Disorders of the Nervous System
Aberrant cortical neuroplasticity in the OSA patient (Commentary on Opie et al.)
Version of Record online: 3 JUN 2013
© 2013 Federation of European Neuroscience Societies and John Wiley & Sons Ltd
European Journal of Neuroscience
Volume 37, Issue 11, page 1843, June 2013
How to Cite
McKenna, J. T., Kocsis, B. and McCarley, R. W. (2013), Aberrant cortical neuroplasticity in the OSA patient (Commentary on Opie et al.). European Journal of Neuroscience, 37: 1843. doi: 10.1111/ejn.12221
- Issue online: 3 JUN 2013
- Version of Record online: 3 JUN 2013
Opie et al. (2013) investigated cortical plasticity impairment in the obstructive sleep apnea (OSA) patient. They found OSA patients have both altered corticospinal excitability and, importantly, decreased long-term depression (LTD) in the motor cortex, induced by theta burst-patterned repetitive transcranial magnetic stimulation (rTMS). These exciting findings further elucidate the relationship between apnea and decreased motor skills, and may be extended to study other apnea-related cognitive complications.
As OSA causes suffering in millions and represents a high cost to society, it is imperative to understand the neurophysiological alterations mediating its behavioral and cardiovascular sequelae. Approximately 7% of the adult population has OSA, defined as abnormal repetitive cessation of breathing during sleep. Apneic moments occur as the airway is obstructed, leading to hypercapnia (increased carbon dioxide), hypoxia (decreased oxygen) and resulting sleep fragmentation as the airway is reestablished. In both animal models and humans, neuronal circuitry abnormalities due to apnea have been shown, as well as physiological consequences including cognitive and motor impairment, hypersomnia and metabolic and cardiovascular complications (Dempsey et al., 2010; Wang et al., 2010; Brown et al., 2012; Lal et al., 2012).
In this paper, the authors investigated the well-established link between apnea and fine motor skill deficits (Beebe et al., 2003). Baseline motor cortex excitability was first evaluated. Motor evoked potential thresholds were elevated, compared to a non-apneic control group, reflecting abnormal corticospinal excitability. The authors then used a specific rTMS protocol to produce LTD in the motor cortex. Previous work in healthy subjects (Huang et al., 2005) showed that short bursts of stimuli (three pulses at 50 Hz intraburst frequency) repeated at theta frequency, i.e. at 5 Hz, induced long-term potentiation when applied in an intermittent pattern or LTD when applied continuously for 40 s, termed continuous theta-burst stimulation (cTBS). Opie et al. (2013) thus applied cTBS to a particular subregion of the motor cortex, shown previously to innervate hand muscles, and in which motor evoked potentials were suppressed in healthy subjects, therefore demonstrating cTBS-induced LTD. Apneic patients, though, showed an abnormal response to cTBS, for motor evoked potentials were not attenuated. The authors ruled out the possibility that intracortical inhibition played a role in the observed impairment, and concluded that the impaired baseline threshold level for evoked motor potentials, as well as the observed LTD impairment, reflected impaired neuroplasticity in the motor cortex.
This exciting and novel investigation by Opie et al. (2013) is the first to use TMS to evaluate cortical neuroplasticity in OSA patients. Although more investigations are needed to describe the mechanism by which cortical neuroplastic changes are induced by cTBS protocols, the results of this study may facilitate OSA treatment. At present, few treatments are available to improve the attentional, mnemonic and/or motor deficits seen in apnea, beyond continuous positive airway pressure (CPAP) treatment. Cortical plasticity in the motor cortex could be evaluated following pharmacological, surgical and/or CPAP treatment, to gauge efficacy of treatment. In future studies, other TMS stimulation protocols may also be applied, such as those that induce long-term potentiation, and alternative cortical regions may also be explored. Of particular interest, a recent investigation in healthy subjects described similar inhibitory cTBS effects on neuroplasticity in the prefrontal cortex (Tupak et al., 2013), an area that may also be affected in apnea and involved in attentional and memory mechanisms. In summary, this paper provides a promising first step in what could be an expansive field of research investigating cortical plasticity in the apneic patient.
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