Schizoaffective disorder


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Introduction


Although no biological laboratory tests exist which confirm schizoaffective disorder, biological tests should be performed to exclude psychosis associated with or caused by substance use, medications, toxins or poisons, surgical complications, or other medical illnesses. Since non-medical mental health practitioners are not trained to exclude medical causes of psychosis, people experiencing psychosis should be referred to an emergency department or hospital.

Delirium should be ruled out, which can be distinguished by visual hallucinations, acute onset and fluctuating level of consciousness, indicating other underlying factors which includes medical illnesses. Blood tests are not usually repeated for relapse in people with an established diagnosis of schizoaffective disorder, unless there is a specific medical indication.

These may include serum BSL if olanzapine has previously been prescribed, thyroid function if lithium has previously been taken to rule out hypothyroidism , liver function tests if chlorpromazine has been prescribed, CPK levels to exclude neuroleptic malignant syndrome , and a urinalysis and serum toxicology screening if substance use is suspected.

Assessment and treatment may be done on an outpatient basis; admission to an inpatient facility is considered if there is a risk to self or others. Because psychosis may be precipitated or exacerbated by common classes of psychiatric medications , such as antidepressants , [41] [42] [43] [44] [45] ADHD stimulant medications , [46] [47] [48] and sleep medications , [49] [50] prescribed medication-induced psychosis should be ruled out , particularly for first-episode psychosis.

Bowers, Jr, MD wrote: Illicit drugs aren't the only ones that precipitate psychosis or mania—prescribed drugs can too, and in particular, some psychiatric drugs. We investigated this and found that about 1 in 12 psychotic or manic patients in an inpatient psychiatric facility are there due to antidepressant-induced psychosis or mania.

That's unfortunate for the field [of psychiatry] and disastrous for some of our patients. It is important to be understood here. I want to call attention to the fact that some persons with a family history of even the subtler forms of bipolar disorder or psychosis are more vulnerable than others to the mania- or psychosis-inducing potential of antidepressants, stimulants and sleeping medications.

While I'm not making a blanket statement against these medications, I am urging caution in their use. I believe [clinicians] should ask patients and their families whether there is a family history of bipolar disorder or psychosis before prescribing these medications.

Most patients and their families don't know the answer when they are first asked, so time should be allowed for the patient to ask family or relatives, between the session when asked by [the clinician] and a follow-up session. This may increase the wait for a medication slightly, but because some patients are vulnerable, this is a necessary step for [the clinician] to take. I believe that psychiatry as a field has not emphasized this point sufficiently.

As a result, some patients have been harmed by the very treatments that were supposed to help them; or to the disgrace of psychiatry, harmed and then misdiagnosed. Substance-induced psychosis should also be ruled out. Both substance- and medication-induced psychosis can be excluded to a high level of certainty while the person is psychotic, typically in an emergency department, using both a. Some dietary supplements may also induce psychosis or mania, but cannot be ruled out with laboratory tests.

So a psychotic person's family, partner, or friends should be asked whether he or she is currently taking any dietary supplements. Common mistakes made when diagnosing psychotic patients include: Only after these relevant and known causes of psychosis have been ruled out can a psychiatric differential diagnosis be made.

A mental health clinician will incorporate family history, observation of a psychotic person's behavior while the person is experiencing active symptoms, to begin a psychiatric differential diagnosis. Diagnosis also includes self-reported experiences, as well as behavioral abnormalities reported by family members, friends, or significant others.

Mistakes in this stage include:. The most widely used criteria for diagnosing schizoaffective disorder are from the American Psychiatric Association 's Diagnostic and Statistical Manual of Mental Disorders The DSM-IV schizoaffective disorder definition was plagued by problems of being inconsistently or unreliably used on patients; [6] when the diagnosis is made, it doesn't stay with most patients over time; [6] and it has questionable diagnostic validity that is, it doesn't describe a distinct disorder, nor predict any particular outcome.

Only when psychotic states persist in a sustained fashion for two weeks or longer without concurrent affective symptoms is the diagnosis schizoaffective disorder, schizophreniform disorder or schizophrenia. The second cardinal guideline in the DSM-5 diagnosis of schizoaffective disorder is one of timeframe. These two changes are intended by the DSM-5 workgroup to accomplish two goals: If the schizoaffective diagnosis is used less often, other diagnoses like psychotic mood disorders and schizophrenia are likely to be used more often; but this is hypothetical until real-world data arrive.

Validity problems with the diagnosis remain and await further work in the fields of psychiatric genetics , neuroimaging , and cognitive science that includes the overlapping fields of cognitive , affective , and social neuroscience , which may change the way schizoaffective disorder is conceptualized and defined in future versions of the DSM and ICD.

One of two types of schizoaffective disorder may be noted in a diagnosis based on the mood component of the disorder: Clinicians adequately trained in diagnosis used the schizoaffective diagnosis too often, [6] largely because the criteria were poorly defined, ambiguous , and hard to use or poorly operationalized.

Carpenter and the DSM-5 schizoaffective disorders workgroup analyzed data made available to them in , and reported in May that: Hence, this unreliable and poorly defined diagnosis is clearly overused. As stated above, the DSM-IV schizoaffective disorder diagnosis is very inconsistently used or unreliable.

In April , Carpenter and the DSM-5 schizoaffective disorder workgroup reported that they were "developing new criteria for schizoaffective disorder to improve reliability and face validity ," and were "determining whether the dimensional assessment of mood [would] justify a recommendation to drop schizoaffective disorder as a diagnostic category. We had hoped to get rid of schizoaffective [disorder] as a diagnostic category [in the DSM-5] because we don't think it's [a] valid [scientific entity] and we don't think it's reliable.

On the other hand, we think it's absolutely indispensable to clinical practice. A major reason why DSM-IV schizoaffective disorder was indispensable to clinical practice is because it offered clinicians a diagnosis for patients with psychosis in the context of mood disorder whose clinical picture, at the time diagnosed, appeared different from DSM-IV "schizophrenia" or "mood disorder with psychotic features.

But DSM-IV schizoaffective disorder carries an unnecessarily worse prognosis than a "mood disorder with psychotic features" diagnosis, [6] because long-term data revealed that a significant proportion of DSM-IV schizoaffective disorder patients had year outcomes indistinguishable from patients with mood disorders with or without psychotic features, [6] [11] even though the clinical picture at the time of first diagnosis looked different from both schizophrenia and mood disorders.

These problems with the DSM-IV schizoaffective disorder definition result in most people the diagnosis is used on being misdiagnosed; [6] furthermore, outcome studies done 10 years after the diagnosis was released showed that the group of patients defined by the DSM-IV and ICD schizoaffective diagnosis had significantly better outcomes than predicted, so the diagnosis carries a misleading and unnecessarily poor prognosis.

The new schizoaffective disorder criteria continue to have questionable diagnostic validity. Instead, questionable diagnostic validity means there are unresolved problems with the way the DSM-5 categorizes and defines schizoaffective disorder. A core concept in modern psychiatry since DSM-III was released in , is the categorical separation of mood disorders from schizophrenia, known as the Kraepelinian dichotomy. Emil Kraepelin introduced the idea that schizophrenia was separate from mood disorders after observing patients with symptoms of psychosis and mood disorder, over a century ago, in This was a time before genetics were known and before any treatments existed for mental illness.

The Kraepelinian dichotomy continues to be used in DSM-5 despite having been challenged by data from modern psychiatric genetics for over eight years, [63] and there is now evidence of a significant overlap in the genetics of schizophrenia and bipolar disorder. The dichotomy at the foundation of the current system forms the basis for a convoluted schizoaffective disorder definition in DSM-IV that resulted in excessive misdiagnosis.

The new definition continues the lack of parsimony of the old definition. More parsimonious definitions than the current one were considered by Carpenter and the DSM-5 workgroup: One option for the DSM-5 would have been to remove the schizoaffective disorder category and to add affective [or mood] symptoms [that is, mania , hypomania , mixed episode , or depression ] as a dimension to schizophrenia and schizophreniform disorder or to define a single category for the co-occurrence of psychosis and mood symptoms.

This option was extensively debated but ultimately deemed to be premature in the absence of sufficient clinical and theoretical validating data justifying such a … reconceptualization.

Additionally, there appeared to be no practical way to introduce affect [or mood] dimensions covering the entire course of illness, that would capture the current concept of periods of psychosis related and unrelated to mood episodes.

Most presenting symptoms of psychosis have little validity in determining diagnosis, prognosis, or treatment response in psychosis. The field of psychiatry has begun to question its assumptions and analyze its data in order to merge closer with evidence-based medicine. For clinicians to make such sizeable errors of misdiagnosis may imply systemic problems with the schizoaffective disorder diagnosis itself. Already, at least one expert believes the new schizoaffective definition hasn't gone far enough to solve the previous definition's problems.

From a scientific standpoint, modern clinical psychiatry is still a very young, underdeveloped medical specialty because its target organ, the human brain, is not yet well understood. Clinical psychiatry, furthermore, has begun to understand and acknowledge its current limitations—but further steps by the field are required to significantly reduce misdiagnosis and patient harm ; this is crucial both for responsible patient care and to retain public trust.

Looking forward, a paradigm shift is needed in psychiatric research to address unanswered questions about schizoaffective disorder. The dimensional Research Domain Criteria project currently being developed by the U. National Institutes of Mental Health, may be the specific problem solving framework psychiatry needs to develop a more scientifically mature understanding of schizoaffective disorder as well as all other mental disorders.

The primary treatment of schizoaffective disorder is medication, with improved outcomes using combined long-term psychological and social supports. Long-term hospitalization is uncommon since deinstitutionalization beginning in the s, although it still occurs.

Evidence indicates that regular exercise has a positive effect on the physical and mental health of those with schizoaffective disorder.

Participating in internet forums is sometimes used by people with schizoaffective disorder in addition to outpatient medication treatment. Skillfully delivered psychosocial treatments are perhaps the most important component of pushing for and encouraging improved overall functioning in schizoaffective disorder.

Supportive psychotherapy and cognitive behavioral therapy are both helpful. High quality psychosocial or psychiatric rehabilitation is very important for recovery from schizoaffective disorder. Psychiatric or psychosocial rehabilitation focuses on solving community integration problems such as obtaining and keeping housing and increasing involvement in positive social groups. It also focuses on improving and increasing activities of daily living ; increasing daily healthy habits such as normalizing sleep-wake cycles ; increasing early morning natural light exposure; increasing moderate exercise [such as 20—30 minutes of moderate to brisk early morning to pre-afternoon walking daily, in order to help normalize circadian rhythms]; helping individuals understand the specific benefits of healthy food choices; increasing stress-reduction activities such as yoga, tai chi, or meditation ; and decreasing unhealthy behaviors such as substance abuse and smoking ; thereby significantly improving quality of life.

High quality psychiatric rehabilitation may also focus on vocational rehabilitation including preparing the client for volunteer, part-time paid work, returning to school for further education, job skills training for full-time flexible or supported employment, and other client self-improvement efforts.

Core principles of effective psychiatric rehabilitation must include providing hope when the client lacks it, respect for the client wherever they are in the recovery process, empowering the client, teaching the client wellness planning , and emphasizing the importance for the client to develop social support networks.

Few medications are approved specifically for schizoaffective disorder. Antipsychotic medication is usually required both for acute treatment and the prevention of relapse.

In people with treatment-refractory psychosis, a clozapine trial should be considered. The management of the bipolar type of schizoaffective disorder is similar to the treatment of bipolar disorder , with the goal of preventing mood episodes and cycling. For depression, if an antidepressant is prescribed, extra attentiveness must be given by the prescribing clinician due its risk for long-term mood cycle acceleration that is, inducing more frequent episodes of depression per unit of time and medication-induced psychosis or mania.

For individuals who experience anxiety, anti-anxiety medications can be used, usually on a short-term basis. Care must be taken when prescribing benzodiazepines due to the risk of the person developing tolerance and dependence.

Electroconvulsive therapy , or ECT, may be considered for patients with schizoaffective disorder experiencing severe depression or severe psychotic symptoms that have not responded to treatment with antipsychotics. Schizoaffective disorder is estimated to occur in 0. The term schizoaffective psychosis was introduced by the American psychiatrist Jacob Kasanin in [78] to describe an episodic psychotic illness with predominant affective symptoms, that was thought at the time to be a good-prognosis schizophrenia.

Other psychiatrists, before and after Kasanin, have made scientific observations of schizoaffective disorder based on assumptions of a biological and genetic cause of the illness. In , German psychiatrist Karl Kahlbaum — described schizoaffective disorders as a separate group in his vesania typica circularis.

Cross-sectional refers to observation of a single, specific episode of the illness, for example, one episode of psychotic depression; while longitudinal refers to long-term observation of many distinct episodes [similar or different] often occurring over the span of years.

In , psychiatrist Emil Kraepelin — , the founder of contemporary scientific psychiatry, observed a "great number" of cases that had characteristics of both groups of psychoses that he originally posited were two distinct and separate illnesses, dementia praecox now called schizophrenia and manic depressive insanity now called bipolar disorders [plural since there are more than one type of bipolar disorder] and recurrent depression.

Kraepelin acknowledged that "there are many overlaps in this area," that is, the area between schizophrenia and mood disorders. The historical clinical observation that schizoaffective disorder is an overlap of schizophrenia and mood disorders is explained by genes for both illnesses being present in individuals with schizoaffective disorder; specifically, recent research shows that schizophrenia and mood disorders share common genes and polygenic variations.

Schizoaffective disorder was included as a subtype of schizophrenia in DSM-I and DSM-II, though research showed a schizophrenic cluster of symptoms in individuals with a family history of mood disorders whose illness course, other symptoms and treatment outcome were otherwise more akin to bipolar disorder than to schizophrenia.

The DSM-5 schizoaffective disorder workgroup analyzed all of the available research evidence on schizoaffective disorder, and concluded that "presenting symptoms of psychosis have little validity in determining diagnosis, prognosis, or treatment response. Presenting symptoms of psychosis describe only presenting symptoms to be treated, and not much more. Evidence is sorely lacking about schizoaffective disorder's likely multiple causes and mechanisms knowing these leads to specific and consistently effective treatments , and about how exactly mood episodes and psychosis are related knowing this may lead to a simpler, clearer, and more usable behavioral definition of the disorder; as well as a better diagnostic system.

Research into the assessment and treatment of schizoaffective disorder will rely less on DSM and ICD criteria as time progresses, and more on the dimensional Research Domain Criteria currently being developed by the U.

From Wikipedia, the free encyclopedia. For other uses, see SAD disambiguation. Acta Psychiatrica Scandinavica Supplement. Radioactivity in the filters was measured by scintillation counting. The inhibitory activity of Cpd 6A on T-lymphocyte proliferation was calculated by the formula:. T cells were collected and total cellular RNA was extracted by TRIzol reagent according to the manufacturer's protocol. The concentration of the extracted RNA was calculated by measuring the optical density at nm.

The ratio of the optical density at nm to that at nm was always higher than 1. The quality of RNA was assessed by the integrity of 28S and 18S bands and lack of degradation on agarose-gel electrophoresis.

The following reagents were added to the tube: The PCR was performed in an air thermocycler according to the manufacturer's instructions, as described previously Kuo et al. All primer pairs for the cytokines and cyclins were designed based on published human cDNA sequence data Gray et al. The c-fos and c-jun specific primers used were: The PCR was carried out under the following conditions: Procedures for cell cycle analysis have been described previously Kuo et al.

The cells were harvested by centrifugation, washed in phosphate-buffered saline PBS; pH 7. Total cellular proteins was extracted from T lymphocytes by a method described previously Kuo et al.

After blocking the filters, the filters were incubated with mouse monoclonal antibodies. Specific reactive proteins were detected by an enhanced chemiluminescence method, employing a rabbit anti-mouse Ig Ab linked to horseradish peroxidase. The total, viable, and nonviable cell numbers were counted under the microscope with the help of a hemocytometer following trypan blue staining.

The viability was calculated as. Reagents were obtained from Sigma or Merck. Rabbit anti-mouse Ig Ab linked to horseradish peroxidase for detection in the Western blots was obtained from Santa Cruz Biotechnology, Inc.

Santa Cruz, CA, U. A voucher specimen No. To extract pure active compounds from the C. The most active compound 15 mg was obtained from the sixth combined fraction as colorless needles with m. NMR and mass spectrum analyses indicated a structure as shown in Figure 1.

The mass and NMR spectra data for the compound were compatible with those previously reported for ergosterol peroxide by Bok et al. The purity of ergosterol peroxide isolated from C. Ergosterol peroxide appeared as a single peak at 6. Treatment with the vehicle DMSO affected neither the tritiated thymidine uptake in the resting state nor that in the stimulated state. While being similar to cyclosporin A in having little effects on tritiated thymidine uptake in resting T cells, both Cpd 6A and cyclosporin A significantly suppressed the enhanced uptake observable in activated cells.

Furthermore, the inhibitory effects of Cpd 6A on activated T cells were concentration dependent. The corresponding degrees of inhibition for 6. The inhibitory effects of Cpd 6A on T cells were not related to direct cytotoxicity, since the viability of resting Inhibitory effects of Cpd 6A on T-lymphocyte proliferation.

Proliferation assay was performed as described in Methods. Each bar represents the mean of three independent experiments. Time-course experiments were performed to determine at what point in the activation process Cpd 6A inhibited T-cell proliferation. Cpd 6A was added to cultures at 0, 2, 4, 6, 8, 12, 16, 24, 36, 48, and 72 h, and the proliferation assay was performed at 88 h. The results indicated that, after stimulation, addition of Cpd 6A between 0 and 24 h appeared to exert the highest suppressory effect on T-cell proliferation Figure 2b.

The addition of Cpd 6A to the cultures at 36, 48, and 72 h postactivation only attenuated the cell proliferation.

The fact that Cpd 6A was inhibitory when added during the first 24 h suggested that the inhibitory effects of Cpd 6A might be related to the blocking of biochemical events or gene expression necessary for T-cell proliferation activated with PHA during this time. We further examined where in the cell cycle of T cells the arrest took place.

After incubation with or without Cpd 6A for 3 days, cell cycle analyses were performed using a commercially prepared propidium iodide reagent for staining nuclear DNA prior to flow cytometry analysis. Ability of Cpd 6A to block T-cell progression into the S phase of the cell cycle. For determining cells entering into the different parts of the cell cycle, cells from a representative subject were stained with propidium iodide, and the DNA content of the cells was analyzed by flow cytometry a.

Each bar is the mean of three independent experiments b. Total cellular proteins were then extracted, and the production of Cyclins D2, E, A1, and B1 in T lymphocytes was assayed by Western blot analyses. By contrast, the stimulated production of 50 kDa Cyclin E in activated T cells was significantly suppressed by Cpd 6A.

Inhibition of cyclin E production and gene expression in T lymphocytes by Cpd 6A. Unstimulated cells lane 1 , unstimulated cells treated with Cpd 6A lane 2 , stimulated cells lane 3 , and stimulated cells in the presence of Cpd 6A lane 4.

The results are representative of three experiments. The exponential phase of amplification was determined by performing for 20, 30, 40, and 50 cycles. To evaluate the relevance of cytokine production to the inhibitory effects of Cpd 6A on T-cell proliferation after stimulation with PHA, T cells were incubated with or without varying concentrations of Cpd 6A for 3 days. As shown in Figure 5a—d , the stimulated production of these cytokines in activated T cells was significantly suppressed by Cpd 6A.

Furthermore, the inhibitory activities of Cpd 6A were concentration dependent. Cytokine production in T lymphoctyes treated with Cpd 6A.

Each point is the mean of three independent experiments. As the production of several cytokines in activated T lymphocytes was decreased by Cpd 6A, we examined whether the expression of cytokine mRNA in activated T cells was affected by Cpd 6A. Laser densitometry analysis demonstrated that the mRNAs of those cytokines were suppressed by Cpd 6A.

Similar results were also obtained from other cytokines data not shown. Graphical representation of laser densitometry of cytokine expression in resting or PHA-stimulated T cells in the presence or absence of Cpd 6A. Each bar is the mean of three independent experiments. Cellular proteins were then extracted, and c-Fos and c-Jun protein levels detected by Western blot analysis. As shown in Figure 7b , analysis of laser densitometry demonstrated that the values for c-Fos and c-Jun proteins in Cpd 6A-treated cells were significantly lower than those in untreated cells.

These results are representative of three separate experiments. The results are representative of three experiments c. Then, total cellular RNA was isolated from T cells at 2 min lane 1 , 30 min lane 2 , 2 h lane 3 , 4 h lane 4 , 6 h lane 5 , and 8 h lane 6 postactivation. T cells were pretreated with or without Cpd 6A for 30 min. These results are shown in Figure 7c. Furthermore, similar results were obtained from the cells treated with PHA and Cpd 6A at the same time data not shown. The data showed that c-fos mRNA was expressed in the cells 30 min after activation, and decreased 6 h after activation Figure 7e.

Then, cell proliferation was determined on the basis of uptake of tritiated thymidine. Flow cytometry was used to analyze the percentage of the cell population that could enter S phase in the presence of these agents. Proliferation assays were performed as described. In the present study, the action mechanisms of Cpd 6A identified from C. The results demonstrated that the growth-suppressive actions of Cpd 6A were not explained by a drug-induced reduction in cell viability and that delayed addition of Cpd 6A reduced its antiproliferative activity.

We suggest that Cpd 6A interferes with some regulatory events required for the entry of PHA-activated T cells into the S phase and then the cell proliferation is suppressed. Cpd 6A is a sterol and has been isolated from many fungi such as Ganoderma carnosum , C. There are several biological functions described for ergosterol peroxide. It possesses an antiviral action Lindequist et al. Ergosterol peroxide is identified as an immunosuppressive component Fujimoto et al. The present results showed that Cpd 6A suppressed the activation and proliferation signals in primary human T lymphocytes induced by PHA.

T-cell proliferation and viability were not changed by DMSO. The morphology and characteristics of T cells treated with or without Cpd 6A were similar, suggesting that the inhibitory effects of Cpd 6A were not related to the pH, osmolarity, or other physiological variables in different preparations data not shown. We cannot exclude the possibility that Cpd 6A may have toxic effects on T cells following chronic treatment or at higher concentrations.

The central event in the generation of immune responses is the activation and clonal expansion of T cells Charles et al. During the process of differentiation, T cells spontaneously arrest in G0 and may remain quiescent for long periods of time, until exposed to specific antigen or mitogens.

Interaction of T cells with antigens or PHA initiates a cascade of biochemical events, which induces the resting T cells to enter the cell cycle and then to proliferate and differentiate Charles, Data from primary human T lymphocytes indicate that cyclin E is likely to play a regulatory role in the cell cycle from G1 transition to the S phase Charles, Inhibition of the function of cyclin E and its related cyclin-dependent kinase cdk2 prevents mammalian cells from entering the S phase Pagano et al.

Subsequent G1 events and initiation of DNA synthesis are dependent on the induction of IL-2 receptor and on a supply of IL-2 from autocrine or external sources.

Although the molecular mechanisms involved in regulating the passage through cell cycle in T cells stimulated with PHA remain largely unknown, growth modulators or other external events that affect the T-cell proliferation are ultimately likely to act by controlling the expression or function of the products of these genes Ajchenbaum et al. Thus, we suggest that the inhibitory effects of Cpd 6A on T-cell proliferation may be related to the reduction of cyclin E gene expression and arrest of cell cycle progression in the cells.

These decreases in cytokine production were related to Cpd 6A suppressing the mRNA transcripts for these cytokines. The c-fos and c-jun genes are required for cell cycle progression and cell proliferation in PHA-stimulated lymphocytes Tay et al. In our studies, although, in some cases, the production and gene expressions of c-fos and c-jun could be detected in unstimulated T cells, both gene products could be significantly increased in the cells after PHA stimulation.

The data demonstrated that Cpd 6A reduced the levels of c-Fos and c-Jun proteins through inhibition of c-fos and c-jun mRNA expressions in activated T cells. Attenuation of c-fos and c-jun gene expression in T cells may be one of the mechanisms by which Cpd 6A suppressed T-cell proliferation induced by PHA.

In summary, we hypothesize that the inhibitory mechanisms of Cpd 6A on T-cell proliferation activated by PHA are, at least in part, related to: Thus, results of the present study indicate that Cpd 6A contained in extracts of C.

Our observations correlate with the putative pharmacological activities attributed to C. Although in vitro studies do not necessarily predict in vivo outcomes, such studies have provided insights into molecular targets, as illustrated by the effects of Cpd 6A on cytokine, cyclins, and AP-1 genes. The relative contributions of these activities to the potent immunosuppression by Cpd 6A in vivo remain to be elucidated.





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