Abstract
Insight into the biological pathomechanism of a clinical syndrome facilitates the development of effective interventions. This paper applies this perspective to the important clinical problem of obsessive-compulsive symptoms (OCS) occurring during the lifetime diagnosis of schizophrenia. Up to 25% of schizophrenia patients suffer from OCS and about 12% fulfil the diagnostic criteria of obsessive-compulsive disorder (OCD). This is accompanied by marked subjective burden of disease, high levels of anxiety, depression and suicidality, increased neurocognitive impairment, less favourable levels of social and vocational functioning, and greater service utilization. Comorbid patients can be assigned to heterogeneous subgroups. It is assumed that second generation antipsychotics (SGAs), most importantly clozapine, might aggravate or even induce second-onset OCS. Several epidemiological and pharmacological arguments support this assumption. Specific genetic risk factors seem to dispose patients with schizophrenia to develop OCS and risk-conferring polymorphisms has been defined in SLC1A1, BDNF, DLGAP3, and GRIN2B and in interactions between these individual genes. Further research is needed with detailed characterization of large samples. In particular interactions between genetic risk constellations, pharmacological and psychosocial factors should be analysed. Results will further define homogeneous subgroups, which are in need for differential causative interventions. In clinical practise, schizophrenia patients should be carefully monitored for OCS, starting with at-risk mental states of psychosis and longitudinal follow-ups, hopefully leading to the development of multimodal therapeutic interventions.
Highlights
Insight into Biological Mechanisms of DiseasesCompared to other medical illnesses and disciplines biological mechanisms of psychiatric disorders are still poorly understood
Poyurovski et al estimated that up to 70% of schizophrenia patients treated with proobsessive SGAs develop secondary OCS [61], while Lykouras et al reviewed published data and reported de novo OCS in 77% of CLZ-treated patients [154]
Schizophrenia, for instance, is commonly perceived as a result of gene and environment interactions (GxEIs), where individual genetic properties dispose to a specific liability and sensitivity for specific stressors
Summary
Compared to other medical illnesses and disciplines biological mechanisms of psychiatric disorders are still poorly understood This leads to a lack of innovative therapeutic interventions in psychiatry compared, for example, to general medicine [1]. Further research seems necessary in order to define molecular targets for interventions This is especially true for major psychiatric conditions such as schizophrenia or obsessive-compulsive disorder (OCD) and even more for their comorbidity. The disease risk is largely determined by genetic factors, but the only linkage finding that has been consistently replicated refers to single nucleotide polymorphism (SNP) in the gene SLC1A1 on chromosome 9p24, encoding the neuronal glutamate transporter EAAC1 (excitatory amino acid carrier 1) [30] This finding supports neurochemical concepts beyond the serotonergic theory of OCD. This review has the intention to summarize the current knowledge of the pathogenesis and therapeutic options of obsessive-compulsive symptoms (OCS) in schizophrenia patients and describes necessary future research perspectives
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