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Results for “Sleep Disorders, Intrinsic”

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PubMed1999

Evoked potentials as a tool for the investigation of human sleep.

This review summarizes studies of evoked potentials (EPs) applied to the investigation of human sleep and of sleep disorders. The first part is devoted to studies dealing with the nature, mechanisms and extent of information processing during sleep. EP studies suggest that the brain's ability to detect salient stimuli persists during even the deepest sleep stages, while discrimination of the stimulus' intrinsic significance and/or semantic content may persist only in stage II and paradoxical sleep (PS). Deviance detection in non-rapid eye movement (NREM) sleep is reflected by amplitude recovery of K-complexes elicited by stimulations that differ from the background. The evoked K-complex appears to be formed by two functionally different modules. The first may be related to the discrimination of relevant information. The second appears more sensitive to stimulus salience than to its intrinsic significance. In PS, the EP signs of stimulus discrimination are similar to those observed during waking. Thus, if the possibilities of information processing are fairly similar during stage II and PS, their respective neural mechanisms are not the same, as judged by their electrophysiological counterparts. The second part of the paper reviews clinical application of EPs to the study of sleep/wake disorders. While early potentials are of little use for diagnosis of sleep disorders, the cognitive P300 may help to quantify cognitive slowing and pathological sleepiness. However, intersubject variability restrains the use of these techniques in individual patients. A promising approach is the utilization of late responses to the study of sleep inertia with the use of "forced awakening" recording paradigms.

Journal Article↗

PubMed1995

Acetylcholine and hallucinations: disease-related compared to drug-induced alterations in human consciousness.

Newly proposed criteria for Lewy body dementia include alterations in consciousness. Lewy body dementia is also associated with a disturbance in cholinergic transmission; neocortical cholinergic deficits in this disorder are more extensive than in Alzheimer's disease and are correlated with symptoms commonly associated with delirium, such as visual hallucinations. The traditional view that derangements of the basal forebrain cholinergic system in Alzheimer's disease relate specifically to memory impairment is assessed in terms of a more general role for cortical acetylcholine in consciousness. This extends the concept that cortical acetylcholine enhances neuronal signal to noise ratio. It is suggested that muscarinic receptor activation in the cortex is involved in confining the contents of the discrete self-reported conscious "stream." In the absence of cortical acetylcholine, currently irrelevant intrinsic and sensory information, which is constantly processed in parallel at the subconscious level, enters conscious awareness. This is consistent with the ability of anti-muscarinic drugs administered medically, recreationally, or ritualistically to induce visual hallucinations and other perceptual disturbances. The hypothesis is explored through comparisons between muscarinic and nicotinic receptor psychopharmacology and between the pathology of the basal forebrain as opposed to pedunculopontine cholinergic systems in different diseases of the human brain affecting consciousness and cognition. The paradoxical effects of muscarinic receptor blockade to induce hallucinations and of REM sleep-associated cholinergic activation of the thalamus to induce dreaming may be related to the differential distribution and activity of muscarinic receptor subtypes or to the differing responses of intrinsic GABA neurons in cortex and thalamus.

Acetylcholine↗

PubMed2005

The human circadian system in normal and disordered sleep.

The human circadian system regulates rhythmicity in the human body and establishes normal sleep and wake phases. The suprachiasmatic nuclei (SCN), located in the hypothalamus above the optic chiasm, make up the human pacemaker known as the circadian or biological clock, but other essential parts of the circadian system include the pineal gland, retina, and retinohypothalamic tract. The importance of light in resetting the intrinsic human circadian cycle, the intrinsic period of which is slightly longer than 24 hours, ensures that the human cycle will stay entrained to the earth's 24-hour daily cycle. Within the SCN neurons, circadian rhythmicity is generated by the regular transcription of proteins. Since the circadian system is the foundation of the sleep-wake cycle, disorders and abnormalities in sleep are often connected with disorders or abnormalities in the circadian system. Circadian rhythm sleep disorders, such as jet lag syndrome and shift work sleep disorder, are those specifically attributed to dysfunctions or insufficiencies in the circadian system. Taking into consideration the preeminence of the circadian clock in timing sleep, it is likely that other sleep disorders, such as insomnia, are also linked to circadian system abnormalities.

Biological Clocks↗

PubMed1997

[Better cure for anxiety, sleep disorders, epilepsy?].

Gamma-aminobutyric acid (GABA), the most important inhibitory neurotransmitter, is characterised by rapid effects that are mediated via GABAA, receptors. These receptors are also targets for many drugs including benzodiazepines, barbiturates and general anaesthetics. Recognition of the heterogeneity of GABAA receptors has opened up new possibilities for the development of more selective therapeutic agents. In particular, subtype-specific receptor ligands varying in intrinsic activity are likely to give rise to fewer side effects than do currently available drugs.

Anti-Anxiety Agents↗

PubMed1997

Secretory profile of immunoreactive growth hormone-releasing hormone (IR-GHRH) during sleep in man and its clinical value.

To clarify the role of growth hormone-releasing hormone (GHRH) in the regulation of the episodic growth hormone (GH) secretion which is known to occur constantly in the initial slow wave stage of nocturnal sleep in man, we studied the relation between the secretions of plasma immunoreactive(IR)-GHRH and GH while recording electroencephalograms. In subjects who showed a normal sleep pattern, the plasma IR-GHRH level increased 3- to 4-fold just before the surge of plasma GH, suggesting that GH release in the initial slow wave stage of sleep is mainly mediated by GHRH. However, when there was an apparent GH surge just before the onset of sleep, the magnitude of the GH response associated with the initial slow wave stage tended to be blunted, even when sufficient IR-GHRH was released. We also observed no appreciable fluctuations of plasma IR-GHRH during nocturnal sleep in a patient diagnosed as having GH-deficient dwarfism, suggesting the primary lesion was on the hypothalamus level, not the pituitary, in such a patient. In a case of multiple endocrine neoplasia (MEN) type I with an ectopic (GHRH-producing pancreatic tumor, no remarkable elevation of plasma IR-GHRH was detected in the initial slow wave stage of nocturnal sleep. We conclude that the present study is significant not only in demonstrating the physiology of GHRH release, but also in establishing a safe, reliable and practical test for routine clinical use to investigate intrinsic ability to release GHRH and the primary lesions in patients with disorders of GH secretion.

Acromegaly↗

PubMed1999

Collapsibility of passive pharynx in patients with acromegaly.

Sleep-disordered breathing (SDB), either central or obstructive in nature, is common in patients with acromegaly. However, no study has systematically examined the collapsibility of the pharynx in acromegaly to date. We evaluated intrinsic mechanical properties of passive pharynx in 10 anesthetized and paralyzed patients with active acromegaly before transsphenoidal adenomectomy for their pituitary adenoma. Static pressure-area relationships of the velopharynx and oropharynx were obtained by step changes in airway pressure during endoscopic cross-sectional area measurement of each segment. Moreover, curve fitting analysis by an exponential function estimated the closing pressure (P'close) of each segment. Preoperative nocturnal oximetry identified five acromegalic patients with an oxygen desaturation index (ODI) greater than 10 h-1 and clinical symptoms suggesting presence of SDB. The pharyngeal airway of all five acromegalic patients with SDB was highly collapsible at both velopharynx and oropharynx with positive P'close. Compared with age-, body mass index (BMI)-, and ODI-matched SDB patients without acromegaly, SDB patients with acromegaly had a higher P'close of the oropharynx, indicating that the etiology of SDB in acromegaly appears to differ from that of ordinary sleep apnea. Our results suggest that anatomic abnormality, especially at the base of the tongue, appears to play a significant role in development of SDB in acromegaly.

Acromegaly↗

PubMed2002

Integration of human sleep-wake regulation and circadian rhythmicity.

The human sleep-wake cycle is generated by a circadian process, originating from the suprachiasmatic nuclei, in interaction with a separate oscillatory process: the sleep homeostat. The sleep-wake cycle is normally timed to occur at a specific phase relative to the external cycle of light-dark exposure. It is also timed at a specific phase relative to internal circadian rhythms, such as the pineal melatonin rhythm, the circadian sleep-wake propensity rhythm, and the rhythm of responsiveness of the circadian pacemaker to light. Variations in these internal and external phase relationships, such as those that occur in blindness, aging, morning and evening, and advanced and delayed sleep-phase syndrome, lead to sleep disruptions and complaints. Changes in ocular circadian photoreception, interindividual variation in the near-24-h intrinsic period of the circadian pacemaker, and sleep homeostasis can contribute to variations in external and internal phase. Recent findings on the physiological and molecular-genetic correlates of circadian sleep disorders suggest that the timing of the sleep-wake cycle and circadian rhythms is closely integrated but is, in part, regulated differentially.

Aging↗

PubMed2003

The upper airway in sleep: physiology of the pharynx.

The upper airway is the primary conduit for passage of air into the lungs. Its physiology has been the subject of intensive study: both passive mechanical and active neural influences contribute to its patency and collapsibility. Different models can be used to explain behavior of the upper airway, including the "balance of forces" (airway suction pressure during inspiration versus upper airway dilator tone) and the Starling resistor mechanical model. As sleep is the primary state change responsible for sleep disordered breathing (SDB) and the obstructive apnea/hypopnea syndrome (OSAHS), understanding its effects on the upper airway is critical. These include changes in upper airway muscle dilator activity and associated changes in mechanics and reflex activity of the muscles. Currently SDB is thought to result from a combination of anatomical upper airway predisposition and changes in neural activation mechanisms intrinsic to sleep. Detection of SDB is based on identifying abnormal (high resistance) breaths and events, but the clinical tools used to detect these events and an understanding of their impact on symptoms is still evolving. Outcomes research to define which events are most important, and a better understanding of how events lead to physiologic consequences of the syndrome, including excessive daytime somnolence (EDS), will allow physiologic testing to objectively differentiate between "normal" subjects and those with disease.

Airway Obstruction↗

PubMed1989

Marked blood pressure fluctuations during narcoleptic attacks alternating with abnormal wakefulness: effects of treatment with clonidine.

A middle-aged man was admitted to our department because of sleep-wake cycle disorders (alternating hypersomnia and sleeplessness), bipolar behavioural disturbances and marked fluctuations in blood pressure and heart rate. Neither evident precipitating stimuli nor an obvious cause for his illness were found. When tests that normally activate intrinsic autonomic responses were performed, two distinct circulatory patterns were recognized. During hypersomnia (phase A), cardiovascular reflex activity was blunted or abolished and orthostasis could not be maintained. The clinical, biochemical, behavioural pictures and the observed decrease in sympathetic outflow resembled the effects of clonidine administration. On the contrary, during sleeplessness (phase B) the autonomic pathways were functionally integral and orthostatic hypotension was not detected. The clinical, biochemical, behavioural features and cardiovascular overactivity closely mimicked the abrupt withdrawal syndrome encountered with clonidine. Three hypothetical mechanisms are advanced to explain this intriguing case as well as the acute and chronic relief of our patient's clinical problem following institution of clonidine therapy (phase C). The role played by central alpha adrenoceptors in integrating sleep-wake, cardiovascular and behavioural functions is also suggested.

Blood Pressure↗

PubMed2003

Interobserver reliability of ICSD-R criteria for REM sleep behaviour disorder.

We estimated the interobserver reliability (IR) of the diagnosis of rapid eye movement (REM) Sleep Behaviour Disorder (RBD) among trained neurologists, with the application of International Classification of Sleep Disorders Revised (ICSD-R), by means of videotaped interviews of people with motor sleep behaviour disorders of different nature. IR of clinical judgement for the diagnosis of RBD was "substantial" (Kappa 0.65); nevertheless, some criteria ('limb or body movement associated with dream mentation', criterion B, and 'sleep behaviours (that) disrupt sleep continuity', criterion C3) showed a 'moderate' IR, resulting from the intrinsic limitations of the patient report and terminological ambiguity. Further clarification of terminology of the ICSD-R criteria would be useful to improve the reliability.

Female↗

PubMed2002

Disorders of the circadian clock: etiology and possible therapeutic targets.

The mammalian circadian clock in the suprachiasmatic nuclei (SCN) of the hypothalamus conveys 24-hr rhythmicity to sleep-wake cycles, temperature, locomotor activity and virtually all other behavioral and physiological processes. In order for these cycles to be adaptive, they must be synchronized, or entrained, to the 24-hr light/dark cycle produced by the rotation of the Earth. The timing of circadian variables relative to the light/dark cycle, i.e., the phase angle of entrainment, is influenced by intrinsic circadian clock properties that are to an extent genetically determined, and thus varies between individuals. In extreme cases (advanced or delayed sleep phase syndrome) or during shift work or jet lag, the phase angle of entrainment may be incompatible with work requirements or other social demands, resulting in negative consequences to health and productivity. This review describes the etiology of circadian disorders within the context of formal circadian clock properties and summarizes studies in humans and in other species which link specific genetic loci to circadian clock function and malfunction. The proteins encoded by these genetic loci play key roles in the intracellular feedback loop that generates circadian rhythms, and thus represent therapeutic targets for the treatment of both endogenous and exogenous circadian disorders.

Animals↗

PubMed2003

Developmental changes in the effects of serotonin on neurons in the region of the pedunculopontine nucleus.

The percent of rapid eye movement (REM) sleep decreases dramatically between 10 and 30 days postnatally in the rat. The pedunculopontine nucleus (PPN) is known to modulate waking and REM sleep. We recorded intracellularly from 127 neurons in the PPN in 12-21-day rat brainstem slices maintained in warmed, oxygenated artificial cerebrospinal fluid. We identified three types of PPN neurons based on intrinsic membrane properties, type I (LTS), type II (A) and type III (A+LTS), as previously described. The percent of type I neurons increased from 6% at 12 days to 17% by 21 days, while the percent of type III neurons decreased from 21% at 12-17 days, to 4% after 17 days. Thus, PPN neurons may differentiate into type I bursting neurons and type II slow-firing neurons across this critical stage in development. The 5-HT1 receptor agonist 5-carboxyamido-tryptamine (5-CT) was found to hyperpolarize 58% of 12-16-day PPN neurons, did not affect 25% and depolarized 17%. However, a higher percentage of 17-21-day PPN neurons were hyperpolarized (85%), and a lower percentage unaffected (10%) or depolarized (5%), suggesting that serotonergic responses switched from both excitatory and inhibitory before, to almost purely inhibitory after, 17 days. These findings indicate a reorganization of PPN intrinsic membrane properties and serotonergic responses occur across this stage, in keeping with the proposed presence of a REM sleep inhibitory process during development. We suggest that disturbances in this developmental process may lead to disorders marked by increased REM sleep drive.

Aging↗

PubMed1988

The intrinsic electrophysiological properties of mammalian neurons: insights into central nervous system function.

This article reviews the electroresponsive properties of single neurons in the mammalian central nervous system (CNS). In some of these cells the ionic conductances responsible for their excitability also endow them with autorhythmic electrical oscillatory properties. Chemical or electrical synaptic contacts between these neurons often result in network oscillations. In such networks, autorhythmic neurons may act as true oscillators (as pacemakers) or as resonators (responding preferentially to certain firing frequencies). Oscillations and resonance in the CNS are proposed to have diverse functional roles, such as (i) determining global functional states (for example, sleep-wakefulness or attention), (ii) timing in motor coordination, and (iii) specifying connectivity during development. Also, oscillation, especially in the thalamo-cortical circuits, may be related to certain neurological and psychiatric disorders. This review proposes that the autorhythmic electrical properties of central neurons and their connectivity form the basis for an intrinsic functional coordinate system that provides internal context to sensory input.

Animals↗

PubMed2005

Dyssomnia in children diagnosed with attention deficit hyperactivity disorder: a critical review.

OBJECTIVE: Studies prior to 1999 reported prevalent sleep disturbances in children diagnosed with attention deficit hyperactivity disorder (ADHD). However, these reports were largely inconclusive and inconsistent in their findings, hence the current review based on studies published thereafter. METHOD: An online research of the National Library of Medicine and the Cochrane Library was conducted using the terms 'attention deficit hyperactivity disorder', 'sleep', 'human', and 'English language'. RESULTS: Sixteen articles met the search criteria with 10 reporting objective measures of sleep characteristics (i.e. polysomnography, actigraphy, and/or video recording). These studies confirm an increase of rapid eye movement (REM) sleep latency and a proportional decrease of REM sleep in children diagnosed with ADHD. Stimulant treatment appears to have little effect on sleep quality while parent's reports of poor sleep in their ADHD-diagnosed offspring was largely inconsistent with the objective measures. CONCLUSIONS: The review demonstrated a link between disturbances in sleep architecture and ADHD. Whether this is of an intrinsic or extrinsic cause remains debateable, as both behavioural (parental reporting) and physiological (objective differences in sleep architecture) factors are indicated. The effect of stimulant medication on sleep also requires further research, as current evidence is limited by study design.

Attention Deficit Disorder with Hyperactivity↗

PubMed2002

[Pharmacological profile and clinical effect of zolpidem (Myslee tablets), a hypnotic agent].

Zolpidem is a non-benzodiazepine hypnotic agent with a chemical structure of imidazopyridine. In vitro and in vivo binding studies, zolpidem exhibits selectivity to omega 1 receptors (GABAA-receptor subtypes containing alpha 1 subunits). Unlike benzodiazepines, zolpidem produces sedative effects in preference to anxiolytic, anticonvulsant and myorelaxant effects in behavioral experiments using mice. Double-blind comparative studies with reference drugs such as triazolam and zopiclone show that zolpidem is an effective and highly safe drug for the treatment of insomnia. In addition, zolpidem does not produce next-day residual effects, rebound insomnia and tolerance. This clinical profile of zolpidem may be related to its selectivity and high intrinsic activity for omega 1 receptors.

Animals↗

PubMed2002

Insomnia in children: when are hypnotics indicated?

Insomnia in children is a nonspecific impairing symptom that may be the result of normal developmental changes, psychosocial duress, a sleep disorder, a psychiatric disorder, other medical disorders, substance misuse, or an adverse effect of medication. Careful clinical assessment of insomnia in children may include the use of symptom rating scales, laboratory testing, or other medical assessment. Short- and long-term treatment of insomnia in children involves management of etiological factors and associated syndromes. Controlled treatment studies of pediatric insomnia are limited to <10 published studies of psychosocial and/or psychopharmacological treatment in young children. Directive parent education and behavior modification techniques have been effective in short-term treatment of insomnia in young children, and may be the preferred treatment of extrinsic insomnia, as well as an important adjunctive treatment of any insomnia symptoms. Two benzodiazepines [flurazepam and delorazepam (chlordesmethyldiazepam)], one antihistamine (niaprazine) and one phenothiazine [alimemazine (trimeprazine)] have been shown to be effective in the short-term treatment of insomnia in young children, although none of these agents have US Food and Drug Administration approval for pediatric insomnia. Short-acting benzodiazepines may have a role in the brief treatment of pediatric insomnia associated with an anxiety or mood disorder, psychosis, aggression, medication- induced activation, or anticipatory anxiety associated with a medical procedure. However, tachyphylaxis and risk of misuse preclude the long-term use of benzodiazepines for the treatment of insomnia in children. Newer hypnotics, which appear better tolerated than the benzodiazepines in studies of adults, may have a role when combined with psychosocial treatments of pediatric insomnia. Treatment of intrinsic pediatric insomnia may additionally involve chronotherapy or medical management.

Adolescent↗

PubMed2000

Effect of anticonvulsants on sleep.

The intensive study of seizures via serial 24-hour EEG-video monitoring has allowed enhanced observation of sleep patterns among epilepsy patients and has revealed that disturbed rest is common in this population. Previous work has shown that sleep deprivation of any type can exacerbate seizure activity, leading to speculation that the intrinsically poor sleep in these patients may serve as a threshold-lowering factor, and that this factor might be partially reversed by effective antiepileptic drugs (AEDs). However, to better understand this interaction, it is necessary to know whether the sleep disorder of epilepsy is caused by repetitive ictal events or whether it is part of a process that causes epilepsy to emerge in the first place. In addition, to separate and analyze the sleep effects of AEDs, one must compare studies of normal controls, which have only rarely been accomplished, with studies of drug-free patients, which are difficult to achieve. As little as is known about the detailed effects of AEDs on sleep architecture, even less is known about the mechanisms by which AEDs might cause such effects. Nevertheless, there is great potential for those undertaking such work, due to the wealth of basic science accumulating in the field of sleep mechanisms and the prodigious amount of information already amassed in the area of anticonvulsant mechanisms.

Anticonvulsants↗

PubMed2006

Inspiratory flow shape clustering: an automated method to monitor upper airway performance during sleep.

We describe an automated method for monitoring airflow dynamics in the upper airway of a sleeping subject. Its main task is to determine a set of inspiratory flow shape representatives and their relative incidence in a given respiratory airflow material. The flow shape clustering aims at reducing redundant information in the data, and thereby decreases the time needed to score overnight sleep recordings. Compared with previous computer-assisted systems, built on a pre-defined classification of prototype shapes, we require no a priori assumptions of the flow shape clusters to be discovered. The intrinsic flow shape clustering is performed with a modification of the Isodata algorithm, and the K-means clustering is used as a reference in comparison studies. The operation of the method is demonstrated on clinical sleep recordings both from patients with nocturnal breathing disorders and from non-symptomatic individuals. The feasible results obtained in the practical research design suggest that application of clustering algorithms to respiratory airflow measurements could give important insights into the subtle flow shape abnormalities underlying obstructive sleep-disordered breathing.

Algorithms↗