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Comorbid Obsessive-Compulsive Symptoms in Schizophrenia: Insight into Pathomechanisms Facilitates Treatment.

Zink M - Adv Med (2014)

Bottom Line: Insight into the biological pathomechanism of a clinical syndrome facilitates the development of effective interventions.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.Results will further define homogeneous subgroups, which are in need for differential causative interventions.

View Article: PubMed Central - PubMed

Affiliation: Central Institute of Mental Health, Department of Psychiatry and Psychotherapy, Medical Faculty Mannheim, Heidelberg University, P.O. Box 12 21 20, 68072 Mannheim, Germany.

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.

No MeSH data available.


Related in: MedlinePlus

Schematic diagram on onset and course of OCS related to stages of schizophrenia. Bright-gray symbols indicate the onset and severity of OCS, dark-gray symbols are related to the at-risk mental state of psychosis (ARMS), the upcoming first episode of schizophrenia or its chronic course. (1) Preexisting and persistent OCS. (2) Intermittent OCS during ARMS or later in the clinical course. (3) OCS onset during ARMS and persistent course, strongly associated with the psychotic symptoms (schizo-obsessive concept). (4) Fluctuating course of OCS. (5) Second-onset OCS during antipsychotic treatment.
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fig2: Schematic diagram on onset and course of OCS related to stages of schizophrenia. Bright-gray symbols indicate the onset and severity of OCS, dark-gray symbols are related to the at-risk mental state of psychosis (ARMS), the upcoming first episode of schizophrenia or its chronic course. (1) Preexisting and persistent OCS. (2) Intermittent OCS during ARMS or later in the clinical course. (3) OCS onset during ARMS and persistent course, strongly associated with the psychotic symptoms (schizo-obsessive concept). (4) Fluctuating course of OCS. (5) Second-onset OCS during antipsychotic treatment.

Mentions: A remarkably large subgroup of patients already suffers from OCS during the ARMS, as recently summarized [83]. The mean prevalence of all reported sample-size weighed rates results in 12.1% (CI: 9.4 to 14.8%) of ARMS patients who report OCS [84–88], whereas 5.2% (CI: 4.1 to 6.3%) fulfil the criteria for OCD [84, 86–92] (Figure 1). In first episode patients slightly higher averaged rates can be found for OCS (17.1%, CI: 14.0 to 20.2) and OCD (7.3%, CI: 5.3 to 9.3%) (Figure 1) [70, 83, 88, 88, 93–95]. Epidemiological data in the referred individual studies largely vary. This might be explained by differences in the ARMS criteria used and differences in the definition and psychometric assessment of OCS or OCD. OCS during the ARMS seems to have an important impact on other clinical variables, but so far findings have been rather heterogeneous. Consistent results have been reported for higher impairment of psychosocial functioning [85, 89, 91, 94] and more severe depressive symptoms [70, 86, 89, 96] in cases with comorbid OCS. In contrast, results investigating the effect of OCS on the transition rates into psychosis [86, 90, 91, 96] have been contradicting. Only preliminary data existed regarding the influence on cognition [85, 96, 97], until the interventional study PREVENT (Secondary Prevention of Schizophrenia: A Randomized Controlled Trial [84]) allowed a multidimensional assessment of a large cohort [83]. Within a sample of 233 ARMS patients 26 patients fulfilled the DSM-IV criteria for concurrent OCD or had a lifetime history of at least subclinical OCS. They were more severely impaired in psychosocial functioning and general psychopathology but not regarding affective symptoms and neurocognitive abilities. Apart from OCS during the ARMS several studies investigated the cooccurrence of OCS during manifest schizophrenia. Whereas some patients experience OCS onset simultaneously with the first episode of psychosis, another and often underestimated subgroup reports OCS development after treatment-start with SGAs. In these cases, a typical order of three events can be observed: first “onset of psychosis,” second “start with SGA treatment,” and subsequently “de novo development of OCS.” This sequence suggests the involvement of pharmacodynamic mechanisms in the pathogenesis of OCS in this subgroup of schizophrenia patients (see Figure 2(5) and detailed description in Section 2.6).


Comorbid Obsessive-Compulsive Symptoms in Schizophrenia: Insight into Pathomechanisms Facilitates Treatment.

Zink M - Adv Med (2014)

Schematic diagram on onset and course of OCS related to stages of schizophrenia. Bright-gray symbols indicate the onset and severity of OCS, dark-gray symbols are related to the at-risk mental state of psychosis (ARMS), the upcoming first episode of schizophrenia or its chronic course. (1) Preexisting and persistent OCS. (2) Intermittent OCS during ARMS or later in the clinical course. (3) OCS onset during ARMS and persistent course, strongly associated with the psychotic symptoms (schizo-obsessive concept). (4) Fluctuating course of OCS. (5) Second-onset OCS during antipsychotic treatment.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4590963&req=5

fig2: Schematic diagram on onset and course of OCS related to stages of schizophrenia. Bright-gray symbols indicate the onset and severity of OCS, dark-gray symbols are related to the at-risk mental state of psychosis (ARMS), the upcoming first episode of schizophrenia or its chronic course. (1) Preexisting and persistent OCS. (2) Intermittent OCS during ARMS or later in the clinical course. (3) OCS onset during ARMS and persistent course, strongly associated with the psychotic symptoms (schizo-obsessive concept). (4) Fluctuating course of OCS. (5) Second-onset OCS during antipsychotic treatment.
Mentions: A remarkably large subgroup of patients already suffers from OCS during the ARMS, as recently summarized [83]. The mean prevalence of all reported sample-size weighed rates results in 12.1% (CI: 9.4 to 14.8%) of ARMS patients who report OCS [84–88], whereas 5.2% (CI: 4.1 to 6.3%) fulfil the criteria for OCD [84, 86–92] (Figure 1). In first episode patients slightly higher averaged rates can be found for OCS (17.1%, CI: 14.0 to 20.2) and OCD (7.3%, CI: 5.3 to 9.3%) (Figure 1) [70, 83, 88, 88, 93–95]. Epidemiological data in the referred individual studies largely vary. This might be explained by differences in the ARMS criteria used and differences in the definition and psychometric assessment of OCS or OCD. OCS during the ARMS seems to have an important impact on other clinical variables, but so far findings have been rather heterogeneous. Consistent results have been reported for higher impairment of psychosocial functioning [85, 89, 91, 94] and more severe depressive symptoms [70, 86, 89, 96] in cases with comorbid OCS. In contrast, results investigating the effect of OCS on the transition rates into psychosis [86, 90, 91, 96] have been contradicting. Only preliminary data existed regarding the influence on cognition [85, 96, 97], until the interventional study PREVENT (Secondary Prevention of Schizophrenia: A Randomized Controlled Trial [84]) allowed a multidimensional assessment of a large cohort [83]. Within a sample of 233 ARMS patients 26 patients fulfilled the DSM-IV criteria for concurrent OCD or had a lifetime history of at least subclinical OCS. They were more severely impaired in psychosocial functioning and general psychopathology but not regarding affective symptoms and neurocognitive abilities. Apart from OCS during the ARMS several studies investigated the cooccurrence of OCS during manifest schizophrenia. Whereas some patients experience OCS onset simultaneously with the first episode of psychosis, another and often underestimated subgroup reports OCS development after treatment-start with SGAs. In these cases, a typical order of three events can be observed: first “onset of psychosis,” second “start with SGA treatment,” and subsequently “de novo development of OCS.” This sequence suggests the involvement of pharmacodynamic mechanisms in the pathogenesis of OCS in this subgroup of schizophrenia patients (see Figure 2(5) and detailed description in Section 2.6).

Bottom Line: Insight into the biological pathomechanism of a clinical syndrome facilitates the development of effective interventions.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.Results will further define homogeneous subgroups, which are in need for differential causative interventions.

View Article: PubMed Central - PubMed

Affiliation: Central Institute of Mental Health, Department of Psychiatry and Psychotherapy, Medical Faculty Mannheim, Heidelberg University, P.O. Box 12 21 20, 68072 Mannheim, Germany.

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.

No MeSH data available.


Related in: MedlinePlus