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October 2001; Volume 3; 80
With Comments by Adriane Fugh-Berman, MD
Source: Comparison of sustained-release nifedipine and temperature biofeedback for treatment of primary Raynaud phenomenon. Results from a randomized clinical trial with 1-year follow-up. Arch Intern Med 2000;160: 1101-1108.
Design/Setting/Subjects: A randomized, controlled clinical trial (double-blind for drug and placebo, not blinded for biofeedback) of 313 subjects (95% white, 70% women) with primary Raynaud’s phenomenon (with at least two attacks/d during the cold season).
Treatment: Subjects were divided into four groups: sustained-release nifedipine (30 mg/d titrated up to 30 mg twice a day if tolerated); placebo; temperature biofeedback; or control biofeedback (electromyographic frontalis muscle biofeedback). Those assigned to biofeedback were asked to attend 10 one-hour sessions over a five- to 10-week period during the winter and spring. Four booster sessions were scheduled in the fall for those who had not successfully learned the technique or who had missed at least half of the spring sessions. Those in the biofeedback groups were asked to utilize the technique in situations perceived as being associated with high probability of causing Raynaud’s phenomenon.
Outcome Measures: The primary endpoint was the number of verified attacks during the one-year assessment. Subjects were given photographs depicting hands with different color changes. "Verified" attacks were recorded attacks with a letter code matching one of photographs depicting true Raynaud’s.
Results: A total of 230 subjects (of 313 randomized) completed the trial. Compared to the placebo group, the nifedipine group experienced a 66% reduction in the number of verified attacks, and the temperature biofeedback group experienced a 32% reduction (the difference between the nifedipine group and the temperature biofeedback group did not reach statistical significance). Temperature biofeedback was not significantly different than control (EMG) biofeedback. Nifedipine-treated subjects had a significantly higher incidence of side effects including edema, flushing, and tachycardia; 15% of subjects in the nifedipine group dropped out due to adverse events.
Funding: Supported by contracts from the National Heart, Lung, and Blood Institute. Nifedipine (Procardia XL) was donated by Pfizer labs.
Comments: Although the authors conclude that temperature biofeedback "is not better than its control treatment and is inferior to sustained-release nifedipine," this is misleading. Nifedipine was clearly more effective than oral placebo, but biofeedback did not receive a fair testing in this trial. In biofeedback training, skin temperature, muscle contractions, brain waves, or other parameters are translated into audio or visual signals that a subject learns to affect using imagery, relaxation techniques, etc. Once a subject can reliably affect the parameter tested, the equipment is no longer needed. There is a great deal of individual variability in how long it takes a subject to learn the technique.
It is incredible that the authors used attendance at biofeedback sessions rather than successful learning as an endpoint for effective training. Only 35% of those in the temperature biofeedback group successfully learned the technique. Subjects were asked to attend 10 biofeedback sessions; 53 of 81 (65%) temperature biofeedback participants completed all 10 sessions (compared with 80% of those in the EMG biofeedback group). "Booster" sessions were scheduled for those who had not successfully learned the technique or who had missed half of the sessions. The researchers deemed minimum biofeedback training to be completion of at least six initial sessions or two booster sessions.
However, it is irrelevant how many sessions were attended if the subjects did not learn the technique. Assessing competence by attendance has obvious drawbacks. The researchers do note that inadequate training may have compromised the results, but acknowledgement of this obvious point is no excuse for poor trial design. The situation is comparable to a medication trial in which two-thirds of the treatment group took no medication.
The selection of EMG biofeedback as a control treatment is odd. Electromyographic frontalis muscle biofeedback is used in the treatment of tension headache, but it also is used for inducing skeletal muscle relaxation, and thus general relaxation. Raynaud’s phenomenon may be triggered by stress, so EMG biofeedback should not have been considered an inactive control. In fact, a biofeedback textbook recommends the combination of frontalis muscle EMG biofeedback and temperature feedback for the treatment of Raynaud’s.1
The question of whether biofeedback is an effective treatment for Raynaud’s will have to await a better trial.
1. Sedlacek K. Biofeedback treatment of primary Raynaud’s disease. In Basmajian, JV, ed. Biofeedback: Principles and Practice for Clinicians. 3rd ed. Baltimore, MD: Williams and Wilkins; 1989:317-321.