PEDIATRICS Vol. 114 No. 3 September 2004, pp. 658-662 (doi:10.1542/peds.2003-0612-L)
Does Sleep or Sleep Deprivation Increase Epileptiform Discharges in Pediatric Electroencephalograms?
From the Division of Neurology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONCONCLUSIONSREFERENCES |
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Objective. Sleep deprivation before obtaining an electroencephalogram (EEG) is believed both to increase the likelihood of sleep during an EEG and to increase the detection of interictal epileptiform discharges. However, depriving a child of sleep poses a burden on both the parent and the child. The objective of this study was to compare the effects of sleep, standard sleep deprivation, partial sleep deprivation, and no sleep deprivation on the odds of an epileptiform abnormality in outpatient pediatric EEGs.
Methods. Data were collected from all pediatric EEGs performed at a busy, university-based neurologic practice during two 2-month periods. During the first period, all EEGs were performed as ordered, either standard sleep-deprived (SSD) or non–sleep-deprived (NSD). During the second 2 months, SSD EEGs were performed per routine. However, non-SSD families were instructed to keep their children awake 2 hours later the night before the EEG. Those who complied were classified as partially sleep-deprived (PSD). Patient characteristics across protocols were compared with 
2 and analysis of variance tests as appropriate. The odds of epileptiform and abnormal findings associated with sleep, NSD, PSD, and SSD EEGs were calculated using logistic regression.
Results. Of 820 eligible EEGs, sleep occurred in 22% of NSD, 44% of PSD, and 57% of SSD EEGs. The sample size of this study allowed for an 85% power, with 
of .05, to detect an absolute increased EEG yield of 10%. Neither the presence of sleep (odds ratio [OR]: 0.99; 95% confidence interval [CI]: 0.69-1.42) nor the use of PSD (OR: 0.90; 95% CI: 0.50-1.62) or SSD (OR: 0.96; 95% CI: 0.63-1.47) protocols increased the odds of epileptiform EEGs.
Conclusions. Sleep deprivation should not be used routinely to increase the yield of pediatric EEGs.
Key Words: EEG • sleep • children • seizure • epilepsy • diagnostic test
Abbreviations: EEG, electroencephalogram • NSD, non–sleep-deprived • PSD, partial sleep-deprived • SSD, standard sleep-deprived • ASD, antiseizure drug • HSD, honestly significantly different • OR, odds ratio
The epilepsies are a heterogeneous group of chronic, potentially life-threatening, yet treatable conditions characterized by recurring unprovoked seizures. The onset is often in childhood.1 Although the diagnosis of epilepsy is clinical, an electroencephalogram (EEG) is commonly performed to gain additional diagnostic or prognostic information.
EEGs have been recommended as a standard of care after a first unprovoked seizure in childhood.2 They may also aid in syndrome diagnosis in new-onset epilepsy.3,4 However, approximately half of routine EEGs in children with clinically diagnosed epilepsy show no abnormalities.5,6
One approach that is believed to increase the likelihood of detecting epileptiform discharges is sleep deprivation.7–10 Sleep-deprived EEG protocols require keeping the patient awake all or part of the night before an EEG. Clinically, sleep deprivation is a trigger of seizures and is believed to increase detection of epileptiform discharges. The American Electroencephalography Society’s Guideline and Technical Standards states that "sleep recordings should be obtained whenever possible."11 However, several studies have questioned the value of sleep deprivation before EEGs.6,12,13 A recent review concluded that there is no consensus as to whether partial sleep deprivation or total, 24-hour sleep deprivation is superior and that "little evidence, informed opinion, or guidance on sleep-deprived EEGs has penetrated to practitioners."14
One common practice is to order a non–sleep-deprived (NSD) EEG first, and if this is normal or fails to show sleep, to obtain a repeat sleep-deprived EEG.15–17 However, in studies showing increased yield of repeat EEGs, some of the additional findings could be attributable to the effect of repeated sampling.17 If the EEG yield is higher with sleep deprivation, then it may be more cost-effective to obtain sleep-deprived EEGs in all patients the first time. Alternatively, if the yield after sleep deprivation is no better than the yield after NSD, then obtaining sleep-deprived EEGs may pose an unnecessary burden to parents and children.
Recently, in hopes of increasing the occurrence of natural sleep during EEGs, our neurophysiology laboratory began instructing parents to keep their children awake an extra 2 hours the night before the EEG, such that there would be partial sleep deprivation. Because the children who received EEGs before and after the change in laboratory policy should not be different clinically, this created a unique opportunity for an observational study to produce an unbiased comparison of the yield of NSD and sleep-deprived EEGs in childhood. The purpose of this study was to estimate and compare the yield of partially sleep-deprived (PSD) and standard sleep-deprived (SSD) versus NSD pediatric outpatient EEGs. We sought to determine whether sleep-deprivation protocols, or the presence of sleep, affect the odds of positive EEGs in children for whom physicians ordered EEGs as part of routine clinical practice.
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METHODS |
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All EEGs were obtained on outpatients who were aged 0 to 18 years. Cincinnati Children’s Hospital Medical Center provides most of the pediatric neurology care in the greater Cincinnati metropolitan area. During the time of this study, there were >10 new patient referrals per week to a "new-onset seizure" clinic. At the request of referring physicians, EEGs were performed on a wide spectrum of cases, including children with unclear spells, first seizure, epilepsy, intractable epilepsy, headaches, and behavior problems. Eighty-three percent of test requisitions in children who are not taking antiseizure drugs (ASDs) and 96% of requisitions in children who are taking ASD state "seizure" as the reason for the EEG. At our institution, 47% of EEGs are ordered by generalists, mainly pediatricians. Overall, 26% of EEGs ordered by neurologists and 10% ordered by pediatricians are sleep-deprived.6
EEGs
All EEGs were performed using a 21-channel digital recording. Standard protocols included 20- to 30-minute EEG tracings, photic stimulation, and hyperventilation in cooperative children. Children did not receive pharmacologic sedation.
EEG results from two 2-month periods were entered into a database and analyzed. During the first 2-month period, October to November 2001, all patients received either an NSD EEG or SSD EEG, as ordered by the primary physician. At our institution, SSD instructions include no naps or caffeine before the EEG, and age-based sleep deprivation: age >11 years, stay awake after 12 AM the night before; age 3 to 11 years, stay awake after 2 AM; age <3 years, stay awake after 4 AM. Sleep-deprived EEGs are performed in the morning.
During the second 2-month period, February to March 2002, subjects for whom a sleep-deprived EEG was ordered by the primary physician received SSD as ordered. Beginning in January 2002, technicians and the scheduling center had been instructed to ask all other families to do PSD EEGs. Instructions for PSD EEGs included no caffeine and no naps the day of the EEG and to stay awake 2 hours past the usual bedtime the night before the EEG for children 2 years and older. Children younger than 2 years could not take a nap before the EEG. One investigator (M.A.B.) questioned families and technicians to determine whether families complied. Those who complied were categorized as PSD; those who did not, for whatever reason, were categorized as NSD.
Data Collection
After all EEGs had been completed and interpreted by the interpreting neurologists as routine clinical studies, data from patients aged 0 to 18 years were extracted directly into data collection forms from the primary EEG report and were de-identified by 1 researcher (M.A.B.). Approval for data collection was granted by the Cincinnati Children’s Hospital Institutional Review Board. Data included age at the time of the EEG, date of study, study period (1 or 2), current use of ASDs (yes/no and number), sleep deprivation protocol (NSD, PSD, SSD), presence of stage II sleep (yes, no), and EEG interpretation (epileptiform discharges yes/no; any abnormality yes/no).
Statistical Analyses
Exploratory univariate analyses, using analysis of variance and 2 as appropriate, were performed comparing characteristics of patients in period 1 versus period 2. Our expectation, because the only known difference between these patients was the month in which the EEG was ordered, was that there would be no significant differences in period 1 versus 2. As an additional check on this assumption, we compared the proportion of EEGs identified as epileptiform across periods, within SSD and NSD protocols, which occurred in both periods.
Next, age and use of ASDs, 2 factors known to influence the odds of epileptiform EEGs, were compared between patients on the 3 protocols. Because patients were not randomly allocated to SSD versus NSD protocols (SSD was ordered specifically), we anticipated that these factors might differ between SSD and other protocols. Also, age and ASD use might have influenced compliance with PSD. Comparisons were made using 2 and analysis of variance, with post hoc bivariate analyses, using Tukey’s honestly significantly different (HSD) P value to correct for multiple comparisons, as needed. ASD and age were included as independent predictors in subsequent regression analyses for the main outcomes of interest.
We were interested in determining whether sleep affected yield differently in subjects who received EEGs for seizures versus subjects who received EEGs for other reasons. Because the majority of children who are not taking ASDs and receive EEGs for which "seizure" is written on the requisition have other types of (nonseizure) spells, the chief complaint is not a good marker of the actual diagnosis.6 Therefore, we compared the frequency of epileptiform EEGs with and without sleep separately for children who were and were not taking ASDs, using the Mantel-Haenszel test.
For the final analysis, there are 3 dichotomous outcomes of interest: presence of sleep, presence of epileptiform discharges, and presence of any EEG abnormality. Crude frequencies of epileptiform discharges and other abnormalities are reported for each protocol, by sleep status, and by ASD and age group. Multivariate logistic regression was performed to estimate the odds of sleep and of positive EEGs by protocol. Adjusted odds ratios (ORs) and 95% confidence intervals were calculated.
Because the occurrence of sleep is not independent of sleep deprivation protocol and may be a pathway variable, regression analyses were performed separately to determine the odds of epileptiform or abnormal EEGs in the presence of stage II sleep and the odds with sleep deprivation protocols. The following regression analyses were performed:
P (stage II sleep) = sleep protocol (NSD, PSD, SSD) + age (<2; >2) + ASD (Y; N)
P (epileptiform discharge) = sleep protocol (NSD, PSD, SSD) + age (<2; >2) + ASD (Y; N)
P (epileptiform discharge) = sleep (Y; N) + age (<2; >2) + ASD (Y; N)
P (abnormal EEG) = sleep protocol (NSD, PSD, SSD) + age (<2; >2) + ASD (Y; N)
P (abnormal EEG) = sleep (Y; N) + age (<2; >2) + ASD (Y; N)
Regressions were also performed with age as a continuous variable. All analyses were performed using SPSS version 11.5 (SPSS Inc, Chicago, IL).
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RESULTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONCONCLUSIONSREFERENCES |
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Subjects, Protocols, Time Periods, and EEGs
There were 820 EEGs in the 2 time periods. In period 1, 402 EEGs were performed, 94 of which were SSD and 308 were NSD. In period 2, 418 EEGs were performed, 129 of which were SSD, 88 were PSD, and 201 were NSD. Compliance with the PSD protocol was poor as a result of patients’ not receiving instructions in a timely manner from the call center, from the EEG technicians, or from the ordering physicians and of families’ choosing not to comply.
Subjects ranged in age from 0 to 18 years (mean: 6.6, standard deviation: 5.2 years). There were no significant differences in the mean ages in period 1 (6.7 years) versus period 2 (6.6 years; P = .74). The proportions of subjects who were taking ASDs in period 1 (27%) versus period 2 (32%) were not significantly different (P = .16). The proportions of NSD EEGs interpreted as epileptiform in period 1 (22%) versus period 2 (27%) were not significantly different (P = .17). The proportions of SSD EEGs interpreted as epileptiform in period 1 (22%) versus period 2 (23%) were not significantly different (P = .98).
There were significant differences in the ages of subjects in the 3 protocols, with age assessed as a continuous variable or dichotomized into categories "<2 years old" versus ">2 years old" (Table 1). Post hoc, SSD patients were significantly older than those in the other 2 protocols (Tukey’s HSD, P < .01 for each). There was no significant difference in age between the PSD and NSD groups (Tukey’s HSD, P = .09). The proportion of subjects who were taking ASDs seemed to be lower in the SSD group (Table 1). However, the difference by protocol was only borderline statistically significant.
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Odds of Sleep by Protocol
Odds of stage II sleep were higher in SSD and PSD protocols, compared with NSD (Table 2). Sleep occurred in 42% of younger children (77 of 183) versus 31% of older children (200 of 637). Sleep was not more likely to occur in children who were taking ASDs.
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Frequencies of Epileptiform and Abnormal EEGs With Sleep, Stratifying for ASD Use
Overall, 43% of EEGs in children who were taking ASDs showed epileptiform discharges, versus 15% of EEGs in children who were not taking ASDs. Overall, 22% of EEG tracings with sleep and 24% of EEGs with no sleep showed epileptiform discharges.
The percentages of epileptiform and abnormal EEGs by presence of sleep, stratified by ASD use, are shown in Table 3. Among 241 subjects who were taking ASDs, 41% of EEGs with sleep showed epileptiform discharges, compared with 44% of EEGs with no sleep. Among 579 patients who were not taking ASDs, 15% of EEGs with sleep showed epileptiform discharges versus 16% of EEGs without sleep (Table 3). Stratifying for use of ASDs, epileptiform discharges were not more common in EEGs with sleep (Mantel-Haenszel 2 = 0.06, P = .8). ORs for epileptiform EEGs were not different by ASD use (Breslow-Day 2 = 0.07, P = .8). Similarly, the probability that any abnormality would be seen on EEG was not higher in EEGs with sleep, stratifying for ASD use (Mantel-Haenszel 2 = 0.95, P = .3). ORs for any abnormality on EEG were not different by ASD use (Breslow-Day 2 = 0.52, P = .5).
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Frequencies of Epileptiform and Abnormal EEGs With Sleep Protocols, Stratifying for ASD Use
Overall, 24% (123 of 509) of NSD, 21% (18 of 88) of PSD, and 23% (52 of 223) of SSD EEGs showed epileptiform discharges. The percentages of epileptiform and abnormal EEGs by protocol, stratified by ASD use, are shown in Table 4. There is no significant association between proportion of EEGs showing epileptiform discharges and sleep protocol in children who were taking ASDs (
2 = 1.5, P = .5) or were not taking ASDs (2 = 3.5, P = .2). The proportion of abnormal EEGs was not significantly associated with sleep protocol in children who were not taking ASDs (2 = 2.4, P = .3). However, among children who were taking ASDs, there seemed to be a significant association between sleep protocol and the proportion of abnormal EEGs (2 = 8.0, P = .02), with abnormal EEGs occurring most commonly in the NSD EEGs.
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Multivariate Analysis of Relationships Between Sleep, Sleep Deprivation Protocols, and Odds of Epileptiform EEGs
Among NSD EEGs, epileptiform discharges were present in 19% (21 of 110) with sleep versus 26% (102 of 399) with no sleep. Among PSD EEGs, epileptiform discharges were present in 26% (10 of 39) with sleep versus 16% (8 of 49) without sleep. Among SSD EEGs, epileptiform discharges were present in 23% (30 of 128) with sleep versus 23% (22 of 95) without sleep.
In the multivariate analyses, after accounting for age and ASD use, there was no evidence that sleep deprivation protocols increased the odds that an EEG would be interpreted as epileptiform (Table 5). Similarly, the adjusted odds of an epileptiform EEG were not greater when stage II sleep was observed (Table 6).
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Relationships Between Sleep, Sleep Deprivation Protocols, and Odds of Abnormal EEGs
Overall, 32% of NSD, 23% of PSD, and 25% of SSD EEGs showed any abnormality. Among NSD EEGs, abnormal discharges were present in 25% (27 of 110) with sleep versus 34% (134 of 399) without sleep. Among PSD EEGs, abnormal discharges were present in 26% (10 of 39) with sleep versus 20% (10 of 49) without sleep. Among SSD EEGs, abnormal discharges were present in 27% (34 of 128) with sleep versus 23% (22 of 95) without sleep.
In the multivariate analyses, after accounting for age and ASD use, there was no evidence that sleep deprivation protocols increased the odds that an EEG would be interpreted as abnormal (Table 5). Similarly, the adjusted odds of an abnormal EEG were no different when stage II sleep was observed (Table 6). The results of these analyses were similar when age was included as a continuous covariate versus a categorical variable (data not shown).
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONCONCLUSIONSREFERENCES |
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Neither sleep deprivation protocols nor the presence of stage II sleep increased the probability of positive EEGs. The only significant effect of sleep deprivation was to increase the odds of sleep occurring.
The sample size of this study allowed for an 85% power, with of .05, to detect an absolute increased EEG yield of 10% as a result of either sleep or sleep deprivation protocol. Thus, this negative finding is robust, with an acceptably low probability of type II error. When we stratified by current use of ASDs, a marker of epilepsy, we found, as expected, a high prevalence of epileptiform and abnormal EEGs, similar to that seen in other pediatric epilepsy studies.17 However, there was no association between achieving sleep and the frequency of epileptiform EEGs in subjects who were or were not taking ASDs. This suggests that our failure to find a relationship between sleep and EEG yield was not caused by case mix or the low pretest probability of positive EEGs.
The results of this study apply to pediatric EEGs in general but do not exclude the possibility that sleep or sleep-deprived EEGs provide useful information in selected circumstances. We did not identify the prevalence of epilepsy syndromes, eg, electrical status epilepticus during slow sleep, diagnosed during sleep EEGs. We also did not address the use of sleep and overnight video/EEGs for evaluating nocturnal epilepsies and parasomnias. Clinical factors that affect the preferred diagnostic approach may be more familiar to practicing neurologists and epileptologists than to nonneurologists.
The overall yield of EEG may reflect the current practice patterns in many communities.6,18–21 Recent clinical practice guidelines for headache22 and developmental delay23 have not supported the routine use of EEGs for nonseizure purposes. We do not believe that EEGs, with or without sleep deprivation, are routinely indicated for nonseizure diagnoses. We believe that a careful clinical evaluation, by a specialist if necessary, should precede the decision to order a sleep-deprived EEG.
The chief limitation of our analysis of the relationship between sleep deprivation protocol and EEG yield is the nonrandom allocation of patients to the SSD protocol. However, because PSD occurred in period 2 as a result of a policy change in our laboratory, we believe that children who receive PSD and NSD EEGs should be clinically similar enough to allow for a valid, unbiased comparison between these groups. It is possible that some subjects who had SSDs have forms of epilepsy in which interictal epileptiform discharges occur less frequently, thereby lowering the apparent yield. In addition, patients with severe epileptic encephalopathies, such as Lennox Gastaut, may have been less likely to have SSD EEGs ordered. These diagnoses represent a small fraction of the outpatient EEGs in this study, however.
This study did not assess the clinical utility of the common practice of obtaining an NSD first and an SSD or a PSD EEG second.15,17 However, in studies in which repeat sleep-deprived EEGs show additional findings, it is not always clear whether the additional findings result from sleep or from obtaining another EEG.
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CONCLUSIONS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONCONCLUSIONSREFERENCES |
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The null associations between the presence of sleep/sleep deprivation and positive EEGs in this study suggest that sleep deprivation is not a simple method of increasing the yield of pediatric EEGs. Therefore, a general practice of obtaining first sleep-deprived EEGs or repeat sleep-deprived EEGs, solely because a first EEG was negative or lacked sleep, is not supported. Patients and families should be subjected to sleep-deprived EEGs in select instances in which a particular epilepsy syndrome diagnosis, suspected or established by a knowledgeable clinician, requires additional electrophysiologic information known to be better achieved in sleep. The most important indications and methods for sleep-deprived EEGs remain a matter of some controversy among neurologists,14 but at present, it seems that there is insufficient evidence of increased diagnostic information to justify a routine approach of depriving a child and a parent of sleep before a pediatric EEG.
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ACKNOWLEDGMENTS |
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Financial support for this study was provided by the Division of Neurology at Cincinnati Children’s Hospital Medical Center (Cincinnati, OH) and through K23 NS41920 (D.L.G.).
We thank Robert Van Howe, MD, and Elaine Caoili, MD, for helpful comments on the manuscript and the expert technicians and neurologists who performed and interpreted the EEGs.
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FOOTNOTES |
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Accepted Feb 17, 2004.
Reprint requests to (D.L.G.) Division of Neurology, Cincinnati Children’s Hospital Medical Center, ML 2015, 3333 Burnet Ave, Cincinnati, OH 45229-3039. E-mail: d.gilbert{at}cchmc.org
This research was presented in part at the 2002 Meeting of the American Epilepsy Society; Dec 6–11, 2002; Seattle, Washington.
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PEDIATRICS (ISSN 1098-4275). ©2004 by the American Academy of Pediatrics
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