Sleep patterns in female adolescents with chronic musculoskeletal pain

This study examined sleep patterns in female adolescents with chronic musculoskeletal pain. Twenty-six participants with chronic musculoskeletal pain completed questionnaires during their clinic visit, and three 24-Hour Sleep Patterns Interviews during the following 2 weeks. Compared to normative data (Acebo & Carskadon, 2002), adolescents with chronic pain reported similar total sleep time (TST) and bedtimes. However, study participants reported significantly longer sleep onset latency, more night wakings, a later morning wake time, and more symptoms of daytime sleepiness. Pain improved after sleep for 27% of the study sample, and was associated with longer TST. Finally, depression and anxiety were related to daytime sleepiness, but not total sleep time or sleep onset latency. Female adolescents with chronic pain either may be more sensitive to the chronic sleep debt that is common in this age group, or they may experience underlying physiological sleep disrupters (e.g., periodic limb movement disorder) or sleep abnormalities (e.g., alpha-delta intrusions) not measured in this study. Additional research is needed to examine the complex relation between sleep and chronic musculoskeletal pain.     

Sleep Patterns in Female Adolescents With Chronic Musculoskeletal Pain

This study examined sleep patterns in female adolescents with chronic musculoskeletal pain. Twenty-six participants with chronic musculoskeletal pain completed questionnaires during their clinic visit, and three 24-Hour Sleep Patterns Interviews during the following 2 weeks. Compared to normative data (Acebo & Carskadon, 2002), adolescents with chronic pain reported similar total sleep time (TST) and bedtimes. However, study participants reported significantly longer sleep onset latency, more night wakings, a later morning wake time, and more symptoms of daytime sleepiness. Pain improved after sleep for 27% of the study sample, and was associated with longer TST. Finally, depression and anxiety were related to daytime sleepiness, but not total sleep time or sleep onset latency. Female adolescents with chronic pain either may be more sensitive to the chronic sleep debt that is common in this age group, or they may experience underlying physiological sleep disrupters (e.g., periodic limb movement disorder) or sleep abnormalities (e.g., alpha–delta intrusions) not measured in this study. Additional research is needed to examine the complex relation between sleep and chronic musculoskeletal pain.     

Possible role for glutamic acid decarboxylase in fibromyalgia symptoms: a conceptual model for chronic pain

Fibromyalgia (FM) is a condition of chronic generalized musculoskeletal pain that is thought to be a disorder of central pain sensitization. A number of neurotransmitters in the ascending and descending pain pathways have been implicated in FM including glutamate and GABA. Glutamic acid decarboxylase (GAD) is the rate-limiting enzyme in the conversion of glutamate to GABA and decreased expression or activity of this enzyme could result in an imbalance of excitatory and inhibitory neurotransmission in the ascending and descending pain pathways. Specifically, the expression and activity of the predominant isoform of GAD (GAD65) is influenced by several factors that are associated with FM such as female sex, poor diet, obesity, sedentary lifestyle, and stress. We hypothesize that decreased GAD expression and/or activity plays a role in the development and exacerbation of FM leading to impairments in the three common domains of FM symptomatology: increased pain (hyperalgesia and allodynia), disrupted sleep, and disturbances in mood (anxiety and depression). There are several lines of evidence that appear to support a role of GAD in FM. First, the defining symptom of FM is pain and GAD65 knockout mice have been shown to exhibit supraspinal hyperalgesia. Second, GAD has been implicated in disorders of muscle stiffness and rigidity and morning stiffness is a common symptom of FM. Third, stress, depression, and anxiety, which are often comorbid with FM, decrease GAD activity. Fourth, FM is associated with poor sleep, specifically disrupted non-rapid eye movement (NREM) sleep, and the pharmacological induction of NREM sleep is associated with the activation of GAD-containing neurons in the preoptic hypothalamus. Fifth, FM is more commonly diagnosed in women than men and the activity of GAD is reduced by low levels of its cofactor pyroxidine, which is less well-absorbed by women and can be further lowered by diet, tobacco, and alcohol intake. Sixth, FM patients tend to be overweight or obese and caloric restriction and exercise have been shown to increase GAD expression and activity. These six general lines of evidence suggest that GAD expression and/or activity might underlie the pathophysiology of FM. If this hypothesis is supported by future empirical studies, our understanding of the etiology of FM could be greatly improved. Moreover, behavioral and pharmacological therapies that modulate or mimic the effects of GAD might hold promise for the treatment of this debilitating and poorly understood disorder.     

Video polysomnographic findings in non‐rapid eye movement parasomnia

Although video polysomnography (vPSG) is not routinely recommended for the evaluation of typical cases of non‐rapid eye movement (NREM) parasomnias, it can aid diagnosis of unusual cases, other sleep disorders and complicated cases with REM behaviour disorder (RBD), and in differentiating parasomnias from epilepsy. In this study, we aimed to assess vPSG findings in consecutive patients with a clinical diagnosis of NREM‐parasomnia covering the whole phenotypic spectrum. Five hundred and twelve patients with a final diagnosis of NREM parasomnia who had undergone vPSG were retrospectively identified. vPSGs were analysed for features of NREM parasomnia and for the presence of other sleep disorders. Two hundred and six (40.0%) patients were clinically diagnosed with sleepwalking, 72 (14.1%) with sleep terrors, 39 (7.6%) with confusional arousals, 15 (2.9%) with sexsomnia, seven (1.4%) with sleep‐related eating disorder, 122 (23.8%) with mixed phenotype, and 51 (10.0%) with parasomnia overlap disorder (POD). The vPSG supported the diagnosis of NREM parasomnia in 64.4% of the patients and of POD in 98%. In 28.9% of the patients, obstructive sleep apnea (OSA) or/and periodic limb movements during sleep (PLMS) were identified, most commonly in older, male, sleepy and obese patients. vPSG has a high diagnostic yield in patients with NREM parasomnia and should be routinely performed when there is diagnostic doubt, or in patients where there is a suspicion of OSA and PLMS.     

PTSD-related hyperarousal assessed during sleep

Posttraumatic stress disorder is widely understood to include "persistent symptoms of increased arousal." This presumption has rarely been tested under conditions in which effects of anticipatory anxiety could be ruled out. In this study, heart rate and electroencephalogram spectral power were assessed during sleep, a state free of most sources of artifact contaminating indices of tonic arousal. Fifty-six unmedicated nonapneic Vietnam combat-related inpatients with posttraumatic stress disorder (PTSD) and 14 controls spent 3 or more nights in the sleep laboratory during which their electrocardiograms and electroencephalograms were continuously recorded. Heart rate and electroencephalogram spectral power were quantified continuously off-line and averaged by sleep stage over all postadaptational nights. Sleep heart rate exhibited no group differences and no covariation with the severity of subjective hyperarousal reported by PTSD patients. PTSD patients exhibited a trend toward reduced low-frequency electroencephalogram spectral power during nonrapid-eye-movement (NREM) sleep. This reduction was significant during slow-wave sleep in those subjects producing scoreable slow-wave sleep. The relationship of rapid-eye-movement (REM) beta-band power to NREM beta-band power was different in PTSD patients and controls, with the patients exhibiting more beta in REM versus NREM sleep than controls. In patients, NREM sleep sigma-band electroencephalogram spectral power exhibited a positive correlation with subjective hyperarousal. Finally, a novel and surprisingly strong inverse correlation between REM-NREM sleep heart rate difference and REM percent of sleep was observed in PTSD patients only. In summary, peripheral and central measures of tonic arousal during sleep demonstrated contrastive relations to PTSD diagnostic and symptom status. The data suggest that more consideration should be directed to mechanisms of central arousal in PTSD.     

Sleep Quality and Psychological Adjustment in Chronic Fatigue Syndrome

Without specific etiology or effective treatment, chronic fatigue syndrome (CFS) remains a contentious diagnosis. Individuals with CFS complain of fatigue and poor sleep—symptoms that are often attributed to psychological disturbance. To assess the nature and prevalence of sleep disturbance in CFS and to investigate the widely presumed presence of psychological maladjustment we examined sleep quality, sleep disorders, physical health, daytime sleepiness, fatigue, and psychological adjustment in three samples: individuals with CFS; a healthy control group; and individuals with a definite medical diagnosis: narcolepsy. Outcome measures included physiological evaluation (polysomnography), medical diagnosis, structured interview, and self-report measures. Results indicate that the CFS sample had a very high incidence (58%) of previously undiagnosed primary sleep disorder such as sleep apnea/hypopnea syndrome and restless legs/periodic limb movement disorder. They also had very high rates of self-reported insomnia and nonrestorative sleep. Narcolepsy and CFS participants were very similar on psychological adjustment: both these groups had more psychological maladjustment than did control group participants. Our data suggest that primary sleep disorders in individuals with CFS are underdiagnosed in primary care settings and that the psychological disturbances seen in CFS may well be the result of living with a chronic illness that is poorly recognized or understood.     

Sleep,neuroimmune and neuroendocrine functions in fibromyalgia and chronic fatigue syndrome

The justification for disordered chronobiology for fibromyalgia and chronic fatigue syndrome (CFS) is based on the following evidence: The studies on disordered sleep physiology and the symptoms of fibromyalgia and CFS; the experimental studies that draw a link between interleukin-1 (IL-1), immune-neuroendocrine-thermal systems and the sleep-wake cycle; studies and preliminary data of the inter-relationships of sleep-wakefulness, IL-1, and aspects of peripheral immune and neuroendocrine functions in healthy men and in women during differing phases of the menstrual cycle; and the observations of alterations in the immune-neuroendocrine functions of patients with fibromyalgia and CFS (Moldofsky, 1993b, d). Time series analyses of measures of the circadian pattern of the sleep-wake behavioural system, immune, neuroendocrine and temperature functions in patients with fibromyalgia and CFS should determine whether alterations of aspects of the neuro-immune-endocrine systems that accompany disordered sleep physiology result in nonrestorative sleep, pain, fatigue, cognitive and mood symptoms in patients with fibromyalgia and CFS.     

Gender-dependent age effects on sleep EEG power density in major depression

Summary Introduction   In the present study, we evaluated the impact of age and gender on EEG spectral power of non rapid eye movement (NREM) sleep in Major depression and hypothesized a gender-dependent age effect as previously observed in healthy controls (more prominent decline of delta activity in male than in female subjects).
Patients and Methods   We spectrally analyzed the NREM sleep EEG of 11 male and 11 female depressed patients, who were carefully pair-matched with regard to age and clinical parameters and were free of any psychoactive drugs for at least 1 week.
Results   Whereas male and female patients did not differ significantly in averaged spectral power, we found a significant decline of delta activity as the main age effect on sleep in men, but not in women.
Conclusion   This clear gender-dependent age effect on the sleep EEG in Major depression contributes to a better understanding of sleep changes with aging and is methodologically important for future sleep studies in psychiatric disorders.     

Polysomnography and self-reported sleep, pain, fatigue, and anxiety in children with active and inactive juvenile rheumatoid arthritis

OBJECTIVE: To compare polysomnography (PSG) and self-reported sleep, symptoms (pain and fatigue), and anxiety between children with active and inactive juvenile rheumatoid arthritis (JRA) and examine relations among sleep, symptoms, and anxiety. METHODS: Two consecutive nights of PSG, self-reported sleep, and symptoms were obtained in 70 children 6-11 years of age with active (n = 35) or inactive (n = 35) JRA. RESULTS: On the second (study) night, PSG and self-reported sleep variables were not different, but pain and fatigue were significantly higher (both p <.02) in children with active compared to inactive disease. In a stepwise regression, age, medications, disease status, anxiety, evening pain, total sleep time, and arousals explained 36% of the variance in fatigue and age, disease status, and evening pain were significant (all p <.04) predictors of fatigue. All children showed longer sleep latency and reduced sleep efficiency on the first night in the laboratory. CONCLUSIONS: Sleep was not altered in children with active JRA, however, the "first night effect" suggests that valid laboratory sleep assessments require an adaptation night.     

Motor dyscontrol in sleep of narcoleptic patients (a lifelong development?)

In our retrospective study 27 narcoleptic patients were divided into two groups: Group A comprised 14 patients (10 male, 4 female) with a history of REM behaviour disorder (RBD) and Group B comprised 13 age- and sex-matched patients (10 male, 3 female) without a history of RBD. Polygraphic and videometry data, medical history, medication, blood chemistry, psychological and neuroradiological data of the two groups of patients were compared. The narcoleptic patients with a history of RBD differed from the narcoleptic control group without history of RBD in that they had: (a) a higher frequency of parasomnias in their history; (b) a higher percentage of stage 1 REM (P < 0.01); (c) a lower number of arousals during REM sleep; (d) fewer sleep stage changes. Compared to the heterogenous RBD patient group of Mahowald and Schenck, the REM behaviour of most of our narcoleptic patients was less violent. Thus it can be speculated that the motor disorder in REM sleep might still be in the process of developing towards a full-blown REM sleep behaviour disorder. In a possible lifelong development of a motor disorder starting in NREM sleep, the onset of narcolepsy might represent the turning point for its intrusion into REM sleep.     

Are microarousals preceded by electroencephalographic slow wave synchronization precursors of confusional awakenings?

The number of microarousals preceded by electroencephalographic (EEG) slow wave synchronization (MAS) and the number not preceded by EEG slow wave synchronization (K-complexes and/or delta groups) (MA) were analyzed during the first night of sleep in nine young patients with somnambulism and/or sleep terrors and in eight age- and sex-matched controls. While MAs peaked in REM ad intermediate sleep, MASs appeared as a phenomenon of NREM sleep, peaking in stage 2. The number of MASs was significantly greater in all stages of NREM sleep in the patient group, but number and distribution of MAs did not differ between the two groups. In the patient group, the MASs occurred in slow wave sleep (stages 3-4 of each sleep cycle); in controls, MASs occurred infrequently. MASs were frequently associated with automatic chewing movements. The higher frequency of microarousals in the patient group did not result in an increase in time awake during the night. The increase in number of microarousals supports Broughton's hypothesis of the presence of some "arousal disorder" in somnambulism and/or sleep terrors. MASs may be predictive markers of ensuing confusional awakenings.     

Spindle frequencies in sleep EEG show U-shape within first four NREM sleep episodes

It has been shown in previous studies on sleep electroencephalogram (EEG) that spindles are slower in the beginning of the night fastening towards the end of the night. Corresponding findings have been obtained by spectral analysis. The present study was based on our preliminary observation that slower spindles are found in the middle of the non-rapid eye movement (NREM) sleep episodes as compared with the beginning or the end of the episodes. Eight healthy female and six male subjects were studied. Sleep spindles were visually selected and spindle frequencies calculated for 11 analysis points in each NREM sleep episode. The median spindle frequencies formed a clear U-shape within NREM sleep episodes with an initial decrease and final increase. The decrease was statistically significant within the first four NREM sleep episodes. It is possible that the spindle frequency pattern could be used to reveal variations in sleep depth within sleep stage 2. In animal studies the spindle frequency has been found to be associated to the duration of the hyperpolarization-rebound sequences of the thalamocortical cells. If it is assumed that the same cellular mechanisms are responsible for spindle frequencies in humans then the study of variations in spindle frequency could be used to examine the NREM sleep process in humans.     

Management of pain and fatigue in the joint hypermobility syndrome (a.k.a. Ehlers-Danlos syndrome, hypermobility type): principles and proposal for a multidisciplinary approach

Joint hypermobility syndrome (JHS), or Ehlers-Danlos syndrome (EDS) hypermobility type (EDS-HT), is a underdiagnosed heritable connective tissue disorder characterized by generalized joint hypermobility and a wide range of visceral, pelvic, neurologic, and cognitive dysfunctions. Deterioration of quality of life is mainly associated with pain and fatigue. Except for the recognized effectiveness of physiotherapy for some musculoskeletal features, there are no standardized guidelines for the assessment and treatment of pain and fatigue. In this work, a practical classification of pain presentations and factors contributing in generating painful sensations in JHS/EDS-HT is proposed. Pain can be topographically classified in articular limb (acute/subacute and chronic), muscular limb (myofascial and fibromyalgia), neuropathic limb, back/neck, abdominal and pelvic pain, and headache. For selected forms of pain, specific predisposing characteristics are outlined. Fatigue appears as the result of multiple factors, including muscle weakness, respiratory insufficiency, unrefreshing sleep, dysautonomia, intestinal malabsorption, reactive depression/anxiety, and excessive use of analgesics. A set of lifestyle recommendations to instruct patients as well as specific investigations aimed at characterizing pain and fatigue are identified. Available treatment options are discussed in the set of a structured multidisciplinary approach based on reliable outcome tools.     

Is fibromyalgia part of the climacteric syndrome?

Fibromyalgia syndrome (FMS) is a disorder usually affecting middle aged women, who complain of diffuse musculoskeletal aches, pains or stiffness associated with tiredness, anxiety and poor sleep. Neurotransmission disorders linked both to pain perception as well as mood, sleep and cognition modulation are involved in FMS etiopathogenesys. Treatments that may be effective to decrease pain and fatigue include tricyclic antidepressants, dual reuptake inhibitors of serotonin/noradrenalin and pregabalin. The climacteric syndrome is a set of symptoms caused by the decline of ovarian hormone levels, which alters brain neurotransmission and provokes musculoskeletal pains, mood disorders, poor sleep quality and hot flushes. The hormone therapy reverses those symptoms and its risks are marginal if women's own hormones are used through transdermal route. Some antidepressants may be useful for patients with climacteric symptoms. We have found it surprising the epidemiological, etiopathogenic, symptomatic and therapeutic similarity between FMS and climacteric that could lead us to hypothesize that FMS is a part of the climacteric syndrome. However, the existence of FMS non-climacteric patients points out that hormone deficit is not the only physiopathological mechanism involved in this syndrome's etiopathogenesys. Nevertheless, it is likely that hormone disorders are involved in the symptoms genesis of most middle aged women with FMS. Keeping this in mind, we see the point in considering the use of HT in climacteric patients with FMS. Studies assessing the FMS clinical response to HT in a prospective manner and with the current diagnose criteria are still required.     

Dreaming during non-rapid eye movement sleep in the absence of prior rapid eye movement sleep

STUDY OBJECTIVES: There is a long-standing controversy surrounding the existence of dream experiences during non-rapid eye movement (NREM) sleep. Previous studies have not answered the question whether this "NREM dream" originates from the NREM sleep mechanism because the subject might simply be recalling experiences from the preceding rapid eye movement (REM) sleep. METHODS: We scheduled 11 healthy men to repeat 20-minute nap trials separated by 40-minute periods of enforced wakefulness across a period of 3 days. At the end of the nap trial, each participant answered questions regarding the formal aspects of his dream experiences during the nap trial, using the structured interviews. RESULTS: We obtained a total of 172 dream reports after naps containing REM sleep (REM naps) and 563 after naps consisting of only NREM sleep (NREM naps). Dream reports from NREM naps were less remarkable in quantity, vividness, and emotion than those from REM naps and were obtained more frequently during the morning hours when the occurrences of REM sleep were highest. CONCLUSIONS: These results suggest that the polysomnographic manifestations of REM sleep are not required for dream experiences but that the mechanisms driving REM sleep alter experiences during NREM sleep in the morning. A subcortical activation similar to REM sleep may occur in human NREM sleep during the morning when REM sleep is most likely to occur, resulting in dream experiences during NREM sleep.     

Development and evaluation of a cognitive-behavioral intervention for juvenile fibromyalgia

OBJECTIVE: To describe the development and test the efficacy of a cognitive-behavioral intervention (CBT) for juvenile fibromyalgia. METHOD: Sixty-seven children with fibromyalgia and their parents were recruited to participate in an 8-week intervention that included modules of pain management, psychoeducation, sleep hygiene, and activities of daily living. Children were taught techniques of cognitive restructuring, thought stopping, distraction, relaxation, and self-reward. Additionally, they kept daily pain and sleep diaries. Children completed questionnaires of pre- and post-treatment measuring physical status and psychological functioning. RESULTS: Following CBT, children reported significant reductions (p < .006) in pain, somatic symptoms, anxiety, and fatigue, as well as improvements in sleep quality. Additionally, children reported improved functional ability and had fewer school absences. CONCLUSION: Children with fibromyalgia can be taught CBT strategies that help them effectively manage this chronic and disabling musculoskeletal pain disorder.     

Sleep-related myoclonus in rheumatic pain modulation disorder (fibrositis syndrome) and in excessive daytime somnolence

We describe a new syndrome, Rheumatic Pain Modulation Disorder (RPMD) ("fibrositis syndrome") with sleep-related myoclonus (involuntary periodic leg movements). Measures of sleepiness, fatigue and pain, before and after sleep, and aspects of sleep of nine subjects (Ss) with RPMD and sleep-related myoclonus were compared to nine subjects with excessive daytime somnolence and sleep-related myoclonus. In eight of the RPMD with sleep-related myoclonus and three of those with daytime sleepiness, an alpha (7.5-11 Hz) EEG Non-Rapid Eye Movement sleep disorder was demonstrated. The RPMD with sleep-related myoclonus group contained a greater number of women, more pain, morning fatigue, and disturbances in sleep (more stage changes and alpha EEG sleep prior to leg myoclonus); but in comparison to the sleep-related myoclonus, daytime somnolent group, there were no differences in evening and morning sleepiness, number of limb movements, movement arousals, awakenings after sleep onset, sleep duration, and percent sleep stages.     

The impact of a 4-hour sleep delay on slow wave activity in twins discordant for chronic fatigue syndrome

OBJECTIVES: Chronic fatigue syndrome (CFS) has been associated with altered amounts of slow wave sleep, which could reflect reduced delta electroencephalograph (EEG) activity and impaired sleep regulation. To evaluate this hypothesis, we examined the response to a sleep regulatory challenge in CFS. DESIGN: The first of 3 consecutive nights of study served as laboratory adaptation. Baseline sleep was assessed on the second night. On the third night, bedtime was delayed by 4 hours, followed by recovery sleep. Total available sleep time was held constant on all nights. SETTING: A research sleep laboratory. PARTICIPANTS: 13 pairs of monozygotic twins discordant for CFS. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Power spectral analysis quantified slow wave activity (SWA) in the 0.5-3.9 Hz band in successive NREM periods (stage 2, 3, or 4) on each night. To ensure comparability, analyses were restricted to the first 4 NREM periods on each night. Data were coded for NREM period and twin pair. Repeated-measures analysis of variance (ANOVA) contrasted sleep delay effects across NREM periods between twin pairs. A second ANOVA calculated the SWA in each NREM period in recovery sleep relative to baseline SWA. The 2 groups of twins were similar on baseline SWA power. After sleep delay, CFS twins exhibited significantly less SWA power in the first NREM period of recovery sleep and accumulated a smaller percentage of SWA in the first NREM period than their co-twins. CONCLUSIONS: CFS is associated with a blunted SWA response to sleep challenge, suggesting that the basic sleep drive and homeostatic response are impaired.     

Insufficient non-REM sleep intensity in narcolepsy-cataplexy

STUDY OBJECTIVES: To compare electroencephalogram (EEG) dynamics during nocturnal sleep in patients with narcolepsy-cataplexy and healthy controls. Fragmented nocturnal sleep is a prominent feature and contributes to excessive daytime sleepiness in narcolepsy-cataplexy. Only 3 studies have addressed changes in homeostatic sleep regulation as a possible mechanism underlying nocturnal sleep fragmentation in narcolepsy-cataplexy. DESIGN, SETTING AND PARTICIPANTS: Baseline sleep of 11 drug-naive patients with narcolepsy-cataplexy (19-37 years) and 11 matched controls (18-41 years) was polysomnographically recorded. The EEG was subjected to spectral analysis. INTERVENTIONS: None, baseline condition. MEASUREMENTS AND RESULTS: All patients with narcolepsy-cataplexy but no control subjects showed a sleep-onset rapid eye movement (REM) episode. Non-REM (NREM)-REM sleep cycles were longer in patients with narcolepsy-cataplexy than in controls (P = 0.04). Mean slow-wave activity declined in both groups across the first 3 NREM sleep episodes (P<0.001). The rate of decline, however, appeared to be steeper in patients with narcolepsy-cataplexy (time constant: narcolepsy-cataplexy 51.1 +/- 23.8 minutes [mean +/- SEM], 95% confidence interval [CI]: 33.4-108.8 minutes) than in controls (169.4 +/- 81.5 minutes, 95% CI: 110.9-357.6 minutes) as concluded from nonoverlapping 95% confidence interval of the time constants. The steeper decline of SWA in narcolepsy-cataplexy compared to controls was related to an impaired build-up of slow-wave activity in the second cycle. Sleep in the second cycle was interrupted in patients with narcolepsy-cataplexy, when compared with controls, by an increased number (P = 0.01) and longer duration (P = 0.01) of short wake episodes. CONCLUSIONS: Insufficient NREM sleep intensity is associated with nonconsolidated nocturnal sleep in narcolepsy-cataplexy. The inability to consolidate sleep manifests itself when NREM sleep intensity has decayed below a certain level and is reflected in an altered time course of slow-wave activity across NREM sleep episodes.