A single low-dose infusion of ketamine, an NMDA receptor antagonist, given after recalling a traumatic memory can weaken the fear response associated with post-traumatic stress disorder. In the study, people who received ketamine showed lower activity in the amygdala and hippocampus when re-exposed to trauma memories, compared to those who received midazolam. Ketamine also reduced communication between the amygdala and hippocampus, without affecting connections to the prefrontal cortex. These changes lasted at least 30 days after treatment, suggesting that human traumatic memories can be altered during a reconsolidation window, potentially offering a new approach to treating PTSD.
A single dose of a dissociative drug altered resting-state functional connectivity between frontal and limbic brain regions in individuals with posttraumatic stress disorder, suggesting a potential mechanism for its therapeutic effects. The randomized controlled pilot study compared drug versus placebo in a small sample, finding changes in connectivity patterns that may relate to symptom reduction. The authors indicate that these preliminary results warrant further investigation in larger trials.
A subanesthetic dose of ketamine did not increase resting-state functional connectivity between the medial prefrontal cortex and amygdala in individuals with PTSD, contrary to prior correlational findings. Instead, ketamine produced a stronger transient decrease in vmPFC-amygdala connectivity compared to the control drug midazolam. These preliminary results from a randomized controlled pilot study challenge the view that dissociation involves emotion overmodulation via increased fronto-limbic connectivity, suggesting a more nuanced neurobiological understanding of dissociative phenomena in PTSD is needed.