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.

Objective To investigate whether providing information about normal findings before a diagnostic test improves patients' reassurance and reduces anxiety about symptoms.Design Randomised controlled trial.Setting Outpatient cardiology clinic.Participants 92 patients with chest pain referred for a diagnostic exercise stress test.Intervention Before undergoing testing patients were randomised to receive standard information (n=28; control group), a pamphlet explaining the function of the test and the meaning of normal test results (n=30; pamphlet group), or the pamphlet and a brief discussion about the meaning of normal test results (n=34; discussion group).Main outcome measures The primary outcome was patients' reported reassurance on a 5 item scale immediately after the test and at one month. Secondary outcomes were the proportion of patients still with chest pain and still taking cardiac drugs at one month.Results The mean levels of reassurance after testing and feedback from the doctor were significantly higher in the discussion group (42.0, 95% confidence interval 39.7 to 44.2) than in the pamphlet (39.2, 36.1 to 42.3) and control groups (35.8, 31.6 to 39.9). This difference was maintained at one month. The proportion of patients still reporting chest pain at one month decreased significantly in the discussion group (to 17%) and pamphlet group (to 28%) but not in the control group (to 36%). A trend was for fewer patients in the discussion group to be taking cardiac drugs at one month.Conclusion Providing patients with information about normal test results before testing can improve rates of reassurance and reduce the likelihood of future reports of chest pain.Trial registration Current Controlled Trials ISRCTN87589121.

A large subgroup of around 25% of schizophrenia patients suffers from obsessive-compulsive symptoms (OCS) and about 12% fulfill the diagnostic criteria of an obsessive-compulsive disorder (OCD). The additional occurrence of OCS is associated with high subjective burden of disease, additional neurocognitive impairment, poorer social and vocational functioning, greater service utilization and high levels of anxiety and depression. Comorbid patients can be assigned to heterogeneous subgroups. One hypothesis assumes that second generation antipsychotics (SGAs), most importantly clozapine, might aggravate or even induce second-onset OCS. Several arguments support this assumption, most importantly the observed chronological order of first psychotic manifestation, start of treatment with clozapine and onset of OCS. In addition, correlations between OCS-severity and dose and serum levels and duration of clozapine treatment hint toward a dose-dependent side effect. It has been hypothesized that genetic risk-factors dispose patients with schizophrenia to develop OCS. One study in a South Korean sample reported associations with polymorphisms in the gene SLC1A1 (solute carrier family 1A1) and SGA-induced OCS. However, this finding could not be replicated in European patients. Preliminary results also suggest an involvement of polymorphisms in the BDNF gene (brain-derived neurotrophic factor) and an interaction between markers of SLC1A1 and the gene DLGAP3 (disc large associated protein 3) as well as GRIN2B (N-methyl-D-aspartate receptor subunit 2B). Further research of well-defined samples, in particular studies investigating possible interactions of genetic risk-constellations and pharmacodynamic properties, are needed to clarify the assumed development of SGA-induced OCS. Results might improve pathogenic concepts and facilitate the definition of at risk populations, early detection and monitoring of OCS as well as multimodal therapeutic interventions.

Background: Epidemiological investigations show that up to 30% of schizophrenic patients suffer from obsessive–compulsive symptoms (OCS) associated with negative impact on the general prognosis. It has been proposed that antiserotonergic second-generation antipsychotics (SGAs) might induce OCS, but investigations of large samples integrating psychopathology, neuropsychology and psychopharmacology are missing.Method: We stratified 70 patients with schizophrenia according to their mode of antipsychotic treatment: clozapine and olanzapine (group I) compared with aripiprazole and amisulpride (group II). The groups were matched according to age, sex, educational levels and severity of the psychotic disorder (Positive and Negative Syndrome Scale). As the primary endpoint, we evaluated OCS severity (Yale–Brown Obsessive–Compulsive Scale).Results: OCS were significantly more prevalent and severe in group I, in which OCS severity correlated with dosage of clozapine and duration of treatment. Pronounced cognitive deficits in group I were found in visuospatial perception and visual memory (Wechsler Adult Intelligence Scale-Revised block design, Rey–Osterrieth Complex Figure Test), impulse inhibition (go/no-go test), higher perseveration scores (Wisconsin Card Sorting Test) and reduced set-shift abilities (Trail Making Test Part B, Set-shift Task). These cognitive domains correlated with OCS severity.Conclusions: 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.