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Positive correlation between left amygdala activation during the perception of increased dyspnea and disease duration in patients with COPD. For visual purposes, activation is thresholded at puncorrected < 0.001 with colorbars indicating T-values. Beta weights (y-axis) of individual subjects' peak voxel used in the scatter plot indicate neural activation using arbitrary units.
Source publication
Background: Dyspnea is the impairing cardinal symptom in COPD, but the underlying brain mechanisms and their relationships to clinical patient characteristics are widely unknown. This study compared neural responses to the perception and anticipation of dyspnea between patients with stable moderate-to-severe COPD and healthy controls. Moreover, ass...
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Citations
... Importantly, it has long been recognized that the "anticipation" or "expectation" of exercise can increase ventilatory demand and the sensation of dyspnea. (74,75) A recent study by Finnegan et al. used neuroimaging to show that specific brain activity associated with the expectation of dyspnea was correlated with symptom intensity.(76) Further, this could be modulated with Dcycloserine,(76) a brain-active drug potentially influencing the mechanisms underlying "expectations". ...
Purpose of review
Exertional dyspnea and exercise intolerance remain key patient-related outcomes in chronic obstructive pulmonary disease (COPD). Improvement in treatment strategies is pendant further understand of their underpinnings across the spectrum of disease severity.
Recent findings
Emerging literature has been reviewed based on a conceptual framework that relates ventilatory demand to capacity under the modulating influence of sub-cortical and cortical centers (symptom perception and affective interpretation). Evidence supporting these fundamental tenets is critically appraised, focusing on mechanistic and interventional studies that shed novel light on the sources of heightened and/or mechanically constrained ventilation. Mechanistic studies using proxies of the inspiratory neural drive (e.g., diaphragm electromyography) were particularly informative, as well as interventional trials aimed at decreasing afferent stimulation and/or symptom perception via pharmacological (e.g., low-dose opiates in selected patients, high flow oxygen, oral nitrate) and nonpharmacological (e.g., novel exercise training paradigms, inspiratory muscle training, breathing techniques) interventions.
Summary
Therapeutic and rehabilitative strategies to lessen dyspnea's devastating impact on quality of life should minimize demand in the setting of reduced capacity and increased sensation awareness in COPD. The most successful attempts so far have amalgamated pharmacological and nonpharmacological approaches tailored to the main underlying mechanisms on an individual basis.
... However, the complex brain processes underlying dyspnoea experiences are still not clearly understood, and require further intensified research efforts. So far, neuroimaging studies from the past three decades, predominantly in healthy samples, have revealed an involvement of senso-motoric as well as cognitive-affective brain networks [23,[29][30][31], with dyspnoeic patients showing some distinct activation patterns within these networks [32][33][34][35]. Among involved brain areas, the thalamus has regularly been implicated during states of experimentally induced dyspnoea, most likely due to its prominent involvement in the neural throughput of afferent sensory signals into higher cortical areas, their respective neural gating and further top-down processes [23,[36][37][38][39][40]. ...
... Consistent evidence shows that dyspnoea occurs concomitantly with the activation of brain networks involving motor, sensory and interoceptive regions [2]. This has been shown using functional magnetic resonance imaging and electroenceophalography during experimental dyspnoea of various types in healthy humans [13][14][15][16], during clinical dyspnoea in patients with chronic respiratory diseases [17][18][19] or under mechanical ventilation [20,21]. This has also been shown during the anticipation of dyspnoea in normal subjects [22,23] and in patients with COPD [18,24]. ...
... This has been shown using functional magnetic resonance imaging and electroenceophalography during experimental dyspnoea of various types in healthy humans [13][14][15][16], during clinical dyspnoea in patients with chronic respiratory diseases [17][18][19] or under mechanical ventilation [20,21]. This has also been shown during the anticipation of dyspnoea in normal subjects [22,23] and in patients with COPD [18,24]. This phenomenon, which can be summarised as "an ensemble of brain responses to abnormal respiratory-related messages" could tentatively be termed "respiratory-related brain suffering". ...
This statement outlines a review of the literature and current practice concerning the prevalence, clinical significance, diagnosis and management of dyspnoea in critically ill, mechanically ventilated adult patients. It covers the definition, pathophysiology, epidemiology, short- and middle-term impact, detection and quantification, and prevention and treatment of dyspnoea. It represents a collaboration of the European Respiratory Society and the European Society of Intensive Care Medicine. Dyspnoea ranks among the most distressing experiences that human beings can endure. Approximately 40% of patients undergoing invasive mechanical ventilation in the intensive care unit (ICU) report dyspnoea, with an average intensity of 45 mm on a visual analogue scale from 0 to 100 mm. Although it shares many similarities with pain, dyspnoea can be far worse than pain in that it summons a primal fear response. As such, it merits universal and specific consideration. Dyspnoea must be identified, prevented and relieved in every patient. In the ICU, mechanically ventilated patients are at high risk of experiencing breathing difficulties because of their physiological status and, in some instances, because of mechanical ventilation itself. At the same time, mechanically ventilated patients have barriers to signalling their distress. Addressing this major clinical challenge mandates teaching and training, and involves ICU caregivers and patients. This is even more important because, as opposed to pain which has become a universal healthcare concern, very little attention has been paid to the identification and management of respiratory suffering in mechanically ventilated ICU patients.
... Consistent evidence shows that dyspnoea occurs concomitantly with the activation of brain networks involving motor, sensory and interoceptive regions [2]. This has been shown using functional magnetic resonance imaging and electroenceophalography during experimental dyspnoea of various types in healthy humans [13][14][15][16], during clinical dyspnoea in patients with chronic respiratory diseases [17][18][19] or under mechanical ventilation [20,21]. This has also been shown during the anticipation of dyspnoea in normal subjects [22,23] and in patients with chronic obstructive pulmonary disease (COPD) [18,24]. ...
... This has been shown using functional magnetic resonance imaging and electroenceophalography during experimental dyspnoea of various types in healthy humans [13][14][15][16], during clinical dyspnoea in patients with chronic respiratory diseases [17][18][19] or under mechanical ventilation [20,21]. This has also been shown during the anticipation of dyspnoea in normal subjects [22,23] and in patients with chronic obstructive pulmonary disease (COPD) [18,24]. This phenomenon, which can be summarised as "an ensemble of brain responses to abnormal respiratory-related messages" could tentatively be termed "respiratory-related brain suffering". ...
This statement outlines a review of the literature and current practice concerning the prevalence, clinical significance, diagnosis and management of dyspnoea in critically ill, mechanically ventilated adult patients. It covers the definition, pathophysiology, epidemiology, short- and middle-term impact, detection and quantification, and prevention and treatment of dyspnoea. It represents a collaboration of the European Respiratory Society (ERS) and the European Society of Intensive Care Medicine (ESICM). Dyspnoea ranks among the most distressing experiences that human beings can endure. Approximately 40% of patients undergoing invasive mechanical ventilation in the intensive care unit (ICU) report dyspnoea, with an average intensity of 45 mm on a visual analogue scale from 0 to 100 mm. Although it shares many similarities with pain, dyspnoea can be far worse than pain in that it summons a primal fear response. As such, it merits universal and specific consideration. Dyspnoea must be identified, prevented and relieved in every patient. In the ICU, mechanically ventilated patients are at high risk of experiencing breathing difficulties because of their physiological status and, in some instances, because of mechanical ventilation itself. At the same time, mechanically ventilated patients have barriers to signalling their distress. Addressing this major clinical challenge mandates teaching and training, and involves ICU caregivers and patients. This is even more important because, as opposed to pain which has become a universal healthcare concern, very little attention has been paid to the identification and management of respiratory suffering in mechanically ventilated ICU patients.
... О поражении вирусом ЦНС и периферической нервной системы также свидетельствует вызванная COVID-19 потеря обоняния (рис.) [48][49][50]. ...
Dyspnea may not be a major symptom of the disease. There are many reports that some patients with COVID-19 did not complain of dyspnea. There is no consensus on the clinical significance of hypoxemia without dyspnea. Several studies suggest that patients with hypoxemia without dyspnea are not protected against the development of adverse COVID-19 outcomes. It is unclear whether hypoxemia with and without dyspnea are two distinct COVID-19 phenotypes or two phases of the disease. There is currently no consensus on the terminology of this condition, its definition, and its mechanisms of formation. It has not been established whether hypoxemia without dyspnea is associated with a favorable outcome of the disease or not. The question of the absence of respiratory response to hypoxia improves the prognosis in such patients remains unresolved. Analysis of currently available data on the mechanisms of hypoxemia development and related manifestations of dyspnea in SARS-CoV-2 virus infection. “Silent hypoxemia” can be observed both in the initial manifestations of respiratory failure and in progression of the disease. Clinical significance of “silent hypoxemia” is that the decrease in physiologic responses and the absence of dyspnea allow patients to feel normal, thus denying the severity of their condition and masking the true severity of the disease. In addition, in elderly patients and patients with diabetes mellitus, suppression of respiratory function in response to hypoxia and the development of “silent hypoxemia” with rapid decompensation should be expected. The attitude to patients with “asymptomatic carriage” of the virus should be reconsidered and comprehensive monitoring of such patients with mandatory pulse oximetry or arterial blood gas test composition should be carried out.
... According to the biopsychosocial model, depression and anxiety may affect disease severity via mechanisms associated with poor treatment adherence and self-care. In addition, several factors such as smoking behaviour [68][69][70], physical activity levels [71,72], brain processes [62,73,74], sleeping patterns [75,76], inflammatory processes [15,77] and activation of cell-mediated immunity [78], fatigue [79] and genetic risk factors [80,81], are most likely involved as contributors or moderators, requiring future systematic studies. Moreover, biological stress systems in the brain (e.g. ...
Psychological distress is prevalent in people with COPD and relates to a worse course of disease. It often remains unrecognised and untreated, intensifying the burden on patients, carers and healthcare systems. Nonpharmacological management strategies have been suggested as important elements to manage psychological distress in COPD. Therefore, this review presents instruments for detecting psychological distress in COPD and provides an overview of available nonpharmacological management strategies together with available scientific evidence for their presumed benefits in COPD. Several instruments are available for detecting psychological distress in COPD, including simple questions, questionnaires and clinical diagnostic interviews, but their implementation in clinical practice is limited and heterogeneous. Moreover, various nonpharmacological management options are available for COPD, ranging from specific cognitive behavioural therapy (CBT) to multi-component pulmonary rehabilitation (PR) programmes. These interventions vary substantially in their specific content, intensity and duration across studies. Similarly, available evidence regarding their efficacy varies significantly, with the strongest evidence currently for CBT or PR. Further randomised controlled trials are needed with larger, culturally diverse samples and long-term follow-ups. Moreover, effective nonpharmacological interventions should be implemented more in the clinical routine. Respective barriers for patients, caregivers, clinicians, healthcare systems and research need to be overcome.
... Indeed, various neuroimaging techniques such as functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) scanning have been used to visualize brain regions wherein neuronal activity is altered in response to the anticipation and/or perception of laboratory-induced breathlessness (Herigstad et al., 2011). Results from multiple studies in healthy adults (Banzett et al., 2000;Brannan et al., 2001;Evans et al., 2002;Faull and Pattinson, 2017;Liotti et al., 2001;Parsons et al., 2001;Pattinson and Johnson, 2014;Peiffer et al., 2001;Stoeckel et al., 2016von Leupoldt et al., 2008von Leupoldt et al., , 2009 or people with COPD (Esser et al., 2017;Finnegan et al., 2021;Herigstad et al., 2015;Reijnders et al., 2020) indicate that breathlessness is processed in distinct affective and sensorimotor-related brain structures ( Fig. 1) (Banzett et al., 2000;Brannan et al., 2001;Esser et al., 2017;Evans et al., 2002;Herigstad et al., 2011;Liotti et al., 2001;Marlow et al., 2019;Parsons et al., 2001;Peiffer et al., 2001;Reijnders et al., 2020;Stoeckel et al., 2016;von Leupoldt and Dahme, 2005;von Leupoldt and Farre, 2020;von Leupoldt et al., 2008von Leupoldt et al., , 2009, most notably and consistently the insular cortex (Banzett et al., 2000;Brannan et al., 2001;Esser et al., 2017;Evans et al., 2002;Herigstad et al., 2011;Liotti et al., 2001;Marlow et al., 2019;Peiffer et al., 2001;Stoeckel et al., 2016;von Leupoldt et al., 2008), the anterior cingulate cortex Esser et al., 2017;Evans et al., 2002;Herigstad et al., 2011;Liotti et al., 2001;Marlow et al., 2019;Stoeckel, Esser, Gamer, Büchel et al., 2018), and the amygdala Esser et al., 2017;Evans et al., 2002;Herigstad et al., 2011;Liotti et al., 2001;Marlow et al., 2019;von Leupoldt et al., 2008). The anterior cingulate cortex has also been implicated in the relief of breathlessness following a decrease in external resistive loading (Peiffer et al., 2008) or in response to intravenous opioid administration (Pattinson et al., 2009) in healthy people. ...
... Indeed, various neuroimaging techniques such as functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) scanning have been used to visualize brain regions wherein neuronal activity is altered in response to the anticipation and/or perception of laboratory-induced breathlessness (Herigstad et al., 2011). Results from multiple studies in healthy adults (Banzett et al., 2000;Brannan et al., 2001;Evans et al., 2002;Faull and Pattinson, 2017;Liotti et al., 2001;Parsons et al., 2001;Pattinson and Johnson, 2014;Peiffer et al., 2001;Stoeckel et al., 2016von Leupoldt et al., 2008von Leupoldt et al., , 2009 or people with COPD (Esser et al., 2017;Finnegan et al., 2021;Herigstad et al., 2015;Reijnders et al., 2020) indicate that breathlessness is processed in distinct affective and sensorimotor-related brain structures ( Fig. 1) (Banzett et al., 2000;Brannan et al., 2001;Esser et al., 2017;Evans et al., 2002;Herigstad et al., 2011;Liotti et al., 2001;Marlow et al., 2019;Parsons et al., 2001;Peiffer et al., 2001;Reijnders et al., 2020;Stoeckel et al., 2016;von Leupoldt and Dahme, 2005;von Leupoldt and Farre, 2020;von Leupoldt et al., 2008von Leupoldt et al., , 2009, most notably and consistently the insular cortex (Banzett et al., 2000;Brannan et al., 2001;Esser et al., 2017;Evans et al., 2002;Herigstad et al., 2011;Liotti et al., 2001;Marlow et al., 2019;Peiffer et al., 2001;Stoeckel et al., 2016;von Leupoldt et al., 2008), the anterior cingulate cortex Esser et al., 2017;Evans et al., 2002;Herigstad et al., 2011;Liotti et al., 2001;Marlow et al., 2019;Stoeckel, Esser, Gamer, Büchel et al., 2018), and the amygdala Esser et al., 2017;Evans et al., 2002;Herigstad et al., 2011;Liotti et al., 2001;Marlow et al., 2019;von Leupoldt et al., 2008). The anterior cingulate cortex has also been implicated in the relief of breathlessness following a decrease in external resistive loading (Peiffer et al., 2008) or in response to intravenous opioid administration (Pattinson et al., 2009) in healthy people. ...
... Indeed, various neuroimaging techniques such as functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) scanning have been used to visualize brain regions wherein neuronal activity is altered in response to the anticipation and/or perception of laboratory-induced breathlessness (Herigstad et al., 2011). Results from multiple studies in healthy adults (Banzett et al., 2000;Brannan et al., 2001;Evans et al., 2002;Faull and Pattinson, 2017;Liotti et al., 2001;Parsons et al., 2001;Pattinson and Johnson, 2014;Peiffer et al., 2001;Stoeckel et al., 2016von Leupoldt et al., 2008von Leupoldt et al., , 2009 or people with COPD (Esser et al., 2017;Finnegan et al., 2021;Herigstad et al., 2015;Reijnders et al., 2020) indicate that breathlessness is processed in distinct affective and sensorimotor-related brain structures ( Fig. 1) (Banzett et al., 2000;Brannan et al., 2001;Esser et al., 2017;Evans et al., 2002;Herigstad et al., 2011;Liotti et al., 2001;Marlow et al., 2019;Parsons et al., 2001;Peiffer et al., 2001;Reijnders et al., 2020;Stoeckel et al., 2016;von Leupoldt and Dahme, 2005;von Leupoldt and Farre, 2020;von Leupoldt et al., 2008von Leupoldt et al., , 2009, most notably and consistently the insular cortex (Banzett et al., 2000;Brannan et al., 2001;Esser et al., 2017;Evans et al., 2002;Herigstad et al., 2011;Liotti et al., 2001;Marlow et al., 2019;Peiffer et al., 2001;Stoeckel et al., 2016;von Leupoldt et al., 2008), the anterior cingulate cortex Esser et al., 2017;Evans et al., 2002;Herigstad et al., 2011;Liotti et al., 2001;Marlow et al., 2019;Stoeckel, Esser, Gamer, Büchel et al., 2018), and the amygdala Esser et al., 2017;Evans et al., 2002;Herigstad et al., 2011;Liotti et al., 2001;Marlow et al., 2019;von Leupoldt et al., 2008). The anterior cingulate cortex has also been implicated in the relief of breathlessness following a decrease in external resistive loading (Peiffer et al., 2008) or in response to intravenous opioid administration (Pattinson et al., 2009) in healthy people. ...
Breathlessness is a centrally processed symptom, as evidenced by activation of distinct brain regions such as the insular cortex and amygdala, during the anticipation and/or perception of breathlessness. Inhaled L-menthol or blowing cool air to the face/nose, both selective trigeminal nerve (TGN) stimulants, relieve breathlessness without concurrent improvements in physiological outcomes (e.g., breathing pattern), suggesting a possible but hitherto unexplored central mechanism of action. Four databases were searched to identify published reports supporting a link between TGN stimulation and activation of brain regions involved in the anticipation and/or perception of breathlessness. The collective results of the 29 studies demonstrated that TGN stimulation activated 12 brain regions widely implicated in the anticipation and/or perception of breathlessness, including the insular cortex and amygdala. Inhaled L-menthol or cool air to the face activated 75% and 33% of these 12 brain regions, respectively. Our findings support the hypothesis that TGN stimulation contributes to breathlessness relief by altering the activity of brain regions involved in its central neural processing.
... Dyspnoea is a symptom but it is also an experience that changes the brain of those afflicted (through memory/ anticipation phenomena, see refs. [5][6][7] ) and therefore shapes their lives. 8,9 This is particularly true when dyspnoea continues despite maximal pathophysiological treatments (persistent dyspnoea). ...
Background
More than a symptom, dyspnoea is an existential experience shaping the lives of those afflicted, particularly when its persistence despite maximal pathophysiological treatments makes it pervasive. It is, however, insufficiently appreciated by concerned people themselves, family members, healthcare professionals and the public (dyspnoea invisibility), limiting access to appropriate care and support.
Aim
To provide a better understanding of dyspnoea experiences and its invisibility.
Design
Interpretative phenomenological analysis of data collected prospectively through in-depth semi-structured interviews.
Setting/Participants
Pulmonary rehabilitation facility of a tertiary care university hospital; 11 people (six men, five women) with severe chronic obstructive pulmonary disease (stages 3 and 4 of the 4-stage international GOLD classification) admitted for immediate post-exacerbation rehabilitation.
Results
We identified several types of dyspnoea invisibility depending on temporality and interlocutors: (1) invisibility as a symptom to oneself; (2) invisibility as a symptom to others; (3) invisibility as an experience that cannot be shared; (4) invisibility as an experience detached from objective measurements; (5) invisibility as an experience that does not generate empathic concern. The notion of invisibility was present in all the identified experiential dimensions of dyspnoea. It was seen as worsening the burden of the disease and as self-aggravating through self-isolation and self-censorship.
Conclusions
The study confirmed that dyspnoea invisibility is a reality for people with advanced chronic obstructive pulmonary disease. It shows dyspnoea invisibility to be a multifaceted burden. Future research should aim at identifying individual and collective measures to overcome dyspnoea invisibility.
... However, interestingly, in the later stages of loading levels, ie, 20 and 30 cmH 2 O, the influence of unwanted sensation weakened, which might be because of subjects' adaptation to the test resulting in an insignificant difference in Borg scores between both devices. Many previous studies have demonstrated that dyspnea among COPD patients could also be attributed to emotional and psychological aspects of the patients, 4,21,28 where the patients were more conscious of dyspnea attention and aversion. Similarly, Esser and his colleagues have found significant involvement of emotional brain regions (hippocampus and amygdala) in the COPD patients before the loading breath test, 21 where they observed no significant difference between the test and rest states of the patients. ...
... Many previous studies have demonstrated that dyspnea among COPD patients could also be attributed to emotional and psychological aspects of the patients, 4,21,28 where the patients were more conscious of dyspnea attention and aversion. Similarly, Esser and his colleagues have found significant involvement of emotional brain regions (hippocampus and amygdala) in the COPD patients before the loading breath test, 21 where they observed no significant difference between the test and rest states of the patients. Since the increase in loading level for I-TLD was gradual, it could be of pivotal importance in reducing the impact of patients' psychological impact on the test. ...
Purpose:
This study aimed to assess the consistency of hand-held electronic incremental threshold loading device (I-TLD) and traditional constant threshold loading device (C-TLD) in measuring the perception of dyspnea (POD) in humans.
Patients and methods:
Thirty-eight patients with stable chronic obstructive pulmonary disease (COPD) and 41 non-COPD subjects were recruited for the study, all of whom were subjected to an external loading breathing test by gradually increasing the inspiratory load starting from 0 to 5, 10, 20, and 30 cmH2O oral pressure using I-TLD and C-TLD. The Borg score measurement was performed immediately after the loading breath of each level. The linear regression slope a of Borg scores vs percentage of oral pressure from the patients' maximum represented patients' POD. The consistency of POD measured by the two devices was analyzed by two Related Samples Wilcoxon test, Spearman correlation analysis, and Bland-Altman analysis.
Results:
There was no significant difference in slope a measured by the two devices in all subjects. The Spearman correlation analysis revealed that the slope a measured by the two devices in the inspiratory loading breath test had a significant correlation: in COPD patients, r = 0.678, (p < 0.001) and in non-COPD subjects, r = 0.603, (p < 0.001). For the results of the Bland-Altman analysis of the whole subjects, 3.8% (3/79) points were outside of the 95% LoA confidence interval (CI) (-10.380, 9.457), and the LoA CI was acceptable, which depicted that the two devices were consistent in their estimation.
Conclusion:
I-TLD was consistent with C-TLD in measuring POD in COPD patients and non-COPD subjects. I-TLD may be used as an alternative method to replace C-TLD to measure POD in COPD patients and non-COPD subjects.
... 69 Dyspnea in COPD patients has been associated with increased activity in anterior cingulate and related medial prefrontal attentional processing regions, 70 and with activation of the thalamus, ACC, insula, and the PFC. 71 In preliminary and exploratory work, the same centers appear to be involved in the perception of cough, 72 nausea, 73 pruritus, 73 and dyspnea. 61,74 Neuroimaging studies of medically unexplained symptoms are still at a very early stage. ...
The mechanism of symptom amplification, developed in the study of somatization, may be helpful in caring for patients with symptoms that, while they have a demonstrable medical basis, are nonetheless disproportionately severe and distressing. Amplified medical symptoms are marked by disproportionate physical suffering, unduly negative thoughts and concerns about them, and elevated levels of health-related anxiety. They are accompanied by extensive and sustained illness behaviors, disproportionate difficulty compartmentalizing them and circumscribing their impact, and consequent problems and dissatisfaction with their medical care. A distinction has long been made between "medically explained" and "medically unexplained" symptoms. However, a more comprehensive view of symptom phenomenology undermines this distinction and places all symptoms along a smooth continuum regardless of cause: Recent findings in cognitive neuroscience suggest that all symptoms-regardless of origin-are processed through convergent pathways. The complete conscious experience of both medically "explained" and "unexplained" symptoms is an amalgam of a viscerosomatic sensation fused with its ascribed salience and the patient's ideas, expectations, and concerns about the sensation. This emerging empirical evidence furnishes a basis for viewing persistent, disproportionately distressing symptoms of demonstrable disease along a continuum with medically unexplained symptoms. Thus, therapeutic modalities developed for somatization and medically unexplained symptoms can be helpful in the care of seriously ill medical patients with amplified symptoms. These interventions include educational groups for coping with chronic illness, cognitive therapies for dysfunctional thoughts, behavioral strategies for maladaptive illness behaviors, psychotherapy for associated emotional distress, and consultation with mental health professionals to assist the primary care physician with difficulties in medical management.
