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PubMed2004

What can neuroimaging findings tell us about sleep disorders?

Models of the pathophysiology of human sleep disorders have only recently been tested using nuclear medicine assessments, which have greatly increased our understanding of the brain mechanisms involved in the human sleep-wake cycle. Dramatic changes in function have been observed in large-scale neuronal networks during sleep. Broad declines in heteromodal-association-cortical function, and relative increases in limbic and paralimbic function have been observed. These cortical areas are responsible for essential aspects of human behavior, allowing us to interact with the world around us and to evaluate the significance of important events in our lives. Preliminary findings suggest that fundamental alterations in the function of these neural systems occur in sleep disorders. In depression, alterations in rapid-eye-movement and slow-wave sleep appear linked to a sleep-related dysfunctional arousal in primary limbic and paralimbic structures (amygdala), and hypofunction in frontal cortical areas. Pharmacologic interventions partially reverse these alterations. Preliminary studies in insomia indicate a subcortical hyperarousal and a failure of sleep to provide normal restoration of function in the prefrontal cortex, leading to chronic sleep deprivation. This review discusses functional neuroimaging data on normal sleep, and on the pathophysiology of insomnia related to depression and primary insomnia.

Brain↗
PubMed2005

Homeostatic regulation of sleep in a genetic model of depression in the mouse: effects of muscarinic and 5-HT1A receptor activation.

In depressed patients, sleep undergoes marked alterations, especially sleep onset insomnia, sleep fragmentation, and disturbances of the Rapid Eye Movement (REM) sleep. Abnormalities of rest-activity rhythms and of hypothalamic-pituitary-adrenocortical function have also been described in these patients. In the present study, we examined the presence of such abnormalities in a recently developed line of mice (Helpless mice-H) that exhibit depression-like behaviors in validated tests, compared to the nonhelpless (NH) line derived from the same colony. Experiments were essentially carried out in females for which previous studies showed marked differences between H and NH lines. Compared to NH mice, the H line exhibited (i) lower basal locomotor activity, (ii) sleep fragmentation, shift towards lighter sleep stages, and facilitation of REM sleep reflected by increased amounts and decreased latency, (iii) larger response to the REM sleep promoting effect of muscarinic receptor stimulation (by arecoline). In contrast, H and NH mice were equally responsive to the REM sleep inhibitory effect of 5-HT1A receptor stimulation (by 8-OH-DPAT). In addition, a deficiency in delta power enhancement after sleep deprivation was observed in the H group, and acute immobilization stress in this group failed to elicit a REM sleep rebound and was associated with a long-lasting raise in serum corticosterone levels. These results further validate H mice as a depression model and suggest they might be of particular interest for investigating the neurobiological mechanisms and possibly genetic substrates underlying sleep alterations associated with depression.

Animals↗
PubMed2005

Stress models of depression: forming genetically vulnerable strains.

Among the most useful models for depressive disorders are those, which involve a stress induced change in behaviour. Learned helplessness is one such model and is induced through exposure to uncontrollable and unpredictable aversive events. Learned helplessness as induced in rats using foot shock is well characterized and has good face validity and predictive validity as a model of depression, including alterations in HPA axis activity and REM sleep characteristic of depression. The data concerning the validity will be briefly reviewed. The model can also be used to look at the role of genetics through selective breeding. These studies will be reviewed and the utility of the genetic strains for understanding the interaction of stress and affect will be examined. A second model of depression using exposure to chronic stress also has high face and predictive validity. A new form of this approach, recently described, also is suitable for the examination of genetic factors leading to depressive like behaviour and this will be presented.

Animals↗
PubMed1998

[Sleep as behavior].

INTRODUCTION: Throughout life human beings maintain an alternating rhythm of two biological rhythms between three states: wakefulness, NREM sleep and REM sleep. These states are quite distinct both with regard to conduct and physiologically. Sleep is an active process during which an amalgam of behavioural and physiological processes occur, together with complex cerebral activity. The universality of sleep or similar resting behaviour in the animal kingdom has encouraged study of its origin and function. The phylogenetics of sleep and the study of behaviour during this state in different species of animals offers ample possibilities to understand its significance. We describe the characteristics of conduct which define the different phases of sleep in adult humans. Motor activity, relationship with the surroundings, perception of and reaction to external stimuli, ability to recognize and remember are all variables which are modified during the transition from wakefulness to sleep, NREM sleep and REM sleep. Changes in behaviour during sleep form a group of pathological conditions with different origins and physiopathological methods involved. The parasomnias are the alterations of behaviour during sleep par excellence. We describe the concept and classification according to current theories.

Adult↗
PubMed1998

[Wake disorders. I. Primary wake disorders].

Primary wake disorders encompass various conditions of excessive daytime sleepiness and/or increased nighttime sleep, of unknown origin beginning most often in adolescence and of chronic or recurrent natural history. The best known of these conditions is narcolepsy associating two major clinical features, irresistible episodes of sleep, sleep onset REM periods and an almost constant association with HLA DR2-DQ1. The prevalence of the condition is close to the one of multiple sclerosis but positive diagnosis requires most often over 10 years to be made. The treatment of excessive daytime sleepiness has recently benefited from a new non-amphetamine awakening compound, modafinil, active in 60 to 70 p. 100 of the cases. The treatment of cataplexy still relies on antidepressants, tricyclics or selective serotonin reuptake blockers. Major advances in pathophysiology and pathogeny have been obtained through a natural model of the disease, canine narcolepsy. Pharmacological studies point to the importance of alpha-1 b adrenergic mechanisms in cataplexy, while dopaminergic systems seem more involved in excessive daytime sleepiness. As concerns genetics, the HLA DQB1*0602 gene predisposes to narcolepsy. In the canine model it is mirrored by an autosomal recessive gene showing a strong homology with the human immunoglobulin gene mu-switch. Familial studies have shown that besides typical phenotypes, attenuated forms of the condition characterized by isolated recurrent daytime naps and/or lapses into sleep do exist. In addition one or several other genes may be involved. Narcolepsy is multifactorial, including one or several genes as well as environmental factors. Idiopathic hypersomnia is noted for very long night sleep, difficulty waking up and more or less constant excessive daytime sleepiness. In contrast with narcolepsy sleep in not refreshing. There is no polysomnographic or immunogenetic special feature. Idiopathic hypersomnia is 10 times less frequent than narcolepsy. It is often overdiagnosed due to insufficient knowledge of other causes of excessive daytime sleepiness such as the upper airway resistance syndrome. Modafinil is also of great value in the treatment of idiopathic hypersomnia. In the absence of an animal model, pathophysiology and pathogeny are still poorly understood. Even rarer is the Kleine-Levin syndrome which is easily distinguishable through its recurrent character and its tendency to progressively disappear. It mainly occurs in early adolescent males. Its main features are episodes of sleep of a week duration recurring at a several months' interval along with disturbances of alimentary and sexual behavior. There is no satisfactory treatment of hypersomniac episodes. On the other hand a prophylactic treatment with carbamazepine or lithium may be active. Pathophysiology remains unsettled in spite of some evidence of a hypothalamic functional disturbance.

Animals↗
PubMed2005

Sleep and pain: interaction of two vital functions.

Disturbed sleep is a key complaint of people experiencing acute and chronic pain. These two vital functions, sleep and pain, interact in complex ways that ultimately impact the biological and behavioral capacity of the individual. Polysomnographic studies of patients experiencing acute pain during postoperative recovery show shortened and fragmented sleep with reduced amounts of slow wave and rapid eye movement (REM) sleep, and the recovery is accompanied by normalization of sleep. Objective assessments of sleep in patients with various chronic pain conditions have been less definitive with some studies showing fragmented and shortened sleep and others showing normal sleep. Although daytime fatigue is a frequent complaint associated with complaints of pain-related disturbed sleep, objective assessments of daytime sleepiness reveal minimally elevated levels of sleepiness and emphasize the importance of distinguishing sleepiness and fatigue. The pain-sleep nexus has been modeled in healthy pain-free subjects and the studies have demonstrated the bidirectionality of the sleep-pain relation. Given this bidirectionality, treatment must focus on alleviation of both the pain and sleep disturbance. Few of the treatment studies have done such, and as a result no clear consensus on treatment approaches, much less on differential etiology-based treatment strategies, has emerged.

Analgesics↗
PubMed2002

Effects of low-dose ketamine on neuropathic pain: An electroencephalogram-electrooculogram/behavioral study.

The aim of the present study was to clarify the neurophysiological changes associated with analgesic and behavioral effects of low-dose ketamine HCl in patients suffering from chronic neuropathic pain. Ten in-patients with neuropathic pain participated in this single-blind, placebo-controlled study after giving written informed consent. Following intravenous injections of a saline solution (placebo), three bolus injections of 5 mg ketamine HCl were administered at 5 min intervals. Changes in pain perception were assessed using a numerical rating scale for pain. Behavioral changes, including psychotomimetic effects, were assessed using the Brief Psychiatric Rating Scale (BPRS). Electroencephalograms (EEG) and electrooculograms (EOG) were recorded continuously throughout the testing period. One minute EEG and closed-eye eye movements were quantified. The effects of ketamine were evaluated by comparing the neurophysiological and behavioral parameters obtained from the placebo and ketamine trials. Pain reduction was significantly correlated with ketamine-induced changes in hallucinatory behavior and excitement as measured by the BPRS. Ketamine injections caused a significant decrease in the EEGalpha amplitude without an accompanying reduction in EEG frequency. The EEGalpha amplitude reduction at the right central electrode was significantly related to subjective pain relief. Subanesthetic doses of ketamine significantly decreased rapid eye movements, but did not initiate slow eye movements. In conclusion, the present EEG-EOG/behavioral results indicate that ketamine-induced failure of neural integration between cortical-subcortical regions induces psychotic symptoms and alters pain perception on neuropathic pain.

Aged↗
PubMed1991

Aging, sleep disorders, and male sexual function.

The relation between age, sleep disorders, nocturnal penile tumescence, and sexual behavior was investigated in 70 healthy married men aged 45-75 years. They had an extensive psychosexual interview, a medical and psychiatric evaluation, and were studied in the sleep laboratory for four nights. Electroencephalogram (EEG), eye movements, muscle tone, and penile tumescence were monitored continuously, and respiratory airflow and bilateral anterior tibialis recordings were obtained during the first sleep session. There was a marked age-related increase in sleep-disordered breathing, but no significant changes in periodic leg movements with age. Respiratory distress and periodic leg movement (PLM) indices were mostly unrelated with nocturnal penile tumescence (NPT) measures as well as with all sexual behavior dimensions when age was taken into account in the analysis of results. Men with a respiratory distress disorder did not differ from a nondisordered group of similar age in NPT and behavioral parameters. Men with PLM disorder differed from their comparison group in only two variables: fewer number of maximum tumescent episodes and less frequent sexual thoughts. Men who met criteria for erectile impotence did not differ significantly in degree of respiratory or PLM disturbances or in the prevalence of sleep disorders when compared to an aged-matched sexually nondysfunctional group. The overall results did not support the notion that sleep disorders are involved in the increased prevalence of erectile impotence in healthy older individuals. Assessment of blood oxygenation and respiratory effort, in addition to airflow, need to be carried out before final conclusions can be drawn on the significance of sleep-disordered breathing in male sexuality.

Age Factors↗
PubMed1994

Twenty-four-hour blood pressure control: effect of cilazapril on continuous arterial blood pressure during sleep, and physical and mental load in patients with arterial hypertension and sleep apnea.

To assess the effectiveness of cilazapril in regulating blood pressure (BP) in patients with sleep-related breathing disorders, 23 male patients (mean age, 50 years; mean body mass index, 32.7 kg/m2) with a mean apnea/hypopnea index of 49.7 and arterial hypertension (163/104 mm Hg) participated in a placebo-controlled, randomized, double-blind study. They received either cilazapril, 2.5 mg/day (n = 12) or placebo (n = 11). The effects of treatment were studied under different conditions of sleep and physical and mental load before and after 8 days of treatment. Measurements by night included cardiorespiratory polysomnography, inductive plethysmography, pulse oximetry and nasal air flow, electroencephalography, (EEG), electrooculography and electromyography, (ECG), and blood pressure (BP). Measurements by day (ECG, heart rate, and BP) were performed at rest and under physical and mental load. Systolic, diastolic, and mean BP (5 min at night; 1 s during the day), heart rate, apnea and hypopnea index, EEG data, and test reaction times were compared in both groups. The systolic and diastolic BP of patients receiving cilazapril was lower compared to baseline for all physical and mental loads. Mean BP reductions over all standardized loads was greater with cilazapril than placebo (-10 vs. -4.3 mm Hg, p < 0.05). These results show that BP is influenced similarly by mental and physical loads, and that behavior [i.e., awake state and non-rapid eye movement and rapid eye movement (NREM and REM) sleep determines BP regulation. Cilazapril is effective in reducing BP in all situations, especially during REM sleep hypertension.

Adult↗
PubMed1995

Arousal fluctuations in non-rapid eye movement parasomnias: the role of cyclic alternating pattern as a measure of sleep instability.

Some non-rapid eye movement (NREM) parasomnias, such as sleep-walking (SW), sleep terror (ST) and, in some aspects, sleep enuresis (SE), are considered "arousal disorders" without significant polysomnographic changes in classic sleep macrostructure. The aim of our study was to evaluate sleep microstructure and oscillations of arousal level by cyclic alternating pattern (CAP) scoring in some NREM parasomnias. Nocturnal polysomnography and videotape recording was used to study 21 patients with motor and behavioral phenomena during sleep: 13 in Group A (seven SW, six ST) with delta sleep-related episodes, eight in Group B with other parasomnias (six sleep bruxism and two SE), and six healthy controls. Classic sleep macrostructural parameters were no different in the parasomniacs and controls. Compared with the controls, our patients' sleep microstructure, scored by CAP analysis, showed increases in CAP rate (a measure of NREM instability with high level of arousal oscillation), in number of the CAP cycles, and in arousals with EEG synchronization, the increases being more significant in Group A than in Group B. An increase in sleep instability and in arousal oscillation seems to be a typical microstructural feature of delta sleep-related parasomnias and probably plays a role in triggering abnormal motor episodes during sleep in these patients.

Adolescent↗
PubMed1975

Neuroregulators and sleep mechanisms.

Information which has emerged thus far relates to the overall transmitter mechanisms of sleep. The data, while conflicting, point to the involvement of many neuroregulators at numerous integrative levels of the process. However the long term question still remain: what triggers and maintain sleep, what stops sleep, what occurs to the body and brain during sleep--in essence, why sleep? These questions are now problems for behavioral neurochemists, whereas in a previous era, they were problems for philosophers. Unfortunately, our answers to date, while in another idiom, have hardly been more complete or satisfying. To answer these questions, it will be necessary to understand, in detail, the manner in which neurobiochemical processes relate to the functional physiology of sleep. Although existing studies have given invaluable insight into the neurochemical anatomy of sleep, we have only recently acquired the technical and biochemical expertise necessary to investigate sleep as it occurs normally. Future research must focus on the dynamic changes associated with the regulatory mechanisms of neurotransmitters. Many questions can be asked. With sleep transitions, what changes occur in transmitter content, synthesis, or release? Are there changes in metabolic pathways, reflecting a shift from intra- to interneuronal metabolism? What changes occur in pre- and postsynaptic neurotransmitter receptors to affect sensitivity? What constraints do genetic (245) and environmental (246) factors impose upon these mechanisms? Knowledge of such parameters will allow us to construct more complete models of the neuroregulatory basis of sleep and waking. However, as we acquire this knowledge, we must avoid the temptation of assuming causation when the evidence merely shows correlation. Neuroregulation are involved in the control of number different behaviors; and, at present, we have few, if any, methods of establishing causative links between a specific neuroregulator and a specific behavioral state. Yet, even without an understanding of what "causes" sleep, we may be able to develop pharmacological agents which permits discrete alteration of sleep mechanisms in a more physiological and specific manner. This potential for manipulation of sleep is of obvious importance in illnesses such as insomnia, narcolepsy, and sleep apnea (247, 248). In addition, it may be valuable in the treatment of such conditions as psychosis and depression, where sleep disturbances are an important component of the illness. For example, delirium tremens might be best understood as a psychotic episode which is the result of an aspect of sleep emerging into wakefulness. The range and breadth of both the basic questions and the potential application of sleep research portend an exciting future for this field.

Acetylcholine↗
PubMed1996

Sleep-related erectile activity.

Sleep-related erections occur in all healthy, potent men in close temporal association with REM sleep. These erections are naturally occurring and can be assessed quantitatively. The nocturnal tumescence cycle seems unaffected by behavioral factors. Furthermore, sleep-related erections are present across the life span with only a slight decline in older healthy people. Analogous phenomena are present in women. The function of sleep-related erections is not known; however, they clearly involve vascular, neurologic, and hormonal mechanisms. Sleep-related erection testing provides a physiologic, objective, diagnostically useful technique for evaluating erectile capacity. Laboratory-based studies with comprehensive polysomnography offer the most complete diagnostic picture of erectile function available. Nonlaboratory procedures require further validation. The sleep-related tumescence pattern contains a wealth of information about the physiology and pathophysiology of erection. The coordination between REM sleep and erection, the differential expansion at the penile base and upper shaft, and the rate of circumference increase and decrease are meaningful indicators for determining if erectile dysfunction exists. Sleep-related erection testing indexes the magnitude and nature of organic involvement and takes the differential diagnosis of impotence beyond a simplistic psychogenic-organic dichotomy.

Adult↗
PubMed2004

Expression of a poly-glutamine-ataxin-3 transgene in orexin neurons induces narcolepsy-cataplexy in the rat.

The sleep disorder narcolepsy has been linked to loss of hypothalamic neurons producing the orexin (hypocretin) neuropeptides. Here, we report the generation of transgenic rats expressing a human ataxin-3 fragment with an elongated polyglutamyl stretch under control of the human prepro-orexin promoter (orexin/ataxin-3 rats). At 17 weeks of age, the transgenic rats exhibited postnatal loss of orexin-positive neurons in the lateral hypothalamus, and orexin-containing projections were essentially undetectable. The loss of orexin production resulted in the expression of a phenotype with fragmented vigilance states, a decreased latency to rapid eye movement (REM) sleep and increased REM sleep time during the dark active phase. Wakefulness time was also reduced during the dark phase, and this effect was concentrated at the photoperiod boundaries. Direct transitions from wakefulness to REM sleep, a defining characteristic of narcolepsy, occurred frequently. Brief episodes of muscle atonia and postural collapse resembling cataplexy were also noted while rats maintained the electroencephalographic characteristics of wakefulness. These findings indicate that the orexin/ataxin-3 transgenic rat could provide a useful model of human narcolepsy.

Animals↗
PubMed2005

The relationship between ictal activity and sleep stages in the newborn EEG.

OBJECTIVE: To verify the relationship of ictal activity and sleep organization (REM/NREM stages) in the neonatal EEG. METHODS: A retrospective study was developed with 41 high-risk newborns, with clinical history suggestive of seizures and ictal activity identified by the EEG. In each EEG, sleep organization and number/duration of sleep stages were determined. Sleep stages (REM, NREM) were scored following behavior and EEG activity. When it was impossible to recognize stages the epoch was classified as unrecognizable sleep stages (UNSS). Ictal activity was classified according to morphology and correlated with sleep epochs. Density of ictal activity was calculated as the duration of the discharge divided by the duration of the sleep epoch. RESULTS: Unrecognizable sleep stages were observed in 21 EEGs (51.2%). Comparing NREM X REM states there was a significant predominance of ictal activity in REM sleep (P = 0.01). Duration of discharges was longer on REM epochs; however, differences were not significant. Considering the type of discharges there was a predominance of monomorphic rhythmic discharges in all sleep epochs. CONCLUSIONS: In this sample, epileptogenic activity occurred more frequently in UNSS, where sleep organization was already disrupted. When it was possible to recognize sleep stages, ictal activity was more frequently during REM sleep. SIGNIFICANCE: This study speculates the relationship between sleep organization and ictal activity and raises the hypothesis that the expression of ictal activity in relation to sleep stages (REM/NREM) may have age-dependent mechanisms in the developing brain.

Action Potentials↗
PubMed2001

Naturally occurring benzodiazepines may codetermine chronotypes.

Determinants of individual differences in sleep-wake cycles and vigilance are being recognized as major factors of influence in both physical and mental health. Alterations of an accustomed circadian sleep-wake rhythm are commonly seen in the early stages of the majority of psychiatric disorders and, by themselves, predispose to significant morbidity even in the absence of an underlying illness. While it is well known that disruptions of sleep respond favourably to benzodiazepines, agents which have been prescribed for insomnia since their industrial synthesis in the early 1960s, little attention has been paid to putative central nervous system effects of naturally occurring benzodiazepines. These molecules were found in various nutritive plants and have been quantified in human brain and peripheral blood of drug-naive individuals at trace amounts. There is agreement that elevated concentrations of naturally occurring benzodiazepines participate in the complex pathophysiology of hepatic encephalopathy, a condition asssociated with progressive impairment of consciousness and, ultimately, coma. In the present study, we address the relationship between naturally occurring benzodiazepines and time-of-day effects on the behavior of healthy subjects.

Adult↗
PubMed2005

Women's sleep in health and disease.

A huge amount of knowledge about sleep has accumulated during the last 5 decades following the discovery of rapid eye movement (REM) sleep. Nevertheless, there are numerous areas of considerable ignorance. One of these concerns the particularities of sleep in women. Most basic and clinical studies have been performed in male subjects, and only very recently research groups around the world have addressed women's sleep in health and disease. In this review, we summarize the present knowledge on the influence of oestrogens on the brain and on the distinctive changes of sleep across the menstrual cycle, during pregnancy and menopause. In addition, studies in female rodents are reviewed as well as the knowledge on female peculiarities regarding the interactions between sleep regulation and age-related changes in circadian rhythms. We also address specific aspects of sleep loss and sleep disorders in women. Finally, very recent studies on the sociology of sleep are summarized and future directions in the field are discussed.

Adult↗
PubMed1993

[Associative networks, formal thought disorders and schizophrenia. On the experimental psychopathology of speech-dependent thought processes].

Association psychology research in psychiatry dates back to Kraepelin, Aschaffenburg and C.G. Jung. Findings of the 1950s and 60s in this field suggest that semantic memory is organized in the form of a network. New results of experimental psychiatric studies indicate that schizophrenic symptoms, in particular formal thought disorders, are in part the result of an unfocussed activation or disinhibition of such associational network structures: The phenomenon of semantic priming is more pronounced in schizophrenic patients than in normals. Moreover, the phenomenon of indirect semantic priming on short stimulus onset asynchrony can be seen only in schizophrenic patients. The study of spontaneous speech further suggests the activation of structures responsible for the storage and processing of meaning. Increase in semantic priming, similar to that observed in schizophrenia, can further be observed in normal subjects on awakening from REM sleep. The findings are discussed in the framework of recent findings on the neurobiological causes of schizophrenia. They can be related structurally to an involvement of the frontal lobe, and functionally to disturbances of dopaminergic transmission. Methods such as the investigation of priming effects in lexical decision tasks, as well as concepts from the domain of cognitive neuroscience such as neural networks and the spreading activation model of lexical access, can help to bridge the gap between phenomenological psychopathology and neurobiology.

Free Association↗
PubMed1984

Rett syndrome--clinical studies and pathophysiological consideration.

Eleven female patients with Rett syndrome were evaluated for detecting the pathogenesis. Clinical symptoms were characterized by their orderly sequence of occurrence of particular symptoms at particular ages starting from early infancy, and their progression. Increment of head circumference tapered from late infancy, resulting in microcephalus which corresponded with the clinical features. Surface EMG revealed the tremulous rhythmic discharge underlying the characteristic stereotyped movement of the hands. Serial polysomnographical examinations showed abnormalities of the tonic and phasic components of sleep and increment of % REM stage with age. The results of these clinical, laboratory and polysomnographical examinations were discussed, comparing with other neurological diseases and knowledge of animal experiments. From these findings the pathophysiology of Rett syndrome could be explained by the early and progressive lesions in the brain stem nuclei, which influence the maturation and function of particular parts of the higher central nervous system. Serotonergic and catecholaminergic neurons might have important roles in the pathophysiology of this syndrome. However, biochemical and histochemical examinations of the brain are necessary for detecting the pathogenesis and etiology. And the cause of gynecopathy also remains to be clarified.

Ammonia↗