PTSD in Court II: Risk factors, endophenotypes, and biological underpinnings in PTSD

The second article in the series of three for the journal on “PTSD in Court” especially concerns the biological bases that have been found to be associated with PTSD (posttraumatic stress disorder). The cohering concepts in this section relate to risk factors; candidate genes; polygenetics; “gene × environment” interactions; epigenetics; endophenotypes; biomarkers; and connective networks both structurally and functionally (in terms of intrinsic connectivity networks, ICNs, including the DMN, SN, and CEN; that is, default mode, salience, and central executive networks, respectively). Risk factors related to PTSD include pre-event, event- and post-event ones. Some of the genes related to PTSD include: FKBP5, 5-HTTLPR, and COMT (which are, respectively, FK506-binding protein 5 gene, serotonin-transporter linked polymorphic region, catechol-O-methyl-transferase). These genetic findings give an estimate of 30% for the genetic influence on PTSD. The typical brain regions involved in PTSD include the amygdala, hippocampus, and prefrontal cortex, along with the insula. Causal models of behavior are multifactorial and biopsychosocial, and these types of models apply to PTSD, as well. The paper presents a multilevel systems model of psychopathology, including PTSD, which involves three levels - a top-down psychological construct one, a bottom-up symptom connection one, and a middle one involving symptom appraisal. Legally, causality refers to the event at issue needing to meet the bar of being materially contributory to the outcome. Finally, this section of the article reviews empirically-supported therapies for PTSD and the dangers of not receiving treatment for it.