Go to the About Us section
Go to the Courses section
Go to the Research section
Go to the Specialist Services & Consultancy section
Go to the Outreach section
Go to the New Students section
You can find details about all the staff in the department below.
return to full list
BSc, PhD, FHEA
Department of Biological and Medical Sciences
Faculty of Health and Life Sciences
Jan'21 -Dec'23 (Director of studies; Self-funded PhD)
Dr. Maria Yermolitska "Inhaled hydroxygas for dyspnoea relief" -(Active)
Sep'20 - Aug'23 (Director of studies; Groome Studentship)
Mr.Tom Chapman "Respiratory control and dysfunction in Parkinson's Disease" -(Active)
Sep’16 – Aug’19 (Director of Studies; Groome Studentship)
Ms. Charlotte Golding “Effects of neurosurgical intervention and neurological damage on dyspnoea“ - (Awarded August 2020)
(currently studying Medicine)
Jan’15 – Jan’21 (Director of Studies; part-time direct PhD)
Dr. Joanna Grogono “Mechanism of dyspnoea in heart failure” -(Awarded February 2021)
Now appointed as a Consultant in Cardiology
Oct’12 – Sep’16 (Director of Studies; Groome Studentship)
Dr. Emmanuel Debrah “Cerebral mechanisms of dyspnoea and its relief” -(Awarded March 2017)
Currently employed as a clinical trials coordinator in Neuroscience
My primary research interest is to find out how breathlessness (‘dyspnoea’) arises so that more effective drugs can be developed to relieve dyspnoea when the underlying disease can’t be cured. The multidisciplinary research involves experiments on healthy volunteers and various patients who are inordinately breathless.
I have tested hypotheses regarding ‘air hunger’ (an unpleasant component of dyspnoea), validated ways to induce specific components of dyspnoea using specially-constructed breathing circuits and developed a unique questionnaire that quantifies overall breathlessness (intensity and unpleasantness) and is based on the language patients use to describe their experience. The work has guided on-going clinical studies including randomised-controlled trials to test novel interventions.
Cardiorespiratory Research Group
British Heart Foundation (Project Grant no. PG/13/84/30486)
“Inhaled frusemide for dyspnoea relief in advanced heart failure”
Mechanisms and management of breathlessness is at the core of the research strategy outlined below. There is an urgent clinical need for effective and safe interventions for breathlessness relief when underlying pathophysiology is incurable. This need has been amplified by the coronavirus pandemic.
I have a three-pronged research strategy:
1) To study patients undergoing neurological interventions or suffering neurological damage in order to better understand neurophysiological mechanisms of breathlessness.
2) To use the improved understanding of neurophysiological mechanisms of breathlessness to identify and trial new pharmacological interventions for intractable breathlessness.
3) To address emerging concerns in clinical physiology, particularly those that have the potential to stretch the NHS to breaking point.
The role of subcortical structures and cerebral cortex in the maintenance of respiratory homeostasis in humans remains poorly understood. Emerging evidence suggests an important role of the anterior cingulate cortex (ACC) in respiratory control. In this study, local field potentials (LFPs) from dorsal ACC were recorded in humans through implanted deep brain electrodes during several breathing activities, including voluntary activities of breath-holding and deep breathing, and involuntary activities of inspiration of varying concentrations of carbon dioxide (1%, 3%, 5% and 7%). We found that the breath-holding task induced significant unilateral left-sided ACC changes in LFP power, including an increased activity in lower frequency bands (3-5 Hz) and decreased activity in higher frequency bands (12-26 Hz). The respiratory task involving reflex increase in ventilation due to hypercapnia (raised inspired CO2 ) was associated with bilateral changes in activity of the ACC (again with increased activity in lower frequency bands and reduced activity in higher frequency bands). The voluntary breathing task with associated hypocapnia (deep breathing) induced bilateral changes in activity within low frequency bands. Furthermore, probabilistic diffusion tractography analysis showed left-sided connection of the ACC with the insula and frontal operculum, and bilateral connections within subsections of the cingulate gyrus and the thalamus. This electrophysiological analysis provides direct evidence for a role of the ACC in respiratory control in humans.
Blood Oxygen Level Dependent (BOLD) fMRI is a common technique for measuring brain activation that could be affected by low-level carbon monoxide (CO) exposure from e.g. smoking. This study aimed to probe the vulnerability of BOLD fMRI to CO and determine whether it may constitute a significant neuroimaging confound. Low-level (6ppm exhaled) CO effects on BOLD response were assessed in 12 healthy never-smokers on two separate experimental days (CO and air control). fMRI tasks were breath-holds (hypercapnia), visual stimulation and fingertapping. BOLD fMRI response was lower during breath holds, visual stimulation and fingertapping in the CO protocol compared to the air control protocol. Behavioural and physiological measures remained unchanged. We conclude that BOLD fMRI might be vulnerable to changes in baseline CO, and suggest exercising caution when imaging populations exposed to elevated CO levels. Further work is required to fully elucidate the impact on CO on fMRI and its underlying mechanisms.
Objective. Respiratory abnormalities such as upper airway obstruction are common in Parkinson's disease (PD) and are an important cause of mortality and morbidity. We tested the effect of pedunculopontine region (PPNr) stimulation on respiratory maneuvers in human participants with PD, and separately recorded PPNr neural activity reflected in the local field potential (LFP) during these maneuvers. Methods. Nine patients with deep brain stimulation electrodes in PPNr, and seven in globus pallidus interna (GPi) were studied during trials of maximal inspiration followed by forced expiration with stimulation OFF and ON. Local field potentials (LFPs) were recorded in the unstimulated condition. Results. PEFR increased from 6.41 ± 0.63 L/sec in the OFF stimulation state to 7.5 L ± 0.65 L/sec in the ON stimulation state (z = −2.666, df = 8, P = 0.024). Percentage improvement in PEFR was strongly correlated with proximity of the stimulated electrode contact to the mesencephalic locomotor region in the rostral PPN (r = 0.814, n = 9, P = 0.008). Mean PPNr LFP power increased within the alpha band (7–11 Hz) during forced respiratory maneuvers (1.63 ± 0.16 μV2/Hz) compared to resting breathing (0.77 ± 0.16 μV2/Hz; z = −2.197, df = 6, P = 0.028). No changes in alpha activity or spirometric indices were seen with GPi recording or stimulation. Percentage improvement in PEFR was strongly positively correlated with increase in alpha power (r = 0.653, n = 14 (7 PPNr patients recorded bilaterally), P = 0.0096). Interpretation. PPNr stimulation in PD improves indices of upper airway function. Increased alpha‐band activity is seen within the PPNr during forced respiratory maneuvers. Our findings suggest a link between the PPNr and respiratory performance in PD.
The cerebral mechanisms of dyspnoea (breathlessness) are not well understood. Neuroimaging studies of experimentally induced dyspnoea in healthy individuals have identified several cortical areas that might form a neural network for perception of dyspnoea , much like those identified for pain perception . However, functional imaging studies alone do not reveal neurophysiological pathways and may miss putative targets for dyspnoea relief. The objective of this study was to assess the effects of Deep Brain Stimulation (DBS) of four different brain nuclei on the sensation of dyspnoea in an individual with Chronic Obstructive Pulmonary Disease (COPD) using an established multidimensional dyspnoea tool .
Background. Inhaled furosemide offers a potentially novel treatment for dyspnoea, which may reflect modulation of pulmonary stretch receptor feedback to the brain. Specificity of relief is unclear because different neural pathways may account for different components of clinical dyspnoea. Our objective was to evaluate if inhaled furosemide relieves the air hunger component (uncomfortable urge to breathe) but not the sense of breathing work/effort of dyspnoea. Methods. A randomised, double blind, placebo-controlled crossover trial in 16 healthy volunteers studied in a university research laboratory. Each participant received 3 mist inhalations (either 40 mg furosemide or 4 ml saline) separated by 30–60 min on 2 test days. Each participant was randomised to mist order ‘furosemide-saline-furosemide’ (n- = 8) or ‘saline-furosemide-saline’ (n = 8) on both days. One day involved hypercapnic air hunger tests (mean ± SD PCO2 = 50 ± 3.7 mmHg; constrained ventilation = 9 ± 1.5 L/min), the other involved work/effort tests with targeted ventilation (17 ± 3.1 L/min) and external resistive load (20cmH2O/L/s). Primary outcome was ratings of air hunger or work/effort every 15 s on a visual analogue scale. During saline inhalations, 1.5 mg furosemide was infused intravenously to match the expected systemic absorption from the lungs when furosemide is inhaled. Corresponding infusions of saline during furosemide inhalations maintained procedural blinding. Average visual analogue scale ratings (%full scale) during the last minute of air hunger or work/effort stimuli were analysed using Linear Mixed Methods. Results. Data from all 16 participants were analysed. Inhaled furosemide relative to inhaled saline significantly improved visual analogues scale ratings of air hunger (Least Squares Mean ± SE − 9.7 ± 2%; p = 0.0015) but not work/effort (+ 1.6 ± 2%; p = 0.903). There were no significant adverse events. Conclusions. Inhaled furosemide was effective at relieving laboratory induced air hunger but not work/effort in healthy adults; this is consistent with the notion that modulation of pulmonary stretch receptor feedback by inhaled furosemide leads to dyspnoea relief that is specific to air hunger, the most unpleasant quality of dyspnoea.
OBJECTIVE: The effects of natural adjuvants on lung inflammation and tracheal responsiveness were examined in sensitized guinea pigs. METHODS: The responses of guinea pig tracheal chains and the serum levels of interleukin-4 and interferon-gamma were examined in control pigs and three other groups of guinea pigs: the sensitized group and two other sensitized groups treated with either adjuvant G2 or adjuvant G2F (n=7 for each group). Sensitization of the animals was achieved by injection and inhalation of ovalbumin. RESULTS: The results showed that sensitized animals had increased tracheal responsiveness and increased serum levels of interleukin-4 and interferon-gamma compared to controls (p<0.05 to p<0.001). Treatments with either G2 or G2F prevented the increase in tracheal responsiveness and serum interleukin-4 (p<0.01 to p<0.001). However, the serum levels of interferon-gamma and the interleukin-4-to-interferon-gamma ratio was increased in the treated groups (p<0.001 for all cases). CONCLUSIONS: These results indicate important preventive effects of two natural adjuvants, particularly G2, on the changes in tracheal responsiveness, serum cytokines and the interleukin-4-to-interferon-gamma ratio (T helper 1/T helper 2 balance) in sensitized guinea pigs.
Objective: To determine the validity and reliability of the Dyspnoea-12 (D-12) for the assessment of breathlessness in patients with interstitial lung disease (ILD). Methods: 101 patients with ILD completed the D-12 (scaling range 0-36, high score indicates worse dyspnea), MRC dyspnea scale, St George" s Respiratory Questionnaire (SGRQ), and Hospital anxiety and depression scale (HADS) at baseline, and 84 patients completed the D- 12 and a global health transition score at follow-up 2-weeks later. D-12 psychometric properties, including floor and ceiling effects, internal consistency, test-retest reliability and construct validity of the D-12 were examined. Results: The D-12 showed good internal consistency (Cronbach" s a =0.93) and repeatability (Intra-class correlation coefficient = 0.94). Its scores were significantly associated with MRC grade (r = 0.56, p<0.001), SGRQ (symptoms r = 0.57; activities r = 0.78; impacts r = 0.75; total r = 0.79, p<0.001). Confirmatory factor analysis confirmed the previously determined structure of the D-12 in this patient group. Conclusion: In patients with ILD, the patient reported D-12 - a patient reported measure of dyspnoea severity that requires no reference to activity, is a reliable and valid instrument. It is short, simple to complete, and easy to score.
Rationale: Dyspnoea is a debilitating and distressing symptom that is reflected in different verbal descriptors. Evidence suggests that dyspnoea, like pain perception, consists of sensory quality and affective components. The objective of this study was to develop an instrument that measures overall dyspnoea severity using descriptors that reflect its different aspects. Methods: 81 dyspnoea descriptors were administered to 123 patients with chronic obstructive pulmonary disease (COPD), 129 with interstitial lung disease and 106 with chronic heart failure. These were reduced to 34 items using hierarchical methods. Rasch analysis informed decisions regarding further item removal and fit to the unidimensional model. Principal component analysis (PCA) explored the underlying structure of the final item set. Validity and reliability of the new instrument were further assessed in a separate group of 53 patients with COPD. Results: After removal of items with hierarchical methods (n=47) and items that failed to fit the Rasch model (n=22), 12 were retained. The"-˜Dyspnoea-12" " had good internal reliability (Cronbach" s alpha=0.9) and fit to the Rasch model (x2 p=0.08). Items patterned into two groups called"-˜physical" " (n=7) and"-˜affective" " ( n=5). In the separate validation study, Dyspnoea-12 correlated with the Hospital Anxiety and Depression Scale (anxiety r=0.51; depression r=0.44, p,0.001, respectively), 6-minute walk distance (r=20.38, p,0.01) and MRC (Medical Research Council) grade (r=0.48, p,0.01), and had good stability over time (intraclass correlation coefficient=0.9, p,0.001). Conclusion: Dyspnoea-12 fulfills modern psychometric requirements for measurement. It provides a global score of breathlessness severity that incorporates both"-˜physical" " and"-˜affective" " aspects, and can measure dyspnoea in a variety of diseases.
Respiratory control and sensation
Dyspnoea (breathlessness) mechanisms, assessment, management
Physiological Society (Full member)
The Dyspnea Society (Nominee for executive committee)
Dyspnea 2021 International Conference -To be hosted at Oxford Brookes in July 2022
1987-1988 Res Technician (Leicester Royal infirmary-Child Health)
1988-1994 Clinical Physiologist (Charing Cross Hospital, London)
1994-1998 PostDoc RA (Imperial College London-Neurophysiology)
1998-2003 Research Scientist (Harvard School of Public Health)
2004-2010 Lecturer (Imperial College London-NHLI)
2010-2011 Research Scientist (Stoke Mandeville Hospital-UKSCIRN)
After graduating in Physiology from King’s College London, I worked as research technician in child health at Leicester Royal Infirmary. In 1988 I became a clinical physiologist at Charing Cross Hospital and began a PhD studying exercise breathing. My first postdoctoral position (also at Charing Cross) involved neurophysiological research on severely brain-injured patients.
In 1998 I moved to Harvard to research mechanisms of breathlessness and returned in 2004 to a lectureship at Imperial College. In 2010 I spent a year as research scientist with UK Spinal Cord Injury Research Network at Stoke Mandeville Hospital before starting my current post.
Oxford BRC Open day -"How long can you hold your breath?"
The Breathlessness Podcast