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Volume 2, Number 4 |
1st December 1999 |
Clapp, LL., Richardson, MT., Smith, JF., Wang, M., Clapp, AJ and Pieroni, RE. Acute effects of thirty minutes of light-intensity, intermittent exercise on patients with chronic fatigue syndrome. Physical Therapy, 1999, 79, 8, 749-756.
This investigation examined whether light-intensity, intermittent physical activity exacerbated symptoms in patients with CFS immediately following exercise and up to 7 days following exercise. Subjects were 9 women and 1 man who met the CDC criteria '94*.
They performed 10 discontinuous 3-minute exercise bouts (separated by 3 minutes of rest, sitting or supine) at a self-selected, comfortable walking pace on a treadmill. Oxygen consumption, minute ventilation, respiratory exchange ratio, and heart rate were measured every minute during the exercise session. To assess the degree of disability, general health status, activity level, symptoms and mood, subjects completed various questionnaires before and after exercise (e.g. Karnofsky Rating Scale, POMS, 20-item MOS). The mean Karnofsky score before the study was 66.67.
The results indicated that degree of disability, general health status and mood did not change immediately and up to 7 days following exercise. There was an increase in fatigue during exercise as well as reports of headaches, leg pain and sore throats but these were not regarded as severe and did not persist. Some symptoms e.g. depression and tension, improved for a short time. The mean Karnofsky score after a week was 67.50.
"Thirty minutes of intermittent walking did not exacerbate symptoms in subjects with CFS. The physiological data did not show any abnormal response to exercise." Although this study did not determine whether 30 minutes of continuous versus intermittent exercise would exacerbate symptoms, all 10 subjects felt that they could not exercise continuously for 30 minutes without experiencing symptom exacerbation. Despite this limitation, the results indicate that some individuals with CFS may be able to use low-level, intermittent exercise without exacerbating their symptoms.
*[Ed. note: This definition does not require the presence of post-exertional fatigue or malaise.]
Scott, LV., Teh, J., Reznek, R., Martin, A., Sohaib, A and Dinan, TG Small adrenal glands in chronic fatigue syndrome: a preliminary computer tomography study. Psychoneuroendocrinology, 1999, 24, 7, 759-768.
Eight patients with post-viral CFS (CDC criteria '94) and no psychiatric disorders, who had a subnormal response on the adrenocorticotropin (ACTH) stimulation test (1µm)*, were recruited from a fatigue clinic. All underwent a computer tomography (CT) adrenal gland assessment. Their results were compared to those of 55 healthy controls.
"The right and left adrenal gland bodies were reduced by over 50% in the CFS subjects indicative of significant adrenal atrophy".
This is the first study to use imaging methods to measure adrenal gland size in CFS. It is a limitation of this study that a selected CFS sample was employed. A future larger study would optimally employ an unselected cohort of CFS patients.
*[Ed. note: This is "a test of adrenal gland functioning".]
Scott, LV., Medbak, S and Dinan, TG. Desmopressin augments pituitary-adrenal responsivity to corticotropin-releasing hormone in subjects with chronic fatigue syndrome and in healthy volunteers. Biological Psychiatry, 1999, 45, 1447-1454.
Corticotropin-releasing hormone (CRH) and vasopressin (VP) are the two principal neuropeptide regulators of the hypothalamic-pituitary-adrenal axis in man, with VP serving to augment CH- induced adrenocorticotropic hormone (ACTH) release. Unlike VP, desmopressin (DDAVP), a synthetic analogue of VP, has not been shown in healthy subjects to have consistent ACTH-releasing properties when administered alone.
100 µg of ovine CRH (oCRH) and 10 µg DDAVP, both alone and in combination, were administered to a group of subjects with CFS (CDC criteria '94, no psychiatric illness), and to a group of healthy volunteers. The aim was to establish the effect of DDAVP on CRH-induced ACTH release in these two groups.
The d-ACTH responses to oCRH were attenuated in the CFS group compared to the control subjects. The d-cortisol responses were also reduced in the CFS group compared to the healthy subjects. The d-ACTH and d-cortisol responses to DDAVP alone did not differ between the two groups. On administration of both CRH and DDAVP no response differences between the two groups for either ACTH or cortisol output were established. Comparing the ACTH and cortisol responses to CRH and CRH/DDAVP in only those individuals from each group who had both tests, the cortisol output to the combination was significantly greater in the CFS compared to the healthy group. The ACTH output was also increased in the former group, though this was not significant.
"DDAVP augments CRH-mediated pituitary-adrenal responsivity in healthy subjects and in patients with CFS. That DDAVP was capable of normalising the pituitary-adrenal response to oCRH in the CFS group suggests there may be increased vasopressinergic responsivity of the anterior pituitary in CFS and/or that DDAVP may be exerting an effect at an adrenal level". DDAVP may enhance ACTH release.
Stewart, JM., Gewitz, MH., Weldon, A and Munoz J. Patterns of orthostatic intolerance. The orthostatic tachycardia syndrome and adolescent chronic fatigue. Journal of Pediatrics, 1999, 135, 2, 218-225.
Using electrocardiography and arterial tonometry, the researchers investigated the heart rate and blood pressure responses during head-up tilt (HUT) in 20 adolescents with orthostatic tachycardia syndrome (OTS) compared with 25 adolescents with CFS (CDC criteria '94), 13 healthy controls and 20 patients with simple faint.
Of the control subjects, 4 of 13 experienced typical vasovagal faints with an abrupt fall in blood pressure and heart rate, and 14 of 20 patients with simple faint experienced similar HUT responses.
All patients with CFS (25/25) experienced severe orthostatic symptoms, with syncope in 2 of 25, early orthostatic tachycardia during HUT in 16 of 23 (13/16 hypotensive), and delayed orthostatic tachycardia in 7 out of 23 (6/7 hypotensive). Acrocyanosis and oedema occurred in 18 of 25.
Early orthostatic tachycardia occurred in 10 of 20 patients with OTS. Of these, 9 of 10 were hypotensive, but hypotension was delayed in 4 of 9. Delayed tachycardia occurred in 10 of 20 (all hypotensive).
Thus acrocyanosis and oedema occurred in most patients with CFS, fewer patients with OTS, and in one patient with simple faint. Orthostatic symptoms were similar but more severe in patients with CFS compared with patients with OTS.
Symptoms and patterns of orthostatic heart rate and blood pressure change in OTS overlap strongly with those of CFS. "Orthostatic intolerance in OTS may represent an attenuated form of chronic fatigue pathophysiology." Deconditioning may contribute to OI in CFS patients but is not important in OTS since many remain active.
There is evidence that adults with significant OI and neurally mediated hypotension represent a subset of people with CFS.
Blenkiron, P., Edwards, R and Lynch, S. Associations between perfectionism, mood, and fatigue in chronic fatigue syndrome. A pilot study. Journal of Nervous and Mental Disease, 1999, 187, 9, 566-570.
Forty CFS sufferers attending a CFS clinic and 31 control healthy subjects completed the Multidimensional Perfectionism Scale (MPS), the Chalder Fatigue Questionnaire (14-item) and the Hospital Anxiety and Depression (HAD) scale.
Total MPS perfectionism scores were lower in the CFS group than the controls, reflecting fewer perfectionistic traits. The scores did not correlate with fatigue, anxiety or depression in either group. Other-oriented MPS scores were significantly lower among CFS sufferers, especially women, and correlated negatively with physical fatigue levels overall (r=-0.27, p=.02). Total and socially prescribed MPS scores correlated with age for the CFS group alone. Thus this study did not confirm a positive association between perfectionism and CFS. The finding that CFS sufferers set lower standards and have lower expectations for significant others may have implications for rehabilitation and recovery from this disorder.
Heijmans, M., de Ridder, D and Bensing, J. Dissimilarity in patients' and spouses' representations of chronic illness. Exploration of relations to patient adaptation. Psychology and Health, 1999, 14, 3, 451-466.
In this cross-sectional study, the illness representations of patients suffering from CFS (n=49) and Addison's Disease (n=52) and those of their spouses were compared.
Couples generally held similar views with regard to the dimensions of illness identity and cause but disagreed on other variables e.g. control/cure, and consequences of the illness.
Dissimilar views were found to have a weak impact on coping and a rather strong impact on adaptive outcome. In general, minimisation of the disorder's seriousness by the spouse was found to have a negative impact on adaptive outcome, although this effect differed with the dimension of illness representation and the type of illness. These results demonstrate the importance of the role of significant others and their beliefs for patient's coping and adaptation with chronic illness.
Powell, P., Edwards, R and Bentall, R. The treatment of wheelchair-bound chronic fatigue syndrome patients: two case studies of a pragmatic rehabilitation approach. Behavioural and Cognitive Psychotherapy, 1999, 27, 249-260.
Two case studies where patients with CFS (Oxford criteria) were successfully treated by a therapist using cognitive behaviour therapy (CBT) and graded exercise. For instance, sessions focused on challenging dysfunctional beliefs (e.g. that headaches were caused by a tumour or that chest pains represented a heart attack). After about 55 to 60 sessions, often by telephone, patients were no longer resting for long periods in bed or using a wheelchair.
Hill, NF., Tiersky, LA., Scavalla, VR., Lavietes M and Natelson BH. Natural history of severe chronic fatigue syndrome. Archives of Physical Medicine and Rehabilitation, 1999, 80, 9, 1090-1094.
Patients with CFS were enrolled from April 1992 to February 1994 and were evaluated three times. Time 1 (at enrolment): history, physical evaluation and psychiatric evaluation; Time 2 (median = 1.6yrs after initial evaluation): postal questionnaire to assess current condition; Time 3 (median = 1.8yrs after Time 2): medical and psychiatric evaluations.
The 23 patients in this study fulfilled the CDC criteria ('88) and had symptom complaints that were substantial or severe. All had been ill for less than 4.5 years; none had a DSM-III-R psychiatric disorder in the 5 years before illness onset and none had substance abuse in the 10 years before enrolment.
Severity of CFS symptoms was assessed by self-report questionnaires, laboratory tests, and medical examination. Psychological status was assessed using the Q-DIS and the Centers for Epidemiological Study-Depression Scale. At each time of evaluation, patients were categorised as severe, slightly improved, improved, and recovered.
Over the 4 years of the study, 13 patients (57%) remained severely ill, 9 improved (29%) although they still fulfilled the '94 criteria, and 1 (4%) recovered. Illness duration, mode of onset, psychiatric status or depressed mood at intake or chemical sensitivity did not predict illness outcome. One patient was diagnosed with an alternate illness, but it probably did not explain her CFS symptoms. Mood improved for those patients whose illness lessened.
"The prognosis for recovery was extremely poor for the severely ill subset of CFS patients. The majority showed no symptom improvement... Illness severity between Times 2 and 3 remained stable".
[Ed. note: There is no information as to treatments tried during this study. The authors only refer to standard medical care.]
Jason, LA., Richman, JA., Rademaker, AW., Jordan, KM., Plioplys, AV., Taylor, RR., McCready, W., Huang, CF and Plioplys, S. A community-based study of chronic fatigue syndrome. Archives of Internal Medicine, 1999, 159, 2129-2137.
Most previous estimates of the prevalence of CFS have derived largely from treated populations, and have been biased by differential access to health care treatment linked with sex, ethnic identification and socio-economic status. The aim of this study was to assess the point prevalence of CFS in an ethnically diverse random community sample.
A sample of 28,673 adults in Chicago, Ill, was screened by telephone, and those with CFS-like symptoms were medically evaluated.
The main outcome measures included self-report questionnaires (phase 1 and 2), psychiatric evaluations (SCID in phase 2), and complete medical examinations with laboratory testing to diagnose patients with CFS (phase 2). Univariate and multivariate statistical techniques were used to delineate the overall rate of CFS (CDC criteria '94) in this population, and its relative prevalence was subcategorised by sex, ethnic identification, age, and socio-economic status.
There was a 65.1% completion rate for the telephone interviews during the first phase of the study. At this stage, 1435 (7.7%) had prolonged fatigue, 780 (4.2%) had chronic fatigue, of whom 39% had a CFS-like illness (not enough minor symptoms to fulfil the CDC criteria), and 52.3% had CFS-like profiles. The latter were invited to participate in phase 2, which included a physical examination, psychiatric interview and medical history form. A control group of 199 screened people with no CFS were included for comparison.
Findings indicated that CFS occurs in about 0.42% (95% confidence interval, 0.29%-0.56%) of this random community-based sample. The highest levels of CFS were consistently found among women, minority groups and persons with lower levels of education and occupational status. People with chronic fatigue and CFS had more fatigue than the controls. There was no significant difference between the chronic fatigue, CFS and CFS-like condition in terms of number of minor symptoms.
"Chronic fatigue syndrome is a common chronic health condition, especially for women, occurring across ethnic groups. Earlier findings suggesting that CFS is a syndrome primarily affecting white, middle-class patients were not supported by our findings."
[Ed. note: Only 75% of the CFS patients reported post-exertional malaise, showing that CFS as currently defined is not the equivalent of ME.]
Ang, DC and Calabrese, LH. A common-sense approach to chronic fatigue in primary care. Cleveland Clinic Journal of Medicine, 1999, 66, 343-346, 349-350, 352.
Short review.
[Ed. note: This article contains an uncritical analysis of the psychiatric literature.]
Scott, LV and Dynan, TG. The neuroendocrinology of chronic fatigue syndrome: Focus on the hypothalamic-pituitary-adrenal axis. Functional Neurology, 1999, 14, 1, 3-11.
Short review of the literature on the functioning of the hypothalamic-pituitary-adrenal axis in CFS. According to the authors, the illness may be triggered by stress.
Starcevic, V. Neurasthenia: Cross-cultural and conceptual issues in relation to chronic fatigue syndrome. General Hospital Psychiatry, 1999, 21, 4, 249-255.
Short article on neurasthenia, noting the different definitions used, and the differences as well as the similarities between neurasthenia and CFS.
Chazotte, B and Pettengill, M. Using membrane potential to follow cytokine effects on mitochondria and possible dysfunction in chronic fatigue syndrome. (Meeting Abstract). Biophysical Journal 1999, 76, 1, A363.
Short report of study focusing on cellular and mitochondrial energy metabolism in individual living cells using laser scanning confocal microscopy. The findings suggested "possible mitochondrial dysfunction. Interferon-a added to cultured human fibroblasts or leukocytes was found to decrease mitochondrial membrane potentials and areas at mitochondrial potentials. Interleukin-2 also affects mitochondrial potentials and may induce an unexplained photosensitivity."
Herrell, R., Buchwald, D., Hartman, S., Belcourt, M., Schmaling, K and Goldberg, J. Chronic fatigue and functional status. A co-twin control study. American Journal of Epidemiology, 1999, 149, 11 Suppl. S44, no 173.
Abstract comparing twins, one of whom suffered from chronic fatigue for six months or more (n=115 pairs). Further analysis compared those who met more stringent criteria (CFS-like illness: n=69 discordant pairs) and cases of CFS who were medically examined (n=19, all monozygotic pairs).
The size of the intra-pair mean difference on the MOS physical health scale was large and increased as the definition of fatigue became more stringent. Differences on the mental health scale were smaller though also related to definition.
Jackson, EL. The effects on siblings in families with a child with chronic fatigue syndrome. Journal of Child Health Care, 1999, 3, 2, 27-32.
Short article on the consequences of having a child with CFS/ME, particularly the effects on siblings.
Marcusson, JA. The frequency of mercury intolerance in patients with chronic fatigue syndrome and healthy controls. Contact Dermatitis, 1999, 41, 1, 60-61.
Letter reporting that more patients with CFS responded to a patch test for metals than a group of controls (26% versus 3%, p<.001). Results from a questionnaire asking about symptoms following removal of amalgam etc., suggest that mercury intolerance may be more prevalent in this patient group than in the general population.
Noah, L. Pigeonholing illness: Medical diagnosis as a legal construct. Hastings Law Journal 1999, 50, 2, 241-307.
Paper on the legal aspects of the classification of disorders.
[Ed. note: This author seems to exaggerate the 'abuse' of the term CFS for financial and personal gain (e.g. to get benefits, and have an acceptable label for emotional distress), citing articles from the Kings College team and people like Shorter.]
Perry, LD. Chronic fatigue syndrome? Pediatrics 1999, 104, 1, 130. Also Plioplys, AV. 130-131. With reply by Krilov, LR, Fisher, M and Friedman, SB 131-132.
Perry and Plioplys respond to a study by Krilov et al (ibid., 1998, 102, 360.) They discuss a number of flaws including possible misdiagnosis, failure to include important variables and misinterpretation of the findings. Krilov et al discuss the points raised and explain their design and conclusions.
Ware, NC. Toward a model of social course in chronic illness: The example of chronic fatigue syndrome. Culture, Medicine and Psychiatry, 1999, 23, 3, 303-331.
Results of a longitudinal study of 66 patients with CFS (CDC criteria '88). The author focuses on the social course of the illness and the problems faced by those affected, e.g. the social isolation, the trivialisation of symptoms, the effects of delegitimation and financial loss.
[Ed. note: Although the influence of American culture means that some observations may not apply to patients elsewhere (e.g. the stress of the multiple activities and high expectations associated with American life), this paper provides many important insights.]
Wessely, S., Nimnuan, C and Sharpe, M. Functional somatic syndromes: one or many? Lancet, 1999, 354, 936-939.
This review suggests that conditions like CFS, hyperventilation syndrome, pre-menstrual syndrome, tension headache, multiple chemical sensitivity, globus syndrome and irritable bowel syndrome (IBS) have "much in common". Functional somatic syndromes (FSS) are defined here as conditions which "after appropriate medical assessment, cannot be explained in terms of a conventionally defined medical disease".
The arguments supporting the view that these syndromes have much in common and might be "different parts of a larger animal" include:
1. an apparent overlap of symptoms;2. patients with one syndrome frequently meet the diagnostic criteria for others;
3. patients with these syndromes share non-symptom characteristics, such as relatively high rates of emotional distress, the "predominance" of women, a history of child abuse and difficulties in the doctor-patient relationship;
4. all functional syndromes tend to respond to the same therapies.
The authors argue that a reclassification of these separate disorders should be considered. They question whether the differences are clinically significant.
[Ed. note ~: It seems that the authors are grouping conditions under one label, largely on the basis of a lack of knowledge and/or understanding. More importantly, they ignore and underplay the various differences. For example, a study on ME found muscle weakness after exercise which increased for at least 24 hours after the exertion had ceased (Paul et al 1999). To my knowledge, this has not been documented in PMS, lBS or hyperventilation syndrome.Their approach reminds me of old-fashioned reductionism. They suggest that as long as there is no reasonable (conventionally defined) explanation, an illness is not a disease. Thus in CFS, the finding of a specific immune abnormality in strictly-defined cases (replicated three times) and the hypoperfusion of the brainstem (replicated twice), are simply ignored. The implication here is that if we don’t know exactly how those changes relate to the symptoms, it’s perfectly valid to classify the illness as ‘unexplained’.
Some have questioned whether we should study and manage the listed disorders primarily according to type. In terms of CFS, this seems a reasonable approach, given the problems documented since the introduction of the Oxford criteria. As Friedberg has noted (see below), the use of such broad definitions has resulted in mixed populations, caused much confusion and made it difficult to interpret the research. Why should we now extend this approach to other conditions? If grouping disorders together did little to increase our understanding of CFS, how will it help us in relation to the other functional syndromes? Isn’t it time to study the differences as well as the similarities?
At the heart of the matter is what constitutes ‘good’ evidence. Should we go ahead and reclassify disorders because most patients report symptoms like fatigue and headaches, or the fact that the majority of those affected are female etc? Is that good evidence? Is it more persuasive than the findings linking CFS with ongoing pathology e.g. Paul et al, Costa et al? Wessely et al obviously believe it is. I do not.
See also Viewpoint/Book Review.]
Proceedings from the Fourth International Conference of the American Association for Chronic Fatigue Syndrome, held in September 1998 in Cambridge, Massachusetts, USA. Journal of Chronic Fatigue Syndrome, 1999, 5, 3/4.
Interesting articles in this issue include:
Jason et al (ibid., 3-33) on the definition and theoretical issues, (with a discussion about the confusion resulting from the use of broad criteria);
Jason et al (ibid., 35-54) on the three phases of CFS: namely crisis, stabilisation and integration;
Racciatti et al (ibid. 61-70) on the heterogeneity of patients with CFS (as defined using the CDC criteria '94);
Donnay and Zien (ibid., 71-80) on the high prevalence rate of CFS (CDC criteria '94) and fibromyalgia among people with multiple chemical sensitivity, and
Walker (ibid., 91-93) on the positive outcomes among patients seen at the University of Michigan, where three-quarters reported feeling better about 14 months after their initial visit. The more severely affected did not differ from the less severely affected in terms of age, activity, exercise and perception of causes.
In the clinical section, Rowe (ibid., 97-107) notes that most patients who completed a trial of gammaglobulin had not deteriorated five years later. Sixty per cent of the participants considered they were 'well' at the last follow-up (45% scored 10/10), although a significant number were still disabled. Cheney and Keever (ibid., 115-116) report that of the 14 patients with CFS who were treated with a growth hormone secretagogue (to raise IGF-1 levels), 57% noted a beneficial response.
In the interdisciplinary section, Friedberg (ibid. 149-159) discusses the reasons why CBT and graded exercise programmes appear to be more effective in British trials than in American or Australian ones. He believes that there are subgroups of CFS patients, and that British researchers have tended to include individuals with chronic fatigue caused by primary psychiatric disorders or psychosocial factors. Indeed, he cites studies suggesting that British research samples show "substantial similarities" to depression, somatisation or phobia patients while the population studied in the States and elsewhere more closely resemble "fatiguing neurological illnesses".
Following a review of the literature, Friedberg concludes that graded exercise and CBT may be most appropriate for low functioning patients with a phobic-like fear of symptom exacerbation. Conversely, high functioning individuals, or low-functioning ones without a disproportionate fear of symptom flare-ups, may show a much more limited response to this type of intervention. He also mentions the follow-up reports on the initial trial of CBT (by Sharpe et al) which showed that outcome improvements had "begun to decline 17 months after treatment termination... suggesting that these patients are not recovered". He recommends a coping skills approach using techniques such as stress management, pleasant mood induction and activity pacing.
Findings from Bazelmans et al (ibid., 175-176) indicate that a woman's double role does not make her more prone to CFS while Prins et al (ibid., 177-178) report that family doctors in Holland would appreciate more information about CFS. A survey found that they tended to attribute the illness primarily to psychosocial factors but that their empathy and understanding was determined by the number of patients and the years in practice.
Johnson et al (ibid. 185-186) compared personality variables of people with CFS and MS. They found a number of similarities, though both groups differed from healthy controls. In their view, the abnormalities were a likely result of "the demoralizing effects of coping with a chronic, disabling illness marked by uncertainty. CFS subjects have the additional burden of an illness that lacks medical legitimacy".
In the microbiology section, Levine (ibid., 199-206) presents data suggesting that Bornavirus may play a role in a small subgroup of CFS patients. Suhadolnik et al (ibid., 223-242, and 243-244) found a significant upregulation in CFS of the 2-5A synthetase/RNase L antiviral pathway. Moreover, there was a significant negative correlation between these findings and disability, as measured by the Karnofsky Performance Score. Other findings also suggest a relationship between the upregulation of the 2-5 A synthetase/RNase L pathway and a lower state of general health, and not just in the most severely affected patients.
Ablashi et al (ibid., 244-245) implicate human herpesvirus-6 (HHV-6) reactivation, while Knox et al (ibid., 245-7) refer to a "persistent infection" with HHV-6. In their view, patients should be assessed using multiple blood samples over a period of weeks or months to obtain more accurate data. Klapow (ibid., 247-8) found evidence of a nematode parasite (C. pulmoni) in a subset of patients, while Peckerman et al (ibid., 252-253) suggest that the more severely affected may have a "low flow circulatory state". Finally, Paul and Wood (ibid., 253-4) report that compared to healthy controls, patients with CFS have poorer balance following exercise, at least when they are tested with their eyes closed.
Andreu, A., Hanna, MG., Reichmann, H., Bruno, C, Penn, AS et al. Exercise intolerance due to mutations in the cytochrome b gene of mitochondrial DNA. New England Journal of Medicine, 1999, 341, 1073-1044.
A study which suggests that mitochondrial myopathy is associated with somatic mutations in the cytochrome b gene of mtDNA. This myopathy is one cause of the common and often elusive syndrome of exercise intolerance.
With editorial by Griggs, RC and Karpati, G. (ibid. 1077-1078).
Hickie, I., Koschera, A., Hadzi-Pavlovic, D., Bennett, B and Lloyd, A. The temporal stability and co-morbidity of prolonged fatigue: a longitudinal study in primary care. Psychological Medicine, 1999, 29, 4, 855-861.
Adults attending primary care completed questionnaires designed to detect cases of prolonged fatigue and psychological distress at presentation and 12 months later. Measures included the General Health Questionnaire-30 (GHQ-30) and Schedule of Fatigue and Anergia (SOFA).
Of the 652 patients, the prevalence rates of 'prolonged fatigue' alone, 'psychological distress' alone, 'prolonged fatigue + psychological distress' and 'no disorder' were 7%, 19%, 15% and 59% respectively at initial assessment. Of those patients with a prolonged fatigue syndrome initially, 58% still reported fatigue 12 months later (representing 13% of the total sample). Most importantly, the risk of developing prolonged fatigue was not increased in patients who initially had psychological distress, neither was the risk of developing psychological distress increased in patients who initially had prolonged fatigue.
"The longitudinal patterns of co-morbidity with psychological distress do not support an aetiological model that proposes a common vulnerability factor for these disorders. Psychiatric classification systems may be better served by treating prolonged fatigue and psychological distress as independent disorders."
Koschera, A., Hickie, I., Hadzi-Pavlovic, D., Wilson, A and Lloyd, A. Prolonged fatigue, anxiety and depression: exploring relationships in a primary care sample. Australian and New Zealand Journal of Psychiatry, 1999, 33, 4, 545-552.
Self report measures of prolonged fatigue (SOFA) and psychological distress (GHQ-30) were administered to consecutive ambulatory care patients attending primary care.
Data from 1593 subjects were obtained. A two-factor principal component solution (varimax rotation) demonstrated a clear separation between fatigue-related items as compared with those items describing anxiety and/or depression. A four-factor solution produced similar results with two factors describing general psychological distress (contrasting anxiety and depression), with two other factors describing the profiles of mental and physical fatigue.
The results lend weight to the argument that prolonged fatigue states can be measured independently of conventional notions of anxiety and depression in patients attending primary care.
Van der Linden, G., Chalder, T., Hickie, I., Koschera, A., Sham, P and Wessely, S. Fatigue and psychiatric disorder: different or the same? Psychological Medicine, 1999, 29, 4, 863-868.
A total of 1177 patients were recruited on attending their general practitioner. Fatigue and psychiatric disorders were measured at three time points with the 12-item GHQ and the 11-item Fatigue Questionnaire (Chalder et al 1993).
Total scores for fatigue and psychiatric disorder did not differ between the three time points and were closely correlated. The association between non-co-morbid ('pure') fatigue and developing psychiatric disorder 6 months later was the same as that for being well and subsequent psychiatric disorder. Similarly, having non-co-morbid psychiatric disorder did not predict having fatigue any more than being well 6 months previously. Between 13 and 15% suffered from non-co-morbid fatigue at each time point and 2.5% suffered from fatigue at two time points 6 months apart. Less than 1% of patients suffered from non-co-morbid fatigue at all three time points.
Non-co-morbid (pure) fatigue did not predict subsequent psychiatric disorder more than the reseverse. Moreover, the data are consistent with the existence of 'pure' independent fatigue state, not associated with psychiatric morbidity. However, this state is unstable and many of the patients become well or, in a small number of cases, are left with emotional distress (GHQ scores only). A persistent, independent fatigue state lasting for 6 months can be identified in the primary-care setting, but it is uncommon - of the order of 2.5% (when lasting 6 months) or under 1% (when lasting longer than 7 months).
Bell, IR et al. Patterns of waking EEG spectral power in chemically intolerant individuals during repeated chemical exposures. International Journal of Neuroscience, 1999, 97, 41-59.
Previous studies indicate that low level chemical intolerance (CI) is a symptom of several different conditions with neuropsychiatric features, e.g., CFS, fibromyalgia, multiple chemical sensitivity, and "Persian Gulf Syndrome". Prior studies suggest that limbic and/or mesolimbic sensitisation may contribute to development of CI. The purpose of this report was to document the waking electroencephalographic (EEG) patterns of individuals with CI during chemical exposures presented over repeated sessions.
Three groups of adult subjects who were recruited from the community participated in the study: self-reported CI who had made associated lifestyle changes due to their intolerance (CI/LSC, n=10), self-reported CI who had not made such changes (CI, n=8), and normal controls without self-reported CI (n=12). Subjects underwent two sessions involving one-minute EEG recordings during exposures to low level chemical odours (a probe for limbic activation).
The EEG data showed that the CI, but not the CI/LSC group "had increased absolute delta power after the chemical exposures during the second, but not the first, session". The findings support the neural sensitisation hypothesis for intolerance to low levels of environmental chemicals in vulnerable individuals. Those with the strongest past history with sensitising agents may not show short-term sensitisation to low level exposures in the laboratory.
The counselling versus antidepressants in primary care study group. How disabling is depression? Evidence from a primary care sample. British Journal of General Practice, 1999, 49, 95-98.
This study revealed differences on various MOS subscales between patients suffering from moderate depression and people with CFS.
Kipen, HM et al. Prevalence of chronic fatigue and chemical sensitivities in Gulf Registry veterans. Archives of Environmental Health, 1999, 54, 5, 313-318.
Postal questionnaires were completed by 1161 veterans from the Gulf War conflict. Of the respondents, 15.7% met the criteria for CFS (CDC '94), 13.1% fulfilled the criteria for multiple chemical sensitivities (MCS) and 3.3% of the respondents had both conditions. Thirty-six per cent of veterans reported being unusually sensitive to certain chemicals. There were no effects of gender, race, branch, duty status, or rank, although MCS was somewhat more prevalent in women and African Americans.
With editorial by Meggs (ibid., 309-311) focusing on chemical sensitivities.
Manu, P. (Ed.) Functional Somatic Syndromes. Etiology, diagnosis and treatment. Cambridge University Press. 1998 Hb. £65.
Functional Somatic Syndromes (FSS) are the latest medical fashion to hit Western psychiatry. The term describes disorders like CFS, fibromyalgia, pre-menstrual syndrome (PMS), multiple chemical sensitivities (MCS), temporomandibular disorders and interstitial cystitis. These conditions can apparently be lumped together because they share "multiple somatic symptoms", they lack "defining structural defects or laboratory abnormalities", there's a "frequent association with psychiatric disorders", an "absence of proven pathophysiological mechanisms" and "a paucity of effective therapeutic interventions". Since I'm not an expert on every disorder described in the book, I can't judge the accuracy and reliability of all the chapters. However, I do have specialist knowledge of PMS and CFS, so in this review, I'll focus on these conditions, as well as the information on definition, aetiology, disability and treatments.
The first thing I noticed about the chapter on PMS is that it fails to differentiate between the clinical condition and a separate research diagnosis known currently as pre-menstrual dysphoric disorder (PMDD). According to experts, PMDD is a "distinct entity with clinical and biologic profiles dissimilar to those seen in other disorders" such as depression (Endicott et al1).
PMS differs from PMDD in that symptoms such as breast tenderness, bloating, cramps and headaches are more common while PMDD is essentially a cyclical mood disorder, dominated by marked tension, irritability or depression.
Although author Teri Pearlstein acknowledges the heterogeneity of the population she describes, she completely ignores this fact when interpreting the research. In my view, such an approach is confusing and misleading. For instance, studies have shown that antidepressants and cognitive therapy help many women with PMDD. However, it doesn't follow that antidepressants should therefore be the "first line treatment for PMS", especially where the main symptom isn't tension or depression but breast pain, dizziness, fainting or headaches2. Laymen may generalise from one subgroup to the population as a whole but scientists shouldn't.
In short, this account of PMS is neither balanced nor particularly authoritative3. Pearlstein doesn't acknowledge the mass of evidence linking PMS with hormonal disturbances, nor does she mention the studies which found no psychological abnormalities in women with PMS. There's also a lack of critical analysis, and no respect for the political influences which have motivated some writers on the subject. For example, Pearlstein cites a certain professor who couldn't tell the difference between normal cyclical changes and PMS. The fact that this professor was a cognitive psychologist who aligned himself with radical feminists, had no clinical experience with PMS and did not, as far as I can recall, actually study women with PMS, is neither here nor there. The point is that his views are noted while those of experts like Professor Backstrom, a gynaecologist who has published a mass of studies on PMS, are not.
The chapter on CFS is even more selective, biased and unfair. Here's just one example of the way author Peter Manu cleverly misleads his readers. On page 22, there's a short section describing two studies on magnetic resonance imaging (MRI). Manu rightly concludes that findings from these types of brain scans tend to be non-specific and thus unhelpful. However, he doesn't mention the much more significant data which have been obtained using SPECT. Did Manu not know about that research? Yes, he did! How can I be so sure? Well, one of the two studies he describes in relation to MRI was actually a comparison of the two techniques (Schwartz et al). In fact, that study revealed abnormalities in 81% of the SPECT scans, and found that "the number of ... abnormalities appeared to correlate with clinical status". Manu also ignores another paper on SPECT, written by the same authors and published in the very same issue. It provided further support for the theory that CFS is linked to infection, as did Costa et al etc. For some reason, Manu doesn't even allude to this work.
As for the rest, there's virtually nothing on the endocrinological findings (which differentiate CFS from depression), and of course, there's no mention of McGarry et al's autopsy report (which provides more evidence of a viral link). There's no distinction made between studies on CFS and general fatigue (probably because there's a closer association between the latter and depression) and no acknowledgement that if a study on CFS includes people with psychiatric disorders, there's a fair chance one will find a statistical relationship between CFS and psychiatric disorders.
Of course, this state of affairs makes a mockery of the editor's claim that the book is based on "the best available publications" and "the principles of evidence-based medicine". No, the chapters I've read suggest that much of the analysis is based on the contributors' personal views and prejudices. Take for example Manu's summary of the research by Friedberg and Krupp. These researchers assessed the effectiveness of cognitive-behaviour therapy (CBT) and found "a trend toward reduced depression symptom scores" but "no significant changes in stress-related symptoms or fatigue severity". This is what Manu makes of the same study: "significant improvement was noted not only for measures of depression but also for fatigue severity and the cognitive and emotional reaction to fatigue" (p. 25). He acknowledges that his comments relate to the patients with CFS and depression. However, he forgot to mention that they represented a subset and that the results he cited did not apply to the group as a whole. That's not objective, dispassionate, evidence-based medicine: that's a case of being highly selective in the course of plugging one particular theory.
Manu concludes that research has "confirmed that the majority of patients with CFS are white middle-aged women with a high prevalence of current major depression and somatisation disorder and abnormal personality traits" (p. 26). Is this a fair representation of the literature? Not in my view (cf. Jason et al above)! I certainly don't think he can justify the link with somatisation disorder (cf. Johnson et al) or abnormal personality traits (cf. Blenkiron et al above). Moreover, one should not simply ignore patients who are older, younger, from a different ethnic background and men. And what about all the methodological flaws which make it difficult to interpret the data? We know that the broad criteria do not differentiate 'pure' post-infectious CFS from clinical depression (cf. Friedberg above). However, all these relevant factors are overlooked. So are the studies which found low rates of psychiatric disorders (e.g. Yeomans and Conway) and the reports suggesting that most psychological abnormalities are a reaction to physical disease (e.g. Stricklin). They're simply not mentioned. Why not? Psychiatrists all have a medical training. Surely they can cope with complicated issues?
A quick dip into the other chapters supports my view that this book is biased and out-of-date. The fairest chapter is the one on assessing disability, which surprised me since the author (Manu) works for an insurance company. Still, his contribution shows once again that the CDC guidelines are not specific enough, and that CFS actually covers a multitude of ills. The most interesting chapter is the review of common denominators, because it really shows just how different these syndromes are. The most out-of-date section must be the account of Gulf War Syndrome which lists the symptoms as fatigue, rash, headache, arthralgias, sleep disturbance, gastro-intestinal complaints and cough. As the rest of us know, some veterans have since died.
I've done my best to consider all the arguments presented in the book. However, I remain unconvinced that FSS is a useful concept. If grey is the new black in fashion, then perhaps these syndromes are the new psychosomatic disorders in medicine. A case of 'new wines in old bottles' perhaps? Or is this an attempt at 'rebranding': a way of avoiding some well-rehearsed criticisms and drawing our attention back to an old though slightly tarnished favourite. Let's face it. Psychosomatic medicine is not what it used to be. We've lost stomach ulcers courtesy of H. Pylori, and we know that headaches are often due to factors other than stress. The subject is in dire need of a new image. Is this supposed to be it?
A second criticism of the book is that it illustrates the 'dumbing-down' of modern psychiatry. On the one hand, the authors claim to be open-minded and evidence-based, but in reality, they are rigidly reductionistic and far from subtle in showing their bias.
I'm appalled by this approach. In relation to CFS, no one noted that when you study mixed populations, there are likely to be several subgroups, each with a different aetiology. More objective observers might have argued that while some subsets may be types of FSS (e.g. TATT), others are not (e.g. ME). As for psychotherapy, if you take any group of patients who've endured years of verbal abuse and insults, shouldn't we expect them to show a positive response to therapists who are kind to them, who acknowledge their suffering and who provide practical advice and handy-hints? Call it CBT, call it counselling, call it what you like. It doesn't prove that most or all cases of CFS (or PMS) are functional somatic syndromes!
To be fair, the book is well-written and eminently readable. However, as a mental health professional, I found it deeply depressing. There are many people who need our help but how on earth can we persuade them that we are well-informed professionals whose clinical judgements are based on a balanced assessment of the evidence, when some of us ignore what we don't like and write so unsympathetically about the individuals concerned? They say they don't blame the victims but on the whole, they do.
I'm not the only specialist who is concerned about this new approach to CFS. Referring to a review of FSS published elsewhere4, Bell and Lapp remind readers that the existence of an illness is not dependent on a reliable, objective marker to identify the condition, or upon knowledge of aetiology. "We accept the existence of a migraine despite the lack of blood tests or x-rays that prove its existence." Besides, "the assertion that there are no markers to identify or study CFS is incorrect." They go on to point out that "unfounded opinions can lead to cutbacks in research funding, erect obstacles to published research, and increase the difficulties of patients who seek compassionate medical care." In these cases, "the authors would be committing gross malfeasance, harming both the medical community and the patients to whom they are dedicated to serve" (AACFS Newsletter 1999, Aug-Sep). In my view, the same can be said about this book.
Doctors should be free to express themselves, but where do we draw the line? Should they be permitted to be so one-sided in their accounts of illness and disability? Is that compatible with their occupation? If you too are fed up with 'opinion-based medicine', write to the appropriate authorities. After all, if psychiatrists are forgetting the rules of science, isn't it up to their colleagues to remind them?
EMG
Notes
1. Journal of Women's
Health & Gender-Based Medicine, 1999, 8, 663-679.
2. There is some evidence
that fluoxetine alleviates breast pain, headaches and bloating in
women with PMDD (e.g. Steiner et al, Biological Psychiatry, 1999, 45,
73S, no. 236) and in mixed populations (e.g. Su et al,
Neuropsychopharmacology, 1997, 16, 5, 346-356). However, in
heterogeneous samples, findings supporting the use of SSRI
antidepressants have been inconsistent (e.g. Veeninga et al,
Psychopharmacology, 1990, 102, 414-416) and there's still little
evidence of a beneficial effect in cases of pure PMS.
3. For a more balanced
view, see Van Leusden, Lancet, 1995, 346, 1443 and Sundstrom et al,
Gynecological Endocrinology, 1999, 13, 206-220.
4. Barsky and Borus.
Archives of Internal Medicine, 1999, 130, 910.
These are the proposed new clinical guidelines for the diagnosis of myalgic encephalopathy/myoencephalopathy (ME). They are based on the criteria for epidemic neuromyasthenia suggested by JR Adamson. New England Journal of Medicine, 1969, 281, 798. Amendments by Gordon Parish.
Epidemic cases may be diagnosed on 4 to 5 criteria including one of the first three. Sporadic cases should be diagnosed on 7 criteria including one of the first three.
Comments from clinicians and researchers are most welcome.
~ Due to the authors' obvious lack of respect towards colleagues with a different view, a draft of these comments was not forwarded for their response.**The opinions expressed are those of the author and do not necessarily reflect the views of the whole editorial team.
This issue was compiled by Dr. EM Goudsmit, Dr. A. Macintyre and Mrs S. Howes. We gratefully acknowledge the help and support from Dr. C. Shepherd, M. Sullivan, Mr. D. Axford and AbilityNet. The ME and CFS Capita Selecta Quarterly was entirely funded by donations.
Copyright EM. Goudsmit 1999.
©
Psychologist/Archivist, London.
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