The amygdala is a region of the brain known for its connections to emotional responses and fear memories, and hyperreactivity of the amygdala is associated with symptoms of PTSD (post-traumatic stress disorder). That said, it’s quite a leap to design neurosurgical ablation of the amygdala to address someone’s PTSD. This type of irreversible intervention could only be considered because of the presence of another brain disorder: epilepsy.
In a case series published in Neurosurgery, Emory investigators describe how for their first patient with both refractory epilepsy and PTSD, observations of PTSD symptom reduction were fortuitous. However, in a second patient, before-and-after studies could be planned. In both, neurosurgical ablation of the amygdala significantly reduced PTSD symptoms as well as reducing seizure frequency.
Violence and trauma are certainly not gifts, but scientifically, the Grady Trauma Project keeps on giving, even after co-director Kerry Resslerâ€™s 2015 move to Massachusetts. Research at Emory on the neurobiology of post-traumatic stress disorder (PTSD) continues. This Nature Communications paper, published in December with VA-based psychiatrist Aliza Wingo as lead author, is an example.
Three interesting things about this paper:
- The focus on PTSD co-occurring with depression. As the authors note, several studies looking at traumatized individuals found PTSD and depression together more often than they were present separately. This was true of Atlanta inner city residents in the Grady Trauma Project, veterans and survivors of the 2001 World Trade Center attack.
- DICER: the gene whose activity is turned down in blood samples from people with PTSD plus depression. Its name evokes one of the three Fates in Greek mythology, Atropos, who cuts the thread of life. DICER is at the center of a cellular network of regulation, because it is part of the machinery that generates regulatory micro-RNAs.
- The findings recapitulate work in mouse models of stress and its effects on the brain, with a connection to the many-tentacled Wnt signaling/adhesion protein beta-catenin.
Some past posts on the Grady Trauma Projectâ€™s scientific fruits follow. Read more
The connection between stress and blood pressure seems like common sense. Of course experiencing stress — like a narrow miss in morning traffic or dealing with a stubborn, whiny child — raises someoneâ€™s blood pressure.
Try reversing the cause-and-effect relationship: not from brain to body, but instead from body to brain. Could medication for controlling blood pressure moderate the effects of severe stress, and thus aid in controlling PTSD symptoms or in preventing the development of PTSD after trauma?
That was the intriguing implication arising from a 2012 paper from Grady Trauma Project investigators led by psychiatrist Kerry Ressler (lab at Yerkes, supported by HHMI).
They had found that traumatized civilians who take either of two classes of common blood pressure medications tend to have less severe post-traumatic stress symptoms. In particular, individuals taking ACE inhibitors (angiotensin converting enzyme)Â or ARBs (angiotensin receptor blockers)Â tended to have lower levels of hyperarousal and intrusive thoughts, and this effect was not observed with other blood pressure medications.
This was one of those observational findings that needs to be tested in an active way: â€œOK, people who are already taking more X experience less severe symptoms. But can we actually use X as an intervention?â€
In mice, it seems to work. Read more