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

Sleep disturbances in psychoses can mean hypo- as well as hypersomnia. In 90% of endogenous depressed patients sleep disturbances were seen, mostly as hyposomnia. In the group of schizophrenic psychotic patients only 30% had sleep disturbances. With polygraphical investigations in endogenous depressed patients a shortening of REM-latency and a disturbed sleep profile, in schizophrenic psychoses a shortened REM-rebound and a reduced amount of stages 3 and 4 were found. The treatment of choice for depressions are antidepressive drugs and sleep deprivation, for schizophrenic psychoses neuroleptic drugs. This treatments improved subjective and objective sleep disturbances with psychopathological remission at the same time. So far, only hypothetical considerations do exist about the relationship between psychopathology and sleep disturbances. It is suspected that etiological relations exist between depression and desynchronization of central sleep mechanisms and between schizophrenia and special disturbances of REM-sleep and stage 3 and 4.
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PMID:[Sleep problems and their treatment in psychosis (author's transl)]. 4 23

Sleep is affected in depression; insomnia is common, sleep of normal duration and hypersomnia less common. All-night studies have shown changes of the two types of sleep. Deep non-REM sleep is abolished during the course of the illness and sometimes also after remission. Paradoxical sleep, which may be reduced or increased in duration, starts sooner after the onset of sleep. According to Kupfler, ease of production of that sleep is specific to primary depression, unipolar or bipolar. A possible relationship between paradoxical sleep and certain types of depression is suggested by the fact that the tricyclic and MAOI antidepressant drugs and lithium reduce or suppress that sleep. Finally, deprivation of paradoxical sleep by repeated waking during the night has been put forward as a form of treatment. Despite the heterogeneous nature of depression, findings at present which show paradoxical sleep pressure provide a pathophysiological basis for the biological problems posed.
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PMID:[Depression and sleep (author's transl)]. 4 63

The authors studied the occurrence of depression in 100 randomly selected patients with narcolepsy and in 30 patients with hypersomnia. In the isolated form of idiopathic narcolepsy (without signs of cataplexy, sleep paralysis or hypnagogic hallucinations) depression occurred 28.6 per cent of cases. In idiopathic narcolepsy with cataplexy or other symptoms of sleep dissociation, depression was found in 17.2 per cent of cases. In idiopathic hypersomnia the occurrence of depression was 26.1 per cent. In the majority of cases the endogenous form of depression was observed. In the symptomatic form of narcolepsy and hypersomnia the occurence of depression has not been noted in any case. In most cases a parallel clincial course has been observed between the manifestation of depression and narcolepsy or hypersomnia. During a remission of the depressive state the hypersomniac symptoms decreased or disappeared totally. The authors furter discuss the possible pathophysiological mechanisms of the above mentioned symptoms. They are of the opinion that an important role is played by the secretion and metabolism of the cerebral monamines.
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PMID:Depresssion in narcolepsy and hypersommia. 16 33

Very few epidemiological surveys have specifically studied relationships between sleep disturbances and psychiatric diseases. In this review, we preferred to use the classification proposed in 1979 by the Association of Sleep Disorders Centers. It includes four main categories: insomnias, excessive sleepiness, troubles of the wake/sleep schedule and parasomnias. Evaluating psychiatric disorders among general populations is easier owing to DSM III and DSM III-R criteria, but there are not equivalent criteria in evaluating sleep disorders. It is almost impossible to realize polysomnographic recordings in large samples, therefore sleep disorders are to be detected by questionnaires. It has been shown that there is a good correlation between self-reports and polysomnographic recordings among clinical and general samples. The prevalence of insomnia, defined as difficulties of initiating and maintaining sleep, is estimated between 9 and 31%. It is higher among women, elderly people, separated and divorced subjects, and low educational levels' groups. It has to be noticed that polysomnographic records of some subjective insomniacs are not different from those of good sleepers, sleep latency excepted. These subjective (and not objective) insomniacs have high scores in anxiety scale, depression scale, or psychologic distress. Insomnia is more frequently noted amongst subjects with psychiatric diagnoses, especially major depressive disorders and anxiety disorders. Depressive disorders are present in 21-40% of insomniacs versus 0-1% of non-insomniacs, and anxiety disorders in 13-24% of insomniacs versus 3-10% of non-insomniacs. In depressive disorders, sleep alterations are frequently noted: they are difficulties of initiating and maintaining sleep, decreasing proportion of slow-wave sleep, decreasing time of REM (rapid eye movement) sleep and REM sleep latency, and increasing density of REM sleep. Of these modifications, the last two ones seem to be specific for depression. The relationships between sleep, aging and depression are more complex than previously noted. For example, differences between depressed and non-depressed subjects depend on the age of the population. The prevalence of hypersomnia is lower than the insomnia's. It varies between 2 and 4%. It is more frequently noted among young people, and never married subjects. Two specific aetiologies must be looked for: sleep apnea syndrome and narcolepsy. These diagnoses are respectively found in 45% and 24% of hypersomniacs examined in American Sleep Centers. Hypersomnias are objectived by the Multiple Sleep Latency Test, which measures the physiologic sleep tendency.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Sleep disorders in psychiatric diseases. Epidemiological aspects]. 129 83

The existence of depression in young individuals has often been denied or at least underestimated particularly during adolescence, to the benefit of such other concepts as morosity, inherent in this period of life, and from which depression should be differentiated. Recent epidemiological investigations in the general population have revealed an approximate 2% and 10% prevalence of depression in the child and the adolescent, respectively. This considerable increase in morbidity is associated with a modification of the sex ratio: more boys are affected before puberty, more girls after puberty. In the present work we shall first deal with the semiology and comorbidity of depression as related with the developmental changes occurring in the child and the adolescent. Thus, several studies have shown that the DSM III criteria for affective disorders are consistently applicable to pre-puberty children and adolescents as well. However, depression in the pre-puberty children may be more ostentatious, manifesting itself by psychomotor agitation, somatic complaints and anxiety comorbidity of the type: Separation Anxiety Disorder and phobias. Depressed adolescents may exhibit more anhedonia, more depressive cognition, hypersomnia, weight variations, more alcohol or drug abuse and suicide attempts, and, in one third of them, greater coexistence of anxiety disorders or behavioural disorders. The course of depression at this age is now known, owing to catamnestic studies that proved methodologically satisfactory (we personally managed the follow-up of 75 depressed adolescents over an average 45 months). Depression in the child and the adolescent is not a benign affection, it is a long-lived, recurrent and disabling illness.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Time and depression in children and adolescents]. 130 45

Various classes of antidepressant drugs with distinct pharmacologic actions are differentially effective in the treatment of classic melancholic depression--characterized by pathological hyperarousal and atypical depression--associated with lethargy, hypersomnia, and hyperphagia. All antidepressant agents exert their therapeutic efficacy only after prolonged administration. In situ hybridization histochemistry was used to examine in rats the effects of short-term (2 weeks) and long-term (8 weeks) administration of 3 different classes of activating antidepressant drugs which tend to be preferentially effective in treating atypical depressions, on the expression of central nervous system genes thought to be dysregulated in major depression. Daily administration (5 mg/kg, i.p.) of the selective 5-hydroxytryptophan (5-HT) reuptake inhibitor fluoxetine, the selective alpha 2-adrenergic receptor antagonist idazoxan, and the nonspecific monoamine oxidase A and B inhibitor phenelzine increased tyrosine hydroxylase mRNA levels by 70-150% in the locus coeruleus after 2 weeks of drug and by 71-115% after 8 weeks. The 3 drugs decreased corticotropin-releasing hormone mRNA levels by 30-48% in the paraventricular nucleus of the hypothalamus. The decreases occurred at 8 weeks but not at 2 weeks. No consistent change in steroid hormone receptor mRNA levels was seen in the hippocampus with the 3 drugs, but fluoxetine and idazoxan increased the level of mineralocorticoid receptor (MR) and glucocorticoid receptor (GR) mRNA, respectively, after 8 weeks of drug administration. Proopiomelanocortin (POMC) mRNA levels in the anterior pituitary and plasma adrenocorticotropic-hormone (ACTH) levels were not altered after 2 or 8 weeks of drug treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The antidepressants fluoxetine, idazoxan and phenelzine alter corticotropin-releasing hormone and tyrosine hydroxylase mRNA levels in rat brain: therapeutic implications. 135 83

Seasonal affective disorder is characterized by recurrent winter depression associated with hypersomnia, overeating, and carbohydrate craving. The severe form of winter depression affects about 5% of the general population and is believed to be caused by light deficiency. About 70%-80% of patients with winter depression experience attenuation of symptoms when exposed to bright light therapy. Hypotheses pertaining to the pathogenesis of winter depression implicate the effects of light on different characteristics of circadian rhythms. One of the environmental factors which may be implicated, in addition to light, in the pathophysiology of winter depression is the geomagnetic field. There is strong indication that the pineal gland is a magnetosensitive system and that changes in the ambient magnetic field alter melatonin secretion and synchronize the circadian rhythms. In man, shielding of the ambient magnetic field significantly desynchronizes circadian rhythms which could be gradually resynchronized after application of magnetic fields. The strength of the environmental magnetic field diminishes during the winter months, leading to increased susceptibility for desynchronization of circadian rhythms. Thus, since the acute application of magnetic fields in experimental animals resembles that of acute exposure to light with respect to melatonin secretion (i.e., suppression of melatonin secretion), magnetic treatment might be beneficial for patients with winter depression. In addition, since the environmental light and magnetic fields, which undergo diurnal and seasonal variations, influence the activity of the pineal gland, we propose that a synergistic effect of light and magnetic therapy in patients with winter depression would be more physiological and, therefore, superior to phototherapy alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Magnetic fields and seasonality of affective illness: implications for therapy. 136 47

From 9 centres 293 patients took part in the WHO-collaborative study on Dexamethasone-Suppression-Test (DST) in depression to examine the relationship of psychopathological and psychiatric history information to cortisol-levels and suppression/non-suppression status. Differences between the centres were large and significant on nearly all of the measures. The predictor analyses generally suffered from numerically weak correlations with many variables correlating to sex and age. Therefore analyses of the data were adjusted for centre-, sex-, and age-influences. The best predicting features of cortisol were 'fitful, restless sleep', 'change of bodyweight' and 'affective disorders in blood relatives'. The last 2 items together with 'hypersomnia' and 'ideas of insufficiency' were the best predictors of suppression/nonsuppression status. However, statistical evidence did not seem to be strong enough to describe a typical symptom profile of a depressive cortisol suppressor or nonsuppressor.
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PMID:Clinical correlates of response to DST. The Dexamethasone Suppression test in depression: a World Health Organisation collaborative study. 143 Jun 64

We used three rating scales to study diurnal variation of mood in 37 patients with major depressive disorder (17 drug-free patients and 20 treatment refractory patients on stable regimens of antidepressant medication). The three rating scales included global self-ratings administered twice a day; an itemized, prospective, observer-rated scale administered twice a day; and the retrospective item on the Hamilton Depression Rating Scale. Z scores and Intraclass Correlation Coefficients demonstrated a poor level of agreement between the itemized, prospective scale and the self-ratings. In addition, stepwise multiple regression analysis and point bi-serial correlation showed no systematic relationship between atypical diurnal variation (i.e., mood worsening in the evening) and atypical depressive symptoms (weight gain, hypersomnia, etc.), or between typical diurnal variation (i.e., mood worsening in the morning) and typical depressive symptoms (weight loss, insomnia, etc.). This lack of relationship was observed in both drug-free and medicated patients using each of the three rating scales. We discuss possible explanations for these negative findings.
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PMID:Diurnal variation: reliability of measurement and relationship to typical and atypical symptoms of depression. 146 Jan 70

At least three categories of atypical depression have been described. The hysteroid dysphoria is characterized by repeated episodes of depressed mood in response to feeling rejected, and a craving for sweets and chocolate. Two other issues are characterized by a cyclical occurrence of changes of mood and appetite, i.e., the late luteal phase dysphoric disorder (DSM-III-R, appendix), or "the premenstrual syndrome" (PMS), and the major depression with seasonal pattern (DSM-III-R), or seasonal affective disorder (SAD). The reactive mood changes are frequently accompanied by features as hypersomnia, lethargy and increased appetite, particularly with a preference for carbohydrates. Central serotonin pathways participate in the regulation of mood and behavioural impulsivity, and modulate eating patterns qualitatively and quantitatively. Depressives with PMS og SAD benefit, in general, from treatments with serotonin potentiating drugs, suggesting that brain serotonin plays a role in the pathophysiology. Ingestion of carbohydrates increases the plasma ratio of tryptophan to other large neutral amino acids in man and animal, and the serotonin synthesis in the rat brain. Based on these findings it has been suggested that the excessive carbohydrate intake by patients with PMS and SAD reflects a self-medication that temporarily relieves the vegetative symptoms via an increased central serotonergic activity.
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PMID:Serotonin, carbohydrates, and atypical depression. 148 May 61


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