September 22, 2003


Study: Paxil aids brain function in PTSD sufferers

By Kathi Baker


Emory researchers have found that paroxetine HCL (Paxil) produces measurable improvement in verbal memory and also increases the size of the hippocampus, a key area of the brain involved in learning and remembering, in persons suffering from post-traumatic stress disorder (PTSD).

Their study, which will be published in the Oct. 1 edition of Biological Psychiatry, also found that Paxil significantly reduces the three main symptom clusters of PTSD: re-experiencing the traumatic event; avoidance and emotional numbing related to experiences that recall the traumatic event; and hyperarousal at inappropriate times.

The study was directed by Douglas Bremner, associate professor of psychiatry and behavioral sciences and director of mental health research at the V.A. Medical Center. Eric Vermetten, former research fellow psychiatry and now at the University of Utrecht in The Nether-lands, was first author. Conducted over a 12-month period, the study examined 23 people who suffered with PTSD from a variety of causes, most commonly childhood abuse.

“Many patients with post-traumatic stress disorder suffer impaired memory, often leading them to experience distorted or fragmented memories of the traumatic event,” Bremner said. “In addition, PTSD patients suffer from problems with new learning and memory as well as concentration. The findings of this study indicate that Paxil may help reverse memory loss and increase hippocampal volume, leading to clinically significant improvements in memory and concentration that will improve their work and social function. It may also be true that improved memory will help trauma survivors reintegrate and work through memories of their own traumatic events.”

Previous studies have demonstrated that patients with PTSD suffer a decrease in volume of the hippocampus, as well as deficits in hippocampal-based learning and memory as measured with neuropsychological testing. Some studies have associated high levels of cortisol, a hormone that regulates stress, with negative effects on this area of the brain. Studies in animals have also shown that medications such as Paxil have a beneficial effect on the growth and structure of hippocampal neurons.

The study participants were all residents of Connecticut. The patients took 10–50 mg of Paxil (average 20 mg) and were evaluated at the end of 36 weeks. No psycho-therapeutic procedure was administered in the study phase, except for supportive therapy. Hippocampal volume was assessed by MRI before and after treatment. Stress parameters and measures of declarative memory function also were evaluated.

Patients in the study experienced significant improvement in verbal declarative memory functions and retention; a 4 percent increase in the right hippocampus, which affects visual/spatial functioning, and a 5.2 percent increase in their left hippocampus, which controls verbal functioning; decreased cortisol levels, a stress regulator, in the brain; and significant relief of each of the three major symptom clusters of PTSD.

“These findings reinforce that post-traumatic stress disorder is caused by biologic changes in the brain, and that medications like Paxil play a neurobiologic role in its treatment,” Bremner said. “This data provides clinicians with insight into the complicated nature of treating PTSD, and the importance of effective treatments.”

Affecting up to 16 million Americans, PTSD is a debilitating condition that develops after experiencing or witnessing a traumatic event. Of people exposed to traumatic events—such as car accidents, natural disasters, physical or sexual assault,
terrorist attack and robbery—as many as 15 percent will develop PTSD. To be diagnosed with PTSD, people must experience intense fear, helplessness or horror and experience each of the three main symptom clusters for more than one month post-exposure to the trauma.