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The effect of sleep deprivation on the rate of focal interictal epileptiform discharges
288
Electroencephalograpto, and clinical Neurophysiology, 1988, 70:288-292 Elsevier Scientific Publishers Ireland, Ltd.
EEG 03571
The effect of sleep deprivation on the rate of focal interictal epilep,qorm disc ges Majid Molaie and Angel Cruz Department of Neurology, S U N Y Health Science Center and Veterans Administration Medical (?enter. 5~vracuse. N Y 13210 (U.S.A.)
(Accepted for publication: 8 March 1988)
Summary Eight men with complex partial seizures who had frequent focal interictal cpileptiform discharges (F1EDs) dunng routine EEGs were selected for all-night EEG recording before, and after 36 h of sleep deprivation. After sleep deprivation 6 of 8 patients showed increased FIEDs. The pooled mean number of FIEDs was greatest during light non-REM stages of sleep, especially stage II. Thus sleep deprivation is an effective activation method in medicated patients with complex partial seizures. However. a significant activation requires recording stage II sleep after sleep deprivation. Key words: Sleep deprivation; Epilepsy; Partial seizure; Sleep stages
The literature regarding the efficacy of sleep deprivation (SD) as an activating procedure for epileptiform activity is voluminous (Ellingson et al. 1984). Estimates of the incidence of activation range from 6.9% (Broeker et al. 1973) to 83% (Spadetta 1971). Some authors suggest that SD is a convenient way of inducing sleep in the EEG laboratory, and that the increased yield of epileptiform discharges is simply due to drowsiness and sleep after SD (White et al. 1962; Gajkowski and Zalejski 1976; Ritter et al. 1977; ScolloLavizzari et al. 1977). However, since seizures can be precipitated by prolonged periods of sleeplessness in persons without a history of epilepsy (Bennett et al. 1964, 1969; Gunderson et al. 1973), activation of epileptiform discharges by SD is not unexpected. The major source of controversy stems from the various uncontrolled methodological approaches to the problem. Ellingson et al. (1984) and Rodin
Correspondence to: Dr. M. Molaie, Neurology Service No. 127, VA Medical Center, Syracuse, NY 13210 (U.S.A.).
(1984) in their comprehensive reviews outlined these methodological shortcomings. For instance, EEG sampling time for pre- and post-SD records, and subjects' compliance to SD had been rarely cited in the literature (Ellingson et al. 1984). Most investigators had studied patients whose pre-SD records showed equivocal or no epileptiform discharges (Mattson et al. 1965; Berti Ceroni et al. 1967; Pratt et al. 1968; Gellar et al. 1969; Spadetta 1971; Bechinger et al. 1973; Scollo-Lavizzari et al. 1975, 1977; Degen 1977; Rumpl et al. 1977; Schwarz and Zangemeister 1978; Tartara et al. 1980; Rowan et al. 1982). Several authors studied known epileptics, but without reporting anticonvulsant blood levels before or after SD (Rodin 1984). Veldhuizen et al. (1983) pointed out that if a population of patients not showing epileptiform activity in the initial EEG is selected for study, a second recording will inevitably demonstrate a higher discharge incidence than the first due to the statistical phenomenon of regression to the mean. Veldhuizen et al. (1983) randomly selected epileptic patients irrespective of whether the initial EEGs contained epileptiform activity. Their re-
0013-4649/88/$03.50 © 1988 Elsevier Scientific Publishers Ireland, Ltd.
289
EFFECT OF SD ON THE RATE OF FIEDs sults indicated no evidence of an overall increase in discharge rate after SD either in waking or sleep records. In our study, we attempted to control the variables that may have led to conflicting results in previous studies regarding the effect of SD as an activating procedure.
Methodology Eight men with complex partial seizures (CPS), who manifested frequent focal interictal epileptiform discharges (FIEDs) during several routine day-time E E G recordings were selected for the study. Mean age was 48 years (range of 29-63 years), and all were taking antiepileptic drugs, six received phenytoin alone or with another anticonvulsant. Causes of seizures, brain CT findings, and other pertinent data are outlined in Table I. All subjects were admitted to the neurology ward in the morning. At 20.00 h, they reported to the sleep laboratory where electrodes were placed on the scalp and face for all night (23.00-6.00 h) continuous EEG, EOG, and E M G recordings. A low intensity light camera mounted in the bedroom ceiling permitted continuous observation of patients on closed circuit TV and video monitoring of the subjects sleeping in the dark. A 7 h awake and sleep recording was performed on the first night which served as a control. Patients were remained awake for 36 h from 11.00 h to 23.00 h the next day. Patients were studied in pairs in order to keep each other awake under supervision of medical staff. Nocturnal recording was repeated after 36 h of SD in a similar fashion as the baseline study. Nocturnal EEGs were scored according to periods of wakefulness and light nonREM (LNREM) (stages I and II), deep non-REM (DNREM) (stages III and IV), and REM stages. FIEDs were calculated visually in the E E G records by two readers who were blind both to the patient identification and to the baseline versus SD records. The number of FIEDs was calculated per unit of time for different stages of sleep during the control night and during the night after SD. Blood was sampled twice in each patient, during
the control night and the night after SD, to measure anticonvulsant drug levels.
Results
Sleep data The pooled mean percentage of sleep stages was not significantly different between the 2 nights except for the percentage of wakefulness which was significantly lower the night after SD (8.52 + 3.27, P < 0.05) than in the control night (13.77 + 5.77, Fig. 1). Six of the 8 patients had increased total number of FIEDs during the night after SD with the ratio ranging from 1.2 to 12.3. Those patients with abundant discharges during the control night had minimal increased ratio (patients no. 1 and 3), and those with minimal number of discharges had maximum increased ratio of FIEDs on the night after SD (patients no. 2 and 4, Table I). The pooled mean percentages of FIEDs per sleep stage did not differ significantly between both nights, but after SD, the pooled mean number of FIEDs showed a significant increase ( P < 0.05) during L N R E M stages of sleep (Fig. 2). The pooled mean number of FIEDs, when adjusted per unit of time for each stage of sleep, showed a significant increase ( P < 0 . 0 5 ) from awake to L N R E M stages of sleep only during the night after SD. Further data analysis revealed that
Percentage of Sleep Stages
/
~ REM / IV I (11.I%)~' (12.7%) ,
\
II
152.0%1
/
/
J
/ /
During the CTR Night
\,\
,
/
During the Night After SD
Fig. 1. Comparison of pooled mean percentage of sleep stages during the control night and the night after SD.
M. MOLAIE, A. CRUZ
290 TABLE I Patients no./age/ rate of FIEDs/
Ratio of FIEDs (SD/CTR)
rain during the CTR night
All night
1/39/10.3
Persistent EEG foci
Cause of seizures
of head
R frontal S and W discharges
CT scan
Antiepileptic drugs
Post-traumatic
Small _Rfrontal hypodensitx,
Phenytoin + carbamazepine
R temporal and central S and W
Post-traumatic
Bifrontal h~podensit 3
Phenytoin-~ phenobarbital
Stage II sleep
1.2
1.5
2/55/'0.1
12.3
27.3
3/63/7.3
0.8
1.3
R temporal S and W
Post-traumatic
Prominent sulci
Phenytoin valproic acid
4/48/0.I
4.3
6.1
1.. temporal S and W
Post-traumatic
Bifrontal hypodensity
Phenytoin + carbamazepine
5/50/0.2
2.1
2.8
_Ltemporal S and W
Unknown
Normal
Carbamazepine
6/61/0.8
1.8
1.3
R temporal S and W
Unknown
Diffuse atrophy
Phenytoin + primidone
7/38/0.7
0.3
0.2
R temporal S and W
Unknown
Mild diffuse atrophy
Phenytoin
8/29/0.2
1.7
2.0
Independent bifrontal S and W
Unknown
Normal
Carbamazepine
FIEDs = focal interictal epileptiform discharges; S and W = spike and waves; SD = the night after sleep deprivation; CTR = the control night.
the differences reached significance only during stage II of sleep (Fig. 3). The pooled mean number of FIEDs per unit of time during wakefulness was not significantly different from D N R E M stages of sleep either during control or after SD
nights. A significant reduction of pooled mean number of FIEDs per unit of time was observed during REM stages of sleep as compared to
The Comparison of the Pooled Mean Number of FIEDs Per Unit of Time During Pre and Post Sleep Deprivation Nights 50
Mean # of Epileptiform Discharge Prior and After S l e e p D e p r i v a t i o n
0809
45
.ff-" "'".....
=~ 35 30
O7
""
tL
25
15 10 03
05
02
(30
. . . .
AWAKE
O 1 OO
I AWAKE *s ignific ant
LNREM at p~ , } 0 5
ONREId
CTR Night
+
III Stages of S+eep
f] Night After SD
IV
REM
*significant at P < 0 0 5
REM
Fig. 2. Comparison of pooled mean number of focal interictal epileptiform discharges (FIEDs) per stage of sleep during the control night and the night after SD.
Fig. 3. Comparison of pooled mean number of FIEDs per minute during each stage of sleep in the control night and the night after SD. Note the significant rise during stage II sleep in the night after SD.
EFFECT OF SD ON THE RATE OF FIEDs
L N R E M ( P < 0 . 0 1 ) and D N R E M stages ( P < 0.02) in both nights. Blood concentration of anticonvulsant drugs showed minimal fluctuations during each night and between the 2 nights.
Discussion
In this study, we intended to exclude the variables that may have affected reliability of previous results regarding the efficacy of SD as an activating procedure for epileptiform discharges. We selected a homogenous population of epileptic patients, similar in gender, age, and seizure type. Patients were studied under uniform conditions which included a similar length of recording times. The reliability of SD in all patients was documented by the medical staff, and EEGs were interpreted blindly and independently by two experts. Despite these efforts, there were still considerable interindividual differences on the efficacy of SD as an activating method. Two patients failed to show any increase on the rate of FIEDs after SD, and others demonstrated a wide range of enhancement. However, it appears that those patients with abundant epileptiform discharges during the control night had a minimal or no increase discharges after SD (patients no. 1 and 3). On the other hand, those with minimal epileptiform discharges during the control night manifested several-fold increase in the rate of discharges after SD (Table I). When the pooled mean number of FIEDs was calculated per unit of time and compared for the waking period and for each of the stages of sleep between 2 nights, a significant rise was observed during LNREM stages in the night after SD. Furthermore, a significant increase of mean number of FIEDs per unit of time from awake to stage II sleep occurred only during the night after SD. Thus, the activation effect of sleep on the rate of FIEDs became apparent only after SD. There were no significant differences between awake and DNREM stages of sleep during either the control night or the night after SD. We were surprised to find a reduction in the number of FIEDs during wakefulness after the period of SD. A similar finding was noted by Veldhuizen et al. (1983) who
291
conducted a well-controlled study of mixed epileptic patients. Our results support the findings by Degen (1980), that an EEG which includes light sleep after SD is an effective activation method for epileptiform activity in patients treated with antiepileptic drugs. Since only stage II sleep contained a statistically significant rise in the number of FIEDs after SD, it should be included in the EEG recording after SD to maximize the efficacy of SD in the evaluation of patients suspected of CPS. References Bechinger, D., Kriebel, J. und Schlager, M. Das SchlafentzugEEG, ein wichtiges diagnostisches Hilfsmittel bei cerebralen Anfallen. Z. Neurol., 1973, 205: 193-206. Bennett, D.R., Mattson, R.H., Ziter, F.A., Calverley, J.R., Liske, E.A. and Pratt, K.L. Sleep deprivation: neurological and electroencephalographic effects. Aerospace Med., 1964, 35: 888-890. Bennett, D.R., Ziter, F.A. and Liske, E.A. Electroencephalographic study of sleep deprivation in flying personnel. Neurology, 1969, 19: 375-377. Berti Ceroni, G., Sabattini, L., Gambi, D. e Lugaresi, E. Effetti della 'sleep deprivation' in epilettici. Riv. Neurol., 1967, 37: 305-320. Broeker, H., Sack, G., Muller, D. und Muller, J. Schlaf-EEG Untersuchungen bei unklaren Anfallszustanden und episodischen Verhaltensstoerungen. Ein vorlaufiger Bericht. Psychiat. Neurol. Med. Psychol. (Lpz.), 1973, 11: 656-660. Degen, R. Die diagnostische Bedeutung des Schlafs nach Schlafentzug unter antiepileptischer Therapie. Nervenarzt, 1977, 48: 314-320. Degen, R. A study of the diagnostic value of waking and sleep EEGs after sleep deprivation in epileptic patients on anticonvulsive therapy. Electroenceph. clin. Neurophysiol., 1980, 49: 577-584. Ellingson, R.J., Wilken, K. and Bennett, D.R. Efficacy of sleep deprivation as an activating procedure in epilepsy patients. J. Clin. Neurophysiol., 1984, 1: 83-101. Gajkowski, K. and Zalejski, S. Comparative evaluation of seizure provocation methods with sleep deprivation and brietal in epileptics. Neurol. Neurochir. Pol., 1976, 10: 267-272. Gellar, M.R., Gourdji, N., Christoff, N. and Fox, E. The effects of sleep deprivation on the EEGs of epileptic children. Dev. Med. Child. Neurol., 1969, 11: 771-776. Gunderson, C.H., Dunne, P.B. and Feher, T.L. Sleep deprivation seizures. Neurology, 1973, 23: 678-686. Mattson, R.H., Pratt, K.L. and Calverley, J.R. Electroencephalograms of epileptics following sleep deprivation. Arch. Neurol., 1965, 13: 310-315.
292 Pratt, K.L., Mattson, R.H., Weikers, N.J. and Williams, R. EEG activation of epileptics following sleep deprivation: a prospective study of 114 cases. Electroenceph. clin. Neurophysiol., 1968, 24: 11-15. Ritter, G., Becker, A. und Duensing, F. Zum diagnostischen Wert des EEGs nach Schlafentzug. Nervenarzt, 1977, 48: 365-368. Rodin, E. Sleep deprivation and epileptological implications. In: R. Degen and E. Niedermeyer (Eds.), Epilepsy-SleepSleep Deprivation. Elsevier, Amsterdam, 1984: 295-302. Rowan, J., Veldhuizen, R.J. and Nagelkerke, N.J.D. Comparative evaluation of sleep deprivation and sedated sleep EEGs as diagnostic aids in epilepsy. Electroenceph. clin. Neurophysiol., 1982, 54: 357-364. Rumpl, E., Lorenzi, E., Bauer, G. und Hengl, W. Zum diagnostischen Wert des EEG nach Schlafentzug. Z. EEGEMG, 1977, 8: 205-209. Schwarz, J.R. and Zangemeister, W.H. The diagnostic value of the short sleep EEG and other provocative methods following sleep deprivation. J. Neurol., 1978, 218: 179-186.
M. MOLAIE, A. CRUZ Scollo-Lavizzari, G., Pralle, W. and De la Cruz, N. Activation effects of sleep deprivation and sleep in seizure patients. Eur. Neurol., 1975, 13:1 5. Scollo-Lavizzari, G., Pralle, W. and Radue, E.W. Comparative study of efficacy of waking and sleep recordings following sleep deprivation as an activating method in the diagnosis of epilepsy. Eur. Neurol.. 1977, 15: 121-123. Spadetta, V. La privazione di sonno nella diagnosi elettroencefalografica di epilessia. Acta Neurol. (Napoli), 1971. 26: 7 13. Tartara, A., Moglia, A., Manni, R. and Corbellini, C. EE(J findings and sleep deprivation. Eur. Neurol., 1980, 19: 330-334. Veldhuizen, R., Binnie, ('.D. and Beintema, D.J. The effect of sleep deprivation on the EEG in epilepsy. Electroenceph. clin. Neurophysiol., 1983, 55: 505-512. White, P., Dyken, M.. Grant, P. and Jackson, L. Electroencephalographic abnormalities during sleep as related to the temporal distribution of seizures. Epilepsia, 1962, 3: 167.-174.
Electroencephalograpto, and clinical Neurophysiology, 1988, 70:288-292 Elsevier Scientific Publishers Ireland, Ltd.
EEG 03571
The effect of sleep deprivation on the rate of focal interictal epilep,qorm disc ges Majid Molaie and Angel Cruz Department of Neurology, S U N Y Health Science Center and Veterans Administration Medical (?enter. 5~vracuse. N Y 13210 (U.S.A.)
(Accepted for publication: 8 March 1988)
Summary Eight men with complex partial seizures who had frequent focal interictal cpileptiform discharges (F1EDs) dunng routine EEGs were selected for all-night EEG recording before, and after 36 h of sleep deprivation. After sleep deprivation 6 of 8 patients showed increased FIEDs. The pooled mean number of FIEDs was greatest during light non-REM stages of sleep, especially stage II. Thus sleep deprivation is an effective activation method in medicated patients with complex partial seizures. However. a significant activation requires recording stage II sleep after sleep deprivation. Key words: Sleep deprivation; Epilepsy; Partial seizure; Sleep stages
The literature regarding the efficacy of sleep deprivation (SD) as an activating procedure for epileptiform activity is voluminous (Ellingson et al. 1984). Estimates of the incidence of activation range from 6.9% (Broeker et al. 1973) to 83% (Spadetta 1971). Some authors suggest that SD is a convenient way of inducing sleep in the EEG laboratory, and that the increased yield of epileptiform discharges is simply due to drowsiness and sleep after SD (White et al. 1962; Gajkowski and Zalejski 1976; Ritter et al. 1977; ScolloLavizzari et al. 1977). However, since seizures can be precipitated by prolonged periods of sleeplessness in persons without a history of epilepsy (Bennett et al. 1964, 1969; Gunderson et al. 1973), activation of epileptiform discharges by SD is not unexpected. The major source of controversy stems from the various uncontrolled methodological approaches to the problem. Ellingson et al. (1984) and Rodin
Correspondence to: Dr. M. Molaie, Neurology Service No. 127, VA Medical Center, Syracuse, NY 13210 (U.S.A.).
(1984) in their comprehensive reviews outlined these methodological shortcomings. For instance, EEG sampling time for pre- and post-SD records, and subjects' compliance to SD had been rarely cited in the literature (Ellingson et al. 1984). Most investigators had studied patients whose pre-SD records showed equivocal or no epileptiform discharges (Mattson et al. 1965; Berti Ceroni et al. 1967; Pratt et al. 1968; Gellar et al. 1969; Spadetta 1971; Bechinger et al. 1973; Scollo-Lavizzari et al. 1975, 1977; Degen 1977; Rumpl et al. 1977; Schwarz and Zangemeister 1978; Tartara et al. 1980; Rowan et al. 1982). Several authors studied known epileptics, but without reporting anticonvulsant blood levels before or after SD (Rodin 1984). Veldhuizen et al. (1983) pointed out that if a population of patients not showing epileptiform activity in the initial EEG is selected for study, a second recording will inevitably demonstrate a higher discharge incidence than the first due to the statistical phenomenon of regression to the mean. Veldhuizen et al. (1983) randomly selected epileptic patients irrespective of whether the initial EEGs contained epileptiform activity. Their re-
0013-4649/88/$03.50 © 1988 Elsevier Scientific Publishers Ireland, Ltd.
289
EFFECT OF SD ON THE RATE OF FIEDs sults indicated no evidence of an overall increase in discharge rate after SD either in waking or sleep records. In our study, we attempted to control the variables that may have led to conflicting results in previous studies regarding the effect of SD as an activating procedure.
Methodology Eight men with complex partial seizures (CPS), who manifested frequent focal interictal epileptiform discharges (FIEDs) during several routine day-time E E G recordings were selected for the study. Mean age was 48 years (range of 29-63 years), and all were taking antiepileptic drugs, six received phenytoin alone or with another anticonvulsant. Causes of seizures, brain CT findings, and other pertinent data are outlined in Table I. All subjects were admitted to the neurology ward in the morning. At 20.00 h, they reported to the sleep laboratory where electrodes were placed on the scalp and face for all night (23.00-6.00 h) continuous EEG, EOG, and E M G recordings. A low intensity light camera mounted in the bedroom ceiling permitted continuous observation of patients on closed circuit TV and video monitoring of the subjects sleeping in the dark. A 7 h awake and sleep recording was performed on the first night which served as a control. Patients were remained awake for 36 h from 11.00 h to 23.00 h the next day. Patients were studied in pairs in order to keep each other awake under supervision of medical staff. Nocturnal recording was repeated after 36 h of SD in a similar fashion as the baseline study. Nocturnal EEGs were scored according to periods of wakefulness and light nonREM (LNREM) (stages I and II), deep non-REM (DNREM) (stages III and IV), and REM stages. FIEDs were calculated visually in the E E G records by two readers who were blind both to the patient identification and to the baseline versus SD records. The number of FIEDs was calculated per unit of time for different stages of sleep during the control night and during the night after SD. Blood was sampled twice in each patient, during
the control night and the night after SD, to measure anticonvulsant drug levels.
Results
Sleep data The pooled mean percentage of sleep stages was not significantly different between the 2 nights except for the percentage of wakefulness which was significantly lower the night after SD (8.52 + 3.27, P < 0.05) than in the control night (13.77 + 5.77, Fig. 1). Six of the 8 patients had increased total number of FIEDs during the night after SD with the ratio ranging from 1.2 to 12.3. Those patients with abundant discharges during the control night had minimal increased ratio (patients no. 1 and 3), and those with minimal number of discharges had maximum increased ratio of FIEDs on the night after SD (patients no. 2 and 4, Table I). The pooled mean percentages of FIEDs per sleep stage did not differ significantly between both nights, but after SD, the pooled mean number of FIEDs showed a significant increase ( P < 0.05) during L N R E M stages of sleep (Fig. 2). The pooled mean number of FIEDs, when adjusted per unit of time for each stage of sleep, showed a significant increase ( P < 0 . 0 5 ) from awake to L N R E M stages of sleep only during the night after SD. Further data analysis revealed that
Percentage of Sleep Stages
/
~ REM / IV I (11.I%)~' (12.7%) ,
\
II
152.0%1
/
/
J
/ /
During the CTR Night
\,\
,
/
During the Night After SD
Fig. 1. Comparison of pooled mean percentage of sleep stages during the control night and the night after SD.
M. MOLAIE, A. CRUZ
290 TABLE I Patients no./age/ rate of FIEDs/
Ratio of FIEDs (SD/CTR)
rain during the CTR night
All night
1/39/10.3
Persistent EEG foci
Cause of seizures
of head
R frontal S and W discharges
CT scan
Antiepileptic drugs
Post-traumatic
Small _Rfrontal hypodensitx,
Phenytoin + carbamazepine
R temporal and central S and W
Post-traumatic
Bifrontal h~podensit 3
Phenytoin-~ phenobarbital
Stage II sleep
1.2
1.5
2/55/'0.1
12.3
27.3
3/63/7.3
0.8
1.3
R temporal S and W
Post-traumatic
Prominent sulci
Phenytoin valproic acid
4/48/0.I
4.3
6.1
1.. temporal S and W
Post-traumatic
Bifrontal hypodensity
Phenytoin + carbamazepine
5/50/0.2
2.1
2.8
_Ltemporal S and W
Unknown
Normal
Carbamazepine
6/61/0.8
1.8
1.3
R temporal S and W
Unknown
Diffuse atrophy
Phenytoin + primidone
7/38/0.7
0.3
0.2
R temporal S and W
Unknown
Mild diffuse atrophy
Phenytoin
8/29/0.2
1.7
2.0
Independent bifrontal S and W
Unknown
Normal
Carbamazepine
FIEDs = focal interictal epileptiform discharges; S and W = spike and waves; SD = the night after sleep deprivation; CTR = the control night.
the differences reached significance only during stage II of sleep (Fig. 3). The pooled mean number of FIEDs per unit of time during wakefulness was not significantly different from D N R E M stages of sleep either during control or after SD
nights. A significant reduction of pooled mean number of FIEDs per unit of time was observed during REM stages of sleep as compared to
The Comparison of the Pooled Mean Number of FIEDs Per Unit of Time During Pre and Post Sleep Deprivation Nights 50
Mean # of Epileptiform Discharge Prior and After S l e e p D e p r i v a t i o n
0809
45
.ff-" "'".....
=~ 35 30
O7
""
tL
25
15 10 03
05
02
(30
. . . .
AWAKE
O 1 OO
I AWAKE *s ignific ant
LNREM at p~ , } 0 5
ONREId
CTR Night
+
III Stages of S+eep
f] Night After SD
IV
REM
*significant at P < 0 0 5
REM
Fig. 2. Comparison of pooled mean number of focal interictal epileptiform discharges (FIEDs) per stage of sleep during the control night and the night after SD.
Fig. 3. Comparison of pooled mean number of FIEDs per minute during each stage of sleep in the control night and the night after SD. Note the significant rise during stage II sleep in the night after SD.
EFFECT OF SD ON THE RATE OF FIEDs
L N R E M ( P < 0 . 0 1 ) and D N R E M stages ( P < 0.02) in both nights. Blood concentration of anticonvulsant drugs showed minimal fluctuations during each night and between the 2 nights.
Discussion
In this study, we intended to exclude the variables that may have affected reliability of previous results regarding the efficacy of SD as an activating procedure for epileptiform discharges. We selected a homogenous population of epileptic patients, similar in gender, age, and seizure type. Patients were studied under uniform conditions which included a similar length of recording times. The reliability of SD in all patients was documented by the medical staff, and EEGs were interpreted blindly and independently by two experts. Despite these efforts, there were still considerable interindividual differences on the efficacy of SD as an activating method. Two patients failed to show any increase on the rate of FIEDs after SD, and others demonstrated a wide range of enhancement. However, it appears that those patients with abundant epileptiform discharges during the control night had a minimal or no increase discharges after SD (patients no. 1 and 3). On the other hand, those with minimal epileptiform discharges during the control night manifested several-fold increase in the rate of discharges after SD (Table I). When the pooled mean number of FIEDs was calculated per unit of time and compared for the waking period and for each of the stages of sleep between 2 nights, a significant rise was observed during LNREM stages in the night after SD. Furthermore, a significant increase of mean number of FIEDs per unit of time from awake to stage II sleep occurred only during the night after SD. Thus, the activation effect of sleep on the rate of FIEDs became apparent only after SD. There were no significant differences between awake and DNREM stages of sleep during either the control night or the night after SD. We were surprised to find a reduction in the number of FIEDs during wakefulness after the period of SD. A similar finding was noted by Veldhuizen et al. (1983) who
291
conducted a well-controlled study of mixed epileptic patients. Our results support the findings by Degen (1980), that an EEG which includes light sleep after SD is an effective activation method for epileptiform activity in patients treated with antiepileptic drugs. Since only stage II sleep contained a statistically significant rise in the number of FIEDs after SD, it should be included in the EEG recording after SD to maximize the efficacy of SD in the evaluation of patients suspected of CPS. References Bechinger, D., Kriebel, J. und Schlager, M. Das SchlafentzugEEG, ein wichtiges diagnostisches Hilfsmittel bei cerebralen Anfallen. Z. Neurol., 1973, 205: 193-206. Bennett, D.R., Mattson, R.H., Ziter, F.A., Calverley, J.R., Liske, E.A. and Pratt, K.L. Sleep deprivation: neurological and electroencephalographic effects. Aerospace Med., 1964, 35: 888-890. Bennett, D.R., Ziter, F.A. and Liske, E.A. Electroencephalographic study of sleep deprivation in flying personnel. Neurology, 1969, 19: 375-377. Berti Ceroni, G., Sabattini, L., Gambi, D. e Lugaresi, E. Effetti della 'sleep deprivation' in epilettici. Riv. Neurol., 1967, 37: 305-320. Broeker, H., Sack, G., Muller, D. und Muller, J. Schlaf-EEG Untersuchungen bei unklaren Anfallszustanden und episodischen Verhaltensstoerungen. Ein vorlaufiger Bericht. Psychiat. Neurol. Med. Psychol. (Lpz.), 1973, 11: 656-660. Degen, R. Die diagnostische Bedeutung des Schlafs nach Schlafentzug unter antiepileptischer Therapie. Nervenarzt, 1977, 48: 314-320. Degen, R. A study of the diagnostic value of waking and sleep EEGs after sleep deprivation in epileptic patients on anticonvulsive therapy. Electroenceph. clin. Neurophysiol., 1980, 49: 577-584. Ellingson, R.J., Wilken, K. and Bennett, D.R. Efficacy of sleep deprivation as an activating procedure in epilepsy patients. J. Clin. Neurophysiol., 1984, 1: 83-101. Gajkowski, K. and Zalejski, S. Comparative evaluation of seizure provocation methods with sleep deprivation and brietal in epileptics. Neurol. Neurochir. Pol., 1976, 10: 267-272. Gellar, M.R., Gourdji, N., Christoff, N. and Fox, E. The effects of sleep deprivation on the EEGs of epileptic children. Dev. Med. Child. Neurol., 1969, 11: 771-776. Gunderson, C.H., Dunne, P.B. and Feher, T.L. Sleep deprivation seizures. Neurology, 1973, 23: 678-686. Mattson, R.H., Pratt, K.L. and Calverley, J.R. Electroencephalograms of epileptics following sleep deprivation. Arch. Neurol., 1965, 13: 310-315.
292 Pratt, K.L., Mattson, R.H., Weikers, N.J. and Williams, R. EEG activation of epileptics following sleep deprivation: a prospective study of 114 cases. Electroenceph. clin. Neurophysiol., 1968, 24: 11-15. Ritter, G., Becker, A. und Duensing, F. Zum diagnostischen Wert des EEGs nach Schlafentzug. Nervenarzt, 1977, 48: 365-368. Rodin, E. Sleep deprivation and epileptological implications. In: R. Degen and E. Niedermeyer (Eds.), Epilepsy-SleepSleep Deprivation. Elsevier, Amsterdam, 1984: 295-302. Rowan, J., Veldhuizen, R.J. and Nagelkerke, N.J.D. Comparative evaluation of sleep deprivation and sedated sleep EEGs as diagnostic aids in epilepsy. Electroenceph. clin. Neurophysiol., 1982, 54: 357-364. Rumpl, E., Lorenzi, E., Bauer, G. und Hengl, W. Zum diagnostischen Wert des EEG nach Schlafentzug. Z. EEGEMG, 1977, 8: 205-209. Schwarz, J.R. and Zangemeister, W.H. The diagnostic value of the short sleep EEG and other provocative methods following sleep deprivation. J. Neurol., 1978, 218: 179-186.
M. MOLAIE, A. CRUZ Scollo-Lavizzari, G., Pralle, W. and De la Cruz, N. Activation effects of sleep deprivation and sleep in seizure patients. Eur. Neurol., 1975, 13:1 5. Scollo-Lavizzari, G., Pralle, W. and Radue, E.W. Comparative study of efficacy of waking and sleep recordings following sleep deprivation as an activating method in the diagnosis of epilepsy. Eur. Neurol.. 1977, 15: 121-123. Spadetta, V. La privazione di sonno nella diagnosi elettroencefalografica di epilessia. Acta Neurol. (Napoli), 1971. 26: 7 13. Tartara, A., Moglia, A., Manni, R. and Corbellini, C. EE(J findings and sleep deprivation. Eur. Neurol., 1980, 19: 330-334. Veldhuizen, R., Binnie, ('.D. and Beintema, D.J. The effect of sleep deprivation on the EEG in epilepsy. Electroenceph. clin. Neurophysiol., 1983, 55: 505-512. White, P., Dyken, M.. Grant, P. and Jackson, L. Electroencephalographic abnormalities during sleep as related to the temporal distribution of seizures. Epilepsia, 1962, 3: 167.-174.