Twenty-one female patients suffering from diagnosed idiopathic Raynaud's Disease were trained to raise digital skin temperature using either autogenic training, progressive muscle relaxation, or a combination of autogenic training and skin temperature feedback. Patients were instructed in the treatment procedures in three one-hour group sessions spaced one week apart. All patients were instructed to practice what they had learned twice a day at home. Patients kept records of the frequency of vasospastic attacks occurring over a four-week baseline period, and during the first four weeks and the ninth week of training. In addition, patients underwent four laboratory cold stress tests during which they were instructed to maintain digital temperature as the ambient temperature was slowly dropped from 260 to 17°C. Cold stress tests were given during week 1 of baseline and during weeks 1, 3, and 5 of training. Results indicated that all patients improved during the first four weeks of training. No significant differences between the three behavioral treatment procedures were obtained. In addition, the ability of patients to maintain digital temperature during the cold stress challenge showed significant improvement from the first to the last tests. Symptomatic improvement was maintained by all patients nine weeks after the start of the training. The implications of these findings for the behavioral treatment of Raynaud's Disease are discussed.DESCRIPTORS: Raynaud's Disease, progressive relaxation training, autogenic training, behavioral medicine, female patients Raynaud's Disease is a painful vasospastic disorder usually affecting the digits in the hands and feet. The etiology of the disorder in its idiopathic form is unclear and the efficacy of current surgical and pharmacologic treatments is questionable (Spittel, 1972). During a vasospastic episode the affected area goes through a three-stage color change; first blanching, then turning cyanotic blue, and finally becoming bright red as the vasospasm is relieved and reactive hyperemia ensues. Although the pathophysiology of the disease is not understood, it is widely accepted that activity of the sympathetic nervous system is a major contributing factor (Spittel, 1972).