Comparing two relaxation procedures to ease fatigue in multiple sclerosis: a single-blind randomized controlled trial.

Background: Various relaxation procedures have been proposed to reduce fatigue in multiple sclerosis (MS). However, it is unknown, which type of relaxation has the largest effect on fatigue reduction and on autonomic nervous system (ANS) activity.

Objective: We aimed to compare two biofeedback-supported relaxation exercises: a deep breathing (DB) exercise and progressive muscle relaxation (PMR), which may ameliorate MS fatigue and alter ANS activity.

Heart rate variability and fatigue in MS: two parallel pathways representing disseminated inflammatory processes?

Background: Fatigue is a disabling symptom of multiple sclerosis. Its biological causes are still poorly understood. Several years ago, we proposed that fatigue might be the subjective representation of inflammatory processes.

Lupus anticoagulant and thrombosis: role of von Willebrand factor multimeric forms.

Objective: Patients with lupus anticoagulant (LA) have an increased incidence of venous and arterial thrombosis whose pathogenesis is still unclear. High molecular weight von Willebrand Factor (vWF) multimers seem to play a causal role in shear stress-induced platelet aggregation and thrombus formation. We studied whether in patients with LA, alterations in the vWF multimers might coexist.

[Anomalies of coagulation and fibrinolytic activity in patients with chronic pulmonary thromboembolism].

Introduction: Haemostatic and fibrinolytic parameters were evaluated in patients with chronic pulmonary hypertension following pulmonary embolism (CPE). The diagnosis of CPE was based on lobar or segmental defects on perfusion lung scans and by pulmonary angiograms which showed complete or partial obstruction of main or segmentary lobar arteries.

Methods: Antithrombin III (AT III), protein C, protein S, and lupus anticoagulant (LA) were assayed in 8 patients with CPE; in 6 out of 8 patients plasma fibrinolytic activity was assessed both under basal conditions and after venous stasis.

Lupus anticoagulant: interference with in vivo prostaglandin production and with platelet sensitivity to prostacyclin.

The hypothesis has been made that inhibition of prostacyclin (PG12) production may play a role in the pathogenesis of thrombosis in patients with the lupus anticoagulant (LA), but so far no evidence of reduced PG12 levels in vivo has been produced. We have tested the plasma levels of PG12 and thromboxane A2 (TXA2) and the platelet sensitivity to PG12 in 14 patients with and without LA and in 14 healthy controls. No significant difference in the prostanoid basal levels was detected among the groups; however, in some patients PG12 increments seemed to parallel the clinical course of the disease.