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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

Adults have an intrinsic body clock which regulates a complex series of rhythms including sleep and wakefulness, fatigue and cognitive ability. This endogenous clock naturally runs more slowly than the solar day and is entrained to a 24-h rhythm primarily by the alternation of light and darkness. Jet lag, shift-work sleep disorder, and some of the chronic insomnias are caused by a temporal discrepancy of the body clock relative to the surrounding environment and social network. The underlying mechanisms and general management are described. Both bright light and melatonin therapy have potential in the management of these disorders. Traditionally, bright light therapy has been used to alleviate the depression associated with seasonal affective disorder. Melatonin has received much ill-formed publicity, it being claimed that it is a panacea and an 'antiageing' treatment. Both of these treatment approaches are reviewed.
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PMID:Disorders of the sleep-wake cycle in adults. 964 Apr 37

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

Seasonal affective disorder (SAD) is characterized by annual major depressive episodes. It occurs most commonly in young women during autumn and winter with full remission during the following spring. The patient's mood is a combination of depression and anxiety accompanied by fatigue, loss of libido, and a reduction of socialization. Most of these patients complain of atypical vegetative symptoms (e.g. hypersomnia, carbohydrate craving, and weight gain). Hypotheses on the underlying mechanisms of these behavioural disorders indicate that environmental variables, e.g. climate, latitude, light, and changes in neurotransmitter function that occur naturally with the seasons, may be important. Phototherapy is being used increasingly for the treatment of SAD. The antidepressant response is contingent on the exposure of the patients' eyes to light. The biological basis of the diverse psychological and biological changes in SAD and the underlying mechanism of action of phototherapy are still unclear and require further study.
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PMID:[Seasonal depression]. 992 Oct 42

There is some evidence that the neurotransmitter serotonin (5-hydroxytryptamine; 5-HT) may be involved in the pathogenesis of seasonal affective disorder (SAD). Short-term tryptophan (TRP) depletion was carried out in 18 drug-free remitted patients who met DSM-IV criteria for SAD. Behavioral effects were measured with the Hamilton Depression Rating Scale (HDRS) both 24 h before and 24 h after TRP depletion. Some of the patients showed behavioral responses such as lowered mood, feelings of guilt, loss of interest, agitation, loss of energy, fatigue, social withdrawal, increased appetite, and carbohydrate craving. It was the aim of our study to investigate whether the genotypes of the serotonin transporter gene were associated with symptoms of transient depressive relapse after TRP depletion. In addition, we matched the SAD patients with healthy control subjects to see if alleles and genotypes of the serotonin transporter gene were associated with SAD. High molecular weight DNA was isolated from peripheral blood leukocytes using standard methods. For the 5-HTT receptor gene, a 17-bp repetitive element of intron 2 was genotyped (variable number tandem repeat, VNTR). Alterations in HDRS scores after TRP depletion showed no significant association with alleles or genotypes of the 5-HTT gene, although heterozygotes showed a trend toward increased HDRS scores. The serotonin transporter is known to play a critical role in the termination of serotonergic neurotransmission by sodium-dependent uptake of 5-HT into the presynaptic neuron. The present study in a small group of SAD patients was unable to demonstrate that the 5-HTT gene plays a role in the pathogenesis of SAD or in short-term depressive relapse after TRP depletion.
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PMID:Behavioral effects of tryptophan depletion in seasonal affective disorder associated with the serotonin transporter gene? 1033 77

Seasonal affective disorder (SAD) is characterized by recurrent episodes of depression in the fall and winter that alternate with nondepressed periods in the spring and summer. Because some symptoms of SAD, such as decreased energy and weight gain, also occur in hypothyroidism, it is possible that individuals with SAD have a subtle decrease in thyroid function. To test this hypothesis, we studied blood levels of free thyroxine (T4) and thyroid-stimulating hormone (TSH) in SAD patients and matched controls in the winter. We found that free T4 blood levels were slightly but significantly lower in patients than in healthy volunteers. The difference between TSH levels in SAD patients and controls was not statistically significant. Future research will be needed to determine whether the difference in thyroid function between SAD patients and controls is an epiphenomenon or is related to the biological mechanisms that cause symptoms of SAD.
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PMID:Free thyroxine and thyroid-stimulating hormone levels in patients with seasonal affective disorder and matched controls. 1070 77

Mood and behavior changes that have a seasonal pattern were first called seasonal affective disorder (SAD) in 1984. SAD, which affects about 5% of Americans, is most common among reproductive-age women. Afflicted patients typically experience debilitating somatic complaints of fatigue, discomfort, lethargy and atypical depressive complaints of hypersomnia, increased appetite, carbohydrate craving, and weight gain. This article presents current issues in the clinical assessment and management of SAD.
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PMID:Diagnosing and managing seasonal affective disorder. 1097 35

The seasonal variation in thyroid function and mood was examined in 10 men and two women who spent the 1997 or 1998 austral winter at McMurdo Station, Antarctica. Serum samples of TSH, free T3 and free T4 were collected each month over a 10-month period (October-August), along with responses to the Profile of Mood States (POMS) and the Center for Epidemiologic Studies - Depression (CES-D) Scale. Both TSH and mood (a summary score created from the POMS depression, anger, fatigue and confusion subscales) exhibited a circannual pattern with peaks during the months of November and July and a trough during the months of March and April. High levels of tension-anxiety and confusion were preceded by declines in free T3 and T4. However, increases in tension-anxiety and total mood disturbance also preceded a decline in free T3 levels, suggesting a feedback of mood on T3 levels. Levels of free T4 were independently associated with preceding increases in anger scores. These results support the hypothesis that the symptoms characteristic of the winter-over syndrome is a state of relative CNS hypothyroidism. This model of seasonal variation in thyroid function and mood also has implications for an understanding of potential mechanisms underlying the association between latitude and SAD or S-SAD.
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PMID:Circannual pattern of hypothalamic-pituitary-thyroid (HPT) function and mood during extended antarctic residence. 1125 61

Atypical depression, somatoform disorder, neurasthenia and fibromyalgia seem to form a spectrum of disorders, who share a common biological basis, i.e. a reduced activity of the hypothalamus-pituitary-adrenocortical (HPA)-system. This is similar to the situation in Cushing's disease, where the central part of the hypothalamus-pituitary-adrenocortical-system is decreased by an increased feedback via increased intracerebral cortisol concentration. Cushing's disease is accompanied by features of atypical depression and of somatisation. Treatment with hypericum seems to disinhibit the hypothalamus-pituitary-adrenocortical-system in healthy subjects and patients with a depression. Furthermore it decreases intracerebral corticosteroids, possibly by increasing the expression of p-glycoprotein at the blood brain barrier. Therefore hypericum might be especially effective in patients with a symptom cluster of atypical depressive features and somatisation. Clinical studies with patients with depression with atypical features like the seasonal affective disorder (SAD) and with patients with a depressive syndrome accompanied by somatic complaints or fatigue support this view.
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PMID:[Atypical depression and related illnesses--neurobiological principles for their treatment with Hypericum extract]. 1224 86


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