Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recurring hypersomnias are described according to 3 etiological groups: 1) idiopathic - the Kleine Levin syndrome and its clinical variants - 2) organic and 3) psychiatric. The typical form of the Kleine Levin syndrome is remarkable for the association of recurring episodes of sleep, overeating and temporary mental disturbances lasting from a few hours to several days. Its diagnosis is mainly based on clinical data Laboratory investigations have so far failed to document specific features. Emphasis is laid on circumstances at onset and pathological studies which could be in favour of a viral origin. Some clinical aspects and polysomnographic features are reminiscent of endogenous depression. The treatments of hypersomniac episodes based on stimulants are often disappointing. On the other hand, the prevention of the hypersomniac episodes of the Kleine Levin syndrome with lithium carbonate has been successful in several well-documented cases as well as the prevention of the hypersomniac episodes of the menstruation related hypersomnia with ovulatory inhibitors. Organic and psychiatric forms of recurring hypersomnias are not well known. Their clinical features are described and their various possible etiologies indicated.
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PMID:[Recurrent hypersomnia]. 304 32

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

The Inventory for Depressive Symptomatology (IDS) is a new measure of depressive signs and symptoms. Both self-report and clinician-rated versions are under development. The IDS-SR (self-report) was completed by 289 patients, 285 of whom were outpatients. Unipolar major depression (n = 174), bipolar disorder (n = 44), euthymic (S/P unipolar or bipolar) depression (n = 33), and other psychiatric disorders (n = 38) were included. The IDS-SR had good internal reliability (coefficient alpha = 0.85), and significantly correlated with both the Hamilton Rating Scale for Depression (HRSD) (r = 0.67) and the Beck Depression Inventory (BDI) (r = 0.78). The clinician-rated IDS (IDS-C) was administered to 82 outpatients (75 with unipolar or bipolar disorder, 5 with other psychiatric disorders, and 2 euthymic (S/P unipolar) depressions). Coefficient alpha (0.88) suggested strong internal consistency. The IDS-C correlated highly with both the HRSD (r = 0.92) and the BDI (r = 0.61). Discriminant and factor analyses provided evidence for construct validity for both the IDS-C and IDS-SR. Both scales significantly differentiated endogenous from nonendogenous depression defined by Research Diagnostic Criteria (RDC). Factor structures for the IDS-SR revealed four factors: mood/cognition, anxiety, selected endogenous symptoms, and hyperphagia-hypersomnia. The IDS appears applicable to both inpatients and outpatients with endogenous, atypical, and nonendogenous major depression, and may have utility with dysthymics.
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PMID:The Inventory for Depressive Symptomatology (IDS): preliminary findings. 373 88

Psychopharacologist have had a longstanding interest in identifying a depressive subtype which selectively benefits from monoamine oxidase inhibitors (MAOIs). A superior rate of improvement with MAOI treatment might help delineate a depressive subgroup with pathophysiology different from other depressive syndromes. Research is described which indicates that patients with reactivity of mood, as well as two of four associated features (hypersomnia, overeating, lethargy, and rejection sensitivity), may have a preferential response to phenelzine as compared with imipramine or placebo. Preliminary data are presented to suggest that patients with reactive mood and only one associated feature may have a preferential response rate to phenelzine compared to imipramine and placebo. Data on patients with reactive mood but no associated features are insufficient at this point to draw any conclusions.
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PMID:Defining the boundaries of atypical depression. 637 82

Atypical depressions are those characterized by high levels of phobic anxiety or by reversed vegetative symptoms such as hypersomnia and hyperphagia. Patients with such depressions may present overtly for treatment. However, they may also present within other diagnostic categories such as personality disorder or somatic complaints. The comparative roles of monoamine oxidase inhibitors, heterocyclic antidepressants, and other biologic treatments for atypical depressions are discussed.
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PMID:Atypical depression. 638 59

Seasonal affective disorder (SAD) is a syndrome characterized by recurrent depressions that occur annually at the same time each year. We describe 29 patients with SAD; most of them had a bipolar affective disorder, especially bipolar II, and their depressions were generally characterized by hypersomnia, overeating, and carbohydrate craving and seemed to respond to changes in climate and latitude. Sleep recordings in nine depressed patients confirmed the presence of hypersomnia and showed increased sleep latency and reduced slow-wave (delta) sleep. Preliminary studies in 11 patients suggest that extending the photoperiod with bright artificial light has an antidepressant effect.
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PMID:Seasonal affective disorder. A description of the syndrome and preliminary findings with light therapy. 658 56

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

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

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


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