Continuous positive airway pressure treatment does not normalize the prolonged reflex inhibition to inspiratory loading in obstructive sleep apnea.

In obstructive sleep apnea (OSA), the short-latency inhibitory reflex (IR) of inspiratory muscles to airway occlusion is prolonged in proportion to the severity of the OSA. The mechanism underlying the prolongation may relate to chronic inspiratory muscle loading due to upper airway obstruction or sensory changes due to chronic OSA-mediated inflammation. Continuous positive airway pressure (CPAP) therapy prevents upper airway obstruction and reverses inflammation. We therefore tested whether CPAP therapy normalized the IR abnormality in OSA. The IR responses of scalene muscles to brief airway occlusion were measured in 37 adult participants with untreated, mostly severe, OSA, of whom 13 were restudied after the initiation of CPAP therapy (usage >4 h/night). Participants received CPAP treatment as standard clinical care, and the mean CPAP usage between initial and subsequent studies was 6.5 h/night (range 4.1-8.8 h/night) for a mean of 19 mo (range 4-41 mo). The duration of the IR in scalene muscles in response to brief (250 ms) inspiratory loading was confirmed to be prolonged in the participants with OSA. The IR was assessed before and after CPAP therapy. CPAP treatment did not normalize the prolonged duration of the IR to airway occlusion (60 ± 21 ms pretreatment vs. 59 ± 18 ms posttreatment, means ± SD) observed in participants with severe OSA. This suggests that the prolongation of IR reflects alterations in the reflex pathway that may be irreversible, or a specific disease trait.

Effect of airway inflammation on short-latency reflex inhibition to inspiratory loading in human scalene muscles.

The short-latency reflex inhibition of human inspiratory muscles produced by loading is prolonged in asthma and obstructive sleep apnoea, both diseases involving airway and systemic inflammation. Both diseases also involve repetitive inspiratory loading. Although airway mucosal afferents are not critical components of the normal reflex arc, during airway inflammation, prolongation of the reflex may be caused by altered mucosal afferent sensitivity, or altered central processing of their inputs. We hypothesised that acute viral airway inflammation would replicate the reflex abnormality. The reflex was tested in 9 subjects with a "common cold" during both the acute infection and when well. Surface electrodes recorded electromyographic (EMG) activity bilaterally from scalene muscles. Latencies of the inhibitory response (IR) did not differ significantly (IR peak 67 vs 70 ms (p=0.12), and IR offset 87 vs 90 ms (p=0.23), between the inflamed and well conditions, respectively). There was no difference in any measure of the size of the reflex inhibition.

Respiratory care of patients with cervical spinal cord injury: a review.

Respiratory complications following cervical spinal cord injury are common and are the leading cause of morbidity and mortality after this type of injury. Impaired mechanics of ventilation, poor cough, increased secretions and bronchospasm predispose to atelectasis, pneumonia and exacerbations of respiratory failure. Prolonged mechanical ventilation and tracheostomy are often required. This review discusses the relevant pathophysiology, various ventilatory strategies and timing of tracheostomy, and examines the evidence surrounding physiotherapeutic and pharmacological treatment options.

Differential effects of low-intensity motor cortical stimulation on the inspiratory activity in scalene muscles during voluntary and involuntary breathing.

To assess the cortical contribution to breathing, low-intensity transcranial magnetic stimulation (TMS) was delivered over the motor cortex in 10 subjects during: (i) voluntary static inspiratory efforts, (ii) hypocapnic voluntary ventilation (end-tidal CO(2), 2.7±0.4% mean±SD), and (iii) hypercapnic involuntary ventilation (end-tidal CO(2), 6.0±0.7%). Electromyographic activity (EMG) was recorded from the scalene muscles (obligatory inspiratory muscles) and was significantly suppressed by TMS at short latency (17.2±1.7ms). The scalene EMG was reduced to 76±8% and 76±7% in voluntary breathing and the static inspiratory effort, respectively, but only to 91±10% during the involuntary ventilation, significantly less than during the two voluntary tasks (p<0.005). Thus, with differences in chemical drive to breathe, TMS shows differences in the cortical contribution to inspiratory activity in scalene muscles. Voluntary breathing showed larger suppression than involuntary breathing, when the suppression was marginal. The results strongly suggest that drive from fast-conducting corticospinal neurones contributes to inspiratory activity in scalenes during voluntary breathing but is not required during involuntary breathing.

Reproducibility of the short-latency reflex inhibition to loading of human inspiratory muscles.

Loading of inspiratory muscles produces a profound short-latency inhibitory response (IR) of the electromyogram (EMG), followed by an excitatory response (ER). Duration of IR correlates positively with the apnoea hypopnoea index in obstructive sleep apnoea (OSA) patients, for whom measurement of this reflex may allow the assessment of a physiological response to therapy. To test the reliability of reflex measurement, we studied 11 human subjects on 4 separate days. Inspiration was transiently occluded during 2 sets of 30 trials on each day. Scalene muscle EMG was rectified and averaged. Ten parameters (4 latencies and 6 EMG sizes) were measured. Reproducibility was analysed by ANOVA, intraclass correlation coefficient (ICC) and coefficient of variation (CV). The mean ICC was 0.56 (range 0.30-0.76) and the mean CV was 25% (range 6.7-48%). These results show good measurement reliability. The abnormalities seen in disease are significantly larger than these CVs. The reflex response to airway occlusion may be assessed reliably using our method.