Anxiety is conceptually closely aligned with fear and stress responses and the concept of arousal level. As with most emotional topics concerning the brain the amygdala is implicated in all of the anxiety disorders (Etkin and Wager, 2007).
Within the lierature there is a lateralisation theory of the amygdala. The left amygdala is chiefly responsible for sustained emotional evaluation and the right short and rapid emotional stimuli detection (Phelps et al 2001; Baas et al. 2004). It is now believed past studies have neglected and dismissed right amygdala activation because of older technologies that used lower temporal resolution.
Stein et al. (2007) provides more up to date fMRI evidence for amygdala activation as described above in anxiety prone individuals versus controls. Further studies have noted gender differences, including increased left activation in war veterans with PTSD diagnoses (Shin et al. 2004). It is possible that this can be explained by gender differences in how emotional memories are constructed: language based-left-female; visual based-right-male.
The anterior cingulate cortex is responsible for motor control, cognition and arousal/drive state. Essentially it is involved in translating intentions into actions and in popular metaphor it is implicated in 'fight or flight' responses.
Lesion studies have revealed arousal dysfunction in the absence of other neuropsychological dysfunction.
The dorsomedial prefrontal cortex has an anxiety inhibiting function when active. Kalisch et al. (2004) evidenced trait anxiety correlations to DmPfC function through animal studies and Etkin (2007) mirrored such findings in human lesion studies. Lesions in the DmPfC tend to flatten anxiety responses although findings are inconsistent and there are methodological limitations to the evidence base.
The ventromedial prefrontal cortex has a top down inhibitory effect upon the amygdala. fMRI evidence shows hypoactivation of VmPc when anxiety is high; thus there is a negative correlation to amygdala activity and PET studies have triangulated this finding (Ahs et al. 2009). In theory amydala lesion would necessitate a lower likelihood of developing anxiety and VmPfc lesion would predict an increased likelihood of anxiety development. However, the evidence base is somewhat contradictory, perhaps providing conceptual support for an emotional regulation model rather than a uni directional model of either excitation/inhibition.
Tuesday, 20 December 2011
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