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PubMed2005

Sleep architecture in children with idiopathic generalized epilepsy.

PURPOSE: Children with epilepsy experience sleep disturbances, behavioral and attentional problems at higher rates than their peers. However, the relation between sleep disturbances and the observed behavioral and attentional abnormalities is poorly defined. METHODS: Children with primary generalized epilepsy who were seizure free and between the ages of 5 and 18 years were matched with age- and gender-matched healthy controls and underwent two consecutive nights of nocturnal polysomnography with extended electroencephalography. Connor's Continuous Performance Test (CPT) was administered to assess daytime attentional function. Parents completed the Child Behavior Checklist (CBCL) to assess their emotional-behavioral status. Two sample t tests were used to examine group differences. Spearman correlations were used to examine the relation between sleep variables and behavior and attention variables. Multiple regression analysis was used to identify independent predictors of abnormal behavior and attention among patients. RESULTS: Eleven children with primary generalized epilepsy and eight age- and sex-matched controls participated in the study. Children with epilepsy had longer stage 1 sleep percentage (7.19 +/- 3.2 vs. 4.8 +/- 3.5; p = 0.05) and latency to rapid-eye-movement (REM) sleep (123.5 +/- 40.1 vs. 101.75 +/- 24.3; p = 0.018) compared with controls. Children with epilepsy had worse attention (CPT index, 10.94 +/- 6.55 vs. 3.42 +/- 4.04; p = 0.004) and exhibited significantly higher CBCL Total Behavior and Internalizing Behavior Problem scales. Whereas regression analysis showed no independent predictors of abnormal behavior and attention, a tendency toward association between CBCL total behavior scale and REM percentage (r= 0.55; p = 0.07), and between CPT overall index and stage 1 sleep percentage (r= 0.40; p = 0.10) was noted. CONCLUSIONS: Sleep architecture is abnormal in children with primary generalized epilepsy. Further studies are needed to determine whether abnormalities in sleep architecture contribute to poor daytime behavior and attention.

Adolescent↗
PubMed1998

[The effects of clomipramine on diurnal sleepiness and respiratory parameters in a a case of Prader-Willi syndrome].

The association of Prader-Willi-syndrome with breathing disturbances such as sleep apnea syndrome and/or hypoxemia during REM sleep, REM sleep abnormalities and excessive daytime sleepiness is well known. We report the case of an 11-year-old boy who presented with Prader-Willi syndrome, obesity (body mass index [BMI] = 45.6), severe obstructive sleep apnea syndrome and significant daytime sleepiness on multiple sleep latency test. Behavioral disorders did not allowed the use of continuous positive pressure in this patient. Therefore, clomipramine (20 mg per day) was administered. Sleep examination over 8 months showed: slight weight loss (BMI = 44.4), persistence of severe obstructive sleep apnea syndrome, slight improvement in nocturnal hypoxemia, and disappearance of excessive daytime drowsiness with mean sleep latency of 15 min 37 s (less than 2 min before treatment) and no diurnal REM sleep periods. However, clomipramine had no effect on hyperphagia.

Child↗
PubMed2002

Rapid-eye-movement sleep in jittery infants.

BACKGROUND: The pathogenesis of neonatal jitteriness (JT) remains unknown. Neonatal JT could be one of the symptoms associated with drug withdrawal syndrome due to maternal medication. To study the influence of chemicals and environment on brain development in the fetal period, Swaab and Mirmiran proposed "behavioral teratology". JT could be one of the targets for this concept. Swaab and Mirmiran postulated that rapid-eye-movement sleep (REM sleep) is useful for studying behavioral teratology. AIM: We aimed to determine the neurophysiological alterations in infants with JT by investigating REM sleep. STUDY DESIGN: Sleep records were obtained three times for each of six jittery infants. The mothers of three infants had been on medication (either alpha-methyl dopa, reserpine or haloperidol) during pregnancy, whereas the mothers of the other three infants took no medication during pregnancy. REM sleep parameters (the amount of REM sleep against the total sleep time, newly designated indices-tonic inhibition index (TII) and phasic inhibition index--, and the incidences of gross movements, phasic chin muscle activity (PCMA), and bursts of rapid eye movements) in the six jittery infants were compared with those in age-matched controls. RESULTS: Regardless of maternal medication, TIIs, which represent the shortening of PCMA during REM sleep, were higher in the jittery infants than in the controls. No other REM sleep parameters showed constant differences between the patients and controls. CONCLUSION: Release of the blockade of dopamine D2 receptors in the fetal brain is considered to be critical for the occurrence of neonatal JT with elevation of TII. Since the abnormal elevation of TII continued after 6 months of age when our patients did not show JT anymore, we have to keep monitoring jittery infants from the standpoint of "behavioral teratology".

Female↗
PubMed2005

REM sleep: a sensitive index of fear conditioning in rats.

To examine the influence of conditioned fear stimuli on sleep-wake states, we recorded sleep in Sprague-Dawley rats after exposure to tones previously paired with footshock. After habituation to a recording chamber and the recording procedure, a baseline sleep recording was obtained the next day. One day later, experimental animals were exposed to shock training designed to induce conditioned fear (FC), consisting of five tone-footshock pairings. The 5-s tones (conditioned stimuli; CS) co-terminated with 1-s footshocks (unconditioned stimuli; US). The next day sleep was recorded for 4 h in the recording chamber after presentation of five CSs alone. Sleep efficiency (total sleep time/recording period) and REM sleep (REM) and non-REM (NREM) measures were determined. While sleep efficiency was not significantly changed after CS presentation, the percentage of total sleep time spent in REM (REM percentage) was reduced in the FC animals. The reduction in REM percentage in the FC animals was due to a decrease in the number of REM bouts. In a separate experiment, we repeated the procedures, except the tones and shocks were presented in an explicitly unpaired (UP) fashion. The next day, presentation of the tones increased REM percentage in the UP group. Results are discussed in terms of the decreases in REM as a response to conditioned fear, and the relevance of these findings to the sleep changes seen in post-traumatic stress disorder (PTSD).

Acoustic Stimulation↗
PubMed2004

Affective state and EEG sleep profile in response to rapid tryptophan depletion in recently recovered nonmedicated depressed individuals.

BACKGROUND: The current study examines whether a tryptophan-free amino acid drink (TFD) causes a transient mood relapse in unmedicated patients recently recovered from major depression. TFD is thought to reduce cerebral serotonin, a neurotransmitter implicated in depression. Some studies report that TFD reverses the antidepressant and REM-suppression effects of selective serotonin reuptake inhibitors (SSRIs). METHODS: Following an average of 10 weeks of Cognitive Behavioral Therapy (CBT), 13 recovered patients who achieved 50% or greater reduction on the initial Hamilton Rating Scale of Depression (HRSD) underwent a double-blind challenge with the TFD and a control drink. In order to demonstrate the central physiological effects of the TFD on REM sleep in these patients, all night polygraphic sleep recordings were obtained before and after the TFD and control drink. RESULTS: Relative to the control drink, TFD decreased REM latency and plasma concentrations of tryptophan but had no statistically significant effect on mood symptoms as measured by the HRSD, Beck Depression Inventory (BDI), and Profile of Mood States (POMS). LIMITATIONS: High participant attrition, a physiologically active control drink, physical side effects in response to both drinks, and low statistical power may be methodological considerations that limit interpretation of findings. CONCLUSIONS: The failure to find a transient mood relapse after the TFD may suggest that: (a) nonpharmacological recovery from depression does not occur via serotonergic mechanisms, (b) participant variables may be operating, or (c) CBT alters psychological responses to unfavorable biological states.

Adult↗
PubMed1991

Sleep, depression, and suicide.

In a retrospective study of the electroencephalographic (EEG) sleep of major depressives with and without a history of suicide attempts, suicide attempters had longer sleep latency, lower sleep efficiency, and fewer late-night delta wave counts than normal controls. Nonattempters, compared to attempters, had less rapid eye movement (REM) time and activity in period 2, but more delta wave counts in non-REM period 4. Although both attempters and nonattempters were like controls in regard to REM period 2, patients with suicide attempts had altered intranight temporal distribution of phasic REM activity, with increased REM activity (by both visual and automated scoring) in REM sleep period 2 (significant group x period interaction). These findings, which may be more traitlike or persistent than state-related, are discussed in the context of current theories on the role of serotonin in the regulation of sleep and in suicidal behavior.

Adult↗
PubMed1999

Narcolepsy in orexin knockout mice: molecular genetics of sleep regulation.

Neurons containing the neuropeptide orexin (hypocretin) are located exclusively in the lateral hypothalamus and send axons to numerous regions throughout the central nervous system, including the major nuclei implicated in sleep regulation. Here, we report that, by behavioral and electroencephalographic criteria, orexin knockout mice exhibit a phenotype strikingly similar to human narcolepsy patients, as well as canarc-1 mutant dogs, the only known monogenic model of narcolepsy. Moreover, modafinil, an anti-narcoleptic drug with ill-defined mechanisms of action, activates orexin-containing neurons. We propose that orexin regulates sleep/wakefulness states, and that orexin knockout mice are a model of human narcolepsy, a disorder characterized primarily by rapid eye movement (REM) sleep dysregulation.

Age of Onset↗
PubMed2003

Distinct narcolepsy syndromes in Orexin receptor-2 and Orexin null mice: molecular genetic dissection of Non-REM and REM sleep regulatory processes.

Narcolepsy-cataplexy, a neurological disorder associated with the absence of hypothalamic orexin (hypocretin) neuropeptides, consists of two underlying problems: inability to maintain wakefulness and intrusion of rapid eye movement (REM) sleep into wakefulness. Here we document, using behavioral, electrophysiological, and pharmacological criteria, two distinct classes of behavioral arrests exhibited by mice deficient in orexin-mediated signaling. Both OX2R(-/-) and orexin(-/-) mice are similarly affected with behaviorally abnormal attacks of non-REM sleep ("sleep attacks") and show similar degrees of disrupted wakefulness. In contrast, OX2R(-/-) mice are only mildly affected with cataplexy-like attacks of REM sleep, whereas orexin(-/-) mice are severely affected. Absence of OX2Rs eliminates orexin-evoked excitation of histaminergic neurons in the hypothalamus, which gate non-REM sleep onset. While normal regulation of wake/non-REM sleep transitions depends critically upon OX2R activation, the profound dysregulation of REM sleep control unique to the narcolepsy-cataplexy syndrome emerges from loss of signaling through both OX2R-dependent and OX2R-independent pathways.

Animals↗
PubMed1998

Diagnostic aspects of narcolepsy.

The diagnostic criteria for narcolepsy continue to evolve as more is learned about the features of this and other sleep disorders. A variety of symptoms have been said to distinguish narcolepsy from other sleep disorders, including cataplexy, character of daytime sleepiness, sleep paralysis, hypnagogic hallucinations, and automatic behavior. Other diagnostic assessments, such as determination of human leukocyte antigen (HLA) haplotype and findings of sleep laboratory assessments, also contribute to the differential diagnosis. As diagnostic and analytic techniques have become more sophisticated, however, it has become apparent that many of the characteristic features of narcolepsy--including the HLA-DR2 haplotype, sleep-onset REM sleep, and short sleep latency--may also be present in other sleep disorders. Although unambiguous cataplexy does not occur with other sleep disorders and is therefore a valuable symptom for diagnosis, it may occur with a few other neurologic disorders. Furthermore, the clinical assessment of cataplexy-like symptoms is not always straightforward. Current evidence suggests there is a fairly well-defined syndrome of narcolepsy-cataplexy that is highly associated with specific HLA markers and REM sleep abnormalities. On the other hand, there is substantial clinical overlap between narcolepsy without cataplexy and idiopathic hypersomnia. Patients with features of narcolepsy who do not have definite cataplexy and patients with features of idiopathic hypersomnia must be assessed thoroughly because of the possibility that other sleep disorders are the cause of the symptoms.

Biomarkers↗
PubMed1992

Biological markers, treatment outcome, and 1-year follow-up in endogenous depression: electroencephalographic sleep studies and response to cognitive therapy.

Although there are now considerable data attesting to the efficacy of several forms of treatment for depression, there is surprisingly little information to guide the selection of the treatment most likely to benefit a given patient. Biologic markers of depression have received much attention for their potential to provide theoretically and clinically meaningful subgroups for specific treatments. The relationship between electroencephalographic (EEG) sleep disturbances, treatment outcome, and 1-year follow-up was examined for a sample of 53 patients with endogenous major depression receiving cognitive-behavioral therapy. Overall, there was little support for the prediction of a difference in short- or long-term outcome between patients with and without EEG sleep disturbances.

Adult↗
PubMed2000

Insomnia in the elderly: a review for the primary care practitioner.

The elderly are known to have a high prevalence of insomnia. Causes of insomnia include: medical, psychiatric, and drug issues; circadian rhythm changes; sleep disorders; and psychosocial factors. The elderly frequently use sleeping aids. Risks associated with elderly patients' use of hypnotic drugs are attributable to concomitant comorbid conditions, use of multiple medications, altered pharmacokinetics, and increased central nervous system sensitivity to these drugs. Treatment options for insomnia include behavior modification and pharmacotherapy. The choice of hypnotics is based on matching the nature of the insomnia to the hypnotic agent. Benzodiazepine receptor agonists are common hypnotics prescribed for insomnia in the elderly. The ideal agent has rapid onset, duration of action that lasts through the night but no residual daytime effects, and no adverse effects. The longer-acting agents have been shown to result in a higher risk of falls and hip fractures in the elderly. This relationship is not apparent with short-acting agents. Zaleplon, the newest benzodiazepine receptor agonist, has the shortest half-life of available agents. Studies have demonstrated that zaleplon is effective in improving sleep latency, duration, and sleep quality in the elderly. Zaleplon does not appear to cause rebound insomnia, residual sedation, or adversely affect psychomotor function. The key for the healthcare professional is finding the appropriate treatment or treatment combination, including behavioral modification and pharmacotherapy. When hypnotics are indicated, the most appropriate short-acting agent should be considered.

Age Factors↗