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 International Conference on Complex Systems (ICCS2007)

Could limbic dysregulation cause increased trait anxiety and schizophrenic symptoms?

Lilianne Mujica-Parodi
Biomedical Engineering and Psychiatry, Stony Brook Universit

Mayuresh Korgaonkar
Department of Biomedical Engineering, Stony Brook University

Bosky Ravindranath
Department of Biomedical Engineering, Stony Brook University

Anca Radulescu
Department of Applied Mathematics, University of Colorado at Boulder

     Full text: Not available
     Last modified: June 30, 2007

Abstract
Our neuroimaging and clinical studies show that the dynamic interaction between limbic regions - rather than their activation amplitudes - discriminates between more global physiological and behavioral features of individuals. This supports the view of limbic dysregulation as a control system with a negative feedback loop, in which the left Amygdala is the primary excitatory component, and Brodmannís Areas 9 and 45 modulate the inhibition. This approach may be clinically meaningful in understanding the interactions between the complex neural and autonomic components of the emotional arousal response.

We use the cross-correlation coefficient as a traditional statistical measure of similarity between two time series, and therefore a gross measure of dysregulation. In healthy controls, higher Amygdala-Brodmann Area 45 dysregulation correlates with increased trait anxiety and its cardiac characteristics, particularly in response to emotionally ambiguous stimuli. Schizophrenic patients show a comparatively different Amygdala-Brodmann Area 9 dynamics in response to affect-valent stimuli. This implicates prefrontal areas previously known as inhibitory units in a more specific modulation of the arousal response based on threat detection.

Schizophrenia could be then viewed as a disease of homeostatic regulation, whose symptoms may constitute an end-stage of a cyclic and neurodegenerative process, in which limbic dysregulation (caused by compromised inhibition of the amygdala) leads to hyper-arousal, leading to hypercortisolemia, leading to neurotoxicity and further degeneration of the inhibitory limbic areas, and thus to further limbic dysregulation.







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