Somatosensory Evoked Potentials (SEPs) and Somatosensory Evoked magnetic Fields (SEFs) to median nerve stimulation at wrist were recorded in 5 healthy subjects and the components between 15 and 30 ms after the stimulus were evaluated on the hemiscalp contralateral to the stimulated wrist. SEPs were measured by means of a 32-channel recorder and compared with SEFs obtained via multiple measurements with a 4-channel sensor. Equivalent dipole localization was carried out for the magnetic components peaking at about 15, 20 and 24 ms. The scalp distribution of SEPs, illustrated by bit mapped color images, were qualitatively explained by three separate sources. The first is described as a tangentially oriented dipole placed behind the Central Sulcus and responsible for the parietal N20-“late P25” waves and for the frontal P20-N30 ones. The second is represented by a radieal dipole placed just in front of the Central Sulcus and pointing towards the motor strip, responsible for the rolandic P22 component. The third is just behind the Central Sulcus and is radically oriented towards the surface of the postcentral sensory area for the “early P25” parietal wave. The SEFs distributions, illustrated by color isofield contour maps, were quantitatively explained by a unique tangential dipole localized, with good resolution, well behind the Sulcus for the 15 ms waves and slightly frontal to this site for the waves peaking at around 20 and 24 ms. The equivalent dipole has been localized at a depth of about 5 cm (15 ms component), 2 cm (20 ms components) and 4 cm (24 ms component), across the studied subjects. It is stressed that the dipole responsible for the magnetic pattern is likely to be the same tangential dipole responsible for a part of the electric pattern. Due to their radieal orientation, the other two dipoles, proposed for the SEPs maps, would be mostly undetectable by a magnetic investigation.

Objective: To investigate whether parathyroidectomy (PTx) reverses risk factors for arrhythmias related to the QT dynamic changes evaluated during bicycle ergometry exercise test (ET).Methods: Twenty-four postmenopausal women with primary hyperparathyroidism (PHPT) (mean age 60.0±8.4 years) and 30 sex- and age-matched controls underwent ET, echocardiography, and biochemical evaluation. The following stages were considered during ET: rest, peak exercise, and recovery. The patients were randomized to two groups: 12 underwent PTx (group A) and 12 were followed-up conservatively (group B). After 6 months, the patients were studied again.Results: Groups A and B showed no differences in mean baseline biochemical values, echocardiographic parameters, and QTc interval. PHPT patients showed an increased occurrence of ventricular premature beats (VPBs) during ET compared with controls (37.0 vs 6.6%,P=0.03). Serum calcium level was a predictor of VPBs (P=0.05). Mean value of QTc was in the normal range at baseline (group A: 401±16.9; group B: 402.25±13.5 ms) but significantly lower than controls (417.8±25.1 ms,P<0.01). A negative correlation was found between QTc and calcium values (P=0.03). Physiological reduction of QTc interval from rest to peak exercise was not observed in PHPT patients before surgery. After PTx, group A had a significant reduction in VPBs compared with baseline (at baseline, 5 of 12 vs none of 12 patients after PTx,P=0.03) and a restored normal QT adaptation during ET. Group B showed no significant changes after a 6-month period.Conclusions: PTx reduces the occurrence of VPBs and restored the QTc adaptation during ET.

Endothelin-1 (ET-1), a novel 21-aminoacid vasoconstrictive peptide secreted by endothelial cells, has been thought to play a role in various forms of vascular disease. Diabetes mellitus is well known for its association with microvascular damage. To investigate whether ET-1 levels may be related to microangiopathy in diabetes mellitus, plasma ET-1 levels were measured in two groups of diabetic patients: A) 47 patients with non-insulin dependent diabetes mellitus (NIDDM) and retinopathy (28 M, 19 F; mean age 60.7 ± 8.5 yrs) but without nephropathy (microalbuminuria < 30 mg/day) and hypertension (SBP < 140, DBP < 90 mmHg); group A was divided in three subgroups based on the severity of retinopathy: a) 16 with background retinopathy; b) 21 with pre-proliferative retinopathy; c) 10 with proliferative retinopathy. B) 8 patients with insulin-dependent diabetes mellitus (IDDM) recently diagnosed (6 M, 2 F; 16.4 ± 3.8 yrs) without complications. C) 28 healthy subjects (HS) (16 M, 12 F; 47.8 ± 11.8 yrs) as controls. In the NIDDM group the ET-1 concentration was significantly higher (17.3 ± 2.4 pg/ml) than both in the HS (8 ± 4.7 pg/ml) and IDDM patients (10.2 ± 3.7 pg/ml) (p < 0.0001). In the subgroups with retinopathy the ET-1 levels were a) 15.1 ± 4.3 pg/ml; b) 22.2 ± 6.8 pg/ml and c) 16.6 ± 5.1 pg/ml. These values were significantly elevated as compared to HS (p < 0.001; p < 0.0001; p < 0.002, respectively), being the highest levels of ET-1 observed in the NIDDM patients with pre-proliferative retinopathy. In conclusion our study revealed that the ET-1 concentrations are elevated in NIDDM patients with retinopathy especially in those patients with pre-proliferative retinopathy.