Cannabis-dependent men show exaggerated cognitive performance deterioration during psychosocial stress compared to controls, despite reporting similar stress levels and cardiovascular responses. Brain imaging revealed that this performance decline was accompanied by reduced activity in the precuneus and increased connectivity between the precuneus and the superior frontal gyrus during stress exposure. The findings provide first evidence linking chronic cannabis use to altered neural stress processing, specifically deficient recruitment of the precuneus, which may underlie stress-induced cognitive impairments in cannabis users.
Treatment-resistant depression lacks a standardized definition, but several promising pharmacological and neuromodulatory options exist. Current research emphasizes fast-acting, well-tolerated treatments beyond the monoamine hypothesis. Esketamine is an established fast-acting and well-tolerated therapy, while psychedelics and esmethadone remain in clinical trials. Off-label compounds like dextromethorphan and anti-inflammatory strategies are also discussed. Pharmacological approaches modulating the glutamatergic system or belonging to the psychedelic class are particularly important for current research, especially those with rapid clinical effects and favorable side-effect profiles.
A single intravenous dose of ketamine (100 ng/ml) impairs metacognitive sensitivity and increases metacognitive bias in healthy young adults during an episodic memory task, without affecting memory performance or reaction times. The drug also increases brain activation in posterior cortical areas associated with consciousness, though this activation is not specific to confidence judgments. Ketamine administered during encoding does not significantly affect performance or brain activation. These findings indicate that ketamine disrupts the ability to accurately monitor one's own memory performance.