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Naranch, K., Repka-Ramirez, SM., Park, Y-J., Velarde, A., Finnegan, R., Murray, J., Pheiffer, A., Hwang, E., Clauw, D., and Baraniuk, JN. Differences in baseline nasal secretions between chronic fatigue syndrome (CFS) and control subjects. Journal of Chronic Fatigue Syndrome, 2002, 10, 1, 3-15.
Objective: To assess potential mechanism(s) for the rhinitis found in CFS (CDC criteria '94).
Methods: The concentrations of mucus constituents were measured in basal nasal lavage fluids of 103 CFS and 92 non-CFS control subjects. Subjects were further characterized by their Rhinitis Score and allergy skin test results into non-allergic and allergic rhinitis, atopic, and negative subgroups to determine if differences were related to atopy. Other questionnaires of irritant sensitivity and medicine use were completed.
Results: Mucin polysaccharide (p=0.043), free hemoglobin (p=0.004), mucin/total protein (p=0.039) and hemoglobin/total protein (p=0.043) were higher in people with CFS than controls. CFS subjects with positive Rhinitis Scores (p=0.023) or skin tests (p=0.047) had higher mucin levels than those with negative values. For all subjects, increased mucin was correlated with total protein (Pearson's r2 =0.188) and inhaled corticosteroid use (r2 =0.091), while hemoglobin was correlated with total protein (r2 =0.082) and elevated Tobacco Scores (r2 =0.061). Other correlations with demographic, medication, or questionnaire responses gave r2 <0.05.
Conclusions: CFS subjects have a higher level of complaints in many systems including the nose. They appear to have an irritant (nonallergic) rhinitis with increased mucin production and mucosal friability (epistaxis of hemoglobin). Nasal and systemic drugs do not explain these significant baseline changes.
Farquhar, WB., Hunt, BE., Taylor, JA., Darling, SE and Freeman, R. Blood volume and its relation to peak O2 consumption and physical activity in patients with chronic fatigue. American Journal of Physiology - Heart Circulatory Physiology, 2002, 282, 1, H66-H71.
Individuals with CFS experience a number of somatic complaints including severe, disabling fatigue, and exercise intolerance. We hypothesized that hypovolemia, through its interaction with central hemodynamics, would contribute to the exercise intolerance associated with this disorder.
We examined blood volume, peak aerobic power, habitual physical activity, fatigue level, and their interrelations to understand the physiological basis of this disorder. Seventeen patients who met the CDC criteria for CFS and 17 age‑matched controls participated in the study. Blood volume was assessed using a single bolus injection of Evans blue dye. Peak oxygen consumption was measured during exercise on an upright cycle ergometer. Supine cardiac output and stroke volumes were measured using CO2 rebreathing. Questionnaires were used to assess habitual physical activity and fatigue.
Patients displayed a trend for a 9% lower blood volume (58.3 +/- 2.1 vs. 64.2 +/- 2.5 ml/kg, p=0.084) and had a 35% lower peak oxygen consumption (22.0 +/- 1.2 vs. 33.6 +/- 1.9 ml/kg, p<0.001). These two variables were highly related within the patients (r=0.835, p<0.001) and the controls (r=0.850, p<0.001). Peak ventilation and habitual physical activity were significantly lower in the patients. Fatigue level was not related to any of the measured physiological parameters within the CFS group.
Individuals with CFS have a significantly lower peak oxygen consumption and an insignificant trend toward lower blood volume compared with controls. These variables were highly related in both subject groups, indicating that blood volume is a strong physiological correlate of peak oxygen consumption in patients with CFS.
Naschitz, JE., Sabo, E., Naschitz, S., Shaviv, N., Rosner, I., Rozenbaum, M., Gaitini, L., Ahdoot, A., Ahdoot, M., Priselac, RM., Eldar, S., Zukerman, E and Yeshurun D. Hemodynamic instability in chronic fatigue syndrome: Indices and diagnostic significance. Seminars in Arthritis and Rheumatism, 2001, 31, 3, 199-208.
To evaluate the cardiovascular response to postural challenge in patients with CFS and to determine whether the degree of instability of the cardiovascular response may aid in diagnosing CFS.
Patients with CFS (n=25) and their age- and gender-matched healthy controls (n=37), patients with fibromyalgia (n=30), generalized anxiety disorder (n=15), and essential hypertension (n=20) were evaluated with the aid of a standardized tilt test. The blood pressure (BP) and heart rate (HR) were recorded during 10 minutes of recumbence and 30 minutes of head-up tilt. We designated BP changes as the differences between successive BP values and the last recumbent BP. The average and standard deviation (SD) were calculated. Time curves of BP differences were loaded into a computerized image analyzer, and their outline ratios and fractal dimensions were measured. HR changes were determined similarly. The average and SD of the parameters were calculated, and intergroup comparisons were performed.
On multivariate analysis, the independent predictors of CFS patients versus healthy controls were the fractal dimension of absolute values of the systolic BP changes (SYST-FD.abs), the standard deviation of the current values of the systolic BP changes (SYST-SD.cur), and the standard deviation of the current values of the heart rate changes (HR-SD.cur). The following equation was deduced to calculate the hemodynamic instability score (HIS) in the individual patient: HIS = 64.3303 + (SYST-FD.abs x -68.0135) + (SYST-SD.cur x 111.3726) + (HR-SD.cur x 60.4164). The best cutoff differentiating CFS from the healthy controls was -0.98. HIS values > -0.98 were associated with CFS (sensitivity 97%, specificity 97%). The HIS differed significantly between CFS and other groups (p<.0001) except for generalized anxiety disorder. Group averages (SD) of HIS were CFS = +3.72 (5.02), healthy = -4.62 (2.26), fibromyalgia = -3.27 (2.63), hypertension = -5.53 (2.24), and generalized anxiety disorder = +1.08 (5.2).
CONCLUSION: The HIS adds objective criteria confirming the diagnosis of CFS.
Sargent., C, Scroop, GC., Nemeth, PM., Burnet, RB and Buckley JD. Maximal oxygen uptake and lactate metabolism are normal in chronic fatigue syndrome. Medicine and Science in Sports and Exercise, 2002, 34, 1, 51-56.
Previous studies in CFS have reported reductions in maximal oxygen uptake (VO2max), yet often the testing procedures have not followed accepted guidelines, and gender data have been pooled. The present study was undertaken to reevaluate exercise capacity in CFS patients by using "gold standard" maximal exercise testing methodology and stratifying results on a gender basis.
Sixteen male and 17 female patients with CFS (CDC criteria '94) and their gender-, age-, and mass-matched sedentary controls performed incremental exercise to volitional exhaustion on a stationary cycle ergometer while selected cardiorespiratory and metabolic variables were measured. Also included were Karnofsky scores.
VO2max in male CFS patients was not different from control values (CFS: 40.5 +/- 6.7; controls: 43.3 +/- 8.6; mL.kg‑1.min‑1) and was 96.3 +/- 17.9% of the age-predicted value, indicating no functional aerobic impairment (3.7 +/- 17.9%). In female CFS patients, VO2max was lower than control values (CFS: 30.0 +/-4.7; controls: 34.2 +/- 5.6; mL.kg‑1.min‑1, p=0.002), but controls were higher than the age-predicted value (112.6 +/- 15.4%, p=0.008) whereas the CFS patients were 101.2 +/- 20.4%, indicating no functional aerobic impairment (-1.2 +/- 20.4%). Maximal heart rate (HRmax) in male CFS patients was lower than their matched controls (CFS: 184 +/- 10; controls: 192 +/- 12; beats.min‑1; p=0.016) but was 99.1 +/- 5.5% of their age-predicted value. In female CFS patients, HRmax was not different from controls (CFS: 183 +/- 11; controls: 186 +/- 10; beats.min‑1) and was 98.9 +/- 5.1% of the age-predicted value. The VO2 at the lactate threshold (LT) in each gender group, whether expressed in mL.kg‑1.min‑1 or as a percentage of VO2max, was not different between CFS patients and controls.
In contrast to most previous reports, the present study found that VO2max, HRmax, and the LT in CFS patients of both genders were not different from the values expected in healthy sedentary individuals of a similar age. The fact that the maximal oxygen uptake was normal and that there was no sign of excessive lactic acidosis is significant and does not support the view that deconditioning is a major determinant of ongoing fatigue.
[Ed. Note: Findings in patients selected using the 1994 criteria tend to be normal. These results may therefore not apply to more strictly-defined groups. On the other hand, most of the research on CBT and GET is based on the view that broadly-defined CFS is perpetuated by factors such as deconditioning.]
Asbring, P and Narvanen, AL. Women's experiences of stigma in relation to chronic fatigue syndrome and fibromyalgia. Qualitative Health Research, 2002, 12, 2, 148-160.
CFS and fibromyalgia are characterized by being difficult to diagnose and having an elusive etiology and no clear-cut treatment strategy. The question of whether these illnesses are stigmatizing was investigated through interviews with 25 women with these illnesses. The women experienced stigmatization primarily before receiving a diagnosis, and the diffuse symptomatology associated with the illnesses were significant for stigmatization. Stigma consisted of questioning the veracity, morality, and accuracy of patient symptom descriptions and of psychologizing symptoms. Coping with stigma was also explored and found to comprise both withdrawal and approach strategies, depending on the individual's circumstances and goals.
DiClementi, JD., Schmaling, KB and Jones, JF. Information processing in chronic fatigue syndrome. A preliminary investigation of suggestibility. Journal of Psychosomatic Research, 2001, 51, 5, 679-686.
This study examines the effects of certain types of information processing on the subjective experience of cognitive deficits in persons with CFS. Two groups of participants, 21 persons with CFS (CDC criteria '88 and '94) and 21 healthy controls, were administered a symptom inventory and measures of intellectual functioning, memory, automatic processing, and suggestibility.
The groups differed significantly on number and severity of reported symptoms and on measures of global suggestibility and automatic processing, but not on measures of intellectual functioning and memory. Suggestibility was related to number and severity of reported symptoms, as well as the inability to inhibit the automatic processing of information.
[Ed. Note: There is no evidence that people with CFS are more suggestible or more likely to accept medical misinformation than patients with other medical disorders. The correlation between errors (misinformation test) and number of symptoms is interesting and suggests that the condition itself may have mediated the result. Findings in a laboratory may not reflect experiences in naturalistic settings.]
Buchwald, D., Herrell, R., Ashton, S., Belcourt, M., Schmaling, K., Sullivan, P., Neale, M and Goldberg, J. A twin study of chronic fatigue. Psychosomatic Medicine, 2001 63, 6, 936-943.
Our objective was to assess the role of genetic and environmental factors in unexplained chronic fatigue.
A classic twin study was conducted using 146 female-female twin pairs, of whom at least one member reported 6 or more months of fatigue. After completing questionnaires on symptoms, zygosity, physical health, and a psychiatric interview, twins were classified using three increasingly stringent definitions: 1) chronic fatigue for 6 or more months, 2) chronic fatigue not explained by exclusionary medical conditions, and 3) idiopathic chronic fatigue not explained by medical or psychiatric exclusionary criteria of the CFS case definition. Concordance rates in monozygotic and dizygotic twins were calculated for each fatigue definition along with estimates of the relative magnitude of genetic and environmental influences on chronic fatigue.
The concordance rate was higher in monozygotic than dizygotic twins for each definition of chronic fatigue. For idiopathic chronic fatigue, the concordance rates were 55% in monozygotic and 19% in dizygotic twins (p =.042). The estimated heritability in liability was 19% for chronic fatigue 6 or more months, 30% for chronic fatigue not explained by medical conditions, and 51% for idiopathic chronic fatigue.
These results provide evidence supporting the familial aggregation of fatigue and suggest that genes may play a role in the etiology of CFS.
Jason, LA., Torres-Harding, SR., Taylor, RR and Carrico, AW. A comparison of the 1988 and 1994 diagnostic criteria for chronic fatigue syndrome. Journal of Clinical Psychology in Medical Settings, 2001, 8, 4, 337-343.
CFS is an illness that involves severe, prolonged fatigue as well as neurological, immunological, and endocrinological system pathology. Because the pathogenesis of CFS has yet to be determined, case definitions have relied on clinical observation in classifying signs and symptoms for diagnosis. In an attempt to address various criticisms and inconsistencies in diagnostic criteria, there have been several revisions of the CFS case definition. The 1994 definition is a response to the view that inclusion of physical symptoms increased the number of people with psychiatric problems. The current investigation examined the differences between 1988 and 1994 definitions as well as participants who had a psychiatric explanation for their fatigue. Dependent measures included psychiatric comorbidity (SCID), symptom frequency, other health indices (MOS SF-36), and functional impairment (VAS). Data was obtained from a community survey. There were 14 patients who met the 1988 criteria, 18 who met the 1994 criteria only and 33 people whose chronic fatigue could be explained by psychiatric problems.
The 1988 criteria, compared to the 1994 criteria, appeared to select a group of participants with more symptomatology and functional impairment, but these groups did not significantly differ in psychiatric comorbidity. The 1988 group reported more sore throats, more lymph node pain and worse general health (MOS). There were no differences in terms of physical functioning, sleep, memory problems, new headaches and muscle pain between the groups.
Jason, LA., Torres-Harding, SR., Carrico, AW and Taylor, RR. Symptom occurrence in persons with chronic fatigue syndrome. Biological Psychology, 2002, 59, 1, 15-27.
This investigation compared differences in the occurrence of symptoms in participants with CFS, melancholic depression, and no fatigue (controls). A range of symptoms were assessed in 32 patients with CFS, 19 people with melancholic depression and 47 controls with no fatigue.
The following Fukuda et al 1994 criteria symptoms differentiated the CFS group from controls, but did not differentiate the melancholic depression group from controls: headaches, lymph node pain, sore throat, joint pain, and muscle pain. In addition, participants with CFS uniquely differed from controls in the occurrence of muscle weakness at multiple sites as well as in the occurrence of various cardiopulmonary, neurological, and other symptoms not currently included in the current case definition.
Adding muscle weakness and intolerance to alcohol may increase specificity of the criteria.
Roy-Byrne, P., Afari, N., Fischer, M., Goldberg, J and Buchwald, D. Chronic fatigue and anxiety/depression: a twin study. British Journal of Psychiatry, 2002, 180, 29-34.
Study of 69 monozygotic and 31 dizygotic female twin pairs where one reported at least six months fatigue. Measures included the GHQ-28, and structured psychiatric interview.
Fatigued twins were more anxious and depressed than the non-fatigued twins. There were non-significant differences for somatic symptoms and anxiety/insomnia subscales. Thus in this sample, chronic fatigue and psychological distress are strongly associated without evidence for genetic covariation. This suggests that the association is environmental or due to overlapping definitions.
[Ed. Note: 43 MZ and 18 DZ met the strict CDC '94 criteria (i.e. not due to medical or psychiatric exclusions). There were no differences on the GHQ compared to people with 6 months or more of fatigue due to other reasons. There is no data on type of somatic symptoms in each group other than those listed in the GHQ, or type of onset. Fatigue was rated on a scale of 0-10.]
Strickland, PS., Levine, PH., Peterson, DL., O'Brien, K and Fears, T. Neuromyasthenia and chronic fatigue syndrome (CFS) in Northern Nevada/California: A ten-year follow-up of an outbreak. Journal of Chronic Fatigue Syndrome, 2001, 9, 3/4, 3-14.
In 1984-87, an outbreak of debilitating fatigue was reported by two physicians in the private practice of internal medicine in Incline Village, Nevada. Follow-up questionnaires were sent in 1995 to the 259 patients in this outbreak. The results were analyzed to determine how many patients met the 1994 CDC case definition for CFS, idiopathic chronic fatigue (ICF), or prolonged fatigue (PF, i.e. fatigue < 6 months). Data were analyzed separately for those living in the Lake Tahoe area and those referred from other areas.
Of those returning questionnaires (123, 58%), 41% met the CDC case definition for CFS, 56% met the criteria for inclusion in the subgroup ICF, and 3% experienced PF. In the population‑based Lake Tahoe group, symptomatic women were more likely to have CFS than ICF whereas symptomatic men were likely to fit ICF criteria. Also in this group, full recovery was reported more often among Lake Tahoe participants classified as having ICF (43%) than participants classified as having CFS (15%).
Few reported sore throats but 70% of those with CFS noted post- exertional fatigue compared to 28% of people with ICF and 25% with PF.
Chalder, T., Tong, J and Deary, V. Family cognitive therapy for chronic fatigue syndrome: an uncontrolled study. Archives of Disease in Childhood, 2002, 86, 95-97.
Aim: To examine the efficacy of family focused cognitive behaviour therapy for 11-18 year olds with CFS (Oxford and CDC '94 criteria).
Methods: Twenty three patients plus family were offered family focused cognitive behaviour therapy (15 one hour sessions face-to-face every fortnight). The main outcome was a fatigue score of less than 4 and attendance at school 75% of the time. Other measures included the HAD. Fatigue was measured by the Chalder fatigue scale.
Results: Twenty patients completed treatment. Eighteen had completed all measures at six months follow up; 15 of these (83%) improved according to our predetermined criterion. Substantial improvements in social adjustment, depression, and fear were also noted. There was no change in attributions however. Most continued to attribute the illness to a viral infection. All were very much or much better at follow-up. All were also satisfied with the treatment.
Conclusions: Family focused cognitive behaviour therapy was effective in improving functioning and reducing fatigue in 11-18 year olds. Gains were maintained at six months follow up.
Deale, A., Husain, K., Chalder, T and Wessely, S. Long-term outcome of cognitive behavior therapy versus relaxation therapy for chronic fatigue syndrome: a 5-year follow-up study. American Journal of Psychiatry, 2001, 158, 2038-2042.
This study evaluated the long‑term outcome of cognitive behavior therapy (CBT) versus relaxation therapy for patients with CFS.
Sixty patients with CFS (Oxford criteria) who participated in a randomized controlled trial of CBT versus relaxation therapy were invited to complete self-rated measures and participate in a 5-year follow-up interview with an assessor who was blind to treatment type.
Results: Fifty-three patients (88%) participated in the follow-up study: 25 received CBT and 28 received relaxation therapy. A total of 68% of the patients who received CBT and 36% who received relaxation therapy rated themselves as "much improved" or "very much improved" at the 5-year follow-up. Significantly more patients receiving CBT, in relation to those in relaxation therapy met the criteria for complete recovery, were free of relapse, and experienced symptoms that had steadily improved or were consistently mild or absent since treatment ended. Similar proportions were employed, but patients in the CBT group worked significantly more mean hours per week. However, few patients crossed the threshold for "normal" fatigue (score <4), despite achieving a good outcome on other measures. CBT was positively evaluated and was still used by over 80% of the patients.
CBT for CFS can produce some lasting benefits but is not a cure. CBT helps to improve activity levels and quality of life. Once therapy ends, some patients have difficulty making further improvements. In the future, attention should be directed toward ensuring that gains are maintained and extended after regular treatment ends.
[Ed. Note: It appears that 38% of the patients still had a psychiatric disorder at follow-up. About half in both groups remained 'cases' on the GHQ. This is noteworthy given CBT is generally useful for people with emotional distress. The majority in both groups continued to report excessive fatigue (Fatigue Scale).
A significant number (56% CBT group, 57% of the controls) received treatment for CFS after the trial including counselling.
There were no significant group differences in the numbers who had normal fatigue scores, scores >83 on the physical functioning scale of the MOS, the number of 'cases' on the GHQ, who were judged to be non-cases on the General Health Questionnaire, and the number who no longer met the Oxford criteria (52% in the CBT group, 39% in the controls). Given the fatigue scores and findings relating to distress, did the improvement scores reflect more confidence in being able to control the illness? If so, counselling would be just as good, cf. Ridsdale et al.
There are no details about somatic symptoms, or indeed, any symptoms other than fatigue. Complete recovery was reported by 24% of the CBT group and 4% of the controls. However, people given CBT felt better, reported more stability, and their symptoms had less impact on their lives five years after treatment. That is a noteworthy finding.]
Masuda, A., Nakayama, T., Yamanaka, T., Hatsutanmaru, K and Tei, C. Cognitive behavioral therapy and fasting therapy for a patient with chronic fatigue syndrome. Internal Medicine, 2001, 40, 11, 1158-1161.
Cognitive behavioral therapy temporarily alleviated symptoms of a CFS patient but the anxiety about rehabilitation into work became stronger and his symptoms worsened. This patient was successfully rehabilitated by fasting therapy. Natural killer cell activity and serum acylcarnitine levels recovered after fasting therapy. Though fasting therapy transiently increased physical and mental subjective symptoms, the patient gained self-confidence by overcoming difficulties after fasting therapy. A combination of cognitive behavioral therapy and fasting therapy is promising as a treatment for CFS.
Rosenbaum, ME., Vojdani, A., Susser M and Watson, CM. Improved immune activation markers in chronic fatigue and immune dysfunction syndrome (CFIDS) patients treated with thymic protein A. Journal of Nutritional and Environmental Medicine, 2001, 11, 241-247.
Thymic protein A, an immune modulator, was tested in 23 patients with CFIDS (one year duration, abnormal CD8+ subpopulations and interferon pathway associated enzyme levels). Sixteen patients experienced normalisation of immune function with a corresponding improvement in symptoms.
Whitehead, L and Campion, P. Can general practitioners manage chronic fatigue syndrome? A controlled trial. [Preliminary Study]. Journal of Chronic Fatigue Syndrome, 2002, 10, 1, 55-64.
CFS/Myalgic Encephalomyelitis (CFS/ME) is now recognised as a condition that results in substantial disability with a prevalence of around 0.6%. This study aimed to test the hypotheses that general practitioners could (a) diagnose and (b) treat patients with the CFS.
All practices in two health authorities were contacted with a 35% uptake. Fifty percent of practices then entered a patient into the study. Practices were randomised to either intervention or control groups, and were encouraged to recruit patients. It was intended that the intervention practices would introduce a form of brief cognitive behavioural therapy. Control practices were invited to manage their patients as usual, which often included referral to secondary care. Measure included the Chalder Fatigue Scale and HAD.
Twenty-six patients with CFS (CDC criteria '94) were recruited for the intervention group and 39 were controls. The aims of treatment were to explore 'negative' thoughts about symptoms and recovery and to gradually increase activity levels. Patients were asked to visit their GP weekly or bi-weekly to discuss progress and goals. In practice, they visited their GP for ten minutes every 3.2 weeks. At six months, follow-up data were obtained from 18 people in the intervention group and 28 controls; at one year, information was obtained from 9 in the former and 21 controls.
The study suffered from both poor recruitment as well as high drop out. However, we were able to show that this intervention had no effect on the illness of the patients enrolled, and that patients with CFS remained highly disabled over the 12 month study period, whatever their treatment.
The study suggests that general practitioners in this study were unable to effectively treat the condition. This accords with the Royal Colleges' report (1996), that the only evidence for effective treatment thus far has come from specialist units. The study suggests that general practitioners are unable to provide a management programme of this nature, and possibly effective treatment programmes for CFS in primary care.
[Ed. note: The results are difficult to reconcile with those of Powell et al who reported that three hours of explanation and encouragement to increase activity helped 70% of their patients.]
Harrison, HH, Berg, DE., Berg, LH and Brewer, J. Increased prevalence of thrombophilia and hypofibrinolysis abnormalities in patients with chronic fatigue syndrome: Identification of probable predisposition factors. American Journal of Human Genetics, 2001, 69, 4 Suppl., 564.
Parker, AJ., Wessely, S and Cleare, AJ. The neuroendocrinology of chronic fatigue syndrome and fibromyalgia. Psychological Medicine, 2001, 31, 8, 1331-1345.
Disturbance of the HPA axis may be important in the pathophysiology of CFS and fibromyalgia. Symptoms may be due to: low circulating cortisol; disturbance of central neurotransmitters; or disturbance of the relationship between cortisol and central neurotransmitter function. Accumulating evidence of the complex relationship between cortisol and 5-HT function, make some form of hypothesis most likely. We review the methodology and results of studies of the HPA and other neuroendocrine axes in CFS.
Medline, Embase and Psychlit were searched using the Cochrane Collaboration strategy. A search was also performed on the King's College CFS database, which includes over 3000 relevant references, and a citation analysis was run on the key paper (Demitrack et al. 1991).
One-third of the studies reporting baseline cortisol found it to be significantly low, usually in one-third of patients. Methodological differences may account for some of the varying results. More consistent is the finding of reduced HPA function, and enhanced 5-HT function on neuroendocrine challenge tests. The opioid system, and arginine vasopressin (AVP) may also be abnormal, though the growth hormone (GH) axis appears to be intact, in CFS.
The significance of these changes, remains unclear. We have little understanding of how neuroendocrine changes relate to the experience of symptoms, and it is unclear whether these changes are primary, or secondary to behavioural changes in sleep or exercise. Longitudinal studies of populations at risk for CFS will help to resolve these issues.
[Ed. note: According to Cleare (2001), activity is not related to cortisol levels. The general consensus among researchers is that low cortisol and other signs of altered HPA activity reflects chronic stress.]
Binder, LM., Storzbach, D., Campbell, KA., Rohlman, DS and Anger, WK. Neurobehavioral deficits associated with chronic fatigue syndrome in veterans with Gulf War unexplained illnesses. Journal of the International Neuropsychological Society, 2001, 7, 7, 835-839.
Gulf War unexplained illnesses (GWUI) are a heterogeneous collection of symptoms of unknown origin known to be more common among veterans of the Gulf War than among nonveterans. In the present study we focused on one of these unexplained illnesses, We tested the hypothesis that in a sample of Persian Gulf War veterans CFS was associated with cognitive deficits on computerized cognitive testing after controlling for the effects of premorbid cognitive differences. We obtained Armed Forces Qualification Test (AFQT) data acquired around the date of induction into the military on 94 veterans of the Gulf War, 32 with CFS and 62 healthy controls. Controls performed better than participants diagnosed with CFS on the AFQT. Cognitive deficits were associated with CFS on 3 of 8 variables after the effect of premorbid AFQT scores was removed with ANCOVA.
Clark, C., Buchwald, D., Macintyre, A., Sharpe, M and Wessely, S. Chronic fatigue syndrome: a step towards agreement. Lancet, 2002, 359, 97-98.
Summary of the CMO's working party Report on CFS, which advocates the name CFS/ME, more research and the provision of increased services.
[Ed. note: the section on pacing acknowledges that there are different views on this but ignores most of them. It does not mention two controlled trials which included pacing. The reference for the London criteria is incorrect and it overlooks the evidence for ongoing infection and the differences between the various fatigue syndromes.]
Eaton, L. Chronic fatigue report delayed as row breaks out over content. British Medical Journal, 2002, 324, 7. (5 January)
News item noting the resignation of members of the CMO's working group who were unhappy with the references to medical aspects of CFS, and the inclusion of pacing.
Endicott, NA. Chronic fatigue syndrome in psychiatric patients: exposure to potentially toxic substances. Journal of Chronic Fatigue Syndrome, 2002, 10, 1, 37-53.
Several investigators have suggested that environmental chemicals or "pollutants" play a significant role in the pathogenesis of CFS. This study compares the reported exposures to environmental chemicals and other potentially toxic environmental factors of psychiatric patients with CFS (CDc criteria '92) and two sets of controls from the same practice who did not meet the criteria for CFS. All comparisons found that CFS patients reported significantly more exposures to potentially toxic substances than any of the control groups.
Goudsmit, E. Response to Stainton Rogers. Health Psychology Update, 2002, 11, 1, 60-64.
Letter responding to an earlier article by Stainton Rogers (ibid, 10, 4, 29-32.
Hamilton, W. Chronic fatigue syndrome. British Journal of General Practice, 2001, 51, 473, 1015.
[Ed. note: Letter responding to previous correspondence. Author assumes that CFS covers a single entity and ignoring evidence of pathology in subgroups.]
Hammond, DC. Treatment of chronic fatigue [syndrome] with neurofeedback and self-hypnosis. NeuroRehabilitation, 2001, 16, 4, 295-300.
A 21 year old patient reported a relatively rapid onset of serious CFS, with her worst symptoms being cognitive impairments. Congruent with research on rapid onset CFS, she had no psychiatric history and specialized testing did not suggest that somatization was likely.
Neuroimaging and EEG research has documented brain dysfunction in cases of CFS. Therefore, a quantitative EEG was done, comparing her to a normative data base. This revealed excessive left frontal theta brainwave activity in an area previously implicated in SPECT research. Therefore, a novel treatment approach was utilized consisting of a combination of EEG neurofeedback and self-hypnosis training, both of which seemed very beneficial.
She experienced considerable improvement in fatigue, vigor, and confusion as measured pre-post with the Profile of Mood States and through collaborative interviews with both parents. Most of the changes were maintained at 5, 7, and 9 month follow-up testing.
Logan, AC and Wong, C. Chronic fatigue syndrome: oxidative stress and dietary modifications. Alternative Medicine Review, 2001, 6, 5, 450-459.
The role of oxidative stress in CFS is an important area for current and future research as it suggests the use of antioxidants in the management of CFS. Specifically, the dietary supplements glutathione, N-acetylcysteine, alpha-lipoic acid, oligomeric proantho-cyanidins, Ginkgo biloba, and Vaccinium myrtillus (bilberry) may be beneficial. In addition, research on food intolerance is discussed, since food intolerance may be involved in CFS symptom presentation and in oxidation via cytokine induction. Finally, recent evidence suggests celiac disease can present with neurological symptoms in the absence of gastrointestinal symptoms; therefore, celiac disease should be included in the differential diagnosis of CFS.
Madioni, F. A clinical approach to chronic fatigue syndrome with special emphasis on psychopathology. (Article, French). Annales Medico-Psychologiques, 2001, 159, 6, 431-436.
According to the author, the presence in these cases of a neurotic disorder sets the indication for a psychotherapy with psychodynamic or existential approach.
Mullington, JM., Hinze-Selch, D ad Pollmacher, T. Mediators of inflammation and their interaction with sleep - Relevance for chronic fatigue syndrome and related conditions. Role of Neural Plasticity in Chemical Intolerance, 2001, 933, 201-210.
In humans, activation of the primary host defense system leads to increased or decreased NREM sleep quality, depending on the degree of early immune activation. Modest elevations of certain inflammatory cytokines are found during experimental sleep loss in humans and, in addition, relatively small elevations of cytokines are seen following commencement of pharmacological treatments with clozapine, a CNS active antipsychotic agent, known to have immunomodulatory properties. Cytokines such as TNF-α, its soluble receptors, and IL-6, present in the periphery and the CNS, comprise a link between peripheral immune stimulation and CNS-mediated behaviors and experiences such as sleep, sleepiness, and fatigue. The debilitating fatigue experienced in CFS and related diseases may also be related to altered cytokine profiles.
Pall, ML and Satterlee, JD. Elevated nitric oxide/peroxynitrite mechanism for the common etiology of multiple chemical sensitivity, chronic fatigue syndrome, and posttraumatic stress disorder. Role of Neural Plasticity in Chemical Intolerance, 2001, 933, 323-329.
Patarca, R. Cytokines and chronic fatigue syndrome. Role of Neural Plasticity in Chemical Intolerance, 2001, 933, 185-200.
CFS patients show evidence of immune activation, as demonstrated by increased numbers of activated T lymphocytes, including cytotoxic T cells, as well as elevated levels of circulating cytokines. Nevertheless, immune cell function of CFS patients is poor, with low natural killer cell cytotoxicity (NKCC), poor lymphocyte response to mitogens in culture, and frequent immunoglobulin deficiencies, most often IgG1 and IgG3. Immune dysfunction in CFS, with predominance of so-called T-helper type 2 and proinflammatory cytokines, can be episodic and associated with either cause or effect of the physiological and psychological function derangement and/or activation of latent viruses or other pathogens. The interplay of these factors can account for the perpetuation of disease with remission/exacerbation cycles. A T-helper type 2 predominance has been seen among Gulf War syndrome patients and this feature may also be present in other related disorders, such as multiple chemical sensitivity. Therapeutic intervention aimed at induction of a more favorable cytokine expression pattern and immune status appears promising.
Richardson, J. Viral isolation from brain in myalgic encephalomyelitis. A case report. Journal of Chronic Fatigue Syndrome, 2001, 9, 3/4, 15-19.
Case report of male patient who met Dr. Richardson's criteria for ME. Autopsy showed enterovirus specific genomic sequences, indicating active infection in the brain.
Richardson, J. Myalgic encephalomyelitis: guidelines for doctors. Journal of Chronic Fatigue Syndrome, 2002, 10, 1, 65-80.
Review of symptoms and possible treatments.
Sachs, L. From a lived body to a medicalized body: diagnostic transformation and chronic fatigue syndrome. Medical Anthropology, 2001, 19, 4, 299-317
This paper addresses the diagnostic dilemma posed by chronic illness that offers no demonstrable evidence of serious physical disorders or pathology. Is a diagnosis such as CFS disabling because it encourages people to identify with it? Does it become a self-fulfilling prophecy? In providing people with a name, and thus allowing them to confirm the legitimacy of their suffering, a diagnosis of CFS may help them to relate to their world and, hence, facilitate their recovery. One of the most relevant questions pertaining to a diagnosis of CFS concerns how people deal with suffering when it does not come with a biomedically established pathology. I draw upon material provided by 21 men and women diagnosed with CFS. My analysis concerns the ambivalence involved in the diagnostic process and its implications for the relationship between self-identity and chronicity.
Stores, G. Disturbances of sleep in the chronic fatigue syndrome. Sleep Disturbances in Children and Adolescents with Disorders of Development: Its Significance and Management,2001, 155, 192-195.
Straus, SE. Caring for patients with chronic fatigue syndrome. Lancet, 2002, 324, 124-125.
Leader noting that the Working Group's "conclusions appear more shaped by anecdote than by evidence". The Report to the CMO mentions the seminal studies on graded activity and GET as well as the possible problems of pacing: "a key recommendation without any proof". On the other hand it endorses the view that doctors should accept the illness now and move on.
Interestingly, Straus refers to CFS, not CFS/ME, except for the first paragraph.
Van Heck, GL and De Vries, J. Quality of life of patients with chronic fatigue syndrome. Journal of Chronic Fatigue Syndrome, 2002, 10, 1, 17-35.
The purpose of this study was to compare quality of life between patients with CFS (n = 73) and healthy controls (n =147), using a broad and generic quality of life assessment instrument, the World Health Organization Quality of Life assessment (WHOQOL-100).
Participants were assessed on the WHOQOL-100, a self-assessment instrument designed for quantifying 24 facets relating to quality of life. These facets are grouped into six larger domains: physical health, psychological health, level of independence, social relationships, environment, and spirituality. The WHOQOL-100 also includes one facet examining overall quality of life and general health perceptions.
Analyses revealed that the group with CFS (CDC criteria '88) reported significantly lower levels of quality of life than the control group on overall quality of life and general health perceptions and on 22 out of the 24 facets of quality of life. Compared to earlier studies that used health-status scales or rather limited quality of life measures, this study generated a more complete picture of the problems of patients with CFS.
The results suggest that the impact of CFS on the patients' lives is very profound. CFS has a quality-of-life burden that affects a wide range of factors inherent to quality of life. Questions that must be addressed by future research are considered.
White, PD., Thomas, JM., Kangro, HO., Bruce-Jones, WDA., Amess, J., Crawford, DH., Grover, SA and Clare, AW. Predictions and associations of fatigue syndromes and mood disorders that occur after infectious mononucleosis. Lancet, 2001, 358, 1946-1954.
This study followed 118 people with glandular fever and 127 people with URTIs. They were interviewed one month, two months and six months after onset. Care records were checked two years following the final interview. Details were obtained relating to symptoms, the infection, bed rest, fitness, personality (emotionality), mood disorders, social adversity and other clinical and psychosocial variables.
CFS was defined empirically (fatigue but no psychiatric disorders?) and according to the Oxford and CDC '94 criteria (allowing psychiatric disorders). No distinction was made between CFS and ICF (CDC criteria '94).
There were no significant differences between the groups in age, gender, personality factors, psychiatric history, or pre-onset social adversity. Past psychiatric history or mood disorder did not predict empirically defined CFS
Predictors of CFS included positive monospot test at onset and fitness (p<.05). Mood disorder at 2 months and emotional personality were predictive for CFS (Oxford criteria only) and pre-morbid mood disorder was predictive for CFS/ICF (CDC criteria). Most CFS patients had a mood disorder prior to infection. Number of symptoms at onset and use of antibiotics were not predictors.
The researchers note that the predictors depend on the definition used and emphasise the possible role of inactivity-deconditioning as a contributing factor for developing CFS.
Kerr, JR., Barah, F., Mattey, DL., Laing, I., Hopkins, SJ., Hutchinson, IV and Tyrrell, DAJ. Circulating tumour necrosis factor-alpha and interferon-gamma are detectable during acute and convalescent parvovirus B19 infection and are associated with prolonged and chronic fatigue. Journal of General Virology, 2001, 82 (Pt 12), 3011-3019.
To investigate whether cytokine responses may have a bearing on the symptoms and outcome of parvovirus B19 infection, circulating cytokines were measured during acute infection (n=51), follow-up of acute infection (n=39) and in normal healthy controls (n=50). At acute B19 virus infection (serum anti-B19 IgM-positive), patients ranged in age from 4 to 54 years, with a mean age of 28-2 years. The male: female ratio was 1:41 and symptoms were rash (n=15), arthralgia (n=31), fatigue (n=8), lymphadenopathy (n=4), foetal hydrops (n=3), transient aplastic crisis (n=2), neutropenia (n=2), myelodysplasia (n=1), thrombocytopenia (n=1) and pancytopenia (n=1). Of these patients, 39 were contacted after a follow-up period of 2-37 months (mean of 22-5 months). In comparison with normal controls, detectable IL-6 was associated with acute B19 virus infection (26%; p=0.0003), but not with follow-up (6%; p=0.16). Detection of interferon (IFN)-gamma was associated with acute B19 virus infection (67%; p<0.0001) and follow-up (67%; p<0.0001). Detection of tumour necrosis factor (TNF)-α was associated with acute B19 virus infection (49%; p<0.0001) and follow‑up (56%; p<0.0001). IL-1 beta was detected in acute infection (20%), but not at follow-up. At acute B19 virus infection, detection of serum/plasma IL-6 was associated with rheumatoid factor (p=0.038) and IFN-gamma (greater than or equal to 7 pg/ml) was associated with fatigue in those patients of >15 years of age (p=0.022). At follow-up, fatigue was associated with IFN-gamma (> 7 pg/ml) and/or TNF‑α (>40 pg/ml) (p=0.0275). Prolonged upregulation of serum IFN-gamma and TNF-α appears to represent a consistent host response to symptomatic B19 virus infection.
Tensing, EK., Solovieva, SA., Tervahartiala, T., Nordstrom, DC., Laine, M., Niissalo, S and Konttinen YT. Fatigue and health profile in sicca syndrome of Sjogren's and non-Sjogren's syndrome origin. Clinical and Experimental Rheumatology, 2001, 19, 3, 313-316.
The aim of this study was to assess the health status and fatigue in sicca patients with or without Sjogren's syndrome (SS) and to test whether the immune-inflammatory activity or the extent of the disease predict fatigue in SS.
The Medical Outcomes Study Short-Form General Health Survey (MOS SF-36) was used in 1 degree SS (n = 90), 2 degrees SS (n = 24), non-SS patients with sicca symptoms (n = 15) and healthy population controls (n = 126). Laboratory values and clinical findings were used to predict fatigue in SS.
It was found that 74% of the SS and 80% of the non-SS sicca patients felt tired. In SS neither hemoglobin, ESR nor CRP predicted fatigue. Surprisingly, high serum IgG (p<0.05), antinuclear antibodies (ANA) (p<0.01) and SS-A antibodies (p<0.05) values correlated positively with vitality. The total number of disease manifestations, and ANA and/or SS-A autoantibodies were the best predictors of fatigue, but explained it only to 17-57%. Fatigue in both SS and non-SS sicca syndrome more likely correlates to other features, such as neuroendocrine aspects of the disease.
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