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At least 415 records · Page 23Linked to original sources
PubMed1997

Effects of thyrotropin-releasing hormone and its analogs on daytime sleepiness and cataplexy in canine narcolepsy.

The therapeutic potential of thyrotropin-releasing hormone (TRH) and TRH analogs in narcolepsy, a sleep disorder characterized by abnormal rapid eye movement (REM) sleep and daytime sleepiness, was examined using the canine model. The effects of TRH and the biologically stable TRH analogs CG3703, CG3509, and TA0910 on daytime sleep and cataplexy, a symptom of abnormal REM sleep, were assessed using polysomnographic recordings and the food elicited cataplexy test (FECT), respectively. CG3703 (100 and 400 microg/kg, i.v.) and TA0910 (100 and 400 microg/kg, i.v.) significantly increased wakefulness and decreased sleep in narcoleptic canines, whereas TRH (400 and 1600 microg/kg, i.v.) had no significant effect. TRH (25-1600 microg/kg, i.v.) and all three TRH analogs, CG3703 (6. 25-400 microg/kg, i.v., and 0.25-16 mg/kg, p.o.), CG3509 (25-1600 microg/kg, i.v.), and TA0910 (25-1600 microg/kg, i.v.), significantly reduced cataplexy in canine narcolepsy. These compounds did not produce any significant side effects during behavioral assays, nor did they alter free T3 and T4 levels in serum even when used at doses that completely suppressed cataplexy. Although more work is needed to establish the mode of action of TRH analogs on alertness and REM sleep-related symptoms, our results suggest a possible therapeutic application for TRH analogs in human sleep disorders.

Animals↗
PubMed2005

[Epilepsy and sleep disorders].

Sleep disorders often occur in patients with epilepsy. Every neurologist is familiar with the postictal drowsiness after tonicoclonic convulsions and likewise with the provocation of an attack after sleep deprivation that is often combined with alcohol consumption. It is more difficult to differentiate between motor disturbances and epileptic episodes during sleep. For example, nocturnal paroxysmal dystonia, which are frequently an expression of frontal lobe epilepsy, are long not recognized as non-epileptic, sleep-associated attacks. In addition, nocturnal episodes in context of a REM sleep behavioral disturbance can occasionally be differentiated from frontal lobe epileptic seizures only with great difficulty. A clear differential diagnostics between epileptic and non-epileptic attacks during sleep is, however, a requirement for a selective treatment.

Anticonvulsants↗
PubMed1988

Delayed sleep phase syndrome in adolescents.

The delayed sleep phase syndrome is characterized by difficulty in falling asleep at a socially acceptable time of night and an inability to be easily aroused in the morning. Most commonly encountered in adolescents, this condition can produce daytime sleepiness and poor school performance, and it can lead to behavioral problems. The clinical features of the syndrome are described in 22 adolescents. Nine subjects participated in a protocol of polysomnographic recordings to simulate habitual "weekday" and "weekend" sleep patterns. There was a significant increase in total sleep time (p less than 0.005) and REM sleep (p less than 0.001) during the "weekend" sleep period. A multiple sleep latency test was performed between the two nights to assess daytime sleep tendency. Daytime sleepiness was maximal in the morning, with a tendency for greater alertness as the day progressed. The reduced amount of REM sleep during the "weekdays" plus the tendency for sleepiness in the mornings may contribute to the behavioral and educational difficulties seen in these patients. Recognition of this syndrome enables a specific sleep schedule change to be made that effectively treats the problem.

Adolescent↗
PubMed2001

Basal forebrain acetylcholine release during REM sleep is significantly greater than during waking.

Cholinergic neurons of the basal forebrain supply the neocortex with ACh and play a major role in regulating behavioral arousal and cortical electroencephalographic activation. Cortical ACh release is greatest during waking and rapid eye movement (REM) sleep and reduced during non-REM (NREM) sleep. Loss of basal forebrain cholinergic neurons contributes to sleep disruption and to the cognitive deficits of many neurological disorders. ACh release within the basal forebrain previously has not been quantified during sleep. This study used in vivo microdialysis to test the hypothesis that basal forebrain ACh release varies as a function of sleep and waking. Cats were trained to sleep in a head-stable position, and dialysis samples were collected during polygraphically defined states of waking, NREM sleep, and REM sleep. Results from 22 experiments in four animals demonstrated that means +/- SE ACh release (pmol/10 min) was greatest during REM sleep (0.77 +/- 0.07), intermediate during waking (0.58 +/- 0.03), and lowest during NREM sleep (0.34 +/- 0.01). The finding that, during REM sleep, basal forebrain ACh release is significantly elevated over waking levels suggests a differential role for basal forebrain ACh during REM sleep and waking.

Acetylcholine↗
PubMed1986

Therapy for sleep disorders in depressives.

The treatment of sleep disorders in depressives depends basically on the nature of the underlying affective disorder (endogenous, organic, psychogenic or constitutional depression). Therapeutic approaches may be categorized in: psychological, somatic and pharmacological ones. The former include psychotherapies and behavioral treatments which are useful in psychogenic and constitutional depressions with sleep-onset insomnia but may also be supportive in endogenous depressions. The basic therapeutic factor common to all is anxiety reduction. Somatic therapies, such as ECT, total, partial and REM-sleep deprivation, sleep schedule shifts and bright light (EL) are utilized mostly in endogenous depressions. Sleep laboratory findings and different hypotheses concerning the mode of action of these alternative treatment methods are reviewed. Somnopolygraphic, psychometric, and neuroendocrinological data of our comparative trial with BL and partial sleep deprivation in normals and patients are discussed. The similarity of changes after BL, antidepressants and lithium points to a chronobiological factor in the pathogenesis and treatment of affective disorders. Electrosleep is still controversial, hydro-, ergo- and physical therapy are supportive therapies and as such indicated in all depressions. Exercise, fatigue and nutritional factors may influence sleep. Psychopharmacological treatment has to be regarded as the most important therapeutic approach for sleep disorders in depressives. Antidepressants are the drugs of choice for most patients. Based on their effects on sleep-induction, -maintenance, and -architecture and REM measures, one may differentiate at least two subtypes: sedative antidepressants of the amitriptyline type and nonsedative antidepressants of the desipramine type. Bedtime infusions of antidepressants may have sleep promoting properties, which was objectivated by an EEG spectral analysis during infusion and subsequently by all night sleep studies. Measures indicative of therapeutic outcome are still controversial. Tranquilizers, hypnotics, neuroleptics and serotonin precursors are utilized if the antidepressants alone do not ameliorate insomnia. However, as evidence of a shared diathesis of origin of depressive and anxiety disorders is building up, benzodiazepines are increasingly prescribed as monotherapy too. Finally, sleep laboratory data concerning the hypnotic properties of a pharmacological 80 mg doses of melatonin are demonstrated.

Depressive Disorder↗
PubMed2006

Behavioral and sleep/wake characteristics of mice lacking norepinephrine and hypocretin.

We investigated the interaction between norepinephrine (NE) and orexin/hypocretin (Hcrt) in the control of sleep behavior and narcoleptic symptoms by creating mice that were deficient in both neurotransmitters. Mice with a targeted disruption of the dopamine beta-hydroxylase (Dbh) gene (deficient in NE and epinephrine) or the Hcrt gene were bred to generate double knockouts (DKOs), each single KO (Dbh-KO and Hcrt-KO), and control mice. The duration of wake, non-rapid eye movement (NREM) and REM sleep were monitored by electroencephalogram (EEG)/electromyogram (EMG) recording over a 24-h period, and the occurrence of behavioral arrests was monitored by video/EEG recording for 4 h. Overall, there was very little interaction between the two genes; for most parameters that were measured, the DKO mice resembled either Dbh-KO or Hcrt-KO mice. REM sleep was increased in both DKO and Hcrt-KO mice at night relative to the other groups, but DKO mice had significantly more REM sleep during the day than the other three groups. Sleep latency in response to saline or amphetamine injections was reduced in Dbh-KO and DKO mice relative to other groups. Behavioral arrests, that are frequent in Hcrt-KO mice, were not exacerbated in DKO mice.

Amphetamine↗
PubMed2001

To eat or to sleep? Orexin in the regulation of feeding and wakefulness.

Orexin-A and orexin-B are neuropeptides originally identified as endogenous ligands for two orphan G-protein-coupled receptors. Orexin neuropeptides (also known as hypocretins) are produced by a small group of neurons in the lateral hypothalamic and perifornical areas, a region classically implicated in the control of mammalian feeding behavior. Orexin neurons project throughout the central nervous system (CNS) to nuclei known to be important in the control of feeding, sleep-wakefulness, neuroendocrine homeostasis, and autonomic regulation. orexin mRNA expression is upregulated by fasting and insulin-induced hypoglycemia. C-fos expression in orexin neurons, an indicator of neuronal activation, is positively correlated with wakefulness and negatively correlated with rapid eye movement (REM) and non-REM sleep states. Intracerebroventricular administration of orexins has been shown to significantly increase food consumption, wakefulness, and locomotor activity in rodent models. Conversely, an orexin receptor antagonist inhibits food consumption. Targeted disruption of the orexin gene in mice produces a syndrome remarkably similar to human and canine narcolepsy, a sleep disorder characterized by excessive daytime sleepiness, cataplexy, and other pathological manifestations of the intrusion of REM sleep-related features into wakefulness. Furthermore, orexin knockout mice are hypophagic compared with weight and age-matched littermates, suggesting a role in modulating energy metabolism. These findings suggest that the orexin neuropeptide system plays a significant role in feeding and sleep-wakefulness regulation, possibly by coordinating the complex behavioral and physiologic responses of these complementary homeostatic functions.

Animals↗
PubMed2002

Management of sleep disorders in fibromyalgia.

In summary, the treatment of patients with FM requires a proper assessment of the reason for the unrefreshing sleep, which is an important component of the FM syndrome. Sleep laboratory investigations provides a suitable rationale for management where a specific primary sleep disorder is determined. Nonspecific treatments include various behavioral approaches to improve sleep hygiene, fitness, and regular proper nutrition that serve to regularize disturbances in circadian sleep-wake rhythms. As yet, no medication is known to improve the EEG sleep arousal disorders that include phasic (alpha-delta), tonic alpha non-REM sleep disorders, or the periodic K alpha cycling alternating pattern disorder. Traditional hypnotic agents, while helpful in initiating and maintaining sleep and reducing daytime tiredness, do not provide restorative sleep or reduce pain. Tricyclic drugs, such as amitriptyline and cyclobenzaprine, may provide long term benefit for improving sleep but may not have a continuing benefit beyond one month for reducing pain. The use of a biologic agent that facilitates sleep-related neuroendocrine functions, for example growth hormone, is reported to improve symptoms but the need for injection and high cost restrict its use. No systematic studies have been reported on the use of remedial measures for the management of PLMS/restless legs syndrome and sleep apnea that occur in some patients with FM.

Fibromyalgia↗
PubMed2006

Narcolepsy and the hypocretins.

Narcolepsy is a chronic neurologic disease characterized by excessive daytime sleepiness and one or more of three additional symptoms (cataplexy, or sudden loss of muscle tone; vivid hallucinations; and brief periods of total paralysis) related to the occurrence of rapid eye movement (REM) sleep at inappropriate times. The daytime sleepiness typically presents as a sudden overwhelming urge to sleep, followed by periods of sleep that last for seconds or minutes, or even longer. During daytime sleep episodes, patients may exhibit "automatic behavior," performing conventionalized functions (eg, taking notes), but not remembering having done so once they are awake. About 10% of narcoleptics are members of familial clusters; however, genetic factors alone are apparently insufficient to cause the disease, inasmuch as the most common genetic disorder, a mutation in chromosome 6 controlling the HLA antigen immune complex, although seen in 90% to 100% of patients, also occurs in as many as 50% of people without narcolepsy. A dog model of narcolepsy exhibits a mutation on chromosome 12 that disrupts the processing of the peptide neurotransmitter hypocretin. No such mutation characterizes human narcolepsy; however, cerebrospinal fluid (CSF) hypocretin levels are profoundly depressed in narcoleptic patients, and a specific reduction in hypocretin-containing neurons has been described. One hypothesis concerning the pathophysiology of narcolepsy proposes that the HLA subtype resulting from the mutation on chromosome 6 increases the susceptibility of hypocretin-containing brain neurons to immune attack. Because hypocretin may normally participate in the maintenance of wakefulness, the loss of neurons that release this peptide might allow REM sleep to occur at inappropriate times, ie, while the patient is awake, in contrast to its normal cyclic appearance after a period of slow-wave sleep. The cataplexy, hallucinations, and/or paralysis associated with REM episodes normally are unnoticed-or, at least, not remembered-when the transition to REM follows slow wave sleep, as is normally the case; however, they are remembered when, in people with narcolepsy, the REM episode starts during a period of wakefulness. The association of narcolepsy with a deficiency in a specific neurotransmitter, in this case, hypocretin, is reminiscent of the associations between Parkinson disease and dopamine, or early Alzheimer disease and acetylcholine.

Animals↗
PubMed1992

The pharmacologic treatment of sleep disorders.

Sleep disorders and disturbances are common problems in children and adolescents and frequently occur concurrently with psychiatric symptomatology. There appears to be a complex relationship between the regulation of sleep and emotional and behavioral problems in children and adolescents. This article focuses on appropriate use of medications in the treatment of these common disorders through a comprehensive approach of careful evaluation, diagnosis, and the use of behavioral and other nonpharmacologic treatments.

Adolescent↗
PubMed2006

Insomnia in the elderly: cause, approach, and treatment.

Insomnia is a prevalent problem in late life. Sleep problems in the elderly are often mistakenly considered a normal part of aging. Insomnia, the most common sleep disorder, is a subjective report of insufficient or nonrestorative sleep despite adequate opportunity to sleep. Despite the fact that more than 50% of elderly people have insomnia, it is typically undertreated, and nonpharmacologic interventions are underused by health care practitioners. This article will review the causes of insomnia in the elderly, the approach to patient evaluation, and the nonpharmacologic and pharmacologic treatment of insomnia.

Acetamides↗
PubMed1975

Sleep EEG and motor activity as indicators in affective states.

This report reviews a number of studies which support our current classification schema for affective disorders. This classification differentiates between an anxious-hyperactive type and an anergic-hypoactive type which are then further subdivided into primary and secondary affective disorders. While the motor and activity measurements are for the most part limited to patients suffering from primary affective disease, current studies under way indicate that secondary affective disorders may also have characteristic biologic changes. EEG sleep and motor activity parameters provide useful pointers for differential diagnosis and treatment while having the added advantage of diminishing the clinician's almost exclusive dependency on amnestic data and the psychological observations made on the patient's behavior.

Adjustment Disorders↗