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Objectives. Neurobiologically, panic disorder (PD) is supposed to be characterised by cerebral hypofrontality. Via functional near-infrared spectroscopy (fNIRS), we investigated whether prefrontal hypoactivity during cognitive tasks in PD-patients compared to healthy controls (HC) could be replicated. As intermittent theta burst stimulation (iTBS) modulates cortical activity, we furthermore investigated its ability to normalise prefrontal activation. Methods. Forty-four PD-patients, randomised to sham or verum group, received 15 iTBS-sessions above the left dorsolateral prefrontal cortex (DLPFC) in addition to psychoeducation. Before first and after last iTBS-treatment, cortical activity during a verbal fluency task was assessed via fNIRS and compared to the results of 23 HC. Results. At baseline, PD-patients showed hypofrontality including the DLPFC, which differed significantly from activation patterns of HC. However, verum iTBS did not augment prefrontal fNIRS activation. Solely after sham iTBS, a significant increase of measured fNIRS activation in the left inferior frontal gyrus (IFG) during the phonological task was found. Conclusion. Our results support findings that PD is characterised by prefrontal hypoactivation during cognitive performance. However, verum iTBS as an “add-on” to psychoeducation did not augment prefrontal activity. Instead we only found increased fNIRS activation in the left IFG after sham iTBS application. Possible reasons including task-related psychophysiological arousal are discussed.

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BackgroundA relevant proportion of patients with panic disorder (PD) does not improve even though they receive state of the art treatment for anxiety disorders such as cognitive-behavioural therapy (CBT). At the same time, it is known, that from a neurobiological point of view, PD patients are often characterised by prefrontal hypoactivation. Intermittent Theta Burst Stimulation (iTBS) is a non-invasive type of neurostimulation which can modulate cortical activity and thus has the potential to normalise prefrontal hypoactivity found in PD. We therefore aimed at investigating the effects of iTBS as an innovative add-on to CBT in the treatment for PD.MethodsIn this double-blind, bicentric study, 44 PD patients, randomised to sham or verum stimulation, received 15 sessions of iTBS over the left prefrontal cortex (PFC) in addition to 9 weeks of group CBT. Cortical activity during a cognitive as well as an emotional (Emotional Stroop) paradigm was assessed both at baseline and post-iTBS treatment using functional near-infrared spectroscopy (fNIRS) and compared to healthy controls.ResultsIn this manuscript we only report the results of the emotional paradigm; for the results of the cognitive paradigm please refer to Deppermann et al. (2014).During the Emotional Stroop test, PD patients showed significantly reduced activation to panic-related compared to neutral stimuli for the left PFC at baseline. Bilateral prefrontal activation for panic-related stimuli significantly increased after verum iTBS only. Clinical ratings significantly improved during CBT and remained stable at follow-up. However, no clinical differences between the verum- and sham-stimulated group were identified, except for a more stable reduction of agoraphobic avoidance during follow-up in the verum iTBS group.LimitationsLimitations include insufficient blinding, the missing control for possible state-dependent iTBS effects, and the timing of iTBS application during CBT.ConclusionPrefrontal hypoactivity in PD patients was normalised by add-on iTBS. Clinical improvement of anxiety symptoms was not affected by iTBS.

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Background: Recently, research into attention-deficit/hyperactivity disorder (ADHD) has focused increasingly on its neurobiological under pinnings, revealing (among other things) frontal lobe alterations. Specifically, action-monitoring deficits have been described, including impaired behavioural adjustments following errors. Our aim was to examine the neurophysiological background of post-error behavioural alterations in an adult ADHD sample for the first time, hypothesizing that people with ADHD would differ from controls in neurophysiological markers of cognitive preparation and stimulus processing, specifically following errors. Methods: In total, 34 people with ADHD and 34 controls participated in an electroencephalography measurement while performing a flanker task. The final number of electroencephalography samples included in the analyses ranged from 23 to 28. We recorded event-related potentials for the erroneous response itself (error-related negativity) and for events following errors (intertrial interval: contingent negative variation; next flanker stimu lus: P300). Results: Over frontal electrode sites, error-related negativity amplitudes were significantly reduced in people with ADHD across response conditions. Both groups showed reduced P300 amplitudes on flanker stimuli following errors. Moreover, during the intertrial interval, patients exhibited significantly reduced contingent negative variation, specifically following errors. At the behavioural level, we observed no significant group differences in post-error data. Limitations: Only adults were examined (no longitudinal data). Conclusion: Based on previous reports of post-error behavioural alterations in childhood samples, we conclude that people with ADHD develop compensatory strategies across the lifespan that lead to inconspicuous post-error behaviour in adulthood. Neurophysiologically, however, subtle alterations remain, indicating a perseverance of at least some frontal lobe deficits in people with ADHD who are partially medicated, particularly with respect to action-monitoring and post-error adaptation.