@misc{SchroederRegnathGlasaueretal., author = {Schr{\"o}der, Lena and Regnath, Franziska and Glasauer, Stefan and Hackenberg, Anna and Hente, Juliane and Weilenmann, Sonja and Pohl, Daniel and K{\"a}nel, Roland von and Lehnen, Nadine}, title = {Altered sensorimotor processing in irritable bowel syndrome: Evidence for a transdiagnostic pathomechanism in functional somatic disorders}, series = {Frontiers in Neuroscience}, volume = {16}, journal = {Frontiers in Neuroscience}, issn = {1662-453X}, doi = {10.3389/fnins.2022.1029126}, abstract = {Objective A recent hypothesis suggests that functional somatic symptoms are due to altered information processing in the brain, with rigid expectations biasing sensorimotor signal processing. First experimental results confirmed such altered processing within the affected symptom modality, e.g., deficient eye-head coordination in patients with functional dizziness. Studies in patients with functional somatic symptoms looking at general, trans-symptomatic processing deficits are sparse. Here, we investigate sensorimotor processing during eye-head gaze shifts in irritable bowel syndrome (IBS) to test whether processing deficits exist across symptom modalities. Methods Study participants were seven patients suffering from IBS and seven age- and gender-matched healthy controls who performed large gaze shifts toward visual targets. Participants performed combined eye-head gaze shifts in the natural condition and with experimentally increased head moment of inertia. Head oscillations as a marker for sensorimotor processing deficits were assessed. Bayes statistics was used to assess evidence for the presence or absence of processing differences between IBS patients and healthy controls. Results With the head moment of inertia increased, IBS patients displayed more pronounced head oscillations than healthy controls (Bayes Factor 10 = 56.4, corresponding to strong evidence). Conclusion Patients with IBS show sensorimotor processing deficits, reflected by increased head oscillations during large gaze shifts to visual targets. In particular, patients with IBS have difficulties to adapt to the context of altered head moment of inertia. Our results suggest general transdiagnostic processing deficits in functional somatic disorders.}, language = {en} } @misc{WerderRegnathSchaeferetal., author = {Werder, Dina von and Regnath, Franziska and Sch{\"a}fer, Daniel and J{\"o}rres, Rudolf and Lehnen, Nadine and Glasauer, Stefan}, title = {Post-COVID breathlessness: a mathematical model of respiratory processing in the brain}, series = {European Archives of Psychiatry and Clinical Neuroscience}, journal = {European Archives of Psychiatry and Clinical Neuroscience}, issn = {0940-1334}, doi = {10.1007/s00406-023-01739-y}, abstract = {Breathlessness is among the most common post-COVID symptoms. In a considerable number of patients, severe breathlessness cannot be explained by peripheral organ impairment. Recent concepts have described how such persistent breathlessness could arise from dysfunctional processing of respiratory information in the brain. In this paper, we present a first quantitative and testable mathematical model of how processing of respiratory-related signals could lead to breathlessness perception. The model is based on recent theories that the brain holds an adaptive and dynamic internal representation of a respiratory state that is based on previous experiences and comprises gas exchange between environment, lung and tissue cells. Perceived breathlessness reflects the brain's estimate of this respiratory state signaling a potentially hazardous disequilibrium in gas exchange. The internal respiratory state evolves from the respiratory state of the last breath, is updated by a sensory measurement of CO2 concentration, and is dependent on the current activity context. To evaluate our model and thus test the assumed mechanism, we used data from an ongoing rebreathing experiment investigating breathlessness in patients with post-COVID without peripheral organ dysfunction (Nā€‰=ā€‰5) and healthy control participants without complaints after COVID-19 (Nā€‰=ā€‰5). Although the observed breathlessness patterns varied extensively between individual participants in the rebreathing experiment, our model shows good performance in replicating these individual, heterogeneous time courses. The model assumes the same underlying processes in the central nervous system in all individuals, i.e., also between patients and healthy control participants, and we hypothesize that differences in breathlessness are explained by different weighting and thus influence of these processes on the final percept. Our model could thus be applied in future studies to provide insight into where in the processing cascade of respiratory signals a deficit is located that leads to (post-COVID) breathlessness. A potential clinical application could be, e.g., the monitoring of effects of pulmonary rehabilitation on respiratory processing in the brain to improve the therapeutic strategies.}, language = {en} }