting patients.
REFERENCES Avoli M, Gloor P. Role of thalamus in generalized penicillin epilepsy: observations on decorticate cats. Exp Neurol 1982; 17:3 8 6 4 2 . Baldy-Moulinier M, Touchon J, Besset A, Billiard M, Cadilhac J, Passouant P. Sleep architecture and epileptic seizures. In: Degen R, Niedermeyer E, eds. Epilepsy, sleep and sleep deprivation. Amsterdam: Elsevier, 1984: 109-18. Besset A. Influence of generalized seizures on sleep organization. In: Sterman MB, Schouse MN, Passouant P, eds. Sleep and epilepsy. New York: Academic Press, 1982:339-46. Billiard M, Besset A, Zachariev Z, Touchon J, Baldy-Moulinier M, Cadilhac J. Relation of seizure discharges to sleep stages. In: Wolf P, Dam M, Janz D, Dreifuss FE, eds. Advances in epileptology, XVIth Epilepsy International Symposium. New York: Raven Press, 1987:665-70. Brougthon RJ. Epilepsy and sleep: a synopsis and prospectus. In: Degen R, Niedermeyer E, eds. Epilepsy, sleep and sleep deprivation. Amsterdam: Elsevier, 1984:317-56. Cadhillac J. Complex partial seizures and REM sleep. In: Sterman MB, Schouse MN, Passouant P, eds. Sleep and epilepsy. New York: Academic Press, 1982:315-24. Dahl M, Dam M. Sleep and epilepsy. Ann Clin R e s 1985;17:23542. Gigli GL, Calia E , Luciani L, et al. Eye-closure sensitivity without photosensitivity in juvenile myoclonic epilepsy: polysomnographic study of EEG epileptiform discharge rates. Epilepsia 1991;32:677-83. Gloor P, Quesney LF, Zumstein H. Pathophysiology of generalized penicillin epilepsy in the cat: the role of cortical and subcortical structures. 11. Topical application of penicillin to the cerebral cortex and to subcortical structures. Electroencephalogr Clin Neurophysiol 1977;43:19-94. Epilepsia, Vol. 33, N o . 5 . 1992
804
G . L . GIGLI ET AL.
Gloor P, Testa GF. Generalized penicillin epilepsy in the cat: effects of intracarotid and intravertebral pentyletetrazol and amobarbital injections. Electroencephalogr Clin Neurophysiol 1974;36:499-5 IS. Halasz P. Generalized epilepsy with spike-wave paroxysms as an epileptic disorder of the function of sleep promotion. A c t a Physiol Acad Sci Hung 1981;57:51-86. Halasz P. Sleep, arousal and electroclinical manifestations of generalized epilepsy with spike wave pattern. In: Degen R, Niedermeyer E, eds. Epilepsy, sleep and sleep deprivation. Amsterdam: Elsevier, 1984:97-107. Janz D. The grand ma1 epilepsies and the sleep-waking cycle. Epilepsia 1962;3:69-109. Janz D. Die Epilepsien. Stuttgart, Thieme, 1969:135-63. Janz D. Epilepsy and the sleep-waking cycle. In: Vinken W, Bruyn GW, eds. Handbook of clinical neurology: Volume 15: the epilepsies. Amsterdam: Elsevier, 1974:457-90. Janz D. Epilepsy with impulsive-petit ma1 (juvenile myoclonic epilepsy). A c t a Neurol Scund 1985;72:449-59. Janz D. Juvenile myoclonic epilepsy. Cleve Clin J M e d 1989;56: S23-33. Montplaisir J, Laverdiere M, Saint-Hilaire JM. Sleep and epilepsy. In: Gotman J, Ives JR, Gloor P, eds. Long-term monitoring and computer analysis of the EEG in epilepsy. Amsterdam: Elsevier, 1985:215-39. Niedermeyer E. Sleep electroencephalograms in petit mal. Arch Neurol 1965;12:625-30. Niedermeyer E. Petit mal, primary generalized epilepsy and sleep. In: Sterman MB, Schouse MN, Passouant P, eds. Sleep and epilepsy. New York: Academic Press, 1982:191207. Niedermeyer E . Awakening epilepsy (“ Aufwach-Epilepsie”) revisited 30 years later. In: Degen R, Niedermeyer E, eds. Epilepsy, sleep and sleep deprivation. Amsterdam: Elsevier, 1984:85-96. Rechtschaffen A, Kales A. A manual of standardized terminolo g y , techniques and scoring system f o r sleep stages of human subjects. Los Angeles: BlSlBRI UCLA Los Angeles, 1968. Shouse MN. Thalamocortical mechanisms of state-dependent seizures during amygdala kindling and systemic penicillin epilepsy in cats. Brain R e s 1987;425:198-203. Stevens JR, Lonsbury BL, Goel SL. Seizure occurrence and interspike interval. Arch Neurol 1972;26:409-19. Terzano MG, Mancia D, Salati MR, Costani G , Decembrino A, Parrino L. The cyclic alternating pattern as a physiologic component of normal NREM sleep. Sleep 1985;8: 137-45. Terzano MG, Parrino L, Spaggiari MC. The cyclic alternating pattern in the dynamic organization of sleep. Electroencephalogr Clin Neurophysiol 1988a;69:437-47. Terzano MG, Parrino L, Piroli A, Spaggiari MC, Anelli S, Arcelloni T. Comparison of cyclic alternating pattern (CAP) parameters in normal sleep of young and aged adults. In: Koella WP, Obal H, Schulz H, Visser P, eds. Sleep ’86. StUttgdrt: Gustav Fischer Verlag, 19886:290-2. Terzano MG, Parrino L, Anelli S, Halasz P. Modulation of generalized spike-and-wave discharges during sleep by cyclic alternating pattern. Epilepsia 1989;30:772-81.
Epilepsia, Vol. 33, No. 5 , 1992
Terzano MG, Parrino L, Spaggiari MC, Barusi K, Simeoni S. Discriminatory effect of cyclic alternating pattern in focal lesional and benign rolandic interictal spikes during sleep. Epilepsia 1991;32:616-28. Terzano MG, Parrino L, Anelli S, Boselli M, Clemens B. Effects of generalized interictal EEG discharges on sleep stability: assessment by means of cyclic alternating pattern. Epilepsia 1992;33:3 17-26. Testa GF, Gloor P. Generalized penicillin epilepsy in the cat: effect of midbrain cooling. Electroencephalogr Clin Neurophysiol I974;36:5 17-24. Touchon J. Effect of awakening on epileptic activity in primary generalized myoclonic epilepsy. In: Sterman MB, Shouse MN, Passouant P, eds. Sleep and epilepsy. New York: Academic Press, 1982:23948.
RESUME Les manifestations cliniques et EEG de l’epilepsie myoclonique juvenile (EMJ) surviennent en stricte relation avec le cycle veille-sommeil, particulitrement avec les phases transitionnelles (reveil, endormissement, relaxation en fin d’apres-midi a p e s le travail, etc . . .). Les manifestations de I’EMJ sont dtsactivees pendant le sommeil. Comme les fluctuations de la vigilance pendant le sommeil lent sont vraisemblablement contrblees par les m&mes mkcanismes neurophysiologiques qui regulent la veille, les auteurs ont etudie la relation entre les patterns cycliques alternants (CAP) (et les manifestations de I’EMJ). Des enregistrements polysomnographiques de nuit pratiques chez 10 patients presentant une EMJ ont 6te analyses pour Ctudier les variations des anomalies EEG paroxystiques en relation avec les stades de sommeil et les diffkrentes variables de la microstructure du sommeil (NCAP, CAP, phase A et B). Les taux de CAP (rapport entre la durCe totale des CAP et la duree totale du sommeil lent) ont Cgalement Cte calcults. Le taux moyen de CAP a ete de 46.7% et il est significativement plus ClevC que dans un groupe contrble (23%). L’analyse macrostructurelle n’a pas montre de c o d a t i o n significative entre le taux des anomalies paroxystiques et les stades de sommeil, avec cependant une tendance vers une discrete predominance des anomalies paroxystiques EEG pendant le sommeil A ondes lentes. L’analyse microstructurelle a confirme la modulation de I’activite EEG paroxystique, avec apparition maximale des anomalies pendant la phase A des CAP (taux normalisC: 4.00 2 0.98) et inhibition importante pendant la phase B (0.06 0.06). Des valeurs intermtdiaires ont CtC trouvCes en pkriode NCAP (0.54 0.27). Les auteurs n’ont pas constate de correlation entre le taux d’anomalies paroxystiques pendant le sommeil lent et le taux de CAP, ce qui indique peut-Ctre que, chez les patients presentant une EMJ, I’augmentation du taux de CAP peut Ctre partiellement independant de I’activitC EEG paroxystique. Ces donnCes suggerent que, chez les patients avec EMJ, les CAP peuvent &treun instigateur neurophysiologique qui organise I’expression des decharges paroxystiques, independamment de la tendance individuelle du patient A produire ce type de dkcharge.
*
*
(P. Genton, Marseille)
