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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bright-light therapy is widely regarded as an effective treatment for winter seasonal affective disorder (SAD). We attempted to identify predictors of light therapy response in 54 depressed, drug-free outpatients diagnosed with SAD by DSM-III-R criteria. After a baseline week, patients were treated for 2 weeks with 2500-lx cool-white fluorescent light exposure from 0600 to 0800 daily. The results showed that light therapy significantly reduced depression scores. Several indices of atypical and typical symptoms correlated with response, but none was clearly superior to the pre-treatment depression score. A multiple regression analysis identified 3 factors (hypersomnia, increased eating and younger age) that predicted light-therapy response. These results suggest that specific symptoms of hypersomnia and hyperphagia are predictors of response to morning bright-light therapy in SAD.
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PMID:Morning light therapy for winter depression: predictors of response. 817 70

This is the first comprehensive description of winter depression (WD), as part of seasonal affective disorder (SAD), from Norway, and one of the very few from so far north. A total of 128 media-recruited people had first been screened with the Seasonal Pattern Assessment Questionnaire and were thereafter personally interviewed. The criteria for DSM-III-R mood disorder, seasonal pattern, were satisfied by 85%, whereas 73% satisfied the criteria of Rosenthal et al. for SAD. Seven percent were diagnosed as subsyndromal SAD. The main characteristics of our patient group were in reasonable accordance with other clinical SAD materials: there were 81% women; the mean age was 44 years (range: 20 to 76); the mean age for SAD debut was 24 years (range: 4 to 71); and the duration of WD was most often from October to March or April. Only 12% had ever been manic or hypomanic in summer. During their WD, most patients suffered at least one of the symptoms hypersomnia, hyperphagia or carbohydrate craving; 16% also had a craving for fatty food in winter, but this may be considered "normal" at this northerly latitude.
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PMID:Characteristics of winter depression in the Oslo area (60 degrees N). 821 3

We report the first double-blind, placebo-controlled continuation study comparison of a neuroleptic (haloperidol < or = 6 mg), monoamine oxidase inhibitor (MAOI) antidepressant (phenelzine < or = 90 mg), and placebo in 54 patients with borderline personality disorder. Continuation medication trials of 16 weeks followed 5 weeks of acute therapy. Haloperidol continued to be effective beyond the acute phase only for the treatment of irritability. Higher levels of depression, hypersomnia, and leaden paralysis were noted in the haloperidol group than in the phenelzine and placebo groups. The dropout rate during the first half (8 weeks) of the continuation study was significantly higher for the haloperidol group (64%) than for the placebo group (28%) (p < .05). Phenelzine demonstrated very modest efficacy beyond that noted in the acute phase for the treatment of depression and irritability. Phenelzine was shown to have an activating effect on measures of excitement and reactivity.
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PMID:Haloperidol vs. phenelzine in continuation therapy of borderline disorder. 829 Jun 83

Thirty-four patients with seasonal affective disorder, winter depression type (WD) were randomly distributed to receive the selective monoamine oxidase-A inhibitor moclobemide (400 mg daily) or placebo in a double-blind, parallel group study lasting for up to 14 weeks. Severity measures were the Montgomery-Asberg Depression Rating Scale (MADRS) extended with characteristic symptoms of WD; summed score of the "atypical" symptoms hypersomnia, hyperphagia and carbohydrate craving; and Clinical Global Impressions (CGI). After 3 weeks, patients with unsatisfactory response were switched to open moclobemide. Three patients on placebo dropped out before 3 weeks. Extended MADRS and CGI showed no significant difference between the groups at 3 weeks, whereas the atypical score was reduced significantly more on moclobemide than on placebo already after one week. Nonresponders after 3 weeks (9 of 16 on moclobemide and 7 of 15 on placebo) improved rapidly after being given open moclobemide. Predictor analysis showed a remarkably high negative correlation between improvement at 3 weeks (extended MADRS) and age in the placebo group and a strong, nonsignificant trend in the same direction in the moclobemide group. Dichotomizing the patients according to the median age (45 years) resulted in a somewhat better effect of moclobemide than placebo in the older age group. There were no significant differences in side effects between moclobemide and placebo.
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PMID:Treatment of winter depression in Norway. II. A comparison of the selective monoamine oxidase A inhibitor moclobemide and placebo. 829 82

Women are affected by winter seasonal affective disorder (SAD) more often than men. The female/male ratio is reported to range from 2:1 to 40:1 in samples of patients with winter SAD. It is suggested that this preponderance of women is based on the action of the ovarian steroid hormones estrogen and progesterone. However, the detailed mechanisms of action are not well understood to date. A new hypothesis claims that, in women with winter SAD, decreased levels of estradiol in the ventromedial hypothalamus are associated with the occurrence of atypical symptoms of depression, including increased daytime sleepiness and hypersomnia during the winter.
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PMID:Estrogen could control photoperiodic adjustment in seasonal affective disorder. 852 74

Hypercortisolism in depression seems to preferentially reflect activation of hypothalamic CRH secretion. Although it has been postulated that this hypercortisolism is an epiphenomenon of the pain and stress of major depression, our data showing preferential participation of AVP in the hypercortisolism of chronic inflammatory disease suggest specificity for the pathophysiology of hypercortisolism in depression. Our findings that imipramine causes a down-regulation of the HPA axis in experimental animals and healthy controls support an intrinsic role for CRH in the pathophysiology of melancholia and in the mechanism of action of psychotropic agents. Our data suggest that hypercortisolism is not the only form of HPA dysregulation in major depression. In a series of studies, commencing in patients with Cushing's disease, and extending to hyperimmune fatigue states such as chronic fatigue syndrome and examples of atypical depression such as seasonal affective disorder, we have advanced data suggesting hypofunction of hypothalamic CRH neurons. These data raise the question that the hyperphagia, hypersomnia, and fatigue associated with syndromes of atypical depression could reflect a central deficiency of a potent arousal-producing anorexogenic neuropeptide. In the light of data presented elsewhere in this symposium regarding the role of a hypofunctioning hypothalamic CRH neuron in susceptibility to inflammatory disease, these data also raise the question of a common pathophysiological mechanism in syndromes associated both with inflammatory manifestations and atypical depressive symptoms. This concept of hypofunctioning of hypothalamic CRH neurons in these disorders also raises the question of novel forms of neuropharmacological intervention in both inflammatory diseases and atypical depressive syndromes.
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PMID:Corticotropin releasing hormone in the pathophysiology of melancholic and atypical depression and in the mechanism of action of antidepressant drugs. 859 44

Since 1984, there has been a great interest in the phenomenon of a particular seasonally recurrent mood disorder called seasonal affective disorder (SAD) or winter depression and its treatment: the phototherapy. Seasonal affective disorder is a syndrome described by Rosenthal in 1984. This mood disorder is characterized by depression with onset recurrent in autumn or winter and spontaneous spring or summer remission. It is associated with hypersomnia, anergia, increased appetite, weight gain and carbohydrate craving. The population prevalence in the north of the USA is estimated between 3 and 5%, but it changes with sex, age and also latitude. A long time ago, we know that animals are photoperiod sensitive and that the melatonin secretion in mammals is suppressed by the light. In 1980, Czeiler reported for the first time that human melatonin secretion can be suppressed by high light exposure (+/- 1500 lux). In 1982, Rosenthal, Lewy and al. reported an antidepressant effect of light exposure of a manic-depressive patient. The phototherapy was born. To treat the SAD, the most common procedure of phototherapy is to expose the subject during 2 hours early in the morning, between 06:00 and 09:00 AM. The subject is sitting before a light screen, he can work and has to fix the screen one time every minute. The most common side effects are headache, eyestrain, muscle pain. The ocular phototoxicity is controversed and it seems to be potentially dangerous if phototherapy is associated with tricyclic antidepressants, neuroleptics and other medication containing a tricyclic, heterocyclic or porphyrin ring system. Since this finding, many questions are asked about photoperiod and its effects in the human being. Lewy proposes for the winter depression the hypothesis of a phase delayed circadian rhythm, that can be treated by a morning light exposure. At the present time, many trials are going on to study the effects of phototherapy in other problems like insomnia, maladaptation to night work, jet lag and Alzheimer disease.
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PMID:[Seasonal affective syndrome and phototherapy: theoretical concepts and clinical applications]. 868 79

The aim of the present study was to examine whether high or low levels of platelet monoamine oxidase (MAO) activity were associated with an increased risk of winter seasonal affective disorder (SAD) or of developing characteristic vegetative symptoms during episodes of the disorder. We also investigated the relationship between MAO activity and the Global Seasonality Scale (GSS), a measure of seasonal variation in sleep length, social activity, mood, weight, appetite, and energy level. Patients with SAD (n = 49), patients with subsyndromal SAD (n = 11), and normal volunteers (n = 25) participated in the study. We found significantly higher levels of platelet MAO activity in females but did not observe significant differences across age groups or between groups of patients tested in different seasons or mood states. MAO activity (whether high or low) was not associated with a significant increase in risk of SAD or of developing hypersomnia, hyperphagia, or carbohydrate craving during episodes of winter depression. We found no significant relationship between GSS and MAO activity. Patients who had made suicide attempts during an episode of SAD had significantly lower mean levels of platelet MAO activity than other patients.
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PMID:Platelet monoamine oxidase activity in patients with winter seasonal affective disorder. 880 38

There is a general tendency to restrict the notion of sleep disorders to insomnia and consequently to limit treatment to the prescription of hypnotics. However, it is very often of benefit to prescribe psychotropic agents, in particular antidepressants, not only in insomnia but also in certain cases of hypersomnia, parasomnia and dysomnia associated with organic diseases. In some conditions, however, antidepressants may either induce or aggravate sleep disorders. This is the case with a number of psychostimulants that occasionally induce insomnia. It is also true of the tricyclic antidepressants, which may worsen or even induce a restlessleg syndrome that is often associated with periodic movement syndrome. On the other hand, the antidepressants may play a therapeutic role in certain sleep disorders : - depression-related insomnia is of course the << primary >> indication for antidepressants. Furthermore, certain antidepressants exhibit a sedative action resulting in a hypnogenic-type effect which appears well before the antidepressant effect; - the other types of insomnia may also often be treated with antidepressants : not acute reactional insomnia, against which hypnotics are remarkably effective, but chronic insomnia. In addition, all antidepressants may eventually correct depressive hypersomnia, but in these cases, it is evidently preferable to prescribe non-sedative drugs. Although some tricyclic antidepressants have been proposed for use in hypersomnia due to sleep apnea, their therapeutic interest is minor compared with mechanical and surgical treatment. In contrast, antidepressants play an important role in the treatment of narcolepsy, particularly for the correction of attacks of cataplexy. Antidepressants have also been used for some time in the treatment of parasomnia related to slow deep sleep (night terrors and sleepwalking), but the antidepressants may also be used in enuresis and in parasomnia related to REM sleep : nightmares, sleep paralysis, behavioral problems associated with REM sleep. Antidepressant (mainly serotoninergic drugs) are often used in the treatment of fibrolitis syndrome. Finally, antidepressants (particularly the serotoninergic antidepressants) play an important role in the drug treatment of fibromyalgia.
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PMID:[Use of antidepressants in sleep disorders: practical considerations]. 892 78

The authors examined the rates of atypical depression and prevalence of specific atypical symptoms in patients with seasonal versus non-seasonal depression. Fifty-three patients with seasonal affective disorder (SAD) were compared to 54 patients with non-seasonal major depressive disorder (MDD) using the atypical depression diagnostic scale (ADDS). SAD patients scored significantly higher than non-seasonal MDD patients in hyperphagia and hypersomnia, and significantly lower in interpersonal sensitivity and other rejection avoidance. There was no difference in the rate of ADDS diagnosis of atypical depression. Differences between atypical depression and SAD suggest that they are separate subtypes of depression with an overlapping symptom picture.
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PMID:Atypical depressive symptoms in seasonal and non-seasonal mood disorders. 918 1


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