Ibogaine is associated with reorganization of high-beta brain networks in veterans with post-traumatic stress disorder

A single dose of the atypical psychedelic ibogaine can be highly effective at treating PTSD in veterans up to twelve months later, according to an observational study of 30 veterans. Using a novel EEG analysis method, researchers found that ibogaine shifted high-beta (24 and 25 Hz) brain networks from frontal areas toward posterior regions, an effect seen both three to four days and one month after treatment. This posterior shift correlated with improvements in PTSD symptoms and was replicated in an independent dataset on ibogaine for opioid use disorder. Neural modeling suggested the shift reflects increased corticocortical, not corticothalamic, connectivity. The reconfiguration of high-beta networks may be a robust biomarker for ibogaine's therapeutic effects.

Study at a glance

Abstract

Abstract Post-traumatic stress disorder (PTSD) is a debilitating condition that affects millions of veterans. A recent observational study in 30 veterans showed that a single dose of the atypical psychedelic ibogaine can be highly effective at treating PTSD up to twelve months later. Although a prior study demonstrated that ibogaine transiently alters electroencephalography (EEG) power in various frequency bands, the long-term, network-level neural mechanisms targeted by ibogaine are unclear. Here, we investigated whether ibogaine-related clinical improvements are associated with the reorganization of certain brain networks. We applied a novel framework, FREQuency-resolved brain Network Estimation via Source Separation (FREQ-NESS), to identify frequency-specific brain networks in resting-state EEG data acquired at baseline, three to four days after treatment (immediate-post), and one month after ibogaine. At both the immediate-post and one month-post timepoints, high-beta (24 and 25 Hz) networks shifted away from frontal areas and towards posterior regions, an effect that was replicated in an independent EEG dataset on ibogaine treatment for opioid use disorder. This posterior shift was significantly correlated with improvements in PTSD symptoms at both timepoints. Neural field modeling demonstrated that these posterior high-beta shifts are associated with increases in corticocortical, but not corticothalamic, connectivity. Our results are consistent with prior evidence implicating aberrant frontal beta-band activity in PTSD. Overall, we demonstrate that the reconfiguration of high-beta brain networks could be a robust biomarker for ibogaine’s therapeutic effects.