Region specific distribution of levomepromazine in the human brain
Journal of Neural Transmission, ISSN: 0300-9564, Vol: 113, Issue: 3, Page: 387-397
2006
- 21Citations
- 17Captures
- 3Mentions
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Metrics Details
- Citations21
- Citation Indexes21
- CrossRef21
- 17
- Captures17
- Readers17
- 17
- Mentions3
- References3
- Wikipedia3
Article Description
Objective: The aim of this study was to examine concentrations of levomepromazine and its metabolite desmethyl-levomepromazine in different regions of human brain and in relationship to drug-free time. Methods: Drug concentrations were measured in up to 43 regions of 5 postmortem human brains of patients previously treated with levomepromazine. To enable statistical comparison across brain regions several smaller brain areas were put together to form larger brain areas (cortex cerebri, limbic system, cerebellum, basal ganglia, thalamus). Mean values of drug concentrations in these larger brain areas were used in a repeated measurement ANOVA to analyze for region specific distribution. The elimination half-life in brain tissue was estimated with a NONMEM population kinetic analysis using the mean value of all brain regions of an individual case. Results: Levomepromazine and desmethyl-levomepromazine appear to accumulate in human brain tissue relative to blood. Mean concentrations differed largely between individual brains, in part due to differences in dose of drug, duration of treatment and drug-free time before death. There was an apparent region-specific difference in levomepromazine concentrations with highest values in the basal ganglia (mean 316∈ng/g) and lowest values in the cortex cerebri (mean 209∈ng/g). The elimination half-life from brain tissue is longer than from blood and was calculated to be about one week. Similar results were obtained with desmethyl-levomepromazine. Conclusions: Levomepromazine shows a region-specific distribution in the human brain with highest values in the basal ganglia. This might be the consequence of low expression of the metabolic enzyme Cyp2D6 in the basal ganglia. If this finding is true also for other neuroleptic drugs it might increase our understanding of preferential toxicity of neuroleptic drugs against basal ganglia structures and higher volumes of basal ganglia of neuroleptic-treated patients. Furthermore, patients exposed to levomepromazine cannot be considered to be free of residual effects of the drug for a number of weeks after withdrawal. © Springer-Verlag 2005.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=32044434685&origin=inward; http://dx.doi.org/10.1007/s00702-005-0331-3; http://www.ncbi.nlm.nih.gov/pubmed/15997416; http://link.springer.com/10.1007/s00702-005-0331-3; http://www.springerlink.com/index/10.1007/s00702-005-0331-3; http://www.springerlink.com/index/pdf/10.1007/s00702-005-0331-3; https://dx.doi.org/10.1007/s00702-005-0331-3; https://link.springer.com/article/10.1007/s00702-005-0331-3
Springer Science and Business Media LLC
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