OBJECTIVES: Abnormal attentional and cognitive processes are thought to increase the risk for depression and anxiety. To improve understanding of brain mechanisms of anxiety and depressive disorders and condition of their comorbidity, the study of early attentional processes was provided. METHODS: Participants were patients with depressive (80 s.), anxiety (69 s.), and comorbid (41 s.) disorders, and healthy volunteers (50 s.). Acoustic startle response (ASR) and P50 component of the auditory event-related potential were recorded. RESULTS: In the ASR model decreased startle response amplitude at the left eye in patients with comorbid disorder was found, and ASR latency was lengthened in all clinical groups. Deficit of prepulse inhibition was unique for comorbid disorder, and might be considered as risk of evolution to more serious condition. Reduced prepulse facilitation was revealed in patients with comorbid and anxiety disorders. In P50 suppression paradigm decreased S1 response amplitude was revealed in all clinical groups, P50 latency was prolonged in depressive and comorbid patients, and P50 suppression deficit was observed in depression and anxiety groups. CONCLUSIONS: The obtained results might be useful for development of integrative neural models of comorbidity of anxiety and depression, and elaboration of diagnostic and therapeutic approaches.
OBJECTIVES:Abnormal attentional and cognitive processes are thought to increase the risk for depression and anxiety. To improve understanding of brain mechanisms of anxiety and depressive disorders and condition of their comorbidity, the study of early attentional processes was provided. METHODS:Participants were patients with depressive (80 s.), anxiety (69 s.), and comorbid (41 s.) disorders, and healthy volunteers (50 s.). Acoustic startle response (ASR) and P50 component of the auditory event-related potential were recorded. RESULTS: In the ASR model decreased startle response amplitude at the left eye in patients with comorbid disorder was found, and ASR latency was lengthened in all clinical groups. Deficit of prepulse inhibition was unique for comorbid disorder, and might be considered as risk of evolution to more serious condition. Reduced prepulse facilitation was revealed in patients with comorbid and anxiety disorders. In P50 suppression paradigm decreased S1 response amplitude was revealed in all clinical groups, P50 latency was prolonged in depressive and comorbid patients, and P50suppression deficit was observed in depression and anxiety groups. CONCLUSIONS: The obtained results might be useful for development of integrative neural models of comorbidity of anxiety and depression, and elaboration of diagnostic and therapeutic approaches.