Multiple neurotoxic effects of haloperidol resulting in neuronal death.
Ann Clin Psychiatry
; 29(3): 195-202, 2017 08.
Article
em En
| MEDLINE
| ID: mdl-28738100
ABSTRACT
BACKGROUND:
Several published studies have reported an association between antipsychotic medications, especially first-generation agents, and a decline in gray matter volume. This prompted us to review the possible neurotoxic mechanisms of first-generation antipsychotics (FGAs), especially haloperidol, which has been widely used over the past several decades.METHODS:
A PubMed search was conducted using the keywords haloperidol, antipsychotic, neurotoxicity, apoptosis, oxidative stress, and neuroplasticity. No restrictions were placed on the date of the articles or language. Studies with a clearly described methodology were included.RESULTS:
Animal, cell culture, and human tissue studies were identified. Thirty reports met the criteria for the search. All studies included haloperidol; a few also included other FGAs (fluphenazine and perphenazine) and/or second-generation agents (SGAs) (aripiprazole, paliperidone, and risperidone). A neurotoxic effect of haloperidol and other FGAs was a common theme across all studies. Minimal (mainly at high doses) or no neurotoxic effects were noted in SGAs.CONCLUSIONS:
A review of the literature suggests that haloperidol exerts measurable neurotoxic effects at all doses via many molecular mechanisms that lead to neuronal death. A similar effect was observed in 2 other FGAs, but the effect in SGAs was much smaller and occurred mainly at high doses. A stronger binding to serotonin 5HT-2A receptors than to dopamine D2 receptors may have a neuroprotective effect among SGAs. Further studies are warranted to confirm these findings.
Buscar no Google
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Antipsicóticos
/
Morte Celular
/
Haloperidol
/
Neurônios
Tipo de estudo:
Prognostic_studies
/
Systematic_reviews
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Ann Clin Psychiatry
Assunto da revista:
PSIQUIATRIA
Ano de publicação:
2017
Tipo de documento:
Article