Biological evidence for the development of posttraumatic stress disorder

Biological evidence for the development of posttraumatic stress disorder

What is the evidence regarding a biological basis for the development of posttraumatic stress disorder (PTSD)? 

The neural circuitry implicated in PTSD has been hypothesized to involve interactions between the thalamus, the hippocampus, the amygdala, the posterior cingulate, parietal and motor cortex, and the medial prefrontal cortex. Structural neuroimaging studies have revealed diminished hippocampal volume, reduced left amygdala volumes, and significantly smaller anterior cingulate cortex in persons with PTSD. 

Functional neuroimaging has further shown hyperresponsive amygdala and dorsal anterior cingulate cortex in PTSD.

However, the most replicated functional neuroimaging finding in PTSD has been the hyporesponsivity of the ventromedial prefrontal cortex (vmPFC).

Increased activity in the amygdala secondary to reduced inhibition by the vmPFC has therefore been suggested as a key component in the development of some PTSD symptoms. 

Patients with PTSD also demonstrate heightened autonomic response and electromyographic reactivity (especially in the facial musculature) to external trauma-related stimuli and to startling stimuli.

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