Ibogaine and High Beta Brain Network Reorganization

Kenneth Shinozuka and colleagues, Stanford University, VA Palo Alto, and collaborating institutions

Kenneth Shinozuka and a large multi-institutional team used EEG to examine what happens to brain network organization after ibogaine treatment in veterans with PTSD and traumatic brain injury.

Instead of simply measuring whether a frequency band became stronger or weaker, the team used a method called FREQ NESS, which looks at how brain regions organize together within very specific frequencies. This lets them ask where an oscillatory network is concentrated and whether that spatial organization changes after treatment.

They found that high beta networks around 24 and 25 Hz shifted away from frontal areas of the brain and toward posterior regions after ibogaine. The shift was present three to four days after treatment and remained detectable one month later. The size of the change was also associated with improvement in PTSD symptoms. The researchers then reproduced the same general network shift in a separate dataset from people treated with ibogaine for opioid use disorder.

Their modeling suggested that the change could be reproduced by reducing corticocortical gain, essentially changing how strongly cortical regions influence one another. The authors propose the high beta shift as a possible objective marker of sustained therapeutic change following ibogaine.

The paper also cites my 2025 reward system paper in its discussion of ibogaine and substance use disorder. This was really exciting for me. The authors acknowledge Dr. Nolan Williams for his central role in conceptualizing and designing the work. Someone I respect deeply.

The connection to Neural Attunement is fairly direct. One of the questions behind that framework is whether the period after the acute psychedelic experience contains measurable signs that the nervous system is reorganizing in a more stable or adaptive direction. This study gives us one possible marker. The change occurs after the acute experience, persists for weeks, and relates to clinical improvement.

That does not establish Neural Attunement. It gives us a measurable phenomenon that can be tested within it.

The authors recommend using task-based EEG or MEG to determine whether the beta changes relate directly to problems such as intrusive memories, impaired attention, and impulse control. I would extend that approach into reward, threat, salience, craving, and cognitive control. If a resting network change also predicts how those systems respond when challenged, it becomes much more useful than a simple marker that someone received treatment.

The version discussed here is a preprint that has not been certified by peer review. The observational design cannot separate treatment effects from expectancy or the treatment setting. The model estimates effective coupling from EEG; it does not directly measure synaptic connections.