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)

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

The Kleine-Levin syndrome is a rare and probably underdiagnosed syndrome. It is characterized by periodic attacks of the triad: hypersomnia, vegative disturbances such as hyperphagia and hypersexuality, psychopathological changes in the level of consciousness and control of emotions. Boys and young men in the age group 10-20 years are most commonly affected. Spontaneous remission with a tendency to remission is observed and the disease "burns out" after a prolonged period of years. The etiology and pathogenesis are unknown. Theories have been propounded suggesting dysfunction of the hypothalamus. No pathognomonic findings have been observed in the early phase of sleep during the daylight hours. Central stimulating drugs have been reported to have some effect on the hypersomnia. The diagnosis is based on the clinical picture. Frequently, a long period can elapse before the diagnosis is established and some cases are never diagnosed. The literature is reviewed and is illustrated by two case reports.
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PMID:[Kleine-Levin syndrome]. 146 86

Seasonal Affective Disorder (SAD) has received formal research attention only within the last eight years. Diagnostic criteria for SAD include many characteristics typical of depression: sadness, low self-esteem, lack of energy, social withdrawal, and suicide ideation, and features of atypical depression: carbohydrate craving, overeating, weight gain, and hypersomnia. Differential diagnosis of the disorder depends on an onset in fall/winter and remission in spring/summer. It was hypothesized that spinal cord injury (SCI) patients would have a higher incidence of the disorder in the northern latitudes because of decreased outdoor activities in winter and because of such light-depriving winter survival tactics as installing opaque plastic for storm windows. SCI patient responded to a postal survey which included Rosenthal's Seasonal Pattern Assessment Questionnaire (SPAQ) and the Beck Depression Inventory (BDI). Results showed a substantially higher rate of SAD among SCI patients than in the normative sample.
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PMID:Seasonal affective disorder in a spinal cord injury population. 158 5

CRH has been shown to produce increased locomotion, arousal, and anorexia in experimental animals. A deficiency of CRH in patients with seasonal affective disorder could contribute to the characteristic lethargy, hypersomnia, and hyperphagia characteristic of this illness. To test this hypothesis, we studied basal plasma ACTH and cortisol levels and their responses to ovine CRH in controls and depressed patients with seasonal affective disorder before and after light treatment. Untreated seasonal affective disorder patients showed normal basal plasma cortisol and ACTH levels, but their responses to CRH tended to be delayed and were significantly reduced. When patients were studied after 9 days of light treatment, a significant increase in plasma ACTH and cortisol responses to CRH was observed. Our findings in untreated patients with seasonal affective disorder are similar to those in patients with Cushing's disease 2 weeks after transsphenoidal hypophysectomy, who uniformly show sustained suppression of their CRH neuron because of long-standing hypercortisolism. This findings suggest that the CRH neuron of patients with seasonal affective disorder is hypofunctional. We postulate that the clinical symptomatology in patients with seasonal affective disorder could reflect deficient activity of this important arousal-producing system.
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PMID:Abnormal pituitary-adrenal responses to corticotropin-releasing hormone in patients with seasonal affective disorder: clinical and pathophysiological implications. 185 Nov 85

This article presents a literature review and description of seasonal affective disorder (SAD). SAD is a newly recognized disorder, differentiated from other affective illnesses by its seasonality (with midwinter dysthymia and spring/summer remission), and its atypical symptoms of hypersomnia and hyperphagia. SAD symptoms remit with travel towards the equator or with bright light treatments, possibly indicating a chronobiological circadian etiology. This article introduces aspects of SAD that are amenable to the nursing process, including assessment of the seasonality of dysthymic symptoms; diagnoses of patient responses; referral, education, and psychotherapeutic interventions; and evaluation of patient responses to interventions. Since SAD is found predominantly in young women, and because symptoms may be exacerbated by rotating shifts, it is possible that nurses may have a higher incidence of SAD, compared with other professions.
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PMID:Seasonal affective disorder, the depression of winter: a literature review and description from a nursing perspective. 219 52

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

Sixty patients who met Research Diagnostic Criteria for major, intermittent, or minor depressive disorder and had reactive mood without atypical symptoms were treated with imipramine hydrochloride, phenelzine sulfate, or a placebo. These patients, referred to as simple mood reactive depressives, were contrasted with previously published data from 180 atypical depressives. Atypical depressives had the presence of at least one vegetative atypical sign (hypersomnia, hyperphagia, leaden feeling, or rejection sensitivity) but were otherwise indistinguishable from simple mood reactive depressives. In contrast to the atypical depressives for whom phenelzine was effective and imipramine was relatively ineffective, both medications were equivalently good in simple mood reactive depressives. Since all groups did poorly when given a placebo and well when given phenelzine, the salient feature of atypical symptoms may be that they predict poor response to imipramine. Since the difference between imipramine and placebo depends on the diagnostic group, pharmacologic dissection suggests that atypical symptoms in patients with nonautonomous mood may delineate a qualitatively distinct subgroup.
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PMID:Phenelzine and imipramine in mood reactive depressives. Further delineation of the syndrome of atypical depression. 267 30

Dysthymic disorder, a chronic disturbance of mood, manifests as depressed mood for most of the day, more days than not, for at least two years. In children, dysthymia may present as irritable mood, and a duration of symptoms of only one year is required to make the diagnosis. By definition, there is no history of a major depressive disorder. Associated symptoms include poor appetite or overeating, insomnia or hypersomnia, poor concentration or difficulty making decisions, low energy, low self-esteem and feelings of hopelessness. Because of the chronic nature of this disorder, treatment requires an understanding approach and continuity of care.
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PMID:Recognition and management of dysthymic disorder. 267 13

A Chinese man with Kleine-Levin syndrome showed evidence of hypothalamic disturbance and damage to the limbic system. He has been free from symptoms of hypersomnia and hyperphagia for 15 years, but now suffers from ejaculatory impotence which is discussed in the light of aetiological theories of this puzzling disorder.
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PMID:Kleine-Levin syndrome 15 years later. 280 55


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