Using stepwise analysis only SNiP was retained as an independent correlate (r2 0.72, p = 0.0009) ( Table 3 and Fig. 2). The acute effect of NIV was studied in six patients who were already established users of nocturnal home NIV. One subject declined to have further stimulations

after the end of the period on ventilation so post-NIV data was only available in 5 subjects. NIV significantly reduced the work of breathing with a decrease in diaphragm pressure time product from 269 ± 45 cm H2O s−1 min−1 to 34 ± 13 cm H2O s−1 min−1 (p = 0.003). End expiratory pressures at which stimulations were delivered did not differ significantly in the three periods ( Table 4). NIV was associated with a significant decrease in normalized selleck products amplitude of the diaphragm MEPTS (p = 0.02), but it did not alter motor threshold or MEP latency ( Table 5). NIV did not alter the excitability of intracortical inhibitory or facilitatory pathways assessed using paired stimulation. NIV was also not associated with significant changes in the amplitude of rectus abdominis MEPTS. The main findings of this study were firstly that the

excitability of corticospinal pathways to the respiratory muscles of patients with COPD who have been established on home NIV did not differ from those who do not require NIV. Secondly, the excitability of intracortical facilitatory and inhibitory circuits assessed using paired stimulation www.selleckchem.com/products/obeticholic-acid.html was strongly correlated with indices of disease severity, namely inspiratory muscle

strength and hypercapnia respectively. Finally, although the acute use of NIV in chronic users did reduce the excitability of the corticospinal pathway to the diaphragm it did not, in contrast to our findings in healthy subjects (Sharshar et al., 2004b), alter the excitability of intracortical inhibitory or facilitatory circuits. By studying an expanded cohort of patients we have been able to establish more clearly the relationship between cortical responses and pathophysiological parameters in patients with COPD. Specifically, Tideglusib decreased intracortical facilitation was most closely related to reduced inspiratory muscle strength while greater intracortical inhibition was associated with higher levels of PaCO2. This suggests that excitatory circuits are influenced predominantly by neuromechanical feedback and inhibitory ones by chemical inputs. It is interesting in this context to note that isocapnic non-invasive ventilation in healthy subjects had a greater effect on intracortical facilitation than on inhibition supporting a role for neuromechanical feedback as the principle driver for this adaptation (Sharshar et al., 2004b).