|Symptoms||Hallucinations, delusions, disorganized thinking, depressed mood, manic behavior|
|Complications||Social isolation, suicide|
|Types||Bipolar type, depressive type|
|Risk factors||Genetics, brain chemistry and structure, stress, drug use|
|Medication||Antipsychotics, mood stabilizers|
Schizoaffective disorder (SZA, SZD or SAD) is a mental disorder characterized by abnormal thought processes and abnormal emotions. The diagnosis is made when the person has features of both schizophrenia (usually psychosis) and a mood disorder—either bipolar disorder or depression—but doesn't meet the diagnostic criteria for schizophrenia or a mood disorder separately. The main criterion for the schizoaffective disorder diagnosis is the presence of psychotic symptoms for at least two weeks without any mood symptoms present. Schizoaffective disorder can often be misdiagnosed when the correct diagnosis may be psychotic depression, psychotic bipolar disorder, schizophreniform disorder or schizophrenia; this is important for patients or consumers because the treatments and prognoses for these other disorders are different from schizoaffective disorder. The DSM-5 criteria revision for schizoaffective disorder is mainly an attempt to reduce the significant problems with misdiagnosis; but whether this has been achieved awaits outcome studies which have not been completed yet.
There are two types of schizoaffective disorder: the bipolar type, which is distinguished by symptoms of mania, hypomania, or mixed episode; and the depressive type, which is distinguished by symptoms of depression only. Common symptoms of the disorder include hallucinations, delusions, and disorganized speech and thinking. The onset of symptoms usually begins in young adulthood, currently with an uncertain lifetime prevalence because the disorder was redefined, but DSM-IV prevalence estimates have been less than one percent of the population, in the range of 0.5 to 0.8 percent. Diagnosis is based on observed behavior and the person's reported experiences.
Genetics, neurobiology, early and current environment, behavioral, social, and experiential components appear to be important contributory factors; some recreational and prescription drugs may cause or worsen symptoms. No single isolated organic cause has been found, but extensive evidence exists for abnormalities in the metabolism of tetrahydrobiopterin (BH4), dopamine, and glutamic acid in people with schizophrenia, psychotic mood disorders, and schizoaffective disorder. People with schizoaffective disorder are likely to have co-occurring conditions, including anxiety disorders and substance use disorders. Social problems such as long-term unemployment, poverty and homelessness are common. The average life expectancy of people with the disorder is shorter than those without it, due to increased physical health problems from an absence of health promoting behaviors such as a sedentary lifestyle, and a higher suicide rate.
The mainstay of current treatment is antipsychotic medication combined with mood stabilizer medication or antidepressant medication, or both. There is growing concern by some researchers that antidepressants may increase psychosis, mania, and long-term mood episode cycling in the disorder. When there is risk to self or others, usually early in treatment, hospitalization may be necessary. Psychiatric rehabilitation, psychotherapy, and vocational rehabilitation are very important for recovery of higher psychosocial function. As a group, people with schizoaffective disorder diagnosed using DSM-IV and ICD-10 criteria have a better outcome than people with schizophrenia, but have variable individual psychosocial functional outcomes compared to people with mood disorders, from worse to the same.[non-primary source needed] Outcomes for people with DSM-5 diagnosed schizoaffective disorder depend on data from prospective cohort studies, which have not been completed yet.
In DSM-5 and ICD-10, schizoaffective disorder is in the same diagnostic class as schizophrenia, but not in the same class as mood disorders. The diagnosis was introduced in 1933, and its definition was slightly changed in the DSM-5, published in May 2013, because the DSM-IV schizoaffective disorder definition leads to excessive misdiagnosis. The changes made to the schizoaffective disorder definition were intended to make the DSM-5 diagnosis more consistent (or reliable), and to substantially reduce the use of the diagnosis. Additionally, the DSM-5 schizoaffective disorder diagnosis can no longer be used for first episode psychosis.
- 1 Signs and symptoms
- 2 Causes
- 3 Diagnosis
- 4 Treatment
- 5 Epidemiology
- 6 History
- 7 Research
- 8 References
- 9 Further reading
- 10 External links
Signs and symptoms
Schizoaffective disorder is defined by mood disorder-free psychosis in the context of a long-term psychotic and mood disorder. Psychosis must meet criterion A for schizophrenia which may include delusions, hallucinations, disorganized speech, thinking or behavior and negative symptoms. Both delusions and hallucinations are classic symptoms of psychosis. Delusions are false beliefs which are strongly held despite evidence to the contrary. Beliefs should not be considered delusional if they are in keeping with cultural beliefs. Delusional beliefs may or may not reflect mood symptoms (for example, someone experiencing depression may or may not experience delusions of guilt). Hallucinations are disturbances in perception involving any of the five senses, although auditory hallucinations (or "hearing voices") are the most common. A lack of responsiveness or negative symptoms include alogia (lack of spontaneous speech), blunted affect (reduced intensity of outward emotional expression), avolition (loss of motivation), and anhedonia (inability to experience pleasure). Negative symptoms can be more lasting and more debilitating than positive symptoms of psychosis.
Mood symptoms are of mania, hypomania, mixed episode, or depression, and tend to be episodic rather than continuous. A mixed episode represents a combination of symptoms of mania and depression at the same time. Symptoms of mania include elevated or irritable mood, grandiosity (inflated self-esteem), agitation, risk-taking behavior, decreased need for sleep, poor concentration, rapid speech, and racing thoughts. Symptoms of depression include low mood, apathy, changes in appetite or weight, disturbances in sleep, changes in motor activity, fatigue, guilt or feelings of worthlessness, and suicidal thinking.
Genetic studies do not support the view that schizophrenia, psychotic mood disorders and schizoaffective disorder are distinct etiological entities, but rather the evidence suggests the existence of common inherited vulnerability that increases the risks for all these syndromes. Some susceptibility pathways may be specific for schizophrenia, others for bipolar disorder, and yet other mechanisms and genes may confer risk for mixed schizophrenic and affective [or mood disorder] psychoses, but there is no support from genetics for the view that these are distinct disorders with distinct etiologies and pathogenesis. Laboratory studies of putative endophenotypes, brain imaging studies, and post mortem studies shed little additional light on the validity of the schizoaffective disorder diagnosis, as most studies combine subjects with different chronic psychoses in comparison to healthy subjects.
Viewed broadly then, biological and environmental factors interact with a person's genes in ways which may increase or decrease the risk for developing schizoaffective disorder; exactly how this happens (the biological mechanism) is not yet known. Schizophrenia spectrum disorders, of which schizoaffective disorder is a part, have been increasingly linked to advanced paternal age at the time of conception, a known cause of genetic mutations. The physiology of people diagnosed with schizoaffective disorder appears to be similar, but not identical, to that of those diagnosed with schizophrenia and bipolar disorder; however, human neurophysiological function in normal brain and mental disorder syndromes is not fully understood.
A clear causal connection between drug use and psychotic spectrum disorders, including schizoaffective disorder, has been difficult to prove. In the specific case of cannabis (marijuana), however, evidence supports a link between earlier onset of psychotic illness and cannabis use. The more often cannabis is used, particularly in early adolescence, the more likely a person is to develop a psychotic illness, with frequent use being correlated with double the risk of psychosis and schizoaffective disorder. A 2009 Yale review stated that in individuals with an established psychotic disorder, cannabinoids can exacerbate symptoms, trigger relapse, and have negative consequences on the course of the illness. While cannabis use is accepted as a contributory cause of schizoaffective disorder by many, it remains controversial, since not all young people who use cannabis later develop psychosis, but those who do use cannabis have an increased odds ratio of about 3.
There is evidence that the two major component cannabinoids in cannabis have different effects: tetrahydrocannabinol (THC), which causes a "high," may increase propensity to psychosis; while cannabidiol (CBD), which doesn't cause a "high" and may have neuroprotective effects—that is, reduce psychosis and have mood stabilizing effects.
About half of those with schizoaffective disorder use drugs or alcohol excessively. There is evidence that alcohol abuse via a kindling mechanism can occasionally cause the development of a chronic substance induced psychotic disorder, i.e. schizoaffective disorder. There is little evidence to suggest that psychotic individuals choose specific drugs to self-medicate; there is some support for the hypothesis that they use drugs to cope with unpleasant states such as depression, anxiety, boredom and loneliness.
Amphetamine, cocaine, and to a lesser extent alcohol, can result in psychosis that presents clinically like psychosis in schizoaffective disorder. It is well understood that amphetamine or methamphetamine and cocaine use can result in stimulant-induced psychosis, respectively, that may persist even when users remain abstinent. Alcohol-induced psychosis can also persist during abstinence, though it appears to do so at a lower rate, than when it is being abused.
Psychosis as a symptom of a psychiatric disorder is first and foremost a diagnosis of exclusion. So a new-onset episode of psychosis cannot be considered to be a symptom of a psychiatric disorder until other relevant and known medical causes of psychosis are excluded, or ruled out. Many clinicians improperly perform, or entirely miss this step, introducing avoidable diagnostic error and misdiagnosis.
An initial assessment includes a comprehensive history and physical examination. 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. Excluding medical illnesses associated with psychosis is performed by using blood tests to measure:
- Thyroid-stimulating hormone to exclude hypo- or hyperthyroidism,
- Basic electrolytes and serum calcium to rule out a metabolic disturbance,
- Full blood count including ESR to rule out a systemic infection or chronic disease, and
- Serology to exclude syphilis or HIV infection.
Other investigations which may be performed include:
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, ADHD stimulant medications, and sleep medications, prescribed medication-induced psychosis should be ruled out, particularly for first-episode psychosis. This is an essential step to reduce diagnostic error and to evaluate potential medication sources of further patient harm. Regarding prescribed medication sources of patient harm, Yale School of Medicine Professor of Psychiatry Malcolm B. Bowers, Jr, MD wrote:[self-published source]
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
- Broad spectrum urine toxicology screening, and a
- Full serum toxicology screening (of the blood).
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:
- Not properly excluding delirium,
- Missing a toxic psychosis by not screening for substances and medications,
- Not appreciating medical abnormalities (e.g., vital signs),
- Not obtaining a medical history and family history,
- Indiscriminate screening without an organizing framework,
- Not asking family or others about dietary supplements,
- Premature diagnostic closure, and
- Not revisiting or questioning the initial diagnostic impression of primary psychiatric disorder.
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:
- Not screening for dissociative disorders. Dissociative identity disorder and psychotic symptoms in schizoaffective disorder have considerable overlap, yet a different overall treatment approach.
The most widely used criteria for diagnosing schizoaffective disorder are from the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders-5.
The DSM-IV schizoaffective disorder definition was plagued by problems of being inconsistently (or unreliably) used on patients; when the diagnosis is made, it doesn't stay with most patients over time; and it has questionable diagnostic validity (that is, it doesn't describe a distinct disorder, nor predict any particular outcome). These problems have been slightly reduced (or "modestly improved") in the DSM-5 according to Carpenter.
When psychotic symptoms are confined to an episode of mania or depression (with or without mixed features), the diagnosis is that of a “psychotic” mood disorder, namely either psychotic bipolar disorder or psychotic major depression. 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.
- DSM-5 requires two episodes of psychosis (whereas DSM-IV needed only one) to qualify for the schizoaffective disorder diagnosis. As such, it is no longer an "episode diagnosis." The new schizoaffective framework looks at the time from "the [first episode of] psychosis up to the current episode [of psychosis], rather than only defining a single episode with [co-occurring] psychotic and mood syndromes." Specifically, one of the episodes of psychosis must last a minimum of two weeks without mood disorder symptoms, but the person may be mildly to moderately depressed while psychotic. The other period of psychosis "requires the overlap of mood [disorder] symptoms with psychotic symptoms to be conspicuous" and last for a greater portion of the disorder.
These two changes are intended by the DSM-5 workgroup to accomplish two goals:
- Increase the diagnosis' consistency (or reliability) when it is used;
- Significantly decrease the overall use of the schizoaffective disorder diagnosis.
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.
- Bipolar type, when the disturbance includes manic episodes, hypomania, or mixed episodes—major depressive episodes also typically occur;
- Depressive type, when the disturbance includes major depressive episodes exclusively—that is, without manic, hypomanic, or mixed episodes.
Problems with DSM-IV schizoaffective disorder
The American Psychiatric Association's DSM-IV criteria for schizoaffective disorder persisted for 19 years (1994–2013). Clinicians adequately trained in diagnosis used the schizoaffective diagnosis too often, largely because the criteria were poorly defined, ambiguous, and hard to use (or poorly operationalized). Poorly trained clinicians used the diagnosis without making necessary exclusions of common causes of psychosis, including some prescribed psychiatric medications. Specialty books written by experts on schizoaffective disorder have existed for over eight years before DSM-5 describing the overuse of the diagnosis.
Carpenter and the DSM-5 schizoaffective disorders workgroup analyzed data made available to them in 2009, and reported in May 2013 that:
a recent review of psychotic disorders from large private insurance and Medicare databases in the U.S. found that the diagnosis of DSM-IV schizoaffective disorder was used for about a third of cases with non-affective psychotic disorders. 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. A diagnosis is unreliable when several different mental health professionals observing the same individual make different diagnoses excessively. Even when a structured DSM-IV diagnostic interview and best estimate procedures were made by experts in the field that included information from family informants and prior clinical records, reliability was still poor for the DSM-IV schizoaffective diagnosis.
The DSM-IV schizoaffective diagnosis isn't stable over time either. An initial diagnosis of schizoaffective disorder during time spent at a psychiatric inpatient facility was stable at 6-month and 24-month follow ups for only 36% of patients. By comparison, diagnostic stability was 92% for schizophrenia, 83% for bipolar disorder and 74% for major depression. Most patients diagnosed with DSM-IV schizoaffective disorder are later diagnosed with a different disorder, and that disorder is more stable over time than the DSM-IV schizoaffective disorder diagnosis.
In April 2009, 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." Speaking to an audience at the May 2009 annual conference of the American Psychiatric Association, Carpenter said:
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, because long-term data revealed that a significant proportion of DSM-IV schizoaffective disorder patients had 15-year outcomes indistinguishable from patients with mood disorders with or without psychotic features, 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; furthermore, outcome studies done 10 years after the diagnosis was released showed that the group of patients defined by the DSM-IV and ICD-10 schizoaffective diagnosis had significantly better outcomes than predicted, so the diagnosis carries a misleading and unnecessarily poor prognosis. The DSM-IV criteria for schizoaffective disorder will continue to be used on U.S. board examinations in psychiatry through the end of 2014; established practitioners may continue to use the problematic DSM-IV definition much further into the future also.
DSM-5 research directions
The new schizoaffective disorder criteria continue to have questionable diagnostic validity. Questionable diagnostic validity does not doubt that people with symptoms of psychosis and mood disorder need treatment—psychosis and mood disorder must be treated. 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 1980, 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 1898. This was a time before genetics were known and before any treatments existed for mental illness. The Kraepelinian dichotomy wasn't used for DSM-I and DSM-II because both manuals were influenced by the dominant psychodynamic psychiatry of the time, but the designers of DSM-III wanted to use more scientific and biological definitions. Consequently, they looked to psychiatry's history and decided to use the Kraepelinian dichotomy as a foundation for the classification system.
The Kraepelinian dichotomy continues to be used in DSM-5 despite having been challenged by data from modern psychiatric genetics for over eight years, and there is now evidence of a significant overlap in the genetics of schizophrenia and bipolar disorder. According to this genetic evidence, the Kraepelinian categorical separation of mood disorders from schizophrenia at the foundation of the current classification and diagnostic system is a mistaken false dichotomy.
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. Real life schizoaffective disorder patients have significant and enduring symptoms that bridge what are incorrectly assumed to be categorically separate disorders, schizophrenia and bipolar disorder. People with psychotic depression, bipolar disorder with a history of psychosis, and schizophrenia with mood symptoms also have symptoms that bridge psychosis and mood disorders. The categorical diagnostic manuals don't reflect reality in their separation of psychosis (via the schizophrenia diagnosis) from mood disorder, nor do they currently emphasize the actual overlap found in real-life patients. Thus, they are likely to continue to introduce either-or conceptual and diagnostic error, by way of confirmation bias into clinicians' mindsets, hindering accurate assessment and treatment.
The new definition continues the lack of parsimony of the old definition. Simpler, clearer, and more usable definitions of the diagnosis were supported by certain members of the DSM-5 workgroup (see next paragraph); these were debated but deemed premature, because more "research [is] needed to establish a new classification system of equal or greater validity" to the existing system. Because of DSM-5's continuing problematic categorical foundation, schizoaffective disorder's conceptual and diagnostic validity remains doubtful. After enough research is completed and data exists, future diagnostic advances will need to either eliminate and replace, or soften and bridge, the hard categorical separation of mood disorders from schizophrenia; most likely using a spectrum or dimensional approach to diagnosis.
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.
[N]o valid biomarkers or laboratory measures have emerged to distinguish between affective psychosis [or psychotic mood disorders] and schizophrenia. To the contrary, the idea of a dichotomy between these types of conditions has proven naïve. [T]he admixture of “schizophrenic” and affective [or mood] symptoms is a feature of many, or even most, cases with severe mental illness. Most presenting symptoms of psychosis have little validity in determining diagnosis, prognosis, or treatment response in psychosis. [U]ltimately a more … dimensional approach [to assessment and treatment] will be required.
The field of psychiatry has begun to question its assumptions and analyze its data in order to merge closer with evidence-based medicine. The removal of the "episode diagnosis," and the addition of two episodes of psychosis, as qualifications for the DSM-5 schizoaffective diagnosis, may improve the diagnosis' consistency over DSM-IV for research purposes, where diagnostic criteria are by necessity followed exactingly. But the new definition remains long, unwieldy, and perhaps still not very useful for community clinicians—with two psychoses, one for two weeks minimum and without mood disorder (but the person can be mildly or moderately depressed) and the other with significant mood disorder and psychosis lasting for most of the time, and with lasting mood symptoms for most of the residual portion of the illness. Community clinicians used the previous definition "for about a third of cases with non-affective psychotic disorders." Non-affective psychotic disorders are, by definition, not schizoaffective disorder. 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. The human brain's neural circuits, for example, are just beginning to be mapped by modern neuroscience in the Human Connectome Project and CLARITY. 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.S. 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. Hospitalization may occur for severe episodes either voluntarily or (if mental health legislation allows it) involuntarily. Long-term hospitalization is uncommon since deinstitutionalization beginning in the 1950s, although it still occurs. Community support services including drop-in centers, visits by members of a community mental health team, supported employment and support groups are common. Evidence indicates that regular exercise has a positive effect on the physical and mental health of those with schizoaffective disorder.
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. Intensive case management (ICM) has been shown to reduce hospitalizations, improve adherence to treatment, and improve social functioning. With ICM, clients are assigned a case manager responsible for coordination of care and assisting clients to access supports to address needs in multiple areas related to well-being, including housing.
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. A long-term goal of psychiatric and vocational rehabilitation is that the client learn and actively engage in active stress management while in education or employment, while receiving treatment.
Psychiatric rehabilitation consists of eight main areas:
- Psychiatric (symptom reduction and management)
- Health and Medical (maintaining consistency of care)
- Housing (safe environments)
- Basic living skills (hygiene, meals [including increasing healthy food intake and reducing processed food intake], safety, planning and chores)
- Social (relationships, family boundaries, communication and integration of client into the community)
- Education and vocation (coping skills, motivation and suitable goals chosen by client)
- Finance (personal budget)
- Community and legal (resources)
Few medications are approved specifically for schizoaffective disorder. In general, medications are chosen to reduce symptoms of psychosis and mood disorder.
Antipsychotic medication is usually required both for acute treatment and the prevention of relapse. There is no single antipsychotic of choice in treating schizoaffective disorder, but atypical antipsychotics should be considered because they have mood-stabilizing activity. Paliperidone is an antipsychotic with FDA approval for the treatment of schizoaffective disorder. Antipsychotics should be used at the minimum dose necessary to control symptoms. Potential side effects include extrapyramidal symptoms, including tremor, muscle stiffness, and restlessness or akathisia. Atypical antipsychotics carry a risk of metabolic syndrome, including weight gain, increased blood sugar, and increased blood cholesterol, so regular monitoring of weight and bloodwork should be carried out. Some atypical antipsychotics, such as ziprasidone and aripiprazole, are associated with less risk than others, such as olanzapine. Medication choice is based on how effectively it reduces symptoms, how few side effects it causes, and cost.
In people with treatment-refractory psychosis, a clozapine trial should be considered. Clozapine is an atypical antipsychotic that is recognized as being particularly effective when other antipsychotic agents have failed. Clozapine should also be considered in people with chronic and persistent suicidal thinking and behaviour, as it has been shown to reduce the risk of suicide in patients with schizoaffective disorder and a history of suicidality. Between 0.5 and 2% of patients taking clozapine may develop a life-threatening complication called agranulocytosis, which is a significant drop in a type of white blood cell. Because of this risk, people taking clozapine must have regular monitoring of blood cell counts.
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. Lithium or anticonvulsant mood stabilizers such as valproic acid, carbamazepine, and lamotrigine are prescribed in combination with an antipsychotic.
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 show emerging psychosis, mania, mixed episode symptoms, or mood cycle acceleration, switching to an antipsychotic plus lithium or lamotrigine is preferable to antidepressants.
For individuals who experience anxiety, anti-anxiety medications can be used, usually on a short-term basis. Benzodiazepines, including lorazepam, clonazepam and diazepam, are types of anti-anxiety medications. 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 0.5 to 0.8 percent of people at some point in their life. It is more common in women than men; however, this is because of the high concentration of women in the depressive subcategory, whereas the bipolar subtype has a more or less even gender distribution.
The term schizoaffective psychosis was introduced by the American psychiatrist Jacob Kasanin in 1933 to describe an episodic psychotic illness with predominant affective symptoms, that was thought at the time to be a good-prognosis schizophrenia. Kasanin's concept of the illness was influenced by the psychoanalytic teachings of Adolf Meyer and Kasanin postulated that schizoaffective psychosis was caused by "emotional conflicts" of a "mainly sexual nature" and that psychoanalysis "would help prevent the recurrence of such attacks." He based his description on a case study of nine individuals.
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 1863, German psychiatrist Karl Kahlbaum (1828–1899) described schizoaffective disorders as a separate group in his vesania typica circularis. Kahlbaum distinguished between cross-sectional and longitudinal observations. (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 1920, psychiatrist Emil Kraepelin (1856–1926), 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. In 1959, psychiatrist Kurt Schneider (1887–1967) began to further refine conceptualizations of the different forms that schizoaffective disorders can take since he observed "concurrent and sequential types". (The concurrent type of illness he referred to is a longitudinal course of illness with episodes of mood disorder and psychosis occurring predominantly at the same time [now called psychotic mood disorders or affective psychosis]; while his sequential type refers to a longitudinal course predominantly marked by alternating mood and psychotic episodes.) Schneider described schizoaffective disorders as "cases in-between" the traditional Kraepelinian dichotomy of 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. DSM-III placed schizoaffective disorder in "Psychotic Disorders Not Otherwise Specified" before being formally recognized in DSM-III-R. DSM-III-R included its own diagnostic criteria as well as the subtypes, bipolar and depressive. In DSM-IV, published in 1994, schizoaffective disorders belonged to the category "Other Psychotic Disorders" and included almost the same criteria and the same subtypes of illness as DSM-III-R, with the addition of mixed bipolar symptomatology.
DSM-IV and DSM-IV-TR (published in 2000) criteria for schizoaffective disorder were poorly defined and poorly operationalized. These ambiguous and unreliable criteria lasted 19 years and led clinicians to significantly overuse the schizoaffective disorder diagnosis. Patients commonly diagnosed with DSM-IV schizoaffective disorder showed a clinical picture at time of diagnosis that appeared different from schizophrenia or psychotic mood disorders using DSM-IV criteria, but who as a group, were longitudinally determined to have outcomes indistinguishable from those with mood disorders with or without psychotic features. A poor prognosis was assumed to apply to these patients by most clinicians, and this poor prognosis was harmful to many patients. The poor prognosis for DSM-IV schizoaffective disorder was not based on patient outcomes research, but was caused by poorly defined criteria interacting with clinical tradition and belief; clinician enculturation with unscientific assumptions from the diagnosis' history (discussed above), including the invalid Kraepelinian dichotomy; and by clinicians being unfamiliar with the scientific limitations of the diagnostic and classification system.
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." Given our understanding of overlapping genetics in bipolar disorders, schizoaffective disorder, and schizophrenia, as well as the overlap in treatments for these disorders; but given the lack of specificity of presenting symptoms for determining diagnosis, prognosis or treatment response in these psychotic illness syndromes, the limits of our knowledge are clearer: Presenting symptoms of psychosis describe only presenting symptoms to be treated, and not much more. Schizoaffective disorder was changed to a longitudinal or life course diagnosis in DSM-5 for this reason.
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). Whether schizoaffective disorder is a variant of schizophrenia (as in DSM-5 and ICD-10 classification systems), a variant of bipolar disorder, or part of a dimensional continuum between psychotic depression, bipolar disorders and schizophrenia is currently being investigated.
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.S. National Institute of Mental Health (NIMH). The Research Domain Criteria initiative, led by Bruce Cuthbert, Ph.D., of NIMH, is the inspiration for the Roadmap for Mental Health Research in Europe (ROAMER). The purpose of the Research Domain Criteria initiative is to address the marked variability and overlap within and among the disorder categories, and to foster development of more effective assessment and treatment for each individual patient. Over the coming decades, advances resulting from the Research Domain Criteria in the U.S. and ROAMER in Europe will be incorporated into future versions of the DSM and ICD, with the hope of eventually leading to personalized mental health of greater diagnostic accuracy and with more targeted and useful treatments, including biomedical, psychosocial, and possibly preventive approaches.
- "Schizoaffective Disorder Overview - Symptoms". www.nami.org.
- "Schizoaffective disorder, bipolar type". www.icd10data.com.
- "Schizoaffective disorder, depressive type". www.icd10data.com.
- "Schizoaffective Disorder Overview - Causes". www.nami.org.
- "F25 Schizoaffective disorders". ICD-10 Version:2010. World Health Organization.
- Malaspina D, Owen MJ, Heckers S, Tandon R, Bustillo J, Schultz S, Barch DM, Gaebel W, Gur RE, Tsuang M, Van Os J, Carpenter W (May 2013). "Schizoaffective disorder in the DSM-5". Schizophrenia Research. 150 (1): 21–5. doi:10.1016/j.schres.2013.04.026. PMID 23707642.
- Kaplan, HI; Saddock, VA (2007). Synopsis of Psychiatry. New York: Lippincott, Williams & Wilkins. ISBN 978-0-7817-7327-0.
- Brannon, Guy E; Bienenfeld, David; Talavera, Francisco (9 September 2013). "Schizoaffective Disorder". Medscape Drugs & Diseases. WebMD.
- Kaplan, HI; Saddock, VA (2007). Synopsis of Psychiatry. New York: Lippincott, Williams & Wilkins. pp. 501–502. ISBN 978-0-7817-7327-0.
- Becker T, Kilian R (2006). "Psychiatric services for people with severe mental illness across western Europe: what can be generalized from current knowledge about differences in provision, costs and outcomes of mental health care?". Acta Psychiatrica Scandinavica Supplement. 113 (429): 9–16. doi:10.1111/j.1600-0447.2005.00711.x. PMID 16445476.
- Jäger M, Bottlender R, Strauss A, Möller HJ (2004). "Fifteen-year follow-up of ICD-10 schizoaffective disorders compared with schizophrenia and affective disorders". Acta Psychiatrica Scandinavica. 109 (1): 30–7. doi:10.1111/j.0001-690x.2004.00208.x. PMID 14674956.
- Heckers S, Barch DM, Bustillo J, Gaebel W, Gur R, Malaspina D, Owen MJ, Schultz S, Tandon R, Tsuang M, Van Os J, Carpenter W (2013). "Structure of the psychotic disorders classification in DSM-5". Schizophrenia Research. 150 (1): 11–4. doi:10.1016/j.schres.2013.04.039. PMID 23707641.
- Jeffrey, Susan (26 May 2009). "APA 2009: DSM on Track for 2012, But Difficult Decisions Lie Ahead". Medscape Medical News. WebMD. Retrieved 3 August 2009.
- Hales E and Yudofsky JA, eds, The American Psychiatric Press Textbook of Psychiatry, Washington, DC: American Psychiatric Publishing, Inc., 2003
- van Os J, Kapur S (August 2009). "Schizophrenia" (PDF). Lancet. 374 (9690): 635–45. doi:10.1016/S0140-6736(09)60995-8. PMID 19700006.
- Picchioni MM, Murray RM (July 2007). "Schizophrenia". BMJ. 335 (7610): 91–5. doi:10.1136/bmj.39227.616447.BE. PMC 1914490. PMID 17626963.
- Brown AS, Schaefer CA, Wyatt RJ, Begg MD, Goetz R, Bresnahan MA, Harkavy-Friedman J, Gorman JM, Malaspina D, Susser ES (September 2002). "Paternal age and risk of schizophrenia in adult offspring". The American Journal of Psychiatry. 159 (9): 1528–33. doi:10.1176/appi.ajp.159.9.1528. PMC 2989614. PMID 12202273.
- Martin LF, Hall MH, Ross RG, Zerbe G, Freedman R, Olincy A (December 2007). "Physiology of schizophrenia, bipolar disorder, and schizoaffective disorder". The American Journal of Psychiatry. 164 (12): 1900–6. doi:10.1176/appi.ajp.2007.06010017. PMID 18056246.
- Large M, Sharma S, Compton MT, Slade T, Nielssen O (June 2011). "Cannabis use and earlier onset of psychosis: a systematic meta-analysis". Arch. Gen. Psychiatry. 68 (6): 555–61. doi:10.1001/archgenpsychiatry.2011.5. PMID 21300939.
- Benjamin Chadwick; Michael L. Miller; Yasmin L. Hurd (2013). "Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review". Frontiers in Psychiatry. 4: 129. doi:10.3389/fpsyt.2013.00129. PMC 3796318. PMID 24133461.
- Moore TH, Zammit S, Lingford-Hughes A, et al. (2007). "Cannabis Use during Adolescent Development: Susceptibility to Psychiatric Illness". Lancet. 370 (9584): 319–328. doi:10.1016/S0140-6736(07)61162-3. PMID 17662880.
- Moore TH, Zammit S, Lingford-Hughes A, Barnes TR, Jones PB, Burke M, Lewis G (March 2005). "Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review". Lancet. 370 (9584): 187–94. doi:10.1016/S0140-6736(07)61162-3. PMID 17662880.
- Sewell RA, Ranganathan M, D'Souza DC (Apr 2009). "Cannabinoids and psychosis". International Review of Psychiatry (Abingdon, England). 21 (2): 152–62. doi:10.1080/09540260902782802. PMID 19367509.
- D'Souza DC, Sewell RA, Ranganathan M (July 2009). "Cannabis and psychosis/schizophrenia: human studies". Eur Arch Psychiatry Clin Neurosci. 259 (7): 413–31. doi:10.1007/s00406-009-0024-2. PMC 2864503. PMID 19609589.
- Henquet C, Di Forti M, Morrison P, Kuepper R, Murray RM (November 2008). "Gene-environment interplay between cannabis and psychosis". Schizophr Bull. 34 (6): 1111–21. doi:10.1093/schbul/sbn108. PMC 2632498. PMID 18723841.
- McLaren JA, Silins E, Hutchinson D, Mattick RP, Hall W (January 2010). "Assessing evidence for a causal link between cannabis and psychosis: a review of cohort studies". Int. J. Drug Policy. 21 (1): 10–9. doi:10.1016/j.drugpo.2009.09.001. PMID 19783132.
- Ben Amar M, Potvin S (Jun 2007). "Cannabis and psychosis: what is the link?". Journal of Psychoactive Drugs. 39 (2): 131–42. doi:10.1080/02791072.2007.10399871. PMID 17703707.
- Castle DJ (January 2013). "Cannabis and psychosis: what causes what?". F1000 Medicine Reports. 5 (1): . doi:10.3410/M5-1. PMC 3544398. PMID 23361396.
- Zuardi AW, Crippa JA, Hallak JE, Moreira FA, Guimarães FS (2006). "Cannabidiol, a Cannabis sativa constituent, as an antipsychotic drug" (PDF). Braz. J. Med. Biol. Res. 39 (4): 421–429. doi:10.1590/S0100-879X2006000400001. PMID 16612464.
- Ashton, C.H., Moore, P. B., Gallagher, P., Young, A. H. (2005). Cannabinoids in bipolar affective disorder: a review and discussion of their therapeutic potential. Journal of Psychopharmacology (U.K).
- Leweke FM, Koethe D, Pahlisch F, Schreiber D, Gerth CW, Nolden BM, Klosterkötter J, Hellmich M, Piomelli D (2009). "S39-02 Antipsychotic effects of cannabidiol". European Psychiatry. 24: S207. doi:10.1016/S0924-9338(09)70440-7.
- Gregg L, Barrowclough C, Haddock G (May 2007). "Reasons for increased substance use in psychosis". Clinical Psychology Review. 27 (4): 494–510. doi:10.1016/j.cpr.2006.09.004. PMID 17240501.
- Alcohol-Related Psychosis at eMedicine
- Leweke FM, Koethe D (June 2008). "Cannabis and psychiatric disorders: it is not only addiction". Addict Biol. 13 (2): 264–75. doi:10.1111/j.1369-1600.2008.00106.x. PMID 18482435.
- Larson, Michael (30 March 2006). "Alcohol-Related Psychosis". eMedicine. WebMD. Retrieved 27 September 2006.
- Mahoney JJ, Kalechstein AD, De La Garza R, Newton TF (2008). "Presence and persistence of psychotic symptoms in cocaine- versus methamphetamine-dependent participants". The American Journal on Addictions. 17 (2): 83–98. doi:10.1080/10550490701861201. PMC 4119877. PMID 18393050.
- Soyka M (March 1990). "Psychopathological characteristics in alcohol hallucinosis and paranoid schizophrenia". Acta Psychiatrica Scandinavica. 81 (3): 255–9. doi:10.1111/j.1600-0447.1990.tb06491.x. PMID 2343749.
- Gossman, William (19 November 2005). "Delirium Tremens". eMedicine. WebMD. Retrieved 16 October 2006.
- Sagud M, Mihaljević-Peles A, Mück-Seler D, et al. (September 2009). "Smoking and schizophrenia" (PDF). Psychiatr Danub. 21 (3): 371–5. PMID 19794359.
- Freudenreich, Oliver (3 December 2012). "Differential Diagnosis of Psychotic Symptoms: Medical "Mimics"". Psychiatric Times. UBM Medica. Retrieved October 2013. Check date values in:
- Preda A, MacLean RW, Mazure CM, Bowers MB (2001). "Antidepressant-associated mania and psychosis resulting in psychiatric admissions". The Journal of Clinical Psychiatry. 62 (1): 30–3. doi:10.4088/JCP.v62n0107. PMID 11235925.
- Fortunati F, Mazure C, Preda A, Wahl R, Bowers M (2002). "Plasma catecholamine metabolites in antidepressant-exacerbated mania and psychosis". Journal of Affective Disorders. 68 (2–3): 331–334. doi:10.1016/S0165-0327(00)00327-X. PMID 12063160.
- A. T. Safeekh; Denzil Pinto (Oct–Dec 2009). "Venlafaxine-induced psychotic symptoms". Indian Journal of Psychiatry. 51 (4): 308–09. doi:10.4103/0019-5545.58301.
- Javelot T, Javelot H, Baratta A, Weiner L, Messaoudi M, Lemoine P (Dec 2010). "Acute psychotic disorders related to bupropion: review of the literature". Encephale. 36 (6): 461–71. doi:10.1016/j.encep.2010.01.005. PMID 21130229.
- Kumar S, Kodela S, Detweiler JG, Kim KY, Detweiler MB (Nov–Dec 2011). "Bupropion-induced psychosis: folklore or a fact? A systematic review of the literature". General hospital psychiatry. 33 (6): 612–7. doi:10.1016/j.genhosppsych.2011.07.001. PMID 21872337.
- Bramness, Jørgen G; Gundersen, Øystein Hoel; Guterstam, Joar; Rognli, Eline Borger; Konstenius, Maija; Løberg, Else-Marie; Medhus, Sigrid; Tanum, Lars; et al. (5 December 2012). "Amphetamine-induced psychosis – a separate diagnostic entity or primary psychosis triggered in the vulnerable?". BMC Medicine. 12 (1): 221. doi:10.1186/1471-244X-12-221. PMC 3554477. PMID 23216941.
- Kraemer M, Uekermann J, Wiltfang J, Kis B (2010). "Methylphenidate-induced psychosis in adult attention-deficit/hyperactivity disorder: report of 3 new cases and review of the literature". Clinical Neuropharmacology. 33 (4): 204–6. doi:10.1097/WNF.0b013e3181e29174. PMID 20571380.
- Berman SM, Kuczenski R, McCracken JT, London ED (2009). "Potential Adverse Effects of Amphetamine Treatment on Brain and Behavior: A Review". Molecular Psychiatry. 14 (2): 123–42. doi:10.1038/mp.2008.90. PMC 2670101. PMID 18698321.
- Markowitz JS, Brewerton TD (June 1996). "Zolpidem-induced psychosis". Annals of Clinical Psychiatry. 8 (2): 89–91. doi:10.3109/10401239609148806. PMID 8807033.
- Chiung-Lei H, Ching-Jui C, Ching-Feng H, Hsi-Len L (May 2003). "Zolpidem-induced distortion in visual perception". Annals of Pharmacotherapy. 37 (5): 683–86. doi:10.1345/aph.1C318.
- Bowers, Malcolm, Jr (2004). The Role of Illicit and Prescribed Drugs in Promoting Psychotic and Manic Disorders. Indiana: Xlibris. ISBN 978-1-4134-2807-0. [self-published source]
- Food and Drug Administration (11 February 2004). "Final rule declaring dietary supplements containing ephedrine alkaloids adulterated because they present an unreasonable risk". Federal Register. 69 (28): 6814, 6818. PMID 14968803. (69 FR 6814 and 69 FR 6818)
- Shibayama M (2011). "Differential diagnosis between dissociative disorders and schizophrenia". Seishin shinkeigaku zasshi=Psychiatria et neurologia Japonica. 113 (9): 906–911. PMID 22117396.
- Malhi GS (Oct 2013). "Making up schizoaffective disorder: Cosmetic changes to a sad creation?". Australian and New Zealand Journal of Psychiatry. 47 (10): 891–4. doi:10.1177/0004867413505522. PMID 24072567.
- "NIMH Director's Blog: Transforming Diagnosis". NIMH Director's Blog. Retrieved October 2013. Check date values in:
- Malhi GS, Green M, Fagiolini A, Peselow ED, Kumari V (February 2008). "Schizoaffective disorder: diagnostic issues and future recommendations". Bipolar Disorders. 10 (1 Pt 2): 215–30. doi:10.1111/j.1399-5618.2007.00564.x. PMID 18199238.
- Marneros, A; Akiskal, HS (2007). The Overlap of Schizophrenic and Affective Spectra. New York: Cambridge University Press. ISBN 0-521-85858-5.
- Goodwin, FK; Jamison, KR (2007). Manic-Depressive Illness: Bipolar Disorders and Recurrent Depression, 2nd Edition. New York: Oxford University Press. ISBN 0-19-513579-2.
- Goodwin, FK; Marneros, A (2005). Bipolar Disorders: Mixed States, Rapid Cycling and Atypical Forms. New York: Cambridge University Press. ISBN 0-521-83517-8.
- Murray WH (2006). Schizoaffective Disorders: New Research. New York: Nova Science Publishers, Inc. ISBN 1-60021-030-9.
- Craddock N, Owen MJ (2010). "The Kraepelinian dichotomy – going, going... But still not gone". The British Journal of Psychiatry. 196 (2): 92–95. doi:10.1192/bjp.bp.109.073429. PMC 2815936. PMID 20118450.
- Mayes R, Horwitz AV (2005). "DSM-III and the revolution in the classification of mental illness". J Hist Behav Sci. 41 (3): 249–67. doi:10.1002/jhbs.20103. PMID 15981242.
- Craddock N, Owen MJ (May 2005). "The beginning of the end for the Kraepelinian dichotomy". Br J Psychiatry. 186 (5): 364–6. doi:10.1192/bjp.186.5.364. PMID 15863738.
- "Mental Health on the Spectrum". Nature. Retrieved September 2013. Check date values in:
- "Introduction to RDoC". NIMH. Retrieved February 25, 2016.
- McGurk SR, Mueser KT, Feldman K, Wolfe R, Pascaris A (Mar 2007). "Cognitive training for supported employment: 2–3 year outcomes of a randomized controlled trial". American Journal of Psychiatry. 164 (3): 437–41. doi:10.1176/appi.ajp.164.3.437. PMID 17329468. Archived from the original on 2007-03-03.
- Gorczynski P, Faulkner G (2010). "Exercise therapy for schizophrenia". Cochrane Database Syst Rev (5): CD004412. doi:10.1002/14651858.CD004412.pub2. PMC 4164954. PMID 20464730.
- "Schizoaffective Disorder Treatment". Psych Central. Self-Help.
- Lawn, Sharon (May 2011). "Self-Management: Supporting People with Mental Health & Physical Health Conditions" (PDF). Mental Illness Fellowship.
- "Schizoaffective Forum". Mental Health Forum.
- BMJ Group, "Schizoaffective disorders: Treatment", 2012
- Dieterich M, Irving CB, Park B, et al. (January 6, 2017). Dieterich M, ed. "Intensive Case Management for Severe Mental Illness". Cochrane Database of Systematic Reviews. 1 (CD007906). doi:10.1002/14651858.CD007906.pub3. PMC 4233116. PMID 28067944.
- PSR/RPS Canada, , "PSR/RPS Canada Core Principles and Values"Archived 24 March 2010 at the Wayback Machine.
- American Psychiatric Association, "Practice Guideline for the Treatment of Patients with Schizophrenia, Second Edition", 2004 Archived 6 March 2014 at Archive.is
- Paliperidone, "Schizoaffective disorders: Treatment", 2013
- Stahl SM, Stahl's Essential Psychopharmacology: Neuroscientific basis and practical applications, New York: Cambridge University Press, 2008
- Stahl, Stephen M. (2002). Essential Psychopharmacology of Antipsychotics and Mood Stabilizers. Cambridge University Press. p. 70. ISBN 0-521-89074-8.
- Lake CR, Hurwitz N (August 2006). "Schizoaffective disorders are psychotic mood disorders; there are no schizoaffective disorders". Psychiatry Research. 143 (2–3): 255–87. doi:10.1016/j.psychres.2005.08.012. PMID 16857267.
- Goodwin & Jamison 2007, p. 102.
- Goodwin & Marneros 2005, p. 190.
- Goodwin & Marneros 2005, p. 189.
- Marneros & Akiskal 2007, pp. 3–4.
- Van Snellenberg JX, de Candia T (July 2009). "Meta-analytic evidence for familial coaggregation of schizophrenia and bipolar disorder". Arch. Gen. Psychiatry. 66 (7): 748–55. doi:10.1001/archgenpsychiatry.2009.64. PMID 19581566.
- "Schizophrenia and bipolar disorder may share genetic origins". Harv Ment Health Lett. 25 (12): 7. June 2009. PMID 19582944.
- Purcell SM, Wray NR, Stone JL, Visscher PM, O'Donovan MC, Sullivan PF, Sklar P (July 2009). "Common polygenic variation contributes to risk of schizophrenia and bipolar disorder". Nature. 460 (7256): 748–52. doi:10.1038/nature08185. PMC 3912837. PMID 19571811.
- Potash JB, Bienvenu OJ (June 2009). "Neuropsychiatric disorders: Shared genetics of bipolar disorder and schizophrenia". Nature Reviews Neurology. 5 (6): 299–300. doi:10.1038/nrneurol.2009.71. PMID 19498428.
- Goodwin & Jamison 2007, p. 96.
- Goodwin & Marneros 2005, p. 192.
- Lake CR, Hurwitz N (2007). "Schizoaffective disorder merges schizophrenia and bipolar disorders as one disease". Current Opinion in Psychiatry. 20 (4): 365–79. doi:10.1097/YCO.0b013e3281a305ab. PMID 17551352.
- "No One Is Abandoning the DSM, but it is Almost Time to Transform It". Scientific American. Retrieved October 2013. Check date values in:
- "Roadmap for Mental Health Research in Europe". ROAMER. Retrieved October 2013. Check date values in: