Comparison of light treatment with citalopram in winter depression: a longitudinal single case study*

Wirz‐Justice, Anna; Velde, P. van der; Bucher, A.; Nil, R.

doi:10.1097/00004850-199207020-00008

Cited by 14 publications

(11 citation statements)

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“…Whether for mood (23,28,75) or circadian disorders (26), light has been shown to be an effective and safe, yet challenging therapy. Multiple modulations have been suggested for the chromaticity (76-78), intensity (79), and pattern (55, 80) of light exposures to render them optimal for clinical and personal use.…”

Section: Discussionmentioning

confidence: 99%

“…Axons emerging from the ipRGCs project to nonimage-forming (NIF) centers in the mammalian brain to evoke subcortical changes that include, but are not limited to, the resetting of circadian timing (1,10,11,16,17), suppression of melatonin production (18), activation of the pupillary light reflex (14,15), change in arousal levels (19,20) and sleep drive (21), alleviation of seasonal depression (22,23), and possibly the induction of migraine headaches (24). Given its NIF implications, light has been used for its considerable therapeutic potential in chronobiological disorders such as jet lag and shift work but has also been used to treat sleep and mood disorders as well as cognitive impairment via correction of circadian misalignment and an acute activating response (22,23,(25)(26)(27)(28)(29)(30)(31)(32).…”

Section: Introductionmentioning

confidence: 99%

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Temporal integration of light flashes by the human circadian system

Najjar¹,

Zeitzer²

2016

Journal of Clinical Investigation

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BACKGROUND.Beyond image formation, the light that is detected by retinal photoreceptors influences subcortical functions, including circadian timing, sleep, and arousal. The physiology of nonimage-forming (NIF) photoresponses in humans is not well understood; therefore, the development of therapeutic interventions based on this physiology, such as bright light therapy to treat chronobiological disorders, remains challenging. METHODS.Thirty-nine participants were exposed to 60 minutes of either continuous light (n = 8) or sequences of 2-millisecond light flashes (n = 31) with different interstimulus intervals (ISIs; ranging from 2.5 to 240 seconds). Melatonin phase shift and suppression, along with changes in alertness and sleepiness, were assessed. RESULTS.We determined that the human circadian system integrates flash sequences in a nonlinear fashion with a linear rise to a peak response (ISI = 7.6 ± 0.53 seconds) and a power function decrease following the peak of responsivity. At peak ISI, flashes were at least 2-fold more effective in phase delaying the circadian system as compared with exposure to equiluminous continuous light 3,800 times the duration. Flashes did not change melatonin concentrations or alertness in an ISI-dependent manner. CONCLUSION.We have demonstrated that intermittent light is more effective than continuous light at eliciting circadian changes. These findings cast light on the phenomenology of photic integration and suggest a dichotomous retinohypothalamic network leading to circadian phase shifting and other NIF photoresponses. Further clinical trials are required to judge the practicality of light flash protocols. light in a nonlinear fashion. Intermittent patterns of light tested thus far fail, however, to elicit greater changes in outcomes when compared with continuous light exposures. Shorter duration of light exposures in the order of microseconds to milliseconds have been tested in rodents (45)(46)(47). While a single 2-millisecond flash of light is insufficient to phase shift the murine circadian system, a sequence of flashes administered once per minute for 60 minutes is sufficient to evoke phase delays (48). This study by Van Den Pol and colleagues, in addition to other published studies in rodents (45)(46)(47), established that the mammalian circadian system has the capacity to respond to a sequence of very brief, millisecond flashes of light.of NIF photoreception in humans remains incompletely understood, as it has wavelength (35-39), intensity (40), duration (41), and pattern (42-44) responses that are considerably distinct from the traditional perceptual image-forming responses, and most knowledge in this field has been imputed from studies of nonhuman mammals. Understanding NIF characteristics and responses to light is crucial for the development and optimization of light therapy strategies. NIF responses to light in humans have mainly been tested using continuous or intermittent light exposures, ranging from the order of minutes up to more than 6 hours of bright light (41...

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Temporal integration of light flashes by the human circadian system

Najjar¹,

Zeitzer²

2016

Journal of Clinical Investigation

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“…To evaluate the responses of the circadian system to changes in light intensity, daily rhythms in locomotor activity were analyzed in animals housed in BLD or DLD, respectively. In addition to the circadian mechanisms, the monoaminergic system has also been implicated in the etiology of SAD [18], [19], [20]. To explore the neural substrates underlying the behavioral changes, the serotoninergic signals were examined in the dorsal raphe nucleus (DRN) and several other brain regions.…”

Section: Introductionmentioning

confidence: 99%

Depression-Like Responses Induced by Daytime Light Deficiency in the Diurnal Grass Rat (Arvicanthis niloticus)

2013

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Seasonal Affective Disorder (SAD) is one of the most common mood disorders with depressive symptoms recurring in winter when there is less sunlight. The fact that light is the most salient factor entraining circadian rhythms leads to the phase-shifting hypothesis, which suggests that the depressive episodes of SAD are caused by misalignments between the circadian rhythms and the habitual sleep times. However, how changes in environmental lighting conditions lead to the fluctuations in mood is largely unknown. The objective of this study is to develop an animal model for some of the features/symptoms of SAD using the diurnal grass rats Arvichantis niloticus and to explore the neural mechanisms underlying the light associated mood changes. Animals were housed in either a 12∶12 hr bright light∶dark (1000lux, BLD) or dim light∶dark (50lux, DLD) condition. The depression-like behaviors were assessed by sweet-taste Saccharin solution preference (SSP) and forced swimming test (FST). Animals in the DLD group showed higher levels of depression-like behaviors compared to those in BLD. The anxiety-like behaviors were assessed in open field and light/dark box test, however no significant differences were observed between the two groups. The involvement of the circadian system on depression-like behaviors was investigated as well. Analysis of locomotor activity revealed no major differences in daily rhythms that could possibly contribute to the depression-like behaviors. To explore the neural substrates associated with the depression-like behaviors, the brain tissues from these animals were analyzed using immunocytochemistry. Attenuated indices of 5-HT signaling were observed in DLD compared to the BLD group. The results lay the groundwork for establishing a novel animal model and a novel experimental paradigm for SAD. The results also provide insights into the neural mechanisms underlying light-dependent mood changes.

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“…Moclobemide 4 weeks 5 Marked and uniform improvement, very few side effects [77] Wirz-Justice et al (1992) Citalopram Citalopram in comparison with BLT 1 Both treatments were effective [78] Heßelmann [80] Clinical trials with active comparator Martinez et al (1994) Hypericum + dim-light versus hypericum + BLT 4 weeks 20 No significant between-group differences [57] Partonen and Lonnqvist (1996) Moclobemide versus fluoxetine 6 weeks 32 No significant between-group differences [55] Ghadirian et al (1998) Tryptophan versus BLT Crossover design: 2 weeks BLT, 4 weeks tryptophan 13 Equal efficacy of tryptophan and BLT, slower relapse after withdrawal of tryptophan [81] Ruhrmann vitality in the subjects with s-SAD compared with placebo. As pathophysiological research has demonstrated a melatonergic dysregulation in SAD patients, it seems to be an interesting target for antidepressant treatment: agomelatine is the prototype of a new class of antidepressants and acts as an agonist at melatonin-1 and -2 binding sites and has antagonistic properties at the 5-HT 2C receptor.…”

Section: Open Studies and Case Reportsmentioning

confidence: 99%

Treatment of seasonal affective disorder

Winkler¹,

Pjrek²,

Iwaki³

et al. 2006

Expert Review of Neurotherapeutics

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Seasonal affective disorder (SAD), winter type, is characterized by the regular annual onset of major depressive episodes during fall or winter, followed by spontaneous remission and sometimes hypomanic or manic episodes during spring and summer. SAD is clinically important, since approximately 2-5% of the general population in temperate climates are affected. Since the first description of the syndrome, researchers have made attempts to elucidate the pathophysiological background of SAD. Bright light therapy has been proposed as the treatment of choice for this disorder. However, numerous studies have also investigated suitable psychopharmacological treatments for SAD. This report is aimed to provide an overview on the clinical management and current therapeutic options for SAD.

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Comparison of light treatment with citalopram in winter depression: a longitudinal single case study*

Cited by 14 publications

References 0 publications

Temporal integration of light flashes by the human circadian system

Temporal integration of light flashes by the human circadian system

Depression-Like Responses Induced by Daytime Light Deficiency in the Diurnal Grass Rat (Arvicanthis niloticus)

Treatment of seasonal affective disorder

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