Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015674 (chronic fatigue syndrome)
 2,978 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

Several of the symptoms involved in chronic fatigue syndrome (CFS) such as fatigue, hypersomnia, hyperphagia, weight gain, and mood show seasonal variations in the general population. The aim of this study was to investigate whether patients with CFS experience seasonal fluctuations in these symptoms as well. Seasonal variation of symptoms was assessed in a group of 41 patients with CFS and 41 controls closely matched for age, gender, and city of residence. Participants were recruited across the US and were asked to complete the Seasonal Pattern Assessment Questionnaire (SPAQ) and the Profile of Mood States (POMS). CFS patients showed significantly lower scores on multiple SPAQ-derived measures as compared with controls. These included seasonal variation in energy, mood, appetite, weight, and sleep length. Patients also reported a significantly reduced sensitivity toward sunny, dry, and long days than controls. No association was noted between intensity of seasonal changes and severity of depressive symptoms. Patients with CFS exhibit an abnormally reduced seasonal variation in mood and behavior and would not be expected to benefit from light therapy.
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PMID:Lack of seasonal variation of symptoms in patients with chronic fatigue syndrome. 954 Nov 42

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

We presented three sheets of growth chart in children with chronic fatigue syndrome. The growth chart in 14-year-old boy (patient 1) showed decreased weight gain because of too much exercise. After that he complained nausea, abdominal pain, sleep disturbance and debilitating fatigue. The growth chart in 12-year-old girl (patient 2) revealed increased weight gain because of overeating due to the divorce of her parents. She developed syncope, sleep disturbance, and fatigue during overeating. The growth chart in 13-year-old girl (patient 3) showed decreased weight gain after she developed lymph node enlargement. We diagnosed her as autoimmune fatigue syndrome because of persistent positive antinuclear antibody. Although growth chart will not be able to detect childhood chronic fatigue syndrome prospectively, the chart may be useful for detecting some life events in these children.
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PMID:[Usefulness of growth chart in children and adolescents with chronic fatigue syndrome]. 1756 6

Interventions based on mindfulness have become increasingly popular. This article reviews the empirical literature on its effects on mental and physical health, discusses presumed mechanisms of action as well as its proposed neurobiological underpinning. Mindfulness is associated with increased well-being as well as reduced cognitive reactivity and behavioral avoidance. It seems to contribute to enhance immune functions, diminish inflammation, diminish the reactivity of the autonomic nervous system, increase telomerase activity, lead to higher levels of plasmatic melatonin and serotonin. It enhances the quality of life for patients suffering from chronic pain, fibromylagia and HIV infection. It facilitates adaptation to the diagnosis of cancer and diabetes. It seems to lead to symptomatic improvement in irritable bowel syndrome, chronic fatigue syndrome, hot flashes, insomnia, stress related hyperphagia. It diminishes craving in substance abuse. The proposed mechanism of action are enhanced metacognitive conscience, interoceptive exposure, experiential acceptance, self-management, attention control, memory, relaxation. Six mechanism of actions for which neurological underpinnings have been published are: attention regulation (anterior cingulate cortex), body awareness (insula, temporoparietal junction), emotion regulation (modulation of the amygdala by the lateral prefrontal cortex), cognitive re-evaluation (activation of the dorsal medial prefrontal cortex or diminished activity in prefrontal regions), exposure/extinction/reconsolidation (ventromedial prefrontal cortex, hippocampus, amygdala) and flexible self-concept (prefrontal median cortex, posterior cingulated cortex, insula, temporoparietal junction). The neurobiological effects of meditation are described. These are: (1) the deactivation of the default mode network that generates spontaneous thoughts, contributes to the maintenance of the autobiographical self and is associated with anxiety and depression; (2) the anterior cingulate cortex that underpins attention functions; (3) the anterior insula associated with the perception of visceral sensation, the detection of heartbeat and respiratory rate, and the affective response to pain; (4) the posterior cingulate cortex which helps to understand the context from which a stimulus emerges; (5) the temporoparietal junction which assumes a central role in empathy and compassion; (6) the amygdala implicated in fear responses. The article ends with a short review of the empirical basis supporting the efficacy for mindfulness based intervention and suggested directions for future research.
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PMID:[Review of the effects of mindfulness meditation on mental and physical health and its mechanisms of action]. 2471 1

Depressive syndromes are a group of heterogeneous disorders. Atypical depression (AD) with reversed vegetative signs, such as hyperphagia or hypersomnia, is traditionally neglected, demonstrated by the fact that in the most widely used depression scales, such as the Hamilton Depression Scale (HAMD), melancholic symptoms have a specific weight, while, by contrast, reversed vegetative signs are not included. However, epidemiologically and phenomenologically related disorders to AD do exist, such as somatoform disorders, neurasthenia (chronic fatigue syndrome) and fibromyalgia (FM). In this spectrum, here called the AD spectrum, instead a decrease in hypothalamus-pituitary-adrenocortical (HPA) axis activity seems to exist. This has similarities to Cushing's disease, where a suppression of central HPA system activity is accompanied by features of AD and somatization in a considerable number of patients. Opposite vegetative features might therefore be related to the opposite dysregulation of the HPA system. The psychopharmacological intervention in the AD spectrum should therefore differ from that used in typical major depression. MAO inhibitors, low-dose tricyclic antidepressants and 5-HT3 antagonists demonstrated therapeutic efficacy, but the existing studies focused on different aspects. Hypericum extracts might be an alternative pharmacological intervention, which demonstrated therapeutic efficacy in the symptom range of the spectrum.
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PMID:Atypical depression spectrum disorder - neurobiology and treatment. 2698 70

Marijuana, derived from the Cannabis sativa plant, is the most commonly abused illicit drug in the United States. Now, more than ever, due to changing regulations, marijuana is more readily available and is known to be habitually used by millions. The neuropsychiatric effects of marijuana are well-known which include chronic fatigue syndrome and polyphagia. However, marijuana is also known to exert cardiac effects, such as tachycardia, hypotension, and hypertension. Marijuana has also been described in association with atrial fibrillation, ventricular tachycardia, and cardiac arrest. However, acute coronary syndromes, such as myocardial infarction in the setting of marijuana use, is rare. Herein, we present the case of a non-ST-elevation myocardial infarction (NSTEMI) in the setting of marijuana use in a 42-year-old African American male with no significant past medical history who presented with chest pain at rest one hour after smoking marijuana.
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PMID:Cannabis-induced Acute Coronary Syndrome: A Coincidence or Not? 3172 Jan 64