What are the characteristics and symptoms of Schizoaffective Disorder?

Schizoaffective Disorder is a complex mental health condition that combines symptoms of both schizophrenia and mood disorders. It is often misunderstood and misdiagnosed, making it a challenging disorder to identify and treat. In this essay, we will explore the characteristics and symptoms of Schizoaffective Disorder, including its diagnostic criteria, prevalence, and distinguishing features from other mental health conditions. By gaining a better understanding of this disorder, we can improve our ability to recognize and support individuals living with Schizoaffective Disorder.

Schizoaffective disorder is a psychiatric diagnosis that describes a mental disorder characterized by recurring episodes of elevated or depressed mood, or of simultaneously elevated and depressed mood, that alternate with, or occur together with, distortions in perception.

Schizoaffective disorder most commonly affects cognition and emotion. Auditory hallucinations, paranoia, bizarre delusions, or disorganized speech and thinking with significant social and occupational dysfunction are typical. The division into depressive and bipolar types is based on whether the individual has ever had a manic, hypomanic or mixed episode. Symptoms usually begin in early adulthood, which makes diagnosis prior to age 13 rare.

In addition to schizophrenia, schizoaffective disorder is part of a “schizophrenic spectrum” (comparable to the autistic spectrum) that includes schizotypal personality disorder. Each named disorder on this continuum shares symptoms with the others, and some professionals (including the working group for the DSM-5) contend that the boundaries are so unclear that separate labels are not necessarily warranted.



The lifetime prevalence of the disorder is probably less than 1 percent, in the range of 0.5 to 0.8 percent. Diagnosis is based on the patient’s self-reported experiences and observed behavior. No laboratory test for schizoaffective disorder currently exists, though extensive evidence exists for abnormalities in the metabolism of tetrahydrobiopterin (BH4), dopamine, and glutamate in people with schizophrenia and schizoaffective disorders. As a group, individuals with schizoaffective disorder have a more favorable prognosis than those with schizophrenia, but a worse prognosis than those with other mood disorders.

Genetics, early environment, neurobiology, psychological and social processes are important contributory factors. Some recreational and prescription drugs may cause or worsen symptoms. Current research is focused on the role of neurobiology, but no single organic cause has been found.

The mainstay of treatment is antipsychotic medication combined with mood stabilizer medication or antidepressant medication, or both. Psychotherapy, and vocational and social/psychiatric rehabilitation are also important for recovery. In cases where there is risk to self and others, brief involuntary hospitalization may be necessary.

People with schizoaffective disorder are likely to have comorbid conditions, including anxiety disorders and substance abuse. 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, due to increased physical health problems and a higher suicide rate.

The diagnosis was introduced in 1933 and may be removed in the next iteration of the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders (DSM-5), to be published in May 2013.


Signs and symptoms

Late adolescence and early adulthood are the peak years for the onset of schizoaffective disorder, although it has been diagnosed (very rarely) in childhood.

Schizoaffective disorder is a mental illness characterized by recurring episodes of mood disorder and psychosis. Psychosis is defined by paranoia, delusions and hallucinations. Mood disorders are defined by discrete periods of clinical depression, mixed episodes and manic episodes. Individuals with the disorder may experience psychotic symptoms before, during or (commonly) after their depressive, mixed or manic episodes.

The illness tends to be difficult to diagnose since the symptoms are similar to other disorders with prominent mood and psychotic symptoms like bipolar disorder with psychotic features, recurrent depression with psychotic features and schizophrenia. By contrast, in schizoaffective disorder, as it is presently defined, psychosis must also occur during periods without mood symptoms. In schizophrenia, mood episodes have been thought to be absent or less prominent than in schizoaffective disorder. Since these differences can be difficult to detect, a firm diagnosis of schizoaffective disorder may thus require an extended period of observation and treatment.

Untreated, the individual with schizoaffective disorder may experience delusions. It should be noted that delusions in schizoaffective disorder are acute manifestations of an active psychosis and are not personality traits; that is, they go away when the psychosis subsides. Manifestations of delusions include the individual being convinced that he or she is Jesus or the Antichrist, has some special purpose or destiny (such as to save the world), or is being monitored, watched or persecuted by something (commonly government agencies), when in reality they often are not. Individuals may also feel extremely paranoid. Other delusions may include the belief that an external force is controlling the individual’s thought processes. (See thought insertion.)

Hallucinations involving all five senses can also occur in untreated or undertreated schizoaffective disorder. That is, the individual may see, hear, smell, feel or taste things that aren’t there. For example, the individual may see overt visual hallucinations such as monsters, the devil or more subtle ones such as shadowy apparitions. Individuals may hear voices or, in some cases, music. Things may look or sound different. Individuals may also experience strange sensations. These hallucinations may worsen when the individual is intoxicated.

The untreated individual may quickly change their mind about their romantic partner, friends or family if they hear something negative being said about them; as a result they may attack or, conversely, isolate themself from the person or group until they regain normal thoughts.

Comorbid or co-occurring anxiety disorders may also play a role in the subjective experience of schizoaffective disorder and thus may shape the individual’s delusional thought content. For example, the individual may feel anxious, have trouble swallowing, and then believe that outside forces are controlling their throat functions. They may also suffer from various phobias which may also manifest as delusions.

There may be a decline in work or school functioning during episodes of illness. As stated above, individuals with schizoaffective disorder may withdraw socially and become isolated.

The untreated individual may sleep too much, or be unable to sleep.

Difficulties with executive function may also be a problem for individuals with schizoaffective disorder. This may include difficulties with concentration, attention, logical reasoning and impulse control.

Without treatment, the individual with schizoaffective disorder may further worsen in their delusional thought processes.

With comprehensive treatment, many individuals with schizoaffective disorder may recover much, most or even all of their functionality.



Diagnosis is based on the self-reported experiences of the person as well as abnormalities in behavior reported by family members, friends or co-workers to a psychiatrist, psychiatric nurse, social worker or psychologist in a clinical assessment. There is a list of criteria that must be met for someone to be so diagnosed. These depend on both the presence and duration of certain signs and symptoms.

As discussed above, there are several psychiatric illnesses which may present with a similar range of psychotic symptoms; these include bipolar disorder with psychotic features, major depression with psychotic features, schizophrenia, drug intoxication, brief drug-induced psychosis, and schizophreniform disorder. These disorders need to be ruled out before a firm diagnosis of schizoaffective disorder can be made.

An initial assessment includes a comprehensive history and physical examination by a physician. Although there are no biological tests which confirm schizoaffective disorder, tests are carried out to exclude medical illnesses which rarely may be associated with psychotic symptoms. These include blood tests measuring TSH 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; two commonly ordered investigations are EEG to exclude epilepsy, and a CT scan of the head to exclude brain lesions. It is important to rule out a delirium which can be distinguished by visual hallucinations, acute onset and fluctuating level of consciousness and indicates an underlying medical illness.

Investigations are not generally repeated for relapse 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, and CPK levels to exclude neuroleptic malignant syndrome. Assessment and treatment are usually done on an outpatient basis; admission to an inpatient facility is considered if there is a risk to self or others.

The most widely-used criteria for diagnosing schizoaffective disorder are from the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, the current version being DSM-IV-TR.


DSM-IV-TR criteria

The following are the revised criteria for a diagnosis of schizoaffective disorder from the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR):

Two (or more) of the following symptoms are present for the majority of a one-month period (or a shorter period of time if symptoms got better with treatment):

  • delusions
  • hallucinations
  • disorganized speech (e.g., frequent derailment or incoherence) which is a manifestation of formal thought disorder
  • grossly disorganized behavior (e.g. dressing inappropriately, crying frequently) or catatonic behavior
  • negative symptoms—e.g., affective flattening (lack or decline in emotional response), alogia (lack or decline in speech), avolition (lack or decline in motivation), anhedonia (lack or decline in ability to experience pleasure), social withdrawal (sometimes called social anhedonia).

Negative symptoms refers to symptoms that are not present or that are diminished in the affected persons but are normally found in healthy persons.

If the delusions are judged to be bizarre, or hallucinations consist of hearing one voice participating in a running commentary of the individual’s actions or of hearing two or more voices conversing with each other, only that symptom is required to meet criterion A above. The speech disorganization criterion is only met if it is severe enough to substantially impair communication. and at some time during the illness there is either one, two or all three of the following:

  • major depressive episode
  • manic episode
  • mixed episode
  • During the illness, delusions or hallucinations were present for a minimum of two weeks, without major mood symptoms.
  • For a substantial part of the overall duration of both the active and residual period of the illness, symptoms meeting criteria for a mood episode are present.
  • Symptoms are not caused by drug abuse, medication or another medical condition.



Two subtypes of schizoaffective disorder exist and may be noted in a diagnosis based on the mood component of the disorder:

Bipolar type

if the disturbance includes

  • a manic episode
  • a mixed episode

Major depressive episodes usually, but not always, also occur in the bipolar subtype, however they are not required for DSM-IV diagnosis.


Depressive type

The depressive type is noted when the disturbance includes major depressive episodes exclusively.

This subtype applies if major depressive episodes only (and no manic or mixed episodes) are part of the presentation.


Controversies and research directions

Citing poor interrater reliability, some psychiatrists have totally contested the concept of schizoaffective disorder as a separate entity. The categorical distinction between mood disorders and schizophrenia, known as the Kraepelinian dichotomy, has also been challenged by data from genetic epidemiology. Consequently, some researchers have disputed that the term “schizoaffective disorder” refers to a well defined condition, and have recommended that the term be removed from or amended in future diagnostic manuals.

In April 2009, the DSM-5 Psychotic Disorders Work Group headed by psychiatrist William T. Carpenter of the University of Maryland, College Park School of Medicine, reported that they will be “developing new criteria for schizoaffective disorder to improve reliability and face validity,” and that they will be “determining whether the dimensional assessment of mood will justify a recommendation to drop schizoaffective disorder as a diagnostic category.” Speaking 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 because we don’t think it’s valid and we don’t think it’s reliable. On the other hand, we think it’s absolutely indispensable to clinical practice.”



Although the causes of schizoaffective disorder are unknown, it is suspected that this diagnosis represents a heterogeneous group of individuals, some with aberrant forms of schizophrenia and some with very serious forms of mood disorders. There is little evidence that schizoaffective disorder is a distinct variety of psychotic illness. Consequently, the disorder appears to be comorbid or (co-occurring) with schizophrenia and mood disorder. Schizoaffective disorder thus appears to exist on a continuum in-between schizophrenia and severe bipolar disorder and severe recurrent unipolar depression. It follows then that the etiology is probably more similar to that of schizophrenia in some cases and more similar to severe mood disorders in other cases.

Many different genes may be contributing to the genetic risk of acquiring this illness. In addition, many different biological and environmental factors are believed to interact with the person’s genes in ways which can increase or decrease the person’s risk for developing schizoaffective disorder. Schizophrenia spectrum disorders (of which schizoaffective disorder is a part) have been marginally linked to advanced paternal age at the time of conception, a common cause of mutations.

The physiology of patients diagnosed with schizoaffective disorder appears to be similar but not identical to that of those diagnosed with schizophrenia and severe bipolar disorder.


Substance abuse

A clear causal connection between drug use and psychotic spectrum disorders, including schizoaffective disorder, has been difficult to prove. The two most often used explanations for this are “substance use causes schizoaffective disorder” and “substance use is a consequence of schizoaffective disorder”, and they both may be correct. In the case of marijuana or cannabis, however, evidence is mounting that it can play a role in the development and morbidity of psychotic disorders, including schizoaffective disorder. For example, a 2007 meta-analysis showed that cannabis use is statistically associated with a dose-dependent increase in risk of development of psychotic disorders, including schizoaffective disorder. Moreover, a 2005 meta-analysis found that cannabis use is a significant independent risk factor for developing psychotic symptoms and psychosis. A 2009 Yale study stated that it is clear

“that in individuals with an established psychotic disorder, cannabinoids can exacerbate symptoms, trigger relapse, and have negative consequences on the course of the illness.”

On the other hand, a meta-analysis published in 2008 concluded that “Confidence that most associations reported were specifically due to cannabis is low. Despite clinical opinion, it remains important to establish whether cannabis is harmful, what outcomes are particularly susceptible, and how such effects are mediated.”

However, despite increases in cannabis consumption in the 1960s and 1970s in western society, rates of psychotic disorders generally remained relatively stable. Also, Sweden and Japan, where self-reported marijuana use is very low, do not have lower rates of psychosis than the U.S. and Canada do. For the theory of causality to be correct, other factors which are thought to contribute to psychosis would have to have converged almost flawlessly to mask the effect of increased cannabis usage. However, there may be other confounding factors, including social structure, family structure, typical diet, and ethnic genetic makeup that preclude a clear 1:1 comparison – either pro or con – between populations from different countries.

There is little evidence to suggest that other drugs including alcohol cause schizoaffective disorder, or that psychotic individuals choose specific drugs to self-medicate; there is some support for the theory that they use drugs to cope with unpleasant states such as depression, anxiety, boredom and loneliness. However, regarding psychosis itself, it is well understood that methamphetamine and cocaine use can result in methamphetamine- or cocaine-induced psychosis which presents very similar symptomatology and may persist even when users remain abstinent. The same can also be said for alcohol-induced psychosis, though to a somewhat lesser extent.



Treatment for schizoaffective disorder consists of a combination of medicine, psychotherapy and psychosocial rehabilitation focused on recovery or symptom management.

A licensed psychiatrist will prescribe (usually combinations of) medicine for the individual. Each person responds differently to medication.

The only medicine that is FDA-approved for Schizoaffective Disorder is paliperidone (Invega). For psychotic symptoms neuroleptic medications such as risperidone may be used.

For manic symptoms, mood stabilizer medications may be prescribed along with a neuroleptic. Examples are:

  • Lithium salt (Lithium)
  • Valproate semisodium (Depakote ER)
  • Carbamazepine (Tegretol)

For depression, antidepressant medications may be prescribed along with a neuroleptic. Examples are:

  • SSRI antidepressants (includes Prozac and Zoloft among others)
  • Lamictal (a mood stabilizer with antidepressant properties)

In schizoaffective individuals with manic symptoms, combining lithium, carbamazepine, or valproate with a neuroleptic has been shown to be superior to neuroleptics alone. Lithium-neuroleptic combinations, however, may produce severe extrapyramidal reactions or confusion in some patients.

When lithium is not effective or well tolerated in manic individuals with schizoaffective disorder, Tegretol or Depakote are frequently used. Granulocytopenia can occur during the first few weeks of carbamazepine treatment, and neuroleptic blood levels may be decreased substantially due to hepatic enzyme induction. Valproate can, in rare cases, cause liver toxicity and platelet dysfunction. Calcium channel blockers such as verapamil may also be an effective treatment for manic symptoms but are seldom prescribed for that purpose. The degree of benefit for an individual should be considered carefully, as each of these medications carries its own risks.

Benzodiazepines such as Ativan and Klonopin are effective adjunctive treatment agents for acute manic symptoms, but long-term use may result in dependency.

In schizoaffective individuals with depressive symptoms, an antidepressant (for example, Prozac or other SSRIs) may be prescribed with a neuroleptic. The SNRI antidepressants and Wellbutrin tend not to be prescribed in schizoaffective disorder because they may cause mixed episode symptoms and induce psychosis, respectively.

The anticonvulsant Lamictal is gaining prominence in treating depressed schizoaffective individuals because antidepressants appear to increase the risk of mood cycling in some individuals, which is a safety concern.

Often a sleeping pill will be prescribed initially to allow the individual rest from his or her anxiety, delusions or hallucinations. Long-term use of sleeping medications can, however, cause dependence and can also cause delusions and hallucinations thereby exacerbating psychosis.



Complications are similar to those for schizophrenia and major mood disorders. These include:

  • Problems following medical treatment and therapy
  • Use of unsanctioned drugs in an attempt to self-medicate
  • Short-term side effects and problems arising from long-term use of prescribed medications, including drug interactions.
  • Problems resulting from manic behavior (for example, spending sprees, sexual indiscretion)
  • Suicidal behavior due to depressive or psychotic symptoms



Estimates of the prevalence of schizoaffective disorder vary widely, but schizoaffective manic patients appear to comprise 3-5% of psychiatric admissions to typical clinical centers. At one point it was widely believed that schizoaffective disorder was associated with increased risk of mood disorders in relatives. This may have been because of the number of patients with psychotic mood disorders who were included in schizoaffective study populations.

The current diagnostic criteria define a group of individuals with a mixed genetic picture. They are more likely to have schizophrenic relatives than individuals with mood disorders but more likely to have relatives with mood disorders than individuals with schizophrenia.



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 etiology 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 disorder and recurrent depression).

Kraeplin acknowledged that “there are many overlaps in this area”, that is, the area between schizophrenia and severe mood disorders. In 1959, psychiatrist Kurt Schneider (1887–1967) can be said to have been the first to begin to conceptualize 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; 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 phenomenological observation that schizoaffective disorder is an overlap of schizophrenia and severe mood disorders has more recently been assumed to be explained by genes for both illnesses being present in individuals with schizoaffective disorder. But recent research shows that schizophrenia and severe mood disorders appear to share common genes and polygenic variations also.

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.


Monothematic delusion

A monothematic delusion is a delusional state that only concerns one particular topic. This is contrasted by what is sometimes called multi-thematic or polythematic delusions where the person has a range of delusions (typically the case of schizophrenia). These disorders can occur within the context of schizophrenia or dementia or they can occur without any other signs of mental illness. When these disorders are found outside the context of mental illness, they are often caused by organic disfunction as a result of traumatic brain injury, stroke, or neurological illness.

People who suffer from these delusions as a result of organic dysfunction often do not suffer from any obvious intellectual deficiency nor do they have any other symptoms. Additionally, a few of these people even have some awareness that their beliefs are bizarre, yet they cannot be persuaded that their beliefs are false.



The delusions that fall under this category are:

  • Capgras delusion: the belief that (usually) a close relative or spouse has been replaced by an identical-looking impostor.
  • Fregoli delusion: the belief that various people who the believer meets are actually the same person in disguise.
  • Intermetamorphosis: the belief that people in one’s environment swap identities with each other whilst maintaining the same appearance.
  • Subjective doubles: a person believes there is a doppelgänger or double of him or herself carrying out independent actions.
  • Cotard delusion: the belief that oneself is dead or does not exist; sometimes coupled with the belief that one is putrifying or missing internal organs.
  • Mirrored self-misidentification: the belief that one’s reflection in a mirror is some other person.
  • Reduplicative paramnesia: the belief that a familiar person, place, object or body part has been duplicated. For example, a person may believe that they are in fact not in the hospital to which they were admitted, but in an identical-looking hospital in a different part of the country.
  • Somatoparaphrenia: the delusion where one denies ownership of a limb or an entire side of one’s body (often connected with stroke).

Note that some of these delusions are sometimes grouped under the umbrella term of delusional misidentification syndrome.



Current cognitive neuropsychology research points toward a two-factor approach to the cause of monothematic delusions. The first factor being the anomalous experience—often a neurological defect—which leads to the delusion and the second factor being an impairment of the belief formation cognitive process.

For example of one of these first factors, several studies point toward Capgras delusion being the result of a disorder of the affect component of face perception. As a result, while the person can recognize their spouse (or other close relation) they do not feel the typical emotional reaction and thus the spouse does not seem like the person they once knew.

As studies have shown, these neurological defects are not enough on their own to cause delusional thinking. An additional second factor, a bias or impairment of the belief formation cognitive process is required to solidify and maintain the delusion. Since we do not currently have a solid cognitive model of the belief formation process, this second factor is still somewhat of an unknown.

Some research has shown that delusional people are more prone to jumping to conclusions and thus they would be more likely to take their anomalous experience as veridical and make snap judgments based on these experiences. Additionally, studies have shown that they are more prone to making errors due to matching bias—indicative of a tendency to try and confirm the rule. These two judgment biases help explain how delusion prone people could grasp onto extreme delusions and be very resistant to change.

Researchers claim this is enough to explain the delusional thinking. However other researchers still argue that these biases are not enough to explain why they remain completely impervious to evidence over time. They believe that there must be some additional unknown neurological defect in the patient’s belief system (probably in the right hemisphere).

Scroll to Top