A randomised trial of peri-operative positive airway pressure for postoperative delirium in patients at risk for obstructive sleep apnoea after regional anaesthesia with sedation or general anaesthesia for joint arthroplasty.

Previous pilot work has established an association between obstructive sleep apnoea and the development of acute postoperative delirium , but it remains unclear to what extent this risk factor is modifiable in the 'real world' peri-operative setting. In a single-blind randomised controlled trial, 135 elderly surgical patients at risk for obstructive sleep apnoea were randomly assigned to receive peri-operative continuous positive airway pressure (CPAP) or routine care. Of the 114 patients who completed the study, 21 (18.4%) experienced delirium. Delirium was equally common in both groups: 21% (12 of 58 subjects) in the CPAP group and 16% (9 of 56 subjects) in the routine care group (OR = 1.36 [95%CI 0.52-3.54], p = 0.53). Delirious subjects were slightly older - mean (SD) age 68.9 (10.7) vs. 64.9 (8.2), p = 0.07 - but had nearly identical pre-operative STOP-Bang scores (4.19 (1.1) versus 4.27 (1.3), p = 0.79). Subjects in the CPAP group used their devices for a median (IQR [range]) of 3 (0.25-5 [0-12]) nights pre-operatively (2.9 (0.1-4.8 [0.0-12.7]) hours per night) and 1 (0-2 [0-2]) nights postoperatively (1.4 (0.0-5.1 [0.0-11.6]) hours per night). Among the CPAP subjects, the residual pre-operative apnoea-hypopnea index had a significant effect on delirium severity (p = 0.0002). Although we confirm that apnoea is associated with postoperative delirium, we did not find that providing a short-course of auto-titrating CPAP affected its likelihood or severity. Voluntary adherence to CPAP is particularly poor during the initiation of therapy.

Clinical practice guideline for the pharmacologic treatment of chronic insomnia in adults: An American Academy of Sleep Medicine clinical practice guideline

INTRODUCTION: The purpose of this guideline is to establish clinical practice recommendations for the pharmacologic treatment of chronic insomnia in adults, when such treatment is clinically indicated. Unlike previous meta-analyses, which focused on broad classes of drugs, this guideline focuses on individual drugs commonly used to treat insomnia. It includes drugs that are FDA-approved for the treatment of insomnia, as well as several drugs commonly used to treat insomnia without an FDA indication for this condition. This guideline should be used in conjunction with other INTRODUCTION: The purpose of this guideline is to establish clinical practice recommendations for the pharmacologic treatment of chronic insomnia in adults, when such treatment is clinically indicated. Unlike previous meta-analyses, which focused on broad classes of drugs, this guideline focuses on individual drugs commonly used to treat insomnia. It includes drugs that are FDA-approved for the treatment of insomnia, as well as several drugs commonly used to treat insomnia without an FDA indication for this condition. This guideline should be used in conjunction with other AASM guidelines on the evaluation and treatment of chronic insomnia in adults. METHODS: The American Academy of Sleep Medicine commissioned a task force of four experts in sleep medicine. A systematic review was conducted to identify randomized controlled trials, and the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) process was used to assess the evidence. The task force developed recommendations and assigned strengths based on the quality of evidence, the balance of benefits and harms, and patient values and preferences. Literature reviews are provided for those pharmacologic agents for which sufficient evidence was available to establish recommendations. The AASM Board of Directors approved the final recommendations. RECOMMENDATIONS: The following recommendations are intended as a guideline for clinicians in choosing a specific pharmacological agent for treatment of chronic insomnia in adults, when such treatment is indicated. Under GRADE, a STRONG recommendation is one that clinicians should, under most circumstances, follow. A WEAK recommendation reflects a lower degree of certainty in the outcome and appropriateness of the patient-care strategy for all patients, but should not be construed as an indication of ineffectiveness. GRADE recommendation strengths do not refer to the magnitude of treatment effects in a particular patient, but rather, to the strength of evidence in published data. Downgrading the quality of evidence for these treatments is predictable in GRADE, due to the funding source for most pharmacological clinical trials and AASM guidelines on the evaluation and treatment of chronic insomnia in adults. METHODS: The American Academy of Sleep Medicine commissioned a task force of four experts in sleep medicine. A systematic review was conducted to identify randomized controlled trials, and the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) process was used to assess the evidence. The task force developed recommendations and assigned strengths based on the quality of evidence, the balance of benefits and harms, and patient values and preferences. Literature reviews are provided for those pharmacologic agents for which sufficient evidence was available to establish recommendations. The AASM Board of Directors approved the final recommendations. RECOMMENDATIONS: The following recommendations are intended as a guideline for clinicians in choosing a specific pharmacological agent for treatment of chronic insomnia in adults, when such treatment is indicated. Under GRADE, a STRONG recommendation is one that clinicians should, under most circumstances, follow. A WEAK recommendation reflects a lower degree of certainty in the outcome and appropriateness of the patient-care strategy for all patients, but should not be construed as an indication of ineffectiveness. GRADE recommendation strengths do not refer to the magnitude of treatment effects in a particular patient, but rather, to the strength of evidence in published data. Downgrading the quality of evidence for these treatments is predictable in GRADE, due to the funding source for most pharmacological clinical trials and the attendant risk of publication bias; the relatively small number of eligible trials for each individual agent; and the observed heterogeneity in the data. The ultimate judgment regarding propriety of any specific care must be made by the clinician in light of the individual circumstances presented by the patient, available diagnostic tools, accessible treatment options, and resources. We suggest that clinicians use suvorexant as a treatment for sleep maintenance insomnia (versus no treatment) in adults. (WEAK). We suggest that clinicians use eszopiclone as a treatment for sleep onset and sleep maintenance insomnia (versus no treatment) in adults. (WEAK). We suggest that clinicians use zaleplon as a treatment for sleep onset insomnia (versus no treatment) in adults. (WEAK). We suggest that clinicians use zolpidem as a treatment for sleep onset and sleep maintenance insomnia (versus no treatment) in adults. (WEAK). We suggest that clinicians use triazolam as a treatment for sleep onset insomnia (versus no treatment) in adults. (WEAK). We suggest that clinicians use temazepam as a treatment for sleep onset and sleep maintenance insomnia (versus no treatment) in adults. (WEAK). We suggest that clinicians use ramelteon as a treatment for sleep onset insomnia (versus no treatment) in adults. (WEAK). We suggest that clinicians use doxepin as a treatment for sleep maintenance insomnia (versus no treatment) in adults. (WEAK). We suggest that clinicians not use trazodone as a treatment for sleep onset or sleep maintenance insomnia (versus no treatment) in adults. (WEAK). We suggest that clinicians not use tiagabine as a treatment for sleep onset or sleep maintenance insomnia (versus no treatment) in adults. (WEAK). We suggest that clinicians not use diphenhydramine as a treatment for sleep onset and sleep maintenance insomnia (versus no treatment) in adults. (WEAK). We suggest that clinicians not use melatonin as a treatment for sleep onset or sleep maintenance insomnia (versus no treatment) in adults. (WEAK). We suggest that clinicians not use tryptophan as a treatment for sleep onset or sleep maintenance insomnia (versus no treatment) in adults. (WEAK). We suggest that clinicians not use valerian as a treatment for sleep onset or sleep maintenance insomnia (versus no treatment) in adults. (WEAK).(AU)

Enantioselective total synthesis of (R)-(-)-complanine.

A route is described for the enantioselective synthesis of (R)-(-)-complanine, a marine natural product isolated from Eurythoe complanata, and known to be a causative agent in inflammation. An organocatalytic, asymmetric oxyamination of a homoconjugated all-Z-dienal intermediate provides versatile and efficient access to the natural product.

Prevalence and comorbidity of nocturnal wandering in the U.S. adult general population.

OBJECTIVE: To assess the prevalence and comorbid conditions of nocturnal wandering with abnormal state of consciousness (NW) in the American general population. METHODS: Cross-sectional study conducted with a representative sample of 19,136 noninstitutionalized individuals of the U.S. general population ≥18 years old. The Sleep-EVAL expert system administered questions on life and sleeping habits; health; and sleep, mental, and organic disorders (DSM-IV-TR; International Classification of Sleep Disorders, version 2; International Classification of Diseases-10). RESULTS: Lifetime prevalence of NW was 29.2% (95% confidence interval [CI] 28.5%-29.9%). In the previous year, NW was reported by 3.6% (3.3%-3.9%) of the sample: 1% had 2 or more episodes per month and 2.6% had between 1 and 12 episodes in the previous year. Family history of NW was reported by 30.5% of NW participants. Individuals with obstructive sleep apnea syndrome (odds ratio [OR] 3.9), circadian rhythm sleep disorder (OR 3.4), insomnia disorder (OR 2.1), alcohol abuse/dependence (OR 3.5), major depressive disorder (MDD) (OR 3.5), obsessive-compulsive disorder (OCD) (OR 3.9), or using over-the-counter sleeping pills (OR 2.5) or selective serotonin reuptake inhibitor (SSRI) antidepressants (OR 3.0) were at higher risk of frequent NW episodes (≥2 times/month). CONCLUSIONS: With a rate of 29.2%, lifetime prevalence of NW is high. SSRIs were associated with an increased risk of NW. However, these medications appear to precipitate events in individuals with a prior history of NW. Furthermore, MDD and OCD were associated with significantly greater risk of NW, and this was not due to the use of psychotropic medication. These psychiatric associations imply an increased risk due to sleep disturbance.

British Association for Psychopharmacology consensus statement on evidence-based treatment of insomnia, parasomnias and circadian rhythm disorders.

Sleep disorders are common in the general population and even more so in clinical practice, yet are relatively poorly understood by doctors and other health care practitioners. These British Association for Psychopharmacology guidelines are designed to address this problem by providing an accessible up-to-date and evidence-based outline of the major issues, especially those relating to reliable diagnosis and appropriate treatment. A consensus meeting was held in London in May 2009. Those invited to attend included BAP members, representative clinicians with a strong interest in sleep disorders and recognized experts and advocates in the field, including a representative from mainland Europe and the USA. Presenters were asked to provide a review of the literature and identification of the standard of evidence in their area, with an emphasis on meta-analyses, systematic reviews and randomized controlled trials where available, plus updates on current clinical practice. Each presentation was followed by discussion, aimed to reach consensus where the evidence and/or clinical experience was considered adequate or otherwise to flag the area as a direction for future research. A draft of the proceedings was then circulated to all participants for comment. Key subsequent publications were added by the writer and speakers at draft stage. All comments were incorporated as far as possible in the final document, which represents the views of all participants although the authors take final responsibility for the document.

The use of valerian in neuropsychiatry.

Valerian is a medicinal agent deriving from the plant Valeriana officinalis L. We reviewed the available literature on the use of valerian preparations in the treatment of neuropsychiatric disorders. Preclinical studies suggest that valerian has sedative and muscle-relaxant effects. Few clinical trials with valerian have been carried out in conditions other than insomnia. The insomnia studies have methodologic shortcomings but suggest that some preparations lead to significant subjective improvement in sleep complaints with remarkably few side effects. Furthermore, some evidence indicates that valerian preparations may have a mechanism of action and clinical characteristics that differ from the benzodiazepine-related sedative/hypnotics, making them more suitable for long-term use. If this safety profile and the plant's sedative/hypnotic efficacy are confirmed in double-blind, placebo-controlled trials with carefully and consistently prepared valerian compounds, then those compounds would fill an important and presently unfilled niche in the treatment of insomnia.

EEG effects of ECT: implications for rTMS.

Electroconvulsive therapy (ECT) involves the use of electrical stimulation to elicit a series of generalized tonic-clonic seizures for therapeutic purposes and is the most effective treatment known for major depression. These treatments have significant neurophysiologic effects, many of which are manifest in the electroencephalogram (EEG). The relationship between EEG data and the response to ECT has been studied since the 1940s, but for many years no consistent correlates were found. Recent studies indicate that a number of specific EEG features recorded during the induced seizures (ictal EEG) as well as before and after a course of treatment (interictal EEG) are related to both the therapeutic efficacy and cognitive side effects. Similar to ECT, repetitive transcranial magnetic stimulation (rTMS), which involves focal electromagnetic stimulation of cortical neurons, has also been studied as an antidepressant therapy and also appears to have neurophysiologic effects, although these have not been as fully investigated as is the case with ECT. Given the similarity of these treatments, it is natural to consider whether advances in understanding the electrophysiologic correlates of the ECT response might have implications for rTMS. The present article reviews the literature on the EEG effects of ECT and discusses the implications in terms of the likely efficacy and side effects associated with rTMS in specific anatomic locations, the potential for producing an antidepressant response with rTMS without eliciting seizure activity, eliciting focal seizures with rTMS, and the possibility of using rTMS to focally modulate seizure induction and spread with ECT to optimize treatment.

ECT stimulus intensity: are present ECT devices too limited?

OBJECTIVE: The maximum output charge for ECT devices is limited to 576 millicoulombs in the United States, although there are no data ensuring that this limit will allow consistently effective treatments. The authors examined whether this limit has a negative impact on therapeutic response and, therefore, whether a higher stimulus charge should be available. METHOD: They retrospectively reviewed the records of 471 patients who received a clinical index course of ECT at Duke University between 1991 and 1998. These patients received conservative stimulus dosing of 2.25 times seizure threshold for unilateral ECT and 1.5 times seizure threshold for bilateral ECT. RESULTS: Seventy-two (15%) of the 471 patients required the maximum stimulus intensity during their index ECT course. Of these, 24 (5% of the total) had either a short EEG seizure (less than 25 seconds) or had no seizure at the maximum level. Strategies to augment therapeutic response with caffeine, ketamine, or hyperventilation were used in 14 of the 24 patients, and data on therapeutic response were available for 22 of the 24. Only seven (32%) of these 22 patients were considered ECT responders, compared with 242 (66%) of the remaining 364 patients for whom data on response to ECT were available. Older age and pre-ECT course EEG slowing were predictors of requiring the maximum stimulus level. CONCLUSIONS: The maximum available stimulus output was therapeutically insufficient for 5% of the patients studied even when available means to augment response were instituted. This percentage would likely be even larger with the use of a less conservative dosing protocol for unilateral ECT. Increases in maximum stimulus output for ECT devices should be considered as a means to ensure adequate treatment response.

Prediction of the utility of a switch from unilateral to bilateral ECT in the elderly using treatment 2 ictal EEG indices.

BACKGROUND: The choice of whether to administer nondominant unilateral (UL) or bilateral (BL) ECT remains controversial. METHODS: A study in which moderately suprathreshold UL nonresponders at treatment 6 were randomized to UL or BL ECT offered the opportunity to explore whether ictal EEG indices at treatment 2 might predict response to UL ECT, and also which UL ECT nonresponders are likely to respond to BL ECT. RESULTS: We found that less postictal suppression in response to the second UL ECT stimulus was predictive of a poorer subsequent therapeutic response to UL ECT, but of a better therapeutic response if switched to BL ECT. A multivariate ictal EEG model was developed that had a significant capacity to differentiate those who will respond to UL ECT versus those who will not respond to UL ECT, but who will be therapeutic responders when switched to BL ECT. CONCLUSIONS: This study raises the possibility that ictal EEG indices at treatment 2 may identify situations when UL ECT is physiologically and therapeutically inadequate, and when BL ECT is likely to be more effective. The determination of whether such predictive physiologic models are of clinical utility for the prediction of outcome awaits further study.

The development and retrospective testing of an electroencephalographic seizure quality-based stimulus dosing paradigm with ECT.

The optimization of electroconvulsive therapy (ECT) stimulus dosing remains uncertain. Previous work suggests the potential utility of ictal EEG models of seizure adequacy, but such models have never been tested for their ability to improve the clinical dosing of ECT treatments. Using data from 149 depressed patients, the authors developed an ictal electroencephalographic (EEG) model that can discriminate seizures produced by more therapeutically effective and less efficacious types of stimuli. They retrospectively determined how stimulus dosing according to this seizure adequacy-based model would have differed from that actually used in an additional 61 patients who received ECT according to a standard clinical dose-titration and EEG seizure duration-based dosing strategy. Although the model indicated an increase in stimulus intensity at some point during the ECT treatment course in 23 of 61 patients, only 5 of these 23 actually received a clinical increase in stimulus intensity. The patients who did not receive this increase had a significantly diminished therapeutic response compared with the other patients. Conversely, the model also indicated that an increase in stimulus intensity that occurred clinically might have been unnecessary to achieve therapeutic efficacy in 11% of the patients. This study provides preliminary evidence that ictal EEG models have the potential to make clinically relevant seizure adequacy distinctions among ECT treatments. Further prospective work is indicated to determine the clinical utility of such models.

EEG correlates of the response to ECT: a possible antidepressant role of brain-derived neurotrophic factor.

Studies on the relationship of electroencephalographic (EEG) data to the therapeutic response to electroconvulsive therapy (ECT) have been carried out since the 1940s, but for many years they did not yield any consistent correlates. Recent studies, however, are providing a growing body of evidence of relationships between the antidepressant response to ECT and both the ictal (recorded during ECT seizures) and interictal (recorded during waking) EEG. These studies appear to be consistent in pointing to the importance of electrophysiologic changes in the prefrontal cortex as a potential mediator of the antidepressant response to ECT. The available findings are reviewed and discussed in light of recent neurophysiologic and neuropsychiatric research, including that related to neurotrophic factors.

New methods of time series analysis of non-stationary EEG data: eigenstructure decompositions of time varying autoregressions.

OBJECTIVE: Those who analyze EEG data require quantitative techniques that can be validly applied to time series exhibiting ranges of non-stationary behavior. Our objective is to introduce a new analysis technique based on formal non-stationary time series models. This novel method provides a decomposition of the time series into a set of 'latent' components with time-varying frequency content. The identification of these components can lead to practical insights and quantitative comparisons of changes in frequency structure over time in EEG time series. METHODS: The technique begins with the development of time-varying autoregressive models of the EEG time series. Such models have been previously used in EEG analysis but we extend their utility by the introduction of eigenstructure decomposition methods. We review the basis and implementation of this method and report on the analysis of two channel EEG data recorded during 3 generalized tonic-clonic seizures induced in an individual as part of a course of electroconvulsive therapy for major depression. RESULTS: This technique identified EEG patterns consistent with prior reports. In addition, it quantified a decrease in dominant frequency content over the seizures and suggested for the first time that this decrease is continuous across the end of the seizures. The analysis also suggested that the seizure EEG may be best modeled by the combination of multiple processes, whereas post-ictally there appears to be one dominant process. There was also preliminary evidence that these features may differ as a function of ECT therapeutic effectiveness. CONCLUSIONS: Eigenanalysis of time-varying autoregressive models has promise for improving the analysis of EEG time series.

The use of flumazenil in the anxious and benzodiazepine-dependent ECT patient.

Many patients who receive electroconvulsive therapy (ECT) are benzodiazepine dependent or are anxious and require benzodiazepine drugs. Because these agents may diminish the therapeutic effectiveness of ECT, we explored the dosing, safety, and efficacy of pre-ECT flumazenil administration, a benzodiazepine-competitive antagonist, in patients receiving benzodiazepine medications. We report our experience with 35 patients who received both flumazenil and benzodiazepine drugs during their ECT course. We compared seizure duration with and without flumazenil and compared treatment efficacy to 49 patients who received ECT without either of these medications. Flumazenil could be safely administered with ECT. A few subjects taking higher chronic benzodiazepine dosages experienced breakthrough anxiety or withdrawal symptoms, which were well managed by dosing flumazenil immediately before the anesthetic agent and by immediate posttreatment benzodiazepine administration. A dose of 0.4-0.5 mg was adequate for all but those taking the highest benzodiazepine dosages, where 0.8-1.0 mg resulted in a clinically more effective reversal. No differences in efficacy or seizure duration were found as a function of flumazenil administration. Flumazenil offers the promise of safe and effective ECT in patients receiving benzodiazepine drugs. Follow-up outcome investigation on a random assignment basis will be necessary for definitive assessment of the value of flumazenil. In addition, the direct effect of benzodiazepine drugs and the flumazenil/benzodiazepine combination on ECT seizures remains to be determined.

Changes in seizure threshold over the course of electroconvulsive therapy affect therapeutic response and are detected by ictal EEG ratings.

Therapeutic effectiveness of electroconvulsive therapy is influenced by the degree to which the stimulus intensity exceeds the seizure threshold. However, the threshold rises variably over the treatment course, confounding maintenance of desired relative stimulus intensity. In 47 depressed patients, decreases in relative stimulus intensity between treatments 1 and 6 were associated with diminished therapeutic response at treatment 6 for unilateral (UL) ECT. A multivariate model including manual ratings of ictal EEG data predicted whether seizure threshold rose with 82% accuracy. The same EEG variables were also significantly related to therapeutic response. Thus, decreases in relative stimulus intensity over the ECT course affect the therapeutic potency of UL ECT. Further, ictal EEG indices have considerable potential for predicting such stimulus intensity changes and their effect on therapeutic outcome.

Sleep in peri-menopausal and post-menopausal women.

Despite the fact that a large number of women report sleep disturbances associated with peri-menopausal and post-menopausal periods, there is a surprising lack of literature related to this issue. In fact, there has not been enough work in this area to even definitively establish whether there is a sleep disorder that is specifically related to these life-stage changes. Herein we review the available literature which suggests that insomnia may be directly linked to the changes that occur during the peri/post-menopausal periods. This insomnia appears to be due to night sweats caused by the hormonal changes which occur and which lead to an increase in arousals. Persistence of insomnia symptoms after adequate hormone replacement therapy may indicate that behavioral conditioning of the insomnia initially triggered by the night sweats may have occurred. Alternatively, such an insomnia in a peri/post-menopausal woman could be due to unresolved grief related to going through menopause or could reflect an independent sleep disorder, such as periodic movements of sleep, sleep apnea, depression, anxiety, etc. Whereas menopausal changes do not directly lead to an increase in sleep apnea they seemingly contribute to an increased risk for this disorder. In view of these considerations, we provide guidelines for the proper diagnosis and treatment of peri/post-menopausal women with sleep complaints.

Neuropsychiatric considerations in the use of electroconvulsive therapy.

ECT is an effective and rapidly acting treatment for certain major psychiatric disorders, even in patients with neurologic illness. Further, in some cases the neurologic illness itself also responds to ECT. Patients with some types of neurologic illness may be at increased risk of neurologic or cognitive side effects from ECT, but these risks can be lowered by careful pre-ECT evaluation and optimal ECT technique.

The largest Lyapunov exponent of the EEG during ECT seizures as a measure of ECT seizure adequacy.

Attributes of the electroencephalogram (EEG) recorded during electroconvulsive therapy (ECT) seizures appear promising for decreasing the uncertainty that exists about how to define a therapeutically adequate seizure. In the present report we study whether one promising and not yet tested ictal EEG measure, the largest Lyapunov exponent (lambda1), is useful in this regard. We calculated lambda1 from 2 channel ictal EEG data recorded in 25 depressed subjects who received right unilateral ECT. We studied the relationship of lambda1 to treatment therapeutic outcome and to an indirect measure of treatment therapeutic potency, the extent to which the stimulus intensity exceeds the seizure threshold. We found lambda1 could be reliably calculated from ictal EEG data and that the global mean, maximum, and standard deviation of lambda1 were smaller in the more therapeutically potent moderately suprathreshold ECT and in therapeutic responders. These results imply a more predictable or consistent pattern of EEG seizure activity over time in more therapeutically effective ECT seizures. These findings also suggest the promise of lambda1 as a marker of ECT seizure therapeutic adequacy and build on our previous work suggesting that lambda1 may be useful for classifying seizures and for reflecting the relative physiologic impact of seizure activity.

A comparison of EEG signal dynamics in waking, after anesthesia induction and during electroconvulsive therapy seizures.

Evidence suggests that quantitative dynamical measures of electroencephalogram (EEG) signals are more appropriate for characterizing the differences between states in an individual rather than as absolute indices. One such measure, the largest Lyapunov exponent (lambda 1), appears to have potential for identifying seizure activity and for being of clinical utility for characterizing electroconvulsive therapy (ECT) seizures. As a result, we compared lambda 1 for the EEG recorded in 8 depressed subjects in 3 states: (1) during right unilateral ECT seizures, (2) during the pre-ECT waking state, and (3) following anesthesia administration but prior to ECT. Spectral amplitude and autocorrelation were also calculated in these states, allowing a comparison of these measures with lambda 1. We hypothesized that lambda 1 would be lowest during the ECT seizures, suggestive of greater EEG signal predictability over time during the seizures. We found that during the seizures lambda 1 was smaller, while spectral amplitude was larger. Significant inter-state differences were not found for the left temporal and occipital regions suggesting that these measures might serve as markers of the degree of seizure involvement of specific brain regions. Spectral amplitude and lambda 1 were uncorrelated and varied independently in some cases. The autocorrelation time was shortest in the waking EEG, and longest for the post-anesthesia EEG, and did not account for the differences seen in lambda 1. In contrast, the persistence of oscillations in the autocorrelation functions was greater for the ictal EEG than the other two states and may relate to lambda 1.