Journal
BIOLOGICAL PSYCHIATRY
Volume 85, Issue 1, Pages 79-87Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.biopsych.2018.07.003
Keywords
Antipsychotic drugs; Dopamine; F-DOPA; Positron emission tomography; Psychosis; Schizophrenia
Categories
Funding
- Medical Research Council [MC-A656-5QD30]
- Maudsley Charity [66]
- U.S. Brain & Behavior Research Foundation
- Wellcome Trust [094849/Z/10/Z]
- National Institute for Health Research Biomedical Research Centre at South London and Maudsley National Health Service Foundation Trust and King's College London
- JMAS Sim Fellowship from the Royal College of Physicians, Edinburgh
- AstraZeneca
- Autifony
- Bristol-Myers Squibb
- Eli Lilly
- Heptares
- Janssen
- Lundbeck
- Lyden-Delta
- Otsuka
- Servier
- Sunovion
- Rand
- Roche
- GlaxoSmithKline
- GW Pharmaceuticals
- Takeda
- MRC [MC_U120097115, MR/N026063/1, G1100809] Funding Source: UKRI
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BACKGROUND: Elevated striatal dopamine synthesis capacity has been implicated in the etiology and antipsychotic response in psychotic illness. The effects of antipsychotic medication on dopamine synthesis capacity are poorly understood, and no prospective studies have examined this question in a solely first-episode psychosis sample. Furthermore, it is unknown whether antipsychotic efficacy is linked to reductions in dopamine synthesis capacity. We conducted a prospective [F-18]-dihydroxyphenyl-L-alanine positron emission tomography study in antipsychotic naive/free people with first-episode psychosis commencing antipsychotic treatment. METHODS: Dopamine synthesis capacity (indexed as influx rate constant) and clinical symptoms (measured using Positive and Negative Syndrome Scale) were measured before and after at least 5 weeks of antipsychotic treatment in people with first-episode psychosis. Data from a prior study indicated that a sample size of 13 would have >80% power to detect a statistically significant change in dopamine synthesis capacity at alpha = .05 (two tailed). RESULTS: A total of 20 people took part in the study, 17 of whom were concordant with antipsychotic medication at therapeutic doses. There was no significant effect of treatment on dopamine synthesis capacity in the whole striatum (p = .47), thalamus, or midbrain, nor was there any significant relationship between change in dopamine synthesis capacity and change in positive (p = .35, p = .13), negative, or total psychotic symptoms. CONCLUSIONS: Dopamine synthesis capacity is unaltered by antipsychotic treatment, and therapeutic effects are not mediated by changes in this aspect of dopaminergic function.
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