Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0015674 (chronic fatigue syndrome)
 2,978 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The use of sustained release tri-iodothyronine (SR-T3) in clinical practice, has gained popularity in the complementary and alternative medical community in the treatment of chronic fatigue with a protocol (WT3) pioneered by Dr. Denis Wilson. The WT3 protocol involves the use of SR-T3 taken orally by the patient every 12 hours according to a cyclic dose schedule determined by patient response. The patient is then weaned once a body temperature of 98.6 degrees F has been maintained for 3 consecutive weeks. The symptoms associated with this protocol have been given the name Wilson's Temperature Syndrome (WTS). There have been clinical studies using T3 in patients who are euthyroid based on normal TSH values. However, this treatment has created a controversy in the conventional medical community, especially with the American Thyroid Association, because it is not based on a measured deficiency of thyroid hormone. However, just as estrogen and progesterone are prescribed to regulate menstrual cycles in patients who have normal serum hormone levels, the WT3 therapy can be used to regulate metabolism despite normal serum thyroid hormone levels. SR-T3 prescription is based exclusively on low body temperature and presentation of symptoms. Decreased T3 function exerts widespread effects throughout the body. It can decrease serotonin and growth hormone levels and increase the number of adrenal hormone receptor sites. These effects may explain some of the symptoms observed in WTS. The dysregulation of neuroendocrine function may begin to explain such symptoms as alpha intrusion into slow wave sleep, decrease in blood flow to the brain, alterations in carbohydrate metabolism, fatigue, myalgia and arthralgia, depression and cognitive dysfunction. Despite all thermoregulatory control mechanisms of the body and the complex metabolic processes involved, WT3 therapy seems a valuable tool to re-establish normal body functions. We report the results of 11 patients who underwent the WT3 protocol for the treatment of CFS. All the patients improved in the five symptoms measured. All patients increased their basal temperature. The recovery time varied from 3 weeks to 12 months.
 ...
PMID:Supraphysiological cyclic dosing of sustained release T3 in order to reset low basal body temperature. 1688 75

Syndromes characterized by pain, fatigue, mood disorder, cognitive dysfunction, and sleep disturbance have been referred to as stress-related somatic disorders by virtue of the observation that onset and exacerbation of symptoms occur with stress. These syndromes include but are not limited to fibromyalgia, chronic fatigue syndrome, temporomandibular disorder, and irritable bowel syndrome. As with most chronic illnesses, genetic susceptibility and lifetime environmental exposures play a role in creating vulnerability to disease. Cumulative lifetime stress has been associated with a number of physiologic changes in the brain and body that reflect dysregulated hormonal and autonomic activity. Exposure to the stressor of violence is likely to create a state of vulnerability for the stress-related somatic syndromes and also to contribute to symptom expression and severity. Understanding the relationship between violence, stress, and somatic syndromes will help in clarifying the consequences of violence exposure to long-term health and health-related quality of life.
 ...
PMID:Violence, stress, and somatic syndromes. 1759 47

The status of chronic fatigue syndrome (CFS) is still under debate. Mainstream views still often consider it as an undetected primary sleep disorder or as the psychosomatic expression of a related anxiety or depression syndrome. Both primary sleep disorder and CFS are often related to unrefreshing sleep and affective daytime symptoms. The present study compares nonrapid eye movement sleep distribution between patients with a primary sleep disorder and "pure" CFS patients without sleep or mood disorders. Intensity measures of affective symptoms are also analyzed. Sleep variables of 32 pure CFS (mean age, 41.9 +/- 8.7 years; 25 women), 30 Sleep Apnea Hypopnea Syndrome patients (mean age, 43.7 +/- 6.7 years; 13 women), and 14 healthy controls (mean age, 40.2 +/- 7.6 years; 9 women) were compared. Related affective symptoms were assessed using the self-reported Zung anxiety and depression scales. The study confirms previous reports on increased slow-wave sleep in CFS patients. Both patient groups showed similar sleep duration and efficiency. Sleep efficiency was lower in both patient groups compared with controls. CFS patients showed a higher microarousal index than controls. Anxiety, but not depression symptoms were more intense in the CFS group. The distribution of nonrapid eye movement sleep in CFS differs sizeably from what can be observed in a primary sleep disorder.
 ...
PMID:High slow-wave sleep and low-light sleep: chronic fatigue syndrome is not likely to be a primary sleep disorder. 1942 87

The last ten years have seen a growing interest in clinical scenarios, where a short QT interval may play a role, especially because of an increased risk of sudden cardiac death in some situations. One such entity is Short QT Syndrome, which has emerged as a rare, but very malignant disease, in particular when the QT interval is very short. A short QT interval has also been noticed in some patients with other arrhythmic syndromes such as Idiopathic Ventricular Fibrillation, Brugade Syndrome and Early Repolarization Syndrome, but the role of a short QT interval in these settings is so far not known. Hypercalcemia often leads to shortening of the QT interval, but there are no data in humans to suggest an increased risk of sudden cardiac death in this setting. In addition, a shorter-than-usual QT interval has been reported in patients with Chronic Fatigue Syndrome and in response to atropine, catecholamine and Hyperthermia. When a short QT interval is encountered in daily clinical practice, these various scenarios needs to be considered, but it is still not possible to come up with clear guidelines for how to work up and risk stratify such individuals. Genetic testing is only useful in very few and the value of an electrophysiologic study, Holter monitoring or stress testing to assess QT adaptation to heart rate and T wave morphology analysis may all be helpful, but not well-established, tests in this setting.
 ...
PMID:Short QT interval in clinical practice. 2066 44

Chronic Fatigue Syndrome (CFS), also referred to as Myalgic Encephalomyelitis (ME), is a disease of unknown origin. It is classified as Post Viral Fatigue Syndrome (PVFS) in the WHO International Classification of Diseases (ICD) and listed as sub-category at G93.3 under chapter G93, other disorders of the brain. ME/CFS is primarily an endemic disorder but occurs in both epidemic and sporadic forms. It affects all racial-ethnic groups and is seen in all socioeconomic strata. A diagnosis of CFS is a diagnosis of exclusion, meaning other medical conditions, including psychiatric disorders, must be first ruled out. CFS is diagnosed if there is no other explanation for the fatigue and if the other symptoms did not develop before the fatigue. The estimated worldwide prevalence of CFS is 0.4?1 percent. The disease predominantly affects young adults, with a peak age of onset of between 20 and 40 years, and women, with a female to male ratio of 6:1. Mean illness duration ranges from 3 to 9 years. The patho-physiological mechanism of CFS is unclear but the immunological pattern of CFS patients gleaned from various studies indicates that the immune system is chronically activated. Besides the role of environmental insults (xenobiotics, infectious agents, stress) the genetic features of patients are studied to evaluate their role in triggering the pathology. At present there are no specific pharmacological therapies to treat the disease but a variety of therapeutic approaches have been described as benefiting patients. Treatment programs are directed at relief of symptoms, with the goal of the patient regaining some level of preexisting function and well-being.
 ...
PMID:Chronic fatigue syndrome/myalgic encephalomyelitis: an update. 2124 47

We report here on a case of severe pervasive refusal syndrome. This is of interest for three reasons. Firstly, most reported cases are adolescent girls; our case is regarding an adolescent boy. Secondly, he was successfully treated at home and thirdly, the serology showed an apparent infective pre-cursor to the illness with evidence of possible autoimmune serology. A 14-year old boy deteriorated from a picture where diagnosed CFS/ME developed into Pervasive Refusal Syndrome. This included the inability to move or speak, with closed eyes, multiple tics, facial grimacing, heightened sensitivity to noise (hyperacusis) and touch (hyperaesthesia), and inability or unwillingness to eat anything except small amounts of sloppy food. Successful rehabilitation is reported. Finally the issue of nomenclature is discussed, raising the question whether Pervasive Refusal Syndrome would be better renamed in a way that does not imply that the condition is always volitional and oppositional, as this can distract focus away from an alliance between family and clinicians.
 ...
PMID:Pervasive refusal syndrome. 2173 31

The objectives of this study are to test the hypothesis that the fatigue and accompanying symptoms of Chronic Myalgic Encephalomyelitis/Fatigue Syndrome are in part due to defects in energy provision at the cellular level, and to understand the pathophysiology of the defects so that effective medical intervention can be implemented. We performed an audit of 138 patients (ages 18-65) diagnosed with ME/CFS and attending a private practice. The patients and 53 normal, healthy controls had the ATP Profile test carried out on neutrophils from a 3-ml venous blood sample. This test yields 6 numerical factors that describe the availability of ATP and the efficiency of oxidative phosphorylation in mitochondria. Other biomedical measurements, including the concentration of cell-free DNA in plasma, were made. The results of the audit are compared with the controls and a previous cohort of 61 patients. We find that all patients tested have measureable mitochondrial dysfunction which correlates with the severity of the illness. The patients divide into two main groups differentiated by how cellular metabolism attempts to compensate for the dysfunction. Comparisons with exercise studies suggest that the dysfunction in neutrophils also occurs in other cells. This is confirmed by the cell-free DNA measurements which indicate levels of tissue damage up to 3.5 times the normal reference range. The major immediate causes of the dysfunction are lack of essential substrates and partial blocking of the translocator protein sites in mitochondria. The ATP Profile is a valuable diagnostic tool for the clinical management of ME/CFS.
 ...
PMID:Mitochondrial dysfunction and the pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). 2283 95

Chronic Fatigue Syndrome (CFS) is defined as greater than 6 months of persistent fatigue that is experienced physically and cognitively. The cognitive symptoms are generally thought to be a mild cognitive impairment, but individuals with CFS subjectively describe them as "brain fog." The impairment is not fully understood and often is described as slow thinking, difficulty focusing, confusion, lack of concentration, forgetfulness, or a haziness in thought processes. Causes of "brain fog" and mild cognitive impairment have been investigated. Possible physiological correlates may be due to the effects of chronic orthostatic intolerance (OI) in the form of the Postural Tachycardia Syndrome (POTS) and decreases in cerebral blood flow (CBF). In addition, fMRI studies suggest that individuals with CFS may require increased cortical and subcortical brain activation to complete difficult mental tasks. Furthermore, neurocognitive testing in CFS has demonstrated deficits in speed and efficiency of information processing, attention, concentration, and working memory. The cognitive impairments are then perceived as an exaggerated mental fatigue. As a whole, this is experienced by those with CFS as "brain fog" and may be viewed as the interaction of physiological, cognitive, and perceptual factors. Thus, the cognitive symptoms of CFS may be due to altered CBF activation and regulation that are exacerbated by a stressor, such as orthostasis or a difficult mental task, resulting in the decreased ability to readily process information, which is then perceived as fatiguing and experienced as "brain fog." Future research looks to further explore these interactions, how they produce cognitive impairments, and explain the perception of "brain fog" from a mechanistic standpoint.
 ...
PMID:Caught in the thickness of brain fog: exploring the cognitive symptoms of Chronic Fatigue Syndrome. 2357 89

We present a description of the Central Sensitivity Syndrome (CSS) and some of its main components such as Multiple Chemical Sensitivity Syndrome, Chronic Fatigue Syndrome and Fibromyalgia. We review the changes in pain perception, describing the physiology and pathophysiology of the painful experience from the medulla horn to the CNS. We explain the theory of central sensitization as the basis to the syndrome. We refer to the differences between fibromyalgia and depressive disorders, is spite of their frequent presentation in comorbidity. We state the main clinical and neurobiological differences. We point out the main psychoneuroimmunoendocrinologic differences such as adrenal activity (hypoactivity vs. hyperactivity, DST hypersuppressive response vs. DST non suppression, hypersensitivity of central glucocorticoid receptors vs. desensitization of these, among others), thyroid (probable reverse T3 vs. flat stimuli TSH response curve) and growth hormone secretion (probable increase vs. disruption of normal circadian rhythm) that makes CSS resemble PTSD. We describe differential changes in sleep patterns (alpha-delta intrusion vs. altered sleep time, REM latency, and stage 3/4) and immunological disturbances almost opposite in each pathological entity. We finally argue which medical specialty should treat these complex syndromes.
 ...
PMID:[Conditions, controversies and contradictions between Central Sensitivity Syndrome and Depressive Disorders]. 2431 23

This review explores the proposal that vulnerability to psychological symptoms, particularly anxiety, originates in constitutional differences in the control of bodily state, exemplified by a set of conditions that include Joint Hypermobility, Postural Tachycardia Syndrome and Vasovagal Syncope. Research is revealing how brain-body mechanisms underlie individual differences in psychophysiological reactivity that can be important for predicting, stratifying and treating individuals with anxiety disorders and related conditions. One common constitutional difference is Joint Hypermobility, in which there is an increased range of joint movement as a result of a variant of collagen. Joint hypermobility is over-represented in people with anxiety, mood and neurodevelopmental disorders. It is also linked to stress-sensitive medical conditions such as irritable bowel syndrome, chronic fatigue syndrome and fibromyalgia. Structural differences in "emotional" brain regions are reported in hypermobile individuals, and many people with joint hypermobility manifest autonomic abnormalities, typically Postural Tachycardia Syndrome. Enhanced heart rate reactivity during postural change and as recently recognized factors causing vasodilatation (as noted post-prandially, post-exertion and with heat) is characteristic of Postural Tachycardia Syndrome, and there is a phenomenological overlap with anxiety disorders, which may be partially accounted for by exaggerated neural reactivity within ventromedial prefrontal cortex. People who experience Vasovagal Syncope, a heritable tendency to fainting induced by emotional challenges (and needle/blood phobia), are also more vulnerable to anxiety disorders. Neuroimaging implicates brainstem differences in vulnerability to faints, yet the structural integrity of the caudate nucleus appears important for the control of fainting frequency in relation to parasympathetic tone and anxiety. Together there is clinical and neuroanatomical evidence to show that common constitutional differences affecting autonomic responsivity are linked to psychiatric symptoms, notably anxiety.
...
PMID:Neurovisceral phenotypes in the expression of psychiatric symptoms. 2571 9


<< Previous 1 2 3 Next >>