No abstract

Research on the aetiology of Raynaud's disease and phenomenon has been hindered by the difficulty of provoking attacks in the laboratory. A study was therefore conducted in which digital and ambient temperatures, electrocardiograms, and stress ratings were obtained during ambulatory monitoring in patients with idiopathic Raynaud's disease, Raynaud's phenomenon secondary to scleroderma, and in normal subjects. In Raynaud's disease about one third of the vasospastic attacks were associated with tachycardia and increased stress ratings without declines in ambient temperature. In contrast, cold alone was enough to provoke most attacks of Raynaud's phenomenon in scleroderma.Chronically increased stress ratings in patients with scleroderma and increased muscle tension in anticipation of a cold stimulus suggest that these patients have different patterns of stress responses from those with Raynaud's disease. IntroductionThe symptoms of Raynaud's disease and phenomenon consist of episodic vasospasms in the fingers and toes precipitated by cold or emotional stress, or both. When these attacks occur in the presence of identifiable pathological processes the term Raynaud's phenomenon is used. This is the case for a variety of diseases such as scleroderma, where Raynaud's attacks occur in over 95% of patients.' When the attacks occur in the absence

Thirty-two subjects with idiopathic Raynaud's disease were randomly assigned to receive finger temperature feedback, finger temperature feedback under cold stress, frontalis electromyographic (EMG) feedback, or autogenic training. Subjects receiving finger temperature feedback demonstrated significant temperature increases, without relaxation, during training and after the removal of feedback. A significant, but smaller response was retained a year later, accompanied by a 66.8% reduction in reported attacks. The addition of training under cold stress to temperature feedback significantly improved retention of voluntary vasodilation at follow-up and produced a significantly greater (92.5%) reduction in symptom frequency. These procedures did not change overall levels of tonic peripheral blood flow, recorded over 24 hours in the natural environment. However, following treatment significantly colder temperatures were needed to produce attacks in these subjects, compared to those who had received EMG feedback or autogenic training. These latter techniques produced the expected signs of decreased arousal but were significantly less effective than temperature feedback in increasing finger temperature or decreasing symptom frequency. The addition of cognitive stress management did not significantly affect any procedure.

Although finger temperature feedback has been used to produce digital vasodilation in normal persons and those with Raynaud's disease, the mechanism and site of this effect have not been studied. In the present investigation, feedback-induced vasodilation was attenuated by brachial artery infusions of propranolol in infused, but not contralateral, hands and was not affected by digital nerve blockade. Quantitative measurements of finger blood flow demonstrated that this vasodilation occurred in arteriovenous shunts in normal persons and in the finger capillary bed in those with Raynaud's disease. Raynaud's disease patients who received finger temperature feedback reported 80 fewer percent symptoms 1 and 2 years after treatment and retained the ability to increase finger temperature and capillary blood flow at these times. These effects were not shown by patients given autogenic training, a relaxation procedure.

Panic disorder patients were compared with normal subjects during intravenous infusion of sodium lactate, isoproterenol, and placebo. Panic attacks meeting the criteria of the Diagnostic and Statistical Manual, vol. 3 [American Psychiatric Association, 1980] occurred during all three conditions in patients and during the lactate and isoproterenol infusions in normals. Patients had significantly higher average levels of skin conductance, heart rate and state anxiety, and significantly lower finger temperatures compared to normal subjects. However, no measure reliably differentiated panic attacks from nonattack periods. It is concluded that the peripheral physiologic responses investigated are neither necessary nor sufficient for the occurrence of panic attacks. It is possible that reports of these attacks represent phobic responses to intense anxiety.