Positron emission tomography and fluorodeoxyglucose studies of metabolic hyperfrontality and psychopathology in the psilocybin model of psychosis.
Franz X. Vollenweider, K L Leenders, C Scharfetter, P Maguire, O Stadelmann, J Angst
Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology May 1997 DOI: 10.1016/s0893-133x(96)00246-1 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Observational cohort Peer reviewed |
|---|---|
| Sample size | 10 |
| Population | Healthy volunteers |
| Intervention | Psilocybin |
| Dose | 15- or 20-mg |
| Topics | Psilocybin |
| Key findings | Psilocybin increased cerebral glucose metabolism globally, most markedly in frontomedial and frontolateral cortex (24.3%), anterior cingulate (24.9%), and temporomedial cortex (25.3%), with increases correlating with psychotic symptom formation. The authors propose that excessive 5-HT2 receptor activation produces a hyperfrontal pattern paralleling acute psychotic episodes in schizophrenia. |
Abstract
The effects of the indolehallucinogen psilocybin, a mixed 5-HT2 and 5-HT1 agonist, on regional cerebral glucose metabolism were investigated in 10 healthy volunteers with PET and [F-18]-fluorodeoxyglucose (FDG) prior to and following a 15- or 20-mg dose of psilocybin. Psychotomimetic doses of psilocybin were found to produce a global increase in cerebral metabolic rate of glucose (CMRglu) with significant and most marked increases in the frontomedial and frontolateral cortex (24.3%), anterior cingulate (24.9%), and temporomedial cortex (25.3%). Somewhat smaller increases of CMRglu were found in the basal ganglia (18.5%), and the smallest increases were found in the sensorimotor (14.7%) and occipital cortex (14.4%). The increases of CMRglu in the prefrontal cortex, anterior cingulate, temporomedial cortex, and putamen correlated positively with psychotic symptom formation, in particular with hallucinatory ego disintegration. The present data suggest that excessive 5-HT2 receptor activation results in a hyperfrontal metablic pattern that parallels comparable metabolic findings associated with acute psychotic episodes in chronic schizophrenics and contrasts with the hypofrontality in chronic schizophrenic patients.