Schizotypal personality disorder: an operational definition of Bleuler's latent schizophrenia?

In spite of the pressure for consensus that operational diagnoses exert, there remains considerable disagreement concerning the marginal syndromes which may be subtypes of schizophrenia or phenomenologically or genetically related. Some clarification of the question may result by returning to Bleuler's "latent schizophrenia," which he observed in the relatives of schizophrenics. Schizotypal personality disorder of DSM-III is only a first approximation of this, and its deficits in this respect are discussed briefly.     

Schizoaffective disorder: a form of schizophrenia or affective disorder?

BACKGROUND: The diagnostic status of schizoaffective disorder continues to be controversial. Researchers have proposed that schizoaffective disorder represents a variant of schizophrenia or affective disorder, a combination of the 2, or an intermediate condition along a continuum between schizophrenia and affective disorder. METHOD: We compared outpatients aged 45 to 77 years with DSM-III-R diagnosis of schizoaffective disorder (N = 29), schizophrenia (N = 154), or nonpsychotic mood disorder (N = 27) on standardized rating scales of psychopathology and a comprehensive neuropsychological test battery. A discriminant function analysis was used to classify the schizoaffective patients based on their neuropsychological profiles as being similar either to schizophrenia patients or to those with nonpsychotic mood disorder. RESULTS: The schizoaffective and schizophrenia patients had more severe dyskinesia, had a weaker family history of mood disorder, had been hospitalized for psychiatric reasons more frequently, were more likely to be prescribed neuroleptic and anticholinergic medication, and had somewhat less severe depressive symptoms than the mood disorder patients. The schizophrenia patients had more severe positive symptoms than the schizoaffective and mood disorder patients. The neuropsychological performances of the 2 psychosis groups were more impaired than those of the nonpsychotic mood disorder patients. Finally, on the basis of a discriminant function analysis, the schizoaffective patients were more likely to be classified as having schizophrenia than a mood disorder. CONCLUSION: These findings suggest that schizoaffective disorder may represent a variant of schizophrenia in clinical symptom profiles and cognitive impairment.     

The negative symptoms of schizophrenia: category or continuum?

Negative symptoms have been considered to be specific to schizophrenia or a subtype of schizophrenia: the deficit syndrome. In other words, these symptoms have been considered to be categorically different from other forms of human behavior and experience, whether they occur in healthy persons or patients with other psychiatric disorders. In this paper, we advocate a dimensional approach to negative symptoms, which is supported by two main arguments. First, enduring negative symptoms can even be observed in a variety of psychiatric disorders and they are not specific to schizophrenia. Second, we review evidence that negative symptoms show a continuous distribution from apparently healthy subjects to those with a fully developed clinical syndrome. Although the evidence does not allow for a definite decision concerning the dimensional distribution of negative symptoms, it certainly justifies exploring a dimensional approach with respect to its clinical and scientific utility. Understanding negative symptoms as a variation of normal mental processes will strengthen the development of neurocognitive models and treatment approaches.     

Can we improve the diagnostic efficiency and predictive power of prodromal symptoms for schizophrenia?

Prodromal symptoms and other variables for a sample of 200 young people who had experienced a first-onset functional psychosis, were analyzed to examine their diagnostic efficiency and predictive power in relation to a diagnosis of schizophrenia. Two different techniques were utilized to generate optimal cut-off points for a number of prodromal symptoms, and optimal decision rules to maximize diagnostic efficiency. The product of the chance-corrected sensitivity and specificity, or the area under the QROC curve, was used to assess the predictive efficiency of a number of prodromal variables, DSM-III-R prodromal variables, pre-psychotic deterioration, pre-morbid functioning, and prodromal duration. The SPAN technique generated a decision rule that performed equivalently to the single variable 'duration of prodrome'. Implications of these results for future research are discussed.     

How does studying schizotypal personality disorder inform us about the prodrome of schizophrenia?

An increasing emphasis in the schizophrenia literature has been on the prodromal phase of the illness. The study of schizophrenia spectrum illness, including schizotypal personality disorder, has added important insight into the etiology, neuropathology, and treatment of schizophrenia, which can facilitate early identification, intervention, and perhaps prevention of the illness. The heterogeneity of the schizophrenia spectrum makes its definition elusive at best. The primary aim of the Cognitive Assessment and Risk Evaluation Program at the authors’ institution is to combine the current knowledge of clinical and demographic risk factors for schizophrenia with the rapidly emerging data on vulnerability markers, or endophenotypes, that are associated with schizophrenia. The use of brain-based vulnerability markers may help to identify neurobiologically and clinically meaningful subgroups within this heterogeneous population of individuals in the early stages of schizophrenia. Another important aim of the Cognitive Assessment and Risk Evaluation program is to thoroughly assess those individuals who have not converted to psychosis to understand potential protective factors, reduce the rate of false positives, and decrease disability. The current review details a strategy for researching the schizophrenia prodrome by using information gained from research in schizotypal personality disorder.     

Pharmacological treatment of negative symptoms of schizophrenia: therapeutic opportunity or Cul-de-sac?

Negative symptoms of schizophrenia are debilitating and they contribute to poor outcome in schizophrenia. Initial enthusiasm that second-generation antipsychotics would prove to be powerful agents to improve negative symptoms has given way to relative pessimism that the effects of current pharmacological treatments are at best modest. METHOD: A review of the current 'state-of-play' of pharmacological treatments for negative symptoms in schizophrenia. RESULTS: Treatment results to date have been largely disappointing. The evidence for efficacy of second-generation antipsychotics is reviewed. CONCLUSION: The measurement and treatment trials methodology for the evaluation of negative symptoms need additional refinement before therapeutic optimism that better treatments for negative symptoms can be realized.     

Is initiation of smoking associated with the prodromal phase of schizophrenia?

OBJECTIVE: Although the association between smoking and schizophrenia is well known, little attention has been paid to the time between initiation of smoking and onset of schizophrenia. Our goal was to study this putative temporal relation among patients with schizophrenia. METHODS: We used data from the Northern Finland 1966 Birth Cohort (n = 11,017) linked with the National Finnish Hospital Discharge Register to study age at initiation of smoking and age at onset of schizophrenia, and we examined associations between family and environmental factors and the retrospectively determined regular smoking among patients with schizophrenia. RESULTS: Our main finding was that the initiation of regular smoking was closely related to the onset of schizophrenia. The mean difference in time between the initiation of regular smoking and the onset of schizophrenia among patients (n = 30) was 2.3 (standard deviation [SD] 6.6) years, which was statistically significantly lower than that for subjects with other psychoses (n = 18) (8.6 [SD 6.3] yr) (p < 0.001). Among patients with schizophrenia, the increased likelihood of smoking was associated only with paternal smoking in the family environment, but not with any other background factors (odds ratio 3.5, 95; confidence interval 1.9-11.3). CONCLUSION: Smoking may be a sign of the prodromal phase of schizophrenia.     

Executive deficits: A continuum schizophrenia–bipolar disorder or specific to schizophrenia?

Executive dysfunction is a core deficit in schizophrenia (SCH). However, some controversy exists when examining such deficits in studies of bipolar disorder (BD). The aim of the present research was to investigate whether executive deficits were similar or distinct in both illnesses. 148 patients with BD, 262 patients with stable SCH and 108 healthy controls (CT) were recruited for the study. The BD patients were also differentiated according to the clinical subtype (BD subtype I, BDI, or subtype II, BDII) they exhibited and according to whether there was a previous history of psychosis. All subjects completed a broad neuropsychological battery. The influences of other clinical data were also evaluated. Both the BD and SCH patients showed widespread deficits in all executive tasks, with no differences between these two groups of patients. BDII patients only showed some selective deficits, and their scores on planning and inhibitory tasks fell on the continuum between the CT, the BDI and the SCH patients. Psychotic phenotypes did not influence the BD patients' performance on the battery. Other clinical variables related to illness severity did influence deficits in any subgroup of patients. Our results point to the existence of common executive disturbances in both diagnostic categories. Moreover, the inclusion of subclinical phenotypes in research may be helpful in cognitive assessment studies.     

Do needs, symptoms or disability of outpatients with schizophrenia influence family burden?

Background  Most needs of outpatients with schizophrenia are met by the family. This could cause high levels of family burden. The objective of this study is to assess the relationship between the patients’ needs and other clinical and disability variables and the level of family burden. Method  A total sample of 231 randomly selected outpatients with schizophrenia was evaluated with the Camberwell Assessment of Needs, Positive and Negative Syndrome Scale, Global Assessment of Functioning and Disability Assessment Scale. A total of 147 caregivers also answered the objective and subjective family burden questionnaire (ECFOS-II). Correlations between total number of needs and family burden, t tests between presence or absence of need for each domain of family burden and regression models between family burden and needs, symptoms, disability and sociodemographic variables were computed. Results  The number of patients’ needs was correlated with higher levels of family burden in daily life activities, disrupted behaviour and impact on caregiver’s daily routine. The patients’ needs most associated with family burden were daytime activities, drugs, benefits, self-care, alcohol, psychotic symptoms, money and looking after home. In a regression model, a higher number of needs, higher levels of psychopathology and disability, being male and older accounted for higher levels of family burden. Conclusion  Patients with schizophrenia with more needs cause greater family burden but not more subjective concerns in family members. The presence of patients’ needs (daytime activities, alcohol and drug), severity of psychotic symptoms and disability are related to higher levels of family burden. The NEDES group is a multidisciplinary group of researchers from Sant Joan de Déu, which includes: S. Araya; P. Asensio; J. Autonell; A. Benito; E. Busquets; C. Carmona; P. Casacuberta; M. Castro; N. Díaz; M. Dolz; A. Foix; J. M. Giralt; A. Gost; J. M. Haro; M. Marquez; F. Martínez; R. Martínez; J. Miguel; M. C. Negredo; S. Ochoa; Y. Osorio; E. Paniego; L. Pantinat; A. Pendàs; C. Pujol; J. Quilez; J. Ramon; M. J. Rodríguez; B. Sánchez; A. Soler; F. Teba; N. Tous; J. Usall; M. Valdelomar; J. Vaquer; E. Vicens; M. Zamora.     

Obsessive compulsive symptoms in bipolar disorder patients: a comorbid disorder or a subtype of bipolar disorder?

概述

在过去十年中，人们越来越关注同时符合两种或两种以上精神障碍诊断标准的患者。上述共病情况之一就是双相障碍合并强迫症，这在以双相障碍为主要诊断的患者中比较常见。但是，关于这种共病的诊断和治疗的研究很少，在中国尤为如此。现有的研究主要集中在小样本的横断面研究，因此它们在对理解这种共病情况的病因和病程作用有限。对有限的文献进行回顾发现这是双相障碍中一种相对严重的、难治性的亚型，只有少数情况可以被认为是一种共病障碍。要阐明这种共病的病因、预后以及合适的治疗方法，则需要大样本的前瞻性研究。

中文全文

本文全文中文版从2015年10月26日起在http://dx.doi.org/10.11919/j.issn.1002-0829.215091可供免费阅览下载 The Forum by Peng and Jiang[1] highlights the lack of literature about comorbid bipolar disorder and obsessive compulsive (OCD) disorder. To provide a preliminary summary of the available English-language literature, a search of PubMed using three relevant keywords (‘bipolar disorder’, ‘obsessive compulsive disorder’, and ‘comorbidity’) was conducted in July 2015. Only a few of the 176 papers retrieved by this search were directly related to the topic of interest: most of the relevant papers described the incidence and clinical features of comorbid bipolar disorder and OCD in relatively small samples of patients; some discussed the etiology and treatment of the comorbid condition; and a few reported on prospective, multi-center studies with relatively large samples. Bipolar-OCD comorbidity was first reported in a 1995 study from Germany[2] which found that more than half of all patients with bipolar disorder had experienced other mental disorders, including OCD, during the course of the bipolar disorder. The study reported that the prevalence of comorbid OCD was higher in patients with unipolar depression than among patients with bipolar disorder. A subsequent systematic review[3] of 64 relevant articles in 2014 reported that from 11 to 21% of persons with bipolar disorder experience comorbid OCD at some time during the course of their bipolar disorder. Most reports indicate that comorbid OCD exacerbates the symptoms of bipolar disorder and makes the diagnosis and treatment of bipolar disorder more difficult. Compared to OCD patients and bipolar disorder patients without other comorbid conditions, bipolar patients with comorbid OCD have: a) higher rates of obsessive ideas about sex and religion and lower rates of ritual checking;[4] b) higher rates of substance abuse (including use of alcohol, sedatives, caffeine, etc.);[5,6] more episodes of depression, higher rates of suicide, and more frequent admissions to hospitals;[7] and d) more chronic episodes and residual symptoms.[8,9] There were no differences between bipolar patients with and without comorbid OCD in age, gender, education, marital status, age of onset of bipolar disorder, personality, prevalence of psychotic symptoms or rapid cycling, history of suicide attempts, the type of initial bipolar episode (i.e., depressed or manic), and the type of episode that was most prevalent throughout the course of bipolar disorder.[9] The systematic review by Amerio and colleagues[3] found that compared to bipolar patients without comorbid OCD, patients with bipolar disorder with comorbid OCD were more likely to experience OCD symptoms during an affective disorder episode (75% v. 3%), had a higher mean (sd) number of depressive episodes (8.9 [4.2] v. 4.1 [2.7] episodes), and were more likely to experience an antidepressant-induced manic episode (39% v. 9%). They also found that among patients with comorbid bipolar disorder and OCD, OCD symptoms were more like to occur during depressive episodes than manic episodes (78% v. 64%). Based on their findings, these authors argue that the obsessive-compulsive symptoms observed in these patients were secondary to bipolar disorder, not a co-occurring independent disorder.[3] Following this logic, I recommend that the occurrence of obsessivecompulsive symptoms during the depressive (or manic) episodes of a bipolar disorder should not be sufficient to merit a diagnosis of comorbid bipolar disorder and OCD; this comorbid diagnosis should be restricted to situations in which a patient with bipolar disorder also meets the full OCD symptomatic and duration criteria when the patient is not experiencing a depressive or manic episode. There are only a few articles about the possible etiology of bipolar-OCD comorbidity. A long-term family study based on a multi-generational dataset[10] (cases registered from January 1969 to 2009 included 19, 814 with OCD, 58, 336 with schizophrenia, 48, 180 with bipolar disorders, and 14, 904 with schizoaffective disorder) found familial associations among individuals with bipolar disorder, OCD, and schizophrenia spectrum disorders. There are also few reports about the long-term prognosis of comorbid bipolar disorder and OCD. One study[11] that followed 20 patients with bipolar disorder without comorbid disorders and 20 patients with comorbid bipolar disorder and OCD for 4 years found no significant differences in the long-term outcomes between the two groups. The treatment of bipolar-OCD comorbidity is difficult because the use of antidepressants to treat obsessive compulsive disorder may induce manic episodes. The existing literature about the treatment is primarily composed of case reports, retrospective cross-sectional studies, and a few treatment studies with small samples. A recent systematic review that combined the results of four treatment studies[12] found that 42% of patients with comorbid bipolar disorder and OCD were simultaneously treated with multiple mood stabilizers and another 10% needed combined treatment with mood stabilizers and anti-psychotic medications. One of the four studies reported that the combined use of antidepressants and mood stabilizers was effective and another study reported that some patients benefitted from the combined use of mood stabilizers and psychological therapy.[11] Based on currently available information, I recommend that patients with comorbid bipolar disorder and OCD be initially treated with mood stabilizers; if mono-therapy with mood stabilizers is ineffective, adjunctive treatment with selective serotonin reuptake inhibitor antidepressants (which are less likely to induce mania) should be considered. In my opinion, the basic treatment for bipolar-OCD is mood stabilizers and could be combined with antidepressants if the patients do not respond to the single treatment (ineffective). Despite ongoing debates about the etiology, diagnosis, and treatment of comorbid bipolar disorder and OCD, the clinicians who regularly treat bipolar patients need more high-quality, evidence-based information to improve their identification and management of this relatively severe and refractory subgroup of bipolar patients. Well-designed prospective studies with relatively large samples that are specifically focused on this important subgroup of bipolar disorder patients are needed.     

Is borderline personality disorder part of the bipolar spectrum?

In recent years, advances in the areas of both bipolar and borderline personality disorders have generated considerable interest in the clinical interface between these two conditions. Developments in the study of the neurobiology of borderline personality disorder suggest that many patients with this diagnosis have etiological features in common with those diagnosed with bipolar disorders. This claim is supported by new insights into the phenomenology of both disorders and by evidence that mood stabilizers are efficacious in the pharmacological management of borderline patients. This area of research is an important one because of the considerable morbidity and public health costs associated with borderline personality disorder. Since borderline patients can be so challenging to care for, it may be that a reframing of the disorder as belonging to the broad clinical spectrum of bipolar disorders holds benefits for patients and clinicians alike.     

Dispute over the multiple personality disorder: theoretical or practical dilemma?

Dissociative identity disorder (DID) could also be referred to as multiple personality disorder (MPD). Due to rare occurrence and difficulty in its' identification it is infrequently diagnosed in Poland. The indicated disorder has been portrayed by the authors throughout the historical context, referring to initial 18th century's references concerning dissociation. A typical dissociatively disordered person has been characterized along with his individual personality categories such as: original personality, altered personality, host and personality fragment. Moreover various diagnosis criterions of DID have been introduced. DID has also been differentiated with other disorders: PTSD (post-traumatic stress disorder) and BPD (borderline personality disorder). A hypothesis has been set up, stating that DID is directly correlated with the trauma experienced during childhood, while PTSD is linked with traumatic lived-through events in the later period of ones' life. The most contemporary and frequently used research tools for DID have been indicated: dissociative experience scale (DES) and somatoform dissociation questionnaire (SDQ-20). Based upon the known literature, the authors have presented treatment methods such as hypnotherapy and recorded therapy sessions. It is the view of the authors that the switching in dissociative identity disorder is of adaptive character (it occurrs depending upon adaptive needs).     

Borderline or bipolar? Distinguishing borderline personality disorder from bipolar spectrum disorders

This article addresses the question whether borderline personality disorder (BPD) can be understood as a variant of bipolar disorder. In the past, borderline pathology has been seen as a variant of psychosis, depression, or posttraumatic stress disorder, but there are important differences between all of these conditions and BPD. The proposal that BPD falls within the bipolar spectrum depends on the assumption that affective instability develops through the same mechanism in both diagnostic categories. There are major differences in phenomenology, family history, longitudinal course, and treatment response between BPD and bipolar disorder, and the findings of comorbidity studies are equivocal. Thus, existing evidence is insufficient to support the concept that BPD falls in the bipolar spectrum.