[Subjective illness in non-malignant chronic pain--working patients are feeling better than sick-listed patients].
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Biomedical subjects
Publications and source records attributed to C Mannheimer.
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Spinal cord stimulation (SCS) can relieve symptoms in patients with severe angina pectoris refractory to conventional medical or surgical therapy. This symptomatic improvement may result from decreased myocardial ischemia. To test this hypothesis, positron emission tomography (PET) and potassium-38 as a flow tracer were used in 8 patients for the quantitative evaluation of regional myocardial perfusion at rest and after exercise, before and during SCS. Potassium uptake was evaluated as myocardial clearance (flow times net extraction) in ml/min/100 g. Tomographic segments were categorized as nonaffected and affected on the basis of the absence or presence of arterial stenosis on coronary angiography and on the basis of thallium scintigraphic data. In nonaffected segments, before SCS, regional myocardial clearance significantly increased from rest (28 +/- 4) to exercise (47 +/- 13 clearance units; p less than 0.004). A similar increase occurred after SCS. In affected segments, before SCS, regional myocardial clearance barely increased (p = 0.065) from rest (26 +/- 6) to exercise (33 less than or equal to 12). In comparison, after SCS, the resting regional myocardial clearance was slightly elevated (29 +/- 8) reflecting an increased double product, but did not increase (p = 0.192) with exercise (34 +/- 12). However, the magnitude and duration of ST-segment depression decreased during treatment with SCS. Anginal pain occurred in all patients during control exercise, but was attenuated in all but one with SCS. These results indicate that SCS improves exercise-induced angina and electrocardiographic signs of ischemia but this influence does not appear to be mediated by changes in regional myocardial perfusion.
The present study investigates the relationships between clinical pain relief, physiological and psychological parameters. Out of 50 patients with long-lasting musculoskeletal neck- and shoulder-pain treated with transcutaneous electrical nerve stimulation (TENS), 21 were selected and classified as responders (n = 13) or non-responders (n = 8). Tooth pain thresholds (PT) were measured before and after an experimental TENS treatment and the relative change in PT following the stimulation was calculated. Three psychometric self-inventories were administered: Zung Depression Scale, Spielberger's Trait Anxiety Scale and the Multidimensional Health Locus of Control Scale. Responders (R) and non-responders (NR) differed significantly from each other in the PT measurements as well as on the psychometric scales. NR exhibited higher levels of anxiety and depression, a more pronounced powerful other orientation and no change or a decrease in PT following TENS compared to R. These findings indicate relationships and interactions between physiological and psychological factors in patients with long-lasting pain.
In order to elucidate the effects of atrial pacing on cardiac catecholamine metabolism, 11 patients were studied during cardiac catheterization. Blood samples were drawn from a peripheral artery and the coronary sinus for estimation of catecholamine concentrations. Heart rate was increased by 10 beats/min each minute, and all patients experienced chest pain at maximal pacing rate. Coronary sinus blood flow rose from 122 +/- 19 at rest to 208 +/- 25 ml/min at final pacing rate, and myocardial lactate extraction ratio decreased. There was no significant change in arterial epinephrine levels, whereas the extraction ratio decreased (p less than 0.05). The norepinephrine arterial levels increased at the final pacing rate (p less than 0.01). The calculated myocardial release increased as well, but not to a statistically significant degree. The exact mechanisms of the rise in sympathetic activity and arterial norepinephrine levels cannot be ascertained with the present study design. Myocardial ischemia with subsequent chest pain seems to be a probably cause for the increased sympathetic outflow.
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The influence of naloxone on the effects of high frequency transcutaneous electrical nerve stimulation in angina pectoris induced by atrial pacing was studied in 11 patients with severe coronary artery disease. The patients were catheterised and treated with transcutaneous electrical nerve stimulation on two occasions, double blind and in random order, with a single intravenous dose of saline or with a single intravenous dose of 50 mg naloxone. Treatment with transcutaneous electrical nerve stimulation increased tolerance to pacing and significantly improved lactate metabolism with placebo and with naloxone. The positive effects of transcutaneous electrical nerve stimulation were thus reproducible and not reversed by single intravenous doses of naloxone. The results indicate that the effects of transcutaneous electrical nerve stimulation on the heart are not mediated by beta endorphin but they do not exclude activation of more short-acting opioids such as delta or kappa receptor agonists (met-enkephalin or dynorphin or both) because naloxone has a low affinity for these receptors. Non-opioid mechanisms may also be important.
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The short term effects of epidural spinal electrical stimulation were studied in 10 patients with angina pectoris of New York Heart Association functional class III or IV. The antianginal pharmacological treatment given at entry to the study was regarded as optimal and was not changed during the study. The effects of epidural spinal electrical stimulation were measured by repeated bicycle ergometer tests. Treatment with epidural spinal electrical stimulation increased the patients' working capacity, decreased ST segment depression, increased time to angina, and reduced the recovery time. The observed effects did not seem to be correlated with any changes in myocardial oxygen demand during epidural spinal electrical stimulation and were additional to the benefits of the pharmacological treatment.
The arterial levels of norepinephrine and epinephrine were estimated in 14 patients with severe coronary artery disease in order to assess the catecholamine metabolism during pacing-induced angina pectoris and to evaluate the effects of transcutaneous electrical nerve stimulation (TENS). Arterial levels of epinephrine and norepinephrine increased significantly during pacing to angina pectoris (p less than 0.05 and p less than 0.001, respectively), indicating that maximal atrial pacing induced an increase in sympathetic tone. At the corresponding pacing rate during TENS, myocardial lactate production was improved (p less than 0.01) and the ST segment depression was less pronounced (p less than 0.05). The maximal pacing rate during TENS was 141 +/- 24 compared to 123 +/- 19 (p less than 0.01) and the heart rate-blood pressure product was also significantly higher (p less than 0.01), suggesting an elevation of the anginal threshold by TENS. Systemic vascular resistance and systolic blood pressure were significantly reduced (both p less than 0.01). These beneficial results may be caused by a decrease in left ventricular afterload as reflected by a fall in systolic blood pressure and may be explained by reduced sympathetic activity. TENS may decrease the sympathetic activity either directly or indirectly as a consequence of pain inhibition. This hypothesis is supported by the fact that arterial levels of epinephrine and norepinephrine dropped during TENS in TENS responders.
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The pain-relieving effects of transcutaneous electrical nerve stimulation (TENS) were investigated in patients with severe angina pectoris first with respect to systemic and coronary hemodynamics and myocardial metabolism during pacing-induced angina and second in a controlled long-term study. Two series of patients with severe angina pectoris (NYHA class III to IV) were studied (13 patients in the pacing study and 23 in the long-term study). In the pacing-induced angina study there was increased tolerance to pacing (142 +/- 23 compared with 124 +/- 20 beats/min tolerated, p less than .001), improved lactate metabolism (2 +/- 36% compared with -18 +/- 43%, p less than .01), and less pronounced ST segment depression (2.3 +/- 1.1 compared with 2.9 +/- 2.6 mm, p less than 0.05) with TENS. In the long study the effects of TENS were measured by means of repeated bicycle ergometer test, frequency of anginal attacks, and consumption of short-acting nitroglycerin. TENS was used regularly for 1 hr three times per day. The TENS treatment group had increased work capacity (637 +/- 308 vs 555 +/- 277 W . min, p greater than .001), decreased ST segment depression (2.3 +/- 1.1 vs 3.6 +/- 1.6 mm, p less than .001), reduced frequency of anginal attacks (p less than .05), and reduced consumption of short-acting nitroglycerin per week (p less than .05) compared with the control group. The observed effects were mainly due to decreased afterload resulting from systemic vascular dilatation.
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The effect of transcutaneous nerve stimulation (TNS) on ischemic pain in the lower extremities was tested. Eleven patients with severe arterial insufficiency were observed before and after TNS. The results indicate pain relief and increased walking distance in all subjects. We interpret the results of this study that ischemic pain can be diminished by TNS.
11 patients with peripheral arterial circulatory insufficiency with ulcers on the big toe or on the heel were given 1 g of cephradine intravenously (i.v.) and later 1 g of cefazolin i.v., two cephalosporins with different degrees of protein binding. Antibiotic concentrations were followed in serum and wound secretions after the injections. The peripheral circulatory state of the patients and the degree of protein binding of the cephalosporins used seemed to be of minor importance for the concentrations of the antibiotics in the ulcers, i.e. the infectious focus, compared to local factors such as the bacterial flora of the ulcers. In-vitro studies with bacterial strains isolated from the ulcers of 2 of the patients indicated that beta-lactamases from gram-negative bacteria might be at least part of the explanation for the low concentrations in wound secretion of one or other of the agents used in 4 out of the 11 patients.
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