Patients describe experiencing personal recovery despite ongoing symptoms of psychosis. The aim of the current research was to perform a meta-analysis investigating the relationship between clinical and personal recovery in patients with schizophrenia spectrum disorders. A comprehensive OvidSP database search was performed to identify relevant studies. Correlation coefficients of the relationship between clinical and personal recovery were retrieved from primary studies. Meta-analyses were performed, calculating mean weighted effect sizes for the association between clinical and personal recovery, hope, and empowerment. Additionally, associations between positive, negative, affective symptoms, general functioning, and personal recovery were investigated. The results show that heterogeneity across studies was substantial. Random effect meta-analysis of the relationship between symptom severity and personal recovery revealed a mean weighted correlation coefficient of r = -.21 (95% CI = -0.27 to -0.14, P < .001). We found the following mean weighted effect size for positive symptoms r = -.20 (95% CI = -0.27 to -0.12, P < .001), negative symptoms r = -.24 (95% CI = -0.33 to -0.15, P < .001), affective symptoms r = -.34 (95% CI = -0.44 to -0.24, P < .001) and functioning r = .21 (95% CI = -0.09 to 0.32, P < .001). The results indicate a significant small to medium association between clinical and personal recovery. Psychotic symptoms show a smaller correlation than affective symptoms with personal recovery. These findings suggest that clinical and personal recovery should both be considered in treatment and outcome monitoring of patients with schizophrenia spectrum disorders.

Obsessive-compulsive disorder (OCD) is rarely associated with schizophrenia, whereas 20 to 30% of schizophrenic patients, suffer from comorbid obsessive-compulsive symptoms (OCS). So far no single pathogenetic theory convincingly explained this fact suggesting heterogeneous subgroups. Based on long-term case observations, one hypothesis assumes that second-onset OCS in the course of schizophrenia might be a side effect of second generation antipsychotics (SGA), most importantly clozapine (CLZ). This review summarizes the supporting epidemiological and pharmacological evidence: Estimations on prevalence of OCS increase in more recent cross-sectional studies and in later disease stages. Longitudinal observations report the de novo-onset of OCS under clozapine treatment. This association has not been reported with first generation antipsychotics (FGA) or SGAs with mainly dopaminergic mode of action. Finally, significant correlations of OCS-severity with duration of treatment, dose and serum levels suggest clozapine-induced OCS. However, supposed causal interactions need further verifications. It is also unclear, which neurobiological mechanisms might underlie the pathogenetic process. Detailed genotypic and phenotypic characterizations of schizophrenics with comorbid OCS regarding neurocognitive functioning and activation in sensitive tasks of functional magnetic imaging are needed. Multimodal large-scaled prospective studies are necessary to define patients at risk for second-onset OCS and to improve early detection and therapeutic interventions.

OCS in schizophrenia are associated with antiserotonergic SGA treatment, but longitudinal studies have to prove causality. Before starting treatment with antiserotonergic SGAs, specific neurocognitive domains should be evaluated, as visuospatial learning and impulse inhibition performance might allow early detection of OCS secondary to antipsychotic treatment in schizophrenia.