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At least 19 recordsLinked to original sources

[Role of melatonin in human physiology and pathology. II. Involvement of melatonin in pathogenesis of affective and chronobiological disorders. Melatonin and the aging process. Melatonin and neoplasms].

In the second part of this review the role of melatonin in pathogenesis of affective diseases and chronobiological disorders is discussed. Current views on melatonin involvement in aging are presented. Clinical experiments on the possible usefulness of melatonin in treatment of various types of cancers and hypothetical mechanisms of oncostatic influence of melatonin are also summarized.

Aging↗

Dim light melatonin onset (DLMO): a tool for the analysis of circadian phase in human sleep and chronobiological disorders.

The circadian rhythm of melatonin in saliva or plasma, or of the melatonin metabolite 6-sulphatoxymelatonin (aMT6S) in urine, is a defining feature of suprachiasmatic nucleus (SCN) function, the endogenous oscillatory pacemaker. A substantial number of studies have shown that, within this rhythmic profile, the onset of melatonin secretion under dim light conditions (the dim light melatonin onset or DLMO) is the single most accurate marker for assessing the circadian pacemaker. Additionally, melatonin onset has been used clinically to evaluate problems related to the onset or offset of sleep. DLMO is useful for determining whether an individual is entrained (synchronized) to a 24-h light/dark (LD) cycle or is in a free-running state. DLMO is also useful for assessing phase delays or advances of rhythms in entrained individuals. Additionally, it has become an important tool for psychiatric diagnosis, its use being recommended for phase typing in patients suffering from sleep and mood disorders. More recently, DLMO has also been used to assess the chronobiological features of seasonal affective disorder (SAD). DLMO marker is also useful for identifying optimal application times for therapies such as bright light or exogenous melatonin treatment.

Animals↗

Delayed sleep phase syndrome. A chronobiological disorder with sleep-onset insomnia.

We describe a new syndrome called "delayed sleep phase insomnia." Thirty of 450 patients seen for a primary insomniac complaint had the following characteristics: (1) chronic inability to fall asleep at a desired clock time; (2) when not on a strict schedule, the patients have a normal sleep pattern and after a sleep of normal length awaken spontaneously and feel refreshed; and (3) a long history of unsuccessful attempts to treat the problem. These patients were younger than the general insomniac population and as a group did not have a specific psychiatric disorder. Six patients' histories are described in detail, including the successful nonpharmacological chronotherapy regimen (resetting the patients' biological clock by progressive phase delay). Delayed sleep phase insomnia is proposed to be a disorder of the circadian sleep-wake rhythm in which the "advance" portion of the phase response curve is small.

Adolescent↗

Melatonin, light and chronobiological disorders.

Human plasma melatonin concentrations can be measured accurately and sensitively by gas chromatography-negative chemical ionization mass spectrometry. With this assay, we have shown that: in rats and in humans, plasma melatonin is exclusively derived from the pineal gland; propranolol and clonidine reduce melatonin levels in human; some blind people appear to have free-running melatonin secretory circadian rhythms; bright light can acutely suppress human melatonin production according to a linear fluence-response relationship; manic-depressive patients appear to be supersensitive to light, even when they are well; melatonin levels are greater in manic patients than in depressed patients; in experiments to test the clock-gate model and the hypothesized phase-response curve, two different effects of light appear to present in humans: an acute suppressant effect (mainly in the evening during long photoperiods) and an entrainment effect (particularly during the morning but also in the evening). When blood is sampled for measuring melatonin levels as a marker for circadian phase position, bright light should be avoided after 5 p.m. (the dim light melatonin onset). Bright-light exposure in the morning appears to advance circadian rhythms, whereas bright-light exposure in the evening appears to delay them. Once a patient has been 'phase typed' (phase-advanced vs. phase-delayed), predictions can be made about whether morning or evening light would be more effective in treating the sleep or mood disorder.

Circadian Rhythm↗

Nocturnal headache-hypertension syndrome: a chronobiologic disorder.

The study of blood pressure (BP) monitoring in essential hypertensive patients recurrently suffering from nocturnal headache revealed a rhythmic elevation of sphygmomanometric values during the night. Such a finding was not detected in essential hypertensive patients suffering from occasional headache. The nocturnal elevation of BP was seen to be paralleled by the circadian peak of heart rate, suggesting that the disorder is a systemic phenomenon. Importantly, the headache episodes were seen to disappear after antihypertensive therapy that was adjusted to lower the nocturnal increase of BP. The therapeutic results suggested that the nocturnal headache was dependent on the phasic elevation of BP. The beneficial effects further suggested that the nocturnal headache and the nocturnal elevation of BP may represent a particular syndrome with a cause-effect relationship. The term "nocturnal headache-hypertension syndrome" is proposed.

Adolescent↗

[Chronobiological sleep disorders and their treatment possibilities].

A temporal discrepancy between the endogenous sleep-wake cycle and the daily structure of the surrounding social network are characteristic for chronobiological sleep disturbances. Activity rhythms that are in abnormal relation to the environment are more frequent than commonly assumed. They can arise either from external causes (such as shift-work or jet-lag) or as a result of internal changes promoting abnormal sleep behaviour. Structuring daily activities by paying attention to natural daylight (dawn and dusk) and to the social routine strengthen the synchronizing effect of external timekeepers necessary for the concordance between inner and outer rhythmic phenomena. Treatment of chronobiological sleep/wake-cycle disturbances require correct diagnosis and modification of their causes, particularly changes in habits consolidating such disturbances. Early recognition of a chronobiological sleep disorder can reduce the risk of misuse of sleeping pills, caffeine and nicotine. Recently developed treatment approaches such as bright light, the pineal hormone melatonin and vitamin B12 have provided promising results.

Biological Clocks↗

Sleep-wake cycle, sleep-related disturbances, and sleep disorders: a chronobiological approach.

There is convincing evidence that the functions of sleep include restoration of brain energy storage and memory consolidation. The circadian timing system (CTS) is involved in the daily variation of almost any physiological and psychological variable evaluated thus far. Disturbances of the CTS can be clinically observed by their influence on the sleep-wake cycle, hormones, body temperature, and locomotor activity. This article reviews the basic mechanisms of circadian rhythm sleep disturbances, names the applicable diagnostic tools and specific therapeutic strategies, and thereby hints at the impact of circadian rhythm sleep disturbance on psychiatric disorders, especially disorders of affect and cognition. In light of the preventive, diagnostic, and therapeutic tools now available, a new round of chronobiological studies in psychiatry seems justified, promising, and necessary.

Brain↗

Depression, circadian rhythms and trimipramine.

During depression, chronobiological disorders occur, such as disturbances in body temperature and early urinary excretion of a noradrenaline metabolite. Sleep patterns are disturbed in 90% of depressed patients; early REM sleep and shortened slow-wave sleep (stages 3 and 4), resulting in an increase in REM sleep, have been observed. Thus, an increase in REM sleep may be an indication of depression. Chronic insomnia is characterised by irregular sleep behaviour, an anxious attitude to sleep and increased cognition before sleep onset. Patients with this disorder can be divided into those with a disturbed ultradian rhythm (less than 2 REM-NREM cycles) and those with regular sleep structure (greater than 2 REM-NREM cycles). Most antidepressants reduce REM sleep, an effect evident from day 1 of administration. Trimipramine is an exception in that it has antidepressant and sedative effects without modifying REM sleep, and it possesses a different pharmacodynamic profile. Trimipramine is effective in depressed patients with chronobiological disorders such as chronic insomnia, although its mechanism of action is not fully understood.

Circadian Rhythm↗

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.

Animals↗

The role of chronobiology in sleep disorders medicine.

This review is concerned with circadian (approximately 24 h) aspects of chronobiology, and how they relate to sleep disorders medicine. We begin with an introduction to the key concepts and paradigms of circadian rhythms research in general, including a description of homeostatic and circadian determinants of sleep timing. This is followed by a brief history of chronobiology in relation to sleep disorders medicine. Both animal and human circadian rhythm studies are considered. We trace historical changes in the relative emphasis placed on social contacts, light, and melatonin in human circadian rhythms research. Special attention is given to free-running, forced desynchrony, and ultra-short sleep/wake cycle findings of particular relevance to sleep disorders medicine. The latter part of the review comprises a description of the circadian rhythm sleep disorders, highlighting insights derived from basic circadian rhythms research, including recent advances in molecular genetics. We conclude that the role of chronobiology in sleep disorders medicine is profound and pervasive, and that the two disciplines will move ever closer as a natural function of important new insights into sleep and sleep disorders provided by basic circadian rhythms research.

Chronobiology Phenomena↗

Headache and sleep.

Headache and sleep have long been recognised as being interdependent due to specific causative factors. Yet, the precise understanding of the roles played by these factors in this interdependency remains elusive. Many observations have suggested a reciprocal relationship between headache and sleep; however, these hypotheses have only been partially substantiated by robust findings. Being so, additional well-designed clinical and laboratory studies are required to confirm these relationships. Nonetheless, sleep and headache are known to be related in several ways: primary headache such as migraine, cluster headache (CH) and hypnic headache (HH) can be triggered by sleep, while chronic morning headaches can be caused by sleep disorders such as sleep apnoea and insomnia. Furthermore, headache and sleep disorders can also be symptoms of other underlying pathologies. Migraine, CH and HH seems to be related to sleep stages suggesting that they may in fact be a chronobiological disorder. Patients suffering from chronic morning or nocturnal headache should be considered for the presence of possible sleep disturbances.

Headache↗

Treatment of seasonal affective disorder: unipolar versus bipolar differences.

Evidence-based treatments for seasonal affective disorder (SAD) include light therapy and pharmacotherapy. We briefly review the diagnosis and treatment of SAD, focusing on clinical and treatment differences between patients with unipolar and bipolar illness. Special considerations for the management of SAD in patients with bipolar disorder are discussed, including the need to monitor for emergence of manic and hypomanic mood switches, to use mood stabilizers in patients with bipolar I disorder, and to be aware of potential interactions between bright light and medications used in treating bipolar disorder. Chronobiological treatments such as bright light therapy may be combined with pharmacotherapy to enhance therapeutic effects, reduce adverse side effects, and optimize treatment in patients with seasonal and nonseasonal bipolar disorder.

Antidepressive Agents↗

The circadian basis of winter depression.

The following test of the circadian phase-shift hypothesis for patients with winter depression (seasonal affective disorder, or SAD) uses low-dose melatonin administration in the morning or afternoon/evening to induce phase delays or phase advances, respectively, without causing sleepiness. Correlations between depression ratings and circadian phase revealed a therapeutic window for optimal alignment of circadian rhythms that also appears to be useful for phase-typing SAD patients for the purpose of administering treatment at the correct time. These analyses also provide estimates of the circadian component of SAD that may apply to the antidepressant mechanism of action of appropriately timed bright light exposure, the treatment of choice. SAD may be the first psychiatric disorder in which a physiological marker correlates with symptom severity before, and in the course of, treatment in the same patients. The findings support the phase-shift hypothesis for SAD, as well as suggest a way to assess the circadian component of other psychiatric, sleep, and chronobiologic disorders.

Adult↗

[Seasonal affective disorders, a new clinical category].

Seasonal affective disorders have recently been individualized by American authors. According to these authors, this subgroup of affective diseases deserve to be regarded as a clinical category owing to its specific symptoms, its epidemiological features and its response to treatment. They are characterized by the triad: hypersomnia, hyperoxia, weight gain, associated with usual symptoms of depression. Moreover, contrary to the bipolar manic-depressive psychosis, they seem to predominate among women. Finally, phototherapy, the various protocols of which are discussed here, is said to be effective. The influence of latitude combined with the effectiveness of phototherapy has led to original pathogenic hypotheses, among which the presence of a chronobiological disorder (abnormality of the season-induced circadian rhythm), although attractive and supported by a strict clinical study, has yet to be demonstrated. Also hypothetical is the role played by melatonin: is this hormone the principal "mediator" or an epiphenomenon?

Adult↗