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Background. Globus is the uncomfortable feeling of a lump in the throat. Although a lot of research has been done on the subject, the etiology remains unclear. Chen et al. (2009) suggested visceral hypersensitivity and aberrant symptom referral as a possible cause. Aim. To assess differences in perception thresholds and symptom location during repeated esophageal and UES balloon distension in subjects with and without globus.Methods. 44 globus patients and 25 healthy controls participated. Perception and discomfort thresholds were assessed using stepwise isobaric esophageal balloon distensions (2mmHg/30sec). The barostat balloon was located in the UES and in the esophageal body 10 cm below the UES. Both tests were repeated, with the second measurement immediately following the first. Location of perception was indicated on a body map. A mixed procedure, two-way ANOVA, was used to analyze the data. Results. Patients showed more proximal discomfort during the second esophageal distension in comparison the first distension (1.62 cm vs. 2.39 cm above the xyphoid, p=0.0030), whereas controls showed no significant changes. Patients showed lower discomfort thresholds at second distension (sensitization, from 21.41 mmHg vs. 17.19 mmHg, p<.0001) whereas controls did not show any significant changes. Combined, this indicates that the lower the discomfort thresholds, the higher patients perceive the sensation of discomfort, as confirmed by mixed regression analysis. Conclusion. Globus patients perceive the sensation evoked by repeated esophageal balloon distension significantly higher than healthy control. In addition, patients show lowered discomfort thresholds during the second compared to the first distension sequence, whereas controls show no significant changes. We can conclude that the globus patients are characterized by sensitization upon repeated esophageal distension, corresponding with increased height of symptom perception.

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The interaction between stress and fear conditioning serves as an illuminating model in the understanding of anxiety disorders. Previous work has shown that stress may change subsequent fear acquisition and extinction learning, likely through the stress hormone cortisol. However, variable effects have been described, ranging from facilitative, inhibitory, to null effects. In this article, we first performed a systematic review on the association of stress on subsequent fear acquisition and extinction learning in men. Then, we performed secondary analysis on an existing dataset comprising 133 men who underwent the Maastricht Acute Stress Test (MAST) prior to completing a fear acquisition and extinction task. We examined whether cortisol response trajectories derived from latent-class growth analysis (mild responders (n = 15), moderately-low responders (n = 46), moderately-high responders (n = 48), and hyper responders (n = 24)) could predict the rate of fear acquisition and/or extinction learning, as assessed by US expectancy ratings and skin conductance responses (SCRs). Our systematic review did not reveal a clear consensus pertaining to the association of stress on subsequent fear acquisition. For fear extinction, a negative association of stress exposure, and thus greater extinction resistance, was indicated. In our analysis, we found no significant associations between cortisol response trajectories in response to the MAST and subsequent fear acquisition. We did find an association with extinction learning as assessed by US expectancy ratings, suggesting better safety learning in participants with a hyper-responder cortisol trajectory participant. In addition, during extinction learning, higher overall SCRs were observed in these hyper-responders, indicating greater general arousal during extinction learning independent of stimulus type. These results demonstrate that cortisol responsiveness to a psychosocial stressor interferes with rate of extinction learning at the subjective level and promoted general arousal during this phase at the physiological level. As extinction learning is the theoretical model of exposure therapy, these findings could have clinical implications.

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Introduction Irritable bowel syndrome (IBS) and its comorbidities are thought to be associated with a dysfunction of the stress system. Tools like the Montreal Imaging Stress Task (MIST) and the Maastricht Acute Stress Test (MAST) have been developed to assess the response to experimental stress induction. The main aim of this pilot study is to investigate the effectiveness of these instruments in inducing stress in the population of IBS patients. Methods For both stress tasks, we included 9 patients diagnosed with irritable bowel syndrome according to the Rome IV criteria, regardless of the presence of any comorbidities. The MIST involved the performance of mental arithmetic in an MRI-scanner, with the temporary addition of stress provoking elements during the so-called ‘stress blocks’. During the MAST, stress was induced by alternating hand immersion trials in cold water and mental arithmetic, with a social evaluative component. The perceived stress during both tasks was assessed by means of short questionnaires and Visual Analogue Scales (VAS). Results Both the MIST and the MAST seemed to be effective in eliciting subjective stress. In our small patient samples, not all effect sizes were large enough to be significant, presumably partly due to the presence of anticipatory stress at the moment the first VAS in the MAST protocol was completed. Interestingly, the functional brain images primarily revealed stress-induced activation of the cerebellum, more specifically at the level of the left crus I and the right lobule VI. Discussion We can proceed using these tools for stress induction in the population of IBS patients, provided that subjective scores continue to be monitored. Furthermore, we suggest the addition of a baseline VAS in the MAST protocol, to reduce the effect of anticipatory stress. The interesting finding of cerebellar activation during stress supports existing hypotheses of an underestimated role for the cerebellum in the stress system and in the IBS pathophysiology.