Table 1.

SGAs induce or aggravate OCS.

Clinical observations and epidemiological arguments
(I)	The prevalence rates of OCS in schizophrenia increased after market approval of SGAs such as clozapine.
(II)	The comorbidity rates in later stages of schizophrenia are higher than during the ARMS or at first manifestation of psychosis.
(III)	In parallel to antipsychotic treatment OCS manifest de novo or show a marked aggravation.
(IV)	High prevalence rates of OCS are observed during CLZ treatment.
(V)	Schizophrenia patients with SGA-induced OCS markedly contribute to the entire sample of comorbid patients.
Evidence derived from pharmacological considerations
(I)	Pharmacodynamic properties modulate the risk for OCS: marked difference between samples treated with first generation antipsychotics or mainly dopaminergic SGAs (such as aripiprazole or amisulpride) compared to CLZ.
(II)	OCS manifest as an unfavourable drug effect de novo during treatment with potent antiserotonergic SGAs such as CLZ.
(III)	Indicators of a dose-effect relation: the severity of OCS is positively correlated with duration, dosage, and serum levels of CLZ treatment.
(IV)	OCS severity persists over time in patients under stable CLZ treatment.
(V)	The severity of OCS improves after reduction of CLZ dosage to minimally sufficient levels (due to augmentation or combination).

Summary of epidemiological and pharmacological arguments supporting the induction or at least marked aggravation of OCS by SGA treatment as an unfavourable side effect. CLZ: clozapine, OCS: obsessive-compulsive symptoms, and SGA: second generation antipsychotic agents.