An increase of regional cerebral blood flow (rCBF) has been shown to occur in man during spinal cord stimulation (SCS) by Hosobuchi (1986) and by Meglio et al. (1988) using the 133-Xenon wash-out technique. In this paper we report the effects of SCS on CBF as measured by two different techniques: 8 patients were studied with the 133-Xe method and 28 with the transcranial doppler sonography (TCD), in two cases both studies were performed. The aim of our study was to: 1-verify the effect of SCS on CBF, 2-compare observations made by two different methods, and 3-evaluate a possible correlation between the stimulated spinal segmental level and the modification of CBF. The results of our study confirm that SCS interacts with the mechanisms of regulation of CBF. The stimulation of different spinal cord levels in the same patient can produce different effects and such effects are reproducible. An increase of CBF is more likely to occur with the stimulation of the cervical spinal cord. In patients studied by both methods the sign of CBF changes induced by SCS was the same. Finally, in two patients the effect of SCS on CO2 autoregulation was studied with TCD. The results of such a study, although preliminary, suggest that CO2 and SCS have a competitive effect upon the mechanisms of regulation of CBF.

The effect of spinal cord stimulation (SCS) on heart rate (HR) was studied in 25 patients without cardiological symptoms, who were undergoing SCS for various reasons. HR at rest signifïcantly decreased during SCS. Physiological and pharmacological maneuvers of sympathetic and parasympathetic activation or blockade before and during SCS indicate that SCS interferes with the central mechanisms of regulation of HR mainly by inducing a functional sympathectomy, and that such an effect is mediated by an action on spinal cord ascending fibers.

The possible relationship between diabetic autonomic neuropathy, circadian blood pressure changes, and echocardiographic parameters was investigated in 27 normotensive diabetic patients (10 with and 17 without autonomic neuropathy) who underwent 24 h noninvasive ambulatory blood pressure monitoring and M-mode echocardiographic recording. The two groups were comparable for age, sex, duration of diabetes, body mass index, and metabolic control. There were no significant differences in 24 h average and diurnal values of systolic, diastolic, or mean blood pressure. The percent changes from day to night of systolic, diastolic, and mean blood pressures were significantly lower in diabetics with neuropathy than in those without (P < .04 or less). Increased left ventricular mass index (LVMI) (135.4 +/- 10.2 v 102.9 +/- 6.3; P < .005), septal wall thickness, and posterior wall width were observed in neuropathic patients. Fractional shortening, peak velocity of early left ventricular filling (E), peak velocity of late ventricular filling (A), and their ratio (E/A) were similar in the two groups. The increased LVMI we observed may represent a possible link between diabetic autonomic neuropathy, nocturnal blood pressure levels, and higher cardiovascular mortality rate.

In previous works we have demonstrated that Coenzyme Q10 (CoQ10) levels have a significant inverse correlation with thyroid hormone concentration in patients with spontaneous hyper- or hypothyroidism. In order to verify whether this correlation is maintained in patients on long-term amiodarone therapy, in whom thyroid metabolism is altered by the iodine contained in the drug, we have studied 30 patients with thyroid dysfunction induced by chronic amiodarone treatment. We have distinguished four groups of patients: group A (n = 8): patients with true hyperthyroidism induced by drug administration; group B (n = 11): patients with mild hyperthyroid symptoms, but isolated thyroxine increase or dissociation between different indexes of thyroid function; group C (n = 5): patients with normal thyroid hormone levels, but increased TSH levels; group D (n = 6): patients who appeared really clinically euthyroid, with normal thyroid hormone levels and normal TSH response to TRH. In group A patients, plasma CoQ10 levels averaged 0.49 +/- 0.03 micrograms/ml, significantly lower than those in normal subjects and similar to those observed in spontaneous hyperthyroid patients. In group B patients, CoQ10 levels were in the normal range (0.88 +/- 0.10 microgram/ml). In group C patients, CoQ10 levels were lower than those in normal subjects and similar to those of group A patients (0.49 +/- 0.04 microgram/ml); they differed, in regards to CoQ10 values, in comparison with spontaneous primary hypothyroid patients, who had very high levels of plasma CoQ10. Finally, in group D patients, CoQ10 levels were in the normal range (0.77 +/- 0.04 microgram/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

We have studied with seriated controls for a period of 9 days 18 patients admitted to our hospital for acute myocardial infarction (AMI). Slight, but non significant variations in thyroidal hormone pattern were observed: slight decrease of T3 and T4 levels, increase of reverse T3 on day 3, low free T4 levels, slight increase of TSH levels until the 3rd day. However, hormonal pattern was clearly different in patients who presented a clinical improvement (group 1a) and in patients who died for AMI (group 1b). In fact, a significant TSH increase was recorded in patients of group 1a; on the contrary, a significant decrease of TSH, T4 and free T4 concentrations was observed for subjects of group 1b, suggesting an inadequate response of pituitary-thyroid axis. In conclusion, the evaluation of thyroid hormones and thyrotropin levels can be of clinical usefulness in the management of patients with AMI. The decrease of plasma T4 and free T4 concentrations, accompanied with low TSH levels, can be associated with unfavorable course of the disease and therefore can be considered a bad prognostic sign.