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)

Similar symptomatology has been described for both seasonal affective disorder (SAD) and atypical depression. For example, hyperphagia, hypersomnia, and intense lethargy are common to both, suggesting that they might be subtypes of the same disorder. If SAD and atypical depression are different manifestations of the same underlying pathophysiology, treatment effective for one might also benefit the other. Bright artificial lights (2500 lux, 6-8 a.m. and p.m.) were significantly less effective in treating eight patients diagnosed as having atypical depression without a seasonal pattern than 25 SAD patients. Differential treatment outcome suggests that SAD and atypical depression are separate disorders.
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PMID:Is seasonal affective disorder a variant of atypical depression? Differential response to light therapy. 224 88

Winter depression, a form of seasonal affective disorder, is a common condition that increases in prevalence in northern areas and in regions with a high proportion of overcast fall and winter days. Parts of Ohio are high-risk areas given the high percentage of overcast days. Winter depression is marked by the onset of recurrent episodes of major depression each fall or winter which spontaneously remit in the spring. The depressive syndrome is often characterized by sadness, anxiety, decreased involvement in work and social activities, increased appetite, carbohydrate craving, weight gain, hypersomnia and psychomotor retardation. This syndrome often responds to treatment with two to six hours per day of full-spectrum bright artificial light. The efficacy of drugs in the treatment of this condition is now being studied at The Ohio State University. A monoamine oxidase inhibitor is effective.
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PMID:The naturally occurring rhythm of blues: winter depression. 240 29

Symptoms of so-called atypical depression, such as hypersomnia and lethargy, may accompany specific sleep disorders. It is often difficult to determine which disorder is "primary". The authors examine three cases of depression with atypical features associated with specific sleep disorders and report a favorable response to valproate. Some clinical features of the cases suggest a primary sleep disorder with secondary affective symptoms. However, valproate may have direct mood-altering effects as well as effects on sleep physiology. The implications of these findings for diagnosis and treatment are discussed.
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PMID:Sleep disorders and depression with atypical features: response to valproate. 250 91

Depressed inpatients have a DST non-suppression rate that is several times greater than that of depressed outpatients. To explore what clinical features of depression might explain this difference, 25 depressed inpatients who were DST non-suppressors were compared with 16 DST suppressors, using 70 clinical variables. Those variables that were different between these two groups of inpatients were then used to compare depressed inpatients and outpatients. Three variables that were significantly associated with DST status in depressed inpatients were also found to differentiate between depressed inpatients and depressed outpatients. DST suppression was associated with a family history of alcoholism, with the symptom hypersomnia, and with a younger age at index interview.
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PMID:Is DST status associated with depression characteristics? 252 15

Bright white light (500lx) for 4 h/day was applied to seven narcoleptic patients (age 47-65 years, mean 55 years). The effects of the light on the disturbed sleep-wake cycle in narcoleptics were investigated by the measurement of the following parameters: (1) excessive daytime sleepiness and sustained attention (multiple sleep latency test); (2) rest-activity cycles; (3) self-ratings (mood, anxiety, tiredness); (4) urinary cycles of 6-OH melatonin sulphate and cortisol; (5) sleep EEG. Treatment with bright light showed neither objective nor subjective changes in the clinical symptoms of narcolepsy. While similar "dosage" light applications can phase shift human circadian rhythms and improve depression and hypersomnia in winter depression, it is not an appropriate treatment for narcolepsy.
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PMID:Bright white light does not improve narcoleptic symptoms. 275 54

Morning plasma cortisol response to the 1 mg dexamethasone suppression test along with cortisol levels in blood, cerebrospinal fluid (CSF), and urine were measured in hospitalized male and female patients with primary major depressive disorder who reported hypersomnia (n = 23), or increase in appetite (n = 22). Comparisons were drawn to cortisol levels in patients with primary major depressive disorder who did not report hypersomnia or appetite increase (n = 23) and to normal controls (n = 23), all age- and sex-matched. Depressives with hypersomnia or increased appetite showed higher than normal 24-h urinary free cortisol concentrations. Depressed patients without hypersomnia or appetite increase had in addition to elevated free urinary cortisol concentrations higher than normal morning plasma cortisol levels before and after dexamethasone administration and a higher incidence of cortisol non-suppression after dexamethasone compared to normal subjects. The findings provide preliminary evidence that HPA activation in depression is diminished in the presence of hypersomnia and/or an increased appetite. Studies of the hypothalamic-pituitary-adrenal axis may be useful for differentiating subtypes of depression characterized by hypersomnia or enhanced appetite.
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PMID:Cortisol measures in primary major depressive disorder with hypersomnia or appetite increase. 297 83

Seasonal affective disorders are mood disturbances that occur with a change in season. The most common form is winter depression, marked by sadness, anxiety, decreased physical activity, increased appetite, carbohydrate craving, weight gain, hypersomnia, decreased libido, worsening of premenstrual symptoms, impaired work performance and interpersonal conflict. This syndrome often responds to daily exposure to bright artificial light.
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PMID:Seasonal depression. 305 74

The utility of bipolar type II affective disorder subgrouping is discussed. There is low diagnostic agreement among clinicians for this putative condition. However, the clustering of cases in families and the poor response to standard treatments suggest that it is a distinct subgroup. The clinical features of the depressive phase of this condition including chronicity, intermittency, hyperphagia, hypersomnia, and reactivity relate it to the constructs of "hysteroid dysphoria," atypical depression, and seasonal affective disorder. Its association to several abnormal motivated behaviors such as alcoholism and eating disorders allows the speculation that a distinct morbid mechanism involving serotonin may underlie it and that new serotonin reuptake blocking drugs may be useful in treating it. Finally, the genetic identity of this subgroup in all likelihood will be established or rejected by genetic linkage studies utilizing the restriction fragment length polymorphism map of the genome.
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PMID:Therapeutic and genetic prospects of an atypical affective disorder. 332 66

Besides sleep apnea, the main disorders of excessive daytime sleepiness include narcolepsy and hypersomnia. Narcolepsy is characterized by periods of irresistible sleepiness and sleep attacks of brief duration and, most often, by one or more of the auxiliary symptoms: cataplexy, sleep paralysis, and hypnogogic hallucinations. Generally, sleepiness and sleep attacks in hypersomnia are of longer duration and are more resistible than in narcolepsy; also, the auxiliary symptoms are absent. There are three types of hypersomnia: idiopathic, secondary, and periodic. Nocturnal sleep is typically disrupted in narcolepsy, whereas in idiopathic hypersomnia it is prolonged and in secondary hypersomnia it is variable. The exact causes of narcolepsy and idiopathic hypersomnia are unknown; however, there is evidence for genetic predisposition for either disorder. In secondary hypersomnia causative factors include: neurologic, such as head injuries, cerebrovascular insufficiency, and brain tumors; general medical, such as metabolic disorders, various intoxications, and conditions leading to brain hypoxia; and psychiatric, most notably depression. Although the cause of periodic hypersomnia is unclear, most research supports the notion of underlying organic disease. Often, the evaluation of patients with excessive daytime sleepiness can be completed in the office setting, based on the sleep history and a thorough neurologic, general medical, and psychiatric assessment. Whenever indicated, ancillary laboratory studies, such as computed tomography and magnetic resonance scans, should be performed. Sleep laboratory recordings generally are not necessary unless there is suspicion of sleep apnea or narcolepsy in the absence of auxiliary symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Disorders of excessive sleepiness: narcolepsy and hypersomnia. 333 60

Recurrent episodes of depression accompanied by mild hypersomnia after each respiratory tract infection in an adolescent girl, 10 years old at the first onset, are described. Each episode lasted about 1 week, and she had 11 such episodes up to the age of 14 years, when lithium was prescribed. While on lithium, she suffered three times from febrile and once from afebrile upper respiratory tract infection, but these episodes were not followed by depression or hypersomnia.
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PMID:Depression after each respiratory tract infection in an adolescent girl. 341 32


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