Neuro endocrinology letters · 2015
Predictors of poor treatment response to additional CBT in real panic disorder patients: The role of DLPF, orbitofrontal cortex, parietal lobule, frontal eye field and amygdala in PD.
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Grambal Aleš, Tüdös Zbyněk, Hok Pavel, Kamarádová Dana, Divéky Tomáš, Hluštík Petr, Praško Ján
Аннотация
OBJECTIVE: Previous functional brain imaging studies have described various and contradictory activation findings in patients with panic disorder (PD). Our study focused on patients with a chronic PD, who were investigated and treated in a conventional manner, which represents the real PD patients in clinical practice.
METHODS: Continuing their medication, patients were included in a six-week cognitive-behavioral therapy (CBT) program in the psychiatry department. At the onset of the study, participants underwent clinical evaluation using standard scales and were examined using fMRI while listening to verbal threat-related stimuli contrasted to neutral words. According to the therapeutic outcome, they were subsequently divided into two groups, responders, and nonresponders and the two groups were mutually compared.
RESULTS: In non-responders compared to responders, we found increased pre-treatment activation in dorsolateral prefrontal cortex bilaterally, left orbitofrontal cortex, left frontal eye field, right parietal lobule and left amygdala. In addition, both groups showed negative fMRI BOLD correlation with BAI improvement and positive correlation with CGI improvement across the ROIs. We suggest that DLPFC over-activation may reveal a lack of cognitive control over emotional processing, which makes subsequent CBT less effective.
CONCLUSION: Despite several limitations, we found neuroimaging predictors of poor CBT response, under the conditions of standard clinical practice, in real PD patients.
METHODS: Continuing their medication, patients were included in a six-week cognitive-behavioral therapy (CBT) program in the psychiatry department. At the onset of the study, participants underwent clinical evaluation using standard scales and were examined using fMRI while listening to verbal threat-related stimuli contrasted to neutral words. According to the therapeutic outcome, they were subsequently divided into two groups, responders, and nonresponders and the two groups were mutually compared.
RESULTS: In non-responders compared to responders, we found increased pre-treatment activation in dorsolateral prefrontal cortex bilaterally, left orbitofrontal cortex, left frontal eye field, right parietal lobule and left amygdala. In addition, both groups showed negative fMRI BOLD correlation with BAI improvement and positive correlation with CGI improvement across the ROIs. We suggest that DLPFC over-activation may reveal a lack of cognitive control over emotional processing, which makes subsequent CBT less effective.
CONCLUSION: Despite several limitations, we found neuroimaging predictors of poor CBT response, under the conditions of standard clinical practice, in real PD patients.