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. 2005 Dec;28(12):1547-53.

Cortical excitability in obstructive sleep apnea syndrome: transcranial magnetic stimulation study

Affiliations
  • PMID: 16408414

Cortical excitability in obstructive sleep apnea syndrome: transcranial magnetic stimulation study

Antonello Grippo et al. Sleep. 2005 Dec.

Abstract

Study objective: To investigate cortical motor area function in patients with obstructive sleep apnea syndrome (OSAS) during the daytime.

Design: The day after a nocturnal polysomnography, transcranial magnetic stimulation (TMS) of the motor cortex was performed recording Motor Evoked Potential from the first dorsal interosseous muscle of the dominant hand. We evaluated: 1) the relaxed motor threshold (RMT), 2) the threshold of the cortical silent period (CSP), 3) the duration of CSP elicited by five stimulus intensities (95%,100%,105%,130%, and 150% of RMT). To estimate the influence of waking on TMS, recordings were performed five times in a day. The Epworth Sleepiness Scale (ESS), and Stanford Sleepiness Scale (SSS) were also measured.

Setting: The study was carried out in the Sleep and Evoked Potentials laboratories of the Don C. Gnocchi Foundation (ONLUS IRCCS) Pozzola tico, (Florence), Italy.

Patients: 10 patients with OSAS and 10 healthy volunteers.

Intervention: N/A Measurements and Results: In OSAS patients, ESS and SSS were significantly higher than in controls. Patients had a longer duration of CSP at 95%,100% and 105% RMT intensity at almost recording hours; with 130% of RMT stimuli intensity OSAS patients were significantly different at 10AM from controls and with 150% of RMT intensity the difference did not reach significativity. PaCO2 was significantly correlated with CSP duration elicited at 10AM with 95%, 100% and 105% of RMT stimulus intensities.

Conclusions: We found alterations of motor cortical excitability in OSAS patients during the daytime. We believe that PaCO2 levels, acting probably on various ion channels or metabolic pathways, may change the excitability of motor cortex modifying excitatory and inhibitory cortical circuits.

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