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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Schizophrenia is noted for the remarkably high prevalence of substance use disorders (SUDs) including nicotine (>85%), alcohol and stimulants. Mounting evidence supports the hypothesis that the endophenotype of schizophrenia involves hypofunction of a subpopulation of cortico-limbic NMDA receptors. Low doses of NMDA receptor antagonists such as ketamine replicate in normal volunteers positive, negative and cognitive symptoms of schizophrenia as well as associated physiologic abnormalities such as eye tracking and abnormal event related potentials. Genetic studies have identified putative risk genes that directly or indirectly affect NMDA receptors including D-amino acid oxidase, its modulator G72, proline oxidase, mGluR3 and neuregulin. Clinical trials have shown that agents that directly or indirectly enhance the function of the NMDA receptor at its glycine modulatory site (GMS) reduce negative symptoms and in the case of D-serine and sarcosine improve cognition and reduce positive symptoms in schizophrenic subjects receiving concurrent anti-psychotic medications. Notably, the GMS partial agonist D-cycloserine exacerbates negative symptoms in clozapine responders whereas full agonists, glycine and D-serine have no effects, suggesting clozapine may act indirectly as a full agonist at the GMS of the NMDA receptor. Clozapine treatment is uniquely associated with decreased substance use in patients with schizophrenia, even without psychologic intervention. Given the role of NMDA receptors in the reward circuitry and in substance dependence, it is reasonable to speculate that NMDA receptor dysfunction is a shared pathologic process in schizophrenia and co-morbid SUDs.
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PMID:Substance use disorders and Schizophrenia: a question of shared glutamatergic mechanisms. 1719 72

The most widely cited road block to successful treatment outcomes for psychological and substance use disorders has been described as the return to the previous behavior, or "relapse." The operational definition of "relapse" varies from study to study and between clinicians, but in general the term is used to indicate the return to previous levels of symptomatic behavior. One explanation for the variation in the operationalization of relapse is the wide variety of behaviors for which the term is applied, including (but not limited to): depression, substance abuse, schizophrenia, mania, sexual offending, risky sexual behavior, dieting, and the anxiety disorders. A second explanation for the multitude of definitions for relapse is the inherent complexity in the process of behavior change. In this paper we present the most recent treatment outcome research evaluating relapse rates, with a special focus on the substance use disorders. Following this review of the literature we present an argument for the operationalization of relapse as a dynamic process, which can be empirically characterized using dynamical systems theory. We support this argument by presenting results from the analysis of alcohol treatment outcomes using catastrophe modeling techniques. These results demonstrate the utility of catastrophe theory in modeling the alcohol relapse process. The implications of these analyses for the treatment of alcohol use disorders, as well as a discussion of future research incorporating nonlinear dynamical systems theory is provided.
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PMID:Modeling the complexity of post-treatment drinking: it's a rocky road to relapse. 1735 97

For diagnosis of patients with comorbid psychotic symptoms and substance use disorders (SUDs), Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, makes clear distinctions between independent psychotic disorders (eg, bipolar disorder, schizophrenia) and substance-induced syndromes (eg, delirium, dementias). Most substance-induced psychotic symptoms are considered to be short lived and to resolve with sustained abstinence along with other symptoms of substance intoxication and withdrawal. These guidelines are challenged by practical difficulties in distinguishing between substance-induced and independent psychoses and by mounting evidence that marijuana use may be a contributing cause of schizophrenia. To inform the diagnostic distinction between substance-induced vs independent psychotic symptoms, 2 kinds of information could be sought from longitudinal research: (a) identification of early markers that clearly differentiate the 2 conditions and (b) more precise information about duration of psychotic symptoms induced by different substances. Evidence of this type could emerge from reanalysis of existing data from large-scale longitudinal studies of community samples. To inform possible nosological changes related to the possible schizophrenia-inducing role of marijuana (eg, designating a "cannabis-induced" subtype), a wide range of research evidence will be needed to clarify the relationship between effects of cannabis and schizophrenia symptoms. Ultimately, the ideal psychiatric nomenclature will define syndromes on the basis of established etiology and/or pathophysiology. Given the strong association between SUDs and psychotic disorders, research on the neurobiology of psychotic disorders could fruitfully include subjects with comorbid SUDs to shed light on shared etiology and pathophysiology.
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PMID:DSM-V research agenda: substance abuse/psychosis comorbidity. 1755 51

High rates of pathological gambling are found in psychiatric populations, including those with mood or substance use disorders. The extent to which individuals with schizophrenia exhibit the symptoms of pathological gambling has not been adequately investigated. This paper examines the case of a 40-year-old schizophrenic female with a four-year history of gambling. The characteristics of possible interactions between pathological gambling and schizophrenic symptom profiles are outlined in order to propose better treatments for this group of patients.
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PMID:Schizophrenia and pathological gambling. 1766 Nov 94

This study examines the specificity and impact of comorbid disorders in probands on the familial transmission of panic and social anxiety disorders. It employs a contemporary family study design with 225 probands (with and without panic and social anxiety disorders) sampled from outpatient clinics and the local community. Their 1053 adult first-degree relatives were assessed for lifetime disorders, based on best estimate diagnoses derived from semi-structured psychiatric diagnostic interviews (Schedule for Affective Disorders and Schizophrenia), multi-informant family history information, and medical records. Generalized estimating equations were used to examine the familial aggregation of panic and social anxiety disorders, and the contributions of comorbid disorders. Results show specificity of familial aggregation of both panic disorder and social anxiety in probands and relatives (i.e., panic odds ratio=3.7, 95%CI 1.5-9.3; social anxiety odds ratio=1.8, 95%CI 1.1-2.9) after controlling for comorbid disorders. There was no contribution of common comorbid disorders (depression, alcoholism, generalized anxiety disorder and agoraphobia) in probands on the familial aggregation of either disorder. These findings confirm prior studies of specificity of familial transmission of panic and social anxiety disorders, and demonstrate that the association between these disorders in probands is not attributable to comorbid mood, anxiety or substance use disorders. Therefore, despite the high magnitude of co-occurrence of panic disorder and social anxiety, there may be distinct etiologic factors underlying each disorder. These findings have implications for studies of the etiology, genetics, and treatment of these disorders.
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PMID:Specificity of familial transmission of anxiety and comorbid disorders. 1770 72

Substance abuse is highly prevalent in schizophrenia and associated with numerous negative consequences. While studies have regularly reported more severe depressive symptoms in addicted schizophrenia patients relative to non-abusing patients, some studies have not corroborated this finding. The current meta-analysis was performed to quantify the relative severity of depressive symptoms in dual-diagnosis schizophrenia. A search of the literature using computerized engines was undertaken. Studies were retained in the analysis if (i) they assessed depressive symptoms using validated scales specific to depression (e.g. Hamilton Depression Rating Scale); and (ii) groups of schizophrenia patients were divided according to substance use disorders (alcohol, amphetamines, cannabis, cocaine, hallucinogens, heroin and/or phencyclidine). According to the inclusion criteria, 20 studies were available for mathematical analysis. A small, positive and significant effect size estimate (n =3283; 1680 dual diagnosis; 1603 single diagnosis; adjusted Hedges's g =0.292; p =0.003) was obtained, within a random-effect model, suggesting that some dual-diagnosis patients experience more severe depressive symptoms than single-diagnosis patients. This significant difference was found only for studies using the Hamilton Depression Rating Scale but not for other depression scales. The results of the present meta-analysis suggest that addicted schizophrenia patients experience more severe depressive symptoms compared to non-abusing patients, but that the difference is smaller than commonly assumed. The meta-analysis also shows that the significance of results is related to the scale used to measure depressive symptoms. These results have methodological implications for future studies of depressive symptoms in dual-diagnosis patients, and potential implications for the prevention and treatment of depressive symptoms in schizophrenia.
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PMID:Meta-analysis of depressive symptoms in dual-diagnosis schizophrenia. 1782 52

Substance use disorder is the most frequent and clinically significant comorbidity among schizophrenia patients today. All schizophrenia patients should be assessed and monitored carefully regarding their substance use. Those with any regular use of alcohol or other drugs should be considered at risk for multiple adverse effects. As therapies for co-occurring substance use disorders have evolved over the past 20 years, medication management, psychosocial interventions, and rehabilitation models have increasingly emphasized the integration of mental health and substance abuse treatments, attention to group and residential interventions, matching interventions to stage of treatment, comprehensiveness, and long-term perspectives on recovery. Clinicians should understand the implications of each of these principles of care.
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PMID:Management of substance use disorder in schizophrenia patients: current guidelines. 1793 87

MDD and anxiety disorders are highly prevalent among persons who have MS and have been associated with decreased adherence to MS treatment and poorer functional status and quality of life. Effective treatment is available for MDD, but this disorder continues to be underdetected and undertreated by MS providers. Treatment with pharmacotherapy is particularly challenging in this patient population, given the somatic symptom overlap between MS and depression and the increased burden of side effects. Larger randomized, controlled trials are needed to elucidate further the effectiveness of pharmacotherapy and to identify subgroups of patients who would benefit from this type of treatment for depression. There have been few rigorous studies of the prevalence and impact of anxiety disorders, substance use disorders, or serious mental illness such as bipolar disorder or schizophrenia, in MS samples.
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PMID:Psychiatric issues in multiple sclerosis. 1793 46

Anticonvulsants are being used clinically as monotherapy and adjuncts in mental illnesses other than affective disorders. This review focuses on the literature for anticonvulsants and lithium in substance use disorders, anxiety disorders, and schizophrenia. Given the abuse potential and other difficulties with prescribing benzodiazepines for alcohol and benzodiazepine withdrawal, anticonvulsants have been considered as an alternative. Promising therapeutic effects have been demonstrated in many of the anxiety disorders, with the greatest number of trials and positive results in posttraumatic stress disorder. Although anticonvulsant and lithium augmentation for schizophrenia is common in practice and has been studied in double-blind, randomized, controlled trials, the sum of the evidence has been inconclusive.
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PMID:Update: new uses for lithium and anticonvulsants. 1822 41

Disturbances in the endogenous cannabinoid (ECB) system in schizophrenia may contribute to their enhanced sensitivity to psychoactive substances, and the beneficial effects of second-generation antipsychotics for substance abuse in schizophrenia may involve modulatory effects on ECB. To verify these two assumptions, 29 patients (24 completers) with schizophrenia and substance use disorders (SUD) were treated with quetiapine for 12 weeks, and peripheral ECB levels were measured, using high-performance liquid chromatography/mass spectrometry, in patients (weeks 0, 6 and 12) and 17 healthy volunteers. Baseline anandamide levels were significantly higher in patients, relative to controls. This result is consistent with studies describing ECB dysfunctions in schizophrenia. SUD parameters improved during treatment, but no changes in ECB occurred over time. Improvements in substance abuse were probably not mediated by modulatory effects of quetiapine on ECB. Lastly, baseline anandamide predicted endpoint SUD scores (alcohol/ cannabis). Anandamide is a potential target for medications aimed at relieving SUD in schizophrenia.
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PMID:Endogenous cannabinoids in patients with schizophrenia and substance use disorder during quetiapine therapy. 1830 2


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