Schizoaffective disorder

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https://en.wikipedia.org/wiki/Schizoaffective_disorder

Schizoaffective disorder
Specialty	Psychiatry
Symptoms	Hallucinations, delusions, disorganized thinking, depressed mood, manic behavior
Complications	Social isolation, suicide
Types	Bipolar type, depressive type
Causes	Unknown
Risk factors	Genetics, brain chemistry and structure, stress, drug use, trauma from abuse
Medication	Antipsychotics, mood stabilizers

Schizoaffective disorder (SZA, SZD or SAD) is a mental disorder characterized by abnormal thought processes and an unstable mood. The diagnosis is made when the person has symptoms of both schizophrenia (usually psychosis) and a mood disorder—either bipolar disorder or depression—but does not meet the diagnostic criteria for schizophrenia or a mood disorder individually. 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. It is imperative for providers to accurately diagnose patients, as treatment and prognosis differs greatly for each of these diagnoses.

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. Auditory hallucinations, or "hearing voices," are most common. The onset of symptoms usually begins in young adulthood.

Genetics (researched in the field of genomics); problems with neural circuits; chronic early, and chronic or short-term current environmental stress appear to be important causal factors. 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.

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 that were diagnosed using DSM-IV and ICD-10 criteria (which have since been updated) have a better outcome, but have variable individual psychosocial functional outcomes compared to people with mood disorders, from worse to the same. Outcomes for people with DSM-5 diagnosed schizoaffective disorder depend on data from prospective cohort studies, which have not been completed yet. The DSM-5 diagnosis was updated because DSM-IV criteria resulted in overuse of the diagnosis; that is, DSM-IV criteria led to many patients being misdiagnosed with the disorder. DSM-IV prevalence estimates were less than one percent of the population, in the range of 0.5–0.8 percent; newer DSM-5 prevalence estimates are not yet available.

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.

DSM-5 states that if a patient only experiences psychotic symptoms during a mood episode, their diagnosis is Mood Disorder with Psychotic Features and not Schizophrenia or Schizoaffective Disorder. If the patient experiences psychotic symptoms without mood symptoms for longer than a two-week period, their diagnosis is either Schizophrenia or Schizoaffective Disorder. If mood disorder episodes are present for the majority and residual course of the illness and up until the diagnosis, the patient can be diagnosed with Schizoaffective Disorder.

Causes

A combination of genetic and environmental factors are believed to play a role in the development of schizoaffective disorder.

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.

— According to William T. Carpenter the head of the University of Maryland, Baltimore School of Medicine DSM-5 psychotic disorders workgroup, and others. 

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.

Substance abuse

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. Certain drugs can imitate symptoms of schizophrenia (which we know has similar symptoms to schizoaffective disorder). This is important to note when including that substance-induced psychosis should be ruled out when diagnosing patients so that patients are not misdiagnosed.

Diagnosis

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:

• EEG to exclude epilepsy, and an
• MRI or CT scan of the head to exclude brain lesions.

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:

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.

DSM-5 criteria

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.

Types

One of two types of schizoaffective disorder may be noted in a diagnosis based on the mood component of the disorder:

• 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.

Emil Kraepelin's dichotomy (c. 1898) continues to influence classification and diagnosis in psychiatry

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.

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.

[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.

Treatment

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.

Participating in internet forums is sometimes used by people with schizoaffective disorder in addition to outpatient medication treatment.

Therapy

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)

Medication

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 blood work 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

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.

Epidemiology

Schizoaffective disorder is estimated to occur in 0.5 to 0.8 percent of people at some point in their life. 30% of cases occur between the ages of 25 and 35. 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.

History

The term schizoaffective psychosis was introduced by the American psychiatrist Jacob Kasanin in 1933^[65] 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.

Karl Kahlbaum (1828–1899)

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.

Emil Kraepelin (1856–1926) Embracing the Kraepelinian dichotomy in DSM-III in 1980, while a step forward from psychodynamic explanations of the disorder, introduced significant problems in schizoaffective disorder diagnosis, as explained recently by the DSM-5 workgroup

 

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.

Research

Evidence is 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.

Gray's biopsychological theory of personality

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Gray%27s_biopsychological_theory_of_personality

The biopsychological theory of personality is a model of the general biological processes relevant for human psychology, behavior, and personality. The model, proposed by research psychologist Jeffrey Alan Gray in 1970, is well-supported by subsequent research and has general acceptance among professionals.

Gray hypothesized the existence of two brain-based systems for controlling a person's interactions with their environment: the behavioural inhibition system (BIS) and the behavioural activation system (BAS). BIS is related to sensitivity to punishment and avoidance motivation. BAS is associated with sensitivity to reward and approach motivation. Psychological scales have been designed to measure these hypothesized systems and study individual differences in personality. Neuroticism, a widely studied personality dimension related to emotional functioning, is positively correlated with BIS scales and negatively correlated with BAS scales.

History

The biopsychological theory of personality is similar to another one of Gray's theories, reinforcement sensitivity theory. The Biopsychological Theory of Personality was created after Gray disagreed with Hans Eysenck's arousal theory that dealt with biological personality traits. Eysenck looked at the ascending reticular activating system (ARAS) for answering questions about personality. The ARAS is part of the brain structure and has been proposed to deal with cortical arousal, hence the term arousal theory. Eysenck compared levels of arousal to a scale of introversion versus extraversion. The comparison of these two scales was then used to describe individual personalities and their corresponding behavioral patterns. Gray disagreed with Eysenck's theory because Gray believed that things such as personality traits could not be explained by just classical conditioning. Instead, Gray developed his theory which is based more heavily on physiological responses than Eysenck's theory.

Gray had a lot of support for his theories and experimented with animals to test his hypotheses. Using animal subjects allows researchers to test whether different areas of the brain are responsible for different learning mechanisms. Specifically, Gray's theory concentrated on understanding how reward or punishment related to anxiety and impulsivity measures. His research and further studies have found that reward and punishment are under the control of separate systems and as a result people can have different sensitivities to such rewarding or punishing stimuli.

Behavioral inhibition system

The behavioral inhibition system (BIS), as proposed by Gray, is a neuropsychological system that predicts an individual's response to anxiety-relevant cues in a given environment. This system is activated in times of punishment, boring things, or negative events. By responding to cues such as negative stimuli or events that involve punishment or frustration, this system ultimately results in avoidance of such negative and unpleasant events. According to Gray's Theory, the BIS is related to sensitivity to punishment as well as avoidance motivation. It has also been proposed that the BIS is the causal basis of anxiety. High activity of the BIS means a heightened sensitivity to nonreward, punishment, and novel experience. This higher level of sensitivity to these cues results in a natural avoidance of such environments in order to prevent negative experiences such as fear, anxiety, frustration, and sadness. People who are highly sensitive to punishment perceive punishments as more aversive and are more likely to be distracted by punishments.

The physiological mechanism behind the BIS is believed to be the septohippocampal system and its monoaminergic afferents from the brainstem. Using a voxel-based morphometry analysis, the volume of the regions mentioned was assessed to view individual differences. Findings may suggest a correlation between the volume and anxiety-related personality traits. Results were found in the orbitofrontal cortex, the precuneus, the amygdala, and the prefrontal cortex.

Behavioral activation system

The behavioral activation system (BAS), in contrast to the BIS, is based on a model of appetitive motivation - in this case, an individual's disposition to pursue and achieve goals. The BAS is aroused when it receives cues corresponding to rewards and controls actions that are not related to punishment, rather actions regulating approachment type behaviors. This system has an association with hope. According to Gray's theory, the BAS is sensitive to conditioned appealing stimuli, and is associated with impulsivity. It is also thought to be related to sensitivity to reward as well as approach motivation. The BAS is sensitive to nonpunishment and reward. Individuals with a highly active BAS show higher levels of positive emotions such as elation, happiness, and hope in response to environmental cues consistent with nonpunishment and reward, along with goal-achievement. In terms of personality, these individuals are also more likely to engage in goal-directed efforts and experience these positive emotions when exposed to impending reward. The physiological mechanism for BAS is not known as well as BIS, but is believed to be related to catecholaminergic and dopaminergic pathways in the brain. Dopamine is a neurotransmitter commonly linked with positive emotions, which could explain the susceptibility to elation and happiness upon achieving goals which has been observed. People with a highly active BAS have been shown to learn better by reward than by punishment, inverse to BIS as mentioned above. BAS is considered to include trait impulsivity that is also related to psychopathological disorders such as ADHD, drug abuse, and alcohol abuse. The higher the BAS score, or the higher the impulsive, the more it is likely to be related to psycho-pathological or dis-inhibitory disorders. Certain aspects of the dopaminergic reward system activate when reward cues and reinforcers are presented, including biological rewards such as food and sex. These brain areas, which were highlighted during multiple fMRI studies, are the same areas associated with BAS. 

Compare and contrast

Together, the two systems work in an inverse relationship. In other words, when a specific situation occurs, an organism can approach the situation with one of the two systems. The systems will not be stimulated at the same time and which system is dominant depends on the situation in terms of punishment versus reward. This phenomenon of the differentiation between the two systems is thought to occur because of the distinct areas in the brain that becomes activated in response to different stimuli. This difference was noted years ago through electrical stimulation of the brain.

The behavioral activation system and behavioral inhibition system differ in their physiological pathways in the brain. The inhibition system has been shown to be linked to the septo-hippocampal system which appears to have a close correlation to a serotonergic pathway, with similarities in their innervations and stress responses. On the other hand, the activation, or reward system, is thought to be associated more with a mesolimbic dopaminergic system as opposed to the serotonergic system.

The two systems proposed by Gray differ in their motivations and physiological responses. Gray also proposed that individuals can vary widely in their responsiveness of the behavioral inhibition system and the behavioral activation system. It has been found that someone who is sensitive to their BIS will be more receptive to the negative cues as compared to someone who is sensitive to their BAS and therefore responds more to cues in the environment that relate to that system, specifically positive or rewarding cues. Researchers besides Gray have shown interest in this theory and have created questionnaires that measure BIS and BAS sensitivity. Carver and White have been the primary researchers responsible for the questionnaire. Carver and White created a scale that has been shown to validly measure levels of individual scores of BIS and BAS. This measure focuses on the differences in incentive motivations and aversive motivations. As previously mentioned these motivations correlate to impulsivity and anxiety respectively.

Applications

Since the development of the BAS and BIS, tests have been created to see how individuals rate in each area. The questionnaire is called the Behavioral Inhibition System and Behavioral Activation System Questionnaire.

People can be tested based on their activation of either systems by using an EEG. These tests will conclude whether a person has a more active BIS or BAS. The two systems are independent of each other.

These tests can determine different things about a person's personality. They can determine if a person has more positive or negative moods. Using psychological test scales designed to correlate with the attributes of these hypothesized systems, neuroticism has been found to be positively correlated with the BIS scale, and negatively correlated with the BAS scale.

According to Richard Depue's BAS dysregulation theory of bipolar disorders, now doctors and other professionals can determine if a person with bipolar disorder is on the brink of a manic or depressive episode based on how they rate on a scale of BAS and BIS sensitivity. Essentially, this dysregulation theory proposes that people with BAS dysregulation have an extraordinarily sensitive behavioral activation system and their BAS is hyper-responsive to behavioral approach system cues. If a person with bipolar disorder self-reports high sensitivity to BAS, it means that a manic episode could occur faster. Also, if a person with bipolar disorder reports high sensitivity to BIS it could indicate a depressive phase. A better understanding of BAS dysregulation theory can inform psychosocial intervention (e.g. cognitive behavioral therapy, psychoeducation, interpersonal and social rhythm therapy, etc.).

The BAS/BIS Questionnaire can also be used in the cases of criminal profiling. Previous research as reported by researchers MacAndrew and Steele in 1991 compared two groups on opposite spectrum levels of fear and the response of a variety of questions. The two groups in the study varied on levels of BIS, either high or low, and were selected by the researchers. One group was composed of women who had experienced anxiety attacks and together made up the high BIS group. The low BIS group was composed of convicted prostitutes who had been found to take part in illegal behavior. Main findings showed that the responses to the questionnaires were distinctly different between the high BIS group and the low BIS group, with the convicted women scoring lower. Results from this study demonstrate that questionnaires can be used as a valid measurement to show differences in the behavioral inhibition systems of different types of people. Gray also introduced his SPSRQ questionnaire to measure sensitivity to reward (SR) and sensitivity to punishment (SP) in anxiety (2012). It is a specifically designed questionnaire linking to Gray's theory referencing the SR to the BAS and the SP to the BIS.

Future research or implications

As mentioned previously, psychological disorders have been analyzed in terms of the behavioral inhibition and activation systems. Understanding the differences between the systems may relate to an understanding of different types of disorders that involve anxiety and impulsivity. To date, there are many types of anxiety disorders that deal with avoidance theories and future research could show that the behavioral activation system plays a large role in such disorders and may have future implications for treatment of patients.

Trait theory

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Trait_theory 

In psychology, trait theory (also called dispositional theory) is an approach to the study of human personality. Trait theorists are primarily interested in the measurement of traits, which can be defined as habitual patterns of behavior, thought, and emotion. According to this perspective, traits are aspects of personality that are relatively stable over time, differ across individuals (e.g. some people are outgoing whereas others are not), are relatively consistent over situations, and influence behavior. Traits are in contrast to states, which are more transitory dispositions. 

In some theories and systems, traits are something a person either has or does not have, but in many others traits are dimensions such as extraversion vs. introversion, with each person rating somewhere along this spectrum. 

There are two approaches to define traits: as internal causal properties or as purely descriptive summaries. The internal causal definition states that traits influence our behaviours, leading us to do things in line with that trait. On the other hand, traits as descriptive summaries are descriptions of our actions that don't try to infer causality.

History

Gordon Allport was an early pioneer in the study of traits. This early work was viewed as the beginning of the modern psychological study of personality. He also referred to traits within his work as dispositions. In his approach, "cardinal" traits are those that dominate and shape a person's behavior; their ruling passions/obsessions, such as a need for money, fame etc. By contrast, "central" traits such as honesty are characteristics found in some degree in every person - and finally "secondary" traits are those seen only in certain circumstances (such as particular likes or dislikes that a very close friend may know), which are included to provide a complete picture of human complexity.

A wide variety of alternative theories and scales were later developed, including:

• Raymond Cattell's 16PF Questionnaire
• J. P. Guilford's Structure of Intellect
• Henry Murray's System of Needs
• Timothy Leary's Interpersonal circumplex
• Myers–Briggs Type Indicator
• Gray's Biopsychological theory of personality

Currently, two general approaches are the most popular:

• Eysenck Personality Questionnaire, (EPQ) ("the three-factor model"). Using factor analysis Hans Eysenck suggested that personality is reducible to three major traits: neuroticism, extraversion, and psychoticism.
• Big Five personality traits, ("the five-factor model"). Many psychologists currently believe that five factors are sufficient: neuroticism, extraversion, openness to experience, agreeableness, and conscientiousness.

Trait theory in cross-cultural use

Cultures are widely known and accepted as being different in varying degrees. This can make the study of personality difficult as meaning and the expression of traits may be different within cultural groups. Trait theory uses a hierarchy of traits in order to separate culture from the traits, it can be said the culture is ignored in order to focus of the individual traits and how they are connected to the individual. Gordon Allport's trait theory not only served as a foundational approach within personality psychology, but also is continued to be viewed and discussed by other disciplines such as anthropology because of how he approached culture within trait theory.

Trait theory tends to focus on the individual over the situation in which they are in. This focus has relaxed within modern studies allowing for a consideration of the external factors outside of the self. As the focus becomes more relaxed (but still prominent as it is a main part of the theory) research expands. 

Comparing EPQ and Big Five

Testing methodology, and factors

Both the EPQ and Big Five approaches extensively use self-report questionnaires. The factors are intended to be orthogonal (uncorrelated), though there are often small positive correlations between factors. The five factor model in particular has been criticized for losing the orthogonal structure between factors. Hans Eysenck has argued that fewer factors are superior to a larger number of partly related ones. Although these two approaches are comparable because of the use of factor analysis to construct hierarchical taxonomies, they differ in the organization and number of factors.

Whatever the causes, psychoticism marks the two approaches apart, as the five factor model contains no such trait. Moreover, psychoticism, unlike any of the other factors in either approach, does not fit a normal distribution curve. Indeed, scores are rarely high, thus skewing a normal distribution. However, when they are high, there is considerable overlap with psychiatric conditions such as antisocial and schizoid personality disorders. Similarly, high scorers on neuroticism are more susceptible to sleep and psychosomatic disorders. Five factor approaches can also predict future mental disorders.

Lower-order factors

Similarities between lower-order factors for psychoticism and the facets of openness, agreeableness, and conscientiousness (from Matthews, Deary & Whiteman, 2003)

 

There are two higher-order factors that both taxonomies clearly share: extraversion and neuroticism. Both approaches broadly accept that extraversion is associated with sociability and positive affect, whereas neuroticism is associated with emotional instability and negative affect.

Many lower-order factors, or facets, are similar between the two taxonomies. For instance, both approaches contain factors for sociability/gregariousness, for activity levels, and for assertiveness within the higher order factor extraversion. However, there are differences too. First, the three-factor approach contains nine lower-order factors and the five-factor approach has six.

Eysenck's psychoticism factor incorporates some of the polar opposites of the lower order factors of openness, agreeableness and conscientiousness. A high scorer on tough-mindedness in psychoticism would score low on tender-mindedness in agreeableness. Most of the differences between the taxonomies stem from the three factor model's emphasis on fewer high-order factors. 

Causality

Although both major trait models are descriptive, only the three-factor model offers a detailed causal explanation. Eysenck suggests that different personality traits are caused by the properties of the brain, which themselves are the result of genetic factors. In particular, the three-factor model identifies the reticular system and the limbic system in the brain as key components that mediate cortical arousal and emotional responses respectively. Eysenck advocates that extraverts have low levels of cortical arousal and introverts have high levels, leading extraverts to seek out more stimulation from socializing and being venturesome. Moreover, Eysenck surmised that there would be an optimal level of arousal, after which inhibition would occur and that this would be different for each person.

In a similar vein, the three-factor approach theorizes that neuroticism is mediated by levels of arousal in the limbic system and that individual differences arise because of variable activation thresholds between people. Therefore, highly neurotic people when presented with minor stressors, will exceed this threshold, whereas people low in neuroticism will not exceed normal activation levels, even when presented with large stressors. By contrast, proponents of the five-factor approach assume a role of genetics and environment but offer no explicit causal explanation.

Given this emphasis on biology in the three-factor approach, it would be expected that the third trait, psychoticism, would have a similar explanation. However, the causal properties of this state are not well defined. Eysenck has suggested that psychoticism is related to testosterone levels and is an inverse function of the serotonergic system, but he later revised this, linking it instead to the dopaminergic system.

List of personality traits

Personality traits

Openness to experience	Composed of two related but separable traits, Openness to Experience and Intellect. Behavioral aspects include having wide interests, and being imaginative and insightful, correlated with activity in the dorsolateral prefrontal cortex. Considered primarily a cognitive trait.
Conscientiousness	Scrupulous, meticulous, principled behavior guided or conforming to one's own conscience. Associated with the dorsolateral prefrontal cortex.
Extraversion	Gregarious, outgoing, sociable, projecting one's personality outward. The opposite of extraversion is introversion. Extraversion has shown to share certain genetic markers with substance abuse. Extraversion is associated with various regions of the prefrontal cortex and the amygdala.
Agreeableness	Refers to a compliant, trusting, empathic, sympathetic, friendly and cooperative nature.
Neuroticism	Identifies people who are prone to psychological distress. Individuals who are high in neuroticism tend to be anxious, depressed, self-conscious, impulsive, vulnerable and display angry hostility. "Neuroticism is the major factor of personality pathology" (Eysenck & Eysenck, 1969). Neuroticism has been linked to serotonin transporter (5-HTT) binding sites in the thalamus: as well as activity in the insular cortex. Neuroticism also predicts the occurrence of more negative life experiences.
Honesty-humility	Tendency towards sincerity, modesty, fairness, and greed avoidance. Those who score high on this trait feel little desire to manipulate others or to break the rules for personal gain.
Self-esteem (low)	A "favorable or unfavorable attitude toward the self" (Rosenberg, 1965). An individual's sense of his or her value or worth, or the extent to which a person values, approves of, appreciates, prizes, or likes him or herself" (Blascovich & Tomaka, 1991).
Harm avoidance	A tendency towards shyness, being fearful and uncertain, tendency to worry. Neonatal complications such as preterm birth have been shown to affect harm avoidance. People affected by eating disorders exhibit high levels of harm avoidance. The volume of the left amygdala in girls was correlated to levels of HA, in separate studies HA was correlated with reduced grey matter volume in the orbitofrontal, occipital and parietal regions.
Novelty seeking	Impulsive, exploratory, fickle, excitable, quick-tempered, and extravagant. Associated with addictive behavior.
Sensory processing sensitivity (SPS)	The defining trait of highly sensitive persons, characterized by the increased depth of processing of sensory input that underlies HSPs' greater proclivity to overstimulation, emotional reactivity and empathy, and sensitivity to stimuli.
Perfectionism	"I don't think needing to be perfect is in any way adaptive." (Paul Hewitt, PhD) Socially prescribed perfectionism – "believing that others will value you only if you are perfect." Self-oriented perfectionism – "an internally motivated desire to be perfect." Perfectionism is one of the traits associated with obsessional behavior and like obsessionality is also believed to be regulated by the basal ganglia.
Alexithymia	The inability to express emotions. "To have no words for one's inner experience" (Rený J. Muller PhD). In studies done with stroke patients, alexithymia was found to be more prevalent in those who developed lesions in the right hemisphere following a cerebral infarction. There is a positive association with post-traumatic stress disorder (PTSD), childhood abuse and neglect and alexithymia. Utilizing psychometric testing and fMRI, studies showed positive response in the insula, posterior cingulate cortex (PCC), and thalamus.
Rigidity	Inflexibility, difficulty making transitions, adherence to set patterns. Mental rigidity arises out of a deficit of the executive functions. Originally termed frontal lobe syndrome it is also referred to as dysexecutive syndrome and usually occurs as a result of damage to the frontal lobe. This may be due to physical damage, disease (such as Huntington's disease) or a hypoxic or anoxic insult.
Impulsivity	Risk taking, lack of planning, and making up one's mind quickly (Eysenck and Eysenck). A component of disinhibition. Abnormal patterns of impulsivity have been linked to lesions in the right inferior frontal gyrus and in studies done by Antonio Damasio author of Descartes Error, damage to the ventromedial prefrontal cortex has been shown to cause a defect in real-life decision making in individuals with otherwise normal intellect. Those who sustain this type of damage are oblivious to the future consequences of their actions and live in the here and now.
Disinhibition	Behavioral disinhibition is an inability or unwillingness to constrain impulses, it is a key component of executive functioning. Researchers have emphasized poor behavioral inhibition as the central impairment of ADHD. It may be symptomatic of orbitofrontal lobe syndrome, a subtype of frontal lobe syndrome which may be an acquired disorder as a result of traumatic brain injury, hypoxic ischemic encephalopathy (HIE), anoxic encephalopathy, degenerative diseases such as Parkinson's, bacterial or viral infections such as Lyme disease and neurosyphilis. Disinhibition has been consistently associated with substance abuse disorders, obesity, higher BMI, excessive eating, an increased rate of eating, and perceived hunger.
Psychoticism	Psychoticism is a personality pattern typified by aggressiveness and interpersonal hostility, one of four traits in Hans Eysenck's model of personality. High levels of this trait were believed by Eysenck to be linked to increased vulnerability to psychosis such as schizophrenia. He also believed that blood relatives of psychotics would show high levels of this trait, suggesting a genetic basis to the trait.
Obsessionality	Persistent, often unwelcome, and frequently disturbing ideas, thoughts, images or emotions, rumination, often inducing an anxious state. Obsessionality may result as a dysfunction of the basal ganglia.

Mania

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Mania

Mania
Other names	Manic syndrome, manic episode
Graphical representation of mania and hypomania
Specialty	Psychiatry

Mania, also known as manic syndrome, is a state of abnormally elevated arousal, affect, and energy level, or "a state of heightened overall activation with enhanced affective expression together with lability of affect." Although mania is often conceived as a "mirror image" to depression, the heightened mood can be either euphoric or irritable; indeed, as the mania intensifies, irritability can be more pronounced and result in anxiety, or violence.

The symptoms of mania include elevated mood (either euphoric or irritable), flight of ideas and pressure of speech, increased energy, decreased need and desire for sleep, and hyperactivity. They are most plainly evident in fully developed hypomanic states. However, in full-blown mania, they undergo progressively severe exacerbations and become more and more obscured by other signs and symptoms, such as delusions and fragmentation of behavior.

Causes and Diagnosis

Mania is a syndrome with multiple causes. Although the vast majority of cases occur in the context of bipolar disorder, it is a key component of other psychiatric disorders (such as schizoaffective disorder, bipolar type) and may also occur secondary to various general medical conditions, such as multiple sclerosis; certain medications may perpetuate a manic state, for example prednisone; or substances prone to abuse, especially stimulants, such as caffeine and cocaine. In the current DSM-5, hypomanic episodes are separated from the more severe full manic episodes, which, in turn, are characterized as either mild, moderate, or severe, with certain diagnostic criteria (e.g. catatonia, psychosis). Mania is divided into three stages: hypomania, or stage I; acute mania, or stage II; and delirious mania (delirium), or stage III. This "staging" of a manic episode is useful from a descriptive and differential diagnostic point of view.

Mania varies in intensity, from mild mania (hypomania) to delirious mania, marked by such symptoms as disorientation, florid psychosis, incoherence, and catatonia. Standardized tools such as Altman Self-Rating Mania Scale and Young Mania Rating Scale can be used to measure severity of manic episodes. Because mania and hypomania have also long been associated with creativity and artistic talent, it is not always the case that the clearly manic/hypomanic bipolar patient needs or wants medical help; such persons often either retain sufficient self-control to function normally or are unaware that they have "gone manic" severely enough to be committed or to commit themselves. Manic persons often can be mistaken for being under the influence of drugs.

Classification

Mixed states

In a mixed affective state, the individual, though meeting the general criteria for a hypomanic (discussed below) or manic episode, experiences three or more concurrent depressive symptoms. This has caused some speculation, among clinicians, that mania and depression, rather than constituting "true" polar opposites, are, rather, two independent axes in a unipolar—bipolar spectrum.

A mixed affective state, especially with prominent manic symptoms, places the patient at a greater risk for completed suicide. Depression on its own is a risk factor but, when coupled with an increase in energy and goal-directed activity, the patient is far more likely to act with violence on suicidal impulses.

Associated disorders

A single manic episode, in the absence of secondary causes, (i.e., substance use disorders, pharmacologics, or general medical conditions) is often sufficient to diagnose bipolar I disorder. Hypomania may be indicative of bipolar II disorder. Manic episodes are often complicated by delusions and/or hallucinations; and if the psychotic features persist for a duration significantly longer than the episode of typical mania (two weeks or more), a diagnosis of schizoaffective disorder is more appropriate. Certain obsessive-compulsive spectrum disorders as well as impulse control disorders share the suffix "-mania," namely, kleptomania, pyromania, and trichotillomania. Despite the unfortunate association implied by the name, however, no connection exists between mania or bipolar disorder and these disorders. Furthermore, evidence indicates a B₁₂ deficiency can also cause symptoms characteristic of mania and psychosis.

Hyperthyroidism can produce similar symptoms to those of mania, such as agitation, elevated mood, increased energy, hyperactivity, sleep disturbances and sometimes, especially in severe cases, psychosis.

Signs and symptoms

A manic episode is defined in the American Psychiatric Association's diagnostic manual as a "distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased activity or energy, lasting at least 1 week and present most of the day, nearly every day (or any duration, if hospitalization is necessary)," where the mood is not caused by drugs/medication or a non-mental medical illness (e.g., hyperthyroidism), and: (a) is causing obvious difficulties at work or in social relationships and activities, or (b) requires admission to hospital to protect the person or others, or (c) the person is suffering psychosis.

To be classified as a manic episode, while the disturbed mood and an increase in goal directed activity or energy is present, at least three (or four, if only irritability is present) of the following must have been consistently present:

1. Inflated self-esteem or grandiosity.
2. Decreased need for sleep (e.g., feels rested after 3 hours of sleep).
3. More talkative than usual, or acts pressured to keep talking.
4. Flights of ideas or subjective experience that thoughts are racing.
5. Increase in goal directed activity, or psychomotor acceleration.
6. Distractibility (too easily drawn to unimportant or irrelevant external stimuli).
7. Excessive involvement in activities with a high likelihood of painful consequences.(e.g., extravagant shopping, improbable commercial schemes, hypersexuality).

Though the activities one participates in while in a manic state are not always negative, those with the potential to have negative outcomes are far more likely.

If the person is concurrently depressed, they are said to be having a mixed episode.

The World Health Organization's classification system defines a manic episode as one where mood is higher than the person's situation warrants and may vary from relaxed high spirits to barely controllable exuberance, is accompanied by hyperactivity, a compulsion to speak, a reduced sleep requirement, difficulty sustaining attention and/or often increased distractibility. Frequently, confidence and self-esteem are excessively enlarged, and grand, extravagant ideas are expressed. Behavior that is out of character and risky, foolish or inappropriate may result from a loss of normal social restraint.

Some people also have physical symptoms, such as sweating, pacing, and weight loss. In full-blown mania, often the manic person will feel as though his or her goal(s) are of paramount importance, that there are no consequences or that negative consequences would be minimal, and that they need not exercise restraint in the pursuit of what they are after. Hypomania is different, as it may cause little or no impairment in function. The hypomanic person's connection with the external world, and its standards of interaction, remain intact, although intensity of moods is heightened. But those who suffer from prolonged unresolved hypomania do run the risk of developing full mania, and indeed may cross that "line" without even realizing they have done so.

One of the signature symptoms of mania (and to a lesser extent, hypomania) is what many have described as racing thoughts. These are usually instances in which the manic person is excessively distracted by objectively unimportant stimuli. This experience creates an absent-mindedness where the manic individual's thoughts totally preoccupy him or her, making him or her unable to keep track of time, or be aware of anything besides the flow of thoughts. Racing thoughts also interfere with the ability to fall asleep.

Manic states are always relative to the normal state of intensity of the afflicted individual; thus, already irritable patients may find themselves losing their tempers even more quickly, and an academically gifted person may, during the hypomanic stage, adopt seemingly "genius" characteristics and an ability to perform and articulate at a level far beyond that which they would be capable of during euthymia. A very simple indicator of a manic state would be if a heretofore clinically depressed patient suddenly becomes inordinately energetic, enthusiastic, cheerful, aggressive, or "over happy". Other, often less obvious, elements of mania include delusions (generally of either grandeur or persecution, according to whether the predominant mood is euphoric or irritable), hypersensitivity, hypervigilance, hypersexuality, hyper-religiosity, hyperactivity and impulsivity, a compulsion to over explain (typically accompanied by pressure of speech), grandiose schemes and ideas, and a decreased need for sleep (for example, feeling rested after only 3 or 4 hours of sleep). In the case of the latter, the eyes of such patients may both look and seem abnormally "wide open", rarely blinking, and may contribute to some clinicians’ erroneous belief that these patients are under the influence of a stimulant drug, when the patient, in fact, is either not on any mind-altering substances or is actually on a depressant drug. Individuals may also engage in out-of-character behavior during the episode, such as questionable business transactions, wasteful expenditures of money (e.g., spending sprees), risky sexual activity, abuse of recreational substances, excessive gambling, reckless behavior (such as extreme speeding or other daredevil activity), abnormal social interaction (e.g. over familiarity and conversing with strangers), or highly vocal arguments. These behaviours may increase stress in personal relationships, lead to problems at work, and increase the risk of altercations with law enforcement. There is a high risk of impulsively taking part in activities potentially harmful to the self and others.

Although "severely elevated mood" sounds somewhat desirable and enjoyable, the experience of mania is ultimately often quite unpleasant and sometimes disturbing, if not frightening, for the person involved and for those close to them, and it may lead to impulsive behaviour that may later be regretted. It can also often be complicated by the sufferer's lack of judgment and insight regarding periods of exacerbation of characteristic states. Manic patients are frequently grandiose, obsessive, impulsive, irritable, belligerent, and frequently deny anything is wrong with them. Because mania frequently encourages high energy and decreased perception of need or ability to sleep, within a few days of a manic cycle, sleep-deprived psychosis may appear, further complicating the ability to think clearly. Racing thoughts and misperceptions lead to frustration and decreased ability to communicate with others.

Mania may also, as earlier mentioned, be divided into three “stages”. Stage I corresponds with hypomania and may feature typical hypomanic characteristics, such as gregariousness and euphoria. In stages II and III mania, however, the patient may be extraordinarily irritable, psychotic or even delirious. These latter two stages are referred to as acute and delirious (or Bell's), respectively.

Cause

Various triggers have been associated with switching from euthymic or depressed states into mania. One common trigger of mania is antidepressant therapy. Studies show that the risk of switching while on an antidepressant is between 6-69 percent. Dopaminergic drugs such as reuptake inhibitors and dopamine agonists may also increase risk of switch. Other medication possibly include glutaminergic agents and drugs that alter the HPA axis. Lifestyle triggers include irregular sleep-wake schedules and sleep deprivation, as well as extremely emotional or stressful stimuli.

Various genes that have been implicated in genetic studies of bipolar have been manipulated in preclinical animal models to produce syndromes reflecting different aspects of mania. CLOCK and DBP polymorphisms have been linked to bipolar in population studies, and behavioral changes induced by knockout are reversed by lithium treatment. Metabotropic glutamate receptor 6 has been genetically linked to bipolar, and found to be under-expressed in the cortex. Pituitary adenylate cyclase-activating peptide has been associated with bipolar in gene linkage studies, and knockout in mice produces mania like-behavior. Targets of various treatments such as GSK-3, and ERK1 have also demonstrated mania like behavior in preclinical models.

Mania may be associated with strokes, especially cerebral lesions in the right hemisphere.

Deep brain stimulation of the subthalamic nucleus in Parkinson's disease has been associated with mania, especially with electrodes placed in the ventromedial STN. A proposed mechanism involves increased excitatory input from the STN to dopaminergic nuclei.

Mania can also be caused by physical trauma or illness. When the causes are physical, it is called secondary mania.

Mechanism

The mechanism underlying mania is unknown, but the neurocognitive profile of mania is highly consistent with dysfunction in the right prefrontal cortex, a common finding in neuroimaging studies. Various lines of evidence from post-mortem studies and the putative mechanisms of anti-manic agents point to abnormalities in GSK-3, dopamine, Protein kinase C and Inositol monophosphatase.

Meta analysis of neuroimaging studies demonstrate increased thalamic activity, and bilaterally reduced inferior frontal gyrus activation. Activity in the amygdala and other subcortical structures such as the ventral striatum tend to be increased, although results are inconsistent and likely dependent upon task characteristics such as valence. Reduced functional connectivity between the ventral prefrontal cortex and amygdala along with variable findings supports a hypothesis of general dysregulation of subcortical structures by the prefrontal cortex. A bias towards positively valenced stimuli, and increased responsiveness in reward circuitry may predispose towards mania. Mania tends to be associated with right hemisphere lesions, while depression tends to be associated with left hemisphere lesions.

Post-mortem examinations of bipolar disorder demonstrate increased expression of Protein Kinase C (PKC). While limited, some studies demonstrate manipulation of PKC in animals produces behavioral changes mirroring mania, and treatment with PKC inhibitor tamoxifen (also an anti-estrogen drug) demonstrates antimanic effects. Traditional antimanic drugs also demonstrate PKC inhibiting properties, among other effects such as GSK3 inhibition.

Manic episodes may be triggered by dopamine receptor agonists, and this combined with tentative reports of increased VMAT2 activity, measured via PET scans of radioligand binding, suggests a role of dopamine in mania. Decreased cerebrospinal fluid levels of the serotonin metabolite 5-HIAA have been found in manic patients too, which may be explained by a failure of serotonergic regulation and dopaminergic hyperactivity.

Limited evidence suggests that mania is associated with behavioral reward hypersensitivity, as well as with neural reward hypersensitivity. Electrophysiological evidence supporting this comes from studies associating left frontal EEG activity with mania. As left frontal EEG activity is generally thought to be a reflection of behavioral activation system activity, this is thought to support a role for reward hypersensitivity in mania. Tentative evidence also comes from one study that reported an association between manic traits and feedback negativity during receipt of monetary reward or loss. Neuroimaging evidence during acute mania is sparse, but one study reported elevated orbitofrontal cortex activity to monetary reward, and another study reported elevated striatal activity to reward omission. The latter finding was interpreted in the context of either elevated baseline activity (resulting in a null finding of reward hypersensitivity), or reduced ability to discriminate between reward and punishment, still supporting reward hyperactivity in mania. Punishment hyposensitivity, as reflected in a number of neuroimaging studies as reduced lateral orbitofrontal response to punishment, has been proposed as a mechanism of reward hypersensitivity in mania.

Diagnosis

In the ICD-10 there are several disorders with the manic syndrome: organic manic disorder (F06.30), mania without psychotic symptoms (F30.1), mania with psychotic symptoms (F30.2), other manic episodes (F30.8), unspecified manic episode (F30.9), manic type of schizoaffective disorder (F25.0), bipolar affective disorder, current episode manic without psychotic symptoms (F31.1), bipolar affective disorder, current episode manic with psychotic symptoms (F31.2). 

Treatment

Before beginning treatment for mania, careful differential diagnosis must be performed to rule out secondary causes.

The acute treatment of a manic episode of bipolar disorder involves the utilization of either a mood stabilizer (valproate, lithium, lamotrigine, or carbamazepine) or an atypical antipsychotic (olanzapine, quetiapine, risperidone, or aripiprazole). Although hypomanic episodes may respond to a mood stabilizer alone, full-blown episodes are treated with an atypical antipsychotic (often in conjunction with a mood stabilizer, as these tend to produce the most rapid improvement).

When the manic behaviours have gone, long-term treatment then focuses on prophylactic treatment to try to stabilize the patient's mood, typically through a combination of pharmacotherapy and psychotherapy. The likelihood of having a relapse is very high for those who have experienced two or more episodes of mania or depression. While medication for bipolar disorder is important to manage symptoms of mania and depression, studies show relying on medications alone is not the most effective method of treatment. Medication is most effective when used in combination with other bipolar disorder treatments, including psychotherapy, self-help coping strategies, and healthy lifestyle choices.

Lithium is the classic mood stabilizer to prevent further manic and depressive episodes. A systematic review found that long term lithium treatment substantially reduces the risk of bipolar manic relapse, by 42%. Anticonvulsants such as valproate, oxcarbazepine and carbamazepine are also used for prophylaxis. More recent drug solutions include lamotrigine and topiramate, both anticonvulsants as well. 

In some cases, long-acting benzodiazepines, particularly clonazepam, are used after other options are exhausted. In more urgent circumstances, such as in emergency rooms, lorazepam has been used to promptly alleviate symptoms of agitation, aggression, and psychosis. Sometimes atypical antipsychotics are used in combination with the previous mentioned medications as well, including olanzapine which helps treat hallucinations or delusions, asenapine, aripiprazole, risperidone, ziprasidone, and clozapine which is often used for people who do not respond to lithium or anticonvulsants. 

Verapamil, a calcium-channel blocker, is useful in the treatment of hypomania and in those cases where lithium and mood stabilizers are contraindicated or ineffective. Verapamil is effective for both short-term and long-term treatment.

Antidepressant monotherapy is not recommended for the treatment of depression in patients with bipolar disorders I or II, and no benefit has been demonstrated by combining antidepressants with mood stabilizers in these patients. Some atypical antidepressants, however, such as mirtazepine and trazodone have been occasionally used after other options have failed.

Society and culture

In Electroboy: A Memoir of Mania by Andy Behrman, he describes his experience of mania as "the most perfect prescription glasses with which to see the world... life appears in front of you like an oversized movie screen". Behrman indicates early in his memoir that he sees himself not as a person suffering from an uncontrollable disabling illness, but as a director of the movie that is his vivid and emotionally alive life. There is some evidence that people in the creative industries suffer from bipolar disorder more often than those in other occupations. Winston Churchill had periods of manic symptoms that may have been both an asset and a liability.

English actor Stephen Fry, who suffers from bipolar disorder, recounts manic behaviour during his adolescence: "When I was about 17 ... going around London on two stolen credit cards, it was a sort of fantastic reinvention of myself, an attempt to. I bought ridiculous suits with stiff collars and silk ties from the 1920s, and would go to the Savoy and Ritz and drink cocktails." While he has experienced suicidal thoughts, he says the manic side of his condition has had positive contributions on his life.

Etymology

The nosology of the various stages of a manic episode has changed over the decades. The word derives from the Ancient Greek μανία (manía), "madness, frenzy" and the verb μαίνομαι (maínomai), "to be mad, to rage, to be furious".