[Prefrontal and superior temporal lobe hyperactivity as a biological substrate of generalized anxiety disorders].

OBJECTIVE:To explore the potential mechanism of generalized anxiety disorders (GAD). METHODS:Ten GAD patients and 10 sex- and age-matched healthy persons underwent functional magnetic resonance imaging (fMRI) study in 2 stages by block design: auditory presentation of the stimulation task. In experiment 1 emotionally neutral words were given and then alternated with a no word period for 8 cycles. In experiment 2 emotionally neutral words and threat-related words were given alternately for 8 cycles. The subjects were asked to listen carefully and then judge their subjective feeling in mind. By the end of experiment they were asked to fill in a state anxiety inventory (STAI-S) so as to calculate the STAI-S scores. RESULTS:The mean STI-S score of the patients in the experiment 1 was 57 +/- 5, significantly higher than that of the healthy persons (37 +/- 3, P < 0.01); and the mean STAI-S score in the experiment 2 of the patients was 66 +/- 6, significantly higher than that of the healthy persons (41 +/- 4, P < 0.01). The fMRI findings showed that in the experiment 1 the activated cerebral regions of the 2 groups were mostly overlapped, including bilateral superior temporal gyri (BA22/42) and middle temporal gyri (BA21), premotor areas (B46), and supplementary motor areas (BA6), and cerebellar hemisphere, and left inferior prefrontal gyrus (BA44/45). However, the activation intensity levels (mean T values) of the bilateral superior temporal gyri of the patients were both significantly higher than those of the control (for the left side: P = 0.051, and for the right side: P = 0.035). In addition, activation of the dorsal lateral prefrontal cortex (BA8/9) and bilateral inferior parietal lobules (BA39/40). In the experiment 2 activation of brain areas could be seen only in the patients, including bilateral superior temporal gyri, middle temporal gyri, inferior prefrontal gyri, inferior parietal lobules, anterior motor areas, supplemental motor areas, and anterior cingulate gyri (BA8/24/32), and left dorsal lateral prefrontal cortex. No significantly activated brain area could be shown in the control at the same stringent statistic level (P < 0.01, uncorrected); however, when the threshold value (P value) was reduced to 0.01, the left anterior cingulate gyrus (BA24/32), posterior cingulate gyrus (BA29/30), and inferior parietal lobules (BA40) were all significantly activated. CONCLUSION:Dysfunction of superior temporal lobe and dorsal prefrontal cortex, characterized by hyperactivity in response to outer stimuli, may play an important role in the psychopathologic mechanism of GAD.