Dopamine supersensitivity psychosis (DSP) is observed in patients with schizophrenia under antipsychotic treatment, and it is characterized by rebound psychosis, an uncontrollable psychotic episode following a stable state and tardive dyskinesia. DSP, first described in patients taking typical antipsychotics in the late 1970s, sometimes appears even in patients who are treated with current atypical antipsychotics. It was recently demonstrated that DSP can have a negative impact on the long-term prognosis of schizophrenia patients and that DSP could be involved in the etiology of some cases of treatment-resistant schizophrenia. Accumulating evidence suggests that an up-regulation of dopamine D2 receptors (DRD2) in the brain caused by long-term exposure to antipsychotics is related to the DSP phenomenon. The present review describes the clinical characteristics and the etiology of DSP in the era of second-generation antipsychotics for patients with schizophrenia. Based on the mechanism of DSP, several potential treatments for patients presenting with a DSP episode or the dopamine supersensitivity state are also discussed.
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http://dx.doi.org/10.1177/0269881117728428 | DOI Listing |
Behav Brain Res
September 2024
Department of Statistics, College of Arts and Sciences, University of Kentucky, Lexington, KY 40504, United States; Department of Pharmaceutical Sciences, College of Pharmacy, University of Kentucky, Lexington, KY 40504, United States.
An escalating trend of antipsychotic drug use in children with ADHD, disruptive behavior disorder, or mood disorders has raised concerns about the impact of these drugs on brain development. Since antipsychotics chiefly target dopamine receptors, it is important to assay the function of these receptors after early-life antipsychotic administration. Using rats as a model, we examined the effects of early-life risperidone, the most prescribed antipsychotic drug in children, on locomotor responses to the dopamine D/D receptor agonist, apomorphine, and the D/D receptor agonist, quinpirole.
View Article and Find Full Text PDFJ Neurosci
June 2024
Department of Neurology, Center for Neurodegeneration and Experimental Therapeutics, University of Alabama at Birmingham, Birmingham, Alabama 35294
l-DOPA-induced dyskinesia (LID) is a debilitating motor side effect arising from chronic dopamine (DA) replacement therapy with l-DOPA for the treatment of Parkinson's disease. LID is associated with supersensitivity of striatal dopaminergic signaling and fluctuations in synaptic DA following each l-DOPA dose, shrinking the therapeutic window. The heterogeneous composition of the striatum, including subpopulations of medium spiny output neurons (MSNs), interneurons, and supporting cells, complicates the identification of cell(s) underlying LID.
View Article and Find Full Text PDFPsychopharmacology (Berl)
June 2024
Department of Medical and Clinical Pharmacology, Centre of PharmacoVigilance and Pharmacoepidemiology, Faculty of Medicine and Toulouse University Hospital (CHU), 37 Allées Jules-Guesde 31000, Toulouse, France.
Psychopharmacology (Berl)
February 2024
Pharmacy Department, Maudsley Hospital, London, SE5 8AZ, UK.
Rationale: Dopamine antagonists induce dopamine receptor supersensitivity. This may manifest in late-appearing movement disorders (tardive dyskinesia (TD). VMAT-2 inhibitors reduce dopaminergic transmission but have limited activity at postsynaptic receptors and so may have antipsychotic activity with lower risk of tardive dyskinesia.
View Article and Find Full Text PDFBMJ Case Rep
October 2023
BC Centre on Substance Use, The University of British Columbia, Vancouver, British Columbia, Canada
Antipsychotic medications exert their effects via dopamine antagonism and are widely used off-label among persons with substance use disorders (SUD). While dopamine antagonists are recognised to stimulate food craving and weight gain, outside of possibly increasing nicotine craving and use, their impact on other SUD outcomes is poorly recognised. In this context, research has demonstrated that antipsychotic therapy can produce 'supersensitivity' to dopamine, enhancing the motivational effects of addictive drugs.
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