Bidirectional interactions between the baroreceptor reflex and arousal: An update

Studies involving genetic engineering on animal models and mathematical analysis of cardiovascular signals on humans are shedding new light on the interactions between the arterial baroreceptor reflex (baroreflex) and arousal. Baroreceptor stimulation, if very mild or performed under anaesthesia, may inhibit cortical arousal. However, substantial increases or decreases in baroreflex activation cause arousal in animal models and human subjects in physiological conditions. On the other hand, cardiovascular changes during autonomic arousals and between the states of wakefulness and sleep involve changes in the baroreflex set point and balance with central autonomic commands. Neural connectivity and functional data suggest that the nucleus of the solitary tract, adrenergic C1 neurons of the medulla, and the parabrachial nucleus of the pons mediate the bidirectional interactions between the baroreflex and arousal. These interactions may constitute a positive feedback loop that facilitates sharp and coordinated brain state and autonomic transitions upon arousal: upon arousal, central autonomic commands may increase blood pressure, thereby loading baroreceptors and further increasing arousal. Anomalies of this feedback loop may play a role in the pathophysiology of disease conditions associated with cardiovascular and sleep-wake cycle alterations. These conditions include: obstructive sleep apnoea syndrome, with its association with excessive daytime sleepiness and baroreflex impairment; and insomnia, with its association with autonomic hyperarousal and hypertension. When faced with disorders associated with cardiovascular and sleep-wake cycle alterations, clinical reasoning should entertain the possibility that both conditions are strongly influenced by anomalies of baroreflex function

Stridor in multiple system atrophy: Consensus statement on diagnosis, prognosis, and treatment

Multiple system atrophy (MSA) is a neurodegenerative disorder characterized by a combination of autonomic failure, cerebellar ataxia, and parkinsonism. Laryngeal stridor is an additional feature for MSA diagnosis, showing a high diagnostic positive predictive value, and its early occurrence might contribute to shorten survival. A consensus definition of stridor in MSA is lacking, and disagreement persists about its diagnosis, prognosis, and treatment. An International Consensus Conference among experts with methodological support was convened in Bologna in 2017 to define stridor in MSA and to reach consensus statements for the diagnosis, prognosis, and treatment. Stridor was defined as a strained, high-pitched, harsh respiratory sound, mainly inspiratory, occurring only during sleep or during both sleep and wakefulness, and caused by laryngeal dysfunction leading to narrowing of the rima glottidis. According to the consensus, stridor may be recognized clinically by the physician if present at the time of examination, with the help of a witness, or by listening to an audio recording. Laryngoscopy is suggested to exclude mechanical lesions or functional vocal cord abnormalities related to different neurologic conditions. If the suspicion of stridor needs confirmation, drug-induced sleep endoscopy or video polysomnography may be useful. The impact of stridor on survival and quality of life remains uncertain. Continuous positive airway pressure and tracheostomy are both suggested as symptomatic treatment of stridor, but whether they improve survival is uncertain. Several research gaps emerged involving diagnosis, prognosis, and treatment. Unmet needs for research were identified