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Biomedical subjects

A Wirz-Justice

Publications and source records attributed to A Wirz-Justice.

At least 19 recordsLinked to original sources
PubMed1999

Sleep deprivation in depression: what do we know, where do we go?

Manipulations of the sleep-wake cycle, whether of duration (total or partial sleep deprivation [SD]) or timing (partial SD, phase advance), have profound and rapid effects on depressed mood in 60% of all diagnostic subgroups of affective disorders. Relapse after recovery sleep is less when patients are receiving medication; it may be prevented by co-administration of lithium, pindolol, serotonergic antidepressants, bright light, or a subsequent phase advance procedure. Diurnal and day-to-day mood variability predict both short-term response to SD and long-term response to antidepressant drug treatment. These mood patterns can be understood in terms of a "two-process model of mood regulation" based on the model well established for sleep regulation: the interaction of circadian and homeostatic processes. The therapeutic effect of SD is postulated to be linked to changes in disturbed circadian- and sleep-wake-dependent phase relationships and concomitant increase of slow-wave-sleep pressure; additionally, SD-induced sleepiness may counteract the hyperarousal state in depression. This model has the advantage of providing a comprehensive theoretical framework and stringent protocols ("constant routine," "forced desynchrony") to dissect out specific disturbances. Many aspects tie in with current serotonergic receptor hypotheses of SD action. A treatment inducing euthymia in severely depressed patients within hours is an important therapeutic option that has come of age for clinical use.

Antidepressive Agents↗
PubMed1999

A rapid-cycling bipolar patient treated with long nights, bedrest, and light.

BACKGROUND: Stabilization of rapid-cycling bipolar disorder is extremely difficult. METHODS: A refractory bipolar I rapid-cycling patient on valproate was treated with long "nights" (extended sleep in darkness) and daytime light therapy. RESULTS: Rapid cycling immediately stopped on initiation of a 10 hour dark/rest period. This was extended to 14 hours (plus a self-selected 1 hour midday nap) without problems. Depression gradually improved when midday light therapy was added; near-euthymia was attained after light therapy was shifted to the morning. CONCLUSIONS: Nonpharmacological chronobiological treatments may be a means to interrupt rapid cycling.

Activity Cycles↗
PubMed1999

Accelerated post-glucose glycaemia and altered alliesthesia-test in Seasonal Affective Disorder.

BACKGROUND: Little is known about the link between mood, food and metabolic function in Seasonal Affective Disorder (SAD). METHODS: We investigated this link in a combined glucose tolerance-alliesthesia test in eight SAD patients in winter before and after one week light therapy, and in summer. RESULTS: SAD patients exhibited faster post-glucose glycaemic and insulin responses (p <0.05), and increased hedonic ratings of high concentrated sucrose solutions (p <0.035) when depressed in winter than when euthymic (one week after light treatment or in summer). CONCLUSIONS: The rapid glycaemic and insulin responses to an oral glucose load may be a result of accelerated gastric emptying. LIMITATIONS: The number of studied patients was rather small and no control group was studied in parallel. CLINICAL RELEVANCE: the more rapid post-glucose glycaemia may impair glucose homeostasis in depressed SAD patients.

Adolescent↗
PubMed1998

Sleep deprivation response in seasonal affective disorder during a 40-h constant routine.

BACKGROUND: There are no controlled studies investigating the response of patients with seasonal affective disorder (SAD) to a total sleep deprivation (SD). METHODS: The clinical response to SD of patients with SAD in winter was investigated under the stringently controlled conditions of a 40-h constant routine protocol. RESULTS: 52% of the SAD patients (N=11 women) improved, using a mean of a multiple ratings. This is in the range of response found for non-seasonal major depression. In contrast, controls (N=8 women) showed less improvement of mood (29%). CONCLUSION: SAD patients respond to SD as do non-seasonal major depressives. The best discrimination of response was obtained in an observer rating (Clinical Global Impression: global severity improvement), and the morning values of two different self ratings (v. Zerssen depression scale, 100 mm VAS with the criterion of > or =10 mm improvement). LIMITATION: A more reliable estimate of the SD response rate in SAD patients would require a larger group. CLINICAL RELEVANCE: SAD patients do not differ from other subgroups of major depression in their response to SD, and therefore this is an additional treatment option to light therapy.

Adult↗
PubMed1998

Evening administration of melatonin and bright light: interactions on the EEG during sleep and wakefulness.

Both the pineal hormone melatonin and light exposure are considered to play a major role in the circadian regulation of sleep. In a placebo- controlled balanced cross-over design, we investigated the acute effects of exogenous melatonin (5 mg p.o. at 20.40 hours) with or without a 3-h bright light exposure (5000 lux from 21.00 hours-24.00 hours) on subjective sleepiness, internal sleep structure and EEG power density during sleep and wakefulness in healthy young men. The acute effects of melatonin, bright light and their interaction were measured on the first day (treatment day), possible circadian phase shifts were assessed on the post-treatment day. On the treatment day, the evening rise in subjective sleepiness was accelerated after melatonin and protracted during bright light exposure. These effects were also reflected in specific changes of EEG power density in the theta/alpha range during wakefulness. Melatonin shortened and bright light increased sleep latency. REMS latency was reduced after melatonin administration but bright light had no effect. Slow-wave sleep and slow-wave activity during the first non-rapid eye movement (NREMS) episode were suppressed after melatonin administration and rebounded in the second NREMS episode, independent of whether light was co-administered or not. Self rated sleep quality was better after melatonin administration whereas the awakening process was rated as more difficult after bright light. On the post-treatment day after evening bright light, the rise in sleepiness and the onset of sleep were delayed, independent of whether melatonin was co-administered or not. Thus, although acute bright light and melatonin administration affected subjective sleepiness, internal sleep structure and EEG power density during sleep and wakefulness in a additive manner, the phase shifting effect of a single evening bright light exposure could not be blocked by exogenous melatonin.

Adult↗
PubMed1997

A schizophrenic patient with an arrhythmic circadian rest-activity cycle.

A haloperidol-treated patient with chronic schizophrenia had a near-arrhythmic circadian rest-activity cycle, whereas rhythms of 6-sulphatoxy-melatonin and core body temperature were of normal amplitude and phase-advanced. Sleep electroencephalography measured throughout a 31-h 'constant-bedrest' protocol revealed a phase-delayed sleep-wake propensity cycle, low sleep continuity (ultradian 'bouts'), and very little slow-wave sleep and slow-wave activity (0.75-4.5 Hz). Switching treatment to the atypical neuroleptic clozapine improved both the circadian organization of the rest-activity cycle and the patient's clinical state. This observation can be conceptualized in terms of the two-process model of sleep regulation. High-dose haloperidol treatment may have lowered the circadian alertness threshold, whereas clozapine augmented circadian amplitude (perhaps through its high affinity to dopamine D4 and serotonin 5HT7 receptors in the suprachiasmatic nuclei). Measurement of the circadian rest-activity cycle may be a useful non-invasive method to follow functional consequences of neuroleptic treatment.

Adult↗
PubMed1997

The hypothermic effect of late evening melatonin does not block the phase delay induced by concurrent bright light in human subjects.

This constant routine study (n = 9 men) compared the phase delay of the circadian system induced by a single pulse of evening light (5000 lx at 2100-2400 h) in the presence or absence of exogenous melatonin (5 mg p.o. at 2040 h). On the treatment day, light and melatonin protracted and accelerated, respectively, the evening decline in core body temperature (CBT). Subjective sleepiness ratings showed parallel shifts, the earlier the decline in CBT, the sleepier. On the post-treatment day, light induced a phase delay in the mid-range crossing time of CBT decline independent of whether melatonin was co-administered or not. Subjective sleepiness was delayed in parallel. The phase delay of the circadian system by evening light appears to be independent of an immediate hyperthermic effect and is not mediated by melatonin.

Adult↗
PubMed1997

Early evening melatonin and S-20098 advance circadian phase and nocturnal regulation of core body temperature.

The phase-shifting capacity and thermoregulatory effects of a single oral administration at 18 h of melatonin (5 mg) or S-20098, a melatonin agonist (5 or 100 mg), was investigated in eight healthy young men in a double-blind placebo crossover design. The unmasking conditions of a shortened constant-routine protocol (mini-CR) were used to collect evening phase markers of physiological parameters. In comparison to placebo, all three drug administrations induced an earlier dim-light melatonin onset (DLMO), an earlier increase in distal skin temperature, and an earlier decrease in core body temperature (CBT), heart rate, and proximal skin temperature. This indicates that administration at 18 h of both melatonin and S-20098 (more pronounced with 100 than 5 mg) induced an earlier regulation of the endogenous circadian nocturnal decline in CBT. On the posttreatment day a second mini-CR revealed persistent significantly phase-advanced circadian rhythms as estimated by DLMO, as well as by the midrange crossing time of CBT and heart rate decline. There were no significant differences between the two doses of S-20098. The data suggest that, in addition to immediate thermoregulatory changes, a phase advance of the circadian system had occurred and that the phase advance could still be measured on the posttreatment day.

Acetamides↗
PubMed1997

Melatonin and S-20098 increase REM sleep and wake-up propensity without modifying NREM sleep homeostasis.

The pineal hormone melatonin has been implicated in the circadian regulation of sleep. In a crossover design, we investigated the effect of acute administration of 5 mg melatonin and a melatonin agonist (S-20098, 5 and 100 mg) in healthy young men when given 5 h before bedtime on sleep structure and electroencephalogram (EEG) power density. Each trial comprised a baseline, a treatment, and a posttreatment sleep episode. Relative to the placebo condition, all treatments phase advanced the core body temperature rhythm [Kräuchi, K., C. Cajochen, D. Möri, C. Hetsch, and A. Wirz-Justice. Sleep Res. 24: 526, 1995; and Kräuchi, K., C. Cajochen, D. Möri, and A. Wirz-Justice. Am. J. Physiol. 272 (Regulatory Integrative Comp. Physiol. 41): R1178-1188, 1997]. Rapid eye movement (REM) sleep was increased after both melatonin and S-20098. This increase in REM sleep was most pronounced in the first REM sleep episode. On the posttreatment night after melatonin and S-20098 administration, more wakefulness was present in the latter one-half of the sleep episode. EEG power density between 0.25 and 20 Hz during either non-REM (NREM) or REM sleep did not differ from placebo. Thus a single early evening dose of melatonin or the agonist S-20098 increases REM sleep propensity and advances sleep termination while, at the same time, the EEG in NREM sleep remains unaffected.

Acetamides↗
PubMed1997

A relationship between heat loss and sleepiness: effects of postural change and melatonin administration.

Both the pineal hormone melatonin (Mel) and postural changes have thermoregulatory sequelae. The purpose of the study was to evaluate their relationship to subjective sleepiness. Eight healthy young men were investigated under the unmasking conditions of a constant routine protocol. Heart rate, rectal temperature (Tre), skin temperatures (foot, Tfo; and stomach), and subjective sleepiness ratings were continuously recorded from 1000 to 1700. Mel (5 mg po) was administered at 1300, a time when Mel should not phase shift the circadian system. Both the postural change at 1000 from upright to a supine position (lying down in bed) and Mel administration at 1300 reduced Tre and increased Tfo in parallel with increased sleepiness. These findings suggest that under comfortable ambient temperature conditions, heat loss via the distal skin regions (e.g., feet) is a key mechanism for induction of sleepiness as core body temperature declines.

Adult↗
PubMed1997

Follow-up study of seasonal affective disorder in Switzerland.

Of 39 diagnosed Seasonal Affective Disorder (SAD) patients who were interviewed 2-5 years after participation in a light therapy trial, 10 continued to have recurrent major depressive episodes in winter, and 17 manifested sub-syndromal SAD (2 patients also had recurrent brief depression, seasonal type). 8 patients had recovered, and 4 had shifted in symptomatology. Thus, over a number of years, the clinical diagnosis changed for the better in 64% of the patients, suggesting that SAD is not a prodromal form of a more chronic major affective disorder, and that light therapy (and perhaps also light-oriented behaviour) reduced the incidence and depth of subsequent depressive episodes. Further evidence for this was the large reduction in use of conventional antidepressant drugs (from 17 to 1) during the follow-up period. Diagnosis of SAD was stable and reliable.

Adolescent↗
PubMed1997

Homeostatic versus circadian effects of melatonin on core body temperature in humans.

Evidence obtained in animals has suggested a link of the pineal gland and its hormone melatonin with the regulation of core body temperature (CBT). Depending on the species considered, melatonin intervenes in generating seasonal rhythms of daily torpor and hibernation, in heat stress tolerance, and in setting the CBT set point. In humans, the circadian rhythms of melatonin is strictly associated with that of CBT, the nocturnal decline of CBT being inversely related to the rise of melatonin. Whereas there is inconsistent evidence for the suggestion that the decline of CBT may prompt the release of melatonin, conversely, stringent data indicate that melatonin decreases CBT. Administration of melatonin during the day, when it is not normally secreted, decreases CBT by about 0.3 to 0.4 degree C, and suppression of melatonin at night enhances CBT by about the same magnitude. Accordingly, the nocturnal rise of melatonin contributes to the circadian amplitude of CBT. The mechanisms through which melatonin decreases CBT are unclear. It is known that melatonin enhances heat loss, but a reduction of heat production cannot be excluded. Besides actions on peripheral vessels aimed to favor heat loss, it is likely that the effect of melatonin to reduce CBT is exerted mainly in the hypothalamus, where thermoregulatory centers are located. Recent observations have shown that the acute thermoregulatory effects induced by melatonin and bright light are independent of their circadian phase-shifting effects. The effect of melatonin ultimately brings a saving of energy and is reduced in at least two physiological situations: aging and the luteal menstrual phase. In both conditions, melatonin does not exert its CBT-lowering effects. Whereas in older women this effect may represent an age-related alteration, in the luteal phase this modification may represent a mechanism of keeping CBT higher at night to promote a better embryo implantation and survival.

Body Temperature↗
PubMed1997

The acute soporific action of daytime melatonin administration: effects on the EEG during wakefulness and subjective alertness.

Melatonin has been reported to have soporific effects; following daytime administration, it induces sleepiness and reduces sleep onset latency. However, subjective sleepiness is masked by a variety of stimuli and behaviors; thus, it is important to be able to delineate objective psychophysiological sequelae of melatonin administration. Alertness decrements during wakefulness are correlated with augmented theta/alpha power in the waking electroencephalogram (EEG). This has been validated in a constant routine protocol. In a variety of experiments with melatonin administration (5 mg), the authors have shown that the EEG changes can be measured immediately, before any subjective soporific effects are recognized. These increases in theta/alpha power occur when melatonin is administered during the day (1300 or 1800 h) but are less visible when near the endogenous melatonin rise in the evening (2040 h). Importantly, both subjective and objective measures of sleepiness are suppressed when subjects change posture from supine to standing.

Animals↗