Autonomic nervous system dysfunction in narcolepsy type 1: time to move forward to the next level?
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EDITORIAL
Autonomic nervous system dysfunction in narcolepsy type 1: time to move forward to the next level? Alessandro Silvani1 Received: 29 October 2020 / Revised: 30 October 2020 © Springer-Verlag GmbH Germany, part of Springer Nature 2020
Keywords Autonomic · Sleep · Narcolepsy · Sudoscan · Electrochemical skin conductance Narcolepsy, although a rare disease, is one of the most common causes of chronic sleepiness. Patients with narcolepsy type 1 (NT1) typically show cataplexy and a dramatic reduction in the cerebrospinal fluid concentration of the neuropeptide orexin A (hypocretin 1), which results from extensive loss of the orexin-producing neurons in the hypothalamus [1]. The orexin neurons are a critical component of the sleep control circuits and an integral part of the central autonomic network [1, 2]. In 1982, Sachs and Kaiser reported smaller increases in heart rate (HR) and blood pressure (BP) at the handgrip test and smaller changes in HR during deep breathing and the Valsalva maneuver, but no significant alteration at the head-up tilt test (HUTT) and the cold face test [3], in patients with NT1 compared with healthy controls. However, their findings were not confirmed in later studies by different groups [4, 5]. On the other hand, higher scores of a questionnaire on autonomic symptoms (the Scales for Outcomes in Parkinson’s Disease–Autonomic Dysfunction, SCOPA-AUT) have been recently reported in patients with NT1 than in healthy controls, with significant impairments in the gastrointestinal, urinary, cardiovascular, thermoregulatory, pupillomotor, and sexual subdomains [6]. In this issue of Clinical Autonomic Research, Rocchi and colleagues improved over previous work by administering a comprehensive set of autonomic cardiovascular function tests, an electrochemical skin conductance (ESC) test of sudomotor function, and the SCOPA-AUT questionnaire to a sample of patients with NT1 and controls [7]. They found that, compared with controls, patients with NT1 * Alessandro Silvani [email protected] 1
Department of Biomedical and Neuromotor Sciences, University of Bologna, Piazza di Porta San Donato 2, 40126 Bologna, Italy
showed significantly higher systolic BP during supine rest and HUTT, significant HR alterations during HUTT, the cold-face test, the Valsalva maneuver, and deep breathing, significantly lower ESC in the hands, and higher scores for all SCOPA-AUT subdomains. Based on these results, Rocchi and colleagues concluded for the occurrence of blunted parasympathetic activity during wakefulness, mild sudomotor dysfunction, and a large variety of autonomic symptoms in patients with NT1 [7]. The study by Rocchi and colleagues has limitations, acknowledged by the authors [7]. Patients who smoked or had an apnea–hypopnea index greater than five or assumed drugs to treat NT1 were excluded from the study [7]. This was both a point of strength and a limitation, as it decreased within-group variability at the expense of the generalizability of the findings, with a potential for underesti
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