Brown et al. studied hypoglossal nerve function in acute stroke patients.[1] They demonstrated a high prevalence of nerve dysfunction and a significant correlation with the severity of sleep-disordered breathing (SDB). The authors, due to the recording technique, did not classify this SDB as central or obstructive. As cases affected by previous peripheral neuropathy or OSA were excluded, what might have caused the deficit? Hypoglossal nerve function and upper airways patency are regulated by serotonin (5HT). Several studies have demonstrated that altered central networks, particularly serotoninergic, can contribute to OSA [2] as well as to central sleep apnea. [3] Moreover, Sunderram et al. [4] observed that a selective serotonin reuptake inhibitor (SSRI), paroxetine hydrochloride, may activate motor neurons in the hypoglossal nucleus and increase genioglossal electromyographic (EMG) activity. We hypothesize that the hypoglossal nerve dysfunction observed in the study is --at least par

Hypoglossal nerve dysfunction in patients with acute stroke and sleep disordered breathing: a serotoninergic hypothesis.

SACCHETTI, Maria Luisa;
2014

Abstract

Brown et al. studied hypoglossal nerve function in acute stroke patients.[1] They demonstrated a high prevalence of nerve dysfunction and a significant correlation with the severity of sleep-disordered breathing (SDB). The authors, due to the recording technique, did not classify this SDB as central or obstructive. As cases affected by previous peripheral neuropathy or OSA were excluded, what might have caused the deficit? Hypoglossal nerve function and upper airways patency are regulated by serotonin (5HT). Several studies have demonstrated that altered central networks, particularly serotoninergic, can contribute to OSA [2] as well as to central sleep apnea. [3] Moreover, Sunderram et al. [4] observed that a selective serotonin reuptake inhibitor (SSRI), paroxetine hydrochloride, may activate motor neurons in the hypoglossal nucleus and increase genioglossal electromyographic (EMG) activity. We hypothesize that the hypoglossal nerve dysfunction observed in the study is --at least par
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11573/558492
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