Clozapine in the Treatment of Obsessive-compulsive Symptoms in Schizophrenia Patients: A Case Series Study

doi:10.1055/s-2004-815525

Cited by 51 publications

(18 citation statements)

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“…In addition to the association with duration of treatment, a positive correlation between dose or serum levels of CLZ and severity of OCS has been reported in independent samples [3,41,63]. In line with these previous results, we found positive correlations between the daily dose of CLZ and OCS severity [62].…”

Section: Influence Of Treatment Dose and Blood Serum Levels Of Clz Onsupporting

confidence: 91%

“…In addition, the substance embarks important protective effects against suicidal behaviour resulting in lowest mortality of schizophrenics as documented in the large, naturalistic FIN11-study [48]. However, the de novo occurrence or exacerbation of OCS has most often been observed during treatment with CLZ [39,41] and several epidemiological and pharmacological arguments support the attribution of pro-obsessive effects.This review aims at summarizing the evidence for OCS-induction by CLZ in order to provide a basis for pathogenetic considerations and the design of further clinical trials. For this task, we systematically screened medical databases (Medline OVID, PSYNDEX and PsycINFO) for publications until June 2011 using the keywords (“schizophrenia” or “Psychosis” or “psychotic disorder”) linked with (“OCD” or “obsessive” or “compulsive”).…”

Section: Second-onset Ocs Induced By Antiserotonergic Antipsychoticsmentioning

confidence: 99%

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Clozapine-Induced Obsessive-Compulsive Symptoms in Schizophrenia: A Critical Review

Schirmbeck¹,

Zink

2012

110

104

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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.

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Section: Influence Of Treatment Dose and Blood Serum Levels Of Clz Onsupporting

confidence: 91%

Section: Second-onset Ocs Induced By Antiserotonergic Antipsychoticsmentioning

confidence: 99%

Clozapine-Induced Obsessive-Compulsive Symptoms in Schizophrenia: A Critical Review

Schirmbeck¹,

Zink

2012

110

104

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“…Since then several studies show a clear association and possible causal interaction between SGA-treatment, most importantly CLZ (Schirmbeck and Zink, 2012), and the de novo occurrence of OCS (de Haan et al, 2004; Reznik et al, 2004; Kwon et al, 2009b; Schirmbeck et al, 2011). …”

Section: Ocs Induced By Second-generation Antipsychoticsmentioning

confidence: 99%

“…In addition, the substance demonstrates important anti-suicidal effects resulting in low mortality rates of CLZ-treated schizophrenia patients (Tiihonen et al, 2009). However, within a variety of other important side effects (Asenjo Lobos et al, 2010), the de novo occurrence or exacerbation of OCS under antipsychotic treatment has most often been observed with CLZ (Lykouras et al, 2003; Reznik et al, 2004; Schirmbeck and Zink, 2012). Due to a lack of controlled clinical trials, proposed causal interrelations cannot be confirmed, according to the general criteria suggested by Bradford Hill (2011).…”

Section: Ocs Induced By Second-generation Antipsychoticsmentioning

confidence: 99%

“…Several authors demonstrated positive correlations between dose or serum levels of CLZ and severity of OCS (Lin et al, 2006; Reznik et al, 2004; Mukhopadhaya et al, 2009; Schirmbeck et al, 2011). Similarly, a reduction of daily CLZ-dosage, for instance through the combinations with another SGA, such as APZ, resulted in an alleviation of OCS severity (Rocha and Hara, 2006; Zink et al, 2006; Englisch et al, 2009).…”

Section: Ocs Induced By Second-generation Antipsychoticsmentioning

confidence: 99%

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Comorbid obsessive-compulsive symptoms in schizophrenia: contributions of pharmacological and genetic factors

Schirmbeck¹,

Zink²

2013

Front. Pharmacol.

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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.

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Interventions for obsessive compulsive symptoms in people with schizophrenia

Mohan

Farooq²

2005

Cochrane Database of Systematic Reviews

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This is the protocol for a review and there is no abstract. The objectives are as follows: 1. Primary objectives To evaluate clinically meaningful benefits of interventions used to treat clinically significant obsessive compulsive symptoms occurring in people with schizophrenia with regard to global improvement, changes in mental state, hospitalisation, behaviour and functioning in the short term (less than six weeks), medium term (six weeks to six months) and long term (more than six months). In this review we specifically addressed the efficacy and safety of the following when used to treat clinically significant obsessive compulsive symptoms occurring in people with schizophrenia: 1.1 Conventional and newer (or atypical) antipsychotic drugs 1.2 Conventional and newer antidepressant drugs 1.3 Any other drug or pharmacologically active substance 1.4 Non-pharmacological interventions In future versions of this review we will cover the use of psychosurgery, deep brain stimulation or other invasive interventions for this purpose. 2. Secondary objectives To determine whether these interventions would have a differential effect: 2.1 In people with schizophrenia in whom obsessive compulsive symptoms preceded the onset of symptoms of schizophrenia as opposed to those in whom obsessive compulsive symptoms occurred in the prodromal stages or after the symptoms of schizophrenia were firmly established 2.2 In people with obsessive compulsive symptoms as opposed to obsessive compulsive disorder as defined by diagnostic criteria

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Clozapine in the Treatment of Obsessive-compulsive Symptoms in Schizophrenia Patients: A Case Series Study

Abstract: Further controlled investigations in a larger cohort of OC schizophrenic patients are needed to substantiate our hypothesis. OCD:Obsessive-compulsive disorder OCS:Obsessive-compulsive symptoms SRI:Serotonin reuptake inhibitors

Cited by 51 publications

References 11 publications

Clozapine-Induced Obsessive-Compulsive Symptoms in Schizophrenia: A Critical Review

Clozapine-Induced Obsessive-Compulsive Symptoms in Schizophrenia: A Critical Review

Comorbid obsessive-compulsive symptoms in schizophrenia: contributions of pharmacological and genetic factors

Interventions for obsessive compulsive symptoms in people with schizophrenia

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