Brain activation differences in PTSD
> 2/6/2006 8:36:26 PM

The understanding of the clinical syndrome we know today as Post Traumatic Stress Disorder (PTSD) has been a work in progress since the Civil War. A study published by J.M. DaCosta M.D. described in his 1871 paper "On Irritable Heart; A Clinical Study of a Form of Functional Cardiac Disorder and Its Consequences." Soon labeled DaCosta's syndrome, the irritable heart lineage can be traced through the soldier's heart, the effort syndrome, and neurocirculatory asthenia in World War I, anxiety neurosis in World War II, and the mitral valve prolapse syndrome in the second half of the 20th century.

Anyone who has worked with veterans knows that the syndrome of PTSD is real but is also subject to those who would label suffering Vets as "malingerers". These confusing biases are prominent especially when Vets apply to receive "service connection compensation" from the Veterans Administration. The ability to elucidate the changes in brain functioning for those veterans suffering from PTSD would greatly legitimize their suffering and help to rule out the very rare occurrence of the “malingerer”. Veterans need to not be subject to this kind of doubt that is unfortunately common amongst family, employers and even medical personnel. Hope is emerging from studies using PET and fMRI’s brain scans of PTSD sufferers.

A study published this month in the Archives of General Psychiatry demonstrates the value of such studies in expanding our neurophysiologic understanding of PTSD.

The authors discuss their perspective and findings:
“Posttraumatic stress disorder (PTSD) can occur after trauma exposure (eg, combat, assault, and disasters), and it is characterized by various altered emotional responses. Patients with PTSD not only experience intense negative emotional reactions when reminded of their trauma but also report anhedonia, social withdrawal, isolation, and decreased emotional expressivity, referred to as "emotional numbing."

In conclusion, the present study investigated the neural basis of general affective experience in PTSD. By studying controls with and without previous traumatic exposure compared with PTSD patients, we can start differentiating trauma- and PTSD-specific brain activation changes. Ventral MPFC and amygdala hypoactivity to emotional pictures seems to be specifically related to PTSD. These findings prompt future neuroimaging studies to study general emotional processing and the relationship between prefrontal cortical regions and the amygdala to deepen our understanding of the neural circuitry in PTSD”.

Figure 403501

Figure. Statistical parametric brain activation t map of the regional cerebral blood flow response to emotionally negative pictures showing activation in the ventral medial prefrontal cortex (vMPFC) and amygdala (A) greater in normal controls than in posttraumatic stress disorder (PTSD) patients (A) and activation in the amygdala (A) greater in combat controls than in PTSD patients (B). Regional cerebral blood flow data are projected onto a canonical Montreal Neurologic Institute brain.

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