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Supplementary Material for: Antipsychotic-Induced Dopamine Supersensitivity Psychosis: Pharmacology, Criteria, and Therapy
<p>The first-line treatment for psychotic disorders remains antipsychotic drugs with receptor antagonist properties at D<sub>2</sub>-like dopamine receptors. However, long-term administration of antipsychotics can upregulate D<sub>2</sub>
receptors and produce receptor supersensitivity manifested by
behavioral supersensitivity to dopamine stimulation in animals, and
movement disorders and supersensitivity psychosis (SP) in patients.
Antipsychotic-induced SP was first described as the emergence of
psychotic symptoms with tardive dyskinesia (TD) and a fall in prolactin
levels following drug discontinuation. In the era of first-generation
antipsychotics, 4 clinical features characterized drug-induced SP: rapid
relapse after drug discontinuation/dose reduction/switch of
antipsychotics, tolerance to previously observed therapeutic effects,
co-occurring TD, and psychotic exacerbation by life stressors. We review
3 recent studies on the prevalence rates of SP, and the link to
treatment resistance and psychotic relapse in the era of
second-generation antipsychotics (risperidone, paliperidone,
perospirone, and long-acting injectable risperidone, olanzapine,
quetiapine, and aripiprazole). These studies show that the prevalence
rates of SP remain high in schizophrenia (30%) and higher (70%) in
treatment-resistant schizophrenia. We then present neurobehavioral
findings on antipsychotic-induced supersensitivity to dopamine from
animal studies. Next, we propose criteria for SP, which describe
psychotic symptoms and co-occurring movement disorders more precisely.
Detection of mild/borderline drug-induced movement disorders permits
early recognition of overblockade of D<sub>2</sub> receptors,
responsible for SP and TD. Finally, we describe 3 antipsychotic
withdrawal syndromes, similar to those seen with other CNS drugs, and we
propose approaches to treat, potentially prevent, or temporarily manage
SP.</p