Number 4 |
1st November 2008 |
NEUROLOGY
|
Neary, JP., Roberts, ADW., Leavins, N., Harrison, M
F., Croll., JC and Sexsmith, JR. Pre-frontal cortex oxygenation during incremental exercise in chronic fatigue syndrome. Clinical Physiology Functional Imaging, 2008 Jul 29. [Epub ahead of print]. DOI: 10.1111/j.1475-097X.2008.00822.xThis study examined the effects of maximal incremental exercise on cerebral oxygenation in CFS subjects. Furthermore, we tested the hypothesis that CFS subjects have a reduced oxy-gen delivery to the brain during exercise.
Six female patients with CFS (CDC criteria ’94) and eight control (CON) subjects (similar in height, weight, body mass index and physical activity level) performed an incremental cycle ergometer test to exhaustion, while changes in cerebral oxy-haemoglobin (HbO2), deoxyhaemoglobin (HHb), total blood volume (tHb = HbO2 + HHb) and O2 saturation [tissue oxygenation index (TOI), %)] was monitored in the left prefrontal lobe using a near-infrared spectrophotometer. Heart rate (HR) and rating of perceived exertion (RPE) were recorded at each workload throughout the test.
Predicted VO2peak in CFS (1331 + 377 ml) subjects was significantly (p< .05) lower than the CON group (1990 + 332 ml), and CFS subjects achieved volitional exhaustion significantly faster (CFS: 351 + 224 s; CON: 715 + 176 s) at a lower power output [W = watts] (CFS: 100 + 39 W; CON: 163 + 34 W). CFS subjects also exhibited a significantly lower maximum HR (CFS: 154 + 13 bpm; CON: 186 + 11 bpm) and consistently reported a higher RPE at the same absolute workload when compared with CON subjects. Prefrontal cortex HbO2, HHb and tHb were significantly lower at maximal exercise in CFS versus CON, as was TOI during exercise and recovery. The CFS subjects exhibited significant exercise intolerance and reduced prefrontal oxygenation and tHb response when compared with CON subjects.
These data suggest that the altered cerebral oxygenation and blood volume may contribute to the reduced exercise load in CFS, and supports the contention that CFS, in part, is mediated centrally. “These data support previous research that cerebral oxygenation is reduced...
Taken together, these results indicate that blood flow was likely compromised during incremental exercise in the CFS subjects, as reflected by less change in tHb (NIRS-generated tHb has been used as an indirect measure of blood flow..., and less oxygen transport and utilization (extraction) by the brain (as reflected by the lesser change in HbO2 and HHb in the CFS group)... In support of our observations, and under conditions of orthostatic intolerance, Tanaka et al. (2002) also used non-invasive NIRS to show that the majority of the CFS subjects in their study had decreased oxy-Hb concentration ([oxy-Hb]) in the brain during upright posture. They hypothesized that a reduced perfusion pressure and cerebral vasoconstriction may partly explain the reduction in [oxy-Hb]. This would support recent research by Rasmussen et al. (2007), which showed that a reduced cerebral oxygen delivery had a direct effect on motor performance. Thus, it is likely that the impaired motor performance demonstrated in that study... as a result of the inadequate oxygen delivery to the brain resulted in the observed early onset of central fatigue that we observed in our CFS subjects in the current study, as demonstrated by the reduction in HbO2, tHb and HHb in comparison with the CON subjects. Research has shown that cerebral blood flow is reduced in subjects with CFS when using transcranial Doppler sonography (Ichise et al., 1992; Yoshiuchi et al., 2006). In particular, Ichise et al. (1992) showed a significant blood-flow reduction in multiple regions of the brain of CFS subjects, including the prefrontal cortex... Because cerebral autoregulation, metabolic regulation of O2 and CO2-mediated vasodilation are the most important mechanisms to ensure cerebral blood flow..., our results would support the premise that the central nervous system of CFS subjects is somehow altered, and support previous research that suggests a CNS mechanism(s) is implicated in the pathogenesis of CFS (Georgiades et al., 2003; Chaudhuri & Behan, 2004; Siemionow et al., 2004b).[Ed. Note: Measures during recovery were limited to 60 seconds. However, the findings are consistent with those of Hyde 1992 and others.]
Hoad, A., Spickett, G., Elliott, J and Newton, J. Postural orthostatic tachycardia syndrome is an under-recognized condition in chronic fatigue syndrome. Quarterly Journal of Medicine, 2008 Sep 19. [Epub ahead of print]. doi:10.1093/qjmed/hcn123.
It has been suggested that postural orthostatic tachycardia syndrome (POTS) be considered in the differential diagnosis of those with CFS/myalgic encephalomyelitis (CFS/ME). Currently, measurement of haemodynamic response to standing is not recommended in the UK NICE CFS/ME guidelines. The objectives were to determine the prevalence of POTS in patients with CFS/ME in an observational cohort study.
Fifty-nine patients with CFS/ME (CDC criteria ‘94) and 52 age- and sex-matched controls underwent formal autonomic assessment in the cardiovascular laboratory with continuous heart rate and beat-to-beat blood pressure measurement. Haemodynamic responses to standing over 2 minutes were measured. POTS was defined as symptoms of orthostatic intolerance associated with an increase in heart rate from the supine to upright position of >30 beats per minute or to a heart rate of >120 beats per minute on standing.
Maximum heart rate on standing was significantly higher in the CFS/ME group compared with controls (p=0.02). Of the CFS/ME group, 27% (16/59) had POTS compared with 9% (5) in the control population (p=0.006). This difference was predominantly related to the increased proportion of those in the CFS/ME group whose heart rate increased to >120 beats per minute on standing (p=0.0002). Increasing fatigue was associated with increase in heart rate (p=0.04; r2 = 0.1).
POTS is a frequent finding in patients with CFS/ME. We suggest that clinical evaluation of patients with CFS/ME should include response to standing. Studies are needed to determine the optimum intervention strategy to manage POTS in those with CFS/ME.
Miwa, K and Fujita, M. Small heart syndrome in patients with chronic fatigue syndrome. Clinical Cardiology, 2008, 31, 7, 328-333.
Small heart syndrome has previously been reported as neurocirculatory asthenia, associated with a small heart shadow on a chest roentgenogram. This is characterized as weakness or fatigue even after ordinary exertion, palpitation, dyspnoea, and fainting, resembling patients with CFS. Hypothesis: Small heart syndrome may be prevalent in patients with CFS.
The study population consisted of 56 patients (<50 years) with CFS, and 38 control subjects who were given chest roentgenographic, echocardiographic, and physical examinations.
Small heart syndrome (cardiothoracic ratio <=42%) was significantly more prevalent in the CFS group (61%) than in the control group (24%) (p<0.01). In CFS patients with a small heart (n=34), narrow chest (88%), orthostatic dizziness (44%), foot coldness (41%), pretibial pitting oedema (32%), r-kidney palpability (47%), and mitral valve prolapse (29%), were all significantly more prevalent than in the control group, and also in the CFS patients without small heart syndrome. Echocardiographic examination demonstrated significantly smaller values of both the left ventricular (LV) end-diastolic dimensions and end-systolic, and stroke volume and cardiac indexes in CFS with a small heart, as compared with control subjects with a normal heart size (42% < cardiothoracic ratio < 50%).
A considerable number of CFS patients have a small heart. Small heart syndrome may contribute to the development of CFS as a constitutional factor predisposing to fatigue, and may be included in the genesis of CFS.
Chew-Graham, CA., Cahill, G., Dowrick, C., Wearden, A and Peters, S. Using multiple sources of knowledge to reach clinical understanding of chronic fatigue syndrome. Annals of Family Medicine, 2008, 6, 4, 340-348.
CFS or myalgic encephalitis (ME) is a contentious condition and often a diagnosis of exclusion. Current policy in the United Kingdom recommends management in primary care. We explored how patients with CFS/ME (Oxford criteria) and family physicians understand this condition and how their understanding might affect the primary care consultation.
We undertook a qualitative study with patients and family physicians from North West England participating in a primary care-based randomized controlled trial (FINE Trial). Data were collected through purposive sampling and in-depth semi-structured interviews with 24 patients and 14 family physicians. We analyzed interview transcripts using constant comparison methods.
Family physicians access social and cultural knowledge to reach a clinical understanding of CFS/ME and its management. Patients recognize the difficulties family physicians encounter in understanding their symptoms and access similar non-clinical sources of information. We suggest that both patients and physicians use biomedical discourse within the consultation: the physician to maintain the position as an expert, the patient to engage the physician.
Family physicians obtain information about CFS/ME from their non-professional world, which they incorporate into their professional realm. Patients and physicians describe the use of the discourse of science within consultations about CFS/ME. This form of shared understanding could lead to a positive collaborative interaction. Family physicians need a biomedical, evidence-based knowledge about CFS/ME. There is potential to use the rich knowledge base that patients can bring to consultations in training initiatives directed at family physicians.
www.annfammed.org/cgi/reprint/6/4/340
[Ed. Note: ME refers to myalgic encephalomyelitis.]
Dancy, CP and Friend, J. Symptoms, impairment and illness intrusiveness - their relationship with depression in women with CFS/ME. Psychology and Health, 2008, 23, 8, 983-999.
CFS/ME is an illness in which physiological and psychological factors are believed to interact to cause and maintain CFS/ME in an individual predisposed to it. The various symptoms and impairments associated with CFS/ME have a large impact on quality of life. The purpose of the present study was to identify the extent to which the core symptoms and impairments associated with CFS/ME relate to depression in women with CFS/ME, and to discover whether these relationships were mediated by illness intrusiveness.
The sample comprised 140 women with CFS (CDC criteria ’94) recruited from two CFS charities. The mean illness intrusiveness rating scale (IIRS) score was 65.84 (SD= 13.91.)
CFS/ME was found to be a highly intrusive illness, intruding into more life domains and to a greater degree than other illnesses. The effects of both symptoms and impairment on depression were, in part, mediated by illness intrusiveness. Although symptoms severity and impairment had both direct and indirect effects on depression, illness intrusiveness was the strongest predictor of depression.
[Ed. Note: A smaller study which assessed patients with ME (criteria consistent with Ramsay definition) revealed a total mean IIRS score of 63.27 (n=15), and for ME plus co-morbid disorders, the mean score was 72 (n=8). The combined mean was 66.30. This suggests that there is no significant difference between the impact of ME and CFS as currently defined. See Goudsmit et al, ME Research Online. http://freespace.virgin.net/david.axford/melist.htm, and J Health Psychology, March 2009. The scores for CFS and ME exceed those documented for all other conditions, except anorexia nervosa, (mean=69.61, cf. Carter et al, J. Psychosom Res 2008, 64, 519-526.)]
Knoop, H., Van der Meer, JWM and Bleijenberg, G. Guided self-instructions for people with chronic fatigue syndrome: randomised controlled trial. British Journal of Psychiatry, 2008, 193, 340-341.
Short report. A minimal intervention, based on cognitive–behavioural therapy (CBT) for CFS and consisting of self-instructions combined with email contact, was tested in a randomised controlled trial. A total of 171 patients with CFS (CDC criteria ’94) participated in the trial: 85 were allocated to the intervention condition and 86 to the waiting-list condition. An intention-to-treat analysis showed a significant decrease in fatigue and disability after self-instruction. The level of disability was negatively correlated with treatment outcome. Guided self-instructions are an effective treatment for patients with relatively less severe CFS.
[Ed. Note: the post-treatment MOS scores showed significant disability, i.e., 65.9 versus 60.2 for the waiting list controls. Of those in the treatment condition, 66% emailed and 6% used the telephone to contact the therapist. The drop out rate was low (5%).]
Priebe, S., Fakhoury, WKH and Henningsen, P. Functional incapacity and physical and psychological symptoms: How they interconnect in chronic fatigue syndrome. Psychopathology, 2008, 41, 339-345.
It has been argued that perceived functional incapacity might be a primary characteristic of CFS and could be explained by physical symptoms. If so, it could be expected to be closely associated with physical, but not psychological symptoms. The study tests this hypothesis.
The sample consisted of 73 patients with a diagnosis of CFS (Oxford criteria), randomly selected from clinics in the Departments of Immunology and Psychiatry at St. Bartholomew’s Hospital, London. The degree of fatigue experienced by patients was assessed using the Chalder Fatigue Questionnaire (mean: 9.0) and a visual analogue scale. Self-rated instruments were used to measure physical and social functioning, quality of life, and physical and psychological symptoms, as well as trait anxiety.
Principal-component analysis of all scale scores revealed 2 distinct components, explaining 53% of the total variance. One component was characterized by psychological symptoms and generic quality of life indicators, whilst the other component was made up of physical symptoms, social and physical functioning and indicators of fatigue.
The findings suggest that perceived functional incapacity is a primary characteristic of CFS, which is manifested and/or explained by physical symptoms.
Aspler, AL., Bolshin, C., Vernon, SD and Broderick, G. Evidence of inflammatory immune signaling in chronic fatigue syndrome: A pilot study of gene expression in peripheral blood. Behavioral and Brain Functions, 2008, 4:44, doi:10.1186/1744-9081-4-44. Genomic profiling of peripheral blood reveals altered immunity in CFS, however interpretation remains challenging without immune demographic context. The object of this work is to identify modulation of specific immune functional components and restructuring of co-expression networks characteristic of CFS using the quantitative genomics of peripheral blood. Gene sets were constructed a priori for CD4+ T cells, CD8+ T cells, CD19+ B cells, CD14+ monocytes and CD16+ neutrophils from published data. A group of 111 women were classified using the empiric case definition (CDC) and unsupervised latent cluster analysis (LCA). The empiric classification resulted in the differentiation between 39 people with CFS, 37 non- fatigued (NF) controls, and 35 subjects with insufficient symptoms or fatigue (ISF). The second classification identified the following groups: Obese subjects with prominent post-exercise fatigue, hypnoea and disturbed sleep formed Class 1. Reasonably healthy subjects with few symptoms, low depression scores and good sleep composed Class 2. Subjects in Class 3 resembled those in class 1 but also displayed low heart rate variability during sleep and low 24-hour cortisol levels. Class 4 was populated with healthier, less depressed individuals having restful sleep but suffering muscle pain. Finally
Classes 5 and 6 both captured less obese but highly symptomatic and depressed individuals with prominent post-exercise fatigue. Individuals in Class 6 also displayed disturbed sleep with low heart rate variability and low cortisol. Microarray profiles of peripheral blood were analyzed for expression of leukocyte-specific gene sets and characteristic changes in coexpression identified from topological evaluation of linear correlation networks. Together LCA classes 1 (40%) and 5 (26%) contained two thirds of the subjects assigned to the empiric CFS class. However ISF subjects were distributed almost equally across LCA classes 1 (23%), 3 (31%), and 4 (26%). Conversely most LCA class 3 and 4 subjects were identified as ISF and most subjects in LCA classes 1, 5 and 6 were assigned an empiric CFS classification. The median expression of the CD19+ B cell up-regulated gene set was significantly lower in CFS (p=0.01) and ISF (p=0.05) subjects when compared to the NF group. Expression of this gene set was also significantly repressed in LCA class 3 (p=0.04) and marginally so in LCA class 5 (p=0.09) when compared to control subjects in LCA classes 0 and 2. Recall that 11 of 17 cases in LCA class 3 were also designated ISF. Similarly 10 of the 14 LCA class 5 cases were designated CFS. NK gene set expression was marginally increased in the CFS group (p=0.07). Though not significant, the null probability for NK cell expression was lowest among the LCA classes for LCA-3 (p=0.11). Finally expression of the T regulatory set (FoxP3) was marginally repressed in LCA class 1 (p=0.09) which contained 40% of the CFS subjects though no significant difference was found for the larger CFS group (p=0.31). In addition a detailed analysis of individual genes in the CD19+ up-regulated
set indicated that no single gene was differentially expressed even though the parent set was expressed at the p=0.01 level. This reaffirms that high levels of measurement noise can be effectively ma-naged by aggregating genes into biologically relevant sets. “Specifically in the empiric CFS class we found a significant decrease in the median expression for a set of 6 genes preferentially up-regulated in isolated CD19+ B cells compared to non-fatigued controls. Expression of this CD19+ B cell up-regulated gene set also discriminated ISF from controls at 0.05 confidence level. In a recent study of CFS occurrence both in the presence and absence of viral infection Racciati et al... found no significant differences in CD19+ cell abundance. Robertson et al. ... recently reported significantly higher abundance of CD20+/CD5+ B cells, a subset associated with the production of auto-anti-bodies, in patients with depression. These findings together with our observations of depressed CD19+ gene expression and altered association between up and down-regulated B cell functions would suggest that the function of these cells might be compromised in CFS subjects.” Although no other gene set was differentially expressed at p<0.05, patterns of co-expression in each group differed markedly. Significant co-expression of CD14+ monocyte with CD16+ neutrophil (p=0.01) and CD19+ B cell sets (p=0.00) characterized CFS and fatigue phenotype groups. Also in CFS was a significant negative correlation between CD8+ and both CD19+ up-regulated (p=0.02) and NK gene sets (p=0.08). These patterns were absent in controls.GENETICS
“Therefore our observations supported findings of increased suppression of cytotoxic activity in CFS and hinted at increased Th2 activity though the latter were not specifically addressed in this analysis... a preliminary examination of cytokine data collected in the Wichita study pointed to an increase in TNF-α in CFS subjects (data not shown) as documented previously by Moss et al...”
Dissection of blood microarray profiles points to B cell dysfunction with co-ordinated immune activation supporting persistent inflammation and antibody-mediated NK cell modulation of T cell activity. This has clinical implications as the CD19+ genes identified could provide robust and biologically meaningful basis for the early detection and unambiguous phenotyping of CFS.
http://www.behavioralandbrainfunctions.com/content/4/1/44
Price, JR., Mitchell, E., Tidy, E and Hunot, V. behaviour therapy for chronic fatigue syndrome in adults. Cochrane Database of Systematic Reviews 2008, Issue 3. Art. No.: CD001027. DOI: 10.1002/14651858.CD001027.pub2.
CFS is a common, debilitating and serious health problem. CBT may help to alleviate the symptoms of CFS.
Objectives were to examine the effectiveness and acceptability of CBT for CFS, alone and in combination with other interventions, compared with usual care and other interventions. CCDANCTR-Studies and CCDANCTR-References were searched on 28/3/2008. We conducted supplementary searches of other bibliographic databases. We searched reference lists of retrieved articles and contacted trial authors and experts in the field for information on ongoing/completed trials.
Selection criteria: Randomised controlled trials involving adults with a primary diagnosis of CFS, assigned to a CBT condition compared with usual care or another intervention, alone or in combination.
Data collection and analysis: Data on patients, interventions and outcomes were extracted by two review authors independently, and risk of bias was assessed for each study. The primary outcome was reduction in fatigue severity, based on a continuous measure of symptom reduction, using the standardised mean difference (SMD), or a dichotomous measure of clinical response, using odds ratios (OR), with 95% confidence intervals (CI).
Results: Fifteen studies (1043 CFS participants) were included in the review. When comparing CBT with usual care (six studies, 373 participants), the difference in fatigue mean scores at post-treatment was highly significant in favour of CBT (SMD -0.39, 95% CI -0.60 to -0.19), with 40% of CBT participants (four studies, 371 participants) showing a clinical response in contrast with 26% in usual care (OR 0.47, 95% CI 0.29 to 0.76). Findings at follow-up were inconsistent. For CBT versus other psychological therapies, comprising relaxation, counselling and education/support (four studies, 313 participants), the difference in fatigue mean scores at post-treatment favoured CBT (SMD -0.43, 95% CI -0.65 to -0.20). Findings at follow-up were heterogeneous and inconsistent. Only two studies compared CBT against other interventions and one study compared CBT in combination with other interventions against usual care.
CBT is effective in reducing the symptoms of fatigue at post-treatment compared with usual care, and may be more effective in reducing fatigue symptoms compared with other psychological therapies. The evidence base at follow-up is limited to a small group of studies with inconsistent findings. There is a lack of evidence on the comparative effectiveness of CBT alone or in combination with other treatments, and further studies are required to inform the development of effective treatment programmes for people with CFS.
[Ed. Note: This review ignores the problems associated with the scientific process, e.g. the tendency not to publish trials challenging the CBT model in mainstream UK journals. It also does not address flaws such as the use of scales with a low ceiling (cf. Chalder Fatigue Scale), non-specific definitions, lack of measures dealing with symptoms other than fatigue, e.g. somatic and cognitive symptoms, and the failure to assess activity levels objectively. The studies comparing CBT and counselling have tended to find few differences, which, according to a recent study, is because good outcome is largely related to the opportunity to express emotional distress (Godfrey et al, 2007). NB, the review appears to have focused on RCTs on CBT only, thus it is not possible to draw conclusions about the effectiveness of alternatives which were tested on their own.]
Lorusso, L., Mikhaylova, SV., Capelli, E., Ferrari, D., Ngonga, GK and Ricevuti, G. Immu-nological aspects of chronic fatigue syndrome. Autoimmunity Reviews, 2008 Sep 15. [Epub ahead of print]. doi:10.1016/j.autrev.2008.08.003.
“Various studies have sought evidence for a disturbance in immunity in people with CFS. An alteration in cytokine profile, a decreased function of natural killer (NK) cells, a presence of auto-antibodies and a reduced responses of T cells to mitogens and other specific antigens have been reported. The observed high level of pro-inflammatory cytokines may explain some of the manifestations such as fatigue and flu-like symptoms and influence NK activity. Abnormal activation of the T lymphocyte subsets and a decrease in antibody-dependent cell-mediated cytotoxicity have been described. An increased number of CD8+ cytotoxic T lymphocytes and CD38 and HLA-DR activation markers have been reported, and a decrease in CD11b expression associated with an increased expression of CD28+ T subsets has been observed. This review discusses the immunological aspects”.
Stordeur, S., Thiry, N., and Eyssen, M. Chronisch Vermoeidheidssyndroom: diagnose, behandeling en zorgorganisatie. Health Services Research (HSR). Brussel: Federaal Kenniscentrum voor de Gezondheidszorg (KCE); 2008. KCE reports 88A. (D/2008/10.273/58)
[Ed. Note: Review of information on CFS guided by adherents of the CBT-model (though using information on pacing from Goudsmit and Howes), to help decision makers determine future funding of the Belgian CFS clinics which offer primary CBT/GET. With a description of the Belgian centres. Review is written primarily in English.]
http://www.kce.fgov.be/index_nl.aspx?SGREF=5260&CREF=11648
Bains, W. Treating chronic fatigue states as a disease of the regulation of energy metabolism. Medical Hypotheses, 2008, 71, 4, 481-488.
CFS is a physiological state in which the patient feels high levels of fatigue without an obvious organic cause, which affects around 1 in 400 people in the developed world. A wide range of causes have been suggested, including immune or hormonal dysfunction, viral or bacterial infection, and psychological somatization. It is likely that several causes are needed to trigger the disease, and that the triggers are different from the mechanisms that maintain fatigue over months or years. Many treatments have been tested for CFS, with very limited success - a programme of combined CBT and graded exercise shows the most effect. I suggest that patients with CFS have a reduced ability to increase mitochondrial energy production when exertion requires it, with fewer mitochondria that are each more efficient, and hence nearer to their maximum energy output, than normal. A range of indirect evidence suggests that the renin-angiotensin system stimulates mitochondrial responsiveness and reduces mitochondrial efficiency: chronic under-stimulation of this system could contribute to CFS aetiology. If correct, this means that CFS can be successfully treated with RAS agonists (eg angiotensin mimetics), or adrenergic agonists. It also suggests that there will be a positive link between the use of adrenergic- and RAS-blocking drugs and CFS incidence, and a negative link between adrenergic agonist use and CFS.
Ed. Note: the author claims that patents have normal muscle strength and that any evidence of abnormalities are linked to deconditioning.][
Bramsen, I. Can CBT substantially change grey matter volume in chronic fatigue syndrome? Brain Advance Access published on August 29, 2008. doi:10.1093/brain/awn207.
Letter questioning the conclusions by De Lange et al 2008. For example, she notes: “
First, the authors did not include a control group of patients receiving no treatment or a different treatment. Therefore, the increase in GMV [grey matter volume, ed.] cannot be attributed to the CBT treatment given. It is possible that the natural course of and fluctuations in the illness are responsible for this result. In addition, it might be possible that other treatments than CBT would have resulted in the same, or even better, results. Second, even if the results were indeed to be attributed to changes in lifestyle brought about by CBT, several questions still remain. To name a few, first, the increase in volume of <1% is very modest. Therefore, the question is whether, although statistically significant, this small increase is also of clinical significance. Second, if CBT brings about changes in lifestyle, and these changes are responsible for small improvements in the patients’ brain and activity levels, are these changes structural and related to the primary disease process? An alternative interpretation is that changing the lifestyle of patients, influences their quality of life, activity patterns and GMV, while the underlying disease process is not influenced.Another critical remark relates to the fact that the authors in their paper do not mention the proportion of absolute increase in GMV of 0.7%, but rather report that the initial between-group difference between patients and healthy controls decreases with 12%. For readers, it is important to realize that the measure of change reported by the authors is influenced by the absolute size of the between-group difference: the smaller, and therefore less relevant, this difference is, the larger the reported proportion becomes, thereby making less relevant results looking more impressive.”
With reply by De Lange et al. Ibid, doi:10.1093/brain/awn208. Extract: “
Dr Bramsen neglects the fact that the reported increase in grey matter volume was largely regionally specific, confined to left and right lateral prefrontal cortex [see Fig. 3 of de Lange et al. (2008)]. The increase in grey matter volume might appear numerically modest when expressed in terms of whole brain grey matter volume. Yet, when relating the change to a more specific anatomical structure (the lateral prefrontal cortex), the increase in grey matter volume was on average 8%. Nevertheless, we prefer to focus on whole-brain grey matter volume as a dependent measure, as it is a reliable, sensitive and unbiased measure of overall cerebral morphology.“Original paper; De Lange et al, Ibid, 2008, 131, 2172-2180.
Bhattacharjee, M., Botting, CH and Sillanpää, MJ. Bayesian biomarker identification based on marker-expression proteomics data, Genomics, 2008, doi:10.1016/j.ygeno.2008.06.006.
Fisher, M.McD and Rose, M. Anaesthesia for patients with idiopathic environmental intolerance and chronic fatigue syndrome. British Journal of Anaesthesia, 2008, 101, 4, 486-91.
Idiopathic environmental intolerance syndrome (IEI), formerly known as multiple chemical sensitivity syndrome (MCSS), and CFS are controversial diseases and there is little information in the literature regarding the appropriate conduct of anaesthesia in such patients.
We studied 27 patients referred to our anaesthetic allergy clinic with IEI and CFS (n=9) and performed literature and web searches on anaesthesia in these disorders. The patients had a significant incidence of adverse events related to anaesthesia which were not allergic in nature. The adverse effects usually occurred postoperatively and were self limiting. Patients with IEI and CFS are not at risk of anaphylaxis and there is no scientific evidence that any drug or technique is excessively hazardous. Neither our patients nor the review of the scientific literature supported available web-based recommendations for the anaesthetic management of patients with IEL and CFS.
We suggest that the anaesthetist may best use the technique they would use if the patient did not have CFS or IEI but avoid drugs to which there is a history of adverse response. Anaesthesia is likely to be associated with adverse effects in these patients but the effects are not likely to be severe. A series of recommendations for the safe and harmonious conduct of anaesthesia in patients with CFS and IEI are provided.
Fuite, J., Vernon, SD and Broderick, G. Neuroendocrine and immune network re-modeling in chronic fatigue syndrome: An exploratory analysis. Genomics, 2008 Sep 4. [Epub ahead of print]
This work investigates the significance of changes in association patterns linking indicators of neuroendocrine and immune activity in patients with CFS. Gene sets preferentially expressed in specific immune cell isolates were integrated with neuroendocrine data from a large population-based study. Co-expression patterns linking immune cell activity with
hypothalamic-pituitary-adrenal (HPA), thyroidal (HPT) and gonadal (HPG) axis status were computed using mutual information criteria. Networks in control and CFS subjects were compared globally in terms of a weighted graph edit distance. Local re-modeling of node
connectivity was quantified by node degree and eigenvector centrality measures.
Results indicate statistically significant differences between CFS and control networks determined mainly by re-modeling around pituitary and thyroid nodes as well as an emergent immune sub-network. Findings align with known mechanisms of chronic inflammation and
support possible immune-mediated loss of thyroid function in CFS exacerbated by blunted HPA axis responsiveness.
Gadalla, T. Association of comorbid mood disorders and chronic illness with disability and quality of life in Ontario, Canada. Chronic Diseases in Canada, 2008, 28, 4,148-154.
Mood disorders are more prevalent in individuals with chronic physical illness compared to individuals with no such illness. These disorders amplify the disability associated with the physical condition and adversely affect its course, thus contributing to occupational impairment, disruption in interpersonal and family relationships, poor health and suicide. This study used data collected in the Canadian Community Health Survey, cycle 3.1 (2005) to examine factors associated with co-morbid mood disorders and to assess their association with the quality of life of individuals living in Ontario. Results indicate that individuals with CFS, FM, bowel disorder or stomach or intestinal ulcers had the highest rates of mood disorders. The odds of having a co-morbid mood disorder were higher among women, the single, those living in poverty, the Canadian born and those between 30 and 69 years of age. The presence of co-morbid mood disorders was significantly associated with short-term disability, requiring help with instrumental daily activities and suicidal ideation. Health care providers are urged to proactively screen chronically ill patients for mood disorders, particularly among the subgroups found to have elevated risk for these disorders.
www.phac-aspc.gc.ca/publicat/cdic-mcc/28-4/pdf/cdic28-4-4eng.pdf
Goudsmit, EM., Stouten, B and Howes, S. Fatigue in Myalgic Encephalomyelitis.
Bulletin of The IACFS/ME, 2008, 16, 3-10.The objectives of this study were to measure fatigue in patients with well-defined Myalgic Encephalomyelitis (ME) and to assess if there are any problems associated with the Chalder Fatigue Scale, which has been widely used to assess fatigue in patients with chronic fatigue syndrome (CFS).
Twenty-six patients were recruited from a local support group. All had been diagnosed by physicians and met research criteria for ME. They completed the 11-item Chalder Fatigue Scale and were also asked to rate the severity of their illness. The fatigue scores were calculated using both the Likert method (0,1,2,3) and the bimodal method (0,0,1,1,).
The mean Likert score was 26.65 (SD 5.36) and the mean bimodal score was 9.81 (SD 2.04). Fifty per cent of the patients recorded the maximum score using the bimodal method and 77% recorded the two highest scores. Moreover, there was a marked overlap between those who rated themselves as moderately or severely ill. These findings are indications of a low ceiling.
The findings from this study using the Chalder Fatigue Scale show that the low ceiling associated with the bimodal method means that this scoring system is not suitable for use in clinical trials. Researchers may wish to consider alternative instruments to obtain a more accurate measure of fatigue in patients with moderate to severe ME and similar conditions.
http://www.iacfsme.org/BULLETINFALL2008/Fall08GoudsmitFatigueinMyalgicEnceph/tabid/292/Default.aspx
Hempel, S., Chambers, D., Bagnall, A.M. and Forbes, C. Risk factors for chronic fatigue syndrome/myalgic encephalomyelitis: a systematic scoping review of multiple predictor studies. Psychological Medicine, 2008, 38, 7, 915-926.
The aetiology of CFS/ME is still unknown. The identification of risk factors for CFS/ME is of great importance to practitioners. A systematic scoping review was conducted to locate studies that analysed risk factors for CFS/ME using multiple predictors. We searched for published and unpublished literature in 11 electronic databases, reference lists of retrieved articles and guideline stakeholder submissions in conjunction with the development of a forthcoming national UK guideline. Risk factors and findings were extracted in a concise tabular overview and studies synthesized narratively.
Eleven studies were identified that met inclusion criteria: two case-control studies, four cohort studies, three studies combining a cohort with a case-control study design, one case-control and twin study and one cross-sectional survey. The studies looked at a variety of demographic, medical, psychological, social and environmental factors to predict the development of CFS/ME. The existing body of evidence is characterized by factors that were analysed in several studies but without replication of a significant association in more than two studies, and by studies demonstrating significant associations of specific factors that were not assessed in other studies. None of the identified factors appear suitable for the timely identification of patients at risk of developing CFS/ME within clinical practice.
Various potential risk factors for the development of CFS/ME have been assessed but definitive evidence that appears meaningful for clinicians is lacking.
Hollingsworth, KG., Newton, JL., Taylor, R., McDonald, C., Palmer, JM., Blamire, AM and Jones DE. Pilot study of peripheral muscle function in primary biliary cirrhosis: potential implications for fatigue pathogenesis. Clinical Gastroenterology and Hepatology, 2008, 6, 9, 1041-1048.
Primary biliary cirrhosis (PBC) is characterized in 95% of patients by autoantibody responses directed against the mitochondrial antigen pyruvate dehydrogenase complex (PDC). Although anti-PDC inhibits PDC function in vitro, mitochondrial function in vivo in PBC has not been examined. 31P magnetic resonance spectroscopy was performed in PBC patients (n=15) and fatigued (CFS/ME, n=8), cholestatic (primary sclerosing cholangitis [PSC], n=4), and normal (n=8) controls to define mitochondrial function and pH regulation in peripheral muscle during exercise at 25% and 35% of maximum voluntary contraction.
Normal, CFS/ME and PSC subjects all showed close correlation between kinetics of adenosinediphosphate (ADP) and phosphocreatine (PCr) recovery after low-impact exercise, reflecting the normal tight regulation of PCr "response" by mitochondria to ADP "drive." This relationship was lost in PBC patients, indicating mitochondrial dysfunction (normal r2 = 0.78, p<.005; PBC r2= 0.007, P = ns). Ratio between PCr and ADP recovery half-times (constant in controls, indicating normal mitochondrial responsivity) was significantly elevated in PBC patients (but not PSC) and was associated with anti-PDC levels. At higher levels of exercise PBC (but not PSC) patients showed excess muscle acidosis, with pH correlating with elevation of PCr/ADP recovery ratio, indicating a link to mitochondrial dysfunction. PBC patients alone also showed significant prolongation of muscle pH recovery time after exercise (unrelated to mitochondrial function), which correlated with clinical fatigue.
PBC patients exhibit a variable degree of muscle mitochondrial dysfunction that manifests as excess acidosis after exercise. The extent to which patients can recover rapidly from acidosis appears to determine whether they are clinically fatigued.
Majer, M., Welberg, LAM., Capuron, L., Miller, AH., Pagnoni, G and Reeves, WC. Neuropsychological performance in persons with chronic fatigue syndrome: Results from a population-based study. Psychosomatic Medicine, 2008, 70, 829-836.
The objective was to examine the neuropsychological function characterized in subjects with CFS at the same time controlling for relevant confounding factors. CFS is associated with symptoms of neuropsychological dysfunction. Objective measures of neuropsychological performance have yielded inconsistent results possibly due to sample selection bias, diagnostic heterogeneity, co-morbid psychiatric disorders, and medication usage.
CFS subjects (CDC criteria ’94, operationalised, n=58) and well controls (n=104) from a population-based sample were evaluated, using standardized symptom severity criteria. Subjects who had major psychiatric disorders or took medications known to influence cognition were excluded. Neuropsychological function was measured using the Cambridge Neuropsychological Test Automated Battery (CANTAB).
Compared with controls, CFS subjects exhibited significant decreases in motor speed as measured in the simple and five-choice movement segments of the CANTAB reaction time task. CFS subjects also exhibited alterations in working memory as manifested by a less efficient search strategy on the spatial working memory task, fewer % correct responses on the spatial recognition task, and prolonged latency to a correct response on the pattern recognition task. A significantly higher percentage of CFS subjects versus controls exhibited evidence of neuropsychological impairment (defined by performance 1 standard deviation below the CANTAB normative mean) in tasks of motor speed and spatial working memory. Impairment in CFS subjects versus control subjects ranged from 20% versus 4.8% in five-choice movement time (p = .002) to 27.8% versus 10.6% in search strategy on the spatial working memory task (p = .006).
These results confirm and quantify alterations in motor speed and working memory in CFS subjects independent of co-morbid psychiatric disease and medication usage.
Metzger, K., Frémont, M., Roelant, C and De Meirleir, K. Lower frequency of IL-17F sequence variant (His161Arg) in chronic fatigue syndrome patients. Biochemical and Biophysical Research Communications, 2008, 376, 1, 231-233.
CFS is characterized by immune dysfunctions including chronic immune activation, inflammation, and alteration of cytokine profiles. T helper 17 (Th17) cells belong to a recently identified subset of T helper cells, with crucial regulatory function in inflammatory and autoimmune processes. Th17 cells are implicated in allergic inflammation, intestinal diseases, central nervous system inflammation, disorders that may all contribute to the pathophysiology of CFS. IL-17F is one of the pro-inflammatory cytokines secreted by Th17 cells.
We investigated the association between CFS and the frequency of rs763780, a C/T genetic polymorphism leading to His161Arg substitution in the IL-17F protein. Patients were 89 patients with CFS (CDC criteria ’94) and the results were compared with those of 56 age-matched controls.
The His161Arg variant (C allele) antagonizes the pro-inflammatory effects of the wild-type IL-17F. A significantly lower frequency of the C allele was observed in the CFS population, suggesting that the His161Arg variant may confer protection against the disease. These results suggest a role for Th17 cells in the pathogenesis of CFS.
Miwa, K and Fujita, M. Increased oxidative stress suggested by low serum vitamin E concentrations in patients with chronic fatigue syndrome. International Journal of Cardiology, 2008 Aug 4. [Epub ahead of print].doi
:10.1016/j.ijcard.2008.04.051.Serum α-tocopherol concentrations were determined in 50 patients with CFS (CDC criteria ’94) and 40 control subjects (Controls). Prevalence of each or any coronary risk factor was not significantly different between CFS and Controls. CFS had significantly lower α-tocopherol concentrations than Controls. The concentrations were significantly lower in the subjects with any coronary risk factors than those without in CFS as well as Controls. Even among the subjects with any coronary risk factors and also among those without, CFS had significantly lower α-tocopherol concentrations than Controls. In conclusion, CFS had significantly lower α-tocopherol concentrations irrespective of coronary risk factors than Controls, suggesting the presence of increased oxidative stress in CFS.
Neustadt, J and Pieczenik, SR. Medication-induced mitochondrial damage and disease. Molecular Nutrition & Food Research, 2008, 52, 7, 780-788.
Since the first mitochondrial dysfunction was described in the 1960s, medicine has advanced in its understanding of the role mitochondria play in health and disease. Damage to mitochondria is now understood to play a role in the pathogenesis of a wide range of seemingly unrelated disorders such as schizophrenia, bipolar disease, dementia, Alzheimer's disease, epilepsy, migraine headaches, strokes, neuropathic pain, Parkinson's disease, ataxia, transient ischemic attack, cardiomyopathy, coronary artery disease, CFS, FM, retinitis pigmentosa, diabetes, hepatitis C, and primary biliary cirrhosis. Medications have now emerged as a major cause of mitochondrial damage, which may explain many adverse effects. All classes of psychotropic drugs have been documented to damage mitochondria, as have statin medications, analgesics such as acetaminophen, and many others. While targeted nutrient therapies using antioxidants or their precursors (e.g., N-acetylcysteine) hold promise for improving mitochondrial function, there are large gaps in our knowledge. The most rational approach is to understand the mechanisms underlying mitochondrial damage for specific medications and attempt to counteract their deleterious effects with nutritional therapies. This article reviews our basic understanding of how mitochondria function and how medications damage mitochondria to create their occasionally fatal adverse effects.
Nijs, J and Thielemans, A. Kinesiophobia and symptomatology in chronic fatigue syndrome: A psychometric study of two questionnaires. Psychology & Psychotherapy, 2008, 81(Pt 3):273-283.
The aims of the study were to examine the reliability of the Dutch and French versions of the Tampa scale kinesiophobia (TSK) version CFS, and to examine the reliability and validity of the Dutch and French versions of the CFS symptom list. This was a repeated-measures design.
The results are in support of the psychometric properties of the French and Dutch versions of both the TSK-CFS and the CFS symptom list for assessing kinesiophobia and symptom severity, respectively.
Reynolds, F., Vivat, B and Prior, S. Women's experiences of increasing subjective well-being in CFS/ME through leisure-based arts and crafts activities: A qualitative study. Disability & Rehabilitation, 2008, 30, 17, 1279 – 1288.
The purpose of this study was to understand the meanings of art-making among a group of women living with the occupational constraints and stigma of CFS/ME. The study explored their initial motives for art-making, and then examined how art-making had subsequently influenced their subjective well-being.
Ten women with CFS/ME were interviewed; three provided lengthy written accounts to the interview questions.
The illness had resulted in devastating occupational and role loss. Participants took many years to make positive lifestyle changes. Art-making was typically discovered once participants had accepted the long-term nature of CFS/ME, accommodated to illness, and reprioritized occupations. Several factors then attracted participants specifically to art-making. It was perceived as manageable within the constraints of ill-health. Participants also tended to be familiar with craft skills; had family members interested in arts and crafts, and some desired a means to express grief and loss. Once established as a leisure activity, art-making increased subjective well-being mainly through providing increased satisfaction in daily life, positive self-image, hope, and contact with the outside world. Participants recommended provision of occupational/recreational counselling earlier in the illness trajectory.
Scheeres, K., Wensing, M., Bleijenberg, G and Severens, JL. Implementing cognitive behavior therapy for chronic fatigue syndrome in mental health care: a costs and outcomes analysis. BMC Health Services Research, 2008, 8(1):175.
This study investigated the costs and outcomes of implementing CBT for CFS in a mental health center (MHC). CBT is an evidence-based treatment for CFS that was scarcely available until now. To investigate the possibilities for wider implementation, a pilot implementation project was set up. Costs and effects were evaluated in a non-controlled before- and after study with an eight months time-horizon. Both the costs of performing the treatments and the costs of implementing the treatment program were included in the analysis. The implementation interventions included: informing general practitioners (GPs) and CFS patients, training therapists, and instructing the MHC employees. Given the non-controlled design, cost outcome ratio's (CORs) and their acceptability curves were analyzed. Analyses were done from a health care perspective and from a societal perspective. Bootstrap analyses were performed to estimate the uncertainty around the cost and outcome results.
125 CFS patients [GP diagnosis based on the CDC criteria ’94, ed.] were included in the study. After treatment 37% had recovered from CFS and the mean gained QALY was 0.03. Costs of patients' health care and productivity losses had decreased significantly. From the societal perspective the implementation led to cost savings and to higher health states for patients, indicating dominancy. From the health care perspective the implementation revealed overall costs of €5.320 per recovered patient, with an acceptability curve showing a 100% probability for a positive COR at a willingness to pay threshold of €6.500 per recovered patient.
Implementing CBT for CFS in a MHC appeared to have a favourable cost outcome ratio (COR) from a societal perspective. From a health care perspective the COR depended on how much a recovered CFS patient is being valued. The strength of the evidence was limited by the non-controlled design. The outcomes of this study might facilitate health care providers when confronted with the decision whether or not to adopt CBT for CFS in their institution.
http://www.biomedcentral.com/content/pdf/1472-6963-8-175.pdf
Schrijvers, D., Van Den Eede, F., Maas, Y., Cosyns, P., Hulstijn, W and Sabbe, BGC. Psychomotor functioning in chronic fatigue syndrome and major depressive disorder: A comparative study. Journal of Affective Disorders, 2008 Sep 23. [Epub ahead of print].
doi:10.1016/j.jad.2008.08.010.Studies comparing CFS and major depressive disorder (MDD) reported similarities as well as differences between the two disorders. However, whereas psychomotor symptoms have been studied extensively in MDD, such research in CFS is more limited. Moreover, the few studies that compared cognitive and motor performance in MDD and CFS yielded inconsistent results. Hence this study directly compares fine psychomotor functioning in both syndromes.
Thirty-eight patients diagnosed with CFS (CDC criteria ’94) without a current major depressive episode (MDE), 32 MDD patients with a current MDE and 38 healthy controls performed two computerized copying tasks differing in complexity: a line-copying task that mainly requires motor effort and a figure-copying task requiring additional cognitive efforts. All participants were female. A multivariate general linear model was used to compute group differences.
Overall, both patient groups performed more slowly than the controls. Compared to CFS patients, patients with MDD needed significantly more time to copy the single lines but no such between-group performance difference was observed for the figure reproductions. In this latter copying task, the increasing complexity of the figures resulted in prolonged reaction times for all three participant groups with the effect being larger and the magnitude similar for the two patient groups.
Limitations: All patients were female and most were on psychotropic medication.
In conclusion, both the MDD and CFS patients tested demonstrated an overall fine motor slowing, with the motor component being more affected in the MDD patients than in the CFS patients while both patient groups showed similar cognitive impairments.
The following conditions were present in the CFS group: FM (n=18), somatization disorder (n=7), current anxiety disorder (n=11) and history of one or more depressive episodes (n=19). At the time of testing 16 CFS patients were taking one or more antidepressants (selective serotonin reuptake inhibitor: n=9; tricyclic antidepressant: n=3; mirtazapine or trazodone: n=11) and 11 patients had taken a benzodiazepine the evening before testing (clonazepam: n=4; tetrazepam: n=2; lorazepam: n=1; lormetazepam: n=2; alprazolam: n=1; prazepam: n=1).][Ed. Note:
Swoboda, DA. Negotiating the diagnostic uncertainty of contested illnesses: physician practices and paradigms. Health (London), 2008, 12, 4, 453-478.
In the absence of scientific consensus about contested illnesses such as CFS, Multiple Chemical Sensitivities (MCS), and Gulf War Syndrome (GWS), physicians must make sense of competing accounts and develop practices for patient evaluation. A survey of 800 United States physicians examined physician propensity to diagnose CFS, MCS, and GWS, and the factors shaping clinical decision making. The sample included 108 non-experts, 129 CFS experts and 119 MCS experts.
Results indicated that a substantial portion of physicians, including non-experts, are diagnosing CFS, MCS, and GWS. Diagnosing physicians manage the uncertainty associated with these illnesses by using strategies that enhance bounded rationality and aid in thinking beyond current disease models. Strategies include consulting ancillary information sources, conducting analytically informed testing, and considering physiological explanations of causation. By relying on these practices and paradigms, physicians fit CFS, MCS, and GWS into an explanatory system that makes them credible and understandable to them, their patients, and the medical community. Findings suggest that physicians employ rational decision making for diagnosing contested illnesses, creating a blueprint of how illnesses lacking conclusive pathogenic and etiological explanations can be diagnosed. Findings also suggest that patients with contested illnesses might benefit from working with physicians who use these diagnostic strategies, since they help manage the complexity and ambiguity of the contested illness diagnostic process and aid in diagnosis. In addition, findings provide a window into how emerging illnesses get diagnosed in the absence of medical and scientific consensus, and suggest that diagnosing physicians advance the legitimacy of controversial illnesses by constructing the means for their diagnosis.
Torres-Harding,S., Sorenson, M., Jason, LA., Maher, K and Fletcher, MA. Evidence for T-helper 2 shift and association with illness parameters in chronic fatigue syndrome (CFS). Bulletin of The IACFS/ME, 2008, 16, 3.
Few immunological markers have been consistently reported in CFS. However, a shift to a T-helper 2 (Th2) type immune response has been hypothesized for individuals with CFS. The current study investigated whether individuals with CFS who exhibited a stronger shift towards a Th2 type of immune response would also exhibit more severe symptoms, poorer neurocognitive functioning, and poorer physical and psychosocial functioning. The current investigation measured the percentage of Th1-like and Th2-like memory cells using cell surface flow cytometry in 114 individuals with CFS (CDC criteria ’94). The associations between the ratio of Th1 and Th2 memory cells and various illness parameters measures were then examined, including symptom severity, psychiatric functioning, neurocognitive functioning, salivary cortisol levels, and chronic pain status. Results indicated that individuals who exhibited a more extreme shift towards a Th2 immune response also exhibited poorer sleep and high levels of basal salivary cortisol. The implications of these findings are discussed.
http://www.iacfsme.org/BULLETINFALL2008/tabid/290/Default.aspx
Van den Eede, F and Moorkens, G. HPA-axis dysfunction in chronic fatigue syndrome: clinical implications. Psychosomatics, 2008, 49, 5, 450.
Letter. http://psy.psychiatryonline.org/cgi/content/full/49/5/450
“Patients with CFS frequently adopt a somatic theory with regard to their illness, which can have negative impact on their prognosis. The stress model allows for bridging the dualism between "body" and "mind" in CFS by integrating physical and psychological stress as predisposing, precipitating, and perpetuating factors. In this model, the disturbances of the HPA axis can be considered as a final common pathway and as a physiological link to immunological disturbances.
Furthermore, the search for biological markers is required for diagnostic management and for therapeutic monitoring in CFS. We need to assess the validity of challenge tests such as the test involving the administration of low-dose dexamethasone (to examine the glucocortocoid-feedback function). In the absence of any biological marker, cognitive-behavioral therapy and graded exercise are the only evidence-based treatment options in CFS. Future studies could examine the effect of these interventions on HPA-axis disturbances, as well the effect of these disturbances on the prognosis of CFS.”
[Ed. Note: Patients with CFS frequently adopt a somatic theory because it matches their experience and given the literature, may well be accurate.]
Veldman, J., Van Houdenhove, B and Verguts, J. Chronic fatigue syndrome: a hormonal origin? A rare case of dysmenorrhea membranacea. Archives of Gynecology and Obstetrics, 2008 Sep 12. [Epub ahead of print].
[Ed. Note: Case history illustrating the deficiencies of the current criteria for CFS and risk of misdiagnosis on basis of ‘symptom counting’. Side-effects of the oral contraceptive pill can produce symptoms similar to CFS.]
Ward, T., Hogan, K., Stuart, V and Singleton, E. The experiences of counselling for persons with ME. Counselling and Psychotherapy Research, 2008, 8, 2, 73-79.
A number of studies have evaluated counselling interventions for people with myalgic encephalitis, but few report client perceptions in any detail. This study seeks to explore client perceptions using a qualitative methodology. A sample of 25 individuals with myalgic encephalitis were interviewed (by telephone) about their experiences in counselling. The interviews were transcribed and subjected to thematic analysis using grounded theory principles. The analysis showed that people with myalgic encephalitis endure significant changes to their lives, often involving great loss and trauma. After seeking help through counselling, participants had experienced a wide variety of approaches and there were positive and negative perceptions of each. Other perceptions related to therapist characteristics and the way in which interventions were carried out. Recommendations for practitioners are given.
“The counselling experiences of people with ME as described in this paper point to a need for counsellors to be able to offer a range of interventions, including CBT and person-centred interventions (and from our own experience with clients, psychodynamic perspectives can be useful too). Ideally this integration should be client driven: the counsellor will offer interventions based on client need and in consultation with the client. All counsellors should be familiar with the concept of pacing and how to help clients work on this coping technique. Given that the majority of clients are unlikely to recover fully, counsellors should be willing to address client expectations in a realistic way. In this study, none of the participants felt that they had achieved a full recovery, and a number expressed the view that they were concerned that approaches were often presented as a possible cure. As Song and Jason (2005) point out, those clients that do recover may not have had ‘pure’ ME, and may therefore be improving because the CBT addresses some other underlying issue. The notion that counselling can somehow ‘cure’ ME seems therefore somewhat unrealistic (Deale et al., 2001). However, we feel that counsellors would be justified in saying to clients that counselling may positively impact on issues arising from ME such as grief, loss, anxiety, and depression...
Counsellors should have a good understanding of ME to work with this population. Counselling interventions are most usefully targeted at helping clients cope with their condition, rather than correcting fundamental aetiological factors. . An integrative stance may be best able to meet the diverse needs of the population.”[Ed. Note: This study indicates a confusion between ME, myalgic encephalitis [this, we believe should be encephalomyelitis, ed.] and CFS. Participants were not assessed using criteria and there is a lack of clarity about the type and nature of counselling received. Some reported having had CBT and psychodynamic psycho-therapy. The most useful strategy for activity management was “pacing” but the details suggest some had GET. Discussing the past was generally viewed negatively.]
Chen, R., Moriya, J., Luo, X., Yamakawa, JI., Takahashi, T., Sasaki, K and Yoshizaki, F. Hochu-Ekki-to combined with Interferon-Gamma moderately enhances daily activity of chronic fatigue syndrome mice by increasing NK cell activity, but not neuroprotection. Immunopharmacology and Immunotoxicology, 2008 Sep 12:1-15. [Epub ahead of print]. doi: 10.1080/08923970802391525.
The purpose of this study was to evaluate the beneficial effect of Hochu-ekki-to (TJ-41), an extract of 10 medicinal plants, combined with interferon-γ (IFNγ) on daily activity, immuno-logical and neurological alternation in a mouse model of CFS. CFS was induced by 6 times of repeated injection of Brucella abortus antigen every 2 weeks. Both single TJ-41 and TJ-41 combined with IFNγ increased running activity and thymus weight of CFS mice, while thicker thymic cortex together with elevation of natural killer cell activity was only found in the combined treatment group. No significant improvement was observed in the atrophic brain and decreased expression level of brain-derived neurotrophic factor and Bcl-2 mRNA in hippocampus in both treatment groups. Our results suggest that TJ-41 combined with IFNγ might have a protective effect on the marked reduction in the activity in a model of CFS via normalization of host immune responses, but not neuroprotection.
[Ed. Note: It is questionable whether one can induce CFS in mice, given diagnosis relies on the report of five symptoms. The number of mice per group was very small.]
Goudsmit, EM and Howes, S. Is multiple chemical sensitivity a result of expectations and beliefs? A critical evaluation of provocation studies. Journal of Nutritional & Environmental Medicine, iFirst. 30th September.
http://www.informaworld.com/smpp/content~content=a903527516~db=all~order=pubdate
A systematic review of provocation studies concluded that while persons with multiple chemical sensitivities (MCS) react to chemical challenges, these responses occur more often when they can discern differences between active and sham substances. The authors of the review interpreted these findings as evidence that the symptoms may not be specific to the chemical but related to expectations and prior beliefs. Given the complexity of the subject matter, we re-examined the studies using additional criteria.
Our analysis revealed a number of methodological weaknesses which do not appear to have been given due consideration by the authors when interpreting the findings. In light of these shortcomings, we believe that their conclusions may have overstated the role of psychological factors in the aetiology of MCS.
Pall, ML. Post-radiation syndrome as a NO/ONOO- cycle, chronic fatigue syndrome-like disease. Medical Hypotheses, 2008, 71, 4, 537-541.
Post-radiation syndrome is proposed to be CFS or a chronic fatigue syndrome-like illness, initiated by exposure to ionizing radiation. This view is supported by the nitric oxide/peroxynitrite (NO/ONOO-) cycle mechanism, the putative etiologic mechanism for CFS and related illnesses. Ionizing radiation may initiate illness by increasing nitric oxide levels via increased activity of the transcription factor NF-ΚB and consequent increased synthesis of the inducible nitric oxide synthase.
Two types of components of the nitric oxide/peroxynitrite cycle have been studied in post-radiation syndrome patients and shown to be elevated. The symptoms and signs of post-radiation syndrome and its chronicity are similar or identical to those of CFS and can be explained as being a consequence of nitric oxide/peroxynitrite cycle etiology. While the data available to test this view are limited, it provides for the first time a comprehensive explanation for post-radiation syndrome.
[Ed. Note: View based on a broad concept of CFS.]
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