Discussion in 'General Treatment' started by snowathlete, Jun 30, 2011.
Just wondering, does anyone know where/who this idea came from?
My guess is the wessely school. It's been around for a long time, it was around in 1992.
Not sure when the GET name was first applied to a formalised system, but GET is simply a standardised physiotherapy approach developed from rehabilitation programmes and extended to chronic conditions ( e.g http://ajp.physiotherapy.asn.au/AJP/51-2/AustJPhysiotherv51i2Geraets.pdf ). Anyone who has gone through post surgery rehabilitation will know that physiotherapy operates on a high expectation phliosophy (going beyond the limits set by pain and discomfort ) so there were always going to problems adapting it to relevence to M.E/CFS. The 'negotiated' approach used in the Frenchay CBT study which was conducted in the Pain Management Clinic and incorporated GET (term used was graded activity scheduling !) suggested a degree of usefulness in terms of addressing deconditioning issues for some M.E/CFS patients. It's important to note that the Frenchay study never talked about 'cure' and was focussed on participant evaluations of benefit.
Thanks, so does anyone know who first started applying it in the case of ME/CFS patients as a cure or treatment?
They suddenly discovered a little ability to move about again (after any illness) was gods gift to man and pronounced "we've got it". Must be the answer to everything. Rant over - it's simply common sense (if possible) to move as/when able - (Physios) but ME literature is full of the damage done by "exercise".
I'd have thought it was a fairly natural treatment to try with patients suffering from chronci faituge - I expect it was being used prior to the creation of 'ME' or 'CFS' as terms.
The promotion of it as a cure seems to have been driven by the belief that this was a 'healthy' thing for patients to believe, rather than because anyone thought that it was really true - this sort of cognitive approach was driven by Chalder, Wessely, etc, but I don't know if they were truly the first.
Not sure about this but Dr. Benjamin Levine developed an exercise program for POTS: http://www.theheart.org/article/1241927.do
Exercise training effective for treating postural orthostatic tachycardia syndrome
JUNE 20, 2011 | Michael O'Riordan
Dallas, TX - Exercise, rather than the beta blocker propranolol, is better at improving upright hemodynamics, normalizing renal-adrenal responsiveness, and improving quality of life in patients with postural orthostatic tachycardia syndrome (POTS), according to the results of a new study . Investigators report that increases in physical fitness with exercise improved the function of the renin-angiotensin-aldosterone system (RAAS) and patient quality of life, whereas lowering heart rate with propranolol did not.
"After doing the study, we found that patients treated with beta blockers did lower their heart rates, but it didn't make them feel any better," senior investigator Dr Benjamin Levine (University of Texas Southwestern Medical Center, Dallas, TX) told heartwire. "The patients who underwent the exercise training program, though, also lowered their heart rate, not to the same extent, but ultimately had an improved quality of life."
The results of the study, with first author Dr Qi Fu (University of Texas Southwestern Medical Center, Dallas), are published online June 20, 2011 in Hypertension.
Increases of more than 30 beats per minute while standing
Patients diagnosed with POTS experience increases of more than 30 beats per minute when standing for more than five minutes. The syndrome, said Levine, can be extremely incapacitating, with some individuals unable to work, attend school, or even stand in line at the grocery checkout counter. Past research has shown that POTS patients have a blunted aldosterone response to increases in renin, resulting in a reduced aldosterone-renin ratio while standing. For patients with a racing heart rate, clinicians typically use beta blockers to attempt to control the symptoms.
Levine told heartwire that a reduced aldosterone-renin ratio has been observed in patients undergoing extended bed rest. In addition, astronauts typically return to Earth with POTS-like symptoms, with these individuals often unable to stand for stretches of 10 minutes upon their return to Earth. As a result, there is speculation that cardiovascular deconditioning contributes to the blunted adrenal response in POTS patients.
"We kept coming back to the primary physiology," said Levine. "Stroke volume is too low in the upright position. The approach with exercise is to increase stroke volume. We wanted to see if we could make their hearts bigger and make the condition go away."
In this study, 19 patients, all of whom completed a double-blind drug trial comparing propranolol and placebo for four weeks, underwent exercise training for a three-month period. The program included an extended base training period, with individuals initially trained using the recumbent bicycle, rowing machine, or swimming. Patients were trained in the seated position for at least one month, sometimes two, and exercise duration and intensity increased as the patients became fitter. Upright exercise, include biking, walking, or jogging, was added to the exercise program as tolerated, as was resistance training.
Treatment with propranolol and exercise training significantly lowered standing heart rate. Standing stroke volume remained stable, and cardiac output was slightly lower following exercise training. Training attenuated plasma renin activity increases but had no effect on the aldosterone increases. As a result, the aldosterone-renin ratio increased modestly following training. Assessments on the short-form health survey revealed significant improvements in quality of life.
Treatment with propranolol, assessed after the four-week trial period, lowered heart rate but did not increase stroke volume. The aldosterone-renin ratio remained unchanged after treatment, and there was no impact on patient quality of life.
Levine said that this study does not exclude the use of beta blockers in some patients, especially in patients with a symptomology dominated by increased heart rates who don't have increased levels of fatigue. He noted that patients with POTS can have significant problems with fatigue, and adding a beta blocker can make this symptom significantly worse. However, without fatigue, a beta blocker might be an option, he noted.
The Institute for Exercise and Environmental Medicine at the University of Texas Southwestern Medical Center is currently enrolling patients in an international POTS registry. According to Levine, physicians interested in enrolling patients can contact THRIEEMPOTSRegistry@texashealth.org.
Marquis De Sade, France, Charenton Asylum, 1789
As I said I am sure it was the Wessely school that brought it in for ME/CFS and from what I have read it was around 1988 or 1989 just after the name change and when Simon Wessely was brought into the picture.
This is from hooper biomedical:
If you read that whole page you will see there has been research clearly showing muscle abnormalities in ME/CFS patients and that CBT/GET are useless and dangerous since the 1980's, yet doctors still pump out the bullcrap that it helps us and is "safe". There is nothing "safe" about exercising when your mitachondria is low and you are killing your own dna, that just equals death.
The stupidity of a large number of the medical profession never ceases to amaze me. Sometimes I think cfs should be changed to "chronic stupid doctor syndrome", shortened to SDS.
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