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Dokumen 1 dari 1 Dyspnea and emotional states in health and disease Link dokumen ProQuest Abstrak: Anxiety and depression can increase the intensity of dyspnea out of proportion to the impairment incardiorespiratory function and may contribute to the degree of disability associated with dyspnea. The effect ofanxiety/depression on the sensory and affective components of reported dyspnea in patients with respiratorydisorders might be of particular importance in improving the accuracy of the diagnostic process. However, theexact cause-relationship between dyspnea and anxiety/depression are unclear. A multidimensional model ofdyspnea subsuming sensory components (i.e. intensity and quality) and affective components has recentlybeen proposed. Affective responses drive patients to seek treatment which can cause them to alter their lifestyleto avoid dyspnea. Brain imaging techniques help identify distinct cortical structures involved in processing thediscrete components of dyspnea. Teks lengkap: Introduction The influence of emotional states on symptom perception in respiratory disease is a topic of growing interest toresearchers and clinicians. Patients with chronic lung disease who suffer from dyspnea often exhibit anxiety ordepressive symptoms.1-4 These emotional states have been shown to predict poorer quality of life and functionalstatus5-11 and likely contribute to the degree of disability associated with dyspnea and increased use of medicalservices.12 Emotional states may shape the quality and intensity of dyspnea at a given level of respiratoryactivity and partly explain why the relationship between dyspnea and the degree of impairment in lung functionis not strong.13 Although anxiety and depression may lead to worsening of dyspnea, the exact causerelationships and direction of causality between dyspnea and anxiety/depression are unclear.14,15 Surprisingly, despite frequent discrepancies between respiratory patients' self-reported dyspnea and the extentof underlying pathophysiology, few studies have investigated the effect of psychopathology on ratings ofperceived dyspnea by applying psychophysical methods, that is, the quantitative study of the relationshipbetween stimuli and the evoked conscious sensory response. A critical appraisal of symptoms can only comewith application of psychophysical techniques applied within the framework of respiratory and sensoryphysiology. As with pain, dyspnea should been measured adequately. A consensus statement of the AmericanThoracic Society (ATS) 13 has recently proposed that "instruments or section of instruments pertaining todyspnea should be classified as addressing domains of sensory-perceptual experience, affective distress, orsymptom/disease impact or burden". Sensory-perceptual measures include ratings of intensity (real-timedyspnea measures), and sensory quality. Affective distress can pertain to either a perception of immediateunpleasantness or to a cognitive-evaluative response to or judgment about the possible consequence of what isperceived. Impact measures, although very important, do not directly assess "what breathing feels like". 13 This review focuses on the following: (i) The effect of anxiety/depression on perceived dyspnea in health anddisease, (ii) Differentiation between sensory and affective components in patients with respiratory disorders,and (iii) Brain processing of the discrete components of dyspnea. Effects of emotional states on dyspnea perception Chronic obstructive pulmonary disease (COPD) The greatest attention has been focused on the psychological parameters of COPD.15-17 A systematic review of64 studies focusing on patients with severe disease, indicated that the level of anxiety and depression in COPDpatients was comparable to or higher than the levels detected in cancer, AIDS, renal and cardiac patients.17 Thequestion arises as to whether anxiety and depression can intensify dyspnea out of proportion to the level ofimpairment evidenced by the cardiorespiratory function.18,19 Dahlen et al.20 investigated whether psychologicalfactors assessed by the hospital anxiety and depression (HAD) scale were correlated to the risk of relapse in

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patients with acute exacerbation of asthma and COPD. In their series patients with probable anxiety and/ordepression had the same dyspnea score as patients without anxiety or depression. Also, the risk of treatmentfailure was significantly related to HAD, but not to dyspnea. More recently, it has been shown that the degree ofchronic exertional dyspnea assessed by a graded scale does not differ between non-depressed and depressedCOPD patients 11 with similar levels of airway obstruction but a greater level of anxiety in the latter group. Otherstudies15 have shown a significant association between anxiety/depression (HAD scale) and increase inintensity of dyspnea at rest and after 6 min walking test in patients with mild to moderate COPD. A pulmonaryrehabilitation program (PRP) reduced both dyspnea and anxiety/depression but this association remainedstable over the course of PRP even when improvements in the outcomes were achieved during PRP. 15 Inaddition the negative association between anxiety/depression and dyspnea is not thought to provide proof ofcausality between these variables.15 Further studies are needed to determine a specific cause-effectrelationship. A recent study has shown that the presence of panic attacks (i.e. acute intense anxiety associated with physicalsymptoms and cognitive fears) or panic disorders in individuals with COPD may be associated with aheightened perception of dyspnea.14 Livermore et al.14 compared the perceptual response to a resistive load inCOPD patients with panic attack (PA) or panic disorders (PD) and healthy subjects. The dyspnea ratingincreased linearly for all groups with increasing the resistive load. Patients with PA or PD rated their level ofdyspnea significantly higher than did other subjects. In addition, the higher the levels of depression between thegroups, the greater the rating of dyspnea as the magnitude of resistive load increased. So the diagnosis ofpanic attack/disorder should be carefully considered in patients with respiratory obstructive disorders. Asthma Janson et al.21 have documented correlations between depression/anxiety (HAD scale) and the report ofasthma-related symptoms, such as attacks of breathlessness during rest and activity, and waking with eitherattacks of breathlessness or chest tightness. On the other hand, Chetta et al. 22 were not able to find anyrelationship between personality profile by applying the Minnesota Multiphasic Personality Inventory (MPI)questionnaire, and perceived dyspnea on a Borg scale at 20% FEV1 (forced expiratory volume in 1 s) fall duringa bronchial provocation test. By contrast, significantly higher levels of perceived breathlessness have beenreported during induced bronchoconstriction in asthmatics with comorbid panic disorders. 23 In patients withnear-fatal asthma psychological disturbances might affect asthma control. In a study by Boulet et al.24 patientswith near-fatal asthma exhibited more psychological problems than the non-asthmatic group. However, anincrease in Borg was associated with a concurrent decrease in peak expiratory flow (PEF %pred) similarly in thetwo groups. Also, perception of dyspnea on a Borg scale at 20% fall in FEV1 during methacholine-inducedbronchoconstriction was similar in near-fatal and non-near-fatal asthma groups (3 vs 2.5, Borg units,respectively). Although the ventilatory response to inspiratory loads is governed primarily by respiratory system mechanicsand reflexes, behavioral or cognitive factors may play a role in this response as well. Lavietes et al.25

hypothesised that patients with a specific psychological trait will associate a greater degree of dyspnea duringloaded breathing task than otherwise healthy control subjects. They recruited subjects with Chronic FatigueSyndrome (CFS), and normal healthy subjects. The choice of CFS was motivated by the fact that somatisationwas thought to explain in part the symptom of CFS. Subjects were divided into two groups. The "responder"group reported Borg scores higher than those of the second "non responder" group at all times during resistivebreathing protocol. Responders presented higher depression scores (Center for Epidemiologic Studydepression scale) than did non-responders. Of note a greater percentage of patients (42%) with psychologicalproblems were in the "responder" group than in the "non-responder" group (17%). On the other hand, nodifferences on depression scale were found in control subjects, regardless of load response. Thus the diagnosisof panic attack/disorder should be carefully considered in patients with severe respiratory obstructive disorders.

Affective components of dyspnea and brain processing Any assessment of dyspnea should try to measure the intensity and quality of the sensation of respiratorydiscomfort and the emotional and behavioral response to the breathing discomfort.13 Pivotal studies26-28 haveprovided compelling evidence that sensory intensity and the unpleasantness of pain are discrete dimensionssince they can be independently manipulated in laboratory and clinical situations. They even appear to besubserved by separate neural pathways, a lateral thalamic system that projects to the primary sensory cortexand subserves sensory aspects, and a medial thalamic system that projects to the limbic cortex and subservesaffective aspects. 26 Further development regarding the affective dimensions of pain has been divided into aninitial stage A1 of immediate unpleasantness or discomfort, and later stage A2 of cognitively mediatedemotional reactions such as depression, anxiety, fear, etc., that may lead to behavioral outcomes. 28 Recently,brain image techniques have been used to identify distinct cortical structures and pathways that have beenshown to be more involved in either sensory or affective aspects of pain.27,29 It has been postulated (but notdefinitely proven) that these structures might also process the discrete components of dyspnea.30,31 In thisregard Davenport and Reep32 have described the two major pathways suggested to process respiratorysensation to the sensory cortex. The first pathway arises predominantly from respiratory muscle afferents, isrelayed to the brainstem medulla, and projects to the ventroposterior thalamus area, from where thalamocorticalprojections ascend to the primary and secondary somatosensory cortex. The second pathway includes mainlyvagal afferents from the lungs and airways which are relayed in the brainstem medulla. Brainstem projectionsascend to the amygdala and medial dorsal area of the thalamus and further to the insula and cingulate cortex. First evidence has suggested similar multidimensionality in the perception of both pain and dyspnea.29-33 VonLeupoldt and Dahme34 have recently shown in healthy subjects breathing against increased inspiratory loadsthat with increasing intensity of dyspnea the perceived unpleasantness increased stronger than the perceivedintensity, indicating that the sensory and the affective dimensions of dyspnea can be differentiated similarly tothe perception of pain. These findings help clarify and explain old and recent data. Boulet et al.35 were able to show that perception ofairflow obstruction and breathlessness following methacholine challenge testing were correlated with eachother. Mean perception scores were higher for asthmatics than controls but anxiety levels during methacholinewas low in both groups and did not correlate with dyspnea. However, it must be noted that perception of airwayobstruction was defined as a sensation of a change in breathing pattern while dyspnea was defined as anunpleasant sensation associated with bronchoconstriction. We argue against this contention as unpleasantnessis likely to define the affective component while intensity of dyspnea (Borg scale) defines one of the two aspectsof the sensory component. More recently De Peuter et al.36 have calculated the linear slope between a 20% fall in FEV1 and the increase inthe symptom scores of intensity and affectivity during a histamine bronchial provocation test in patients withasthma. Sensitivity appears to be positively related to trait anxiety, state anxiety, daily asthma symptoms andcatastrophic thinking during an asthma exacerbation in daily life. These relationships were overall stronger foraffective than for sensory symptom slopes. By applying stepwise multiple regression analysis, the state ofanxiety was the best predictor of the affective symptom slopes, whereas catastrophic thinking during an asthmaexacerbation was the best predictor for the sensory symptom slopes. In contrast, the relation between stateanxiety and sensory symptoms was not significant. These results have clinical implications. A high sensitivityseems favorable because it allows the early detection of deteriorating lung function and quick medication relief.A moderate degree of asthma-specific anxiety is adaptive because it may be associated with enhancedperception of bronchoconstriction. In contrast, absence of anxiety may lead to indifference and neglect ofsymptoms. 37 A differentiation between the sensory and affective components of reported dyspnea in patients with comorbiddepression might be of particular importance and improve the accuracy of the diagnostic process, symptom

perception, and therapeutic interventions. This has been pointed out in previous studies 36,38,39 demonstratingthat high negative affectivity reduces the accuracy of global rating of dyspnea perception. This might lead to anincreased use of health care resources to find relief from the overly negatively perceived symptom. Put et al.39

found that asthmatics with high negative affectivity had overall more intense dyspnea than patients scoring lowaffectivity; in addition negative affectivity modulated the effects of suggestions on dyspnea. In this regard,Davenport et al.,40 used respiratory-related evoked potential (RREp) methodology in a group of asthmaticchildren with a story of life-threatening asthma. They found an absence of P1 component after respiratoryocclusion (i.e. the dyspneic sensory signal was not activating the somatosensory cortex). These data suggestthe presence of an asthma-specific deficit in the latter cortical processing of respiratory load information.Nonetheless, it might be interesting in this regard to examine whether patients with blunted perception ofdyspnea have a specific deficit in the affective rather than the sensory aspects of their perceptual processing. A multidimensional model of dyspnea subsuming sensory components (i.e. intensity and quality) and affectivecomponents has recently been proposed.33,41 Affective responses are a major stimulus for learning strategies toavoid biologically threatening sensations; they also drive patients to seek treatment and can cause them to altertheir lifestyle to avoid dyspnea. An exaggerated perception of dyspnea, which may lead to excessive use ofmedical resources, may be an over-response in the affective dimension. In this connection, it has beenhypothesised that the affective dimension of dyspnea (unpleasantness, emotional response) does not strictlydepend on the intensity of dyspnea. Banzett and co-workers 41 tested the hypothesis that the ratio of immediateunpleasantness (A1) to sensory intensity (SI) would vary, depending on the type of dyspnea. Three differentstimuli were applied to healthy subjects. The first (maximal hyperpnea against inspiratory resistance) evokedwork and effort sensations with relatively low unpleasantness (mean A1/SI = 0.64). The second stimulus(hypercapnia with restricted ventilation), titrated to produce dyspnea ratings similar to those obtained byapplying the first stimulus; it evoked air hunger and produced significantly greater unpleasantness (mean A1/SI= 0.95). The third stimulus (further increase of the second stimulus, maximal hypopnea) was even higher untilair hunger was intolerable, evoking the highest intensity and unpleasantness ratings and ratio (A1/SI = 1.09).The data show that: 1. unpleasantness of dyspnea can vary independently from perceived intensity, this isconsistent with the prevailing model of pain, 2. multiple dimensions of dyspnea exist and can be measured.Determining whether a change in dyspnea reflects a change in the primary sensation or an affective responsemay inform us about the role of the psychological state of the patient in ratings respiratory discomfort and helpguide therapies so as to reduce the A1/SI ratio and subsequent discomfort. Additional studies from von Leupoldt et al.42 in healthy subjects breathing against inspiratory load duringattention and distraction indicate that while subjects attend their breathing only intensity score on VASinfluences Borg scale ratings. In contrast, only the VAS unpleasantness scores influences Borg scale ratingwhen subjects are distracted. Directing the patient's attention away from respiratory sensation decreasesunpleasantness but not intensity, even if the difference in A1/SI is quite small. Carrieri-Kohlman et al.43 have shown no correlation between patients' state of anxiety and their anxietyassociated with dyspnea during treadmill testing. Also, exercise training decreased dyspnea and relatedanxiety. These data indicate that the decrease in anxiety is specific for dyspnea and not related to a decrease inoverall anxiety. The same group demonstrated that in COPD patients the relationship between affective andsensory dimensions can be changed within individual subjects. The authors pointed out that a supervisedexercise training program reduced dyspnea-related anxiety more than the intensity of breathing effort. 44 Thisalso suggests that the affective state can limit a patient's exercise tolerance during pulmonary rehabilitation, byreducing its beneficial effect.45 Negative affective states, when compared with positive affective states, increase the perception of dyspneaduring cycling exercise in patients with COPD. The affective unpleasantness of dyspnea during exercise ispredictive of a greater symptom burden in patients' everyday life and a greater reduction in their health-related

quality of life. 46 In other words, those patients experiencing their dyspnea as very unpleasant showed greatersymptom burden in their everyday life. No such effect was found for sensory intensity of dyspnea. Limbic structures have been identified as brain structures involved in the perception of pain.27,29 Banzett et al.30,47 and Evans et al.48 speculated that limbic structures were also involved in the perception of dyspnea. Theyfound activation of mid/anterior insula during severe air hunger. In a functional imaging study (Pet) Peiffer et al.49 were able to identify an area in the right posterior cingulated cortex during loaded breathing-induced dyspneawhich they hypothesised to be associated with affective cognitive factors. Several regions in the posteriorcingulated gyrus have indeed been previously been shown to be activated by various predominantly unpleasantsensory affective functions such as pain, emotion, anxiety, and related symptoms. Von Leupoldt et al.investigated the cortical area associated with the processing of affective unpleasantness of dyspnea bymagnetic resonance imaging (MRI) in healthy subjects. 50 Dyspnea was induced by inspiratory resistivebreathing with concomitant positive and negative emotional stimulation. The BOLD (blood oxygen level-dependent contrast) technique showed that negative emotional situations were associated with similar levels ofintensity but higher unpleasantness of dyspnea when compared with concomitant positive emotionalstimulation. 50 Higher unpleasantness was associated with neural activation of limbic system (anterior insula andamygdala). The data suggest that unpleasantness but not intensity is processed in the human anterior insulaand amygdala, and that different pathways might process affective and sensory dimensions of perceiveddyspnea. 50 The same group51 has recently shown that lesions of the right anterior insula cortex are associatedwith reduced sensitivity for the perception of dyspnea and pain, especially for their perceived unpleasantness.This study supports the theoretical assumption of a dual cortical processing of respiratory signals of dyspnea. Von Leupoldt et al.52 have also shed light on the underlying brain mechanisms of perceived dyspnea in patientswith asthma. Using function fMRI, they compared neural responses to experimentally-induced dyspnea byresistive load breathing and brain activation with neural responses evoked by heat pain induced by contactthermode in patients with asthma and healthy controls. Patients and controls rated the sensory intensity of bothsensations similarly, while the affective unpleasantness of dyspnea and pain was reduced only in asthmaticpatients. The perceptual differences were mirrored by a decrease in insula cortex activity, but with an increasein periaqueductal gray activity in asthmatic patients during both increased dyspnea and pain. 52 These resultssuggest a down-regulation of affect-related insula cortex activity by periaqueductal gray activity during bothsensations in patients with asthma. Moreover, a longer duration of asthma was correlated with a greaterdecrease in insula cortex response during increasing dyspnea. According to these authors this might representa brain habituation mechanism that reduces the affective unpleasantness of dyspnea in patients with mild tomoderate asthma. It is worth noting that reduced brain activation during dyspnea might constitute an importantrisk factor in asthma. In a more recent study of the same group 53 a negative relationship was found betweenincreased volume of periaqueductal gray and reduced reports of affective unpleasantness. These alterationsare likely to contribute to the blunted perception of dyspnea, at least in patients with mild to moderate asthma. Inturn, increased periaqueductal gray activity might lead to increased inhibition of dyspneic sensory afferent to theinsular cortex with reduced insular activation without structural change in this area. It is not understood,however, how the insula gives rise to perceptions of breathlessness. Given the complexity of the sensation,activation of the insular cortex during dyspnea probably occurs in concert with a larger neural networkfunctioning with the insula to mediate dyspnea perception. 29,31,48,54 Neural circuitry underlying stress and emotion can regulate inflammation,55,56 and peripheral inflammatorymediators can influence mood and cognitive function.57 The body of evidence establishes bi-directional causallinks between inflammation and psychological state.58 Asthma, like many inflammatory disorders, is affected bypsychological stress-suggesting that reciprocal modulation may occur between peripheral factors regulatinginflammation and the central neural circuitry underlying emotion and stress reactivity.59 The neural circuitryinvolved remains, however, elusive and conjectural. Rosenkrantz et al.59 used the late phase component of an

allergic reaction as a model to identify brain regions activated by emotional and physiological cues. Using fMRI,they showed that activity of the anterior cingulated cortex (ACC) and insula to asthma-relevant emotional stimuliis associated with markers of inflammation and airway obstruction in asthmatic subjects exposed to antigen. Inparticular, greater signal changes in the ACC and insula in response to antigen asthma-relevant stimuli areassociated with larger increase in eosinophils and are correlated negatively with FEV1. According toRosenkranz et al. 54,59 these results suggest a neural basis for emotion-induced modulation of airway disease inasthmatic patients. More recently the same group measured neural signal (fRMI) in response to asthmaemotional cues, following allergen exposure in asthmatics with a dual response to allergen challenge,asthmatics with only an immediate response and healthy controls. Insula was activated by asthma-relevantcues (emotional stimuli) compared to general negative cues during the late phase of dual response inasthmatics. 60 Like in the previous study59 the degree of this differential activation predicted changes in airwayinflammation and the decrease in lung function. These findings suggest that changes in neural activity are likelyto reflect both afferent and efferent processes. If the late phase response to allergen depends, at least in part,on neural responsivity to disease-relevant information, then reducing this responsivity should decrease themagnitude of the latter phase response. Thus far, whether functional brain imaging of the interaction betweenemotion and inflammation reflects an asthma neurophenotype remains to be defined. Conclusions Anxiety/Depression are likely contributors to the degree of disability associated with dyspnea in patients withchronic respiratory disease. However, a reciprocal interaction between the perception of Anxiety/Depressionand dyspnea should be taken into account. A differentiation between the sensory and affective components ofthe reported dyspnea in these patients might be of particular importance and improve the accuracy of thesymptom perception. Neuroimaging studies have shed light on the brain networks involved in the perception ofsensory and affective components of dyspnea. Whether this can contribute to the development of more effectivetherapeutic strategies for dyspneic patients remains to be elucidated. Conflict of interest We wish to confirm that there are no known conflicts of interest associated with this publication and there hasbeen no significant financial support for this work that could have influenced its outcome. We confirm that the manuscript has been read and approved by all named authors and that there are no otherpersons who satisfied the criteria for authorship but are not listed. We further confirm that the order of authorslisted in the manuscript has been approved by all of us. We confirm that we have given due consideration to the protection of intellectual property associated with thiswork and that there are no impediments to publication, including the timing of publication, with respect tointellectual property. In doing so, we confirm that we have followed the regulations of our institutions concerningintellectual property. We understand that the Corresponding Author is the sole contact for the Editorial process (including EditorialManager and direct communications with the office). She is responsible for communicating with the otherauthors about progress, submission of revisions and final approval of proofs. We confirm that we have provideda current, correct email address which is accessible by the Corresponding Author. References 1 A.G. Gift, S.M. Plaut, A. Jacox, Psychologic and physiologic factors related to dyspnea in subjects withchronic obstructive pulmonary disease, Heart Lung, Vol. 15, 1986, 595-601 2 A.G. Gift, C.A. Cahill, Psychophysiologic aspects of dyspnea in chronic obstructive pulmonary disease: a pilotstudy, Heart Lung, Vol. 19, 1990, 252-257 3 D.L. Dudley, C.J. Martin, T.H. Holmes, Dyspnea: psychological and physiologic observations, J PsychosomRes, Vol. 11, 1968, 325-339 4 V. Carrieri-Kohlman, S. Janson-Bjerklie, Strategies patients use to manage the sensation of dyspnea, West J

Nurs Res, Vol. 8, 1986, 284-305 5 P. Yellowlees, J. Alpers, J. Bowden, G. Bryant, R. Ruffin, Psychiatric morbidity in patients with chronic airflowobstruction, Med J Aust, Vol. 146, 1987, 305-307 6 G. Brenes, Anxiety and chronic obstructive pulmonary disease: prevalence, impact and treatment, PsychosomMed, Vol. 65, 2003, 963-970 7 R. Andenaes, M. Kalfoss, A. Wahl, Psychological distress and quality of life in hospitalized patients withchronic obstructive pulmonary disease, J Adv Nurs, Vol. 46, 2004, 523-530 8 M. Kunik, K. Roundy, C. Veazey, J. Souchek, P. Richardson, N. Wray, Surprisingly high prevalence of anxietyand depression in chronic breathing disorders, Chest, Vol. 127, 2005, 1205-1211 9 A. Yohannes, R. Baldwin, M. Connolly, Depression and anxiety in elderly outpatients with chronic obstructivepulmonary disease: prevalence, and validation of the BASDEC screening questionnaire, Int J GeriatrPsychiatry, Vol. 15, 2005, 1090-1096 10 G. Gudmundsson, T. Gislason, C. Janson, E. Lindberg, C. Ulrik, E. Brondum, Depression, anxiety and healthstatus after hospitalisation for COPD: a multicentre trial in the Nordic countries, Respir Med, Vol. 100, 2006, 87-93 11 T. Ng, M. Niti, W. Tan, Z. Cao, K. Ong, P. Eng, Depressive symptoms and chronic obstructive pulmonarydisease: effect on mortality, hospital readmission, symptom burden, functional status, and quality of life, ArchIntern Med, Vol. 167, 2007, 60-67 12 M. Williams, P. Cafarella, T. Olds, J. Petkov, P. Frith, Affective descriptors of the sensation of breathlessnessare more highly associated with severity of impairment than physical descriptors in people with COPD, Chest,Vol. 138, 2010, 315-322 13 American Thoracic Society Committee on Dyspnea, An official American Thoracic Society statement: updateon the mechanisms, assessment, and management of dyspnea, Am J Respir Crit Care Med, Vol. 185, 2012,435-452 14 N. Livermore, J.E. Butler, L. Sharpe, R.A. McBain, S.C. Gandevia, D.K. McKenzie, Panic attacks andperception of inspiratory resistive loads in chronic obstructive pulmonary disease, Am J Respir Crit Care Med,Vol. 178, 2008, 7-12 15 A. Von Leupoldt, K. Taube, K. Lehmann, A. Fritzsche, H. Magnussen, The impact of anxiety and depressionon outcomes of pulmonary rehabilitation in patients with COPD, Chest, Vol. 140, 2011, 730-736 16 J. Maurer, V. Rebbapragada, S. Borson, R. Goldstein, M.E. Kunik, Anxiety and depression in COPD: currentunderstanding, unanswered questions, and research needs, Chest, Vol. 134, 2008, 43-56 17 J.P. Solano, B. Gomes, I.J. Higginson, A comparison of symptom prevalence in far advanced cancer, IDS,heart disease, chronic obstructive pulmonary disease and renal disease, Pain Symptom Manage, Vol. 31, 2006,58-69 18 J.A. Cully, D.P. Graham, M.A. Stanley, C.J. Ferguson, A. Sharafkhaneh, J. Souchek, M.E. Kunik, Quality oflife in patients with chronic obstructive pulmonary disease and comorbid anxiety or depression,Psychosomatics, Vol. 47, 2006, 312-319 19 W. Katon, E.H. Lin, K. Kroenke, The association of depression and anxiety with medical symptom burden inpatients with chronic medical illness, Gen Hosp Psychiatry, Vol. 29, 2007, 147-155 20 I. Dahlen, L. Westin, A. Adolfsson, Experience of being a low priority patient during waiting time at anemergency department, Chest, Vol. 5, 2002, 1-9 21 C. Janson, E. Bjrnsson, J. Hetta, G. Boman, Anxiety and depression in relation to respiratory symptomsand asthma, Am J Respir Crit Care Med, Vol. 149, 1994, 930-934 22 A. Chetta, G. Gerra, A. Foresi, A. Zaimovic, M. Del Donno, B. Chittolini, Personality profiles andbreathlessness perception in outpatients with different gradings of asthma, Am J Respir Crit Care Med, Vol. 1,1998, 116-122

23 A.S. Van Peski-Oosterbaan, P. Spinhoven, A.J.W. Van Der Does, N.A. Luuk, L.N.A. Willems, P.J. Sterk,Behav Res Ther, Vol. 34, 1996, 333-340 24 L.P. Boulet, F. Deschesnes, H. Turcotte, F.J. Gignac, Near-fatal asthma: clinical and physiologic features,perception of bronchoconstriction, and psychologic profile, Allergy Clin Immunol, Vol. 88, 1991, 838-846 25 M. Lavietes, C. Sanchez, L. Tiersky, N. Cherniack, B. Natelson, Psychological profile and ventilatoryresponse to inspiratory resistive load testing, Am J Respir Crit Care Med, Vol. 161, 2000, 737-744 26 D.D. Price, Psychological mechanism of pain and analgesia, 1999, IASP Press, Seattle 27 P. Rainville, G.H. Duncan, D.D. Price, B. Carrier, M.C. Bushnell, Pain affect encoded in human anteriorcingulate but not somatosensory cortex, Sci, Vol. 277, 1997, 968-971 28 D.D. Price, Psychological and neural mechanisms of the affective dimension of pain, Sci, Vol. 288, 2000,1769-1772 29 A. Von Leupoldt, T. Sommer, S. Kegal, H.J. Baumann, H. Close, B. Dahme, C. Buchel, Dyspnea and painshare emotion-related brain network, NeuroImage, Vol. 48, 2009, 200-206 30 R.B. Banzett, J.A. Dempsey, D.E. O'Donnell, M.Z. Wamboldt, Symptom perception and respiratory sensationin asthma, Am J Respir Crit Care Med, Vol. 162, 2000, 178-182 31 C. Peiffer, Am J Respir Crit Care Med, Vol. 177, 2008, 937-938 32 P.W. Davenport, R.L. Reep, Cerebral cortex and respiration, J.A. Dempsey, A.I. Pack, Regulation ofbreathing, 1995, Dekker, New York, NY, 365-388 33 R.W. Lansing, R.H. Gracely, R.B. Banzett, The multiple dimensions of dyspnea: review and hypotheses,Respir Physiolo Neurobiol, Vol. 167, 2009, 53-60 34 A. Von Leupoldt, B. Dahme, Differentiation between the sensory and affective dimension of dyspnea duringresistive load breathing in normal subjects, Chest, Vol. 128, 2005, 3345-3349 35 L.P. Boulet, I. Cournoyer, F. Deschesnes, P. Leblanc, A. Nouwen, Perception of airflow obstruction andassociated breathlessness in normal and asthmatic subjects: correlation with anxiety and bronchodilator needs,Thorax, Vol. 49, 1994, 965-970 36 S. De Peuter, V. Lemaigre, I. Van Diest, G. Verleden, M. Demedts, O. Van den Bergh, Differentiationbetween the sensory and affective aspects of histamine-induced bronchoconstriction in asthma, Respir Med,Vol. 101, 2007, 925-932 37 S. De Peuter, I. Van Diest, V. Lemaigre, G. Verleden, M. Demedts, O. Van den Bergh, Dyspnea: the role ofpsychological processes, Clin Psychol Rev, Vol. 24, 2004, 557-581 38 S. Rietveld, Symptom perception in asthma: a multidisciplinary review, J Asthma, Vol. 35, 1998, 137-146 39 C. Put, O. Van den Bergh, E. Van Ongeval, S. De Peuter, M. Demedts, G. Verleden, Negative affectivity andthe influence of suggestion on asthma symptoms, J Psychosom Res, Vol. 57, 2004, 249-255 40 P.W. Davenport, M. Cruz, A.A. Stecenko, Y. Kifle, Respiratory-related evoked potentials in children with life-threatening asthma, Am J Respir Crit Care Med, Vol. 161, 2000, 1830-1835 41 R.B. Banzett, S.H. Pedersen, R.M. Schwartzstein, R.W. Lansing, Am J Respir Crit Care Med, Vol. 177,2008, 1384-1390 42 A. Von Leupoldt, A. Vovk, M.M. Bradley, P.J. Lang, P.W. Davenport, Habituation in neural processing andsubjective perception of respiratory sensations, Psychophysiology, Vol. 48, 2011, 808-812 43 V. Carrieri-Kohlman, J.M. Gormley, M.K. Douglas, S.M. Paul, M.S. Stulbarg, Exercise training decreasesdyspnea and the distress and anxiety associated with it. Monitoring alone may be as effective as coaching,Chest, Vol. 110, 1996, 1526-1535 44 V. Carrieri-Kohlman, J.M. Gormley, S. Eiser, S. Demir-Deviren, H. Nguyen, S.M. Paul, Dyspnea and theaffective response during exercise training in obstructive pulmonary disease, Nurs Res, Vol. 50, 2001, 136-146 45 L. Nici, C. Donner, E. Wouters, R. Zuwallack, N. Ambrosino, J. Bourbeau, Am J Respir Crit Care Med, Vol.173, 2006, 1390-1413

46 A. Von Leupoldt, K. Taube, M. Henkhus, B. Dahme, H. Magnussen, The impact of affective states on theperception of dyspnea in patients with chronic obstructive pulmonary disease, Biol Psychol, Vol. 84, 2010, 129-134 47 R.B. Banzett, H.E. Mulnier, K. Murphy, S.D. Rosen, R.J.S. Wise, L. Adams, Breathlessness in humansactivates insular cortex, Brain Imaging, Vol. 11, 2000, 2117-2120 48 K.C. Evans, R.B. Banzett, L. Adams, L. McKay, R.S. Frackowiak, D.R. Corfield, BOLD fMRI identifies limbic,paralimbic, and cerebellar activation during air hunger, J Neurophysiol, Vol. 88, 2002, 1500-1511 49 C. Peiffer, J.B. Poline, L. Thivard, M. Aubier, Y. Samson, Neural substrates for the perception of acutelyinduced dyspnea, Am J Respir Crit Care Med, Vol. 163, 2001, 951-957 50 A. Von Leupoldt, T. Sommer, S. Kegat, H.J. Baumann, H. Klose, B. Dahme, The unpleasantness ofperceived dyspnea is processed in the anterior insula and amygdala, Am J Respir Crit Care Med, Vol. 177,2008, 1026-1032 51 D. Schn, M. Rosenkranz, J. Regelsberger, B. Dahme, C. Bchel, A. von Leupoldt, Reduced perception ofdyspnea and pain after right insular cortex lesions, Am J Respir Crit Care Med, Vol. 178, 2008, 1173-1179 52 A. Von Leupoldt, T. Sommer, S. Kegat, F. Eippert, H.J. Baumann, H. Klose, Down-regulation of insularcortex responses to dyspnea and pain in asthma, Am J Respir Crit Care Med, Vol. 180, 2009, 232-238 53 A. Von Leupoldt, S. Brassen, H.J. Baumann, H. Klose, C. Bchel, Structural brain changes related todisease duration in patients with asthma, PLoS One, Vol. 6, 2011, 237-239 54 M. Rosenkranz, R.J. Davidson, Affective neural circuitry and mind-body influences in asthma, NeuroImage,Vol. 47, 2009, 972-980 55 P.H. Black, Stress and the inflammatory response: a review of neurogenic inflammation, Brain BehavImmun, Vol. 16, 2002, 622-653 56 R.R. Donahue, S.C. LaGraize, P.N. Fuchs, Electrolytic lesion of the anterior cingulate cortex decreasesinflammatory, but not neuropathic nociceptive behavior in rats, Brain Res, Vol. 897, 2001, 131-138 57 S.F. Maier, Bi-directional immune-brain communication: implications for understanding stress, pain, andcognition, Brain Behav Immun, Vol. 17, 2003, 69-85 58 N.A. Harrison, L. Brydon, C. Walker, M.A. Gray, A. Steptoe, Inflammation causes mood changes throughalteration in subgenual cingulated activity and mesolimbic connectivity, Biol Psychiatry, Vol. 66, 2009, 407-414 59 M. Rosenkranz, W.W. Busse, T. Johstone, C.A. Swenson, G.M. Crisafi, M.M. Jackson, Neural circuitryunderlying the interaction between emotion and asthma symptom exacerbation, Proc Natl Acad Sci U S A, Vol.102, 2005, 13319-13324 60 M. Rosenkranz, W.W. Busse, J.F. Sheridan, G.M. Crisafi, R.J. Davidson, PloS One, Vol. 7, Iss. 8, 2012,e40921 Subjek: Studies; Respiratory diseases; Airway management; Respiratory system; Chronic obstructivepulmonary disease; Anxieties; Intellectual property; Load; MeSH: Anxiety -- complications, Asthma -- complications, Asthma -- psychology, Brain -- physiopathology, BrainMapping, Depression -- complications, Dyspnea -- etiology, Dyspnea -- physiopathology, Humans, Dyspnea --psychology (utama), Emotions (utama) Judul: Dyspnea and emotional states in health and disease Pengarang: Scano, Giorgio; Gigliotti, Francesco; Stendardi, Loredana; Gagliardi, Elisa Judul publikasi: Respiratory Medicine Volume: 107 Edisi: 5

Halaman: 649-55 Tahun publikasi: 2013 Tanggal publikasi: May 2013 Tahun: 2013 Penerbit: Elsevier Limited Tempat publikasi: Oxford Negara publikasi: United States Subjek publikasi: Medical Sciences--Respiratory Diseases ISSN: 09546111 Jenis sumber: Scholarly Journals Bahasa publikasi: English Jenis dokumen: Journal Article DOI: http://dx.doi.org/10.1016/j.rmed.2012.12.018 Nomor aksesi: 23347530 ID dokumen ProQuest: 1324273494 URL Dokumen: http://search.proquest.com/docview/1324273494?accountid=38628 Hak cipta: Copyright Elsevier Limited May 2013 Terakhir diperbarui: 2014-03-09 Basis data: ProQuest Nursing & Allied Health Source

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