Friday, March 14, 2008

Majority of CFS Patients Negatively Affected by CBT (Dutch Study)

Majority of ME/CFS patients negatively affected by Cognitive Behaviour Therapy

A recent pilot study (Koolhaas, et al., 2008, Netherlands) reports that only 2% of ME/CFS patients are cured by CBT, while the greatest share (38%) are adversely affected - most reporting substantial deterioration. It is especially notable that employment and education are negatively affected. This is in sharp contrast to the claims of psychiatrists and the Dutch Health Council that 70% of patients improve. Previous studies have also ignored or denied the negative affects of CBT on ME/CFS patients. The pilot study, recently published in the Dutch Medical Magazine, Medisch Contact, concludes that the previously reported claims of 70% improvement in ME/CFS patients receiving CBT are vastly overstated and misleading.

The following summary is from page 4 of the Dutch-language study. http://home.planet.nl/~koolh222/cgtbijmecvsvanuitperspectiefpatient2008.pdf

Cognitieve gedragstherapie bij het chronische vermoeidheidssyndroom (ME/CVS) vanuit het perspectief van de patiënt

Drs. M.P. Koolhaas, H. de Boorder, prof. dr. E. van Hoof Date: February 2008 ISBN: 978-90-812658-1-2 The Netherlands

*SUMMARY*

*Background *In recent years, Chronic Fatigue Syndrome, also known as Myalgic Encephalomyelitis (ME/CFS), has been getting a lot of attention in scientific literature. However its aetiology remains unclear and it has yet to be clarified why some people are more prone to this condition than others. Furthermore, there is as yet no consensus about the treatment of ME/CFS. The different treatments can be subdivided into two groups, the pharmacological and the psychosocial therapies. Most of the scientific articles on treatment emphasize the psychosocial approach.

The most intensively studied psychological therapeutic intervention for ME/CFS is cognitive behaviour therapy (CBT). In recent years several publications on this subject have been published. These studies report that this intervention can lead to significant improvements in 30% to 70% of patients, though rarely include details of adverse effects. This pilot study was undertaken to find out whether patients' experiences with this therapy confirm the stated percentages. Furthermore, we examined whetherthis therapy does influence the employment rates, and could possibly increase the number of patients receiving educational training, engaged in sports, maintaining social contacts and doing household tasks.

*Method *By means of a questionnaire posted at various newsgroups on the internet, the reported subjective experiences of 100 respondents who underwent this therapy were collected. These experiences were subsequently analysed.

*Results *Only 2% of respondents reported that they considered themselves to be completely cured upon finishing the therapy. Thirty per cent reported 'an improvement' as a result of the therapy and the same percentage reported no change. Thirty-eight percent said the therapy had affected them adversely, the majority of them even reporting substantial deterioration. Participating in CBT proved to have little impact on the number of hours people were capable of maintaining social contacts or doing household tasks. A striking outcome is that the number of those respondents who were in paid employment or who were studying while taking part in CBT was adversely affected. The negative outcome in paid employment was statistically significant. CBT did, however, lead to an increase in the number of patients taking up sports.

A subgroup analysis showed that those patients who were involved in legal proceedings in order to obtain disability benefit while participating in CBT did not score worse than those who were not. Cases where a stated objective of the therapy was a complete cure, did not have a better outcome. Moreover, the length of the therapy did not affect the results.

*Conclusions *This pilot study, based on subjective experiences of ME/CFS sufferers, does not confirm the high success rates regularly claimed by research into the effectiveness of CBT for ME/CFS. Over all, CBT for ME/CFS does not improve patients' well-being: more patients report deterioration of their condition rather than improvement. Our conclusion is that the claims in scientific publications about the effectiveness of this therapy based on trials in strictly controlled settings within universities, has been overstated and are therefore misleading. The findings of a subgroup analysis also contradict reported findings from research in strictly regulated settings.

For more information, please contact:

Drs. M.P. Koolhaas

Email: m.p.koolhaas@consunet.nl

* * *

One suggestion for the drop-off in hours worked was that the effort of getting to/from the therapy sessions was at the expense of being able to use that energy to work.

That sounds reasonable to me. CFS patients are proven to have a Daily Activity Limit, so any activity requires a trade-off – if I’m going to spend time cleaning, then I’d better have something for dinner that requires almost no effort because I won’t have it in me to cook if I’ve used my energy to clean.

Someone has suggested that CFS be compared to a debit card: you have $100 (or 100 energy credits) to spend. You can spend them any way you want to, but once you’ve spent them, you’re bankrupt and can’t spend any more until you replenish. You can wisely spend that 100 energy credits 5 at a time for meals, brushing your teeth, combing your hair, toileting, etc., and have enough to get through the day. Or you can blow the whole 100 at once by exercising for an hour, and then you will need to ask someone else to cook your meals and spoon-feed you. Or you can blow 50 on dinner and a movie and not have enough left to shower and change into your pajamas when you come home, and have to sleep in your clothes.

Too many people can’t fathom the notion that I have to let the little niceties slide because I need to conserve energy for more important things. Normal people don’t have to choose between writing checks for bills and writing birthday cards, but if I have only 2 energy credits left after taking care of meals and hygiene, it’s more important to write the checks. It’s more important to me to fix 3 healthy meals each day than to put my hair in curlers and apply makeup and nail polish. Not getting dressed up and made up every day is not a matter of being depressed and not caring what I look like, but of making the conscious choice to save those energy credits to do something more practical, like load/unload the dishwasher.

Patients get WORSE with Therapy (Tom's translation)

Majority of ME/CFS patients negatively affected by Cognitive Behaviour Therapy

(Excerpts from Tom’s attempt at translation)

Cognitieve gedragstherapie bij het chronische vermoeidheidssyndroom (ME/CVS) vanuit het perspectief van de patient

(Cognitive behaviour therapy for chronic fatigue syndrome from the patient’s perspective)

http://home.planet.nl/~koolh222/cgtbijmecvsvanuitperspectiefpatient2008.pdf

I was alerted to this on Friday by Ellen Goudsmit. It had a lot of tables that looked interesting so I tried to read through it using the online translator Babelfish. They talked a bit about the Belgian CBT/GET rehab clinics so I translated that also.

Tom

Average age in years (standaardafwijking (standard deviation I presume)) 39 (11,8) percentage women 84%

ME/CFS 100%

diagnoses has put doctor 98% (doctor gave diagnosis)

complaints worsens after effort 99%

has no effort fear 77%

has been motivated to treatment started 96%

treatments under accompaniment therapeut 99% (treatments done under a therapist, I presume)

had physical oefenprogramma (GET) 88%

treatments 6 months or longer 64%

durations in avance indicated therapeut 62% (the length of treatment was decided in advance)

had been involved in procedure (WAO INCAPACITY BENEFIT) 25%

had other treatment beside CBT (1) 25%

therapy has finished 70% entirely

1) 13 Different therapies and/or types medicijngebruik were in sum called. Most attentive physiotherapy were (9 time). Also mentioned antibiotics (1), fitness (1), psychotherapy (2), hydrotherapy (3), entertainment exercises (1), diet (1), Ritalin (1), sport practising programmes (1), holopathie (2), osteopathy (1), Carnitine (1) and relaxation (1) became.

Reasons prematurely strike therapy (Reason why therapy was stopped prematurely) in the inquiry 5 different reasons had been incorporated for outburst (5 different reasons were given why it was stopped prematurely) . Because more reasons are conceivable, were possible moreover are also not given up reasons called in the inquiry. The 30 persons who drops out called 38 time a reason for premature suspension. In sum it 11 concerned different reasons. In table 2 stand by the respondents reasons given up for striking the therapy.

Table 2: Given up reasons for prematurely props therapy (N=30; 38 time a reason given up)

too heavy because of travel to meetings 5 17% (the travel to the sessions was too much)

too heavy because of physical oefenprogramma 8 27% (the physical exercise program was too hard/much)

stepped no progress aim in advance on 3 10% (had made no progress towards advance aims)

went only reverse 15 50% (was only going backwards)

put for commencement had been gained 1 3%

? other reason (en) 6 20%

Objective therapy it has been confessed that are generally put at CBT before the therapy several, sometimes individual aims. This proves has been at 92% of the respondents also indeed the case. Thereby it was to learn handle the complaints the most attentive doestelling (TK: most common objective) (39%). Personal objectives for (32%) less frequently came or in avance complete convalescence as an objective were stipulated (21%) (TK: complete recovery was stipulated as an objective in 21% of cases) In table 3 we have reflected by the respondents communicated objectives.

Table 3: Objectives CBT (N=100),

certain in advance, complete convalescence/cicatrisation 21%

personal objective, e.g. (partly) work 32%

better to learn handle complaints, restrictions 39%

aims in avance no put 8% (no aims decided in advance)

General impact CBT in the previous paragraph we have mentioned the objectives at the beginning of the therapy. To what extent these are gained becomes clear from table 4. only 2% of the respondents communicates that the therapy to entirely has conducted repaired. In sum (total) 30% improvements communicate without convalescence has been reached. A just as large group communicates no change. Reverse gear became by 38% declared (TK: 38% said they became worse). Remarkably the large group patients, who have deteriorated by the therapy strongly, is (29%) (TK: Remarkably a large group, 29%, got much worse as a result of the therapy). By remainder more patients by this therapy reverse has gone then ahead.

Table 4: Reaches result after suspension CBT (N=100). (1)

Entirely repaired 2%

considerably improved, but do not heal 15%

something improved 15%

rights remained 30%

something deteriorated 9%

strongly deteriorated 29%

1) The group afvallers has been also incorporated in this table. In paragraph 5.3 we make still a splitting up between both groups.

5.2 Impact on social and social activities in this paragraph examines we the impact of CBT on five important social and social activities, namely knows performing paid work, following a study, practising sport, it maintaining social contacts and performing domestic tasks.

Influence CBT at paid work (TK: Influence of CBT on paid work) a rather large minority (41 persons) appears average almost 25 perform hours per week for commencement of CBT still whole or partially paid work. It is striking that after the therapy this number has decreased up to 31: 16 participants, who worked preceding the therapy still, no longer do this after the therapy. The other way around started or resume after the therapy 6 participants paid work. (TK: Out of 41 worked at the start working on average 25 hours per week, 15 gave up; while 6 who hadn't been working started to work). Moreover appears still that this group workers is average 5 hours less will work (TK: Moreover of those that were still working, on average they worked 5 hours less). The total number of decreases hours worked of the group concerned as a result, with almost 40% (TK: This meant that in total, the total number of hours decreased by 40%). The difference appears significant (Paired Twosample t-test, two-sided; t(92)=3.04; p<0.005). CBT appear therefore for working participants a strongly negative impact on the possibilities of performing work have paid. (TK: Therefore CBT appears to have a strongly negative impact on paid work performance/similar).

Table 5: Number of patients hours per week before and after CBT, worked with paid work and number of hours [TK: Observation: The top group is 32.5-40 hours per week. Before it, 13 people were doing this; after it, there were only 4!. For the 24.5-32 hour group it went from 6 to 2. So in total, for 25 hours or more, it went from 19 to 6!]

5.3 Results of subgroup analysis

Aforementioned results have been obtained simply tallying the scores of the 100 respondents. We have however also examined if there possible differences certain subgroups be to find. Thus it is conceivable that the rather large group patients who CBT not to end has been possible accomplish,

the results has negatively influenced(TK: it is conceivable that the results could have been influenced by the rather large group who didn't finish the CBT). Also we have examined if patients whom at the time of the therapy involved products in WAOprocedure, the results have influenced (TK: we have examined if the results could have been influenced by the patients who, at the time of the therapy, were involved products in applying for disability payments). If lying behind idea is, however, suggested that these patients their complaints necessary to prove their revendications on a wao-uitkering (prins e.a., 2002) and therefore would show none or less improvement by CBT [TK: (something like) this is based on the idea that has been suggested that patients who have to prove they have sufficient symptoms/complaints for a disability payment would show none or less improvement by CBT]

Influence persons who drops out (The influence of people who drop out)

Like on the basis of table 2 can be expected is the impact of CGT significantly worse at the patients, whom the therapy has not completed (chi^2(4)=15,01; p<0.01) (TK: As is clear from Table 2, somebody was more likely to have said they were made worse by CBT if they didn't finish it). The most called reason for premature suspension of the therapy was deterioration of the health situation. The results of the group which the therapy is completed because of this something improve then which of the total group (TK: Because of this, the results of the group who completed the therapy are therefore better because of this). It is remarkable however that also 18.6% of the respondents who completed the therapy indicates strongly by the therapy having deteriorated

(1) For the small number of perceptions in the group repaired "entirely" we have added this group for the statistic tests to the group "considerably improved".

Table 11: Impact CBT treatment split up in afvallers and voltooiers (Impact of CBT broken down into completers (people who did the whole course) and those that dropped out

Reported impact Slimmed (TK: Dropped out) (N) a f fallen (TK: Dropped out) (%) accomplished (completed) (N) accomplished (%) total (N) total (%)

Entirely repaired 0 0% 2 2.9% 2 2%

considerably improved 1 3.3% 14 20.0% 15 15%

something improved 4 13.3% 11 15.7% 15 15%

rights remained 6 20.0% 24 34.3% 30 30% (TK: remained the same)

something deteriorated 3 10.0% 6 8.6% 9 9%

strongly deteriorated 16 53.3% 13 18.6% 29 29%

Totals 30 100% 70 100% 100 100%

Influence WAO incapacity benefit procedure

It is frequently put that patients show involved in a WAO incapacity benefit procedure worse outcomes at CBT (TK: It is frequently claimed that patients involved in a WAO incapacity benefit procedures have worse outcomes with CBT). The figures from this inquiry do not support this assumption however: the impact of CBT is at this group not significant worse (chi^2(4) = 2.77; P=0,60).

Table 12: Impact CGT split up in patients, who were, and were not involved with WAO incapacity benefit procedures

Reported impact WAO incapacity benefit procedure (N) Idem (%) no procedure (N) idem (%) total (N) total (%)

entirely repaired 0 0% 2 2.7% 2 2%

considerably improved 6 24% 9 12.0% 15 15%

something improved 5 20% 10 13.3% 15 15%

rights remained 7 28% 23 30.7% 30 30%

something deteriorated 1 4% 8 10.7% 9 9%

strongly deteriorated 6 24% 23 30.7% 29 29%

totals 25 100% 75 100% 100 100%

Influence other treatment beside CBT

A number of patients followed other treatment still one or more or used medicines beside CBT. Between both groups no significant difference could be found (chi^2(4) = 2.27; P=0,69). We have examined this because it is sometimes put at CBT as condition that patients can no other therapies follow or medicines simultaneously to use.

Table 13: Impact simultaneously present other therapies/medicatie on outcome CBT

Reported impact other treatment beside CBT (N) idem (%) no other treatment (N) idem (%) total (N) total (%)

repaired entirely 0 0% 2 2.7% 2 2%

considerably improved 4 16% 11 14.7% 15 15%

something improved 6 24% 9 12.0% 15 15%

rights remained 6 24% 24 32.0% 30 30%

something deteriorated 2 8% 7 9.3% 9 9%

strongly deteriorated 7 28% 22 29.3% 29 29%

totals 25 100% 75 100% 100 100%

Influence physical oefenprogramma (Influence of a physical exercise program)

In the Netherlands CBT are generally combined with Graded Exercise Therapy (GET), physical oefenprogramma (exercise program), in which the physical activity is systematically intensified according to a diagram in avance established. We have examined if the outcomes differed from the therapy for the group from and without such a programme. There no significant difference could be shown (chi^2(4) = 7.69; P=0,10). Must registered become that in only 12 cases GET no component of the therapy determined. (It should be stated that GET was not involved in only 12 of the cases)

Table 14: Impact CBT without and with physical oefenprogramma (GET)

Reported impact no GET (N) Idem (%), however, GET (N) idem (%) total (N) total (%) 0 0%

entirely repaired 2 2.3% 2 2%

considerably improved 0 0% 15 17.0% 15 15%

something improved 1 8.3% 14 15.9% 15 15%

rights remained 7 58.3% 23 26.1% 30 30%

something deteriorated 0 0% 9 10.2% 9 9%

strongly deteriorated 4 33.3% 25 28.4% 29 29%

totals 12 100% 88 100% 100 100%

(The) Influence (of) objectives

It is, however, put at CBT that how higher the put aim is, how larger the impact of the treatment is because put aims could not reached (prins e.a., 2006) (TK: It is claimed that for CBT the higher the stated aim, the larger impact of the treatment is because one won't aim for things if one doesn't try (or something like that) (prins e.a., 2006)]. The two patients, who have communicated complete convalescence, indeed fall in the group where complete convalescence had been in avance put as an aim, but tevens can in table 15 it see that almost half of the patients in this group reported CGT to a strong reverse gear. This impact was exactly not significant (TK: not quite significant) (chi^2 (4) = 8.49; P=0,075).

Table 15: Impact CBT in objective complete convalescence split up and other Objectives

Reported impact aim complete convalescence (N) idem (%) other aim (N) idem (%) total (N) total (%)

entirely repaired 2 9.5% 0 0% 2 2%

considerably improved 3 14.3% 12 15.2% 15 15%

something improved 1 4.8% 14 17.7% 15 15%

rights remained 5 23.8% 25 31.6% 30 30% (TK: remain the same)

something deteriorated 0 0% 9 11.4% 9 9%

strongly deteriorated 10 47.6% 19 24.1% 29 29%

totals 21 100% 79 100% 100 100%

Influence expensive therapy (TK: influence of length of therapy)

Finally we in this subgroup analysis has examined if a longer duration from the therapy to better outcomes has conducted. We have not taken the afvallers (TK: dropouts) because of them it is only confessed how long they have followed the therapy, but not how long the therapy will have lasted if they had completed that. Although in by far the most cases the therapy lasted 6 months or longer prove to be this impact do not improve then at a therapy duration of shorter than 6 months (chi^2 (4) = 3.47; P=0,48).

Table 16: Impact expensive CBT split up in shorter than 6 months and 6 months or longer

Reported impact. shorter than 6 months (N) idem (%) 6 months shorter or longer (N) idem (%) total (N) total (%)

Entirely repaired 0 0% 2 3.8% 2 2.9%

considerably improved 3 17.6% 10 18.9% 13 18.6%

something improved 4 23.5% 8 15.1% 12 17.1%

right remained 6 35.3% 18 34.0% 24 34.3%

something deteriorated 0 0% 7 13.2% 7 10.0%

strongly deteriorated 4 23.5% 8 15.1% 12 17.1%

total 17 100% 53 100% 70 100%

Also from Belgium some figures have been confessed with regard to the effectiveness of CBT in practice. In this country a number of years has been suffered so-called reference centres in use for ME/CFS patients taken in these centres patients standard with CBT/GET is treated.

In 2006 evaluation report, appeared Belgian reference centres (riziv, 2006) (pag. 58) is: read "as far as an comparison is possible lijken the treatment results of the CFS centres therefore less well than the results of the published evidence based studies in which a positive treatment impact of cognitive behaviour therapy or progressive physical rehabilitation was shown". In terms of life quality 48% of the patients (N=403) experienced an improvement by the therapy, 22% found that these equal had remained and 30% communicated reverse have will (pag. 52). these figures be something more positive than those in our study.

Concerning return to work in this report (pag. 55) is read: by the rehabilitation the patients (N=563) perform paid professional activities during on average 18.3% of 38-hour-week. A significant improvement of the socioprofessionele functions of the patients is in accordance with the agreement one of the objectives of the rehabilitation. From the data becomes clear however that the average paid percentage professional activities still decreases up to 14.9% at the end of the rehabilitation. 6% of the patients work more than by the rehabilitation, 10% less. For 84% of the patients does not modify the percentage paid professional activities. Here too appear have contributed CBT/GET positively to an increase of ME/CFS patients to performing paid work, on the contrary. This negative impact was however less strong than in our research.

A variety of patient perspectives

Tom points out:

A case control study of premorbid and currently reported physical activity levels in chronic fatigue syndrome Wayne R Smith , Peter D White and Dedra Buchwald BMC Psychiatry 2006, 6:53doi:10.1186/1471-244X-6-53 http://www.biomedcentral.com/1471-244X/6/53  

But the annoying thing is a lot of the paper involves them impugning the patients perceptions (after they asked the patients about their current and previous activity levels), saying who can trust these patients perceptions for reasons x, y, z, etc. This is despite them admitting, which they slip in in the first paragraph, that "The high levels of physical activity reported by patients have been corroborated by their spouses, partners, or parents [13]." So despite them knowing that, and the data they collected, they spend most of the time trying to build up a case to say the perceptions are likely dodgy without any data to show this. This is despite them not collecting any data in the study to show the patients perceptions were wrong.

 

Michelle writes:

I keep trying to wrap my mind around what happens to these doctors/researchers also. I listened to James Jones's talk that you posted on Co-Cure a few weeks ago and have been meaning to blog about it. It starts out well enough, but eventually his talk becomes peppered with "these people" and before you know it, he's talking about how it's important to train "these people" to understand that activity is good and laying on the couch is bad. It made me wonder if researchers like he and White have internalized some strain of Calvinism in which they can't handle the idea of people not working

At one point Jones gives a case study of a woman diagnosed with CFS who spent all her time on her couch or in bed and left her children "to their own devices." Now, add to this that a lot of us with ME/CFS are overweight (which may well be part of the pathology of the disease) and I do wonder if physicians and researchers like White, Jones or Buchwald can't *not* think of this illness as some pathological form of laziness -- that we just give up on trying – even if White or Jones may have come around to Reeves's view (which also may be grudgingly) that this is a seriously disabling disease.

Of course, my own experience is that we constantly need to be told that it's *okay* to lay on the couch. And, again, when I do slow down and sleep a lot, I actually start feeling *better*. Not cured, mind you. But better.

Btw, thanks for taking the time to put that Dutch study on Co-Cure through Bablefish. Initially it didn't sound all that significant since the abstract made it sound like it was just a study of ME/CFSpatients saying CBT didn't help. But the fact that more patient were not working by the end of the study than were working or had gone back to work was very significant.

 

Erik observes:

"CFS" was intentionally initiated as a "start from scratch" syndrome in order to set aside the possibility that ME and CFS were connected. This was SUPPOSEDLY done in the name of science and research - as if "We don't KNOW if they are connected, so we are starting afresh" but the REALITY of the identifiable immune abnormalities that had to be excluded in order to devise this "CFS research tool" indicate that overlooking the ME connection cannot have been any kind of mistake. Once you "know something", you cannot "unknow it" unless you have Alzheimers.

The pretense that the CDC was unaware of these immune abnormalities is proof of their information suppressing intentions. It amazes me that after twenty years of CFSers watching the CDC "unknow" information, that CFSers still speak of this as if it were an oversight or honest mistake that is waiting to be corrected.

Have you seen my story of the very first "CFS" meeting? It would have been so easy to stop that lone denialist doctor who came to Incline to apprise us that our illness was nothing more than mass delusion through collusion with two suggestible doctors. All we would have to have done is point at the immune abnormalities that Dr Cheney and Dr Peterson identified and demand that the "trivializer" account for these before he did any more theorizing. Instead, the group told those of us who TRIED to speak out, "don't argue with the doctor. It won't do any good. That attitude won't help".

We had him entirely outnumbered, yet by virtue of the group mentality, his view dominated us all - even though we had the facts and he did not. All we had to do was stand up for the truth, but everybody sat down. This is how we got to where we are.

-Erik

"All that is necessary for the triumph of evil is that good men do nothing." - Edmund Burke, Irish orator, philosopher, & politician (1729 - 1797)

 

For Research on Chronic Fatigue Syndrome ( CFS ), visit the List's Website at: http://www.cfsresearch.org/  

From Jean Harrison:

Someone kindly sent me a link to another article about Cher. This time it mentions that she was diagnosed with Epstein Barr in the 1980's. Of course the name CFS did not come to use officially until 1988: "I was sick a long time," she says. "I went to Germany for some medicine and treatment. They have things overseas we never dreamed existed. When I was first diagnosed in the late '80s, I had doctors telling me I was crazy. I was sick constantly and almost died from pneumonia. You never lose it, and it really takes the life out of you." http://www.usatoday.com/life/music/news/2008-02-06-cher-side_N.htm  The more the article is emailed, the more importance the news media gives the subject. Also there is an area in which you can add your comment. What was it she found in Germany? What ever it was seems to have helped her a great deal. Also it's very obvious from this article that Cher is thrilled to be able to work again. And that she hates being sick. Jean Harrison

* * *

I’m glad that Cher has finally admitted that she was diagnosed with CFS. The question is, whether she will "do the right thing" and like Michael J. Fox (Parkinson’s) and David Hyde Pierce (Alzheimer’s), throw her considerable star power behind an effort to publicize and fundraise to help the rest of us, or whether she thinks she has done enough just by coming clean in an interview.

If anyone knows how to contact Cher or her agent/manager, please get that contact information to me. You can post it as a comment to the blog or e-mail it to me privately.

Thursday, March 13, 2008

2 Quickies each on Fibro and CFS

[Muscular strength in patients with fibromyalgia. A literature review] [Article in Danish] Ugeskr Laeger. 2008 Jan 21;170(4):217-24. Dombernowsky T, Dreyer L, Bartels EM, Danneskiold-Samsøe B. Frederiksberg Hospital, Parker Instituttet, Rigshospitalet, Frederiksberg. PMID: 18282450

Do patients with fibromyalgia (FM) have reduced muscular strength?

We examined 22 articles and conclude from the results of these that FM patients have reduced muscular strength in their hands and quadriceps. The material also suggests generalised reduced muscular strength. However, the studies have several methodological shortcomings and future studies should be carefully designed with respect to patients as well as the control group and should be larger. To avoid CNS influence from e.g. fatigue and pain, muscular electro-stimulation may be used to ensure that the actual maximal muscular strength is also measured.

 

A Psychophysical Study of Auditory and Pressure Sensitivity in Patients With Fibromyalgia and Healthy Controls. J Pain. 2008 Feb 14 [Epub ahead of print] Geisser ME, Glass JM, Rajcevska LD, Clauw DJ, Williams DA, Kileny PR, Gracely RH. Chronic Pain and Fatigue Research Center, Department of Internal Medicine, Division of Rheumatology, University of Michigan, Ann Arbor; Department of Physical Medicine and Rehabilitation, University of Michigan, Ann Arbor. PMID: 18280211

Fibromyalgia (FM) is characterized by widespread tenderness. Studies have also reported that persons with FM are sensitive to other stimuli, such as auditory tones. We hypothesized that subjects with FM would display greater sensitivity to both pressure and auditory tones and report greater sensitivity to sounds encountered in daily activities. FM subjects (n = 30) and healthy control subjects (n = 28) were administered auditory tones and pressure using the same psychophysical methods to deliver the stimuli and a common way of scaling responses. Subjects were also administered a self-report questionnaire regarding sensitivity to everyday sounds. Participants with FM displayed significantly greater sensitivity to all levels of auditory stimulation (Ps < .05). The magnitude of difference between FM patients' lowered auditory sensitivity (relative to control subjects) was similar to that seen with pressure, and pressure and auditory ratings were significantly correlated in both control subjects and subjects with FM. FM patients also were more sensitive to everyday sounds (t = 8.65, P < .001). These findings support that FM is associated with a global central nervous system augmentation in sensory processing. Further research is needed to examine the neural substrates associated with this abnormality and its role in the etiology and maintenance of FM.

PERSPECTIVE: Muscle tenderness is the hallmark of FM, but the findings of this study and others suggest that persons with FM display sensitivity to a number of sensory stimuli. These findings suggest that FM is associated with a global central nervous system augmentation of sensory information. These findings may also help to explain why persons with FM display a number of comorbid physical symptoms other than pain.

 

Chronic fatigue syndrome: characteristics and possible causes for its pathogenesis. Journal: Isr Med Assoc J. 2008 Jan;10(1):79-82. Authors: Bassi N, Amital D, Amital H, Doria A, Shoenfeld Y. Affiliation: Department of Rheumatology, University of Padova, Padova, Italy. NLM Citation: PMID: 18300582

Chronic fatigue syndrome is a heterogeneous disorder with unknown pathogenesis and etiology, characterized by disabling fatigue, difficulty in concentration and memory, and concomitant skeletal and muscular pain. Several mechanisms have been suggested to play a role in CFS, such as excessive oxidative stress following exertion, immune imbalance characterized by decreased natural killer cell and macrophage activity, immunoglobulin G subclass deficiencies (IgG1, IgG3) and decreased serum concentrations of complement component. Autoantibodies were also suggested as a possible factor in the pathogenesis of CFS. Recent studies indicate that anti-serotonin, anti-microtubule-associated protein 2 and anti-muscarinic cholinergic receptor 1 may play a role in the pathogenesis of CFS. It has been demonstrated that impairment in vasoactive neuropeptide metabolism may explain the symptoms of CFS.

The full text of Chronic fatigue syndrome: characteristics and possible causes for its pathogenesis. Journal: Isr Med Assoc J. 2008 Jan;10(1):79-82. Authors: Bassi N, Amital D, Amital H, Doria A, Shoenfeld Y. is available for free at: http://www.ima.org.il/imaj/ar08jan-21.pdf  

 

TESTING, TESTING, TESTING:

Excuse the long-suffering tones but I, like many of you, am just pig sick of hearing of folk "instantly" cured of "ME" when, by implication, they did not have the disease and had been deluded into merely thinking they had it. It is simply basic medical and scientific sense to actually examine patients adequately and to apply rigorous taxonomic disease criteria: Testing, testing, testing and separating the proverbial sheep from the goats. Then, and only then, will we know who the genuine Myalgic Encephalomyelitis patients are and who are something different.

Increasingly in the UK however, instead of such genuine science-based medical integrity we are subjected to the Alice-in-Wonderland policies of a corporate-hijacked New Labour spin machine that is increasingly Orwellian.Who knows, maybe the current profiteer's war between purveyors of CBT and purveyors of SSRI's will one day soon result in an oligopolist's truce? Perhaps selling a combined CBT-LSD "Cognitive Leary Therapy": where "CFS/ME" patients are told to turn on, tune in and drop-out of the benefits system?

To be serious though, the current "CFS/ME" situation, where the one-size-fits-all shotgun approach to diagnosis & treatment is fed from on high to supine nodding-dog "medical" professionals is a tragedy as well as a travesty. The result is, that on the one extreme we had psychiatric patients mislabeled as having ME and for years denied the psychotherapy they so desperately needed, the other extreme being genuine WHO-recognised ME patients suffering inhuman abuse and neglect.

The root of all of this rubbish is the undermining of genuine science by the monopolistic capitalist profit motive: and I would direct any ME patient or medical professional to the outstanding non-Marxian documentary film entitled THE CORPORATION. It is perfect for understanding the root malaise facing humanity that is placing ME patients in the front line. If you have not yet seen it you simply MUST! www.thecorporation.com/  

K. Short. (Myalgic Encephalomyelitis Patient. Norfolk, UK). Permission to repost.

Globe&Mail on CFS

(excerpts)

Chronic fatigue syndrome is a true mystery. Some experts feel the affliction has always been with us, but it first came to the attention of medical science midway through the 20th century as a bizarre, debilitating condition sparked by an initial flu-like illness. Preliminary investigations suggested the fatigue was linked to inflammation in the brain and spinal cord, and the condition was dubbed "myalgic encephalomyelitis" (ME), as it is still known in England.

But no symptoms were visible. All that seemed to unite its victims was their exhaustion. (Even now, there is no diagnostic test for it.) So, in 1970 two psychiatrists writing in the British Medical Journal dismissed the condition as mere hysteria, an assessment that stuck for decades. Young doctors were taught that CFS was "hysterical nonsense, a non-disease," says Charles Shepherd, medical adviser to the ME Association in Britain. "So it became something that few people were willing to investigate," and retained its "psychosomatic" status through the 1980s when it was derided as the "yuppie flu" suffered by self-obsessed hypochondriacs.

"But now the research shows that this is undoubtedly not a psychological problem," Dr. Shepherd says.

CFS researcher Anthony Komaroff, a professor of medicine at Harvard Medical School, agrees, pointing to clear evidence of "objective, biological differences" between chronic-fatigue sufferers and the rest of the population.

"The central nervous system and the immune system are measurably different," Dr. Komaroff says. People with CFS have less grey matter in their brains and abnormal functioning of the hypothalamus, as well as elevated levels of cytokines (proteins released by the immune system), impaired white blood cells and lower adrenalin levels. And now researchers have found genetic differences, which may lead to a gene-based diagnostic test.

CFS is now taken so seriously that Statistics Canada estimates as many as 1.3 per cent of Canadians suffer from it and the U.S. Centers for Disease Control and Prevention has launched a public-awareness campaign to dispel the "psychosomatic" stigma.

Still, there is no "cure." The few drugs commonly prescribed can only address the symptoms, such as pain and sleep deprivation. And few of the many alternative remedies available offer much relief.

Most sufferers hope that by looking after themselves and pacing their activity, they can manage the illness. But for some that simply isn't enough.

What makes a person prone to chronic fatigue syndrome?

The answer is written in our genes, researcher Anthony Komaroff says.

"The disease is a consequence of some biological vulnerability that patients are born with," explains Dr. Komaroff, a professor of medicine at Harvard Medical School, "and then something in their environment exposes that vulnerability."

Scientists now believe the sequence is something like this: First, a viral infection leads to a flu-like illness - for example, studies have linked CFS to a number of viruses (including those for Type 6 herpes and its cousin Epstein-Barr, a common cause of another exhausting illness, mononucleosis). Although in most cases, the immune system responds and the people recover, for an unfortunate few, the illness persists, and the immune response never shuts down.

It appears that the fatigue becomes chronic because of malfunctions that occur in a number of cranial control centres, but there remains a great deal that doctors don't know.

 

ASSUME makes an @$$ out of U and ME

The importance of 'assuming' - and how important it is to persist
when you KNOW something is very wrong.      LKW
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~


"I Was Exhausted All The Time"
    By Catherine Winters

Fatigued and out of breath, Karen McGinnis nonetheless kept passing medical tests with flying colors.

What's Wrong With Me?

On New Year's Eve 2005, Karen McGinnis headed for the movies with a friend.
McGinnis, a 47-year-old resident of West Deptford, New Jersey, was
looking forward to 2006. She was six months into a new job in advertising sales for
a local newspaper, active in her church and enjoyed the company of a circle
of friends.

After the movie McGinnis was suddenly too tired to go out to dinner and
opted for Chinese takeout at her pal's house. During the meal McGinnis
could barely stay awake and wondered if she'd caught some kind of respiratory
infection. Over the next six weeks she developed flu-like symptoms in
addition to the exhaustion. She felt headachy and stuffed up. Her chest
felt as though a weight were resting on it, and she had trouble breathing even
when she was inactive, including sitting or lying down. One day in late
February her supervisor at the newspaper took one look at her pale skin and
glassy eyes and sent her home. She didn't know it then, but she would not
return to work for five months.

Before leaving the office McGinnis called her primary-care physician and
described her symptoms. Suspecting an infection of some kind, he told her
he'd order her a prescription for antibiotics at the local pharmacy. That
night McGinnis climbed into bed, assuming the medicine would soon kick in.
"Two days later I could still barely breathe," she recalls. She again
called her doctor, who advised her to head to the emergency room.

The Search For Help

At the ER, doctors put McGinnis on oxygen to help her breathe. Meanwhile,
they examined her but could find no connection between her current symptoms
and her medical history, which over the past decade had included a bout
with Lyme disease, chronic fatigue syndrome, four back surgeries following a car
accident and the diagnosis of a mild heart murmur.

Baffled -- and concerned -- they admitted her to the hospital for further
evaluation. Over the course of a week, McGinnishad a battery of tests. To
examine her heart, doctors performed an echocardiogram, which uses sound
waves to produce images of the heart in motion, its chambers squeezing and
relaxing, its valves opening and closing. She had a chest X-ray and a
pulmonary ventilation scan to assess her lungs. All the scans appeared to
show that McGinnis's heart and lungs were functioning just as before.

The doctors did notice, however, that her voice was raspy, and she was
responding to the oxygen. On the basis of these signs, they guessed that
McGinnis had a viral infection in her lungs that wasn't showing up on the
X-ray; alternately, they conjectured, she was experiencing adult-onset
asthma or allergies. She was discharged with prescriptions for medications
to open her airways and reduce any inflammation in them.

Back home, McGinnis went to bed with the worst fatigue she'd ever
experienced. Going to work was out of the question.

At the end of March 2006 her symptoms suddenly worsened, and she returned
to the ER. Again, she was admitted to the hospital, where she passed a stress
test that involved walking on a treadmill while an electrocardiogram (ECG)
gauged the response of her heart to the activity. After five days she was
discharged without a definitive diagnosis. "When you go to the hospital,
you expect to find out what's wrong with you," says McGinnis. "If you don't,
you start to think you're imagining it all." A woman who prides herself on
being strong, McGinnis decided to tough it out.

By April, though, she could no longer ignore her wheezing and shortness of
breath. McGinnis recalls meeting with a pulmonologist and undergoing a
three-hour test to find out whether the ER doctors' theory that she had
adult-onset asthma was correct. She says she was startled by the conclusion
that her lungs were fine.

That was it. McGinnis concluded that her symptoms had to be psychosomatic.
"I decided my body had given out from all the stress I'd experienced in my
life," she says. "I wasn't 20, I had a demanding job, I was entering
menopause." She'd wait out her symptoms, hoping they would eventually
subside.

She returned to work in mid-June. Later that month, while she was driving
to work, her wheezing and difficulties breathing -- though already bad -- took
a turn for the worse. When she got to the office she was gasping for air,
and concerned colleagues phoned 911.

A Diagnosis

McGinnis recalls rushing to the ER, calling a friend and pleading, "I can't
do this anymore. Somebody has to find out what's wrong with me."
Her friend
knew of a health center that focused on both heart and lung diseases. To
McGinnis, a place with those two specialties under one roof sounded just
right. Her primary-care doctor called the center and arranged to have her
transported there right away.

At this facility, McGinnis underwent another ECG. This time, the scan
indicated the presence of a leak in her heart's aortic valve, through which
blood travels on its way to the rest of the body. Doctors also performed a
heart catheterization, a test that gives them a look inside the heart and
measures its efficiency.

A thin plastic tube, or catheter, was inserted into McGinnis's leg artery
and advanced to her heart. A dye to highlight the organ was injected
through the tube, and X-ray images were taken.

In a normal heart, oxygen-rich blood arrives from the lungs, passes through
the heart's chambers and travels out to the body via the aorta. In
McGinnis's case, her aortic valve wasn't closing completely and blood was
leaking back into her heart, causing it to work harder, depriving her blood
of the oxygen it needed and making her feel breathless.

After six months of suffering and anxiety, McGinnis finally had her
diagnosis: severe aortic-valve insufficiency. She was immediately scheduled
for open-heart surgery to replace the damaged valve with an artificial one.

The operation took place on July 3, 2006 -- a little more than six months
after McGinnis's health problems had begun -- and appeared to be successful.

A Second Opinion

McGinnis understood that the typical recovery time for valve replacement
was six to eight weeks. But she didn't improve; in fact, her presurgical
symptoms persisted. Back home now and in the care of a local cardiologist,
McGinnis had a follow-up ECG in August. The specialist didn't like what he
saw. The artificial valve wasn't working properly, and a subsequent
catheterization showed it was too small. This patient prosthetic mismatch,
or PPM, had occurred because the size of McGinnis's valve opening was
relatively small, causing her surgeon to think she needed a small valve.
The result? Not enough blood was getting through.

Then McGinnis learned that alleviating her problem required more-complex
surgery than the operation to replace the faulty valve in the first place.
Desperate to find a surgeon who could handle the procedure, McGinnis began
an Internet search. Typing in the words "patient prosthetic mismatch"
yielded the name of the Cleveland Clinic. For every question McGinnis had
about PPM, she found an answer on the Ohio hospital's Web site. Her own
doctor confirmed that the facility is highly rated, so McGinnis called the
clinic, spoke with a staff member and shipped her medical records there.

Several months later she got the good news: Her surgery was a go. "I had a
second chance at life," she says.

On October 15, 2007, cardiac surgeon Nicholas Smedira performed a
painstaking six-hour operation, during which he replaced the mismatched
aortic valve with a larger one. "I knew the new valve would make Karen
better," says Dr. Smedira.

The replacement surgery was a success. But Mc- Ginnis's medical odyssey
wasn't quite over. A follow-up echocardiogram indicated a leak in her
mitral valve, which funnels blood into the heart's left ventricle, in preparation
for it to be pumped out to the body. This was likely due to demands being
placed on it by the new aortic valve. Ten days later Dr. Smedira repaired
the mitral valve. "We understood how much Karen had suffered," he says. "We
wanted to give her back her life."

Home in New Jersey, McGinnis is recovering from her ordeal and considering a
new career as a patient advocate. Though attention is finally being paid to
women's hearts nowadays, she has learned firsthand that many female cardiac
problems are still elusive and hard to diagnose. Where heart health is
concerned, McGinnis says, women need to persist:

"Nobody knows your body like you do."


Originally published in Ladies' Home Journal, February 2008.

© Copyright 2008 Meredith Corporation. All Rights Reserved.

Neuroticism as Consequence of Illness

Contrary to those who would like to tell you that CFS is caused by psychological problems, Dr. Goudsmit proves that it's the other way around -- being chronically ill can cause you to develop psychological problems.

Posted on behalf of Ellen Goudsmit (UK)

Neuroticism as a consequence of illness

Today, BMJ rapid responses (letters) published the study of patients with ME (Ramsay defined), MS and healthy controls showing that raised scores documented in the literature are almost certainly due to the duration of illness and the inclusion of five confounding items, e.g. questions asking about symptoms like dizziness and lethargy. The N score of the ME group was similar to that of the group with MS.

See http://www.bmj.com/cgi/eletters?lookup=by_date&days=1

Text:

We were interested in the findings from Hickie et al (1) that
neuroticism (N) scores, recorded shortly after diagnosis of a viral
infection, were not a risk factor for chronic fatigue syndrome
(CFS)
at six and 12 months. This led us to re-examine the N scores we had
collected in 1987 from people with myalgic encephalomyelitis (ME), a
condition similar to and researched before the introduction of the
term CFS. We limited the statistical analysis to 48 patients who had
been diagnosed by physicians, who had been ill for at least six
months, were not taking psychotropic drugs and who had listed either
fatigue or muscle weakness following exertion as a main symptom. All
were recruited by a psychologist (EG) or through an advertisement in
the ME Association magazine. Participants were asked to complete the
Eysenck Personality Inventory (EPI) Form B (2) and to pass on a
second form to a close relative or friend of a similar age and
background, who could act as a healthy control. We also obtained N
scores from 50 patients with multiple sclerosis (MS), who were
recruited through various support groups.
The aims of this study were to measure neuroticism in patients with a
condition similar to those assessed by Hickie et al, to examine the
impact of time and to evaluate the influence of five items in the EPI
which enquired about somatic symptoms commonly reported by patients
with ME and CFS that might reflect disease rather than a personality
trait
(items 16, 35, 38, 45, 47).
The mean N score of the ME group was 12.31 (SD 5.40), the mean of the
MS group was 14.24 (SD 4.78) and the mean of the healthy controls was
9.35 (SD 4.77). The difference between the three groups was highly
significant, F(2,143) =11.874, p<0.0005. However, post hoc analysis
using Tukey's HSD test found no significant difference between the
two patient groups (p=0.139). A similar pattern was observed when the
five somatic items were removed, although the effect was greater for
the groups with ME and MS than the controls
(mean difference: 2.60,
2.34 versus .92 respectively). Using the revised scores, Tukey's HSD
test revealed a significant difference between the patients with MS
and controls (p<0.0005) and between the two patient groups (p=0.029)
but not between the ME group and controls (p=0.304). Thus while the N
scores were higher in the chronically ill groups, the omission of the
five items had the effect of reducing the difference between the ME
group and the controls, while increasing the difference between the
patients with ME and MS.
To assess the effect of the duration of illness, we compared the
scores of the patients who had been ill between 6 months and five
years with those who had been unwell for six years or more. The mean
N score for the former was 11.3 (SD 5.37), while that for the latter
was 15.29 (SD 4.30). The difference between the groups was
significant, both for N (t=2.3, p=0.028) and the revised scores
(t=2.19, p=0.036).
We conclude that raised neuroticism scores documented in ME and CFS (3) may reflect both the length of time which a patient has been ill,
and the inclusion of somatic items which confound the results.

References:
1. Hickie, I, Davenport T, Wakefield D, Vollmer-Conna, U, Cameron B,
Vernon, SD, et al. Post-infective and chronic fatigue syndromes
precipitated by viral and non-viral pathogens: prospective cohort
study. BMJ 2006; 333: 575
2. Eysenck HJ, Eysenck SB. Manual of the Eysenck personality
questionnaire. London: Hodder and Stoughton, 1964.
3. Buckley L., MacHale SM., Cavanagh JTO, Sharpe M., Deary IJ, Lawrie
SM. Personality dimensions inchronic fatigue syndrome and
depression. J Psychosom Res 1999; 46(4): 395-400.
Competing interests: None declared

Goudsmit, EM, Sneddon, P, Shepherd, C and Howes, S.

The Trouble with Psychotherapy

[This is largely to do with the methodology of research methods (incl
outcome measures) used in psychotherapy trials.  Given how many times we are
told CBT is an "evidence-based" treatment for CFS, some people may find it
of interest/use. Thanks to Doug Fraser for drawing my attention to it. Tom
K.]


http://tinyurl.com/2yl9jj 
i.e.
http://www.bps.org.uk/downloadfile.cfm?file_uuid=D9C851D3-1143-DFD0-7E1E-72A47D702AB8&ext=pdf

Clinical Psychology Forum 162 - June 2006

The trouble with psychotherapy

Paul Moloney

The supposedly sound evidence base for the effectiveness
of the psychological therapies may be far more
questionable than is widely supposed.

The term `psychotherapy' refers to a
broad family of talking treatments for
personal distress which are of proven
effectiveness, where some approaches are
helpful for certain kinds of personal difficulty,
and where accredited professional
training will confer particular expertise and
skill (see McLeod, 1994).

The assumptions
contained within this statement are unlikely
to meet with dissent from the average person
in the street (see Furedi, 2003), and in one
form or another constitute the taken for
granted world of the psychotherapy professionals
themselves.

For example, they are
endorsed in the training programmes of
clinical and counselling psychology (BPS,
2002, 2004), in central government recommendations
for the use of psychological therapies
in the NHS (DoH, 2001) and most
recently in calls by Richard Layard - one of
the UK government's key economic consultants
- for psychological therapy to be made
`available to all', as the main answer to the
personal and social malaise which seems to
be afflicting us at record levels (see Roth &
Stirling, 2006).

In contrast to this warmly consensual
picture, the enduring reality is that the psychotherapy
outcome literature offers precious
little support for any of the above notions.

This is an observation that surely
has some importance for any profession that
concernsitself with the understanding and
alleviation of personal distress, and yet it is
one that seems to have been consistently
ignored.

In this paper I critically review some of
the key psychotherapy outcome literature and
ask why it has been so hard for psychologists
to acknowledge the poor evidence on therapy
outcome.

Does therapy work?

It is widely recognised that there are numerous
and complex difficulties in assessing the
effects of psychological therapies, and that
one of the best ways of doing this is by means
of the randomised placebo control trial (or
RPCT).

A large number of such investigations
have been conducted over the last halfcentury
or more, and although the results of
these studies have often been extremely variable,
so called meta-analyses - in which the
findings of large numbers of studies are
aggregated and then analysed - suggest that
most forms of psychological therapy are at
least mildly helpful.

Effect sizes upward of
half a standard deviation or more are routinely
touted.

That is to say, undergoing psychological
therapy is claimed to reliably lead
to significant improvement in the mental
health of up to a quarter or above of all
recipients (Smith et al., 1980).

This compares
favourably with other psychiatric treatments
that may themselves have a large
placebo component, such as antidepressant
medication (Breggin & Cohen, 1999).

Not surprisingly perhaps, these claims
seem to be authorised by the core psychotherapy
professions (see Fonagy & Roth,
1996).

Yet there are a number of serious
methodological problems associated with
attempts to assess the effectiveness of counselling
or psychotherapy in this way.

So much
so that at least some academics and practitioners
admit that it is hard to decide
whether these studies as a whole do or do
not support the notion that psychotherapy
or counselling is generally helpful (McLeod,
1994).

To begin with, the field has long suffered
from a bias toward the selective reporting
and publication of those studies that show
only the desired positive results (Boyle, 2002).

Many psychotherapy RPCT trials have
included inadequate control groups for
comparison purposes, often consisting of
individuals who remain on a waiting list or
who receive a less credible form of pseudotherapy,
delivered with visibly limited commitment
by the researchers (Holmes, 2002;
Mair, 1992).

Conversely, there has been a
trend toward excessive reliance upon
selected research populations, such as university
students or individuals with less severe
problems than are typically found in clinical
settings.

A large proportion of studies have
also suffered from systematic participant
attrition or selection effects that make the
results hard to interpret (Dineen, 1999;
Eisner, 2000).

Statistically significant differences
in outcome between participant
groups have often concealed large numbers
of people for whom psychotherapy has been
ineffective
, while assessments of outcome
have tended to use abstract numerical measurements
and preset diagnostic inventories
that leave little room for subjective experience,
and which may therefore have limited
personal or even clinical meaning (Kline,
1988, and see Tolman, 1994),

Aside from these far from minor difficulties,
this literature may suffer from an even
more pervasive problem.

This is the tendency
to rely almost exclusively upon the
reports of participants - including the client,
the clinician and workers from the agencies
and institutions that support the therapeutic
work - in the absence of any fully independent
check upon the treated person's progress
in the world outside the consulting room
( Eisner, 2000; Epstein, 1996).

This is a serious
issue in psychotherapy research, because of
the range of powerful social and interpersonal
influences are likely to be in play, in
what is in many ways a unique situation in
our culture: part confessional, part ritual of
healing and social affirmation, and m u c h
else besides (Frank & Frank, 1991).

On this
basis, it may be worth discussing the question
of bias in client reports in more detail.

To start at the most basic level, both c l i e n t
and clinician will from the outset usually
desire the same broad result: an improvement
improvement
in the former's mental health, whether
this is defined as happiness, adjustment or
relative freedom from distress.

The patient's
cooperation towards this aim will be engaged
through the practitioner's efforts to establish
a therapeutic relationship, which implicitly
entrains the client into the given therapeutic
model.

For instance, many humanist therapists
seek to build a relationship with their
client that is intense and deep enough to
exceed most ordinary professional-layperson
encounters (e.g. Mearns, 1994).

Other practitioners
may emphasise the complexities of
the psychodynamic transference relationship
(e.g. Casement, 1995) or the alleged scientific
and technical authority for what they do - as
in cognitive behavioural therapy (e.g. Hawton
et al., 1989).

As a result, the client will likely have invested
a great deal of trust and hope in the
person of the practitioner.

All the more so,
perhaps, for having disclosed worries and fears
hitherto shared with few others.

Both parties
may also share potent, culturally sanctioned
beliefs, which equate failure to benefit from
therapy with the client's wilful rescinding of
the inner strength or discipline needed to
overcome adversity (Cushman, 1995).

For
the latter, these factors may combine to render
any admission of failure in the therapeutic
process a sign of personal inadequacy and
a source of anxiety about earning the tacit
disapproval of their therapist.

It therefore
seems reasonable to think that such admissions
of disappointment might be avoided or
denied by many clients: even - or perhaps
especially - to themselves (Epstein, 2006;
Kline, 1988).

And indeed at least some clinicians
felt that they have observed this process
in action (Kelly, 2000).

The key question, of course, is to what
extent the claims for psychotherapy effectiveness
might be distorted by this shaping of
client self-report.

As William Epstein points
out, the scale of this problem becomes apparent
when estimates of psychotherapy effect
size are compared with estimates of so-called
`demand characteristics'.

These are the expectations
that researchers can unconsciously
convey to participants in laboratory based
psychological experiments.

In the absence of
thorough controls such demand factors can
typically account for between 0.70 and 1.0
standard deviation of the reported effect
sizes.

This is for situations that are relatively
impersonal and short term in comparison to
most psychotherapeutic interventions, and
in which the participants might therefore be
expected to have a much lower stake in the
final outcome (see Rosenthal & Rubin, 1978).

Nevertheless, Epstein notes that these estimates
of researcher influences at least equal
(and often surpass) the average gains reported
for psychotherapy, even for the bettercontrolled
studies.

This is obviously a basic issue for the psychotherapy
field, where therapist expectations
of client improvement are inbuilt for
virtually every approach.

Yet rather than getting
to grips with these findings, the whole
area seems instead to have continued to rely
upon the reports of clients (and other
closely involved parties) in the absence of
any form of investigation that is external to
the therapeutic process or the organisations
that sponsor it.

The result being that
researcher expectancy cues are inseparable
from virtually all of the RPCT research to
date, and may confound it.

In the end, the
clear possibility remains that most of the
claimed benefits of psychotherapy might reside
in placebo effects (Epstein, 2006, 1996).

This last prospect is strongly underscored
by four further lines of evidence.

These are,
first, that, aside from (decidedly) modest indications
for the greater efficacy of behavioural
approaches in relation to phobias, the
comparative research literature seems to
offer little support for the idea that any one
treatment is more effective than another
(Assay & Lambert, 1999).

This observation
seems hard to reconcile with the confident
assertions of therapeutic potency and specificity
that are often trumpeted by adherents
of the mainstream therapies (Hansen et al.,
2003).

Yet, within the field, `there is tremendous
resistance to accepting this finding
as a legitimate one' (Bergin & Garfield, 1994,
p.822).

Second, the available evidence suggests
that, rather than specific techniques, a range
of so-called `non-specific' factors may account
for most of the beneficial effects of psychological
treatments.

Among these features,
the client's wider life circumstances and the
quality of the therapeutic relationship seem
to be the most important by far (Bohart, 2000;
Bergin & Garfield, 1994; Mahrer, 1998).

Third, comparisons of qualified practitioners
with amateurs who have received no
specific training in therapeutic models or
methods suggest that there are few real differences
between them in effectiveness
, however
this is measured.

This is a surprisingly
robust (though, again, seldom acknowledged)
finding, which is supported by 39 separate
research studies conducted over more than a
decade (Dawes, 1994; Stivers, 1999).

Fourth, a reliable trend within the psychotherapy
outcome literature is that the
closer the study comes to real life clinical settings,
then the less significant the outcomes
tend to be (Epstein, 1996).

For instance, the
recent American multi-centre research trial
known as the `Fort Bragg demonstration
project' involved the analysis of the treatment
of 42,000 clients (who were largely
children) over a span of five years.

Yet the
results were disappointing in that there was
no evidence that psychological therapy led to
improvement in the lives of these recipients,
many of whom were struggling with significant
social adversities.

As the clinical psychologist
Tana Dineen (1999, p.128) observes :

these results should raise serious doubts about
some current clinical beliefs about the effectiveness
of psychological services . there is
scant evidence of its effectiveness in real life
settings.

What then can we conclude about the
effectiveness of psychotherapy?

Overall, the findings examined in this paper
highlight the overwhelming import of `nonspecific
effects' in psychological treatment
on the one hand, and of the frequently
flawed nature of RPCT methodology, on the
other.

None of which seems to be very encouraging
for the official view of psychological
therapy as a well-validated body of effective
clinical treatments.

Instead of engagement,
however, the tendency inside the main ther
apeutic professions seems to have been to
ignore or downplay these considerations
(see Howard, 2005), and it therefore seems
worth asking why this is so.

Personal conviction
is doubtless one of the reasons.

Within
the confines of the consulting room both
therapists and their clients will often observe
that the latter seem to undergo a significant
relief from their distress.

As already indicated,
this is one instance where immediate personal
experience can be compelling but also
highly deceptive, especially when backed up
by prevalent cultural myths.

Another element in this situation may be
the reliance of the field upon large-scale
meta-analytic studies, a trend that is reinforced
by the accumulating NICE guidelines
on psychotherapeutic practice in the NHS.

Although officially presented as both definitive
and authoritative (see for example,
NICE, 2003) such methods are notoriously
prone to generating misleading or inconclusive
data, as the previous discussion has
shown.

The meta-analytic approach simply
fails to capture the way in which knowledge
is developed and validated within the wider
scientific community.

When pursued in good
faith, scientific knowledge emerges from a
craft-like exploration and sifting of ideas
against the limits of personal experience and
of reasoned reflection - and not from managerial
directives or the behest of professional
interest groups, operating under the guise of
impersonal authority (Charlton, 2000; and
see Polanyi, 1955).

The significance of all this becomes clearer
when set against the evidence that - contrary
to the claims of Layard - our current social
arrangements may continue to underpin
much of the distress that brings people to
the consulting room (see, for example,
Perelman, 2005; Vail et al., 1999; Wilkinson,
1996).

In this situation, the interests of the
therapeutic professions are likely to dovetail
only too well with those of a political order
that is intent upon convincing its citizens
that their private troubles have little connection
with events in the public realm.

And in
this respect, the myth of individual psychological
therapy as cure fits the bill admirably.

Affiliation

Adult Learning Disability Service, Telford.
Address

Adult Learning Disability Service, 40 Tan
Bank, Wellington, Telford, Shropshire
TF1 1HW

References

Assay, T.P. & Lambert, M.J. (1999). The empirical
case for common factors in therapy: Quantitative
findings. In M.A. Hubble, B.L. Duncan, & S.D.
Miller (Eds.) The heart and soul of change: What
works in therapy (pp. 33-56). Washington DC:
American Psychological Association.
Bergin, A. & Garfield, S. (1994). Handbook of psychotherapy
and behaviour change. New York: John
Wiley.
Bohart, A.C. (2000). The client is the most important
common factor: Clients' self-healing capacities and
psychotherapy. Journal of Psychotherapy Integration,
10(2), 127-149.
Boyle, M. (2002). Schizophrenia: A scientific delusion?
(second edition). London: Routledge.
Breggin, P. & Cohen, D. (1999). Your drug may be your
problem: How and why to stop taking psychiatric drugs.
Reading, MA: Perseus Books.
British Psychological Society (2002). Criteria for the
accreditation of postgraduate training programmes in
clinical psychology. Leicester: British Psychological
Society (Division of Clinical Psychology).
British Psychological Society (2004). Board of Examiners
in Counselling Psychology: Regulations and syllabus for
the qualification in counselling psychology. Leicester:
British Psychological Society.
Casement, P. (1995). Further learning from the patient:
The analytic space and process. London: Tavistock.
Charlton, B. G. (2000). The new management of scientific
knowledge: A change in direciton with
profound implications. In A. Miles, J.R. Hampton
& B. Hurwitz (Eds.) NICE, CHI and the NHS reforms:
Enabling excellence or imposing contro l ? London:
Aesculapius Medical Press (pp.13-32).
Cushman, P. (1995). Constructing the self, constructing
America. Cambridge, MA: Perseus Publishing.
Dawes, R. (1994). House of cards: Psychology and psychotherapy
built on myth. New York: Macmillan.
Department of Health (2001). Treatment choice in psychological
therapies and counselling. London: HMSO.
Dineen, T. (1999). Manufacturing victims: What the
psychology industry is doing to people. L o n d o n:
Constable.
Eisner, D. (2000). The death of psychotherapy: From Freud
to alien abductions. New York: Preager.
Epstein, W. (2006). The civil divine: Psychotherapy as
religion. Reno, NV: University of Nevada Press.
Epstein, W. (1996). The illusion of psychotherapy. New
York: Transaction.
Frank, J.D. & Frank J.B. (1991). Persuasion and healing:
A comparative study of psychotherapy. Baltimore,
MD: Johns Hopkins University Press.
Fonagy, T. & Roth, A. (1996) What works for whom? A
critical review of psychotherapy research. New York:
Guilford Press.
Furedi, F. (2003). Therapy culture: Cultivating vulnerability
in an uncertain age. London: Routledge.
Hansen, S., McHoul, A. & Rapley, M. (2003). Beyond
help: A consumer's guide to psychology. Ross-on-Wye:
PCCS Books.
Hawton, K., Salkovskis, P., Kirk, J. & Clarke, D. (1989).
Cognitive behaviour therapy for psychiatric problems: A
practical guide. Oxford University Press.
Holmes, J. (2002). `All you need is cognitive behaviour
therapy?' British Medical Journal, 324, 288-291.
Howard, A. (2005). Identity and counselling. London:
Palgrave.
Kelly, A.E. (2000). `A self-presentational view of psychotherapy'.
Psychological Bulletin, 126(4), 475-494.
Kline, P. (1988). Psychology exposed or The Emperor's new
clothes. London: Routledge.
Mahrer, A. (1998). `Embarrassing problems for the
field of Psychotherapy'. BPS Psychotherapy Section
Newsletter, 23(3), 3-25.
Mair, K. (1992). The myth of therapist expertise. In
W. Dryden & C. Feltham (Eds.) Psychotherapy and
its discontents. Buckingham: Open University.
Mcleod, J. (1994). Doing counselling research. London:
Sage.
Mearns, D. (1994). Developing person-centred counselling.
London: Sage.
National Institute for Clinical Excellence (2003).
D e p ression: The management of depression in primary
and secondary care (second consultation draft,
December). London: NICE.
Perleman, R. (2005). Manufacturing discontent: The trap
of individualism in corporate society. London: Pluto
Press.
Polanyi, M. (1955). Personal knowledge: Towards a postcritical
philosophy. London: Routledge.
Roth, T. & Stirling, P. (2006). Expanding the availability
of psychological therapy. Retrieved 12
February 2006 from www.bps.org.uk/dcp/news/
layard.cfm.
Smith, M.L., Glass, G.V & Miller, T.I. (1980). The benefits
of psychotherapy. Baltimore MD: Johns Hopkins
University.
Stivers, R. (1999). Technology as magic: The triumph of
the irrational. New York: Continuum.
Rosenthal, R. & Rubin, D.B. (1978). Interpersonal expectancy
effects: The first 345 studies. Behavioural
and Brain Sciences, 3, 377-415.
Tolman, C. (1994). Psychology, society and subjectivity: An
introduction to German critical psychology. London:
Routledge.
Vail, J. (1999). Insecure times: Living with insecurity in
contemporary society. London: Routledge.
Wilkinson, R. (1996). Unhealthy societies: The afflictions
of inequality. London: Routledge

Fuzzy Logic in CFS

Thanks to Tom K for finding this one:

Full text at: http://jech.bmj.com/cgi/content/full/62/3/273

Journal of Epidemiology and Community Health 2008;62:273-278;
doi:10.1136/jech.2007.063644
Copyright C 2008 by the BMJ Publishing Group Ltd.

---------------------

THEORY AND METHODS

Methodological insights: fuzzy sets in medicine
P Vineis

Correspondence to:
Paolo Vineis, Imperial College London, Department of Epidemiology and Public
Health, Norfolk Place, London W2 1PG, UK; p.vineis@imperial.ac.uk


Accepted for publication 3 July 2007


In this paper I wish to introduce some ideas about scientific reasoning that
have reached the epidemiological community only marginally. They have to do
with how we classify things (diseases), and how we formulate hypotheses
(causes). According to a simplified and currently untenable model, we come
to defining what a disease, or a protone or a chromosome, is by progressive
simplification-that is, by extracting an essence from the individual
characters of disease. At the end of this inductive process a single
element, which guarantees the unequivocal inclusion in the category, is
identified. This is what has been called "Merkmal-definition" (Merkmal
meaning distinctive sign)-that is, the definition of disease would be
allowed by the isolation of a crucial property, a necessary and sufficient
condition, which makes that disease unique (and a chair out of a chair, a
proton out of a proton, etc). However many objections have been raised by
Wittgenstein, Eleanor Rosch and others to this idea: a Merkmal is not always
identifiable, and more often a word is used to indicate not a homogeneous
and unequivocal set of observations, but a confused constellation with
blurred borders. This constellation has been called a fuzzy set and is at
the basis of the semantic theory of metaphors proposed by MacCormac and the
prototype theory proposed by Rosch. In this way the concept of disease, for
example, abandons monothetic definitions, amenable to a necessary and
sufficient characteristic, to become "polythetic." I explain how these
concepts can help medicine and epidemiology to clarify some open issues in
the definition of disease and the identification of causes, through examples
taken from oncology, psychiatry, cardiology and infectious diseases. The
definition of a malignant tumour, for example, seems to correspond to the
concept of "family resemblance," since there is no single criterion that
allows us to define unequivocally the concept of cancer: not morphology
(there are borderline situations between benign and malignant), not clinical
features, not biochemical or molecular lesions. In the case of
schizophrenia, the problem of indetermination, as it has been defined, is
even stronger. Mental disease probably cannot be distinguished from health
in a clearcut way (according to a minimum set of necessary criteria), but it
would have a fuzzy border with mental conditions that characterise normal
subjects, through intermediate linking conditions.

[..]

We can imagine a historical reconstruction of causality in medicine
according to two vectors, the definition of the causal agent and the
diagnostic process, and considering the transition from monothetic to
polythetic concepts along both vectors. Smallpox is a monothetic disease
both according to the definition vector (the poxvirus) and for symptoms and
signs; tuberculosis is monothetic on the aetiological axis but polythetic on
the symptoms/signs axis. And many "new" diseases (bulimia, psychiatric
diseases, autoimmune disorders) are polythetic along both vectors. Some
diseases have shifted from a monothetic form (with a "typical" presentation,
characterised by evident symptoms, easily interpretable) to polythetic or
borderline forms: one example is diabetes, which centuries ago was diagnosed
by the sweet taste of urine and now is at the border of normality through an
intermediate category (glucose intolerance). A very clear example of such a
transition is told by Aronowitz, "from myalgic encephalitis to yuppie
flue."12
In 1934 in California there was an apparent epidemic of
poliomyelitis, with as many as 2648 cases reported in the first seven months
of the year. In fact, the symptoms were mild (it was not the classic
paralytic form), to the point that several commentators spoke of "collective
hysteria." Something very similar happened in the 1980s with the "chronic
fatigue syndrome," a condition characterised by weakness and muscle pain,
which arose mainly after a viral infection in middle-class subjects. Also in
this case the lack of objective signs and, therefore, of a diagnostic test,
and the lack of an aetiological explanation, make of the disease a typically
polythetic condition, which includes probably both genuine post-viral
syndromes and psychological distress, or even a specific chronic tiredness
(the yuppie disease).

[12) Aronowitz RA. Making sense of illness: science, society and disease
Cambridge: Cambridge University Press, 1998.]

* * *

This has been the problem -- because of the way the revised criteria were written, "both genuine post-viral syndromes and psychological distress" have been lumped into CFS, making it impossible to find one cause or one cure, because they're looking at so many different things masquerading under one name.

As one of the original Incline Village patients continually reminds us, the Incline Village disease (which was actually M.E.) is what name ORIGINALLY applied to.  Anything else being passed off as CFS is a misnomer; whether intentional (to "prove" we're just nutjobs) or accidental (doctors who don't know anything about CFS except "fatigue").

Another CFS blog, and info on petitions (UPDATED 3/18)

Mary writes:

I have created a blog to discuss adopting the Canadian consensus diagnostic and treatment criteria in the United States, along with the name used in that document, Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (which can be found in G93.3 in the World Health Organization's codes of diseases, ICD-10).

The blog is here:

http://canadaconsensus.ning.com/

(Please forgive the stupid ads; I haven't figured out how to get rid of them yet!)

Eventually (when I figure out how to do it) there will be a petition and a vote.  But the decision about the name and its meaning will not have been made in advance by a committee. 

I only ask that those who participate be as polite as if they were all sitting in the same room.  If not, I will not hesitate to delete a rude post - although I will suggest a more polite rephrasing to the poster. 

ALL subjects relating to the name are open, including the combination names that some have preferred - neuro-endocrine-immune disorder, for example. 

I was hoping not to have to restart this debate, but there are issues that need to be discussed before the Fair Name petition http://www.afairname.org/index.cfm  proceeds further.  I had myself signed the petition assuming it referred to the Canadian consensus name, which is Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.  I would not have signed it had I thought "M.E." stood for whatever you wanted it to. 

But this is a choice, and not just mine to make.  So - go get a name, a password (write the password down in your home phone book!) and ... post away.   Have fun, but play nice.

Mary Schweitzer, Ph.D.

---

THIS EMAIL MAY BE FREELY CIRCULATED, UNEDITED. -- Mary Schweitzer

Announcing a new online petition for adopting the international (Canadian) Consensus Document for M.E./CFS in the United States.  Go here:

      http://www.ipetitions.com/petition/consensusdoc/index.html

Information that is not required is still helpful in being able to use the petition with Congress, and only your name shows up on the list of petition signatures. 

Everyone is welcome to download the petition and collect real signatures, which are actually more influential in Congress.  If you do so, try to at least get the state down so that we have information to present to specific Senators.

Discussion about this and the two other petitions on the name of the disease can be found here:
       http://canadaconsensus.ning.com/

Thank you -- Mary Schweitzer

------------------------------  Contents of Petition --------------------------------

http://www.ipetitions.com/petition/consensusdoc/index.html

We, the undersigned, respectfully request that the United States health agencies adopt the international “Consensus Document” for the diagnosis and treatment of the disease therein named Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, or “ME/CFS”.

In the late 1980s, a large number of cluster outbreaks of a mysterious disease appeared throughout the United States. Many patients seemed to have a chronic form of Epstein-Barr Virus, or mononucleosis, but others tested negative for the condition. Experts from both inside and outside the United States suggested that these outbreaks were the same disease that was first named “atypical polio” in Los Angeles in 1934, then called “epidemic neuromyesthenia” in the United States (1950s-1980), and “myalgic encephalomyelitis (M.E.)” in Canada, the UK, and other nations (1950s-present).

The U.S. CDC insisted that these outbreaks represented a new disease entity entirely, and in 1988 named the disease “chronic fatigue syndrome (CFS).” Today there are no fewer than seven different definitions for “CFS” worldwide, some of which directly conflict with each other. All focus on the single symptom “fatigue,” which is a characteristic of any serious illness.

The international Consensus Document for diagnosing and treating ME/CFS was written in response to the placement of both M.E. and CFS in the neurological category, G93.3, by the World Health Organization in ICD-10. The committee who wrote the document came from the United States, Canada, and overseas: Bruce M. Carruthers, Anil Kumar Jain, Kenny L. De Meirleir, Daniel L. Peterson, Nancy G. Klimas, A. Martin Lerner, Alison C. Bested, Pierre Flor-Henry, Pradip Joshi, AC Peter Powles, Jeffrey A. Sherkey, and Marjorie I. van de Sande. The document was published by the Journal of Chronic Fatigue Syndrome in 2003.

A summary written by Bruce Carruthers and Marjorie van de Sande is available through the National ME/FMS Action Network of Canada at the following website:

     http://www.mefmaction.net/Portals/0/docs//ME-CFS%20Overview.04-07.pdf

We believe that adoption of this international Consensus Document by the United States would aid greatly in the efforts to find and treat those who suffer from this devastating and confounding disorder. The Consensus Document not only offers objective measures and biomarkers, but also suggests treatments. The Consensus Document concludes with a bibliography of peer-reviewed journal articles supporting the information presented therein.

A team of researchers at DePaul University found the document to be superior to the CDC’s research criteria in identifying patients with serious physical symptoms and functional impairments, as opposed to those with primary psychopathologies [Jason et al, Journal of CFS 2004]. The patients who most need to be reached would be better served by adopting the Consensus Document. A committee of the IACFS/ME (dedicated to research into CFS and M.E.) has already adopted a version of the Consensus Document for pediatric diagnosis and care [Journal of CFS, 2006].

In the 20 years since the name CFS was created, very little has changed for patients diagnosed with this disease in the U.S. Indeed, the CDC itself admits that no more than 15 percent of patients who have the disease even have a diagnosis.

According to CDC studies, the nation loses at least $20 billion per year in national product, and $7 billion in lost income tax revenues per year, because so many patients with this disease are unable to hold a job. The individual suffering of patients and families forced into poverty by this illness can only be imagined by those who have not experienced it.

The CDC’s informational website for the disease states: “There are no tests and there are no treatments.” What can patients, or their physicians, do?

We, the undersigned, believe it is time for the United States to directly address the needs of one million Americans suffering from a poorly understood, debilitating illness. The best way to begin would be by adopting the existing international Consensus Document for diagnosing and treating ME/CFS.

UPDATE 3/18

I am mortified to have to tell everyone that the petition website where the petition to adopt the Canadian (international) consensus document in the United 'States has been housed is - well, in my opinion, wholly unethical and I have had to take the petition down. 

After about two weeks, and without warning me, the company running the website inserted a request for funding for THEM!  I learned that people would sign the petition, and as soon as they did that, the website would shift to one with different amounts of donations listed - and one person who vetted it for me said that they already had the amount checked and it didn't seem to be uncheckable.

Every type of dispicable practice on internet seems legal.  They probably buried this in fine print somewhere.

I want to assure ANYONE who signed that petition and then got asked to donate money that:

**** The money did not go to me or to M.E. or CFS advocacy.  It went to the website company. ****

Perhaps we can circulate a petition the old-fashioned way, getting signatures wherever people gather.  This was a most disheartening experience.

If you want to discuss the issue (including the other petitions), my other website is still working fine at ning.com -
http://canadaconsensus.ning.com/

ANYONE who actually gave money after signing the petition should contact me ASAP. 

Mary Schweitzer



Fibromyalgia and Sleep

Zeroing in on Fibromyalgia
                  by John D. Zoidis, MD

                  Recent studies provide objective characterizations of sleep disturbances associated with an often misdiagnosed syndrome.

                      
                  Many patients with fibromyalgia-a multisystem illness of unknown etiology that is characterized by generalized muscle and joint pain, sleep disturbances, and fatigue-have faced the question of whether the condition is real. Fibromyalgia often has been misdiagnosed as arthritis or even a psychological issue. Increasingly, though, scientific research is leading to a greater understanding of diagnosing and characterizing sleep disturbances in patients with fibromyalgia.

                  PATHOPHYSIOLOGY
                  While the precise etiology of fibromyalgia is unknown, a growing body of evidence implicates disturbances in the neuroendocrine axis as a primary cause,1-4 particularly with regard to the sleep disturbances that are characteristic of the syndrome. Sleep electroencephalograms of patients with fibromyalgia typically show disturbance of non-rapid eye movement (REM) sleep by intrusions of alpha waves and infrequent progression to Stage 3 and Stage 4 sleep.5

                  Additional derangements of the endocrine and neurologic systems in patients with fibromyalgia have been observed. For example, the concentration of substance P (a neurotransmitter associated with enhanced pain perception) in the cerebrospinal fluid has been found to be up to three times greater than normal in patients with fibromyalgia.6 Dysregulation of the hypothalamic-pituitary-adrenal axis has been noted, with reduced production of cortisol by the adrenal glands.7 These observations suggest that some aberration in the endocrine and/or neurologic response to stress may exist in patients with fibromyalgia.

                  DIAGNOSIS
                  The diagnosis of fibromyalgia is generally a diagnosis of exclusion, and is based on the presence ofwidespread pain. Diagnostic criteria developed by the American College of Rheumatology (ACR) include diffuse soft tissue pain for 3 months or longer and pain on palpation in at least 11 of 18 specific muscle-tendon sites.8 Pain syndromes typical of fibromyalgia are shown in Figure 1, and include any combination of headaches, pain in the jaw, shoulder stiffness when waking up, chronic muscle and joint pain, diarrhea or constipation, sensitivity to chemicals or skin contact, numbness and tingling in the extremities, menstrual cramping, and generalized fatigue. Symptoms are often exacerbated by exertion, stress, lack of sleep, and weather changes. Associated symptoms usually include sleep disturbances and fatigue, and also may include irritable bowel syndrome, depression, and anxiety. Less common associated features include abdominal pain, bloating, dry eyes, dry mouth, and palpitations. Precipitating factors for fibromyalgia include flu-like viral illness, rheumatic disorders, human immunodeficiency virus infection, Lyme disease, physical trauma, emotional trauma, and medications (particularly corticosteroid withdrawal).

                  Initial routine laboratory tests typically include a complete blood count, standard blood chemistries, erythrocyte sedimentation rate, and thyroid function studies. These studies are normal in fibromyalgia, and facilitate a diagnosis by exclusion of fibromyalgia. Other laboratory studies are usually obtained only if there is clear suspicion from the history or physical examination of another disease.

                  CHARACTERIZATION OF SLEEP DISTURBANCES IN FIBROMYALGIA

                      
                        Figure 1. Pain syndromes typical of fibromyalgia. ©morefocus 2004, www.mindbodyfocused.com  
                  The pattern of sleep disturbance may facilitate the diagnosis of fibromyalgia. Patients with fibromyalgia often report early-morning awakenings; awakening feeling tired or unrefreshed; insomnia; and mood and cognitive disturbances related to poor quality of sleep.9 They also may experience primary sleep disorders such as sleep apnea.10 Interestingly, a distinct relationship has been noted between poor sleep quality and pain intensity.9-11 Although a history of sleep disorder is often present in patients with fibromyalgia, the use of sleep studies is controversial.

                  A growing body of evidence suggests that sleep studies are important for determining the underlying reason for the poor sleep in patients with fibromyalgia, and perhaps even for confirming a diagnosis of fibromyalgia.12 Recently, a sleep index has been used to characterize and quantify the sleep complaints of patients with fibromyalgia.13 The Pittsburgh Sleep Quality Index (PSQI) is an instrument used to measure the quality and patterns of sleep in older adults. It differentiates "poor" from "good" sleep by measuring seven sleep domains: subjective sleep quality, sleep latency, sleep duration, habitual sleep efficiency, sleep disturbances, use of sleeping medication, and daytime dysfunction over the last month. Patients self-rate each of these seven areas. Scoring of answers is based on a 4-point numeric scale (0 = strongly disagree; 3 = strongly agree). A global total score of > 5 indicates a "poor" sleeper. In the study, the PSQI was applied to 30 patients with fibromyalgia based on the ACR classification criteria, and to 30 healthy control subjects: The median global PSQI score in the fibromyalgia patients and healthy controls was 12.0 and 3.0, respectively (P<0.001). All PSQI component scores except sleep medications were significantly greater in fibromyalgia patients than controls. Sleep latency, sleep disturbances, and daytime dysfunction were the most frequent sleep difficulties experienced by patients with fibromyalgia. This study suggests that the PSQI is a useful instrument for characterizing and quantifying sleep disturbances in patients who have fibromyalgia.

                  In another study, pain and sleep symptoms of 40 female patients with fibromyalgia and 43 healthy control subjects were studied before and after overnight polysomnography in an effort to characterize the patterns of alpha electroencephalographic sleep and their associations with pain and sleep in patients with fibromyalgia.14 In this study, blinded analyses of alpha activity in non-REM sleep were performed using time domain, frequency domain, and visual analysis techniques. Three distinct patterns of alpha sleep activity were detected amongthe patients with fibromyalgia: phasic alpha (simultaneous with delta activity) in 50% of patients, tonic alpha (continuous throughout non-REM sleep) in 20% of patients, and low alpha activity in the remaining 30% of patients. On the other hand, low alpha activity was exhibited by 84% of control subjects (P<0.01). All fibromyalgia patients who displayed phasic alpha sleep activity reported worsening of pain after sleep, compared with 58% of patients with low alpha activity (P<0.01), and 25% of patients with tonic alpha activity (P<0.01). A post-sleep increase in the number of tender points occurred in 90% of patients with phasic alpha activity, 42% of patients with low alpha activity, and 25% of those with tonic alpha activity (P<0.01). Self-ratings of poor sleep were reported by all patients with phasic alpha activity, 58% of patients with low alpha activity (P<0.01), and 13% of those with tonic alpha activity (P<0.01). Patients with phasic alpha activity reported longer duration of pain than patients in other subgroups (P<0.01). Moreover, patients with phasic alpha sleep activity exhibited less total sleep time than those in other subgroups (P<0.05), as well as lower sleep efficiency (P<0.05) and less slow-wave sleep (P<0.05) than patients with a tonic alpha sleep pattern. This study adds considerably to our understanding of the patterns of sleep disturbances in patients with fibromyalgia, including the relationship of specific sleep-disturbance patterns to pain.

                  TREATMENT
                  The treatment of fibromyalgia is largely empiric. There is no Food and Drug Administration-approved treatment specifically indicated for fibromyalgia. Frequently employed therapeutic approaches include antidepressants, nonsteroidal anti-inflammatory agents, and exercise. More extreme approaches include chronic opioid analgesic therapy with or without psychotherapy. Behavioral therapy may help patients with fibromyalgia who experience work or social difficulties because of poor symptom control.,15,16 Recent evidence suggests that acupuncture may significantly reduce pain in patients with fibromyalgia.17 Early study suggests that pulsed electromagnetic fields may have therapeutic value in fibromyalgia.18

                  SUMMARY
                  Fibromyalgia has been classically viewed as a subjective diagnosis. All patients with fibromyalgia, by definition, experience pain, and most experience sleep disturbances. Over the past several years, new studies have provided needed insight into the characterizations of sleep disturbances in patients with fibromyalgia and the relationship between these patterns and the occurrence of pain. With further study, we may identify sleep-disturbance parameters, with suitably high selectivity and specificity, that can actually be used in the diagnosis of the syndrome. Clearly, sleep study is becoming increasingly recognized as an important component of the work-up of patients with known or suspected fibromyalgia.

                  John D. Zoidis, MD, is a contributing writer for Sleep Review. He can be reached at .

                  Search Sleep Review's online archives for more information on fibromyalgia. Go to the search box at the top of the page and type in "fibromyalgia."

                  REFERENCES
                    1.. McBeth J, Chiu YH, Silman AJ, et al. Hypothalamic-pituitary-adrenal stress axis function and the relationship with chronic widespread pain and its antecedents. Arthritis Res Ther. 2005;7:R992-R1000.
                    2.. Adler GK, Geenen R. Hypothalamic-pituitary-adrenal and autonomic nervous system functioning in fibromyalgia. Rheum Dis Clin North Am. 2005;31:187-202.
                    3.. Gur K, Cevik R, Sarac AJ, Colpan L, Em S. Hypothalamic-pituitary-gonadal axis and cortisol in young women with primary fibromyalgia: the potential roles of depression, fatigue, and sleep disturbance in the occurrence of hypocortisolism. Ann Rheum Dis. 2004;63:1504-1506.
                    4.. Pillemer SR, Bradley LA, Crofford LJ, Moldofsky H, Chrousos GP. The neuroscience and endocrinology of fibromyalgia. Arthritis Rheum. 1997;40:1928-1939.
                    5.. Moldofsky H. Sleep and fibrositis syndrome. Rheum Dis Clin North Am. 1989;15:91-103.
                    6.. Russell IJ, Orr MD, Littman B, et al. Elevated cerebrospinal fluid levels of substance P in patients with the fibromyalgia syndrome. Arthritis Rheum. 1994;37:1593-1601.
                    7.. Demitrack MA, Crofford LJ. Evidence for and pathophysiologic implications of hypothalamic-pituitary-adrenal axis dysregulation in fibromyalgia and chronic fatigue syndrome. Ann N Y Acad Sci. 1998;840:684-697.
                    8.. 8. Wolfe F, Smythe HA, Yunus MB, et al. The American College of Rheumatology 1990 Criteria for the Classification of Fibromyalgia. Report of the Multicenter Criteria Committee. Arthritis Rheum. 1990;33:160-172.
                    9.. Harding SM. Sleep in fibromyalgia patients: subjective and objective findings. Am J Med Sci. 1998;315:367-376.
                    10.. Cote KA, Moldofsky H. Sleep, daytime symptoms, and cognitive performance in patients with fibromyalgia. J Rheumatol. 1997;24:2014-2023.
                    11.. Brecher LS, Cymet TC. A practical approach to fibromyalgia. J Am Osteopath Assoc. 2001;101(suppl):S12-S17.
                    12.. Moldofsky H. Management of sleep disorders in fibromyalgia. Rheum Dis Clin North Am. 2002;28:353-365.
                    13.. Osorio CD, Gallinaro AL, Lorenzi-Filho G, Lage LV. Sleep quality in patients with fibromyalgia using the Pittsburgh Sleep Quality Index. J Rheumatol. 2006;33:1863-1865.
                    14.. Roizenblatt S, Moldofsky H, Benedito-Silva AA, Tufik S. Alpha sleep characteristics in fibromyalgia. Arthritis Rheum. 2001;44:222-230.
                    15.. Singh BB, Berman BM, Hadhazy VA, Creamer P. A pilot study of cognitive behavioral therapy in fibromyalgia. Altern Ther Health Med. 1998;4:67-70.
                    16.. Sandström MJ, Keefe FJ. Self-management of fibromyalgia: the role of formal coping skills training and physical exercise training programs. Arthritis Care Res. 1998;11:432-447.
                    17.. Martin DP, Sletten CD, Williams BA, Berher IH. Improvement in fibromyalgia symptoms with acupuncture: results of a randomized controlled trial. Mayo Clin Proc. 2006;81:749-757.
                    18.. Shupak NM, McKay JC, Nielson WR, Rollman GB, Prato FS, Thomas AW. Exposure to a specific pulsed low-frequency magnetic field: a double-blind placebo-controlled study of effects on pain ratings in rheumatoid arthritis and fibromyalgia patients. Pain Res Manag. 2006;11:85-90.

* * *

My doctors claimed that the only reason for a sleep study was if the patient had sleep apnea.  Obviously, once again, they were misinformed ... or lying to me because they didn't want to see proof that I was actually sick and not "just depressed".

Insist on a sleep study.  It will be one more piece of objective evidence to the judge that you're not exaggerating the extent of your sleep disturbance.