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Chronic Fatigue Syndrome
On Chronic Fatigue Syndrome
An Overview
Definition: Chronic Fatigue Syndrome (CFS) is a.k.a (also known as) Myalgic Encephalomyelitis in many countries outside the United States. It used to be called "Chronic Epstein-Barr Virus" (CEBV) but a study by Straus indicated that EBV has nothing to do with the illness. Supposedly, suppressed viruses, such as EBV, CMV and HHV 6, are reactivated due to a dysfunctional immune system. That is why many patient groups call it Chronic Fatigue Immune Dysfunction Syndrome (CFIDS).
"Chronic fatigue syndrome is a clinically defined condition characterized by severe disabling fatigue and a combination of symptoms that prominently features self-reported impairments in concentration and short-term memory, sleep disturbances, and musculoskeletal pain. Diagnosis of the chronic fatigue syndrome can be made only after alternative medical and psychiatric causes of chronic fatiguing illness have been excluded.
No pathognomonic signs or diagnostic tests for this condition have been validated in scientific studies; moreover, no definitive treatments for it exist. Recent longitudinal studies suggest that some persons affected by the chronic fatigue syndrome improve with time but that most remain functionally impaired for several years." Centers for Disease Control and Prevention - 1994.
Center for Current Reseach Report
General Summary
Summary of Current Research
Bodily Effects
Sources
GENERAL SUMMARY
Chronic Fatigue Syndrome (CFS) was perceived to be an imagined illness among young, overworked professionals. It was dubbed the "yuppie flu," but recently was given credence by the Centers for Disease Control (CDC).
Chronic fatigue syndrome (CFS) was formally defined in 1988, and revised in 1992, to describe a syndrome of severe and disabling fatigue of uncertain etiology associated with a number of physical and/or psychological symptoms.
CFS has been reported in most industrialized countries and is most prevalent in women aged between 20 and 50 years.
Seventy percent of CFS patients have allergies. CFS is also associated with depression in 60% to 80% of cases. Seventy percent of patients have abnormalities in cranial blood flow.
Experts doubt CFS is contagious, but it does seem to run in some families. Symptoms (as defined by the CDC) include an abrupt onset of flu-like symptoms with overwhelming fatigue lasting for at least six months and the absence of any other medical disorder that may explain it. These two criteria must be accompanied by at least eight other criteria, including fever, sore throat, tender lymph nodes, muscle and joint pain, severe headaches, sleep disturbance and significant memory and reasoning lapses.
The cause of CFS remains a mystery. A virus or viruses, bacterium, allergens or environmental toxins may precipitate CFS according to some experts. Evidence suggests that CFS patients have an overactive immune system that produce immune proteins long after a viral threat is over.
There are no tests which conclusively diagnose CFS. Diagnosis is made by ruling out other possible causes of fatigue. The basis of treatment is establishing the diagnosis and educating the patient about the illness.
Most patients undertake a trial of antidepressant therapy, even if major depression is not present. Avoidance of strenuous exercise and administration of symptom-specific drug therapy is often prescribed.
The best advice is to get plenty of rest and eat a nutritious diet. Full recovery, if it occurs, usually takes 18 months to 2 years, but can take much longer in some patients.
CURRENT RESEARCH
Chronic fatigue syndrome is an illness of unknown origin, but much of the most recent research is focusing on determining the cause. According to the authors of a recent review, in the present state of research no infectious or immunological cause has been demonstrated conclusively, although a persistent enterovirus or herpesvirus type 6 infection or a state of chronic immune activation seem to be present in some cases (Cathebras, 1993).
There is no specific treatment of CFS, but antidepressants, cognitive-behavioral therapy and perhaps certain immuno-modulators can be useful. In another 1993 review the authors note that the pathophysiology of CFS remains unknown.
The syndrome often follows a recognized or presumed infection and the disorder may therefore result from a disordered immune response to a precipitating infection or antigenic challenge (Lloyd, 1993). They conclude that the pattern of abnormalities reported in immunological testing in patients with CFS is consistent with the changes seen during the resolving phases of acute viral infection. These data provide circumstantial support for the hypothesis that CFS results from a disordered immune response to an infection.
Although abnormalities in tests of immune function and cerebral imaging have been described in variable numbers of CFS patients, such findings have been inconsistent and cannot be relied upon, either to establish or exclude the diagnosis (Blondel-Hill and Shafran, 1993). These authors further state that the mainstay of treatment is establishing the diagnosis and educating the patient about the illness.
An empathetic clinician can stop further consultations elsewhere ("doctor shopping") and subsequent excessive investigations, which frequently occur in such patients. Most patients should undertake a trial of antidepressant therapy, even if major depression is not present. The choice of antidepressant drug should tailor the tolerability profile to relief of particular CFS symptoms, such as insomnia or hypersomnia. Failure to improve within 12 weeks warrants an alternative antidepressant agent of another class (Blondel-Hill and Shafran, 1993).
Identification and management of persistent fatigue in primary care may prevent the secondary disabilities seen in patients with chronic fatigue syndromes (McDonald, 1993). Sufferers may find help through support organizations like the Chronic Fatigue Immune Dysfunction Syndrome Association in Charlotte, North Carolina, and the Chronic Fatigue Syndrome Society in Portland, Oregon (Poston, 1989).
BODILY EFFECTS
Although CFS is characterized by debilitating fatigue made worse by exercise recent studies indicate that there is no physiological change occurring in the muscle of the CFS patient.
In a study of muscle tissue from 108 patients with CFS or muscle pain and 22 normal volunteers by light and electron microscopy (Edwards, 1993 there was no consistent correlation between symptoms and changes in fibre type prevalence, fibre size, degenerative or regenerative features, glycogen depletion, or mitochondrial abnormalities seen.
Physiological contractile properties of quadriceps (maximal isometric force generation, frequency: force characteristics and relaxation rate) were also examined before and for up to 48 hours after a symptom-limited incremental cycle ergometer exercise test in 12 CFS patients and 12 normal volunteers.
Voluntary and stimulated force characteristics were normal at rest and during recovery. Exercise duration was similar in the two groups although CFS patients had higher perceived exertion scores in relation to heart rate during exercise, indicating a reduced effort sensation threshold.
On physiological and pathological grounds it is clear that CFS is not a myopathy. Psychological/psychiatric factors appear to be of greater importance in this condition, according to the authors.
In another study (Kent-Braun, 1993) the extent of fatigue, metabolic response, and changes in both M-wave amplitude and twitch tension during exercise were similar in patients and controls. The response to systemic exercise was also normal in the patients. However, voluntary activation of the tibialis muscle was significantly lower in the patients during maximal sustained exercise. The results indicate that patients with CFS have (1) normal fatigability and metabolism at both the intracellular and systemic levels, (2) normal muscle membrane function and excitation-contraction coupling, and (3) an inability to fully activate skeletal muscle during intense, sustained exercise. This failure of activation was well in excess of that found in controls, suggesting an important central component of muscle fatigue in CFS, the authors report.
SOURCES
Blondel-Hill, and Shafran, 1993. Treatment of the chronic fatigue syndrome. A review and practical guide. Drugs (October 1993), volume 46(4), pages 639-651.
Cathebras, Bouchou, Charmion, and Rousset, 1993. Chronic fatigue syndrome: a critical review. La Revue de Medecine Interne (April 1993), volume 14(4), pages 233-242.
Kent-Braun, Sharma, Weiner, Massie, and Miller, 1993. Central basis of muscle fatigue in chronic fatigue syndrome. Neurology (January 1993), volume 43(1), pages 125-131.
Lloyd, Wakefield, and Hickie, 1993. Immunity and the pathophysiology of chronic fatigue syndrome. CIBA Foundation Symposium (1993), volume 173, pages 176-187.
Kroenke, 1991. Chronic fatigue syndrome: is it real? Post Graduate Medicine (February 1991), volume 89(2), pages 44-46, 49- 50, 53-55.
McDonald, David, Pelosi, and Mann, 1993. Chronic fatigue in primary care attenders. Psychological Medicine (November 1993), volume 23(4), pages 987-998.
Schwartz, Komaroff, Garada, Gleit, Doolittle, Bates, Vasile, and Holman, 1994. SPECT imaging of the brain: comparison of findings in patients with chronic fatigue syndrome, AIDS dementia complex, and major unipolar depression. American Journal of Roentgenology (April 1994), volume 162(4), pages 943-951.
Chronic Fatigue Syndrome
Chronic fatigue syndrome (CFS) is a common neurological disorder which is becoming recognized as a major health hazard. Its central symptom is overwhelming, persistent, fatigue, lasting for > 6 months and often worsening after exertion.
A diagnosis is made essentially on the absence of other illness and the exclusion of other causes of fatigue. Often, CFS affects people in their most productive years, and the syndrome has a significant morbidity. The symptoms of fatigue in CFS suggest a central cause and are identical to the fatigue seen in people with post-polio syndrome, multiple sclerosis, or idiopathic Parkinson's disease.
The illness is now defined by Centers of Disease Control criteria and the prevalence in the US is estimated to be 4-10 cases per 100 000 adults. No CFS laboratory test has been developed, but rating scales are available to assess symptom severity.
Cases of CFS often follow an infection, usually respiratory or gastro-intestinal. Some cases occur after severe acute stress; others may be initiated by trauma. Symptoms of the Gulf War syndrome are similar to CFS, and it is clinically identical to a neurobehavioural syndrome that occurs after chronic low-dose exposure to organophosphate. CFS may follow exposure to other toxins (e.g. ciquatera fish poisoning and botulinism) but there is no apparent relationship between the severity of poisoning and the subsequent development of CFS.
Neuroscientific research has looked for peripheral clues to the aetiology of CFS. Impaired oxidative muscle metabolism has been shown using nuclear magnetic resonance (NMR) spectroscopy and confirmed by the detection of metabolic abnormalities in long-term muscle cell cultures. Patients with CFS may have a wide defect in cellular metabolism other than skeletal muscles. Striking defects in thallium-201 cardiac scans have been documented in patients with CFS who have no evidence of ischaemic heart disease . Cardiac thallium 2001 single photon computed tomography (SPECT) longitudinal slices through the left ventricle in a normal male (left) and a male with CFS (right). SPECT imaging is a nuclear medicine technique whereby the radioactive tracer thallium 201 is injected intravenously at stress and then again at rest. The thallium behaves similarly to potassium, in that it rapidly leaves the vascular spaced and accumulates in lean tissue including the myocardium. SPECT imaging of the myocardium with a gamma camera then provides 3-D information about the thallium activity in the left ventricle. In the figure, the image is orientated with the apex at the top of the image, with the lateral wall to the right and the septum to the left. It can be seen that the thallium uptake in the left ventricle of the male with CFS is markedly more irregular than in the normal left ventricle. In a Series of 10 subjects with CFS, seven had abnormal cardial thallium 201 SPECT scans. 1
A reduction in total body potassium has been found and increases or abnormalities in resting energy expenditure have been demonstrated. This and other data is suggestive of an abnormal cell membrane disorder. A significant number of patients who develop syndrome X have similar thallium-201 scan abnormalities and go on to develop CFS. Such patients, interestingly, have identical NMR muscle findings and abnormal potassium channel ionophores. Abnormal ionophore function could explain the observed changes in the central nervous system in CFS patients (e.g. abnormal regional hypoperfusion in SPECT scans).
Accruing data indicate subtle hypothalamic dysfunction in CFS. Patients with CFS have abnormal water metabolism and there is an association between the disorder and idiopathic cyclic oedema. Many neuronendocrine studies have shown dysregulation of the neurohypophysis (ADH secretion) and of the hypothalamic-pituitary-adrenal axis (loss of pituitary responsiveness to CRH and adrenal supersensitivity to ACTH). In addition, both pyridostigmine-induced growth hormone release and buspironeinduced prolactin release show exaggerated responses, suggestive of changes in synaptic sensitivity to acetylcholine and serotonin, respectively. Furthermore, neurophysiological studies have demonstrated pronounced hypotension in table tilt manoeuvre neurally-mediated hypotension, in keeping with the reduction in afferent vagal tone supported in other studies of respiratory muscle activity during exercise.
The key to any successful treatment would be the relief of fatigue as the primary outcome measurement and major clinical trials in CFS are in progress. Preliminary trial results may be discussed during the CFS symposium at the forthcoming WCN. This symposium is a recognition of the importance of CFS; indeed, helping to solve the mystery of the fatigue in CFS may have important connotations for other fatigue states.
Peter Behan
Southern General Hospital, Glasgow, UK
Reference
Chauethuri A, Watson WS, Behan PO.
Arguments for a role of abnormal ionophore function in chronic fatigue syndrome.
In: Chronic Fatigue Syndrome (Yehuda and Mostofsky, eds) New York: Plenum Press. 1997.
CHRONIC FATIGUE SYNDROME
Center for Disease Control Article
Cheney Clinic Information Service
"The largest and oldest clinic in the United States serving the world wide CFS community."
A Need for Balance
Bulletins
A new study in the American Journal of Psychiatry (1997;154:408-414), indicates that cognitive behavior therapy (CBT), which focuses on how people think about themselves, is more effective than relaxation therapy; 70% in a CBT group showed improvement, compared to 19% in the relaxation group.
An Overview
Definition: Chronic Fatigue Syndrome (CFS) is a.k.a (also known as) Myalgic Encephalomyelitis in many countries outside the United States. It used to be called "Chronic Epstein-Barr Virus" (CEBV) but a study by Straus indicated that EBV has nothing to do with the illness. Supposedly, suppressed viruses, such as EBV, CMV and HHV 6, are reactivated due to a dysfunctional immune system. That is why many patient groups call it Chronic Fatigue Immune Dysfunction Syndrome (CFIDS).
"Chronic fatigue syndrome is a clinically defined condition characterized by severe disabling fatigue and a combination of symptoms that prominently features self-reported impairments in concentration and short-term memory, sleep disturbances, and musculoskeletal pain. Diagnosis of the chronic fatigue syndrome can be made only after alternative medical and psychiatric causes of chronic fatiguing illness have been excluded.
No pathognomonic signs or diagnostic tests for this condition have been validated in scientific studies; moreover, no definitive treatments for it exist. Recent longitudinal studies suggest that some persons affected by the chronic fatigue syndrome improve with time but that most remain functionally impaired for several years." Centers for Disease Control and Prevention - 1994.
Center for Current Reseach Report
General Summary
Summary of Current Research
Bodily Effects
Sources
GENERAL SUMMARY
Chronic Fatigue Syndrome (CFS) was perceived to be an imagined illness among young, overworked professionals. It was dubbed the "yuppie flu," but recently was given credence by the Centers for Disease Control (CDC).
Chronic fatigue syndrome (CFS) was formally defined in 1988, and revised in 1992, to describe a syndrome of severe and disabling fatigue of uncertain etiology associated with a number of physical and/or psychological symptoms.
CFS has been reported in most industrialized countries and is most prevalent in women aged between 20 and 50 years.
Seventy percent of CFS patients have allergies. CFS is also associated with depression in 60% to 80% of cases. Seventy percent of patients have abnormalities in cranial blood flow.
Experts doubt CFS is contagious, but it does seem to run in some families. Symptoms (as defined by the CDC) include an abrupt onset of flu-like symptoms with overwhelming fatigue lasting for at least six months and the absence of any other medical disorder that may explain it. These two criteria must be accompanied by at least eight other criteria, including fever, sore throat, tender lymph nodes, muscle and joint pain, severe headaches, sleep disturbance and significant memory and reasoning lapses.
The cause of CFS remains a mystery. A virus or viruses, bacterium, allergens or environmental toxins may precipitate CFS according to some experts. Evidence suggests that CFS patients have an overactive immune system that produce immune proteins long after a viral threat is over.
There are no tests which conclusively diagnose CFS. Diagnosis is made by ruling out other possible causes of fatigue. The basis of treatment is establishing the diagnosis and educating the patient about the illness.
Most patients undertake a trial of antidepressant therapy, even if major depression is not present. Avoidance of strenuous exercise and administration of symptom-specific drug therapy is often prescribed.
The best advice is to get plenty of rest and eat a nutritious diet. Full recovery, if it occurs, usually takes 18 months to 2 years, but can take much longer in some patients.
CURRENT RESEARCH
Chronic fatigue syndrome is an illness of unknown origin, but much of the most recent research is focusing on determining the cause. According to the authors of a recent review, in the present state of research no infectious or immunological cause has been demonstrated conclusively, although a persistent enterovirus or herpesvirus type 6 infection or a state of chronic immune activation seem to be present in some cases (Cathebras, 1993).
There is no specific treatment of CFS, but antidepressants, cognitive-behavioral therapy and perhaps certain immuno-modulators can be useful. In another 1993 review the authors note that the pathophysiology of CFS remains unknown.
The syndrome often follows a recognized or presumed infection and the disorder may therefore result from a disordered immune response to a precipitating infection or antigenic challenge (Lloyd, 1993). They conclude that the pattern of abnormalities reported in immunological testing in patients with CFS is consistent with the changes seen during the resolving phases of acute viral infection. These data provide circumstantial support for the hypothesis that CFS results from a disordered immune response to an infection.
Although abnormalities in tests of immune function and cerebral imaging have been described in variable numbers of CFS patients, such findings have been inconsistent and cannot be relied upon, either to establish or exclude the diagnosis (Blondel-Hill and Shafran, 1993). These authors further state that the mainstay of treatment is establishing the diagnosis and educating the patient about the illness.
An empathetic clinician can stop further consultations elsewhere ("doctor shopping") and subsequent excessive investigations, which frequently occur in such patients. Most patients should undertake a trial of antidepressant therapy, even if major depression is not present. The choice of antidepressant drug should tailor the tolerability profile to relief of particular CFS symptoms, such as insomnia or hypersomnia. Failure to improve within 12 weeks warrants an alternative antidepressant agent of another class (Blondel-Hill and Shafran, 1993).
Identification and management of persistent fatigue in primary care may prevent the secondary disabilities seen in patients with chronic fatigue syndromes (McDonald, 1993). Sufferers may find help through support organizations like the Chronic Fatigue Immune Dysfunction Syndrome Association in Charlotte, North Carolina, and the Chronic Fatigue Syndrome Society in Portland, Oregon (Poston, 1989).
BODILY EFFECTS
Although CFS is characterized by debilitating fatigue made worse by exercise recent studies indicate that there is no physiological change occurring in the muscle of the CFS patient.
In a study of muscle tissue from 108 patients with CFS or muscle pain and 22 normal volunteers by light and electron microscopy (Edwards, 1993 there was no consistent correlation between symptoms and changes in fibre type prevalence, fibre size, degenerative or regenerative features, glycogen depletion, or mitochondrial abnormalities seen.
Physiological contractile properties of quadriceps (maximal isometric force generation, frequency: force characteristics and relaxation rate) were also examined before and for up to 48 hours after a symptom-limited incremental cycle ergometer exercise test in 12 CFS patients and 12 normal volunteers.
Voluntary and stimulated force characteristics were normal at rest and during recovery. Exercise duration was similar in the two groups although CFS patients had higher perceived exertion scores in relation to heart rate during exercise, indicating a reduced effort sensation threshold.
On physiological and pathological grounds it is clear that CFS is not a myopathy. Psychological/psychiatric factors appear to be of greater importance in this condition, according to the authors.
In another study (Kent-Braun, 1993) the extent of fatigue, metabolic response, and changes in both M-wave amplitude and twitch tension during exercise were similar in patients and controls. The response to systemic exercise was also normal in the patients. However, voluntary activation of the tibialis muscle was significantly lower in the patients during maximal sustained exercise. The results indicate that patients with CFS have (1) normal fatigability and metabolism at both the intracellular and systemic levels, (2) normal muscle membrane function and excitation-contraction coupling, and (3) an inability to fully activate skeletal muscle during intense, sustained exercise. This failure of activation was well in excess of that found in controls, suggesting an important central component of muscle fatigue in CFS, the authors report.
SOURCES
Blondel-Hill, and Shafran, 1993. Treatment of the chronic fatigue syndrome. A review and practical guide. Drugs (October 1993), volume 46(4), pages 639-651.
Cathebras, Bouchou, Charmion, and Rousset, 1993. Chronic fatigue syndrome: a critical review. La Revue de Medecine Interne (April 1993), volume 14(4), pages 233-242.
Kent-Braun, Sharma, Weiner, Massie, and Miller, 1993. Central basis of muscle fatigue in chronic fatigue syndrome. Neurology (January 1993), volume 43(1), pages 125-131.
Lloyd, Wakefield, and Hickie, 1993. Immunity and the pathophysiology of chronic fatigue syndrome. CIBA Foundation Symposium (1993), volume 173, pages 176-187.
Kroenke, 1991. Chronic fatigue syndrome: is it real? Post Graduate Medicine (February 1991), volume 89(2), pages 44-46, 49- 50, 53-55.
McDonald, David, Pelosi, and Mann, 1993. Chronic fatigue in primary care attenders. Psychological Medicine (November 1993), volume 23(4), pages 987-998.
Schwartz, Komaroff, Garada, Gleit, Doolittle, Bates, Vasile, and Holman, 1994. SPECT imaging of the brain: comparison of findings in patients with chronic fatigue syndrome, AIDS dementia complex, and major unipolar depression. American Journal of Roentgenology (April 1994), volume 162(4), pages 943-951.Mental Impairment And Functional Incapacity Linked In Chronic Fatigue

~~~~~~~~~

LONDON, ENGLAND -- April 9, 1998 -- The degree of functional incapacity resulting from chronic fatigue syndrome parallels the level of cognitive impairment, finds a study in the Journal of Neurology, Neurosurgery, and Psychiatry. Furthermore, psychiatric factors do not explain these findings.
Researchers assessed the mental and physical capacities of 53 patients with the syndrome and 32 healthy people who did not exercise regularly, using questionnaires and a battery of standardised neuropsychological tasks. The tasks focused on verbal and visual memory as well as attention and concentration.
The results showed that patients with higher numbers of failed scores reported significantly more days of inactivity in the previous month than those with fewer failed scores. Patients with failing verbal memory scores were particularly functionally disabled compared with those who passed this test.
The significance of the association was not simply a consequence of psychiatric factors -- anxiety, panic and phobias -- and depression, the results showed. There was absolutely no evidence to suggest that the cognitive impairments caused the functional disability.
The link between the neuropsychological deficits and the functional impairment in patients with chronic fatigue syndrome is similar to findings in patients with HIV, multiple sclerosis, Alzheimer's disease and stroke, explained the authors.
Websites with excellent information
Harvard Neurology Forums for Chronic Fatigue Syndrome visit: http://neuro-www.mgh.harvard.edu/forum/ChronicFatigueMenu.html
Chronic Fatigue Syndrome visit: http://www.cais.net/cfs-news/cfs-news.htm
Excellent website: http://www.cais.net/cfs-news/cfs-news.htm