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(2008) tested auditory sensory gating with a paired click paradigm in patients with OCD and found a disrupted P50 S2/S1 ratio. Ghisolfi et al. (2004), using auditory stimulation, reported significantly greater S2/S1 ratios in post-traumatic stress disorder (PTSD) patients, compared to controls. Moreover, Nanbu et al. (2010) found an impaired P50 gating function in the OCD patients represented by elevated S2/S1 ratios with auditory stimuli compared to the HCs. Taken together, these past and the present findings suggest that impaired gating functions in anxiety disorders are not specific for one sensory modality, but can be observed across different interoceptive as well as exteroceptive modalities. Some cautions need to be exercised when generalizing the results of the present study. Firstly, the study participants only self-reported to have no diagnosis of a MAO respiratory disease or acute respiratory symptoms on the test day, such as experiencing a cold. Secondly, our study did not differentiate between patients with shorter disease duration and those with longer disease duration. Since it is sometimes observed by clinicians that patients with longer disease duration might also report rather reduced levels of respiratory sensations than those with shorter disease duration, future studies are encouraged to examine effect of disease duration on respiratory sensory gating. Finally, we cannot fully rule out residual effects of long-term anxiolytic, antidepressant, or antipsychotic medications in the GAD group. Previous studies have indeed demonstrated the potential modulating effects of medications on sensory gating in patients with anxiety disorders (Siegel et al., 2005; de Leeuw et al., 2010). Although our participants were asked to refrain from medication intake 12 h before the experiments, effects of long-term treatments remain unclear. Future studies are, therefore, encouraged to systematically examine the various potential effects of different treatments on respiratory sensory gating. In summary, the present study suggests that patients with GAD show a larger S2/S1 ratio for the RREP N1 peak, which is suggestive of reduced respiratory sensory gating. Whether this pattern of neural processing of respiratory information varies between subgroups of GAD patients and the degree of anxiety requires more investigation. Future research is needed to clarify the effects of respiratory symptoms, medications, and duration of the disease on respiratory sensory gating in patients with GAD. Finally, GAD specific responses to the first of two paired respiratory stimuli and the respective impact on the subsequent gating ratio need further investigation. Conflict of Interest Statement The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.