Corticoperipheral neuromuscular disconnection in obstructive sleep apnoea

Abstract

<jats:title>Abstract</jats:title> <jats:p>The roles of central nervous mechanisms and cortical output in obstructive sleep apnoea remain unclear. We addressed corticomuscular coupling between cortical sensorimotor areas and lower facial motor units as a mechanistic pathway and as a possible surrogate marker of corticoperipheral motor control in obstructive sleep apnoea. In this exploratory cross-sectional retrospective study, we analysed EEG (C3 and C4 leads) and chin EMG from polysomnography recordings in 86 participants (22 females; age range: 26–81 years): 27 with mild (respiratory disturbance index = 5–15 events/h), 21 with moderate (15–30 events/h) and 23 with severe obstructive sleep apnoea (&amp;gt;30 events/h) and 15 control subjects (&amp;lt;5 events/h). By computing C3-/C4-EEG–chin EMG coherence of signal dynamics in time and frequency domains, we investigated corticomuscular coupling between cortical sensorimotor areas and lower facial motor units with increasing obstructive sleep apnoea severity during the entire sleeping time, during different sleep stages and during obstructive respiratory events, including 5 s before (stable breathing) and after events (breathing resumption). In addition, we studied a possible influence of body mass index and autonomic nervous system activation. We found that both average and respiratory event-specific corticomuscular coupling between cortical sensorimotor areas and lower facial motor units weakened significantly with increasing obstructive sleep apnoea severity, was strongest during N3 and weakened in N1, N2 and rapid eye movement stages (in decreasing order). Coupling increases significantly during the obstructive respiratory events compared with coupling just before and following them. Results were independent of body mass index or autonomic nervous system activation. We conclude that obstructive respiratory events in obstructive sleep apnoea are very strongly associated both quantitatively and temporally with the degree of disconnection within the cortical sensorimotor areas—lower facial motor units pathway. This quite coordinated activity pattern suggests a cortical sensorimotor area-driven obstructive respiratory event pattern generator and a central motor output disorder in obstructive sleep apnoea.</jats:p>

Psychiatric disorders associated with PCSK9 inhibitors: A real‐world, pharmacovigilance study

“…27 However, none of the available literature on the target and mechanism studies of alirocumab explicitly identifies the larynx as a site of toxicity. We also 28,29 and is particularly susceptible to altered upper airway anatomy and defective compensatory neuromuscular activity. 30 Diseases associated with neuromuscular injury also predispose to obstructive sleep apnoea syndrome, progressive respiratory muscle weakness and chronic hypercapnic respiratory failure.…”

“…Unexpectedly, however, there was no convincing clinical evidence of an association between PCSK9i and obstructive sleep apnoea syndrome. Obstructive sleep apnoea syndrome is characterized by recurrent collapse of the upper airway and neuromuscular dysfunction of the upper airway dilator muscles (especially the genioglossus) during sleep, 28,29 and is particularly susceptible to altered upper airway anatomy and defective compensatory neuromuscular activity 30 . Diseases associated with neuromuscular injury also predispose to obstructive sleep apnoea syndrome, progressive respiratory muscle weakness and chronic hypercapnic respiratory failure 31 .…”

Sensorimotor Cortical Activity during Respiratory Arousals in Obstructive Sleep Apnea

“…All PSG data were collected using the Alice ® LE system (Philips Respironics, as supplied by Loewenstein Medical, Bad Ems, Germany) and was subsequently converted and stored in the European Data Format (EDF). The EEG data obtained from C3 and C4 electrodes were used for analysis [27]. The EOG data which recorded vertical and horizontal movements for the right and left eye were collected using self-adhesive electrodes, and ECG collected using 12 disposable electrodes was used to record and monitor the heart activity.…”

“…In this study, we investigated the entropies related to respiratory arousals in OSA to examine the central motor activity in the brain during sleep-associated respiratory events. We have previously shown the involvement of cortical sensorimotor areas in motor control pathways associated with obstructive respiratory events in OSA patients using EEG recordings of standard polysomnography (PSG) [27]. Here, we hypothesize that arousal EEG signals have a specific pattern, which would be repeated in the different time interval around the arousals.…”

Drug-Induced Sleep Endoscopy Findings and Hypoglossal Nerve Stimulation Therapy Outcomes

“…There are well-known anatomic (ones related to the passive critical closing pressure of the upper airway (Pcrit)) and nonanatomic (reduced genioglossus muscle responsiveness, low arousal threshold, and reduced respiratory control stability/increased loop gain) contributions to OSA [ 4 ]. In addition, the degree of the reduction in the connectivity between the sensorimotor neural output units and the mechanical upper-airway muscular units explains the degree of respiratory disturbance in treatment-naive obstructive sleep apnea patients [ 5 ].…”