Anxiety Disorders: Huey ED

Huey ED, Zahn R, Krueger F, Moll J, Kapogiannis D, Wassermann EM, Grafman J. · The National Institute of Neurological Disorders and Stroke, Cognitive Neuroscience Section, NIH/NINDS, Bethesda, MD 20892-1440, USA. · J Neuropsychiatry Clin Neurosci. · Pubmed #19196924 No free full text.

Abstract: Imaging, surgical, and lesion studies suggest that the prefrontal cortex (orbitofrontal and anterior cingulate cortexes), basal ganglia, and thalamus are involved in the pathogenesis of obsessive-compulsive disorder (OCD). On the basis of these findings several models of OCD have been developed, but have had difficulty fully integrating the psychological and neuroanatomical findings of OCD. Recent research in the field of cognitive neuroscience on the normal function of these brain areas demonstrates the role of the orbitofrontal cortex in reward, the anterior cingulate cortex in error detection, the basal ganglia in affecting the threshold for activation of motor and behavioral programs, and the prefrontal cortex in storing memories of behavioral sequences (called "structured event complexes" or SECs). The authors propose that the initiation of these SECs can be accompanied by anxiety that is relieved with completion of the SEC, and that a deficit in this process could be responsible for many of the symptoms of OCD. Specifically, the anxiety can form the basis of an obsession, and a compulsion can be an attempt to receive relief from the anxiety by repeating parts of, or an entire, SEC. The authors discuss empiric support for, and specific experimental predictions of, this model. The authors believe that this model explains the specific symptoms, and integrates the psychology and neuroanatomy of OCD better than previous models.

Koenigs M, Huey ED, Raymont V, Cheon B, Solomon J, Wassermann EM, Grafman J. · Cognitive Neuroscience Section, National Institute of Neurological Disorders and Stroke, US National Institutes of Health, 10 Center Drive, MSC 1440, Bethesda, Maryland, 20892-1440, USA. · Nat Neurosci. · Pubmed #18157125 links to  free full text

Abstract: Post-traumatic stress disorder (PTSD) is an often debilitating mental illness that is characterized by recurrent distressing memories of traumatic events. PTSD is associated with hypoactivity in the ventromedial prefrontal cortex (vmPFC), hyperactivity in the amygdala and reduced volume in the hippocampus, but it is unknown whether these neuroimaging findings reflect the underlying cause or a secondary effect of the disorder. To investigate the causal contribution of specific brain areas to PTSD symptoms, we studied a unique sample of Vietnam War veterans who suffered brain injury and emotionally traumatic events. We found a substantially reduced occurrence of PTSD among those individuals with damage to one of two regions of the brain: the vmPFC and an anterior temporal area that included the amygdala. These results suggest that the vmPFC and amygdala are critically involved in the pathogenesis of PTSD.