Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A clinically relevant sleep-wake disturbance is found in up to half the patients with dementia, and the sundowning agitation is a common cause of institutionalisation of demented geriatric patients. The circadian rhythm of demented patients is levelled off with increased daytime sleep and disrupted night sleep. Particularly in vascular dementia, Korsakow syndrome, Parkinson's disease, and depression the alteration of sleep architecture may be pronounced, whereas in Alzheimer's disease prominent hypersomnolence or insomnia is typically only found in later stages of the diseases. Greatly increased daytime sleepiness or striking insomnia at the very beginning of suspected dementia should thus prompt the search for other, possibly treatable causes of dementia. Neuropathological and neurophysiological studies support the hypothesis of a deteriorated hypothalamic suprachiasmatic nucleus (harbouring the biological clock) as a cause for the deranged circadian sleep-wake system in dementia. Management of sundowning behaviour includes restriction of daytime sleep, exposure to bright lights, and social interaction schedules during the day. The benzodiazepines and analogues usually not being sufficiently effectual, low doses of mild neuroleptics are often needed. Whether recent reports on efficacy of melatonin in elderly insomniacs also apply to demented patients is yet uncertain. The careful search and treatment of possible extracerebral physiologic factors causing reversible hypersomnia or insomnia is an important requisite. Polysomnographic studies are needed to recognise treatable sleep disturbance which could deteriorate or mimic dementia and sundowning. Particularly, a sleep-apnea-hypopnea syndrome must be searched for at the beginning of a suspected dementia, when successful treatment is still possible. Sleep studies should also identify periodic leg movements of sleep with restless legs and/or increased daytime sleepiness, and hyperkinetic parasomnias such as REM sleep behaviour disorder which may complicate or imitate sundowning.
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PMID:[Sleep disorders and dementia]. 938 Oct 26

This study was designed to evaluate the antidepressant effect of negative ions in the ambient air as a potential treatment modality for seasonal affective disorder. Twenty-five subjects with winter depression underwent a double-blind controlled trial of negative ions at two exposure densities, 1 x 10(4) ions/cm3 or 2.7 x 10(6) ions/cm3, using an electronic negative ion generator with wire corona emitters. Home treatments were taken in the early morning for 30 min over 20 days, followed by withdrawals. The severity of depressive symptoms (prominently including the reverse neurovegetative symptoms of hypersomnia, hyperphagia, and fatigability) decreased selectively for the group receiving high-density treatment. Standard depression rating scale assessments were corroborated by clinical impressions. When a remission criterion of 50% or greater reduction in symptom frequency/severity was used, 58% of subjects responded to high-density treatment while 15% responded to low-density treatment (chi 2 = 5.00, df = 1, p = 0.025). There were no side effects attributable to the treatment, and all subjects who responded showed subsequent relapse during withdrawal. Treatment with a high-density negative ionizer appears to act as a specific antidepressant for patients with seasonal affective disorder. The method may be useful as an alternative or supplement to light therapy and medications.
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PMID:Treatment of seasonal affective disorder with a high-output negative ionizer. 939 4

Seasonal affective disorder (SAD) is a condition characterized by annually occurring major depressive episodes which was described by Rosenthal et al. in 1984. It occurs most commonly in women and the onset usually being in early adulthood. These episodes are regularly occurring in fall and winter with full remission during the following spring and summer. The patient's mood is a combination of depression and mild anxiety accompanied by fatigue, loss of libido, and a profound reduction of socialisation. During winter depression, most of these patients complain of atypical vegetative symptoms accompanied by hypersomnia, hyperphagia, carbohydrate craving, and weight gain. Hypotheses on the underlying mechanisms of these behavioral and neurovegetative disorders indicate that environmental variables, e.g., climate, latitude, light, and changes in neurotransmitter fraction that naturally occur with the seasons may be important. Phototherapy is being increasingly used for the treatment of seasonal affective disorder. The antidepressant effect of light therapy in the treatment of SAD has been widely shown. The response in patients with SAD is contingent on the exposure of the patients' eyes to light. Further important factors are the duration of daily treatment and light intensity. However, the role of timing of phototherapy remains controversial. The biological basis of the diverse psychological and biological changes in SAD and the underlying mechanisms of action of phototherapy are still unclear and require further study.
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PMID:[Seasonal depression]. 945 88

Winter depression (seasonal affective disorder, SAD) is characterised by a seasonal major depressive episode in the last 2 years. Hypersomnia, carbohydrate-craving and weight-gain are specific traits. These patients preferentially seek help from their General Practitioner. Current research on the aetiology of SAD covers fields such as retinal deficiency, phase-disturbance of the internal circadian rhythms given by internal oscillators and neuro-endocrinologically expressed disorders, assuming that melatonin is the main mediator of human circadian systems in the CNS. Disorders of neurotransmitters (serotonin) are another cue. Recent longitudinal studies show a prevalence of seasonal depressive symptoms in up to 10% of the general population. Among patients treated for depression, the prevalence of SAD is even higher. The SAD sex-ratio of women to men of 3 to 1 is found repeatedly. SAD becomes rare above the age of 50. Effectiveness of phototherapy is showed in nearly all controlled studies. Bright light appears to be most effective for patients with mild SAD. Hypersomnia and hyperphagia seem to be predictors of response to bright light therapy. To enable evaluation of unspecific therapeutic factors in phototherapy a true placebo for bright light-studies is still to be found. Possible new indications for photo therapy are currently being explored. Bright light for non- seasonal depression has been tested with encouraging results; panic disorders seem to have features in common with SAD; effectiveness in bulimia has been suggested and recently sleep disorders in elderly patients have been successfully and substantially diminished.
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PMID:[Winter depression and phototherapy. The state of the art]. 952 84

Seasonal affective disorder is a pattern of major depressive episodes that occur and remit with changes in seasons. It may be seen in major depressive or bipolar disorders, as described in the Diagnostic and Statistical. Manual of Mental Disorders (DSM-IV). The most recognized form of seasonal affective disorder, "winter depression," is characterized by recurrent episodes of depression, hypersomnia, augmented appetite with carbohydrate craving, and weight gain that begin in the autumn and continue through the winter months. Physicians have many options for treating seasonal affective disorder. While questions regarding the validity of seasonal affective disorder as a syndrome and the mechanism of action of light therapy continue to be investigated, the established effectiveness of light therapy in patients with winter depression supports the usefulness of assessment for this seasonal pattern and consideration of light therapy as an option in addition to existing treatment choices.
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PMID:Seasonal affective disorders. 953 16

Mood changes synchronised to the seasons exist on a continuum between individuals, with anxiety and depression increasing during the winter months. An extreme form of seasonality is manifested as the clinical syndrome of seasonal affective disorder (SAD) with carbohydrate craving, hypersomnia, lethargy, and changes in circadian rhythms also evident. It has been suggested that seasonality and the symptoms of SAD may be due to changing levels of vitamin D3, the hormone of sunlight, leading to changes in brain serotonin. Forty-four healthy subjects were given 400 IU, 800 IU, or no vitamin D3 for 5 days during late winter in a random double-blind study. Results on a self-report measure showed that vitamin D3 significantly enhanced positive affect and there was some evidence of a reduction in negative affect. Results are discussed in terms of their implications for seasonality, SAD, serotonin, food preference, sleep, and circadian rhythms.
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PMID:Vitamin D3 enhances mood in healthy subjects during winter. 953 54

Sleep disturbances are an integral feature of depressive disorders. Like the disorders themselves, the sleep disturbances associated with depression are heterogeneous, ranging from hypersomnia to marked difficulties maintaining sleep. These difficulties are to some extent age dependent and reflect abnormalities of central nervous system arousal. Moreover, the sleep disturbances associated with depression have both reversible, or state-dependent, and more persistent trait-like characteristics. Polysomnographic recordings can be used to document sleep maintenance difficulties, and they often also reveal reduced slow wave sleep, an early onset of the first episode of rapid eye movement (REM) sleep, and increased phasic REM sleep. A deficit of serotonergic neurotransmission, a relative increase in pontine cholinergic activity, and, perhaps, an excess of noradrenergic and corticotropin-releasing hormone activity have been implicated in the pathogenesis of the sleep disturbances of more severe depressive disorders. Antidepressant medications have class- and compound-specific effects on polysomnographic profiles. Unlike other antidepressants, bupropion may increase or intensify REM sleep. While no single effect of antidepressants on sleep neurophysiology is necessary or sufficient for treatment efficacy, differences in drug effects may provide important clues to selection of specific medications for particular patients.
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PMID:Depression, sleep, and antidepressants. 955 22

The study was designed to test the efficacy of desipramine in adolescents with major depression (MDD). In addition, we assessed the presence of atypical features of MDD, consisting of mood reactivity and two of four associated features (rejection sensitivity, hyperphagia, hypersomnia, and leaden paralysis). Patients were randomized to desipramine (DMI) or placebo for 6 weeks, provided they failed to improve (e.g., meeting MDD criteria and a Hamilton Depression Scale score > or = 18) after 2 weeks on single blind placebo. Of 94 adolescents (ages 13-18) who were diagnosed as having MDD, 64 entered the study and 62 received placebo for 2 weeks. Of these, 45 were randomized to DMI or placebo. Completed analyses did not reveal significant improvement for the active treatment compared to the placebo. A large proportion of adolescents responded to placebo (50%), suggesting the need for very large samples to detect differential treatment efficacy, should it exist. A relatively high rate of atypical depression was observed (47% in the 64 patients entered). In view of the demonstrated specificity of monoamine oxidase inhibitor efficacy in adults with atypical features of MDD, this clinical subtype may have relevance to future investigation of therapeutic interventions in adolescent MDD.
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PMID:Adolescent depression: controlled desipramine treatment and atypical features. 959 29

This paper reviews recent literature which suggests that sleep disturbance in members of the general population, whether or not they have ever had a formal psychiatric disorder, is a risk factor for the onset of a formal psychiatric diagnosis at a later time. Based upon the current literature, the strongest link is between subjective insomnia, lasting at least 2 weeks, and the later onset of depression. Less well-established data suggest that lifetime reports of at least 2 weeks of insomnia, hypersomnia, or both hypersomnia and insomnia, are risk factors for the later development of depression, anxiety disorders or substance abuse. More tentatively, preliminary data suggest that increasing subjective sleep disturbance may signal a relapse in remitted depressed patients. Sleep disturbances are common manifestations of major depressive and anxiety disorders. Therefore, sleep complaints may be among the most robust prodromal symptoms reflecting partial depressive or anxiety disorders, which eventually declare themselves as full-blown clinical episodes.
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PMID:Are sleep disturbances risk factors for anxiety, depressive and addictive disorders? 977 46

This study aimed to determine symptom patterns in patients with chronic fatigue syndrome (CFS), in summer and winter. Comparison data for patients with seasonal affective disorder (SAD) were used to evaluate seasonal variation in mood and behavior, atypical neurovegetative symptoms characteristic of SAD, and somatic symptoms characteristic of CFS. Rating scale questionnaires were mailed to patients previously diagnosed with CFS. Instruments included the Personal Inventory for Depression and SAD (PIDS) and the Systematic Assessment for Treatment Emergent Effects (SAFTEE), which catalogs the current severity of a wide range of somatic, behavioral, and affective symptoms. Data sets from 110 CFS patients matched across seasons were entered into the analysis. Symptoms that conform with the Centers for Disease Control and Prevention (CDC) case definition of CFS were rated as moderate to very severe during the winter months by varying proportions of patients (from 43% for lymph node pain or enlargement, to 79% for muscle, joint, or bone pain). Fatigue was reported by 92%. Prominent affective symptoms included irritability (55%), depressed mood (52%), and anxiety (51%). Retrospective monthly ratings of mood, social activity, energy, sleep duration, amount eaten, and weight change showed a coherent pattern of winter worsening. Of patients with consistent summer and winter ratings (n = 73), 37% showed high global seasonality scores (GSS) > or = 10. About half this group reported symptoms indicative of major depressive disorder, which was strongly associated with high seasonality. Hierarchical cluster analysis of wintertime symptoms revealed 2 distinct clinical profiles among CFS patients: (a) those with high seasonality, for whom depressed mood clustered with atypical neurovegetative symptoms of hypersomnia and hyperphagia, as is seen in SAD; and (b) those with low seasonality, who showed a primary clustering of classic CFS symptoms (fatigue, aches, cognitive disturbance), with depressed mood most closely associated with irritability, insomnia, and anxiety. It appears that a subgroup of patients with CFS shows seasonal variation in symptoms resembling those of SAD, with winter exacerbation. Light therapy may provide patients with CFS an effective treatment alternative or adjunct to antidepressant drugs.
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PMID:Chronic fatigue syndrome and seasonal affective disorder: comorbidity, diagnostic overlap, and implications for treatment. 979 Apr 93


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