Obsessive-Compulsive Symptoms During Treatment With Olanzapine and Risperidone

Haan, Lieuwe de; Beuk, Nico; Hoogenboom, Britt; Dingemans, Peter; Linszen, Don

doi:10.4088/jcp.v63n0203

Cited by 92 publications

(5 citation statements)

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“…Recently, interest in this area has increased considerably, probably due to the recognition of higher-than-expected comorbidity rates and the observation of emergence, or exacerbation, of OCS during treatment with AAP. (Ghaemi et al, 1995; Khullar et al, 2001; de Haan et al, 2002; Lykouras et al, 2003; Alevizos et al, 2004). …”

Section: Methodsmentioning

confidence: 99%

“…Recent studies reported that approximately 8–26% of schizophrenic patients met the DSM-IV criteria for OCD (Eisen et al, 1997; Porto et al, 1997; Poyurovsky et al, 1999, 2001; Bermanzohn et al, 2000; Tibbo et al, 2000; de Haan et al, 2002; Nechmad et al, 2003; Ohta et al, 2003; Byerly et al, 2005). However, other investigators have reported rates up to 59.2% (Bland et al, 1987).…”

Section: Methodsmentioning

confidence: 99%

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Obsessive–Compulsive Disorder Comorbidity: Clinical Assessment and Therapeutic Implications

Pallanti¹,

Grassi²,

Sarrecchia³

et al. 2011

Front. Psychiatry

112

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Obsessive–compulsive disorder (OCD) is a neuropsychiatric disorder affecting approximately 1–3% of the population. OCD is probably an etiologically heterogeneous condition. Individuals with OCD frequently have additional psychiatric disorders concomitantly or at some time during their lifetime. Recently, some authors proposed an OCD sub-classification based on comorbidity. An important issue in assessing comorbidity is the fact that the non-response to treatment often involves the presence of comorbid conditions. Non-responsive patients are more likely to meet criteria for comorbid axis I or axis II disorders and the presence of a specific comorbid condition could be a distinguishing feature in OCD, with influence on the treatment adequacy and outcome.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Obsessive–Compulsive Disorder Comorbidity: Clinical Assessment and Therapeutic Implications

Pallanti¹,

Grassi²,

Sarrecchia³

et al. 2011

Front. Psychiatry

112

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“…Schirmbeck et al reported a positive correlation between OCS severity and duration of CLZ-treatment (Schirmbeck et al, 2011). Accordingly, de Haan et al reported this association for OLZ (de Haan et al, 2002). …”

Section: Ocs Induced By Second-generation Antipsychoticsmentioning

confidence: 89%

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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“…This heterogeneity suggests multiple interacting pathways [8]. For the subgroup of patients, who develop OCS subsequent to their first psychotic episode and initiation of antipsychotic treatment, increasing evidence strongly suggests a “pro-obsessive” effect of certain second-generation antipsychotics (SGAs), especially clozapine [9, 10] and olanzapine [11]. Clozapine, and similarly olanzapine, exerts its effects via a relatively low affinity to dopamine D 2 receptors combined with strong antagonism at 5-HT 1C , 5-HT 2A and 5HT 2C receptors [12, 13].…”

Section: Introductionmentioning

confidence: 99%

Reduced activity and connectivity of left amygdala in patients with schizophrenia treated with clozapine or olanzapine

Mier

Schirmbeck

Stoessel

et al. 2018

Eur Arch Psychiatry Clin Neurosci

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Obsessive–compulsive symptoms (OCS) in patients with schizophrenia are a common co-occurring condition, often associated with additional impairments. A subgroup of these patients develops OCS during treatment with second-generation antipsychotics (SGAs), most importantly clozapine and olanzapine. So far, little is known about possible neural mechanism of these SGAs, which seem to aggravate or induce OCS. To investigate the role of SGA treatment on neural activation and connectivity during emotional processing, patients were stratified according to their monotherapy into two groups (group I: clozapine or olanzapine, n = 20; group II: amisulpride or aripiprazole, n = 20). We used an fMRI approach, applying an implicit emotion recognition task. Group comparisons showed significantly higher frequency and severity of comorbid OCS in group I than group II. Task specific activation was attenuated in group I in the left amygdala. Furthermore, functional connectivity from left amygdala to right ventral striatum was reduced in group I. Reduced amygdala activation was associated with OCS severity. Recent literature suggests an involvement of an amygdala–cortico–striatal network in the pathogenesis of obsessive–compulsive disorder. The observed differential activation and connectivity pattern of the amygdala might thus indicate a neural mechanism for the development of SGA-associated OCS in patients with schizophrenia. Further neurobiological research and interventional studies are needed for causal inferences.

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Obsessive-Compulsive Symptoms During Treatment With Olanzapine and Risperidone

Cited by 92 publications

References 0 publications

Obsessive–Compulsive Disorder Comorbidity: Clinical Assessment and Therapeutic Implications

Obsessive–Compulsive Disorder Comorbidity: Clinical Assessment and Therapeutic Implications

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

Reduced activity and connectivity of left amygdala in patients with schizophrenia treated with clozapine or olanzapine

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