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Process of CBT for CFS: Which perpetuating cognitions & behaviour changes related to fatigue reductn

Dolphin

Senior Member
Messages
17,567
It's a pain: they only give the results in figures:
Heins2013_zps8d05aabf.jpg


Response groups and trajectories of process variables Based on their level of fatigue at the different measurements, 42 patients were classified as fast-responders (fatigue <35 at first interim measurement), 44 as mid-term responders (fatigue <35 at second interim measurement), 17 as slow-responders (fatigue <35 at third interim measurement), 24 as very slow responders (fatigue <35 at post-measurement) and 52 as non-responders (fatigue >=35 at post-measurement). Four patients could not be assigned to a subgroup because of missing data. We combined the slow and very-slow responders into one group of slow responders to obtain four groups of sufficient sample size. Becausewe combined the slowand very slowresponders, we also combined the change scores between interimmeasurement 2 and the post-measurement. Mean values of the potential process variables in the different response groups during therapy are depicted in Fig. 3. Patterns of change in all process variables resembled that of fatigue, except for actual objective activity. At post-treatment, non-responders differed significantly from the other groups on all process variables.

This means it is possible for a responder to only drop one point (out of 56) and be counted as a responder as the entry criteria require a fatigue score >=35.
 
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Dolphin

Senior Member
Messages
17,567
Fatigue did actually correlate with objective activity on completion, although it didn't at baseline or at the two interim time points:
Heins2013-Table2_zps754aa38f.jpg
 

Dolphin

Senior Member
Messages
17,567
This study didn't use a SF-36 physical functioning threshold for entry.

The mean (SD) SF-36 physical functioning scores at baseline were 57.5 (20.1). This is close to the "normal functioning" threshold of SF-36 PF>=60 that was used in the PACE Trial (one could also be recovered with a score of 60). This means that probably somewhere close to 50% of those with CFS (Fukuda) had "normal functioning" at baseline (i.e. before any therapy) if one uses the PACE threshold!
 

Dolphin

Senior Member
Messages
17,567
I tried to make an estimate of objective figures.
On completion, it looks like something like:
non-responders (n=52): 67.6
fast (n=42): 76.7
mid-term (n=44): 76.7
slow (n=41): 78.04
Gives a mean of: 74.36.

This contrasts with a mean of 91 in healthy controls reported in Wiborg et al (2010):

The Actometer is described in more detail by van der Werf et al. (2000). They found a significant difference between the mean Actometer score of CFS patients which was 66 (S.D.= 22) and healthy controls who had a mean Actometer score of 91 (S.D.=25).

The baseline scores in this study are a little higher here - I'm too tired to try to calculate - maybe around 67.5-68.
 

Dolphin

Senior Member
Messages
17,567
Here's talk about deconditioning/increasing exercise:

Introduction:

Recently,Wiborg et al. developed a comprehensive treatmentmodel of CBT for CFS [15], based on the model of Vercoulen et al. [7]. For their analyses they used data from previous randomised controlled trials (RCTs) testing the efficacy of CBT for CFS. Wiborg et al. first tested for each variable in the model of Vercoulen whether it was a mediator of CBT for CFS, i.e. whether it changed more in patients receiving CBT than in the control group and whether it indirectly explained (part of) the effect of treatment on symptom change. Two adaptations were made to the original variables: somatic attributions were not analysed, as previous research had shown that somatic attributions do not change during treatment [10], so they could never be a mediator of CBT; and perceived problems with activity were analysed, rather than objective activity assessed with actigraphy, as previous research had shown that objective activity or physical fitness do not mediate the effect of CBT for CFS [16] and other behavioural interventions for chronic fatigue [17,18]. In the final model, the decrease in fatigue is explained by an increased sense of control over fatigue, an increase in perceived activity, and improved physical functioning.

[15] Wiborg JF, Knoop H, Frank LE, Bleijenberg G. Towards an evidence-based treatment model for cognitive behavioral interventions focusing on chronic fatigue syndrome. J Psychosom Res 2012;72:399–404 [Epub 2012/04/04].

[16] Wiborg JF, Knoop H, Stulemeijer M, Prins JB, Bleijenberg G. How does cognitive behaviour therapy reduce fatigue in patients with chronic fatigue syndrome? The role of physical activity. Psychol Med 2010;40:1281–7 [PubMed PMID: 20047707].

[17] Puetz TW, Flowers SS, O'Connor PJ. A randomized controlled trial of the effect of aerobic exercise training on feelings of energy and fatigue in sedentary young adults with persistent fatigue. Psychother Psychosom 2008;77:167–74. http://dx.doi.org/10.1159/ 000116610 [Epub 2008/02/16. doi: 000116610, PubMed PMID: 18277063].

[18] Moss-Morris R, Sharon C, Tobin R, Baldi JC. A randomized controlled graded exercise trial for chronic fatigue syndrome: outcomes and mechanisms of change. J Health Psychol 2005;10:245–59 [PubMed PMID: 15723894].

Methods:

Patients did not receive feedback on their activity level during the measurements, but they were told their activity level after the baseline measurement.

Results:

Regression analyses in which changes in process variables between the previous and current measurements were added showed different results (Table 4). Lower levels of fatigue were related to increases in perceived activity, physical functioning and sense of control over fatigue together with decreases in focusing on symptoms. Changes in objective activity did not predict levels of fatigue.

Lower pre-treatment objective activity predicted lower fatigue at the first interim measurement. This finding is difficult to explain. Levels of objective activity during treatment were not related to subsequent levels of fatigue at other measurements. In the early phases of treatment, even patients who remain severely fatigued after treatment increase their level of physical activity (see Fig. 3). So an increase in physical activity per se does not seem sufficient to reduce fatigue. An increase in perceived activity, however, does seem important.

Discussion:

However, in our study, average levels of activity pre-treatment were not very low* and the lack of a relationship between objective activity and fatigue makes it unlikely that physical deconditioning is a fatigue perpetuating factor. Our results indicate that rather than objective activity, it might be low perceived activity that perpetuates fatigue. This should be taken with caution, as a distinction has to be made between models trying to explain the persistence of symptoms in CFS and those trying to explain the treatment processes. Besides, we did not measure physical fitness directly and physical deconditioning may still play a role in low active patients.
*Average levels of activity were similar (a few percentage points higher) to the pre-treatment levels in the three studies looked at in Wiborg et al. (2010) and Van der Werf (2000) also had similar scores to Wiborg et al. (2010). All a long way from the mean healthy controls of 91.

In conclusion, levels of fatigue during CBT for CFS do not seem to be related to objective physical activity, whereas they do seem related to a change in cognitive factors such as the sense of control over fatigue, focusing on symptoms, perceived activity and physical functioning.
 
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13,774
Was unsure whether it would be worth starting a new thread on this paper from 2009. Didn't look revelatory, but still relevant to the objective capacity vs subjective fatigue thing:

http://www.pmrjournal.org/article/S1934-1482(09)00436-5/abstract

Exploratory Analysis of the Relationships between Aerobic Capacity and Self-Reported Fatigue in Patients with Rheumatoid Arthritis, Polymyositis, and Chronic Fatigue Syndrome
Received 29 July 2008; accepted 22 April 2009.

Objective
To determine if self-reported levels of physical activity and fatigue are related to peak oxygen uptake (VO2peak) and whether these relationships differ among the patient groups (rheumatoid arthritis [RA], polymyositis [PM], and chronic fatigue syndrome [CFS]).

Design
Correlational investigation.

Setting
Two ambulatory research clinics at the National Institutes of Health, Clinical Center, Bethesda, MD.

Participants
There were 9 patients with PM, 10 with RA, and 10 with CFS. All patients met case criteria for their respective diagnoses.

Methods/Main Outcome Measurements
VO2peak during bicycle ergometry and self-reported fatigability, fatigue, and physical activity. VO2peak was used as the criterion measurement of physiological fatigue with which the self-reported variables were compared.

Results
The Pearson r revealed that self-reported physical activity correlated with VO2peak (r = 61, P = .01). However, fatigability and fatigue did not correlate with VO2peak. Linear regression analysis was performed to assess the effects of diagnosis group, self-reported activity level or fatigue, and their interaction. A trend in the data showed a distinctive relationship between fatigue/fatigability within the 3 groups. In addition, when controlling for group status, self-reported activity predicted aerobic capacity as measured by VO2peak.

Conclusions
This study confirms that patients with chronic, but stable RA, PM, or CFS are fatigued and have significantly decreased aerobic capacity. Self-reports of physical activity predicted VO2peak, and may be used as an indicator of activity-based aerobic capacity. Self-reports of fatigue, however, did not correlate with VO2peak and hence are assessing something other than an index of aerobic capacity, and provide additional information about patients' perceptions, which will require further investigation.
 

Snow Leopard

Hibernating
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5,902
Location
South Australia
With respect to the aforementioned paper by Esther, is it necessarily that fatigue was not correlated with VO2 peak, or that fatigue questionnaires are not precise enough/of sufficient quality (too vague etc) to be correlated with VO2 peak...
 

A.B.

Senior Member
Messages
3,780
With respect to the aforementioned paper by Esther, is it necessarily that fatigue was not correlated with VO2 peak, or that fatigue questionnaires are not precise enough/of sufficient quality (too vague etc) to be correlated with VO2 peak...

There is no reason to assume that fatigue should correlate well with VO2 peak in the first place.
 

Firestormm

Senior Member
Messages
5,055
Location
Cornwall England
What might be the impact of us adapting our abilities to our condition, when we are told to 'exercise to the max'? What I mean to say is, I have been adapting to my health restrictions - and pushing against them - improving and relapsing as I am permitted - but have I adapted to such an extent that this has impacted on my ability now to 'exercise'? Has my body accommodated itself? And if, you caught me in a period of relative 'remission' what impact might that have on any physiological measure for ME? Or perhaps this can be said to have been taken into account in these kind of studies? :)
 
Messages
15,786
What might be the impact of us adapting our abilities to our condition, when we are told to 'exercise to the max'? What I mean to say is, I have been adapting to my health restrictions - and pushing against them - improving and relapsing as I am permitted - but have I adapted to such an extent that this has impacted on my ability now to 'exercise'?
Deconditioning has very little impact on ME/CFS patients, as evidenced by our ability to instantly function pretty normally during abrupt remissions.

It's also been shown in two-day CPET tests that the reaction of ME/CFS patients to repeated maximal exertion is strikingly different from that of deconditioned (sedentary) controls. Deconditioned people have improved performance on the 2nd day, whereas ME/CFS patients get much worse.
 

Firestormm

Senior Member
Messages
5,055
Location
Cornwall England
Deconditioning has very little impact on ME/CFS patients, as evidenced by our ability to instantly function pretty normally during abrupt remissions.

It's also been shown in two-day CPET tests that the reaction of ME/CFS patients to repeated maximal exertion is strikingly different from that of deconditioned (sedentary) controls. Deconditioned people have improved performance on the 2nd day, whereas ME/CFS patients get much worse.

But what I am saying - being cack-handed as usual - is that the 'disease' that is ME may not be playing a role here (or indeed it might). Rather, this testing is measuring our functional abilities - and those might have been compounded by our efforts to adapt. Say, you do this test (I think you have), and I do it (I haven't). We both have and can meet the various diagnoses for ME. But, I know that you have more 'things wrong with you' than I do, and so we will both have a different functional capacity unrelated - I think at least it is fair to say - to our ME. Or it can't be said that ME is exclusively the cause of our functional impairments. Unless the inability to meet the results of those without a diagnosis of ME, can be discovered to be a direct result of our primary (perhaps) diagnosis...

I'll come back to that. Sorry. Am a bit BLURGH this morning :)
 
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15,786
We both have and can meet the various diagnoses for ME. But, I know that you have more 'things wrong with you' than I do, and so we will both have a different functional capacity unrelated - I think at least it is fair to say - to our ME. Or it can't be said that ME is exclusively the cause of our functional impairments. Unless the inability to meet the results of those without a diagnosis of ME, can be discovered to be a direct result of our primary (perhaps) diagnosis...
If we both have ME/CFS (which should include PEM) then we should both have reduced VO2max results on day 2 compared to our results for day 1. How bad our results are, either at the 1st day or compared to the 1st day, would vary from patient to patient. Gender, for example, has a huge impact.

I suppose it would be possible that some actual deconditioning in reflected in the results. But since results are much worse on day 2 (whereas merely deconditioned controls improve), it would seem that the PEM-inducing disease process is having a much bigger impact than deconditioning. If both influences were roughly the same, I'd expect ME patients to see little change on day 2, as the conditioning effects of day 1 would approximately balance out the decrease in function caused by the disease.

But because there is a large decline in VO2max the 2nd day, this suggests that deconditioning is having a negligible impact in counter-acting the decline shown in the day 2 results.
 
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