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. 2016 Dec 26;40(3):zsw069. doi: 10.1093/sleep/zsw069

Sleep Perception and Misperception in Chronic Cocaine Users During Abstinence

Sarah E Hodges 1, Brian Pittman 1, Peter T Morgan 1,✉
PMCID: PMC5806585  PMID: 28364419

Abstract

Study Objectives:

During abstinence, chronic cocaine users experience an objective worsening of sleep that is perceived as qualitatively improving. This phenomenon has been termed “occult insomnia.” The objective of this study was to determine whether chronic cocaine users experience positive sleep state misperception during abstinence.

Methods:

Forty-three cocaine-dependent persons were admitted to an inpatient research facility for 12 days and 11 nights to participate in a treatment study of modafinil. Polysomnographic sleep recordings were performed on study nights 3, 4, 10, and 11, when participants were on average 1 and 2 weeks abstinent from cocaine. Participants also completed sleep diary questionnaires every evening before bed and every morning upon awakening. Polysomnographic and sleep diary measurements of total sleep time, sleep latency, time awake after sleep onset, and time in bed after final awakening were compared.

Results:

Chronic cocaine users accurately reported total sleep time after 1 week of abstinence but overreported total sleep time by an average of 40 min after 2 weeks of abstinence. Underestimating sleep latency and time spent awake after sleep onset were responsible for this difference.

Conclusions:

Positive sleep state misperception is revealed in chronic cocaine users after 2 weeks of abstinence and is consistent with the previously identified “occult insomnia” in this population.

Keywords: sleep state misperception, positive sleep state misperception, primary subjective insomnia, occult insomnia, sleep, insomnia, cocaine.

Statement of Significance

Positive sleep state misperception occurs at one end of a spectrum of sleep state perception, with somewhat greater frequency in conditions like insomnia or periodic leg movement disorder, but is not known to be characteristic of any particular condition. The present work found that such overreporting of sleep times is a characteristic feature of prolonged abstinence from chronic cocaine use. This finding suggests that positive sleep state misperception may occur in other conditions and more commonly than previously thought. Given the importance of sleep to health and the reliance on self-report in the routine assessment of sleep, it will be important to identify where positive sleep state misperception occurs, so that previously unrecognized poor sleep may be better addressed.

INTRODUCTION

Paradoxical insomnia (also referred to as primary subjective insomnia) is a form of sleep state misperception in which the sleeper believes they are awake during periods of sleep.1 This phenomenon has been demonstrated in polysomnographic studies and is considered to occur regularly in people with primary insomnia.2,3 In contrast, positive sleep state misperception,1 or reverse sleep state misperception,4 refers to the misperception of physiological wakefulness as sleep. Apparently much less common than paradoxical insomnia, this type of sleep state misperception nevertheless does occur at the other end of the sleep perception spectrum.2–6 However, work in this area—largely on persons who have presented for a medically indicated sleep assessment1—has not identified any particular clinical population in which positive sleep state misperception is characteristic.

One group that may experience positive sleep state perception routinely is chronic users of cocaine. Like chronic users of other substances including alcohol, opiates, and cannabis,7–15 chronic cocaine users have severely disrupted sleep16,17 that may persist for weeks, months, or even longer (for review, see Angarita et al.18). Over the first several weeks of abstinence, polysomnographically (PSG) measured sleep in chronic cocaine users worsens, with shortening total sleep time, diminishing REM sleep (rapid eye movement sleep; a sleep phase characterized by rapid and random eye movements, muscle inhibition, and brain waves similar to those exhibited during wakefulness) time, increasing sleep latency, and chronically decreased slow-wave sleep time.16,17,19–26 However, such findings are in contrast with seminal studies characterizing cocaine withdrawal and abstinence, which found self-reported (SR) improvements in sleep quality and related SR measures over a similar time frame.27,28 Studies that combined PSG and SR qualitative measures reconciled these findings by showing that chronic cocaine users are largely unaware of their worsening sleep, with SR measures of sleep quality at their best when PSG-measured sleep times and sleep latency are at their worst,17 and not different from sleep quality measures reported by healthy sleepers.24

This coincidence of improving SR sleep quality with poor and worsening sleep was termed “occult insomnia”17 to reflect the relative lack of awareness of what appears to be severely disrupted sleep. Importantly, the polysomnographic insomnia observed in abstinent cocaine users is accompanied by deficits in sleep-dependent cognitive function,17,29 indicating that the polysomnographic measures were indicative of consequentially poor sleep. What has not been reported, however, is whether the “occult insomnia” in chronic cocaine users is a form of positive sleep state misperception, wherein the actual time spent sleeping is misperceived or whether it reflects an alteration in the inner metric for describing or experiencing sleep quality unrelated to the perception of time spent sleeping.

Answering this question could be important for a number of reasons. Fundamentally, the identification of positive sleep state misperception in a specific clinical population would indicate that this construct is not only one end of a long spectrum of sleep state perception but also a potentially important characteristic of pathological states. If so, its appreciation could have implications for understanding and treating the associated conditions. On a more immediate, practical level, recognizing positive sleep state misperception is important when trying to characterize sleep without polysomnography or other objective measurement.

The work presented herein explores the highly unusual and heretofore uncharacterized observation of sleep time overestimation among chronic cocaine users during abstinence. A better characterization of sleep disruptions associated with cocaine use will provide higher resolution for potential treatment targets, since considerable evidence suggests that improving sleep may promote abstinence and recovery.23,24

METHODS

Participants

Forty-three persons with current cocaine dependence by DSM-IV contributed data to this study. Other data from this study and a comprehensive description of the recruitment methods and participant characteristics have been published previously.23 Briefly, participants had an average age of 44 ± 7 [SD], were 19% female, completed an average of 12 ± 2 years of education, used an average of $360 ± $350 worth of cocaine weekly, had a history of using cocaine for 24 ± 8 years, and were on average 7 ± 3 days abstinent from cocaine on study night 4. Baseline Pittsburgh Sleep Quality Index30 scores averaged 8 ± 5, and the Shipley Institute for Living Scale31 score averaged 88 ± 14.

All participants met DSM-IV criteria for current cocaine dependence as determined by a clinical interview with an experienced psychiatrist, were not currently in treatment, and were between the ages of 25 and 50 inclusive. All participants reported current use of cocaine by smoked or intravenous route at least 1 time each week in the past month and a positive urine test for cocaine metabolite at screening. All participants exhibited dependence on cocaine in the past year as measured by a score ≥3 on the Severity of Dependence Scale27 and by SR use in at least 9 of the past 12 months.

Potential participants were excluded for history or polysomnographic evidence of sleep apnea, narcolepsy, restless leg syndrome, periodic limb movement disorder (PLMD), or REM sleep disorder, pharmacological treatment for insomnia of any type within the past 6 months, or seizure disorder. Participants with medical conditions who were not considered stable as evidenced by changes in treatment or exacerbations of their condition in the past 6 months or who could interfere with the safety of their participation were excluded. Potential participants were also excluded for current dependence on any drugs other than cocaine or nicotine, or for lifetime dependence on alcohol, benzodiazepines, or opiates, or any current, non-substance-related Axis I disorder as determined by structured clinical interview for DSM-IV (SCID). Current use of alcohol in excess of 25 standard drinks/week, or a positive urine test for opiates, methadone, amphetamines, barbiturates, benzodiazepines, PCP, methaqualone, or propoxyphene at any time prior to randomization was exclusionary. History of recent cannabis use was allowed so long as a negative urine test for cannabis use was obtained prior to study start and at the time of inpatient admission.

All participants reviewed and signed a consent form, approved by the local institutional review board, and were assessed in their understanding of the consent form by a short quiz.

Setting

Participants were admitted to a 12-bed research facility for 12 days and 11 nights. All meals and snacks were provided on the caffeine-free unit and 3 times daily, 15-min outdoor breaks allowed smoking (at 8:45 am, 12:45 pm, and 5:45 pm). Participants maintained an 11 pm–7 am time in bed schedule while on the inpatient unit, and were checked by staff every 15 min outside those times; daytime napping was not permitted.

Medication

Participants were randomized in a double-blind fashion to receive either placebo or modafinil, stratified by age, sex, and amount of cocaine used in the past 30 days. All participants took 4 capsules containing placebo each morning of Study Days 2–4. Participants in the placebo group continued taking 4 placebo capsules thereafter. In the modafinil group, placebo capsules were replaced with modafinil capsules such that modafinil participants received 100 mg of modafinil on Day 5, 200 mg on Day 6, and 400 mg daily thereafter. Participants took the medication at 7:30 am while observed by nursing staff.

Objective Sleep Assessment

PSG sleep recordings were performed on Study Nights 3, 4, 10, and 11. These nights were chosen to capture sleep at approximately 1 and 2 weeks of abstinence,17 and to have an accommodation or re-accommodation night (Nights 3 and 10) for each subsequent data night (Nights 4 and 11). On these nights, participants slept in 1 of the 2 sleep laboratory rooms connected to the inpatient unit. Night 3 also served as a screening night for unreported sleep disorders. On Night 3, a full clinical sleep study including electroencephalogram (EEG) leads (C3-A2, C4-A1, F3-A2, F4-A1, O1-A2, and O2-A1), left and right electrooculogram (EOG), a 2-lead chin electromyogram (EMG), 2-lead electrocardiogram (ECG), right and left leg EMGs, finger pulse oximeter, plethysmographic thoracic and abdominal belts, airflow sensor, and snore microphone was performed using the Siesta PSG system (Compumedics). No participants were excluded based on the clinical PSG study. PSG studies on subsequent nights were recorded using a TEMEC 8 Channel Universal system (TEMEC Instrument B.V., Kerkrade, the Netherlands) and consisted of EEG (C3-A2 and C4-A1), left and right EOG, chin EMG, and ECG.

All PSG records were scored according to American Academy of Sleep Medicine guidelines28 by an experienced sleep scorer who was blind to treatment group and study night. Sleep onset latency was defined as time from “lights out” until the first epoch of sleep. Time awake after sleep onset was defined as the time spent awake after the first epoch of sleep until the last epoch of sleep. Time awake after final awakening was defined as the time spent awake after the last epoch of sleep until the recording ended (i.e. at ~7 am and 8 h after recording started). PSG data from Nights 4 (week 1) and 11 (week 2) were used for analysis, with Nights 3 and 10 serving as accommodation nights.

SR Sleep Assessment

Participants completed the Evening-Morning Sleep Ques tionnaire17 every night just before entering bed and every morning upon awakening. Participants reported the time they went to bed (i.e. ~11 pm), how long they felt it took to fall asleep, how much time they spent awake in the middle of the night, and the time of the final awakening and the time they got out of bed (i.e. ~7 am). SR sleep data from Night 4 (week 1) and Night 11 (week 2) are reported here.

Statistical Analysis

Pearson correlations between PSG-measured and SR sleep times were calculated at week 1 and week 2, as were the slopes and intercepts of the least squares best fit lines. Repeated measures analysis of variance (ANOVA) was used to assess differences between PSG-measured and SR sleep times at week 1 and week 2, with post hoc tests performed as indicated. Because differences were found between SR and PSG-measured sleep times at week 2 but not week 1 (when both treatment groups received placebo), subsequent repeated measures ANOVA assessed the possibility of an effect of active modafinil treatment at week 2 on the observed differences. Although there was a weak interaction between modafinil treatment and sleep measurement type at week 2, both the modafinil- and placebo-treated groups exhibited similar differences between SR and PSG-measured sleep time (see Results section). Furthermore, controlling for treatment group assignment with multiple regression analysis did not alter the findings. Hence, analysis of sleep latency, time awake after sleep onset, and time in bed after final awakening (by repeated measures ANOVA) at week 2 was done on the entire sample.

In exploratory analysis, a median split of the data was made to assess for differences in baseline characteristics between persons with high and low levels of positive sleep time misreporting at week 2 (i.e. SR sleep time minus PSG-measured sleep time). Similar analyses were performed to assess possible associations between PSG-measured total sleep times (i.e. total sleep time and time in each sleep stage) and sleep time misreporting, with both median split and Pearson correlation analysis.

Objective sleep time estimates, reflecting the ratio of the SR total sleep time to PSG-measured total sleep time,3 were calculated and binned in 0.025 unit increments.

RESULTS

SR total sleep time and PSG-measured total sleep time were strongly correlated (Pearson R = 0.77, p < .0001) during the first week of inpatient hospitalization, with the best-fit line nearly indistinguishable from y = x over the sampled domain (Figure 1, left panel). SR and PSG-measured sleep time were not as strongly correlated during the second week of inpatient hospitalization (R = 0.46, p = .002), with the slope of the best-fit line (0.45) significantly different from unity (99% confidence interval: 0.09–0.72; Figure 1, right panel).

Figure 1.

Figure 1

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Self-reported (SR) versus polysomnographically (PSG) measured total sleep time during the first (left panel) and second (right panel) week of inpatient hospitalization. Blue circles indicate placebo group participants, red circles (left panel) and squares (right panel) indicate modafinil group participants during placebo and active treatment, respectively. Solid lines indicate best linear fit for all data (first week: y = 0.98x + 17, R2 = 0.60; second week: y = 0.45x + 234, R2 = 0.21). Dotted lines indicate y = x. Insets show mean and standard error. *mean SR total sleep time was greater than PSG-measured total sleep time during the second week (p < .0001).

Repeated measures ANOVA on total sleep times revealed a statistically significant interaction between time (first to second week) and measurement (SR vs. PSG; F[1,42] = 15.81, p = .0003). Post hoc assessment showed no significant difference between SR (402 ± 9 min [SEM]) and PSG (391 ± 7 min) during week 1 but a statistically significant difference during week 2 (SR: 394 ± 8 min, PSG: 354 ± 8 min; p < .0001; Figure 1, insets). No significant difference between SR total sleep times was found between weeks 1 and 2, and (as reported in detail elsewhere23) a decrease in PSG-measured total sleep time was observed from week 1 to week 2 (p < .001).

Possible effects of active treatment with modafinil on the differences between SR and PSG-measured sleep time during week 2 were also assessed with ANOVA. There was no main effect of treatment group on sleep times (F[1,42] = 2.05, p = .16), but there was an effect of measurement as shown above (SR vs. PSG; F[1,43]=22.4, p < .0001) and an interaction effect (F[1,41] = 4.2, p < .05). Post hoc assessment showed a strong difference between PSG (337 ± 13 min) and SR total sleep time (392 ± 12) in the placebo group (p < .0005) and a smaller and nearly significant difference in the modafinil-treated group (PSG: 374 ± 9 min, SR: 395 ± 11 min; p = .051). There was no difference in SR sleep time between treatment groups, but (as reported in detail elsewhere23) PSG sleep times were longer in the modafinil group than in the placebo group (p < .05).

The contributions of sleep latency, time awake after sleep onset (until final awakening), and time spent in bed after final awakening to the difference in total sleep time during week 2 are shown in Figure 2. Repeated measures ANOVA showed an overall difference between PSG and SR measures (F[1,129] = 13.5, p < .0005) and an interaction effect (F[2,126] = 3.1; p < .05). Post hoc tests showed that SR of sleep latency (p < .02) and time awake after sleep onset (p < .00001) were both underestimated compared to PSG measurement. There was no difference between SR and PSG measurement of time in bed after final awakening.

Figure 2.

Figure 2

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Breakdown in self-reported (SR) and polysomnographically (PSG) measured total sleep time difference during week 2 of inpatient hospitalization. WASO: wake time after sleep onset prior to final awakening. TimeAfter: time in bed after final awakening. *, p < .02; **, p < .00001.

A median split of participants by the number of minutes participants positively misreported their sleep time at week 2 (high vs. low) showed no statistically significant differences in age (44 ± 7 [SD] vs. 44 ± 7 years; p > .9), sex (19% female vs. 18% female, p > .9), years of education (12.1 ± 1.5 vs. 12.4 ± 1.7; p = .6), premorbid cognitive ability as measured by the Shipley Institute of Living Scale (87 ± 13 vs. 90 ± 15; p = .6), baseline Pittsburgh Sleep Quality Index score (9.4 ± 5.1 vs. 7.4 ± 3.7; p = .12), amount of cocaine used per week ($400 ± 300 vs. $300 ± 400; p = .4), or years of use (23 ± 8 vs. 25 ± 8; p = .6). However, minutes spent in REM sleep at week 2 was significantly lower (79 ± 27 vs. 92 ± 24; p = .057) among the high misreporters. There were no statistically significant differences in total sleep time (344 ± 60 vs. 364 ± 48; p = .2), N2 sleep time (198 ± 46 vs. 201 ± 43; p = .7), N3 sleep time (39 ± 33 vs. 46 ± 32; p = .7), latency to sleep onset (27 ± 23 vs. 22 ± 16; p = .2), or REM sleep latency (67 ± 41 vs. 59 ± 34; p = 5). Correlation analysis revealed statistically significant associations between the number of minutes participants positively misreported their sleep time at week 2 and both total sleep time (R = −0.53, p = .0002) and REM sleep time (R = −0.51, p = .0005; Figure 3). There were no such associations between the number of minutes participants positively misreported their sleep times and N2 sleep time, N3 sleep time, latency to sleep onset, or REM sleep latency (all R2 < 0.05, all p > .1).

Figure 3.

Figure 3

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Sleep time misperception (the difference between self-reported sleep time and polysomnographically [PSG] measured sleep time) versus PSG-measured rapid eye movement (REM) sleep time during the second week of inpatient hospitalization. Sleep time misperception is negatively correlated with REM sleep time (r = −0.51, p = .0005).

A histogram illustrating the increase in objective sleep time estimates from week 1 to week 2 is shown in Figure 4 along with quartile data from previously published studies for comparison.

Figure 4.

Figure 4

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Distribution of objective sleep time estimates (self-reported sleep time/polysomnographically [PSG] measured sleep time, in 0.025 unit bins) for chronic cocaine users at week 1 and week 2 of abstinence (curves are rolling averages). Inset table shows quartiles for chronic cocaine users at week 2 of abstinence and comparison data from previously published work in persons with insomnia for whom clinical PSG was performed.3 *Seventy persons with combined sleep onset and maintenance insomnia; **Fifty-seven persons with any insomnia and observed periodic leg movements; ***Twenty-five persons with any insomnia believed to have a physical cause.

DISCUSSION

We found that chronic cocaine users correctly report total sleep time at 1 week of abstinence but substantially overreport total sleep time at approximately 2 weeks of abstinence. These findings suggest that the previously identified “occult insomnia” in this population reflects not only an alteration of the qualitative experience of sleep but also a positive misperception of the amount of time spent sleeping. Although misperception of sleep time is not uncommon,1–3overreporting sleep time is unusual1 and has not heretofore been identified as characteristic of any disease or disorder. The present work appears to identify positive sleep state misperception as characteristic of chronic cocaine users after approximately 2 weeks of abstinence and may contribute to a more general understanding of sleep state misperception.

It is perhaps not surprising that positive sleep state misperception would be associated with chronic cocaine use, if it were found to be characteristic of any disease or disorder. Polysomnographic sleep studies in abstinent cocaine users show deterioration of sleep times with progressive abstinence (for review, see reference32), reaching insomnia-like levels after 2–3 weeks of abstinence.25 However, chronic cocaine users typically report improving sleep quality as abstinence progresses from early withdrawal to more sustained abstinence.29,33 These 2 phenomena—improving qualitative sleep and deteriorating sleep times—co-occur over the first 3 weeks of abstinence17 and reflect perceived sleep quality that is similar to that reported by age-matched healthy sleepers (despite sleeping around 100 min less per night on average by the third week of abstinence24). The present work suggests that underlying at least part of the difference in perceived sleep quality may be the misperception of time spent sleeping, with chronic cocaine users overreporting sleep time by about 40 min on average after 2 weeks of abstinence.

Prior work suggests that the observed sleep state misperception could be related to homeostatic sleep drive dysregulation. Morgan et al.17 hypothesized that the dissociation between sleep quality and objective records of sleep was rooted in an inability of chronic cocaine users to mount a normal sleep response to wakefulness during prolonged abstinence. This inability is exemplified by chronically and markedly reduced slow-wave sleep time,17,23,24 increased sleep latency,17 decreased objective daytime sleepiness,24 and decreased total sleep time17,23,24 that manifest with abstinence after the initial withdrawal period. Such dysregulation could be responsible for sleep state misperception,4 contributing in this case to both a qualitative and quantitative “denial” of poor sleep. Notably, in the current study, SR sleep times were unchanged from week 1 to week 2 of abstinence, suggesting that normal sleep perception during week 1 was followed by a lack of appreciation of the shortened sleep time measured by PSG during the second week of abstinence.

The profound dysregulation of sleep in chronic cocaine use also includes alterations in REM sleep time that may affect sleep time perception. Following cessation of cocaine use, chronic users experience a rebound in REM sleep with markedly shortened REM latency and longer REM sleep times.34 With continued abstinence, however, REM sleep times decrease to sub-baseline levels.34 Hence, it is possible that the short REM latency and long REM sleep times of withdrawal and early abstinence contribute to the negative qualitative perception of sleep17 and relatively accurate sleep time perception. In contrast, marked decreases in REM sleep later in abstinence may contribute to a more positive qualitative experience of sleep and a tendency to overreport sleep times. This latter conjecture is supported by the data from the present study, which show a negative correlation between REM sleep time and positive sleep misperception, as well as work in other populations. For example, in persons with depression, REM sleep inhibition contributes to a more positive perception of sleep,35 and in healthy sleepers, experimentally induced REM sleep deprivation causes sleep state misperception.36

If there is a connection between REM sleep and positive sleep state misperception in chronic cocaine users, it could be mediated by dopamine signaling that has been strongly implicated in REM sleep production (e.g.,see reference37 and for review, see reference38). Although positive sleep state has not previously been observed as consistently or to the degree observed here,2–6 one clinical group with relatively elevated sleep time estimates is persons with PLMD.1,3,4 Low dopamine levels have been implicated in the occurrence of PLMD, and dopamine agonists are used to treat PLMD, suggesting a possible connection between sleep state misperception and dopamine. Substantially more research will be required, however, to better assess any role of dopamine signaling in positive sleep state misperception.

Another consideration that may be relevant to the observed sleep state misperception is the effect of wake time after sleep onset on sleep perception more generally. More time awake in bed at any point raises the ceiling on the amount of time that can be misperceived and thereby increases the potential variance in sleep state perception. In a condition where positive sleep state misperception is characteristic, this would be observed as greater overestimates of sleep time when actual sleep times are shorter. This is evident in the present study in the relationship between SR and PSG sleep time during week 2 of abstinence: the best-fit line has a y-intercept greater than 0 and slope less than 1, such that the line is farther from y = x (worse accuracy) at shorter actual sleep times and is closer to y = x (more accuracy) as sleep times increase.

This latter consideration may explain why participants in the modafinil-treated group appeared to overestimate their sleep somewhat less than placebo-treated participants. Morning-dosed modafinil treatment was associated with longer sleep times in these participants23 and in a prior study of chronic cocaine users.24 These longer sleep times reduced the amount of time awake that could be misperceived (see Figure 1, right panel), such that the observed misperception, although present (i.e. a 21-min difference), was less than that observed in the placebo group (i.e. a 55-min difference). If correct, this line of reasoning suggests that modafinil had no direct effect on sleep time perception in this population, consistent with its lack of effect on perceived sleep quality24 and despite its effects on sleep architecture24 and clinical outcome.23

Practically, the data from the current study reinforce the idea that SR sleep times in chronic cocaine users are inaccurate at 2 weeks of abstinence and not likely useful for studying sleep duration. Perhaps surprisingly, SR sleep times around 1 week of abstinence were remarkably accurate, without substantial under- or overreporting. Although sleep in chronic cocaine users at this point of abstinence does not reflect the deterioration that comes with more sustained abstinence,17,18,24 the accuracy of the SR—at least in a sleep laboratory environment with strict time-in-bed controls—suggests that it could nevertheless be useful for studying sleep in this population when more objective measurement is not feasible. However, a greater frequency of PSG measurement of sleep would be required to ascertain, for example, whether sleep time perception is accurate prior to the first point tested in this study and what the time course is for the misperception that was observed at the second time point. All participants had at least 3 days of confirmed abstinence at the first measured time point, leaving a gap of several days in which the accuracy of SR is unknown. It is also worth noting that not all participants exhibited positive sleep state misperception on the night it was tested. This heterogeneity was not related to any measured baseline characteristic but could reflect as an yet unknown trait variability across individuals in their sleep perception. Alternatively, some or all of the observed heterogeneity may reflect night-to-night variability in the sleep experience within individuals.

The present results identify positive sleep state misperception as a characteristic feature of abstinence from chronic cocaine use. However, this study was performed in a predominantly male sample in a condition where numerous sex differences exist, not the least of which is considerable differences in sleep.39 Further study is necessary to explore potential gender differences in sleep misperception in this clinical population and to describe the source of the observed misperception. Such information could be useful in better understanding the pathophysiology of addiction and relapse, as well as contribute substantially to our understanding of sleep disorders like insomnia, and sleep perception more generally.

FUNDING

This work was funded by the National Institute on Drug Abuse (DA011744-PTM), and the State of Connecticut, Department of Mental Health and Addiction Service. This publication was also made possible by CTSA Grant Number UL1 TR000142 from the National Center for Advancing Translational Science (NCATS), components of the National Institutes of Health (NIH), and NIH roadmap for Medical Research. Its contents are solely the responsibility of the authors and do not necessarily represent the official view of NIH.

[Modafinil, Sleep Architecture and Cocaine Relapse; NCT01137396; https://clinicaltrials.gov/ct2/show/NCT01137396]

DISCLOSURE STATEMENT

None declared.

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