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10th International Congress of the International Neuropsychiatric Association (INA)Jerusalem, Israel October 14-16, 2015

Dr. Jesse Viner, Dr. Laura Viner and Leah Klein of Yellowbrick attended the conference. Both Laura Viner and Leah Klein presented.

Their abstract, COMT and Deregulation of the Prefrontal Cortex in PTSD has been accepted for poster presentation.

Dr. Jesse Viner, MD and Laura Viner, PhD

Laura Viner, PhD and Leah Klein

 

COMT and Deregulation of the Prefrontal Cortex in PTSD

Laura Viner, PhD, Jesse Viner, MD, Leah Klein, BS and Emily Rose Kirschenbaum

Dopaminergic inhibition exerts a central role in the modulation of the limbic system and its fear-based attention and response systems implicated in PTSD. Several recent studies suggest that the genomic variant of catechol-O-methyltransferase (COMT), an enzyme responsible for intrasynaptic dopamine degradation, valine (Val/Val) has been linked to faster levels of dopamine degradation in the prefrontal cortex as compared to the methionine (Met/Met) variant. This, in turn, has been implicated in an increased vulnerability to PTSD when exposed to trauma, as compared to the resilience associated with Met/Met. The present study examined the relative association between these two variants of COMT, Val/Val and Met/Met, and the corresponding deregulation/regulation of the prefrontal cortex, in patients who develop PTSD when exposed to trauma, relative to those who do not.

Twenty-eight consecutive patients admitted to Yellowbrick, an intensive supported apartment treatment center, were given extensive initial assessments including SCID diagnoses, genomic analysis using commercially available assays (Assure RX or Genomind), and qEEG studies of localized brain function using the standard 10/20 EEG array during Eyes Closed with Neuroguide software and LORETA 3-dimensional source analysis. Seventeen patients were SCID-diagnosed with PTSD and 11 with trauma but no PTSD. Chi-Square analyses showed that, as expected, a significantly greater percent of patients with the genotype Val/Val had PTSD, whereas Met/Met was greater in those who had trauma without PTSD (p<.01). Also consistent with lower levels of dopamine in the prefrontal cortex, a greater percentage of patients with PTSD showed at least 2 SD greater deregulation of the prefrontal cortex than did patients with trauma but no PTSD (p<.01). These findings have potential implications for both assessment and treatment of trauma and PTSD.

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