M I Polkey

Acute ischaemic hemispheric stroke is associated with impairment of reflex in addition to voluntary cough

Cough function is impaired after stroke; this may be important for protection against chest infection. Reflex cough (RC) intensity indices have not been described after stroke. RC, voluntary cough (VC) and respiratory muscle strength were studied in patients within 2 weeks of hemispheric infarct. The null hypotheses were that patients with cortical hemisphere stroke would show the same results as healthy controls on: 1) objective indices of RC and VC intensity; and 2) respiratory muscle strength tests. Peak cough flow rate (PCFR) and gastric pressure (Pga) were measured during maximum VC and RC. Participants also underwent volitional and nonvolitional respiratory muscle testing. Nonvolitional expiratory muscle strength was assessed by measuring Pga increase after magnetic stimulation over the T10 nerve roots (twitch T10 Pga). Stroke severity was scored using the National Institutes of Health Stroke Scale (NIHSS; maximum = 31). 18 patients (mean±sd age 62±15 yrs and NIHSS score 14±8) and 20 controls (56±16 yrs) participated. VC intensity was impaired in patients (PCFR 287±171 versus 497±122 L·min−1) as was VC Pga (98.5±61.6 versus 208.5±61.3 cmH2O; p<0.001 for both). RC PCFR was reduced in patients (204±111 versus 379±110 L·min−1; p<0.001), but RC Pga was not significantly different from that of controls (179.0±78.0 versus 208.0±77.4 cmH2O; p = 0.266). Patients exhibited impaired volitional respiratory muscle tests, but twitch T10 Pga was normal. VC and RC are both impaired in hemispheric stroke patients, despite preserved expiratory muscle strength. Cough coordination is probably cortically modulated and affected by hemispheric stroke.

Transcranial magnetic stimulation study of expiratory muscle weakness in acute ischemic stroke

Background: Expiratory muscle weakness due to cerebral infarction may contribute to reduced airway clearance in stroke patients. Methods: Transcranial magnetic stimulation (TMS) at the vertex and over each hemisphere and magnetic stimulation over the T10-11 spinal roots (Tw T10) and the phrenic nerves bilaterally (BAMPS) were performed in 15 acute ischemic stroke patients (age 68.9 ± 9.8 years) and 16 matched controls. Surface electrodes recorded motor evoked potentials (MEPs) in the rectus abdominis (RA) and external oblique (EO) muscles bilaterally. Respiratory muscle function was assessed by measuring maximum static expiratory pressure (PEmax) and changes in intragastric (Pgas) and transdiaphragmatic (Pdi) pressure after voluntary cough, TMS, TwT10, and BAMPS. Regression models were used to assess determinants of peak voluntary cough flow rates (PCFR). Results: PCFR, cough Pgas, and vertex TMS Pgas were decreased in stroke patients compared with controls (203.6 ± 151.1 vs 350.8 ± 111.7 L/min, p = 0.004; 72.7 ± 64.5 vs 163.4 ± 55.8 cm H2O, p = 0.0003 and 8.7 ± 3.3 vs 16.7 ± 11.5 cm H2O, p = 0.023, respectively). There were no differences in TwT10 Pgas (25.2 ± 7.8 vs 29.4 ± 12.4 cm H2O, p = 0.153) or BAMPS Pdi (21.6 ± 7.2 vs 19.2 ± 3.4 cm H2O, p = 0.163). TMS Pgas was lower (4.1 ± 2.8 vs 6.1 ± 1.9 cm H2O, p = 0.023) following TMS of the injured compared with the uninjured hemisphere in stroke patients. Age and gender adjusted PCFR correlated with Pgas (r = 0.51, p = 0.009) and PEmax (r = 0.46, p = 0.024). Stroke was an independent determinant of PCFR after adjusting for Pgas and PEmax (p = 0.031). Conclusion: Ischemic cortical injury is associated with expiratory muscle weakness and may contribute to cough impairment in stroke patients. BAMPS = bilateral anterolateral magnetic phrenic stimulation; EO = external oblique; MEP = motor evoked potential; NIHSS = NIH Stroke Scale; Pdi = transdiaphragmatic pressure; Pes = esophageal pressure; Pgas = intragastric pressure; PCFR = peak voluntary cough flow rates; PEmax = maximum static expiratory pressure; POE = point of optimal excitability; RA = rectus abdominis; TMS = transcranial magnetic stimulation.

Improvement in volitional tests of muscle function alone may not be adequate evidence that inspiratory muscle training is effective

In 1976 Leith and Bradley 1 generated the hypothesis that the inspiratory muscles, like other muscles, could be trained. In the now classic study 12 healthy adults were divided into three groups of four. One group underwent strength testing, consisting of maximal voluntary efforts against a closed airway over a range of lung volumes for 30u2005min per day for 5 days a week for 5 weeks. The second group performed voluntary hyperventilation for a similar period and the third group served as controls. They found that subjects undergoing strength training increased strength by 55% while endurance trainers experienced a 15–19% increase in the time that they could sustain maximal and submaximal ventilation. Only minor improvements were seen in control subjects. Since the seminal observations of Leith and Bradley 1 numerous investigators (a PubMed search with the term respiratory muscle training yielded over 1500 citations in September 2003) have explored the field, yet theclinical role of inspiratory muscle training remains controversial.nnIn high income countries chronic obstructive pulmonary disease (COPD) is the most …

Screening for sleep-disordered breathing in neuromuscular disease using a questionnaire for symptoms associated with diaphragm paralysis

Patients with neuromuscular disease (NMD) are at risk of developing sleep-disordered breathing (SDB) following respiratory muscle involvement. We hypothesised that a questionnaire based on clinical symptoms and signs of diaphragm weakness can be used to screen for SDB in such patients. We developed a self-administered multiple choice questionnaire containing five questions (Sleep-Disordered Breathing in Neuromuscular Disease Questionnaire (SiNQ)-5), scoring 0–10 points. 125 patients were enrolled: 32 with respiratory muscle weakness, 35 subjects with normal respiratory muscle strength and 58 patients with obstructive sleep apnoea (OSA). All subjects underwent full polysomnography. NMD patients with involvement of the respiratory muscles scored mean±sd 6.8±2.3 out of 10 points, significantly higher than both OSA patients 2.5±2.3 and normal subjects 1.0±2.0 (p<0.001). A score of five or more points in the SiNQ-5 had a sensitivity of 86.2%, specificity of 88.5%, positive predictive value of 69.4% and a negative predictive value of 95.5% to identify NMD with combined SDB. A short self-administered questionnaire, the SiNQ-5, based on clinical symptoms can reliably screen for SDB in patients with diaphragm weakness. However, comorbidities, such as heart failure, that have symptoms influenced by posture could alter diagnostic accuracy.

Diaphragm electromyograms recorded from multiple surface electrodes following magnetic stimulation

The diaphragm compound-muscle action potential (CMAPdi), elicited by unilateral magnetic stimulation (UMS) of the phrenic nerve can be recorded using surface electrodes. However, there is no consensus on the best positioning of surface electrodes and there are no data on the reproducibility of the signal. Using 36 surface electrode pairs, in five healthy subjects, the CMAPdi elicited by UMS and electrical stimulation (ES) were compared and 12 pairs were identified as providing acceptable signals. The latency and amplitude were measured for each CMAPdi, following UMS at 60–100% of maximal stimulator output, in 12 healthy subjects, on two occasions. Latencies obtained using UMS and ES ranged between 6.1–7.33 and 6.25–7.17u2005ms, respectively. Optimum CMAPdi were not recorded from the same electrode pair in all subjects, or for both hemidiaphragms in each subject. However, the optimal recording site for a particular individual remained unchanged on subsequent testing. When recorded from the optimal site, latencies and amplitudes of CMAPdi elicited on the two occasions were not significantly different. The current study suggests that the use of multiple chest wall electrodes can identify an optimal electrode pair, from which it is possible to obtain reproducible compound-muscle action potential signals.

Effect of brachial plexus co-activation on phrenic nerve conduction time

BACKGROUND Diaphragm function can be assessed by electromyography of the diaphragm during electrical phrenic nerve stimulation (ES). Whether phrenic nerve conduction time (PNCT) and diaphragm electrical activity can be reliably measured from chest wall electrodes with ES is uncertain. METHODS The diaphragm compound muscle action potential (CMAP) was recorded using an oesophageal electrode and lower chest wall electrodes during ES in six normal subjects. Two patients with bilateral diaphragm paralysis were also studied. Stimulations were deliberately given in a manner designed to avoid or incur co-activation of the brachial plexus. RESULTS For the oesophageal electrode the PNCT was similar with both stimulation techniques with mean (SE) values of 7.1 (0.2) and 6.8 (0.2)u2009ms, respectively (pooled left and right values). However, for surface electrodes the PNCT was substantially shorter when the brachial plexus was activated (4.4 (0.1)u2009ms) than when it was not (7.4 (0.2)u2009ms) (mean difference 3.0u2009ms, 95% CI 2.7 to 3.4, p<0.0001). A small short latency CMAP was recorded from the lower chest wall electrodes during stimulation of the brachial plexus alone. CONCLUSIONS The results of this study show that lower chest wall electrodes only accurately measure PNCT when care is taken to avoid stimulating the brachial plexus. A false positive CMAP response to phrenic stimulation could be caused by inadvertent stimulation of the brachial plexus. This finding may further explain why the diaphragm CMAP recorded from chest wall electrodes can be unreliable with cervical magnetic stimulation during which brachial plexus activation occurs.

The case against inspiratory muscle training in COPD

Despite maximal medical therapy, many chronic obstructive pulmonary disease (COPD) patients remain breathless and this has led to persistent and commendable efforts to reduce symptoms and improve exercise performance using nonpharmacological approaches; some of these, for example pulmonary rehabilitation (PR) 1, comprising general exercise and fitness training, are of proven benefit, while others remain controversial.nnInspiratory muscle training (IMT), being cheap and free of side-effects, is intuitively attractive, since improving the capacity of the inspiratory muscles should “make breathing easier” and so improve exercise performance. Enthusiasts do not allow the superficial attractiveness of this proposition to be clouded by aspects of the data. These are that the diaphragm is already working hard and well trained in emphysema, with a shift towards fatigue resistant type I fibres 2, that at a single fibre level it is energetically more efficient 3, that (allowing for hyperinflation) it is not actually weak 4, 5 and that diaphragm fatigue cannot be elicited in patients in vivo 6, 7, even when patients are sufficiently ill to require mechanical ventilation 8. The question of whether the respiratory muscles are weak in COPD seems particularly important in the context of IMT. In the current issue of the European Respiratory Journal , Gosselink et al. 9 cite our paper 5 as evidence that the diaphragm is weak; in fact, we concluded that the major reason for the reduced transdiaphragmatic pressures observed in COPD was hyperinflation, which of course would not be expected to improve with IMT. They also state that inspiratory …

Effect of pattern and severity of respiratory muscle weakness on carbon monoxide gas transfer and lung volumes

In clinical practice, an elevated carbon monoxide (CO) transfer coefficient (KCO) and restrictive ventilatory defect are taken as features of respiratory muscle weakness (RMW). However, the authors hypothesised that both pattern and severity of RMW effect gas transfer and lung volumes. Measurements of CO transfer and lung volumes were performed in patients with isolated diaphragm weakness (n=10), inspiratory muscle weakness (n=12), combined inspiratory and expiratory muscle weakness (n=5) and healthy controls (n=6). Patients with diaphragm weakness and inspiratory muscle weakness had reduced total lung capacity (TLC) (83.6% predicted and 68.9% pred, respectively), functional residual capacity (FRC) (83.9% pred and 83.6% pred) and transfer factor of the lung for CO (TL,CO) (86.2% pred and 66.2% pred) with increased KCO (114.1% pred and 130.2% pred). Patients with combined inspiratory and expiratory muscle weakness had reduced TLC (80.9% pred) but increased FRC (109.9% pred) and RV (157.4% pred) with decreased TL,CO (58.0% pred) and KCO (85.5% pred). In patients with diaphragm weakness, the increase in carbon monoxide transfer coefficient was similar to that of normal subjects when alveolar volume was reduced. However, the increase in carbon monoxide transfer coefficient in inspiratory muscle weakness was often less than expected, while in combined inspiratory and expiratory muscle weakness, the carbon monoxide transfer coefficient was normal/reduced despite further reductions in alveolar volume, which may indicate subtle abnormalities of the lung parenchyma or pulmonary vasculature. Thus, this study demonstrates the limitations of using carbon monoxide transfer coefficient in the diagnosis of respiratory muscle weakness, particularly if no account is taken of the alveolar volume at which the carbon monoxide transfer coefficient is made.

Diaphragm compound muscle action potential measured with magnetic stimulation and chest wall surface electrodes

To seek a method to reliably measure phrenic nerve conduction time (PNCT) with magnetic stimulation we investigated two stimulus sites, placing the magnetic coil at the cricoid cartilage (high position) or close to the clavicle (low position). We also compared compound muscle action potential (CMAP) recorded from three different sites: in the sixth to eighth intercostal spaces in the anterior axillary line (Ant-a); in the 8th intercostal space close to the midclavicular line; and with one electrode at the lower sternum and the other at the costal margin. Fourteen normal subjects were studied. The PNCT measured by magnetic stimulation in the high position recorded from (Ant-a) was 7.6+/-0.6 on the left side and 8.4+/-0.7 on the right. The PNCT recorded from all three sites become much shorter when the magnetic coil was moved from the high to the low position. Our results show that PNCT can be accurately measured with magnetic stimulation when care is taken to avoid coactivation of the brachial plexus.

Neural drive during continuous positive airway pressure (CPAP) and pressure relief CPAP

BACKGROUNDnPressure release continuous positive airway pressure (CPAP) is an evolution of CPAP that has been reported to improve patient comfort. We hypothesised the pressure release would lead to unloading of the inspiratory muscles and therefore conducted a prospective double-blind cross-over physiological study of autotitrating CPAP (APAP) against autotitrating pressure relief CPAP (PR-APAP).nnnMETHODSnEleven patients with severe obstructive sleep apnoea (OSA; mean AHI 74.5+/-14.4/h) were studied. We assessed neural drive by recording the oesophageal pressure, gastric pressure, transdiaphragmatic pressure and the diaphragm EMG during overnight polysomnography.nnnRESULTSnBoth APAP and PR-APAP significantly reduced neural respiratory drive. Transdiaphragmatic pressure swings during apnoea (30.2+/-11.5 cm H2O) before treatment decreased to 9.1+/-5.3 cm H2O for PR-APAP and 8.5+/-3.7 cm H2O for APAP. The transdiaphragmatic pressure and the diaphragm EMG did not differ significantly between APAP and PR-APAP. The gastric pressure swing at expiration phase disappeared during both APAP and PR-APAP when sleep respiratory events were eliminated.nnnCONCLUSIONSnPR-APAP is not superior to APAP in terms of reducing neural respiratory drive. It is unnecessary to replace conventional APAP with PR-APAP for patients who have been successfully treated with traditional APAP.