Diurnal Variations of Mood and Sleep Disturbances during Phototherapy in Major Depressive Disorder

Volz, Hans-Peter; Mackert, A.; Stieglitz, Rolf‐Dieter; Müller‐Oerlinghausen, B.

doi:10.1159/000284720

Cited by 10 publications

(8 citation statements)

References 11 publications

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“…Both interpretations predict that patients' mood may be changed by manipulations of the circadian system by light. This idea was supported by data of Volz et al (1991), who reported a small predictive value of diurnal mood variation with respect to the success of light therapy.…”

mentioning

confidence: 64%

“…Because of the relationship between diurnal mood variation and the sleep-wake cycle, it is supposed that patients with high daily mood variability are likely to suffer from underlying chronobiological disturbances. This idea is supported by the results of Volz et al (1991); in their study, patients with diurnal variations of mood (feeling better in the evening) responded slightly better to 7 days of bright light therapy in the morning than did patients without diurnal mood variations.…”

Section: Introductionmentioning

confidence: 75%

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Testing the Hypothesis of a Circadian Phase Disturbance Underlying Depressive Mood in Nonseasonal Depression

Gordijn¹,

Beersma²,

Korte³

et al. 1998

J Biol Rhythms

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In a crossover design, 8 nonseasonal depressed subjects, selected on the presence of diurnal mood variations, and 8 sex and age-matched controls were exposed to dim light (< 10 lux) in the evening (18:00-21:00 h) and bright light (2500 lux) in the morning (ML, 6:00-9:00 h), to dim light in the morning and bright light in the evening (EL), or to dim light both in the evening and in the morning (DL) during 3 consecutive days in each of these conditions. There were no initial phase differences between depressed and healthy subjects in the timing of dim light melatonin onset, sleep termination, and body temperature. The phase shifts after EL and ML in both healthy and depressed subjects were as expected on the basis of a human phase response curve. On average, there was no therapeutic effect of the light exposure in the depressed patients. Two patients improved, but these effects do not seem to be related to shifts in the circadian system.

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confidence: 64%

Section: Introductionmentioning

confidence: 75%

Testing the Hypothesis of a Circadian Phase Disturbance Underlying Depressive Mood in Nonseasonal Depression

Gordijn¹,

Beersma²,

Korte³

et al. 1998

J Biol Rhythms

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“…Remarkably, as I reviewed earlier, the baseline diurnal variation of mood that is clearly related to TSD effects was not found to be related to the clinical response to light in the Mackert et al (1991) study (data reported separately by Volz et al, 1991). As to how diurnal variation relates to circadian physiology, only the melatonin phase shifts reported by Rao et al (1992) are available.…”

Section: Light Treatmentmentioning

confidence: 91%

“…Apart from some small-scale uncontrolled studies (Yerevanian et al, 1986;Dietzel et al, 1986;Fleishhauer et al, 1988), in which bright light was sometimes reported to be clinically successful, one large-scale study should be mentioned (Mackert et al, 1991). Forty-two patients were exposed to bright white light (2,500 lux at eye level) or dim red light (50 lux at eye level) 2 hr daily for 1 week.…”

Section: Light Treatmentmentioning

confidence: 99%

“…As in the sleep deprivation experiments, proper control for placebo effects is hard to achieve. In the only study in which melatonin was measured (Mackert et al, 1991), it was found that the acrophases of serum melatonin were phase advanced in 64% and 68% of the patients treated with dim and bright light respectively (Rao et al, 1992). Obviously these lighting conditions may evoke different expectations (Eastman, 1990).…”

Section: Light Treatmentmentioning

confidence: 99%

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Chronobiological Theories of Nonseasonal Affective Disorders and Their Implications for Treatment

Hoofdakker

1994

J Biol Rhythms

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Downloaded from 158 &dquo;dysrhythmia&dquo; is the consequence of the disruption of external routines, particularly the social routines that would act as zeitgebers for behavioral and mental rhythms, and the sleep-wake cycle; disordered biological rhythms are in this view the result of abnormal masking influences on what are essentially normally regulated endogenous rhythms. The disorder would be comparable with dysregulations underlying shift-work disturbances. The debate represents one variant of the classical debate in psychiatry between those who emphasize endogenous and exogenous causation. The primary source of the illness is either located internally, that is, in &dquo;the clock,&dquo; or in the environment, that is, in &dquo;the social zeitgebers.&dquo; Both concepts can be reconciled. In the first place, disrupted social routines resulting, for example, in changes in sleep timing might entail changes in light exposure, which then in turn would affect the central pacemaker. In such cases the latter would produce a truly abnormal output. Furthermore, pacemakers may have interand intrapersonal variability in the susceptibility to light and alterations of light schedules.Whatever the cause of the &dquo;dysrhythmia&dquo; (i.e., a primary or a secondary abnormality in the circadian regulation), the existence of it is generally accepted, provided that dysrhythmia is taken as a descriptive term covering a broad variety of abnormalities in form, amplitude, and phase positions of all possible kinds of rhythms. In view of the clinical phenomena, such as diurnal variation of mood and early morning awakening, it is understandable that much attention has been paid to the regulation of the sleep-wake cycle. The attention has grown in light of findings that manipulations of this cycle and exposure to bright light induce considerable changes in disturbed mood. These observations constitute the core arguments underlying chronobiological theories of affective disorders. However, the argumentation is precarious. A number of questionable assumptions are tacitly implied. The first is that the various &dquo;dysrhythmias,&dquo; particularly those concerning the sleep-wake cycle, can be interpreted as products of specifiable anomalies in the regulation of this cycle. The second questionable assumption is that if this were true the clinical effects of the manipulation of sleep-wake cycles or exposure to light are the results of their impact on these regulatory anomalies. The third assumption is that , if the former assumption might be valid, this would prove that the affective disorders are caused by these anomalies. Despite its attractiveness, this reasoning is weak. Even if coherent links between some dysregulation and clinical response to manipulations of sleep-wake cycles or exposure to light would be demonstrated, this would not necessarily imply that this link is causal, nor would it show that affective disorders result from this dysregulation. The latter may still be an epiphenomenon.Nevertheless, in view of the wide dispe...

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Light therapy for non-seasonal depression

Tuunainen

Kripke

Endo³

2004

Cochrane Database of Systematic Reviews

178

110

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For patients suffering from non-seasonal depression, bright light therapy offers modest though promising antidepressive efficacy, especially when administered during the first week of treatment, in the morning, and as an adjunctive treatment to sleep deprivation responders. Hypomania as a potential adverse effect needs to be considered. Due to limited data and heterogeneity of studies these results need to be interpreted with caution.

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Diurnal Variations of Mood and Sleep Disturbances during Phototherapy in Major Depressive Disorder

Cited by 10 publications

References 11 publications

Testing the Hypothesis of a Circadian Phase Disturbance Underlying Depressive Mood in Nonseasonal Depression

Testing the Hypothesis of a Circadian Phase Disturbance Underlying Depressive Mood in Nonseasonal Depression

Chronobiological Theories of Nonseasonal Affective Disorders and Their Implications for Treatment

Light therapy for non-seasonal depression

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