Pharmacopsychiatry
September 1, 2005
Euphrosyne Gouzoulis‐mayfrank, Anna Neukirch, Karsten Heekeren
2 citations
Two classes of hallucinogens—serotonergic agonists like DMT and NMDA antagonists like S-ketamine—produce distinct patterns of psychosis-like symptoms, rather than one being a universally better model of schizophrenia. In a double-blind crossover study with 15 healthy volunteers, DMT more strongly induced positive symptoms such as thought disorder and inappropriate affect, while S-ketamine more strongly induced negative symptoms, attention deficits, body perception disturbances, and catatonia-like motor phenomena. The findings suggest that each drug class models different aspects or subtypes of schizophrenia, not that the NMDA antagonist model is overall superior to the 5-HT2A agonist model.
Pharmacopsychiatry
June 2, 2025
Ludovic C Dormegny-Jeanjean, Suzie Lenoir, Ilia Humbert et al.
1 citation
Ketamine and esketamine, when used alongside non-selective monoamine oxidase inhibitors, do not cause clinically significant increases in blood pressure or heart rate. In 193 esketamine sessions with 13 patients, systolic pressure rose by 8.68 mmHg, diastolic by 6.57 mmHg, and heart rate by 3.5 beats per minute—changes not considered clinically meaningful. The combination of esketamine with monoamine oxidase inhibitors was not linked to elevated blood pressure. These results suggest minimal risk of sympathomimetic synergy with this drug combination, supporting its safe use in treatment-resistant depression.
Pharmacopsychiatry
December 20, 2024
Mu-Hong Chen, Tung-Ping Su, Wei-Chen Lin et al.
1 citation
Low-grade inflammation (LGI) is linked to poor response to standard antidepressants, but its role in ketamine treatment for treatment-resistant depression (TRD) was unclear. In 167 patients with TRD, 46 had LGI (C-reactive protein ≥3 mg/L) and 121 did not. A single low-dose ketamine infusion improved depressive symptoms only in patients without LGI, showing no significant antidepressant effect in those with LGI. However, ketamine reduced suicidal thoughts in both groups. The placebo response was notably greater in patients with LGI, which may explain the lack of observed ketamine effect in that group. Further research is needed to confirm these findings.
Pharmacopsychiatry
July 7, 2026
Kie Nomoto, Yohei Ohtani, Taisuke Yatomi et al.
In a double-blind, randomized, placebo-controlled trial, 34 Japanese patients with treatment-resistant depression received four intravenous doses of either ketamine (0.5 mg/kg) or saline. No significant differences emerged between the groups on objective or subjective cognitive function measures. Among ketamine-treated patients, those who responded to treatment (at least 50% reduction on the Montgomery-Åsberg Depression Rating Scale) showed greater improvement in subjective cognitive function than non-responders. Participants with weaker inhibitory control at baseline experienced larger reductions in depressive symptoms after ketamine. Repeated ketamine administration did not worsen cognitive function compared to placebo, suggesting cognitive safety, and baseline cognitive control deficits may predict better treatment response.
Pharmacopsychiatry
February 26, 2026
Ping-Chung Wu, Wei-Chen Lin, Tung-Ping Su et al.
A combination of clinical markers better predicts which patients with treatment-resistant depression and suicidal thoughts will respond rapidly and durably to a single low-dose ketamine infusion than any single marker alone. The markers include mild or moderate depression severity, a shorter current episode, no more than four prior antidepressant failures, low or moderate current suicide risk, and a history of suicide attempts. The analysis of 67 patients from previous trials used a decision-tree model to identify these predictors. Clinicians can use these findings to select patients most likely to benefit, though further confirmation is needed.
Pharmacopsychiatry
February 5, 2026
Tianyi Xu, Sabrina Wong, Gia Han Le et al.
Lysergic acid diethylamide and 3,4-methylenedioxymethamphetamine activate the 5-hydroxytryptamine 2B receptor, a pathway known to cause drug-induced valvular heart disease. This systematic review of 17 studies found no research on psilocybin, dimethyltryptamine, or mescaline. Both lysergic acid diethylamide and 3,4-methylenedioxymethamphetamine show high or moderate affinity for this receptor and promote signaling linked to fibrotic changes in heart valve tissue. In vivo studies confirm serotonin-induced valvulopathy, and chronic 3,4-methylenedioxymethamphetamine use has been associated with valve abnormalities in humans. No clinical cases of lysergic acid diethylamide-induced valvulopathy have been reported, but preclinical data suggest potential for fibrotic signaling under sustained exposure. Preliminary evidence supports the need for cardiac safety monitoring in psychedelic research.