Imperial College London

ProfessorMichaelPolkey

Faculty of MedicineNational Heart & Lung Institute

Professor of Respiratory Medicine
 
 
 
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Contact

 

+44 (0)20 7351 8029m.polkey

 
 
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Location

 

Respiratory MuscRoyal BromptonRoyal Brompton Campus

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Summary

 

Publications

Publication Type
Year
to

652 results found

Boutou AK, Raste Y, Demeyer H, Troosters T, Polkey M, Vogiatzis I, Louvaris Z, Rabinovich RA, van der Molen T, Garcia-Aymerich J, Hopkinson Net al., 2019, Progression of physical inactivity in COPD patients: the effect of time and climate conditions – a multicentre prospective cohort study, International Journal of COPD, Vol: 14, Pages: 1979-1992, ISSN: 1176-9106

Purpose: Longitudinal data on the effect of time and environmental conditions on physical activity (PA) among COPD patients are currently scarce, but this is an important factor in the design of trials to test interventions that might impact on it. Thus, we aimed to assess the effect of time and climate conditions (temperature, day length and rainfall) on progression of PA in a cohort of COPD patients.Patients and methods: This is a prospective, multicentre, cohort study undertaken as part of the EU/IMI PROactive project, in which we assessed 236 COPD patients simultaneously wearing two activity monitors (Dynaport MiniMod and Actigraph GT3X). A multivariable generalised linear model analysis was conducted to describe the effect of the explanatory variables on PA measures, over three time points (baseline, 6- and 12-month). Results: At 12 months (n=157; Forced Expiratory Volume in 1 second (FEV1) %predicted=57.7±21.9) there was a significant reduction in all PA measures (Actigraph step count (4284±3533 vs. 3533±293), Actigraph moderate- to vigorous-intensity physical activity ratio (8.8 (18.8) vs. 6.1(15.7)), Actigraph vector magnitude units (374902.4 (265269) vs. 336240 (214432)), Minimod walking time (59.1(34.9) vs. 56.9(38.7) minutes) and Minimod PA intensity (0.183(0) vs. 0.181(0)). Time had a significant, negative effect on most PA measures in multivariable analysis, after correcting for climate factors, study centre, age, FEV1 %predicted, 6 Minute Walking Distance and other disease severity measures. Rainfall was the only climate factor with a negative effect on most PA parameters. Conclusions:COPD patients demonstrate a significant decrease in physical activity over 1 year follow up, which is further affected by hours of rainfall, but not by other climate considerations.

Journal article

Patel M, McKie E, Steiner M, Pascoe S, Polkey Met al., 2019, Anaemia and iron dysregulation: untapped therapeutic targets in chronic lung disease?, BMJ Open Respiratory Research, Vol: 6, ISSN: 2052-4439

Hypoxia is common in many chronic lung diseases. Beyond pulmonary considerations, delivery of oxygen (O2)to the tissues and subsequent O2 utilisation is also determined by other factors including red blood cell massand iron status; consequently disruption to these mechanisms provides further physiological strains on analready stressed system. O2 availability influences ventilation, regulates pulmonary blood flow and impactsgene expression throughout the body. Deleterious effects of poor tissue oxygenation include decreasedexercise tolerance, increased cardiac strain and pulmonary hypertension in addition to pathophysiologicalinvolvement of multiple other organs resulting in progressive frailty. Increasing inspired O2 is expensive,disliked by patients and does not normalise tissue oxygenation; thus other strategies that improve O2 deliveryand utilisation may provide a novel therapeutic opportunity in patients with lung disease. In this review, wefocus on the rationale and possibilities for doing this by increasing haemoglobin availability or improving ironregulation.

Journal article

Elbehairy A, Quint J, Rogers J, Laffan M, Polkey M, Hopkinson Net al., 2019, Prevalence of breathlessness and associated consulting behaviour: results of an online survey, Thorax, Vol: 74, Pages: 814-817, ISSN: 1468-3296

The online British Lung Foundation Breath Test provides an opportunity to study the relationship between breathlessness, common sociobehavioural risk factors and interaction with healthcare. We analysed data from 356 799 responders: 71% were ≥50 years old and 18% were smokers. 20% reported limiting breathlessness (Medical Research Council breathlessness score ≥3), and the majority of these (85%) worried about their breathing; of these, 29% had not sought medical advice. Of those who had, 58% reported that the advice received had not helped their breathlessness. Limiting breathlessness was associated with being older, physically inactive, smoking and a higher body mass index. These data suggest a considerable unmet need associated with breathlessness as well as possibilities for intervention.

Journal article

Ciano M, Mantellato G, Connolly M, Paul-Clark M, Mitchell J, Wilson-Owen S, Cookson W, Moffatt M, Hughes S, Polkey M, Kemp P, Natanek Set al., EGF receptor (EGFR) inhibition promotes a slow-twitch oxidative, over a fast-twitch, muscle phenotype, Scientific Reports, ISSN: 2045-2322

A low quadriceps slow-twitch (ST), oxidative (relative to fast-twitch) fiber proportion is prevalent in chronic diseases such Chronic Obstructive Pulmonary Disease (COPD) and is associated with exercise limitation and poor outcomes. Benefits of an increased ST fiber proportion are demonstrated in genetically modified animals. Pathway analysis of published data of differentially expressed genes in mouse ST and FT fibers, mining of our microarray data and a qPCR analysis of quadriceps specimens from COPD patients and controls were performed. ST markers were quantified in C2C12 myotubes with EGF-neutralizing antibody, EGFR inhibitor or an EGFR-silencing RNA added. A zebrafish egfra mutant was generated by genome editing and ST fibers counted. EGF signaling was (negatively) associated with the ST muscle phenotype in mice and humans, and muscle EGF transcript levels were raised in COPD. In C2C12 myotubes, EGFR inhibition/silencing increased ST, including mitochondrial, markers. In zebrafish, egfra depletion increased ST fibers and mitochondrial content. EGF is negatively associated with ST muscle phenotype in mice, healthy humans and COPD patients. EGFR blockade promotes the ST phenotype in myotubes and zebrafish embryos. EGF signaling suppresses the ST phenotype, therefore EGFR inhibitors may be potential treatments for COPD-related muscle ST fiber loss.

Journal article

Kwan HY, Maddocks M, Nolan CM, Jones SE, Patel S, Barker RE, Kon SSC, Polkey MI, Cullinan P, Man WD-Cet al., 2019, The prognostic significance of weight loss in chronic obstructive pulmonary disease-related cachexia: a prospective cohort study., Journal of Cachexia, Sarcopenia and Muscle, Pages: 1-9, ISSN: 2190-6009

BACKGROUND: Cachexia is an important extra-pulmonary manifestation of chronic obstructive pulmonary disease (COPD) presenting as unintentional weight loss and altered body composition. Previous studies have focused on the relative importance of body composition compared with body mass rather than the relative importance of dynamic compared with static measures. We aimed to determine the prevalence of cachexia and pre-cachexia phenotypes in COPD and examine the associations between cachexia and its component features with all-cause mortality. METHODS: We enrolled 1755 consecutive outpatients with stable COPD from two London centres between 2012 and 2017, stratified according to European Respiratory Society Task Force defined cachexia [unintentional weight loss >5% and low fat-free mass index (FFMI)], pre-cachexia (weight loss >5% but preserved FFMI), or no cachexia. The primary outcome was all-cause mortality. We calculated hazard ratios (HRs) using Cox proportional hazards regression for cachexia classifications (cachexia, pre-cachexia, and no cachexia) and component features (weight loss and FFMI) and mortality, adjusting for age, sex, body mass index, and disease-specific prognostic markers. RESULTS: The prevalence of cachexia was 4.6% [95% confidence interval (CI): 3.6-5.6] and pre-cachexia 1.6% (95% CI: 1.0-2.2). Prevalence was similar across sexes but increased with worsening Global Initiative for Chronic Obstructive Pulmonary Disease spirometric stage and Medical Research Council dyspnoea score (all P < 0.001). There were 313 (17.8%) deaths over a median (interquartile range) follow-up duration 1089 (547-1704) days. Both cachexia [HR 1.98 (95% CI: 1.31-2.99), P = 0.002] and pre-cachexia [HR 2.79 (95% CI: 1.48-5.29), P = 0.001] were associated with increased mortality. In multivariable analysis, the unintentional weight loss feature of cachexia was independently associated with mortality [HR 2.16 (95% CI: 1.31-3.08), P&nbs

Journal article

Polkey M, 2019, Respiratory Muscle Assessment in Clinical Practice, CLINICS IN CHEST MEDICINE, Vol: 40, Pages: 307-+, ISSN: 0272-5231

Journal article

Farre-Garros R, Lee J, Natanek S, Connolly M, Sayer A, Patel H, Cooper C, Polkey M, Kemp Pet al., 2019, Quadriceps miR-542-3p and 5p are elevated in COPD and reduce function by inhibiting ribosomal and protein synthesis, Journal of Applied Physiology, Vol: 126, Pages: 1514-1524, ISSN: 8750-7587

Reduced physical performance reduces quality of life in patients with COPD. Impaired physical performance is, in part, a consequence of reduced muscle mass and function, which is accompanied by mitochondrial dysfunction. We recently showed that miR-542-3p and miR-542-5p were elevated in a small cohort of COPD patients and more markedly in critical care patients. In mice these miRNAs promoted mitochondrial dysfunction suggesting that they would affect physical performance in patients with COPD but we did not explore the association of these miRNAs with disease severity or physical performance further. We therefore quantified miR-542-3p/5p and mitochondrial rRNA expression in RNA extracted from quadriceps muscle of patients with COPD and determined their association with physical performance. As miR-542-3p inhibits ribosomal protein synthesis its ability to inhibit protein synthesis was also determined in vitro.Both miR-542-3p and -5p expression were elevated in patients with COPD (5-fold p<0.001) and the degree of elevation associated with impaired lung function (TLCO% and FEV1%) and physical performance (6-minute walk distance %). In COPD patients, the ratio of 12S rRNA to 16S rRNA was suppressed suggesting mitochondrial ribosomal stress and mitochondrial dysfunction and miR-542-3p/5p expression was inversely associated with mitochondrial gene expression and positively associated with p53 activity. miR-542-3p suppressed RPS23 expression and maximal protein synthesis in vitro. Our data show that miR-542-3p and -5p expression is elevated in COPD patients and may suppress physical performance at least in part by inhibiting mitochondrial and cytoplasmic ribosome synthesis and suppressing protein synthesis.

Journal article

Laveneziana P, Albuquerque A, Aliverti A, Babb T, Barreiro E, Dres M, Dube B-P, Fauroux B, Gea J, Guenette JA, Hudson AL, Kabitz H-J, Laghi F, Langer D, Luo Y-M, Neder JA, O'Donnell D, Polkey M, Rabinovich RA, Rossi A, Series F, Similowski T, Spengler C, Vogiatzis I, Verges Set al., 2019, ERS statement on respiratory muscle testing at rest and during exercise, EUROPEAN RESPIRATORY JOURNAL, Vol: 53, ISSN: 0903-1936

Journal article

Liew F, Gargoum F, Potter R, Rosen SD, Ward S, Hind M, Polkey MIet al., 2019, Platypnoea-orthodeoxia syndrome: beware of investigations undertaken supine, Thorax, ISSN: 1468-3296

Platypnoea-orthodeoxia syndrome (POS) is a rare disorder, manifesting as deoxygenation occurring when the patient is in the upright position. Four broad mechanisms for the condition have been described: intracardiac shunts, intrapulmonary shunts, hepatopulmonary syndrome and pulmonary ventilation-perfusion mismatch. Here, we present the first case of POS in a patient with a proven right to left intracardiac shunt occurring in the context of postural hypotension and normal right heart pressures. We highlight the need to carry out investigations in the upright position before discounting intracardiac shunting as a cause for the syndrome. Short-term improvement of the syndrome was obtained with medical management of the patient's orthostatic hypotension and as such suggests a conservative management strategy for similar patients, which may delay the need for invasive procedures to close the anatomical defect.

Journal article

Sharanya A, Ciano M, Withana S, Polkey M, Kemp P, Natanek Set al., 2019, Sex differences in COPD-related quadriceps muscle dysfunction and fibre abnormalities, Chronic Respiratory Disease, Vol: 16, Pages: 1-13, ISSN: 1479-9723

Background: In COPD, lower limb dysfunction is associated with reduced exercise capacity, increased hospitalisations and mortality. We investigated sex differences in the prevalence of quadriceps dysfunction and fibre abnormalities in a large COPD cohort, controlling for the normal sex differences in health. Methods: We compared existing data from 76 male and 38 female COPD patients where each variable was expressed as a function of gender-specific normal values (obtained from 16 male and 14 female controls). Results: Female COPD patients had lower quadriceps muscle strength and peak workload on a maximal incremental cycle ergometry protocol compared to male patients. Female patients had a smaller type II fibre cross-sectional area (CSA) compared to male patients, suggesting a greater female preponderance to fibre atrophy, although this result was largely driven by a few male patients with increased type II fibre CSA. Female patients had significantly higher concentrations of a number of plasma pro-inflammatory cytokines including tumor necrosis factor alpha (TNFα) and interleukin 8 (IL8), but not lower levels of physical activity or arterial oxygenation, compared to males. Conclusions: Our data confirms results from a previous small study and suggests that female COPD patients have a greater prevalence of muscle wasting and weakness. Larger studies investigating sex differences in COPD-related muscle atrophy and weakness are needed, as the results will have implications for monitoring in clinical practice and for design of clinical trials evaluating novel muscle anabolic agents.

Journal article

Kemp P, Griffiths M, Polkey M, 2019, Muscle wasting in the presence of disease, why is it so variable?, Biological Reviews, Vol: 94, Pages: 1038-105, ISSN: 1464-7931

Skeletal muscle wasting is a common clinical feature of many chronic diseases and also occurs in response to single acute events. The accompanying loss of strength can lead to significant disability, increased care needs and have profound negative effects on quality of life. As muscle is the most abundant source of amino acids in the body, it appears to function as a buffer for fuel and substrates that can be used to repair damage elsewhere and to feed the immune system. In essence, the fundamentals of muscle wasting are simple: less muscle is made than is broken down. However, although well‐described mechanisms modulate muscle protein turnover, significant individual differences in the amount of muscle lost in the presence of a given severity of disease complicate the understanding of underlying mechanisms and suggest that individuals have different sensitivities to signals for muscle loss. Furthermore, the rate at which muscle protein is turned over under normal conditions means that clinically significant muscle loss can occur with changes in the rate of protein synthesis and/or breakdown that are too small to be measurable. Consequently, the changes in expression of factors regulating muscle turnover required to cause a decline in muscle mass are small and, except in cases of rapid wasting, there is no consistent pattern of change in the expression of factors that regulate muscle mass. MicroRNAs are fine tuners of cell phenotype and are therefore ideally suited to cause the subtle changes in proteome required to tilt the balance between synthesis and degradation in a way that causes clinically significant wasting. Herein we present a model in which muscle loss as a consequence of disease in non‐muscle tissue is modulated by a set of microRNAs, the muscle expression of which is associated with severity of disease in the non‐muscle tissue. These microRNAs alter fundamental biological processes including the synthesis of ribosomes and mitochondria leading to reduce

Journal article

Fermont JM, Masconi KL, Jensen MT, Ferrari R, Di Lorenzo VAP, Marott JM, Schuetz P, Watz H, Waschki B, Mullerova H, Polkey MI, Wilkinson IB, Wood AMet al., 2019, Biomarkers and clinical outcomes in COPD: a systematic review and meta-analysis, THORAX, Vol: 74, Pages: 439-446, ISSN: 0040-6376

Journal article

Garfield B, Crosby A, Shao D, Yang P, Read C, Sawaik S, Moore S, Parfitt L, Harries C, Rice M, Paul R, Ormiston M, Morrell N, Polkey M, Wort SJ, Kemp Pet al., 2019, Growth/differentiation factor 15 causes TGFβ activated kinase 1 dependent muscle atrophy in pulmonary arterial hypertension, Thorax, Vol: 74, Pages: 164-176, ISSN: 1468-3296

Introduction Skeletal muscle dysfunction is a clinically important complication of pulmonary arterial hypertension (PAH). Growth/differentiation factor 15 (GDF-15), a prognostic marker in PAH, has been associated with muscle loss in other conditions. We aimed to define the associations of GDF-15 and muscle wasting in PAH, to assess its utility as a biomarker of muscle loss and to investigate its downstream signalling pathway as a therapeutic target.Methods GDF-15 levels and measures of muscle size and strength were analysed in the monocrotaline (MCT) rat, Sugen/hypoxia mouse and in 30 patients with PAH. In C2C12 myotubes the downstream targets of GDF-15 were identified. The pathway elucidated was then antagonised in vivo.Results Circulating GDF-15 levels correlated with tibialis anterior (TA) muscle fibre diameter in the MCT rat (Pearson r=−0.61, p=0.003). In patients with PAH, plasma GDF-15 levels of <564 pg/L predicted those with preserved muscle strength with a sensitivity and specificity of ≥80%. In vitro GDF-15 stimulated an increase in phosphorylation of TGFβ-activated kinase 1 (TAK1). Antagonising TAK1, with 5(Z)-7-oxozeaenol, in vitro and in vivo led to an increase in fibre diameter and a reduction in mRNA expression of atrogin-1 in both C2C12 cells and in the TA of animals who continued to grow. Circulating GDF-15 levels were also reduced in those animals which responded to treatment.Conclusions Circulating GDF-15 is a biomarker of muscle loss in PAH that is responsive to treatment. TAK1 inhibition shows promise as a method by which muscle atrophy may be directly prevented in PAH.

Journal article

Polkey MI, Praestgaard J, Berwick A, Franssen FME, Singh D, Steiner MC, Casaburi R, Tillmann H-C, Lach-Trifilieff E, Roubenoff R, Rooks DSet al., 2019, Activin type II receptor blockade for treatment of muscle depletion in COPD: a randomized trial, American Journal of Respiratory and Critical Care Medicine, Vol: 199, ISSN: 1073-449X

RATIONALE: Bimagrumab is a fully human monoclonal antibody that blocks the activin type II receptors, preventing the activity of myostatin and other negative skeletal muscle regulators. OBJECTIVES: To assess the effects of bimagrumab on skeletal muscle mass and function in patients with COPD and reduced skeletal muscle mass. METHODS: Sixty-seven COPD patients (mean FEV1 1.05 L [41.6% predicted]; aged 40-80 years; body mass index <20 kg/m2 or appendicular skeletal muscle mass index ≤7.25 [men] and ≤5.67 [women] kg/m2), received two doses of either bimagrumab 30 mg/kg intravenously (n=33) or placebo (n=34) (Weeks 0 and 8) over 24 weeks. MEASUREMENTS AND MAIN RESULTS: We assessed changes in thigh muscle volume (TMV, cm3) as the primary endpoint along with 6-minute walk distance (6MWD, m), safety, and tolerability. Fifty-five (82.1%) patients completed the study. TMV increased by Week 4 and remained increased at Week 24 in bimagrumab-treated patients, whereas no changes were observed with placebo (Week 4: +5.9% [3.4%, SD] vs. 0.0% [3.3%], P<0.001; Week 8: +7.0% [3.7%] vs. -0.7% [2.8%], P<0.001; Week 16: +7.8% [5.1%] vs. -0.9% [4.5%], P<0.001; Week 24: +5.0% [4.9%] vs. -1.3% [4.3%], P<0.001). Over 24 weeks, 6MWD did not increase significantly in either group. Adverse events in bimagrumab group included muscle-related symptoms, diarrhea, and acne, most of which were mild in severity. CONCLUSIONS: Blocking the action of negative muscle regulators through the activin type II receptors with bimagrumab treatment safely increased skeletal muscle mass but did not improve functional capacity in patients with COPD and low muscle mass. Clinical trial registration available at www.clinicaltrials.gov, ID NCT01669174.

Journal article

Alqurashi Y, Nakamura T, Moss J, Polkey MI, Mandic D, Morrell MJet al., 2019, The Efficacy of a Novel In-ear Electroencephalography (EEG) Sensor to Measure Overnight Sleep in Healthy Participants, International Conference of the American-Thoracic-Society, Publisher: AMER THORACIC SOC, ISSN: 1073-449X

Conference paper

Mohan D, Forman JR, Allinder M, McEniery CM, Bolton CE, Cockcroft JR, MacNee W, Fuld J, Marchong M, Gale NS, Fisk M, Nagarajan S, Cheriyan J, Lomas DA, Calverley PMA, Miller BE, Tal-Singer R, Wilkinson IB, Polkey MIet al., 2018, Fibrinogen does not relate to cardiovascular or muscle manifestations in COPD: cross-sectional data from the ERICA study, THORAX, Vol: 73, Pages: 1182-1185, ISSN: 0040-6376

Journal article

Elbehairy AF, Quint JK, Rogers J, Laffan MJ, Polkey MI, Hopkinson NSet al., 2018, PATTERNS OF BREATHLESSNESS IN THE UK: RESULTS FROM THE BRITISH LUNG FOUNDATION ONLINE BREATH TEST, Winter Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A247-A247, ISSN: 0040-6376

Conference paper

Elbehairy AF, Quint JK, Rogers J, Laffan MJ, Polkey MI, Hopkinson NSet al., 2018, THE BRITISH LUNG FOUNDATION ONLINE BREATH TEST: IMPACT ON HEALTH-CARE BEHAVIOUR, Winter Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A246-A246, ISSN: 0040-6376

Conference paper

Loeckx M, Rabinovich RA, Demeyer H, Louvaris Z, Tanner R, Rubio N, Frei A, De Jong C, Gimeno-Santos E, Rodrigues FM, Buttery SC, Hopkinson NS, Busching G, Strassmann A, Serra I, Vogiatzis I, Garcia-Aymerich J, Polkey MI, Troosters Tet al., 2018, Smartphone-based physical activity telecoaching in chronic obstructive pulmonary disease: Mixed-methods study on patient experiences and lessons for implementation, JMIR mHealth and uHealth, Vol: 6, ISSN: 2291-5222

Background: Telecoaching approaches can enhance physical activity (PA) in patients with chronic obstructive pulmonary disease (COPD). However, their effectiveness is likely to be influenced by intervention-specific characteristics.Objective: This study aimed to assess the acceptability, actual usage, and feasibility of a complex PA telecoaching intervention from both patient and coach perspectives and link these to the effectiveness of the intervention.Methods: We conducted a mixed-methods study based on the completers of the intervention group (N=159) included in an (effective) 12-week PA telecoaching intervention. This semiautomated telecoaching intervention consisted of a step counter and a smartphone app. Data from a project-tailored questionnaire (quantitative data) were combined with data from patient interviews and a coach focus group (qualitative data) to investigate patient and coach acceptability, actual usage, and feasibility of the intervention. The degree of actual usage of the smartphone and step counter was also derived from app data. Both actual usage and perception of feasibility were linked to objectively measured change in PA.Results: The intervention was well accepted and perceived as feasible by all coaches present in the focus group as well by patients, with 89.3% (142/159) of patients indicating that they enjoyed taking part. Only a minority of patients (8.2%; 13/159) reported that they found it difficult to use the smartphone. Actual usage of the step counter was excellent, with patients wearing it for a median (25th-75th percentiles) of 6.3 (5.8-6.8) days per week, which did not change over time (P=.98). The smartphone interface was used less frequently and actual usage of all daily tasks decreased significantly over time (P<.001). Patients needing more contact time had a smaller increase in PA, with mean (SD) of +193 (SD 2375) steps per day, +907 (SD 2306) steps per day, and +1489 (SD 2310) steps per day in high, medium, and low contact

Journal article

Elbehairy AF, Whittaker H, Quint JK, Buttery S, Jordan S, Polkey MIet al., 2018, IDENTIFYING PATIENT SUITABILITY FOR LUNG VOLUME REDUCTION - ESTIMATION OF GAS TRAPPING FROM SPIROMETRY, Winter Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A30-A31, ISSN: 0040-6376

Conference paper

Pavitt MJ, Tanner RJ, Lewis AP, Buttery SC, Mehta B, Jefford H, Curtis KJ, Banya W, Husain S, Satkunam K, Shrikrishna D, Man WD-C, Polkey MI, Hopkinson NSet al., 2018, ORAL DIETARY NITRATE SUPPLEMENTATION TO ENHANCE PULMONARY REHABILITATION IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE: A MULTI-CENTRE, DOUBLE BLIND, PLACEBO-CONTROLLED, PARALLEL GROUP STUDY, Winter Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A3-A3, ISSN: 0040-6376

Conference paper

Alqurashi YD, Nakamura T, Goverdovsky V, Moss J, Polkey MI, Mandic DP, Morrell MJet al., 2018, A novel in-ear sensor to determine sleep latency during the Multiple Sleep Latency Test in healthy adults with and without sleep restriction, Nature and Science of Sleep, Vol: 10, Pages: 385-396, ISSN: 1179-1608

Objectives: Detecting sleep latency during the Multiple Sleep Latency Test (MSLT) using electroencephalogram (scalp-EEG) is time-consuming. The aim of this study was to evaluate the efficacy of a novel in-ear sensor (in-ear EEG) to detect the sleep latency, compared to scalp-EEG, during MSLT in healthy adults, with and without sleep restriction.Methods: We recruited 25 healthy adults (28.5±5.3 years) who participated in two MSLTs with simultaneous recording of scalp and in-ear EEG. Each test followed a randomly assigned sleep restriction (≤5 hours sleep) or usual night sleep (≥7 hours sleep). Reaction time and Stroop test were used to assess the functional impact of the sleep restriction. The EEGs were scored blind to the mode of measurement and study conditions, using American Academy of Sleep Medicine 2012 criteria. The Agreement between the scalp and in-ear EEG was assessed using Bland-Altman analysis.Results: Technically acceptable data were obtained from 23 adults during 69 out of 92 naps in the sleep restriction condition and 25 adults during 85 out of 100 naps in the usual night sleep. Meaningful sleep restrictions were confirmed by an increase in the reaction time (mean ± SD: 238±30 ms vs 228±27 ms; P=0.045). In the sleep restriction condition, the in-ear EEG exhibited a sensitivity of 0.93 and specificity of 0.80 for detecting sleep latency, with a substantial agreement (κ=0.71), whereas after the usual night’s sleep, the in-ear EEG exhibited a sensitivity of 0.91 and specificity of 0.89, again with a substantial agreement (κ=0.79).Conclusion: The in-ear sensor was able to detect reduced sleep latency following sleep restriction, which was sufficient to impair both the reaction time and cognitive function. Substantial agreement was observed between the scalp and in-ear EEG when measuring sleep latency. This new in-ear EEG technology is shown to have a significant value as a convenient measure for sleep lat

Journal article

Shanks A-M, Desai SR, Rice A, Thomas SR, Polkey MI, George PMet al., 2018, Restrictive lung defects: parenchymal, chest wall and neuromuscular, THORAX, Vol: 73, Pages: 989-991, ISSN: 0040-6376

Journal article

Polkey MI, Ambrosino N, 2018, Inspiratory muscle training in COPD: can data finally beat emotion?, THORAX, Vol: 73, Pages: 900-901, ISSN: 0040-6376

Journal article

Pavitt M, Tanner RJ, Lewis AP, Buttery SC, Mehta B, Jefford H, Curtis KJ, Banya W, Husain S, Satkunam K, Shrikrishna D, Man WD, Polkey MI, Hopkinson NSet al., 2018, Late Breaking Abstract - Dietary nitrate supplementation enhances the benefit of pulmonary rehabilitation in people with COPD, 28th International Congress of the European-Respiratory-Society (ERS), Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936

Conference paper

Barker R, Kon SSC, Jones SE, Maddocks M, Gao W, Nolan CM, Patel S, Kwan HY, Clarke SF, Polkey MI, Cullinan P, Man WD-Cet al., 2018, Short Physical Performance Battery and long term prognosis following severe acute exacerbation of COPD: a prospective cohort study, 28th International Congress of the European-Respiratory-Society (ERS), Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936

Conference paper

Fermont J, Fisk M, Bolton C, Cockroft J, Mceniery C, Fuld J, Mohan D, Tal-Singer R, Mullerova H, Wood A, Wilkinson I, Polkey Met al., 2018, The value of short physical performance battery (SPPB) as an alternative component of the BODE Index in predicting death in chronic obstructive pulmonary disease (COPD) in the ERICA cohort., 28th International Congress of the European-Respiratory-Society (ERS), Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936

Conference paper

Pavitt M, Lewis AP, Buttery SC, Fernandez BO, Mikus-Lelinska M, Feelisch M, Polkey MI, Hopkinson NSet al., 2018, Late Breaking Abstract - Dietary nitrate supplementation increases exercise endurance time in COPD patients using ambulatory oxygen, 28th International Congress of the European-Respiratory-Society (ERS), Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936

Conference paper

Watson G, Baker C, Polkey M, Howard Let al., 2018, The impact of obesity on pulmonary haemodynamic interpretation, 28th International Congress of the European-Respiratory-Society (ERS), Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936

Conference paper

Benson V, Mohan D, Allinder M, Galwey N, Mceniery C, Fuld J, Bolton C, Macnee W, Cockcroft J, Wilkinson I, Tal-Singer R, Polkey Met al., 2018, Prevalence of physical limitation in COPD: the short physical performance battery (SPPB), 28th International Congress of the European-Respiratory-Society (ERS), Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936

Conference paper

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