M. Cornelia Stoeckel’s research while affiliated with University Medical Center Hamburg - Eppendorf and other places

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Publications (10)


Breathlessness amplifies amygdala responses during affective processing
  • Article

April 2018

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74 Reads

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13 Citations

Psychophysiology

M. Cornelia Stoeckel

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Breathlessness is an aversive symptom in many prevalent somatic and psychiatric diseases and is usually experienced as highly threatening. It is strongly associated with negative affect, but the underlying neural processes remain poorly understood. Therefore, using fMRI, the present study examined the effects of breathlessness on the neural processing of affective visual stimuli within candidate brain areas including the amygdala, insula, and anterior cingulate cortex (ACC). During scanning, 42 healthy volunteers, mean (SD) age: 29.0 (6.0) years, 14 female, were presented with affective picture series of negative, neutral, and positive valence while experiencing either no breathlessness (baseline conditions) or resistive‐load induced breathlessness (breathlessness conditions). Respiratory measures and self‐reports suggested successful induction of breathlessness and affective experiences. Self‐reports of breathlessness intensity and unpleasantness were significantly higher during breathlessness conditions, mean (SD): 45.0 (16.6) and 32.3 (19.8), as compared to baseline conditions, mean (SD): 1.9 (3.0) and 2.9 (5.5). Compared to baseline conditions, stronger amygdala activations were observed during breathlessness conditions for both negative and positive affective picture series relative to neutral picture series, while no such effects were observed in insula and ACC. The present findings demonstrate that breathlessness amplifies amygdala responses during affective processing, suggesting an important role of the amygdala for mediating the interactions between breathlessness and affective states.


Dyspnea catastrophizing and neural activations during the anticipation and perception of dyspnea

September 2017

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43 Reads

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37 Citations

Psychophysiology

M. Cornelia Stoeckel

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Dyspnea is an aversive symptom in various diseases. High levels of negative affectivity are typically associated with increased dyspnea and changes in its neural processing. Recently, more dyspnea-specific forms of negative affectivity such as dyspnea catastrophizing were suggested to contribute to increased perception of dyspnea beyond effects of rather unspecific negative affectivity such as general anxiety levels. The involved neural mechanisms have not yet been explored. Therefore, the present retrospective analysis examined the associations of dyspnea catastrophizing with neural activations during the anticipation and perception of dyspnea. Sixty-six healthy volunteers underwent 20 blocks of inspiratory resistive load breathing with parallel acquisition of fMRI data. Loads inducing either severe or mild dyspnea (dyspnea conditions) were presented in alternating order, with each condition being visually cued (anticipation conditions). Dyspnea catastrophizing and general trait anxiety were measured with the Breathlessness Catastrophizing Scale (BCS) and the State-Trait Anxiety Inventory, respectively. Correlating the BCS scores with neural activations during the perception of dyspnea yielded no significant results. However, during the anticipation of dyspnea, BCS scores correlated positively with activations of the anterior cingulate cortex (ACC), even after controlling for general anxiety levels. These activations in the ACC were not related to concurrent respiratory parameters. Results suggest that dyspnea catastrophizing in healthy volunteers is associated with stronger ACC recruitment during dyspnea anticipation. Given the established role of the ACC in processing affective states, affect regulation, and antinociception, this might reflect increased affective and/or top-down modulatory processing in individuals with higher dyspnea catastrophizing when anticipating dyspnea.


Supplementary Material
  • Data
  • File available

August 2017

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17 Reads

Download

Diagram of scanning protocol for one trial (out of ten). The entire scan duration was about 13–17 min and differed between participants due to differences in individual rating speed.
Brain activation during the perception of increased dyspnea. (A) Patients with COPD showed significant activation in the supplementary-motor area (SMA), sensorimotor cortices (SMC: primary sensorimotor cortex and secondary somatosensory cortex/operculum), thalamus (Th), anterior cingulate cortex (ACC), dorso-medial prefrontal cortex (dmPFC), and insula. (B) The control group showed significant activation in comparable brain areas. (C) The conjunction analysis (patients ∩ control subjects) revealed shared brain activation during increased dyspnea perception between the patient and control group. For visual purposes, activation is thresholded at puncorrected < 0.001 with colorbars indicating T-values.
Brain areas with significantly higher neural activation in patients with COPD compared to the control group during the anticipation of increased dyspnea. (A) Bilateral hippocampus, (B) right amygdala, and (C) right hippocampus and amygdala. Enhanced neural activation in these brain regions was correlated with patient characteristics such as reduced exercise capacity, higher level of dyspnea, and anxiety in the left hippocampus (A), and reduced quality of life in right hippocampus (B) and right amygdala (C). For visual purposes, activation is thresholded at puncorrected < 0.001 with colorbars indicating T-values. Significant correlations are presented as *p < 0.05, **p < 0.01, ***p < 0.001.
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.
MNI-space peak coordinates, z-values, and p-values for regions showing significant brain activation during increased dyspnea perception in patients with COPD. 
Brain Activation during Perception and Anticipation of Dyspnea in Chronic Obstructive Pulmonary Disease

August 2017

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257 Reads

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51 Citations

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, associations between COPD-specific brain activation and clinical patient characteristics were examined. Methods: During functional magnetic resonance imaging, dyspnea was induced in patients with stable moderate-to-severe COPD (n = 17) and healthy control subjects (n = 21) by resistive-loaded breathing. Blocks of severe and mild dyspnea were alternating, with each block being preceded by visually cued anticipation phases. Results: During the perception of increased dyspnea, both patients and controls showed comparable brain activation in common dyspnea-relevant sensorimotor and cortico-limbic brain regions. During the anticipation of increased dyspnea, patients showed higher activation in hippocampus and amygdala than controls which was significantly correlated with reduced exercise capacity, reduced health-related quality of life, and higher levels of dyspnea and anxiety. Conclusions: This study suggests that patients with stable moderate-to-severe COPD show higher activation in emotion-related brain areas than healthy controls during the anticipation, but not during the actual perception of experimentally induced dyspnea. These brain activations were related to important clinical characteristics and might contribute to an unfavorable course of the disease via maladaptive psychological and behavioral mechanisms.


Brain Responses during the Anticipation of Dyspnea

January 2016

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141 Reads

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58 Citations

Dyspnea is common in many cardiorespiratory diseases. Already the anticipation of this aversive symptom elicits fear in many patients resulting in unfavorable health behaviors such as activity avoidance and sedentary lifestyle. This study investigated brain mechanisms underlying these anticipatory processes. We induced dyspnea using resistive-load breathing in healthy subjects during functional magnetic resonance imaging. Blocks of severe and mild dyspnea alternated, each preceded by anticipation periods. Severe dyspnea activated a network of sensorimotor, cerebellar, and limbic areas. The left insular, parietal opercular, and cerebellar cortices showed increased activation already during dyspnea anticipation. Left insular and parietal opercular cortex showed increased connectivity with right insular and anterior cingulate cortex when severe dyspnea was anticipated, while the cerebellum showed increased connectivity with the amygdala. Notably, insular activation during dyspnea perception was positively correlated with midbrain activation during anticipation. Moreover, anticipatory fear was positively correlated with anticipatory activation in right insular and anterior cingulate cortex. The results demonstrate that dyspnea anticipation activates brain areas involved in dyspnea perception. The involvement of emotion-related areas such as insula, anterior cingulate cortex, and amygdala during dyspnea anticipation most likely reflects anticipatory fear and might underlie the development of unfavorable health behaviors in patients suffering from dyspnea.


Neural correlates of dyspnea in COPD

September 2015

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42 Reads

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2 Citations

European Respiratory Journal

Patients with COPD suffer from chronic dyspnea. Previous studies on the neural mechanisms underlying dyspnea perception were investigated in healthy volunteers only. We tested whether COPD patients compared to healthy controls show different neural responses while anticipating and perceiving dyspnea, and whether neural responses correlate with disease-specific characteristics. Using functional magnetic resonance imaging, 17 stable outpatients with moderate-to-severe COPD were compared with 21 matched controls. Conditions of baseline and inspiratory resistive load-induced dyspnea were repeatedly presented for 24s in alternating order. Each trial was preceded by a 6s anticipation phase, being signalled by specific cues . After each trial subjects provided Borg ratings of perceived dyspnea unpleasantness and intensity. Patients and controls showed comparable ratings of dyspnea unpleasantness and intensity. During dyspnea perception, patients and controls showed comparable activations in sensorimotor and limbic brain regions with known relevance for dyspnea perception. For dyspnea anticipation, patients showed greater neural activation in fear-related brain areas, such as hippocampus and amygdala, when compared to controls. In patients, disease duration and symptom level were positively correlated with neural activity in the amygdala, anterior cingulate, and prefrontal cortex. The present findings suggest that chronic exposure to dyspnea in COPD patients affects mainly neural responses during the anticipation of dyspnea. Correlations between neural activity and disease-specific characteristics might be related to the development of dyspnea-related fear/anxiety, or mirror the neural effort for emotional regulation and control.


Structural Brain Changes in Patients with Chronic Obstructive Pulmonary Disease

July 2015

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66 Reads

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46 Citations

Chest

Patients with Chronic Obstructive Pulmonary Disease (COPD) suffer from chronic dyspnea, which is commonly perceived as highly aversive and threatening. Moreover, COPD is often accompanied by disease-specific fears and avoidance of physical activity. However, little is known about structural brain changes in COPD patients and respective relations with disease duration and disease-specific fears. This study investigated structural brain changes in COPD patients and their relation with disease duration, fear of dyspnea, and fear of physical activity. We used voxel-based morphometric analysis of MRI images to measure differences in generalized cortical degeneration and regional gray matter between 30 patients with moderate-to-severe COPD and 30 matched healthy control subjects. Disease-specific fears were assessed by the COPD anxiety questionnaire. COPD patients showed no generalized cortical degeneration, but decreased gray matter in posterior cingulate cortex (whole brain analysis) as well as in anterior and mid cingulate cortex, hippocampus, and amygdala (regions-of-interest analyses). Patients' reductions in gray matter in anterior cingulate cortex were negatively correlated with disease duration, fear of dyspnea, and fear of physical activity. Mediation analysis revealed that the relation between disease duration and reduced gray matter of the anterior cingulate was mediated by fear of physical activity. COPD patients demonstrated gray matter decreases in brain areas relevant for the processing of dyspnea, fear, and antinociception. These structural brain changes were partly related to longer disease duration and greater disease-specific fears, which might contribute to a less favorable course of the disease.


FIGURE 1 | Early (mean of block 1–5) and late (mean of block 6–10) ratings on dyspnea intensity (A) and unpleasantness (B). The figure shows the change from early ratings (mean set to zero) to late ratings. Red lines thus indicate increases of ratings over time ( " sensitization " ) while green lines indicate decreases ( " habituation " ).  
FIGURE 2 | Trait anxiety as measured by the State-Trait-Anxiety Inventory (STAI-T) correlates significantly with both intensity (r = 0.36, p = 0.007) and unpleasantness (r = 0.46, p = 0.001) of dyspnea ratings (mean late−mean early).  
FIGURE 3 | Localization of correlations between intensity (A) and unpleasantness (B,C) ratings and changes in fMRI activation over time for dyspnea anticipation [(cue dyspnea late−cue baseline late)−(cue dyspnea early−cue baseline early)]. (A) and (B) show negative correlations, while (C) shows positive correlations. Correlations displayed at p uncorr < 0.005 are superimposed on a representative single subjects T1-weighted MR image. Color-bars indicate T-values. OFC, orbitofrontal cortex; PAG, periaqueductal gray; R, right.  
FIGURE 4 | Localization of correlations between intensity (A) and unpleasantness (B,C) ratings and changes in fMRI activation over time for dyspnea perception [(dyspnea late−baseline late)−(dyspnea early−baseline early)]. (A) and (B) show negative correlations, while (C) shows positive correlations. Correlations displayed at p uncorr < 0.005 are superimposed on a representative single subjects T1-weighted MR image. Color-bars indicate T-values. OFC, orbitofrontal cortex; R, right.  
Brain mechanisms of short-term habituation and sensitization toward dyspnea

June 2015

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132 Reads

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26 Citations

Dyspnea is a prevalent and threatening cardinal symptom in many diseases including asthma. Whether patients suffering from dyspnea show habituation or sensitization toward repeated experiences of dyspnea is relevant for both quality of life and treatment success. Understanding the mechanisms, including the underlying brain activation patterns, that determine the dynamics of dyspnea perception seems crucial for the improvement of treatment and rehabilitation. Toward this aim, we investigated the interplay between short-term changes of dyspnea perception and changes of related brain activation. Healthy individuals underwent repeated blocks of resistive load induced dyspnea with parallel acquisition of functional magnetic resonance imaging data. Late vs. early ratings on dyspnea intensity and unpleasantness were correlated with late vs. early brain activation for both, dyspnea anticipation and dyspnea perception. Individual trait and state anxiety were determined using questionnaire data. Our results indicate an involvement of the orbitofrontal cortex (OFC), midbrain/periaqueductal gray (PAG) and anterior insular cortex in habituation/sensitization toward dyspnea. Changes in the anterior insular cortex were particularly linked to changes in dyspnea unpleasantness. Changes of both dyspnea intensity and unpleasantness were positively correlated with state and trait anxiety. Our findings are in line with the suggested relationship between the anterior insular cortex and dyspnea unpleasantness. They further support the notion that habituation/sensitization toward dyspnea is influenced by anxiety. Our study extends the known role of the midbrain/PAG in anti-nociception to an additional involvement in habituation/sensitization toward dyspnea and suggests an interplay with the OFC.


Amygdala response to anticipation of dyspnea is modulated by 5-HTT LPR genotype: Dyspnea and 5-HTTLPR genotype

February 2015

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68 Reads

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17 Citations

Psychophysiology

Dyspnea anticipation and perception varies largely between individuals. To investigate whether genetic factors related to negative affect such as the 5-HTTLPR polymorphism impact this variability, we investigated healthy, 5-HTTLPR stratified volunteers using resistive load induced dyspnea together with fMRI. Alternating blocks of severe and mild dyspnea ("perception") were differentially cued ("anticipation") and followed by intensity and unpleasantness ratings. In addition, volunteers indicated their anticipatory fear during the anticipation periods. There were no genotype-based group differences concerning dyspnea intensity and unpleasantness or brain activation during perception of severe vs. mild dyspnea. However, in risk allele carriers, higher anticipatory fear was paralleled by stronger amygdala activation during anticipation of severe vs. mild dyspnea. These results suggest a role of the 5-HTTLPR genotype in fearful dyspnea anticipation. © 2015 Society for Psychophysiological Research.


Citations (9)


... Importantly, the limbic system is also associated with PTSS [64], with evidence to suggest that interactions between breathlessness and PTSS may manifest in this emotional neural network. For example, breathlessness has been found to heighten amygdala responses during affective processing [65], while negative affect has simultaneously been found to increase breathlessness perception [66]. These findings suggest that there may be a bidirectional link between the negative affect arising due to PTSS and breathlessness. ...

Reference:

The Interactive Effects of Post-Traumatic Stress Symptoms and Breathlessness on Fatigue Severity in Post-COVID-19 Syndrome
Breathlessness amplifies amygdala responses during affective processing
  • Citing Article
  • April 2018

Psychophysiology

... 9,10 It is hypothesized that dyspnea-specific negative affectivity, such as breathlessness catastrophizing, contributes to increased dyspnea perception beyond the effects of general anxiety levels. 11 There are limited options in the literature for determining the extent to which patients with COPD experience dyspnea. The Interpretation of Breathing Problems Questionnaire, which was created for patients with COPD, is hardly utilized because it is challenging to complete in a clinical environment. ...

Dyspnea catastrophizing and neural activations during the anticipation and perception of dyspnea
  • Citing Article
  • September 2017

Psychophysiology

... 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". ...

Brain Activation during Perception and Anticipation of Dyspnea in Chronic Obstructive Pulmonary Disease

... Patients with COPD experience increased dyspnea during daily activities and even at rest, depending on the severity level of the disease. When individuals perceive breathless during activity or at rest, cortical regions associated with their previous dyspnea experience are activated, which stimulates cortical regions processing emotions, such as the insula, anterior cingulate cortex, and amygdala, through neural pathways, thereby triggering the dyspnea-related fear (40). Showing a low-to-moderate significant correlation between kinesiophobia and dyspnea severity, previous studies advocated that dyspnearelated fear in patients with COPD is the main reason for exercise and physical activity avoidance (14,33). ...

Brain Responses during the Anticipation of Dyspnea

... The affective dimension of dyspnea has been related to its association with the activation of limbic cerebral areas. Studies of experimental dyspnea in healthy participants, where breathing discomfort results from the application of mechanical inspiratory loads or from CO 2 stimulation, and studies of clinical dyspnea in patients have shown the involvement of limbic areas such as the anterior and posterior-insula, the cingulate and prefrontal cortices as well as the lateral periaqueductal gray (PAG) (Banzett et al., 2000;Berk et al., 2015;Brannan et al., 2001;Esser et al., 2015;Faull, Jenkinson, Martyn Ezra, & Kyle Ts Pattinson, 2016;Herigstad, Anja Hayen, & Kyle, 2011;Herigstad et al., 2017;von Leupoldt et al. 2008;von Leupoldt and Dahme, 2005;Liotti et al. 2001;Raux et al. 2013;Reijnders et al., 2020;Stewart et al., 2014). These areas are key components of the interoceptive network allowing the conscious monitoring of bodily sensations (Craig, 2002;Critchley, 2004). ...

Neural correlates of dyspnea in COPD
  • Citing Article
  • September 2015

European Respiratory Journal

... The hippocampus is a plastic and vulnerable region of the brain that is especially susceptible to damage [23]. Hippocampal volume loss has been reported in patients with COPD [24,25], in frailty [26,27] and in patients with depression [28]. ...

Structural Brain Changes in Patients with Chronic Obstructive Pulmonary Disease
  • Citing Article
  • July 2015

Chest

... Indeed, OSA patients have an increased drive to breathe (Mezzanotte et al., 1992;Saboisky et al., 2007;Steier et al., 2010) and exhibit a respiratory-related activation of the cerebral cortex visible under the form of slow preinspiratory potentials (PIPs) (Launois et al., 2015), two circumstances generally associated with dyspnea. Respiratory habituation has been described experimentally (Subhan et al., 2003;Von Leupoldt et al., 2011;Wan et al., 2009) and hypothesized to proceed from downregulation of the insular cortex (Stoeckel et al., 2015;Von Leupoldt et al., 2011) or impaired somatosensory processing (Davenport et al., 2000;Fauroux et al., 2007) as it exists in OSA patients (Donzel-Raynaud et al., 2009;Grippo et al., 2011). Demonstrating respiratory habituation in OSA patients would require showing first that a neurophysiological phenomenon usually associated with dyspnea can be evidenced in the absence of dyspnea and second that this phenomenon disappears in response to an intervention associated with "pseudo-relief". ...

Brain mechanisms of short-term habituation and sensitization toward dyspnea

... High anxiety sensitivity is associated with more intense feelings of SOB and additional panic symptoms in response to dyspnea induced through inspiratory resistive loads (110), or tensing respiratory muscles by intercostal muscle biofeedback (97). Neuroimaging studies indicate that habituation to dyspnea is influenced by an individual's level of anxiety in that individuals with low anxiety are more likely to habituate (111). Personality traits such as neuroticism correlate positively with dyspnea intensity (112,113). ...

Amygdala response to anticipation of dyspnea is modulated by 5-HTT LPR genotype: Dyspnea and 5-HTTLPR genotype
  • Citing Article
  • February 2015

Psychophysiology

... Only recently, a first set of respective studies became available, suggesting that experimentally induced dyspnoea might indeed impair different domains of cognitive functioning. For example, JURAVLE et al. [24], demonstrated that resistive loaded breathing impairs the neural processing of affective pictures. Moreover, inspiratory threshold loading decreased the performance in a face recognition task and a locomotor task as suggested by VINCKIER et al. [25] and NIERAT et al. [26]. ...

Investigating the effect of respiratory bodily threat on the processing of emotional pictures
  • Citing Article
  • May 2014

Respiratory Physiology & Neurobiology