Effect of simulated dawn on quality of sleep--a community-based trial. (17/73)

BACKGROUND: Morning light exposure administered as simulated dawn looks a promising method to treat Seasonal Affective Disorder, but it may moreover help with resetting the inaccurate organisation of body clock functions relative to sleep occurring in winter among people in general. Disturbances in sleep patterns are common and may compromise wellbeing even in the short term. Our hypothesis was that simulated dawn could improve the subjective quality of sleep during winter. METHODS: A community-based trial with 100 volunteer subjects provided with dawn simulators. Study period lasted for eight weeks, and subjects used the dawn simulators for two weeks at a time, each subject acting as his own control (ABAB-design). Main outcome measure was subjective quality of sleep recorded each morning with Groningen Sleep Quality Scale. RESULTS: 77 subjects completed the trial. Quality of sleep improved while subjects were using dawn simulator-devices (p = 0.001). The treatment became beneficial after six days' use of dawn simulator, but the effect did not last after the use was ceased. CONCLUSION: Dawn simulation may help to improve the subjective quality of sleep, but the benefits are modest. Further research is needed to verify these findings and to elucidate the mechanism by which dawn simulation acts on the sleep-wake pattern.  (+info)

Drop-out and mood improvement: a randomised controlled trial with light exposure and physical exercise [ISRCTN36478292]. (18/73)

BACKGROUND: Combining bright light exposure and physical exercise may be an effective way of relieving depressive symptoms. However, relatively little is known about individual factors predicting either a good response or treatment failure. We explored background variables possibly explaining the individual variation in treatment response or failure in a randomised trial. METHODS: Participants were volunteers of working-age, free from prior mental disorders and recruited via occupational health centres. The intervention was a randomised 8-week trial with three groups: aerobics in bright light, aerobics in normal room lighting, and relaxation/stretching in bright light. Good response was defined as a 50% decrease in the symptom score on either the Hamilton Depression Rating Scale (HDRS) or 8-item scale of atypical symptoms. Background variables for the analysis included sex, age, body-mass index, general health habits, seasonal pattern, and sleep disturbances. RESULTS: Complete data were received from 98 subjects (11 men, 87 women). Of them, 42 (5 men, 37 women) were classified as responders on the HDRS. Overall, light had a significant effect on the number of responders, as assessed with the HDRS (X2 =.02). The number needed to treat (NNT) for light was 3.8. CONCLUSIONS: We investigated the effect of bright light and exercise on depressive symptoms. Problems with sleep, especially initial insomnia, may predict a good response to treatment using combined light and exercise. Bright light exposure and physical exercise, even in combination, seem to be well tolerated and effective on depressive symptoms.  (+info)

Single photon emission computed tomography (SPECT) of anxiety disorders before and after treatment with citalopram. (19/73)

BACKGROUND: Several studies have now examined the effects of selective serotonin reuptake inhibitor (SSRI) treatment on brain function in a variety of anxiety disorders including obsessive-compulsive disorder (OCD), posttraumatic stress disorder (PTSD), and social anxiety disorder (social phobia) (SAD). Regional changes in cerebral perfusion following SSRI treatment have been shown for all three disorders. The orbitofrontal cortex (OFC) (OCD), caudate (OCD), medial pre-frontal/cingulate (OCD, SAD, PTSD), temporal (OCD, SAD, PTSD) and, thalamic regions (OCD, SAD) are some of those implicated. Some data also suggests that higher perfusion pre-treatment in the anterior cingulate (PTSD), OFC, caudate (OCD) and antero-lateral temporal region (SAD) predicts subsequent treatment response. This paper further examines the notion of overlap in the neurocircuitry of treatment and indeed treatment response across anxiety disorders with SSRI treatment. METHODS: Single photon emission computed tomography (SPECT) using Tc-99 m HMPAO to assess brain perfusion was performed on subjects with OCD, PTSD, and SAD before and after 8 weeks (SAD) and 12 weeks (OCD and PTSD) treatment with the SSRI citalopram. Statistical parametric mapping (SPM) was used to compare scans (pre- vs post-medication, and responders vs non-responders) in the combined group of subjects. RESULTS: Citalopram treatment resulted in significant deactivation (p = 0.001) for the entire group in the superior (t = 4.78) and anterior (t = 4.04) cingulate, right thalamus (t = 4.66) and left hippocampus (t = 3.96). Deactivation (p = 0.001) within the left precentral (t = 4.26), right mid-frontal (t = 4.03), right inferior frontal (t = 3.99), left prefrontal (3.81) and right precuneus (t= 3.85) was more marked in treatment responders. No pattern of baseline activation distinguished responders from non-responders to subsequent pharmacotherapy. CONCLUSIONS: Although each of the anxiety disorders may be mediated by different neurocircuits, there is some overlap in the functional neuro-anatomy of their response to SSRI treatment. The current data are consistent with previous work demonstrating the importance of limbic circuits in this spectrum of disorders. These play a crucial role in cognitive-affective processing, are innervated by serotonergic neurons, and changes in their activity during serotonergic pharmacotherapy seem crucial.  (+info)

The effects of nefazodone on women with seasonal affective disorder: clinical and polysomnographic analyses. (20/73)

OBJECTIVE: To outline the clinical and polysomnographic changes induced by nefazodone in patients with seasonal affective disorder. METHODS: Twelve patients were enrolled, and 9 of them studied, in an open-label trial with objective and subjective measurements. The mean age of the studied patients was 45 (range 35-58) years. They met Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV), criteria for major depressive disorder and current major depressive episode with seasonal patterns. The patients' mean baseline score on the Seasonal Patterns Assessment Questionnaire (SPAQ) was 15.7 (standard deviation [SD] 5.3). The total nefazodone treatment period was 8 weeks, and the daily dosages were 100 mg in week 1, 200 mg in week 2, 300 mg in week 3, and up to 400 mg in weeks 4-8. Each patient received the 29-item version of the Hamilton Rating Scale for Depression (HAM-D), the Hamilton Rating Scale for Anxiety (HAM-A) and 2-night polysomnographic assessments on 3 occasions: before treatment (baseline, W0), at the end of week 4 (W4) and at the end of week 8 (W8). RESULTS: There were statistically significant improvements in depression, anxiety, sleep latency and sleep efficiency during the 8-week treatment protocol. Repeated-measures analysis of variance results indicated that nefazodone has a time-dependent effect on both HAM-D and HAM-A scores. After 8 weeks of nefazodone therapy, HAM-D scores decreased from 33.4 (SD 8.1) to 11.6 (SD 5.6) (F(2,14) = 13.68, p = 0.001) and HAM-A decreased from 26.6 (SD 7.0) to 11.5 (SD 11.1) (F(2,14) = 13.46, p = 0.001). The results of paired t tests show that, compared with baseline, HAM-D and HAM-A scores decreased at both W4 (p = 0.004 and p = 0.002, respectively) and W8 (p = 0.002 and p = 0.005, respectively). The time-dependent effects on stage 1 sleep (F(2,16) = 6.06, p = 0.011) and periodic leg movement index (F(2,16) = 4.31, p = 0.035) were also significant. The mean sleep latency of these patients decreased from 39.9 (SD 32.7) minutes at W0 to 16.6 (SD 15.3) minutes at W8 (p < 0.05). Sleep efficiency increased from 78.8% (SD 14.6%) at W0 to 91.5% (SD 5.5%) at W8 (p < 0.05). Stage 1 sleep decreased from 4.9% (SD 1.9%) at W0 to 3.4% (SD 2.6%) at W8 (p < 0.05). CONCLUSIONS: The results of this preliminary study indicate that nefazodone not only has favourable antidepressant and anxiolytic effects but also enhances sleep efficiency and sleep latency.  (+info)

Melatonin treatment of winter depression following total sleep deprivation: waking EEG and mood correlates. (21/73)

Patients with winter depression (seasonal affective disorder (SAD)) commonly complain of sleepiness. Sleepiness can be objectively measured by spectral analysis of the waking electroencephalogram (EEG) in the 1-10 Hz band. The waking EEG was measured every 3 h in 16 female SAD patients and 13 age-matched control women throughout a total sleep deprivation of 30 h. Melatonin (or placebo) under double-blind conditions was administered subsequently (0.5 mg at 1700 h for 6 days), appropriately timed to phase advance circadian rhythms, followed by reassessment in the laboratory for 12 h. The increase in EEG power density in a narrow theta band (5-5.99 Hz, derivation Fz-Cz) during the 30 h protocol was significantly attenuated in patients compared with controls (difference between linear trends p=0.037). Sleepiness (p=0.092) and energy (p=0.045) self-ratings followed a similar pattern. Six patients improved after sleep deprivation (> or =50% reduction on SIGH-SAD(22) score). EEG power density dynamics was correlated with clinical response to sleep deprivation: the steeper the build-up (as in controls), the better the improvement (p<0.05). There was no differential effect of melatonin or placebo on any measure; both treatments stabilized the improvement. Overall, patients with winter depression manifest similar wake EEG characteristics as long sleepers or late chronotype with respect to an insufficient build-up of homeostatic sleep pressure. Sleep deprivation was an effective antidepressant treatment for some patients, but evening melatonin was not more efficacious than placebo in sustaining this antidepressant effect.  (+info)

Epidemiology, etiology, and natural treatment of seasonal affective disorder. (22/73)

There is much more seasonal difference in higher latitudes than in lower latitudes. In a significant portion of the population of the northern United States, the shorter days of fall and winter precipitate a syndrome that can consist of depression, fatigue, hypersomnolence, hyperphagia, carbohydrate craving, weight gain, and loss of libido. If these symptoms persist in the winter, abate as the days grow longer, and disappear in the summer, the diagnosis of seasonal affective disorder (SAD) can be made. Many hypotheses exist regarding the biochemical mechanisms behind the predisposition toward this disease, including circadian phase shifting, abnormal pineal melatonin secretion, and abnormal serotonin synthesis. Although the mechanism(s) behind this disease is not fully known, one treatment appears to address each of the theories. Light therapy is a natural, non-invasive, effective, well-researched method of treatment for SAD. Various light temperatures and times of administration of light therapy have been studied, and a combination of morning and evening exposure appears to offer the best efficacy. Other natural methods of treatment have been studied, including L-tryptophan, Hypericum perforatum (St. John's wort), and melatonin.  (+info)

The circadian basis of winter depression. (23/73)

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.  (+info)

A birth-season/DRD4 gene interaction predicts weight gain and obesity in women with seasonal affective disorder: A seasonal thrifty phenotype hypothesis. (24/73)

We have recently described an association between the hypofunctional 7-repeat allele (7R) of the dopamine-4 receptor gene (DRD4), weight gain, and obesity in women with seasonal affective disorder (SAD). In the current study, we examined whether season-of-birth might interact with the 7R allele to influence body weight regulation in SAD. In 182 female probands with SAD, we performed an analysis of covariance predicting maximum lifetime body mass index (BMI) with both the exon-3 variable number of tandem repeat polymorphism of DRD4 and season-of-birth as independent variables, and age as the covariate. The overall model was highly significant (F = 4.42, df = 8, 173, p < 0.0001) with season-of-birth predicting maximal lifetime BMI both on its own and in its interaction with the 7R allele. The latter finding was attributable to 7-repeat carriers born in the spring (N = 17), who had a mean maximal lifetime BMI of 33.7 kg/m2 (SD 8.6), compared to 26.7 kg/m2 (SD 5.4) for all other probands combined (N = 165) (F = 20.01, df = 1, 179, p < 0.0001). The lifetime rate of obesity (maximal BMI > 30 kg/m2) was also significantly higher in the 7R/spring birth group (9/17=52.9% vs 32/165=19.4%; chi2 = 9.94, df = 1, p = 0.002; odds ratio = 4.68, 95% CI = 1.67-13.07). These data may reflect a novel gene-environment interaction, during early brain development, which establishes an increased risk for obesity in women with SAD. Although the mechanism for season-of-birth effects in psychiatric disorders is unknown, a characteristic pattern of melatonin exposure during the second and third trimesters may be of particular relevance in this study population. We speculate that these data may reflect the vestigial expression of a seasonal thrifty phenotype that contributed to the positive selection of the 7R allele over the past 40,000 years.  (+info)