Structural and functional plasticity of the human brain in posttraumatic stress disorder

Abstract

Posttraumatic stress disorder (PTSD) is associated with long-term changes in neurobiology. Brain areas involved in the stress response include the medial prefrontal cortex, hippocampus, and amygdala. Neurohormonal systems that act on the brain areas to modulate PTSD symptoms and memory include glucocorticoids and norepinephrine. Dysfunction of these brain areas is responsible for the symptoms of PTSD. Brain imaging studies show that PTSD patients have increased amygdala reactivity during fear acquisition. Other studies show smaller hippocampal volume. A failure of medial prefrontal/anterior cingulate activation with re-experiencing of the trauma is hypothesized to represent a neural correlate of the failure of extinction seen in PTSD. The brain has the capacity for plasticity in the aftermath of traumatic stress. Antidepressant treatments and changes in environment can reverse the effects of stress on hippocampal neurogenesis, and humans with PTSD showed increased hippocampal volume with both paroxetine and phenytoin.

Fig. 1

Effects of a traumatic script on memory recall. There was a significant difference in delayed paragraph recall for paragraphs encoded after exposure to traumatic scripts compared to paragraphs encoded at a pre-stress baseline (t(22) = −3.39, p<0.01). This showed that stress impaired the ability to consolidate declarative memory.

Fig. 2

Relationship between hippocampal volume measured with MRI and dissociative states measured with the CADSS in women with early abuse and the diagnosis of dissociative identity disorder. There was a significant negative correlation between hippocampal volume and dissociative states (r = −0.54; df = 14; p<0.05), suggesting that increased levels of dissociation were related to smaller hippocampal volume. This correlation was not shown for amygdala volume. In addition there was not an association between level of PTSD symptoms and hippocampal volume in these patients.