Structural and functional plasticity of the human brain in posttraumatic stress disorder.
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.
Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA, USA. jdbremn@emory.edu
J Douglas
JD
Bremner
Bernet
B
Elzinga
Christian
C
Schmahl
Eric
E
Vermetten
D000818:Animals; D001921:Brain / Q000473:pathology* / Q000503:physiopathology*; D001923:Brain Chemistry / Q000502:physiology; D005239:Fear / Q000502:physiology; D005971:Glutamates / Q000378:metabolism; D006624:Hippocampus / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D008568:Memory / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology*; D018377:Neurotransmitter Agents / Q000502:physiology; D013313:Stress Disorders, Post-Traumatic / Q000473:pathology* / Q000503:physiopathology*
D005971:Glutamates; D018377:Neurotransmitter Agents