Schizoaffective Disorder Depressed Type Research Articles

Assessing the validity of a self-reported clinical diagnosis of schizophrenia.

The increasing availability of biobanks is changing the way individuals are identified for genomic research. This study assesses the validity of a self-reported clinical diagnosis of schizophrenia. The study included 1744 clinically-ascertained participants with schizophrenia or schizoaffective disorder depressed-type (SA-D) diagnosed by self-report and/or research interview and 1453 UK Biobank participants with self-reported and/or medical record diagnosis of schizophrenia or SA-D. Unaffected controls included a total of 501,837 participants. We assessed the positive predictive values (PPV) of self-reported clinical diagnoses against research interview and medical record diagnoses. Polygenic risk scores (PRS) and phenotypes relating to demographics, education and employment were compared across diagnostic groups. The variance explained (r2) in schizophrenia PRS for each diagnostic group was compared to samples in the Psychiatric Genomics Consortium (PGC). In the clinically-ascertained participants, the PPV of self-reported schizophrenia for a research diagnosis of schizophrenia was 0.70, which increased to 0.81 after expanding the research diagnosis to schizophrenia or SA-D. In UK Biobank, the PPV of self-reported schizophrenia for a medical record diagnosis was 0.74. Compared to participants who self-reported, participants with a clinically-ascertained research diagnosis were younger and more likely to have a high school qualification. Participants with a medical record diagnosis in UK Biobank were less likely to be employed or have a high school qualification than those who self-reported. Schizophrenia PRS did not differ between participants that had a diagnosis from self-report, research diagnosis or medical records. Polygenic liability r2, for all diagnosis definitions, fell within the distribution of PGC schizophrenia cohorts. Self-reported measures of schizophrenia are justified in genomic research to maximise sample size and reduce the burden of in-depth interviews on participants, although within sample validation of diagnoses is recommended.

Schizoaffective Disorder Depressive Type in “The Yellow Wallpaper” by Charlotte Perkins Gilman

Presentation given at the 21th Annual Phi Kappa Phi Student Research and Fine Arts Conference

Examining cognition across the bipolar/schizophrenia diagnostic spectrum.

Cognitive impairments are well-established features of schizophrenia, but there is ongoing debate about the nature and degree of cognitive impairment in patients with schizoaffective disorder and bipolar disorder. We hypothesized that there is a spectrum of increasing impairment from bipolar disorder to schizoaffective disorder bipolar type, to schizoaffective disorder depressive type and schizophrenia. We compared performance on the Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) Consensus Cognitive Battery between participants with schizophrenia (n = 558), schizoaffective disorder depressive type (n = 112), schizoaffective disorder type (n = 76), bipolar disorder (n = 78) and healthy participants (n = 103) using analysis of covariance with post hoc comparisons. We conducted an ordinal logistic regression to examine whether cognitive impairments followed the hypothesized spectrum from bipolar disorder (least severe) to schizophrenia (most severe). In addition to categorical diagnoses, we addressed the influence of symptom domains, examining the association between cognition and mania, depression and psychosis. Cognitive impairments increased in severity from bipolar disorder to schizoaffective disorder bipolar type, to schizophrenia and schizoaffective disorder depressive type. Participants with schizophrenia and schizoaffective disorder depressive type showed equivalent performance (d = 0.07, p = 0.90). The results of the ordinal logistic regression were consistent with a spectrum of deficits from bipolar disorder to schizoaffective disorder bipolar type, to schizophrenia/schizoaffective disorder depressive type (odds ratio = 1.98, p < 0.001). In analyses of the associations between symptom dimensions and cognition, higher scores on the psychosis dimension were associated with poorer performance (B = 0.015, standard error = 0.002, p < 0.001). There were fewer participants with schizoaffective disorder and bipolar disorder than schizophrenia. Despite this, our analyses were robust to differences in group sizes, and we were able to detect differences between groups. Cognitive impairments represent a symptom dimension that cuts across traditional diagnostic boundaries.

S189. CARVING A MORE SPECIFIC SUBTYPE OF SCHIZOPHRENIA FOR GENETIC STUDIES: SPORADIC SCHIZOAFFECTIVE BIPOLAR TYPE

BackgroundSchizophrenia is a heterogeneous group of disorders. The familial-sporadic distinction has been considered under a range of genetic models. Research supports a strong association of de novo copy mutations with sporadic schizophrenia. The aim of the study was to determine a more homogenous phenotype for genetic research via comparison of various clinical and socio-demographic variables in familial and sporadic schizophrenia.MethodsA cross-sectional observational design was used. This study included 384 participants with schizophrenia/schizoaffective disorder from an Afrikaner founder population in South Africa that previously participated in genetic research. A comprehensive data capturing sheet was completed from a pre-existing database that contains information obtained from the Diagnostic Interview for Genetic Studies, chronological clinical summary reports and additional sources of information. The study protocol was approved by the Research Ethics Committee from the Faculty of Health Sciences at the University of Pretoria. Logit models were fitted using the backward elimination procedure to investigate relationships where the dependent variable was binary. Odds ratio estimates were calculated for independent variables that were significant in the model. The Kruskal-Wallis test was conducted to compare the means of groups. For cases where there were significant differences a post-hoc test with a Bonferroni correction was done to determine which groups differ significantly.ResultsThere were 214 familial and 170 sporadic subjects. 279 had a diagnosis of schizophrenia, 66 schizoaffective, bipolar type and 39 schizoaffective disorder, depressive type. 242 were male and 142 female. The age at onset of the primary psychiatric diagnosis, season of birth, co-morbid diagnoses, symptomatology, suicidality history and marital status weren’t significantly different when considering the combined schizophrenia/schizoaffective disorder group and its relationship to familiality. Early deviant behaviour was however decreased in the sporadic group. These findings were replicated when analysing schizophrenia independently from schizoaffective disorder. The sporadic schizoaffective disorder, bipolar type did however have a significantly lower age at onset (mean 20.18 versus 25.07 years), 8.8 times more hallucinations, 6.6 times more odd behaviour before the age of 10 and were 2.8 times more likely to be single. The bipolar type also had 2.9 times more suicide attempts as opposed to ideation. This finding wasn’t statistically significant. The sporadic schizoaffective group overall was 2.2 times more likely to abuse substances. The depressive type didn’t differ significantly with regards to age at onset, season of birth, co-morbidities, early deviant behaviour, symptomatology, suicidality or marital status.DiscussionThe combined schizophrenia/schizoaffective group didn’t differ significantly, nor did schizophrenia and schizoaffective disorder depressive type when analysed independently. The sporadic schizoaffective bipolar type differed significantly on multiple important variables that suggest a poorer prognosis and increased disease severity. The sporadic schizoaffective bipolar type forms a more homogenous group, with genetic studies hinting at relatively specific genetic risk factors. Studies elucidating the genetic architecture of this group could prove invaluable in clarifying the aetiology of schizophrenia.

P.1.j.006 - Examining cognition across the bipolar/schizophrenia diagnostic spectrum

BACKGROUND: Cognitive impairments are well-established features of schizophrenia, but there is ongoing debate about the nature and degree of cognitive impairment in patients with schizoaffective disorder and bipolar disorder. We hypothesized that there is a spectrum of increasing impairment from bipolar disorder to schizoaffective disorder bipolar type, to schizoaffective disorder depressive type and schizophrenia. METHODS: We compared performance on the Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) Consensus Cognitive Battery between participants with schizophrenia (n = 558), schizoaffective disorder depressive type (n = 112), schizoaffective disorder type (n = 76), bipolar disorder (n = 78) and healthy participants (n = 103) using analysis of covariance with post hoc comparisons. We conducted an ordinal logistic regression to examine whether cognitive impairments followed the hypothesized spectrum from bipolar disorder (least severe) to schizophrenia (most severe). In addition to categorical diagnoses, we addressed the influence of symptom domains, examining the association between cognition and mania, depression and psychosis. RESULTS: Cognitive impairments increased in severity from bipolar disorder to schizoaffective disorder bipolar type, to schizophrenia and schizoaffective disorder depressive type. Participants with schizophrenia and schizoaffective disorder depressive type showed equivalent performance (d = 0.07, p = 0.90). The results of the ordinal logistic regression were consistent with a spectrum of deficits from bipolar disorder to schizoaffective disorder bipolar type, to schizophrenia/schizoaffective disorder depressive type (odds ratio = 1.98, p < 0.001). In analyses of the associations between symptom dimensions and cognition, higher scores on the psychosis dimension were associated with poorer performance (B = 0.015, standard error = 0.002, p < 0.001). LIMITATIONS: There were fewer participants with schizoaffective disorder and bipolar disorder than schizophrenia. Despite this, our analyses were robust to differences in group sizes, and we were able to detect differences between groups. CONCLUSION: Cognitive impairments represent a symptom dimension that cuts across traditional diagnostic boundaries.

Ketamine Role in Schizoaffective Disorder Depressive Type

Ketamine use for patients with severe treatment-resistant depression continues to be an area of interest due to the relatively limited number of treatment options for those patients. Although its use as a treatment option for patients with schizophrenia and schizoaffective disorder may seem counterintuitive, in this case report, we explore the efficacy of ketamine for depressive episodes in schizoaffective disorder. This patient who carried a diagnosis of schizoaffective disorder was given 300 mg of intramuscular ketamine for agitation. However, over the course of four days of inpatient stay, her depression drastically improved. She met criteria for remission with the Hamilton Rating Scale for Depression (HAM-D) score of 4, down from an initial score of 21. We advocate for a better understanding of the pros and cons of using ketamine for depression in schizoaffective disorders considering the controversy over the diagnosis of schizoaffective disorder, especially in African American population. At the urging of reducing the risk of suicide among this group and improving their quality of life as well as reducing financial burden by shortening total duration of hospitalization, it may be worthwhile to explore the feasibility of ketamine as a treatment option for severe depression in these patients, possibly as a last resort.

Mania possibly induced by clozapine: a case report

Mania possibly induced by clozapine: a case report Manic shift can be caused by the use of atypical antipsychotics. Hypomanic/manic episodes caused by olanzapine, risperidone, quetiapine, ziprasidone, amisulpride, aripiprazole, zotepine, perospirone, and paliperidone have been frequently described in the literature. The proposed causes of mania/hypomania switching are due to blockages of 5HT2A and D2 receptors, enhancement of 5HT1A receptors, and dopamine release in the prefrontal/frontal regions. There have been no hypomanic/manic episodes described during clozapine use up to the present. A manic shift observed during clozapine use in a 30-yearold woman with schizoaffective disorder depressive type without any history of manic or mixed episodes was presented below.

Genetic associations between neuregulin-1 SNPs and neurocognitive function in multigenerational, multiplex schizophrenia families

Recent work shows promising associations between schizophrenia and polymorphisms in neuregulin-1 (NRG1) and a large literature also finds strong familial relationships between schizophrenia and cognitive deficits. Given the role of NRG1 in glutamate regulation and glutamate's effect on cognition, we hypothesized that cognitive deficits may be related to variation within NRG1, providing a possible mechanism to increase risk for schizophrenia. This study examined the associations between NRG1, cognition, and schizophrenia using a multigenerational multiplex family sample (total N=419, 40 families), including 58 affected participants (schizophrenia or schizoaffective disorder-depressed type) and their 361 unaffected relatives. Participants were genotyped for 40 NRG1 single nucleotide polymorphisms (SNPs), chosen largely based on previous associations with schizophrenia. All participants completed structured diagnostic interviews and a computerized neurocognitive battery assessing eight cognitive domains. Variance component quantitative trait analyses tested for associations between individual NRG1 SNPs and cognitive performance in the total sample, a subsample of healthy participants with no Diagnostic and Statistical Manual of Mental Disorders diagnosis, and using general intelligence as a covariate. Effect sizes (within-family β coefficients) ranged from 0.08 to 0.73, and 61 of these associations were nominally significant (P≤0.05), with 12 associations at P≤0.01, although none achieved the modified Bonferroni significance threshold of P<0.0003. Attention was the most frequently nominally associated domain and rs10503929, a nonsynonymous SNP, was the most frequently nominally associated SNP. Although not significant experiment-wise, these findings suggest that further study of the associations between variation in NRG1 and cognition may be productive.

Diagnostic and therapeutic challenges involving patients with post-traumatic stress disorder and schizoaffective disorder depressive type

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Major depressive disorder as a co-morbid diagnosis in schizophrenia versus the diagnosis of schizoaffective disorder – depressed type

The purpose of this article is to focus on the importance of depressive symptoms in patients suffering from schizophrenia, and the dilemma posed by hierarchical classification methods, which exclude co-morbid diagnoses such as Major Depressive Disorder in patients with schizophrenia. The question arises that if Major Depressive Disorder is only categorized under the diagnosis of Schizoaffective Disorder (depressed type), are we able to recognize these symptoms promptly and treat them sufficiently? The duration of the substantial period of depressed mood referred to in the DSM IV TR criteria for Schizoaffective Disorder is unspecified. We suggest that one should only allocate the latter diagnosis if the substantial period is that of one third or more of the whole duration of the illness. Identification of the optimal cutoff point can generate further hypothesis testing research and refinement of the diagnostic model. It is not only important to refine the diagnosis, but it is even more important to detect these symptoms and treat promptly and effectively. According to the latest literature, the best possible treatment for depression in schizophrenia appears to be the combination of a second-generation antipsychotic and cognitive psychotherapy.

Long-Term Study Confirms DST As Suicide-Prediction Tool

Back to table of contents Previous article Next article Clinical & Research NewsFull AccessLong-Term Study Confirms DST As Suicide-Prediction ToolJoan Arehart-TreichelJoan Arehart-TreichelSearch for more papers by this authorPublished Online:4 May 2001https://doi.org/10.1176/pn.36.9.0040Which depressed persons will ultimately commit suicide? A few psychological or behavioral risk factors have emerged with consistency: hopelessness, suicidal ideation, a history of suicide attempts, being unmarried, living alone, and being male. But suppose doctors had a simple, inexpensive, biological test that could also help them identify such persons?Some studies conducted during the past few years have suggested that such a test indeed exists. And now a new investigation bolsters the argument still further. It was conducted by William Coryell, M.D., a psychiatrist at the University of Iowa College of Medicine in Iowa City, and by Michael Schlesser, M.D., a psychiatrist with Neuropsychiatry Associates in Dallas. They report their favorable study results with the test in the May American Journal of Psychiatry.Depressed persons in especially great danger of committing suicide, various researchers have suspected, might have abnormally high levels of three interacting hormones that mirror the brain’s and body’s reaction to stress. The hormones are the adrenal glands’ cortisol, the pituitary gland’s adrenocorticotropic hormone (ACTH), and the hypothalamus’s corticotropin-releasing factor (CRF). For instance, when the bodies of persons who had died by suicide were compared with those of persons who had died by other violent means, the former were found to have heavier adrenal glands and also higher levels of CRF in their cerebrospinal fluid. So some of these investigators decided to conduct studies to learn whether the dexamethasone suppression test (DST), which measures abnormally high levels of cortisol in the body (and thereby indirectly also abnormally high levels of ACTH and CRF), might predict suicide in depressed persons. Some of these studies (although not all) produced favorable results, suggesting that the DST might indeed be able to predict suicide.One drawback of these investigations, however, is that they were not conducted over the long term. Another drawback was that the apparent predictive value of the DST had not been compared with known psychological and behavioral suicidal risk factors—that is, to known psychological and behavioral predictors. So Coryell and Schlesser decided to conduct a study that would both test the value of the DST over a 15-year period and pit the value of the DST against psychological and behavioral predictors.Between 1978 and 1981, they recruited 78 patients for their study. The patients sought either inpatient or outpatient treatment at the University of Iowa for conditions that met research diagnostic criteria for major depressive disorder, mania, or schizoaffective disorder–depressed type. In addition to providing psychological and behavioral data that indicated whether they might be especially in danger of committing suicide, such as hopelessness, previous suicide attempts, living alone, and so forth, the patients were given the DST.During the test, each patient took 1 mg of dexamethasone orally at 11 p.m., then provided blood samples the next day at 8 a.m. and/or 4 p.m. Cortisol levels in the blood samples were then determined. A cortisol value greater than 5 μg/dl indicated that dexamethasone had failed to suppress cortisol in the patient’s blood—in other words, that test results were abnormal and that the patient’s cortisol level was abnormally high. Thirty-two of the 78 patients, it turned out, showed abnormal DST results.Coryell and Schlesser then followed the fate of the 78 patients over the next 15 years to see how many committed suicide, whether the DST results were predictive of suicide, and how DST predictivity compared with predictivity via psychological and behavioral risk factors. (The study did not influence any depression treatments that the patients received throughout these years, although such therapies were noted.)Of the 78 patients, eight were found to have committed suicide. DST results for seven of the eight had been abnormal. Also telling, survival analyses showed that the estimated risk for eventual suicide in the abnormal DST group was 27 percent, compared with only 3 percent among patients who had normal DST results. When the known psychological and behavioral risk factors for suicide in the 78 patients were examined, none was found to distinguish significantly the eight patients who later committed suicide from those who did not.Yet another intriguing aspect about the DST that emerged from the study is that its ability to predict suicide seemed to remain robust as the years went by.If the DST truly pans out after further study as an effective suicide predictor in depressed patients, it is probably something that psychiatrists could use in their clinical practices, Coryell indicated.The study, “The Dexamethasone Suppression Test and Suicide Prediction,” is posted on the journal’s Web site at http://ajp.psychiatryonline under the May issue. ▪ ISSUES NewArchived

Depressive and negative symptoms in major psychiatric disorders

Among 193 inpatients with Research Diagnostic Criteria (RDC) major psychiatric disorders, the scores in Hamilton's Rating Scale for Depression (HRSD) were higher among those patients with RDC schizoaffective disorder depressed type and major depressive disorder, whereas the scores in the Scale for Assessment of Negative Symptoms (SANS) were higher among patients with these two disorders, as well as those with RDC nonaffective psychoses (schizophrenia and unspecified functional psychosis). The HRSD and SANS items were factor-analyzed, yielding nine factors that discriminated depressive and negative symptoms. These findings suggest that although depressive and negative symptoms frequently coexist, they constitute discrete syndromes.

Clinical course and outcome of schizoaffective disorders. A three-year follow-up study.

Four samples of patients (fulfilling at the index episode, respectively, Research Diagnostic Criteria for schizoaffective disorder manic type, schizoaffective disorder depressed type, manic disorder and major depressive disorder) were followed up for 3 years. At the end of the follow-up period, no significant difference with respect to the mean scores on the Disability Assessment Schedule (DAS) and on the Strauss-Carpenter Outcome Scale was observed between schizomanics and manics (although the global outcome was slightly poorer in the former group). In contrast, significant differences between schizodepressives and depressives were found both on some DAS subscales (the schizodepressives were more socially withdrawn, had less social contacts and poorer work performance) and on the Strauss-Carpenter Outcome Scale (the mean total score and the mean scores on the items "social contacts" and "employment" were significantly lower in schizodepressives). The most frequent pattern of course in patients diagnosed cross-sectionally as schizomanic was a bipolar one. Some patients had only recurrent schizomanic episodes and others more an alternance of schizomanic and schizophrenic episodes. In patients diagnosed cross-sectionally as schizodepressives, the most frequent pattern of course was that characterized by recurrent schizodepressive episodes. In some patients an alternance of schizodepressive and depressive or schizodepressive and schizophrenic episodes was observed. These data confirm that patients diagnosed cross-sectionally as schizoaffective represent a very heterogeneous group when they are studied longitudinally, and support the usefulness of a "multiaxial" approach to the classification of schizoaffective disorders, taking into account both cross-sectional symptomatology and clinical course.