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DOI: 10.1542/peds.2008-0357 2009


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DOI: 10.1542/peds.2008-0357 2009

  1. 1. Effects of Sleep Deprivation on the Pediatric Electroencephalogram Steven T. DeRoos, Kipp L. Chillag, Martina Keeler and Donald L. Gilbert Pediatrics 2009;123;703-708 DOI: 10.1542/peds.2008-0357 The online version of this article, along with updated information and services, is located on the World Wide Web at: PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly publication, it has been published continuously since 1948. PEDIATRICS is owned, published, and trademarked by the American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk Grove Village, Illinois, 60007. Copyright © 2009 by the American Academy of Pediatrics. All rights reserved. Print ISSN: 0031-4005. Online ISSN: 1098-4275. Downloaded from by on October 18, 2010
  2. 2. ARTICLE Effects of Sleep Deprivation on the Pediatric Electroencephalogram Steven T. DeRoos, MDa, Kipp L. Chillag, DOa, Martina Keeler, MDb, Donald L. Gilbert, MDc Divisions of aPediatric Neurology and bPediatric Hospitalists, Helen DeVos Children’s Hospital, Grand Rapids, Michigan; cDivision of Pediatric Neurology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio The authors have indicated they have no financial relationships relevant to this article to disclose. What’s Known on This Subject What This Study Adds Sleep deprivation is thought to increase the yield of epileptiform discharges on pediatric This is the first pediatric study to directly compare sleep deprivation with routine EEG. EEG. ABSTRACT BACKGROUND. The routine electroencephalogram aids in epilepsy syndrome diagnosis. Unfortunately, routine outpatient electroencephalogram results are normal in roughly half of children with epilepsy. To increase the yield, practice guidelines peds.2008-0357 recommend electroencephalograms with sleep and sleep deprivation. The purpose of this study was to rigorously evaluate this recommendation in children. doi:10.1542/peds.2008-0357 The funding source had no involvement in METHODS. We conducted a randomized, blinded comparison of routine electroen- the study design; collection, analysis, or cephalograms versus sleep-deprived electroencephalograms in 206 children aged interpretation of the data; writing of the report; or in the decision to submit the 0 to 18 years. Electroencephalograms were ordered for standard indications after article for publication. a neurologist’s clinical assessment indicated 1 seizure (83%) or unclear spell Key Words (17%). The primary outcome was the proportion of normal routine electroen- EEG, electroencephalogram, epilepsy, cephalogram results versus sleep-deprived electroencephalogram results. Logistic pediatric, seizure, sleep deprivation regression modeling was used to assess the influence of sleep, as well as other Abbreviations clinical factors. EEG— electroencephalogram SDEEG—sleep-deprived RESULTS. Although children with sleep-deprived electroencephalograms had less sleep electroencephalogram REEG—routine electroencephalogram the night before (4.9 vs 7.9 hours) and more sleep during electroencephalograms ASD—antiseizure drug (73% vs 55%), the increase in electroencephalogram yield was borderline significant df— degree(s) of freedom (56% normal sleep-deprived electroencephalogram versus 68% normal routine OR— odds ratio electroencephalogram). Moreover, sleep during the electroencephalogram did not CI— confidence interval increase its diagnostic yield. Sleep-deprived electroencephalogram yield tended to be Accepted for publication Jun 6, 2008 higher in children with preelectroencephalogram clinical diagnosis of seizure(s) and Address correspondence to Steven T. DeRoos, MD, 1300 Michigan, Suite 102, Grand Rapids, at older ages ( 3 years). MI 49503. E-mail: steven.deroos@ CONCLUSIONS. Sleep deprivation, but not sleep during the electroencephalogram, mod- PEDIATRICS (ISSN Numbers: Print, 0031-4005; estly increases the yield of the electroencephalogram in children diagnosed with Online, 1098-4275). Copyright © 2009 by the seizures by neurologists. Compared with a routine electroencephalogram, the num- American Academy of Pediatrics ber needed to test with sleep-deprived electroencephalogram to identify 1 additional child with epileptiform discharges is 11. Pediatrics 2009;123:703–708 T HE ELECTROENCEPHALOGRAM (EEG) is used clinically to aid in epilepsy syndrome diagnosis, thereby aiding in the selection of partial versus generalized epilepsy medications and in predicting prognosis. Unfortunately, approx- imately half of routine EEGs in patients with clinically diagnosed epilepsy show no abnormalities.1–4 Clinical practice guidelines emphasize sleep and pre-EEG sleep deprivation for enhancing the use of an EEG. The American Electroencephalography Society Guideline and Technical Standards states that, “sleep recordings should be obtained whenever possible.”5 Clinical practice guidelines recommend that, when EEGs are negative, repeat EEGs should be obtained with sleep deprivation,6–8 but these recommendations are based on studies for which the designs fall below current standards for rigorously assessing diagnostic tests.9 In this study, we aimed to prospectively and rigorously compare the yield of sleep-deprived EEG (SDEEG) to routine EEG (REEG). There is no reference standard for comparison, such as inpatient video EEG monitoring, that is widely applicable as a standard of care. Rather, in the common clinical setting represented by this study, a higher yield would be clinically useful. We also provided, in a generalizable, neurologist-referred sample of children, estimates of the probability of treatment-relevant EEG findings in SDEEG versus REEG. PEDIATRICS Volume 123, Number 2, February 2009 703 Downloaded from by on October 18, 2010
  3. 3. METHODS Electroencephalograms All of the EEGs were performed by using a 21-channel Subjects digital recording with electrodes placed according to the All of the EEGs were obtained on outpatient subjects international 10 –20 system, with 30-minute EEG trac- aged 5 months to 18 years at the Helen DeVos Chil- ings, photic stimulation, and hyperventilation in coop- dren’s Hospital. This hospital provides most of the erative children. EEGs were read using standard mon- pediatric neurology care in the greater Grand Rapids tages by 5 experienced clinical neurologists: all were metropolitan area. All of the children were referred board certified in neurology; 2 had completed epilepsy for EEG by a pediatric neurologist, and EEGs were fellowships; and years in practice ranged from 2 to 9. In performed as part of routine clinical care, not for the an attempt to avoid false-positives, epileptiform dis- purpose of a study. charges were considered present only if seen recurrently At the time that the individual EEG was ordered, the with a reliable morphology in an area without muscle neurologist decided whether the patient likely had 1 artifact. epileptic seizure, coded as a clinical seizure, or suspicious but diagnostically uncertain events for which it was Data Collection judged that an EEG would be helpful. Patients with After all of the EEGs had been completed and inter- obvious nonseizure diagnoses, like headache, tics, be- preted by 1 of the 5 neurologists, 1 researcher deidenti- havioral outbursts, and syncope, were excluded, because fied and extracted directly into data collection forms EEG is generally not helpful for these diagnoses. from the primary EEG report the following data: study Patients were recruited from December 2004 to No- identification number, age at the time of the EEG, date vember 2006 with the following inclusion criteria: a of study, gender, number of previous EEG studies, clin- diagnosis of first unprovoked seizure, established epi- ical diagnosis (seizure/epilepsy or other), current use of lepsy, or spells being evaluated for seizures. All of the antiseizure drugs (ASDs) (yes or no and number), sleep children were judged by neurologists to be appropriate deprivation protocol (SDEEG or REEG), EEG reader (1– candidates for EEGs (either initial or follow-up study) as 5), presence of stage-2 sleep (yes or no), and EEG inter- part of standard medical practice (not for the purpose of pretation (normal yes or no; epileptiform discharges yes this study). Patients were excluded only if their cognitive or no and focal or generalized; any abnormality yes or no dysfunction made maintaining or assessing arousal dif- and focal or generalized). The protocol blind was broken ficult. Only 2 families declined to participate when at the completion of the study after all of the EEGs were asked. The study was approved by the hospital institu- interpreted and entered into the database. tional review board and informed consent was obtained from parents or guardians of all of the patients. Statistical Analyses Sample Size We determined that a meaningful increase in the yield of Study Design SDEEG versus REEG would be an absolute increased This is a prospective, randomized, physician-blinded yield of 20% (number needed to test: 5). This is a rea- study of partial SDEEGs versus routine, nonsleep depri- sonable difference, because 20% of parents and chil- vation EEGs (REEGs). Subjects were numbered consec- dren report that SDEEG was an inconvenient burden, utively. Before the study, the Rand procedure in Mi- and 50% are fatigued the next day.11 Thus, the primary crosoft Excel (Microsoft Corp, Redmond, WA) was used hypothesis to be tested was a comparison of proportions to generate a series of random numbers to allocate equal of EEG results that are normal (versus abnormal) in numbers of subjects to the REEG or SDEEG protocol. On REEG versus SDEEG groups. We anticipated that the the basis of this allocation, instructions for either proto- majority of children in our sample would have had 1 col were placed in sealed envelopes with the study sub- seizure, and we estimated that 60% of REEG results in ject number on the outside. These envelopes were dis- our sample would be normal. To detect a 20% difference pensed to families after consent, and the families were in the absolute proportion of positive EEGs, assuming a instructed not to reveal the instructions. 2-sided test at P .05, we calculated that a sample size The SDEEG protocol directed children to go to bed at of 98 in each group would provide 80% power. their normal bedtime. Parents were instructed to allow no naps or caffeine before the EEG, and age-based sleep- Random Allocation Test deprivation instructions were as follows: (1) children To assess similarity of characteristics of children ran- aged 11 years were to stay awake after 12:00 AM; (2) domly assigned to SDEEG versus REEG, we performed children aged 3 to 11 years were to stay awake after 2:00 univariate analyses, without correcting for multiple AM; and (3) children aged 3 years were to stay awake comparisons, using t test and 2 as appropriate. EEG after 4:00 AM. Every attempt was made to perform EEGs protocol groups did not differ in age or in the proportion in the morning.10 No sedation was administered. of children with suspected seizures, using ASDs medica- The total number of hours of sleep at home before the tions, or EEG reader assignment (all P values .10). EEG was based on parent recall. This information was However, the proportion of girls was significantly higher obtained by the first author and entered into the data- in the REEG group (P .047), so this was included in base after the neurologist interpreted the EEG. the statistical analyses to assess for confounding. 704 DeROOS et al Downloaded from by on October 18, 2010
  4. 4. Sleep-Deprivation Effectiveness Tests TABLE 1 Clinical Characteristics of the Study Sample We assessed, by using t tests and 2 as appropriate, Factors REEG SDEEG P whether allocation to SDEEG affected sleep. These com- Gender, male, n (%) 44 (44.4) 58 (58.6) .047 parisons addressed the following questions. For the night Age groups, n (%) before the EEG, was there a significant difference in the 2y 18 (18.2) 18 (18.2) .999 mean number of hours of sleep between the SDEEG and 3y 81 (81.8) 81 (81.8) the REEG groups? Did the proportions of children in Seizure, clinically, yes, n (%) 85 (85.9) 79 (79.8) .258 each group who had adequate sleep for age based on age ASD use, n (%) norms12 differ significantly? Did the proportions of chil- No ASD 35 (35.4) 39 (39.4) dren in each group who achieved stage-2 sleep during ASD 64 (64.6) 60 (60.6) .557 the EEG differ? First EEG, n (%) 19 (19.2) 25 (25.3) .305 Age, mean (SD) 8.56 (4.79) 8.47 (4.60) .9 Primary Analysis The primary outcome of interest was dichotomous: pres- seizure or epilepsy in 164 patients (83.0%). Ages ranged ence of no abnormalities (ie, normal EEG results) versus from 0 to 18 years. the presence of any abnormality, for SDEEG versus The 2 EEG protocol groups were similar (see Table 1). REEG. The mean ages were 8.56 years (SD: 4.80 years) in the REEG group and 8.47 years (SD: 4.61 years) in the SDEEG group (P .90). Clinical seizures were diagnosed Secondary Analyses in 86% of the REEG group and 80% of the SDEEG group To assess the influence of protocol more specifically on (P .26). ASDs were already used in 65% of the REEG the EEG results, we also assessed the proportion of EEGs group and 61% of the SDEEG group (P .56). Reader showing (1) any epileptiform discharges, (2) focal epi- assignment and the number of previous EEGs did not leptiform discharges, (3) generalized epileptiform dis- differ between the 2 groups (P .1), but gender did, charges, (4) focal slowing, and (5) any other abnormal- with more boys randomly assigned to the SDEEG (59% ities. For each protocol, we calculated the proportion of vs 41%; P .047). Therefore, gender was analyzed EEGs showing these findings, estimated the 95% confi- alone and in combination with sleep-deprivation proto- dence interval (CI) for these proportions, and compared col. There was no significant effect of gender ( 2 .11; these proportions using 2 or Fisher’s exact test, as ap- degree(s) of freedom [df] 1; P .74), nor was there propriate. Because this was exploratory, we did not cor- significant interaction between gender and protocol (P rect for multiple comparisons. .105). Therefore, gender was not forced into all of the The yield of SDEEG might be higher in certain groups subsequent analyses. of patients. To further determine whether age or other clinical factors might be important, a stepwise logistic Sleep regression was performed. The dependent variable was Overall compliance with the SDEEG protocol was ac- normal EEG results. Categorical factors were seizure ceptable. Before the EEG, the SDEEG group averaged clinically (yes or no), age ( 2 years or 3 years), ASD 4.86 (SD: 2.22) and the REEG group 7.94 (SD: 1.93) use, gender, first EEG, and particular EEG reader. We sleep hours (t196 10.42; P .00001). Surprisingly, on stratified for age on the basis of a previous study that the basis of age norms,12 only 30% of the total sample of showed a much lower yield of EEGs in children 3 years children had adequate sleep for age, but this also differed with first seizure.13 Using the significant clinical/demo- between SDEEG (12%) and REEG (48%) children ( 2 graphic categories from the regression, we used logistic 30.6; df 1; P .0001). A total of 127 children (64%) regression to better understand the role of sleep and fell asleep during their EEG, more often in the SDEEG sleep deprivation on the EEG yield. Four logistic regres- group (stage-2 sleep 73% vs 55%; 2 6.93; df 1; P sions were performed, and sleep was assessed as follows: .009). (1) sleep-deprivation protocol assignment; (2) presence of adequate sleep for age; (3) number of hours of sleep EEG Results reported; and (4) presence of stage-2 sleep on the EEG. At the level of trend, REEG results were normal more often than SDEEG results (67.7% vs 55.6%; 2 3.08; RESULTS df 1; P .08; Fig 1). This 12.1% difference corre- sponds with a number needed to test of 8.3 SDEEGs to Patient and EEG Characteristics identify 1 fewer abnormal EEG result. EEG results, ac- We invited 208 patients, and only 2 families declined to cording to protocol, are shown in Table 2. For the total participate when asked. Eight patients did not comply sample, no specific type of EEG abnormality was signif- with their EEG and did not reschedule. Of those, 3 were icantly more prevalent in the SDEEG group. The number scheduled for sleep deprivation and 5 for nonsleep de- needed to test with SDEEG to identify 1 additional child privation. No further analysis was performed on the 8 with epileptiform discharges on EEG was 11. noncompliant patients. The remaining 198 patients were included in the Secondary Analyses of Clinical Factors study, 99 in each arm. A total of 51.5% of participants Stepwise conditional logistic analysis showed that clini- were boys (n 102). The pre-EEG clinical diagnosis was cal diagnosis of seizure(s) and age group were significant PEDIATRICS Volume 123, Number 2, February 2009 705 Downloaded from by on October 18, 2010
  5. 5. Strengths of our study include the use of random assignment, reader blinding, and assessment of compli- ance. In addition, our sample is both community re- ferred and neurologist assessed.15–17 Clinical diagnoses were recorded independent of EEG findings, and most children were diagnosed with 1 seizure, the clinical setting in which EEGs are most useful.4,17–19 Caution is needed in interpreting certain aspects of our results. First, insufficient sleep in the REEG group may have biased our group comparison results toward the null. However, because the overall prevalence of FIGURE 1 abnormal EEG results in the REEG group is not higher Among children with 1 clinically diagnosed seizure, proportions of normal and abnor- than in other studies, false elevation in this group should mal EEG results in children under the REEG (left) and SDEEG (right) protocols. be minimal. Second, this study was not powered for posthoc analyses for age strata, clinical diagnosis, and other possibly clinically important factors, and, thus, factors, but all of the other clinical and test-related fac- estimates related to these factors are imprecise. In addi- tors were nonsignificant. The odds that an EEG result tion, in children 3 years of age, difficulty with imple- would be interpreted as normal were significantly higher menting sleep deprivation may have affected the results. (odds ratio [OR]: 6.67 [95% CI: 2.27–20.83]; P .001) The findings of the present study differ slightly from in the uncertain-spells patients compared with those results of our 2 previous, larger retrospective studies in with clinically diagnosed seizure(s). Odds of a normal which SD did not increase EEG yield.4,14 We suspect that EEG result were also significantly higher (OR: 2.78 [95% the main source of bias may be referral related: nearly CI: 1.16 – 6.67]; P .022) in the younger ( 3 years) age half of the EEGs were ordered by pediatricians and other group compared with the older children. Comparisons nonneurologists or occurred before a first neurology for specific types of EEG findings are shown in Table 2. clinic visit. Thus, in those samples, the rate of normal EEG results was much higher. Although in this study Secondary Analyses of Sleep and EEG Findings SDEEGs occurred based on random assignment and not Whether the child fell asleep during the EEG did not expert clinician choice, our data support the notion that influence the EEG results. The proportions of EEG re- previous clinical evaluation by a neurologist results in a sults that were normal, epileptiform, or otherwise ab- more appropriate EEG use.17,19 normal were nearly identical in EEGs where sleep oc- The modest increase in the detection of abnormalities curred versus EEGs where sleep did not (Fig 2). with SDEEG is consistent with pediatric first-seizure When age group and clinical diagnosis were added to studies in which, after a normal first EEG, a second the logistic regression model, significantly fewer SDEEG SDEEG did detect additional abnormalities. It is worth results than REEG results were normal (OR: 0.51 [95% noting that these positive repeat SDEEGs did not predict CI: 0.28 – 0.94]; P .032). However, this finding was not higher risk for seizure recurrence.20 Similarly, another robust when sleep was assessed in 3 other ways: (1) study found that SDEEG was superior and was reported number of sleep hours before the EEG (P .114 for to have “92% sensitivity.”21 The authors unconvention- sleep hours as covariate); (2) proportion with inade- ally defined sensitivity as the proportion of positive quate sleep for age (OR: 1.17 [95% CI: 0.61–2.27]; P SDEEGs among epilepsy patients with any positive EEG .64); and (3) presence of stage-2 sleep during the EEG in that study (rather than the proportion of among pa- (OR: 0.80 [95% CI: 0.43–1.51]; P .94). tients with epilepsy) and left out epileptic patients with For the 36 children whose histories were not compel- normal EEG results. In any study of repeat EEGs,20,22,23 it ling for epileptic seizures, 2 (6%) had abnormal EEG should be remembered that some additional findings results (1 REEG and 1 SDEEG). One child had brief may be attributable to repeated sampling,1 not because eye-rolling spells and subsequent generalized discharges. of sleep, or to instability of this test in children.24 The other had brief staring spells without obvious be- havioral arrest or focal epileptiform discharges present, CONCLUSIONS and did subsequently improve with oxcarbazepine. Our results have implications for the use of EEGs in children. First, some clinicians obtain SDEEGs in any DISCUSSION child undergoing an EEG. Our data from this and previ- In this study, we have shown that, in children referred ous studies do not support indiscriminate use of sleep by neurologists, partial sleep deprivation before an out- deprivation for EEGs. Rather, a modest increased yield to patient EEG modestly raises the yield. This effect is more SDEEG may justify its use in selected situations. How- robust in children with 1 clinically diagnosed seizure ever, given the uncertain magnitude of this improve- and in children over the age of 3 years. Consistent with ment, this can be considered a relative benefit. Because our previous retrospective studies,4,14 we found no evi- 1 study estimated that 20% of families consider SDEEGs dence that sleep itself affects the EEG yield. Thus, our to be burdensome,11 the diagnostic gains may not offset data do not support practice guideline recommendations the burden of sleep deprivation to the child and parent. that EEGs should routinely be obtained with sleep. Second, a routine practice of ordering repeat EEGs in 706 DeROOS et al Downloaded from by on October 18, 2010
  6. 6. TABLE 2 Results of REEGs and SDEEGs EEG Results REEGs SDEEGs P n % 95% CI n % 95% CI Entire sample No. 99 99 Normal 67 67.7 58.5–76.9 55 55.6 45.8–65.3 .08 Any abnormality 32 32.3 23.1–41.5 44 44.4 34.7–54.2 Any epileptiform discharges 28 28.3 19.4–37.2 37 37.4 27.8–46.9 NS Focal epileptiform discharges 15 15.2 8.1–22.2 23 23.2 14.9–31.6 NS Generalized epileptiform discharges 14 14.1 7.3–21.0 15 15.2 8.1–22.2 NS Other abnormalities 6 6.1 1.4–10.8 9 9.1 3.4–14.8 NS Focal slowing 2 2.0 0.0–4.8 6 6.1 1.4–10.8 NS Generalized slowing 5 5.1 0.7–9.4 2 2.0 0.0–4.8 NS Clinical seizure only, all ages No. 85 79 Normal 54 63.5 53.3–73.8 38 48.1 37.1–59.1 .047 Any abnormality 31 36.5 26.2–46.7 41 51.9 38.3–60.4 .047 Any epileptiform discharges 27 31.8 21.9–41.7 36 45.6 34.6–56.6 .069 Focal epileptiform discharges 14 16.5 8.6–24.4 22 27.8 18.0–37.7 .079 Generalized epileptiform discharges 13 15.3 7.6–22.9 15 19.0 10.3–27.6 NS Other abnormalities 6 7.1 1.6–12.5 8 10.1 3.5–16.8 NS Focal slowing 2 2.4 0.0–5.6 6 7.6 1.8–13.4 NS Generalized slowing 5 5.9 0.9–10.9 1 1.3 0.0–3.7 NS Suspected spells only, all ages No. 14 20 Normal 13 92.9 79.4–106.3 17 85.0 69.4–100.6 NS Any abnormality 1 7.1 0.0–20.6 3 15.0 0.0–30.6 NS Any epileptiform discharges 1 7.1 0.0–20.6 1 5.0 0.0–14.6 NS Focal epileptiform discharges 1 7.1 0.0–20.6 1 5.0 0.0–14.6 NS Generalized epileptiform discharges 1 7.1 0.0–20.6 0 0.0 — NS Other abnormalities 0 0.0 — 1 5.0 0.0–14.6 NS Focal slowing 0 0.0 — 0 0.0 — NS Generalized slowing 0 0.0 — 1 5.0 0.0–14.6 NS Clinical seizure only, age 3 and over No. 70 64 Normal 42 60 48.5–71.5 28 43.8 31.6–55.9 .06 Any abnormality 28 40 28.5–51.5 36 56.3 44.1–68.4 .06 Any epileptiform discharges 25 35.7 24.5–46.9 32 50.0 37.8–62.3 .095 Focal epileptiform discharges 13 18.6 9.5–27.7 20 31.3 19.9–42.6 .089 Generalized epileptiform discharges 12 17.1 8.3–26.0 14 21.9 11.7–32.0 NS Other abnormalities 5 7.1 1.1–13.2 6 9.4 2.2–16.5 NS Focal slowing 2 2.9 0.0–6.8 5 7.8 1.2–14.4 NS Generalized slowing 4 5.7 0.3–11.2 1 1.6 0.0–4.6 NS Clinical seizure only, age 2 and under No. 15 15 Normal 12 80.0 59.8–100.2 10 66.7 42.8–90.5 NS Any abnormality 3 20.0 0.0–40.2 5 33.3 9.5–57.2 NS Any epileptiform discharges 2 13.3 0.0–30.5 4 26.7 4.3–49.0 NS Focal epileptiform discharges 1 6.7 0.0–19.3 2 13.3 0.0–30.5 NS Generalized epileptiform discharges 1 6.7 0.0–19.3 1 6.7 0.0–19.3 NS Other abnormalities 1 6.7 0.0–19.3 2 13.3 0.0–30.5 NS Focal slowing 0 0.0 — 1 6.7 0.0–19.3 NS Generalized slowing 1 6.7 0.0–19.3 0 0.0 — NS NS indicates not significant; —, no data. any child where a first EEG does not show sleep is not differential effect of SD on generalized versus focal epi- justified, because sleep itself was not linked to more leptiform discharges. However, specific epilepsy syn- positive EEGs. Third, because we found no direct effect dromes, such as benign rolandic epilepsy, were not spe- of the number of hours of sleep before the EEG, partial cifically studied. sleep deprivation, not full-night sleep deprivation, is Finally, it is worth emphasizing that a 50% positive probably adequate to achieve any advantages of sleep rate is still unsatisfactory. Other creative strategies,25 per- deprivation for EEG. That is, the amount of sleep depri- haps using complementary modalities tailored to the vation does not seem to be “dose related.” There was no clinical features, may serve our patients better than the PEDIATRICS Volume 123, Number 2, February 2009 707 Downloaded from by on October 18, 2010
  7. 7. European Affairs: Subcommission on European Guidelines. Acta Neurol Scand. 2002;106(1):1–7 9. Bossuyt PM, Reitsma JB, Bruns DE, et al. Towards complete and accurate reporting of studies of diagnostic accuracy: the STARD initiative. BMJ. 2003;326(7379):41– 44 10. Labate A, Ambrosio R. Gambardella A, Sturniolo M, Pucci F, Quattrone A. Usefulness of a morning routine EEG recording in patients with juvenile myoclonic epilepsy. Epilepsy Res. 2007; 77(1):17–21 11. Nijhof SL, Bakker AL, Van Nieuwenhuizen O, Oostrom K, van Huffelen AC. Is the sleep-deprivation EEG a burden for both child and parent? Epilepsia. 2005;46(8):1328 –1329 FIGURE 2 12. Iglowstein I, Jenni OG, Molinari L, Largo RH. Sleep duration Among children with 1 clinically diagnosed seizure, proportions of normal and abnor- from infancy to adolescence: reference values and generational mal EEG results in children based on presence of stage-2 sleep during the EEG. Left, no trends. Pediatrics. 2003;111(2):302–307 sleep; right, sleep. 13. Shinnar S, Kang H, Berg AT, Goldensohn ES, Hauser WA, Moshe SL. EEG abnormalities in children with a first unpro- ´ voked seizure. Epilepsia. 1994;35(3):471– 476 current practice. We recommend considering SDEEG 14. Gilbert DL, DeRoos S, Bare MA. Does sleep or sleep deprivation increase epileptiform discharges in pediatric electroencephalo- more strongly in children 3 years old and in whom grams? Pediatrics. 2004;114(3):658 – 662 seizures are highly suspected after a neurologist’s assess- 15. Gurbani NS, Gurbani SG, Mittal M, et al. Screening of EEG ment. Incorporating the preference of the family into the referrals by neurologists leads to improved healthcare resource decision is reasonable given the modest increase in yield. utilization. Clin EEG Neurosci. 2006;37(1):30 –33 16. Nicolaides P, Appleton RE. Beirne M. EEG requests in ACKNOWLEDGMENTS paediatrics: an audit. 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  8. 8. Effects of Sleep Deprivation on the Pediatric Electroencephalogram Steven T. DeRoos, Kipp L. Chillag, Martina Keeler and Donald L. Gilbert Pediatrics 2009;123;703-708 DOI: 10.1542/peds.2008-0357 Updated Information including high-resolution figures, can be found at: & Services References This article cites 25 articles, 11 of which you can access for free at: Citations This article has been cited by 2 HighWire-hosted articles: s Subspecialty Collections This article, along with others on similar topics, appears in the following collection(s): Neurology & Psychiatry try Permissions & Licensing Information about reproducing this article in parts (figures, tables) or in its entirety can be found online at: Reprints Information about ordering reprints can be found online: Downloaded from by on October 18, 2010