Journal of psychopharmacology (Oxford, England)
June 5, 2025
Ben Beaglehole, Paul Glue, Shona Neehoff et al.
19 citations
In an open-label extension of a prior crossover trial, oral ketamine was given for six weeks to people with treatment-resistant depression, post-traumatic stress disorder, or obsessive-compulsive disorder. Doses started at 1-1.5 mg/kg and increased to 1.5-2.5 mg/kg, taken one to three times per week. Symptom scores remained low throughout the six weeks, and the oral formulation was well tolerated with few side effects. The findings suggest that oral ketamine can sustain improvements in these treatment-resistant conditions and offers a practical alternative for maintenance therapy.
Journal of psychopharmacology (Oxford, England)
January 1, 2025
Ben Beaglehole, Paul Glue, Shona Neehoff et al.
12 citations
Ketamine reduces obsessive-compulsive symptoms more than a psychoactive control (fentanyl) in people with severe, treatment-resistant OCD. In a small double-blind trial, participants received a single intramuscular dose of either 0.5 mg/kg ketamine, 1.0 mg/kg ketamine, or 50 µg fentanyl. Both ketamine doses produced greater and dose-related reductions on the Yale-Brown Obsessive-Compulsive Scale, with effects separating from fentanyl within 1–2 hours and persisting for up to 168 hours. Ketamine caused short-term dissociative and cardiovascular effects; two of twelve participants dropped out due to not tolerating dissociation. The findings provide preliminary evidence for ketamine's efficacy and tolerability in an outpatient cohort.
BJPsych Open
October 1, 2025
Ben Beaglehole, Paul Glue, Shona Neehoff et al.
5 citations
Intramuscular ketamine shows preliminary effectiveness and is well tolerated by people with posttraumatic stress disorder in a community setting. The findings are encouraging given the known limitations of existing treatments, but more research is needed to determine the best dosing schedule and long-term role of ketamine for PTSD.
The International Journal of Neuropsychopharmacology
July 6, 2026
Shabah M. Shadli, Neda Nasrollahi, Calvin K. Young et al.
Ketamine at low doses (0.5-1.0 mg/kg I.M.) quickly reduces symptoms in treatment-resistant major depressive disorder (TR-MDD), post-traumatic stress disorder (TR-PTSD), and obsessive-compulsive disorder (TR-OCD), but its neural effects differ by diagnosis. EEG recordings of resting frontal activity before and after ketamine or fentanyl showed that TR-PTSD patients had dose- and band-frequency-dependent power changes (especially alpha at 0.5 mg/kg), while TR-MDD patients showed no such changes. TR-OCD responses differed qualitatively from both. Correlations between EEG power changes and symptom scale improvements varied by band and electrode across different disorder-specific scales. Ketamine's effects and their therapeutic links vary by brain site and frequency band depending on the DSM diagnosis, suggesting disorder-specific systems require a ketamine-sensitive factor to generate the disorder.
Journal of the Royal Society of New Zealand
February 1, 2026
Neil McNaughton, Shabah M Shadli, B Beaglehole et al.
Neurotic disorders such as depression, anxiety, and PTSD are diagnosed by symptoms rather than biological causes, making them costly and difficult to treat. Researchers in New Zealand have developed an EEG biomarker for anxiety disorders that can detect resistance to conventional treatments, with similar work underway for depression. Ketamine has been identified as a novel treatment for treatment-resistant neurotic disorders, supported by a proposed "double hit" hypothesis of its mechanisms. Similar results have been obtained with ketamine, LSD, and psilocybin, and treatment-related EEG changes have been demonstrated. These developments, potentially combined with psychotherapy, may lead to faster, broader, and more effective treatments, especially with the recent development of oral tablet delivery for home dosing.
bioRxiv Preprint Server
May 30, 2021
Calvin K. Young, Kachina G. Kinley, Neil McNaughton
preprint
Depression is the leading cause of disability worldwide, yet its biological mechanisms remain poorly understood. This study investigated whether scaffolding proteins in the medial frontal cortex contribute to antidepressant effects. The researchers injected chABC into the infralimbic cortex of animals to remove perineuronal nets and then tested for antidepressant effects using the forced swim test. They also tested whether systemic ketamine injections added to the effect. Preliminary data indicate that neither removing the scaffolding proteins nor ketamine alone decreased depression-like behavior, but the two treatments may interact synergistically to decrease immobility time in the forced swim test.