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Motor cortex plasticity induced by theta burst stimulation is impaired in patients with obstructive sleep apnoea
Author(s) -
Opie George M.,
Catcheside Peter G.,
Usmani Zafar A.,
Ridding Michael C.,
Semmler John G.
Publication year - 2013
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.12203
Subject(s) - ctbs , neuroplasticity , transcranial magnetic stimulation , motor cortex , medicine , stimulation , neuroscience , cardiology , psychology , primary motor cortex , anesthesia
Obstructive sleep apnoea (OSA) is a respiratory condition occurring during sleep characterised by repeated collapse of the upper airway. Patients with OSA show altered brain structure and function that may manifest as impaired neuroplasticity. We assessed this hypothesis in 13 patients with moderate‐to‐severe OSA and 11 healthy control subjects. Transcranial magnetic stimulation was used to induce and measure neuroplastic changes in the motor cortex by assessing changes in motor‐evoked potentials (MEPs) in a hand muscle. Baseline measurements of cortical excitability included active (AMT) and resting motor thresholds (RMT), and the maximal stimulator output producing a 1‐mV MEP. Intracortical inhibition (ICI) was investigated with short‐ and long‐interval ICI paradigms (SICI and LICI, respectively), and neuroplastic changes were induced using continuous theta burst stimulation (cTBS). At baseline, differences were found between groups for RMT (9.5% maximal stimulator output higher in OSA) and 1‐mV MEPs (10.3% maximal stimulator output higher in OSA), but not AMT. No differences were found between groups for SICI or LICI. The response to cTBS was different between groups, with control subjects showing an expected reduction in MEP amplitude after cTBS, whereas the MEPs in patients with OSA did not change. The lack of response to cTBS suggests impaired long‐term depression‐like neuroplasticity in patients with OSA, which may be a consequence of sleep fragmentation or chronic blood gas disturbance in sleep. This reduced neuroplastic capacity may have implications for the learning, retention or consolidation of motor skills in patients with OSA.