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Motor impairment in Parkinson's disease (PD) is partly due to defective central processing of lower limb afferents. Concomitant alterations in cardiovascular autonomic control leading to orthostatic hypotension may worsen motor ability. We evaluated whether mechanical activation of feet sensory afferents could improve gait and modify the response of cardiovascular autonomic control to stressors in 16 patients (age 66 ± 2 yr) with idiopathic PD (Hoehn & Yhar scale 2–3) on their usual therapy. Eight subjects ( group A) were randomized to undergo skin pressure (0.58 ± 0.04 kg/mm2) stimulation at the hallux tip and first metatarsal joint (effective stimulation; ES) of both feet. Eight remaining patients ( group B) underwent sham stimulation (SS) followed by ES. Three-dimensional movement analysis provided quantitative indexes of movement disability before (baseline) and 24 h after ES and SS. Spectral analysis of heart rate and blood pressure variability provided markers of cardiac sympatho-vagal (LF/HF) and vascular sympathetic (LFSAP) modulations. Markers were measured at rest and during 75° head-up tilt, before and 24 h after ES and SS. After ES, step length and gait velocity increased, upright rotation velocity was enhanced, and step number was decreased. After ES, LFSAP declined. The increase in LF/HF and LFSAP induced by tilt was greater than before feet stimulation. No changes in gait and autonomic parameters were observed after SS. Twenty-four hours after ES, patients with PD showed improved gait and increased cardiac and vascular sympathetic modulation during upright position compared with baseline. Conversely, SS was ineffective on both movement and autonomic parameters, indicating a site specificity effect of the stimulation.

Cardiac baroreflex is a fundamental component of the cardiovascular control. The continuous assessment of baroreflex sensitivity (BRS) from spontaneous heart period (HP) and systolic arterial pressure (SAP) variations during general anesthesia provides relevant information about cardiovascular regulation in physiological conditions. Unfortunately, several difficulties including unknown HP-SAP causal relations, negligible SAP changes, small BRS values, and confounding influences due to mechanical ventilation prevent BRS monitoring from HP and SAP variabilities during general anesthesia. We applied a model-based causal closed-loop approach aiming at BRS assessment during propofol anesthesia in 34 patients undergoing coronary artery bypass graft (CABG) surgery. We found the following: 1) traditional time and frequency domain approaches (i.e., baroreflex sequence, cross-correlation, spectral, and transfer function techniques) exhibited irremediable methodological limitations preventing the assessment of the BRS decrease during propofol anesthesia; 2) Granger causality approach proved that the methodological caveats were linked to the decreased presence of bidirectional closed-loop HP-SAP interactions and to the increased incidence of the HP-SAP uncoupling; 3) our model-based closed-loop approach detected the significant BRS decrease during propofol anesthesia as a likely result of accounting for the influences of mechanical ventilation and causal HP-SAP interactions; and 4) the model-based closed-loop approach found also a diminished gain of the relation from HP to SAP linked to vasodilatation and reduced ventricular contractility during propofol anesthesia. The proposed model-based causal closed-loop approach is more effective than traditional approaches in monitoring cardiovascular control during propofol anesthesia and indicates an overall depression of the HP-SAP closed-loop regulation.

It is unclear whether the complexity of the variability of the systolic arterial pressure (SAP) provides complementary information to that of the heart period (HP). The complexity of HP and SAP variabilities was assessed from short beat-to-beat recordings (i.e., 256 cardiac beats). The evaluation was made during a pharmacological protocol that induced vagal blockade with atropine or a sympathetic blockade (beta-adrenergic blockade with propranolol or central sympathetic blockade with clonidine) alone or in combination, during a graded head-up tilt, and in patients with Parkinson's disease (PD) without orthostatic hypotension undergoing orthostatic challenge. Complexity was quantified according to the mean square prediction error (MSPE) derived from univariate autoregressive (AR) and multivariate AR (MAR) models. We found that: 1) MSPEMAR did not provide additional information to that of MSPEAR; 2) SAP variability was less complex than that of HP; 3) because HP complexity was reduced by either vagal blockade or vagal withdrawal induced by head-up tilt and was unaffected by beta-adrenergic blockade, HP was under vagal control; 4) because SAP complexity was increased by central sympathetic blockade and was unmodified by either vagal blockade or vagal withdrawal induced by head-up tilt, SAP was under sympathetic control; 5) SAP complexity was increased in patients with PD; and 6) during orthostatic challenge, the complexity of both HP and SAP variabilities in patients with PD remained high, thus indicating both vagal and sympathetic impairments. Complexity indexes derived from short HP and SAP beat-to-beat series provide complementary information and are helpful in detecting early autonomic dysfunction in patients with PD well before circulatory symptoms become noticeable.

In physiological conditions, heart period (HP) affects systolic arterial pressure (SAP) through diastolic runoff and Starling's law, but, the reverse relation also holds as a result of the continuous action of baroreflex control. The prevailing mechanism sets the dominant temporal direction in the HP-SAP interactions (i.e., causality). We exploited cross-conditional entropy to assess HP-SAP causality. A traditional approach based on phases was applied for comparison. The ability of the approach to detect the lack of causal link from SAP to HP was assessed on 8 short-term (STHT) and 11 long-term heart transplant (LTHT) recipients (i.e., less than and more than 2 yr after transplantation, respectively). In addition, spontaneous HP and SAP variabilities were extracted from 17 healthy humans (ages 21–36 yr, median age 29 yr; 9 females) at rest and during graded head-up tilt. The tilt table inclinations ranged from 15 to 75° and were changed in steps of 15°. All subjects underwent recordings at every step in random order. The approach detected the lack of causal relation from SAP to HP in STHT recipients and the gradual restoration of the causal link from SAP to HP with time after transplantation in the LTHT recipients. The head-up tilt protocol induced the progressive shift from the prevalent causal direction from HP to SAP to the reverse causality (i.e., from SAP to HP) with tilt table inclination in healthy subjects. Transformation of phases into time shifts and comparison with baroreflex latency supported this conclusion. The proposed approach is highly efficient because it does not require the knowledge of baroreflex latency. The dependence of causality on tilt table inclination suggests that “spontaneous” baroreflex sensitivity estimated using noncausal methods (e.g., spectral and cross-spectral approaches) is more reliable at the highest tilt table inclinations.