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Background: The sympathetic baroreflex (sBR) adjusts muscle sympathetic nerve activity (MSNA) in response to arterial pressure changes but the relevance of assessing sBR control complexity is unclear. Objective: We propose a method for the evaluation of sBR control complexity. Approach: The approach comprises the quantification of complexity of the sBR latency regulation and the assessment of complexity of the relationship linking MSNA burst to R-wave peak regardless of the variability of the sBR latency. The Shannon entropy (SE) of the sBR latency distribution is taken as an estimate of complexity of the sBR latency regulation. The conditional entropy (CE) of the beat-to-beat binary series obtained by coding the presence/absence of the MSNA burst after an R-wave peak is taken as an estimate of complexity of the sBR control regardless of the sBR latency variability. Surrogate analysis was utilized to set the level of inactive or impaired sBR. The approach was applied to 10 young healthy subjects undergoing head-up tilt (HUT) followed by lower body negative pressure to evoke presyncope (preSYNC) before and after 21 d head-down bed rest (HDBR), and to five amyotrophic lateral sclerosis (ALS) patients undergoing HUT. Main results: In healthy subjects the surrogate analysis suggested that HUT and preSYNC significantly activated the sBR control but its response was weakened after 21 d HDBR. During preSYNC sBR latency increased significantly only after 21 d HDBR. In ALS patients the complexity of the sBR latency regulation was close to the level set by surrogate analysis and HUT did not trigger any sBR control response. Significance: The proposed method for sBR control complexity quantification was useful in detecting the impairment of the sBR control after 21 d HDBR in healthy subjects and the dysfunction of the sBR regulation in ALS patients. [ABSTRACT FROM AUTHOR]

Although the clinical hallmark of amyotrophic lateral sclerosis (ALS) is a progressive motor weakness, different combinations of autonomic nervous system (ANS) dysfunction have been described. No clear correlation between ANS abnormalities and ALS clinical characteristics has been found so far. We investigated the cardiovascular neural regulation in ALS with a non-invasive methodology, using spectral and complexity analysis of heart rate variability (HRV) and systolic arterial pressure (SAP) variability. In all patients, we found low RR variance and an altered response to orthostasis, witnessed by the indices derived from both spectral and complexity analysis of HRV and SAP variability. Besides, we identified two groups with distinct autonomic profiles at rest, those with higher, and those with lower cardiac sympathetic activity. In both groups the cardiovascular response to tilting was impaired. Our study outlined that ANS is invariably impaired in ALS, and patients can present with different baseline patterns. Our findings suggest important pathophysiological, clinical and prognostic insights. The presence of different autonomic profiles at rest supports the new concept of ALS as a multisystem disorder with phenotypic heterogeneity. Our results are also relevant in clinical practice. They can help to improve patients’ management, and to identify prognostic factors. [ABSTRACT FROM AUTHOR]