Misplaced Pages

This is an old revision of this page, as edited by MarkWood (talk | contribs) at 14:24, 6 June 2007 (→Differential diagnosis: added per talk page). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.

Schizophrenia
Specialty	Psychiatry, clinical psychology

The mental disorder Schizophrenia (from the Greek word σχιζοφρένεια, or schizophreneia, meaning "split mind") is a psychiatric diagnosis characterized by impairments in the perception or expression of reality, most commonly manifest as auditory hallucinations, paranoid or bizarre delusions or disorganized speech and thinking in the context of significant social or occupational dysfunction. Onset of symptoms typically occurs in young adulthood, with approximately 0.4–0.6% of the population affected. Diagnosis is based on the patient's self-reported experiences and observed behavior. No laboratory test for schizophrenia exists.

Studies suggest that genetics, early environment, neurobiology and psychological and social processes are important contributory factors. Current psychiatric research into the development of the disorder often focuses on the role of neurobiology, although a reliable and identifiable organic cause has not been found. Due to the many possible combinations of symptoms, heated debates are ongoing about whether the diagnosis represents a single disorder, or a number of discrete syndromes. For this reason, Eugen Bleuler deliberately called the disease "the schizophrenias" (plural) when he coined the present name. Despite its etymology, "schizophrenia" is not synonymous with dissociative identity disorder, previously known as multiple personality disorder or "split personality"; in popular culture the two are often confused.

One of the more consistent findings is the overactivity of the receptor dopamine in mesolimbic pathway in the brain. The mainstay of treatment is pharmacotherapy with antipsychotic medications; these primarily work by suppressing dopamine activity. Psychotherapy vocational and social rehabilitation are also important. In more serious cases where there is risk to self and others involuntary hospitalization may be necessary, though in general people are hospitalized alot less frequently and for much shorter periods than they were in previous years.

Although the disorder is primarily thought to affect cognition, it also usually contributes to chronic problems with behavior and emotion. Patients diagnosed with schizophrenia are highly likely to be diagnosed with other disorders. The lifetime prevalence of substance abuse is typically around 40%. Comorbidity is also high with clinical depression, anxiety disorders, and social problems, and a generally decreased life expectancy is also present. Patients diagnosed with schizophrenia typically live ten to twelve years less than those without the disorder, owing to increased physical health problems and a high suicide rate. Unemployment and poverty are common.

History

The term "schizophrenia" translates roughly as "splitting of the mind", and comes from the Greek σχίζω (or schizo, "to split" or "to divide") and φρήν (or phrēn, "mind"). Accounts that may relate to symptoms of schizophrenia date back as far as 2000 BC in the Book of Hearts, part of the ancient Ebers papyrus. However, a recent study into the ancient Greek and Roman literature showed that although the general population probably had an awareness of psychotic disorders, there was no recorded condition that would meet the modern criteria for schizophrenia.

This broad concept of "madness" has existed for thousands of years, but schizophrenia was only classified as a distinct mental disorder by Emil Kraepelin in 1893. He was the first to make a distinction in the psychotic disorders between what he called dementia praecox (a term first used by psychiatrist Bénédict Morel 1809–1873) and manic depression. Kraepelin believed that dementia praecox was primarily a disease of the brain, and particularly a form of dementia. Kraepelin named the disorder 'dementia praecox' (early dementia) to distinguish it from other forms of dementia, such as Alzheimer's disease, which occur late in life.

The word "schizophrenia" was coined by Eugene Bleuler in 1908 and was intended to describe the separation of function between personality, thinking, memory, and perception. Bleuler described the main symptoms as 4 "A"'s: flattened Affect, Autism, impaired Association of ideas and Ambivalence. Bleuler realized that the illness was not a dementia as some of his patients improved rather than deteriorated and hence proposed the term schizophrenia instead.

The term 'schizophrenia' is commonly misunderstood to mean that affected persons have a "split personality". Although some people diagnosed with schizophrenia may hear voices and may experience the voices as distinct personalities, schizophrenia does not involve a person changing among distinct multiple personalities. The confusion perhaps arises in part due to the meaning of Bleuler's term 'schizophrenia' (literally 'split' or 'shattered mind'). The first known misuse of "schizophrenia" to mean "split personality" was in an article by the poet T. S. Eliot in 1933.

In the first half of the twentieth century schizophrenia was considered by many to be a "hereditary defect", and individuals affected by schizophrenia became subject to eugenics in many countries. Hundreds of thousands were sterilized, with or without consent, the majority in Nazi Germany, the United States, and Scandinavian countries, Many people diagnosed with schizophrenia, together with other people labeled "mentally unfit", were murdered in the Nazi "Operation T-4" program.

The diagnostic description of schizophrenia has changed over time. It became clear after the 1971 'US-UK diagnostic study' that schizophrenia was diagnosed to a far greater extent in American than in Europe. This was partly due to the difference in diagnostic systems, the US used the DSM-II manual, while Europe used the ICD-9, each of which had different descriptions of schizophrenia. This was one of the factors in leading to the revision not only of the diagnosis of schizophrenia, but the revision of the whole DSM manual, resulting in the publication of the DSM-III.

Signs and symptoms

A person experiencing schizophrenia may demonstrate a variety of symptoms; these may include disorganized thinking, delusions and hallucinations, in particular auditory hallucinations. The current classification of psychoses holds that symptoms need to have been present for at least one month in a period of at least six months of disturbed functioning. A psychosis of shorter duration is termed a schizophreniform disorder. Onset of schizophrenia typically occurs in late adolescence or early adulthood, with males tending to show symptoms earlier than females. No one symptom is diagnostic of schizophrenia, and all can occur in various other medical or psychiatric conditions.

Some symptoms, such as social isolation, may be caused by a number of factors. One possible factor is impairment in social cognition, which is associated with schizophrenia, but isolation may also result from an individual reacting to psychotic symptoms (such as paranoia) or avoiding potentially stressful social situations which may exacerbate mental distress in some people.

Much work in recent years has gone into the prodromal (pre-onset) phase of the illness, which has been detected up to 30 months prior to the onset of symptoms although may be present for longer. Many people later diagnosed with schizophrenia experience difficulties including nonspecific symptoms of social withdrawal, irritability and dysphoria as well as transient or self-limiting psychotic symptoms.

Schneiderian classification

The psychiatrist Kurt Schneider attempted to list the particular forms of psychotic symptoms that he thought were particularly useful in distinguishing between schizophrenia and other disorders that could produce psychosis. These are called first rank symptoms or Schneiderian first rank symptoms and include delusions of being controlled by an external force, the belief that thoughts are being inserted into or withdrawn from one's conscious mind, the belief that one's thoughts are being broadcast to other people and hearing hallucinatory voices which comment on one's thoughts or actions, or may have a conversation with other hallucinated voices. The reliability of 'first rank symptoms' has been questioned, although they have contributed to the current diagnostic criteria.

Positive and negative symptoms

Schizophrenia is often described in terms of "positive" (or productive) and "negative" (or deficit) symptoms. Positive symptoms include delusions, auditory hallucinations and thought disorder and are typically regarded as manifestations of psychosis. Negative symptoms are so named because they are considered to be the loss or absence of normal traits or abilities, and include features such as flat, blunted or constricted affect and emotion, poverty of speech and lack of motivation. Additionally, a 'disorganization syndrome' and neurocognitive deficits may be present. These may take the form of reduced or impaired psychological functions such as memory, attention, problem-solving, executive function or social cognition. A third symptom grouping, the so-called 'disorganization syndrome', includes disorganized speech (thought disorder) and related disorganized behavior.

Diagnosis

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

Although there are no biological tests which confirm schizophrenia, an initial assessment includes a comprehensive physical examination and tests to exclude other causes as rarely a medical illness may present with psychotic symptoms. These include blood tests measuring TSH to exclude hypo- or hyperthyroidism, basic electrolytes and serum calcium to rule out a metabolic disturbance, full blood count to rule out an infective process, and serology to exclude syphilis or HIV infection; two commonly ordered investigations are EEG to exclude epilepsy, and a CT scan of the head to exclude brain lesions. Note that these investigations are not generally repeated for relapse unless there is a specific medical indication. Assessment and treatment are usually done on an outpatient basis; admission to an inpatient facility is considered if there is a risk to self or others.

The most widely used criteria for diagnosing schizophrenia are from the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders (the current version is the DSM-IV-TR) and the World Health Organization's International Statistical Classification of Diseases and Related Health Problems (currently the ICD-10). The ICD-10 criteria are typically used in European countries while the DSM criteria are used in the USA or the rest of the world, although it is more common for research studies to use DSM criteria for consistency. The ICD-10 criteria put more emphasis on Schneiderian 'first rank symptoms' although, in practice, agreement between the two systems is high.

DSM IV-TR Criteria

To be diagnosed with schizophrenia, a person must display:

• Characteristic symptoms: Two or more of the following, each present for a significant portion of time during a one-month period (or less, if successfully treated)
  • delusions
  • hallucinations
  • disorganized speech (e.g., frequent derailment or incoherence; speaking in abstracts). See thought disorder.
  • grossly disorganized behavior (e.g. dressing inappropriately, crying frequently) or catatonic behavior
  • negative symptoms, i.e., affective flattening (lack or decline in emotional response), alogia (lack or decline in speech), or avolition (lack or decline in motivation).

Note: Only one of these symptoms is required if delusions are bizarre or hallucinations consist of hearing one voice participating in a running commentary of the patient's actions or of hearing two or more voices conversing with each other.

• Social/occupational dysfunction: For a significant portion of the time since the onset of the disturbance, one or more major areas of functioning such as work, interpersonal relations, or self-care, are markedly below the level achieved prior to the onset.

• Duration: Continuous signs of the disturbance persist for at least six months. This six-month period must include at least one month of symptoms (or less, if successfully treated).

Additional criteria are also given that exclude a diagnosis of schizophrenia if symptoms of mood disorder or pervasive developmental disorder are present. Additionally a diagnosis of schizophrenia is excluded if the symptoms are the direct result of a substance (e.g., abuse of a drug, medication) or a general medical condition.

Subtypes

Historically, schizophrenia in the West was classified into simple, catatonic, hebephrenic (now known as disorganized), and paranoid. The DSM contains five sub-classifications of schizophrenia:

• paranoid type: where delusions and hallucinations are present but thought disorder, disorganized behavior, and affective flattening are absent (DSM code 295.3/ICD code F20.0)
• disorganized type: named 'hebephrenic schizophrenia' in the ICD. Where thought disorder and flat affect are present together (DSM code 295.1/ICD code F20.1)
• catatonic type: prominent psychomotor disturbances are evident. Symptoms can include catatonic stupor and waxy flexibility (DSM code 295.2/ICD code F20.2)
• undifferentiated type: psychotic symptoms are present but the criteria for paranoid, disorganized, or catatonic types have not been met (DSM code 295.9/ICD code F20.3)
• residual type: where positive symptoms are present at a low intensity only (DSM code 295.6/ICD code F20.5)

The ICD-10 also recognises another two subtypes:

• post-schizophrenic depression: a depressive episode arising in the aftermath of a schizophrenic illness where some low-level schizophrenic symptoms may still be present (ICD code F20.4)
• simple schizophrenia: insidious but progressive development of prominent negative symptoms with no history of psychotic episodes (ICD code F20.6)

Differential diagnosis

In rare instances, medical illnesses may manifest with psychiatric symptoms. These conditions may include delirium or organic conditinos. Once an organic condition is ruled out, there are several psychiatric conditions which may present with psychotic symptoms, such as Schizophrenia. Other conditions that my present with psychotic symptoms include bipolar disorder, borderline personality disorder, drug intoxication, brief drug-induced psychosis, and schizophreniform disorder. Regardless of cause, antipsychotics are the acute treatment of choice for psychotic symptoms although ones with minimal anticholinergic activity, such as haloperidol or risperidone are preferable if a delirium is suspected.

Diagnostic issues and controversies

Schizophrenia as a diagnostic entity has been criticised as lacking in scientific validity or reliability, part of a larger criticism of the validity of psychiatric diagnoses in general. One alternative suggests that the issues with the diagnosis would be better addressed as individual dimensions along which everyone varies, such that there is a spectrum or continuum rather than a cut-off between normal and ill. This approach appears consistent with research on schizotypy and of a relatively high prevalence of psychotic experiences and often non-distressing delusional beliefs amongst the general public.

Another criticism is that the definitions used for criteria lack consistency (for example, see the entries on delusions and thought disorder for a discussion of this issue). More recently, it has been argued that psychotic symptoms are not a good basis for making a diagnosis of schizophrenia as "psychosis is the 'fever' of mental illness — a serious but nonspecific indicator".

Perhaps because of these factors, studies examining the diagnosis of schizophrenia have typically shown relatively low or inconsistent levels of diagnostic reliability. Most famously, David Rosenhan's 1972 study, published as On being sane in insane places, demonstrated that the diagnosis of schizophrenia was (at least at the time) often subjective and unreliable. More recent studies have found agreement between any two psychiatrists when diagnosing schizophrenia tends to reach about 65% at best. This, and the results of earlier studies of diagnostic reliability (which typically reported even lower levels of agreement) have led some critics to argue that the diagnosis of schizophrenia should be abandoned.

In 2004 in Japan, Japanese term of schizophrenia was changed from Seishin-Bunretsu-Byo (mind-split-disease) to Tōgō-shitchō-shō (integration disorder). In 2006, campaigners in the UK, under the banner of Campaign for Abolition of the Schizophrenia Label, argued for a similar rejection of the diagnosis of schizophrenia and a different approach to the treatment and understanding of the symptoms currently associated with it.

Alternatively, other proponents have argued for a new approach that would use the presence of specific neurocognitive deficits to make a diagnosis. These often accompany schizophrenia and take the form of a reduction or impairment in basic psychological functions such as memory, attention, executive function and problem solving. It is these sorts of difficulties, rather than the psychotic symptoms (which can in many cases be controlled by antipsychotic medication), which seem to be the cause of most disability in schizophrenia. However, this argument is relatively new and it is unlikely that the method of diagnosing schizophrenia will change radically in the near future.

The diagnosis of schizophrenia has been abused for political rather than therapeutic purposes. An example of this can be seen in the Soviet Union, where an additional sub-classification of sluggishly progressing schizophrenia was created. Particularly in the RSFSR (Russian Soviet Federated Socialist Republic), this diagnosis was used for the purpose of silencing political dissidents or forcing them to recant their ideas by the use of forcible confinement and treatment. In 2000 similar concerns about the abuse of psychiatry to unjustly silence and detain practitioners of the Falun Gong movement by the Chinese government led the American Psychiatric Association's Committee on the Abuse of Psychiatry and Psychiatrists to pass a resolution to urge the World Psychiatric Association to investigate the situation in China.

Epidemiology

Schizophrenia is typically diagnosed in late adolescence or early adulthood. The peak ages of onset are 20–28 years for men and 26–32 years for women. It is found approximately equally in men and women, though its onset is later on average in women, who tend to experience a better course and outcome. Relatively rare are instances of childhood-onset schizophrenia and late-onset schizophrenia (occurring in old age). The lifetime prevalence of schizophrenia—that is, the proportion of individuals expected to experience the disease at any time in their lives—is commonly given at 1%. A 2002 systematic review of many studies, however, found a lifetime prevalence of 0.55%. The same study found that prevalence may vary greatly among countries, despite the received wisdom that schizophrenia occurs at similar rates throughout the world. Due to this high, although variable incidence, schizophrenia is a major cause of disability. In a 1999 study of 14 countries, active psychosis was ranked the third-most-disabling condition, after quadriplegia and dementia and before paraplegia and blindness.

One particularly stable and replicable finding has been the association between living in an urban environment and schizophrenia diagnosis, even after factors such as drug use, ethnic group and size of social group have been controlled for.

Causes

While the reliability of the diagnosis introduces difficulties in measuring the relative effect of genes and environment (for example, symptoms overlap to some extent with severe bipolar disorder or major depression), evidence suggests that genetic vulnerability and environmental stressors can act in combination to result in onset of schizophrenia. However, the proportion of these factors' influence is widely and hotly debated.

The idea of an inherent vulnerability (or diathesis) in some people which can be unmasked by a biological, psychological or environmental stressor is known as the stress-diathesis model. Evidence suggests that the diagnosis of schizophrenia has a significant heritable component, although this may be significantly influenced by subsequent environmental factors or stressors which trigger or cause illness onset. As an example, monozygotic twins, who have identical genetic material, have a 50% chance of concordance.

Genetic

Schizophrenia is likely a condition of complex inheritance; it is likely that several genes interact to generate risk for schizophrenia or for the separate components that can co-occur to lead to a diagnosis. This, combined with disagreements over which research methods are best, or how data from genetic research should be interpreted, has led to differing estimates over genetic contribution. Molecular genetic studies of schizophrenia attempt to identify specific genes which may increase risk; genes that are thought to be most involved change as new evidence is gathered.

Enviromental

Living in an urban environment is one of the strongest environmental risk factors for schizophrenia. Being a first or second generation immigrant is also a strong risk factor for schizophrenia, for which social adversity, racial discrimination, family dysfunction, unemployment and poor housing conditions have been proposed as contributing factors. Childhood experiences of abuse or trauma have also been implicated as risk factors for a diagnosis of schizophrenia later in life.

Prenatal

It is thought that causal factors can initially come together in early neurodevelopment, including during pregnancy, to increase the risk of later developing schizophrenia. One curious finding is that people diagnosed with schizophrenia are more likely to have been born in winter or spring, (at least in the northern hemisphere). There is now evidence that prenatal exposure to infections increases the risk for developing schizophrenia later in life, providing additional evidence for a link between in utero developmental pathology and risk of developing the condition.

Substance use

The relationship between schizophrenia and drug use is complex, meaning that a clear causal connection between drug use and schizophrenia has been difficult to tease apart. There is strong evidence that using certain drugs can trigger either the onset or relapse of schizophrenia in some people. It may also be the case, however, that people with schizophrenia use drugs to overcome negative feelings associated with both the commonly prescribed antipsychotic medication and the condition itself, where negative emotion, paranoia and anhedonia are all considered to be core features. Amphetamines trigger the release of dopamine and excessive dopamine function is believed to be responsible for many symptoms of schizophrenia (known as the dopamine hypothesis of schizophrenia), amphetamines may worsen schizophrenia symptoms. Schizophrenia can be triggered by heavy use of hallucinogenic or stimulant drugs. There is evidence that cannabis use can contribute to schizophrenia.

Pathophysiology

Differences in the size and structure of certain brain areas have been found in adults diagnosed with schizophrenia. Early findings came from the discovery of ventricular enlargement in people diagnosed with schizophrenia with negative symptoms most prominent. However, this finding has not proved particularly reliable on the level of the individual person, with considerable variation between patients. More recent studies have shown a large number of differences in brain structure between people with and without diagnoses of schizophrenia. However, as with earlier studies, many of these differences are only reliably detected when comparing groups of people, and are unlikely to predict any differences in brain structure of an individual person with schizophrenia.

Studies using neuropsychological tests and brain imaging technologies such as fMRI and PET to examine functional differences in brain activity have shown that differences seem to most commonly occur in the frontal lobes, hippocampus, and temporal lobes. These differences are heavily linked to the neurocognitive deficit often associated with schizophrenia, particularly in areas of memory, attention, problem solving, executive function, and social cognition.

Dopamine

Particular focus has been placed upon the function of dopamine in the mesolimbic pathway of the brain. This focus largely resulted from the accidental finding that a drug group which blocks dopamine function, known as the phenothiazines, could reduce psychotic symptoms. An influential theory—the "dopamine hypothesis of schizophrenia"—proposed that a malfunction involving dopamine pathways was the cause of (the positive symptoms of) schizophrenia. This theory is now thought to be overly simplistic as a complete explanation, partly because newer antipsychotic medication (called atypical antipsychotic medication) can be equally effective as older medication (called typical antipsychotic medication), but also affects serotonin function and may have slightly less of a dopamine blocking effect.

Glutamate

Interest has also focused on the neurotransmitter glutamate and the reduced function of the NMDA glutamate receptor in schizophrenia. This has largely been suggested by abnormally low levels of glutamate receptors found in postmortem brains of people previously diagnosed with schizophrenia and the discovery that the glutamate blocking drugs such as phencyclidine and ketamine can mimic the symptoms and cognitive problems associated with the condition. The fact that reduced glutamate function is linked to poor performance on tests requiring frontal lobe and hippocampal function and that glutamate can affect dopamine function, all of which have been implicated in schizophrenia, have suggested an important mediating (and possibly causal) role of glutamate pathways in schizophrenia. Further support of this theory has come from preliminary trials suggesting the efficacy of coagonists at the NMDA receptor complex in reducing some of the positive symptoms of schizophrenia.

Treatment and services

The concept of a "cure" remains controversial, as there is no consensus on the definition, although some criteria for the remission of symptoms have recently been suggested. The effectiveness of schizophrenia treatment is often assessed using standardized methods, one of the most common being the positive and negative syndrome scale (PANSS). As with many chronic illness, aiming for management of symptoms and improving function is more achievable than a "cure". Treatment was revolutionized in the mid 1950s with the development and introduction of chlorpromazine.

Medication

The mainstay of treatment for schizophrenia is an antipsychotic medication. These are thought to provide symptomatic relief from the positive symptoms of psychosis. Most medications take around 7-14 days to have an antipsychotic effect but indirect symptomatic relief may occur immediately as insomnia and agitation are addressed by nonspecific sedative effects or adjunctive benzodiazepine prescription.

Though expensive, the newer atypical antipsychotic drugs are usually preferred for initial treatment over the older typical antipsychotics; they are generally better tolerated and associated with lower rates of tardive dyskinesia, although they are more likely to induce weight gain and obesity-related diseases. It remains unclear whether the newer antipsychotics reduce the chances of developing neuroleptic malignant syndrome, a neurological disorder most often caused by an adverse reaction to neuroleptic or antipsychotic drugs.

The two classes of antipsychotics are generally thought equally effective for the treatment of the positive symptoms. Some researchers have suggested that the atypicals offer additional benefit for the negative symptoms and cognitive deficits associated with schizophrenia, although the clinical significance of these effects has yet to be established. Recent reviews have refuted the claim that atypical antipsychotics have fewer extrapyramidal side effects than typical antipsychotics, especially when the latter are used in low doses or when low potency antipsychotics are chosen.

Treatment-resistant schizophrenia is a term used for the failure of symptoms to respond satisfactorily to at least two different antipsychotics; patients in this category may be prescribed clozapine, a medication of superior effectiveness but several potentially lethal side effects including cardiomyopathy and agranulocytosis. Monitoring for this latter complication requires weekly blood tests for several months, then monthly indefinitely afterwards. For other patients who are unwilling or unable to take medication regularly, long-acting depot preparations of antipsychotics may be given every two weeks to achieve control. America and Australia are two countries with laws allowing the forced administration of this type of medication on those who refuse but are otherwise stable and living in the community.

A novel approach to medication is the use of omega-3 fatty acids, which are found in foods such as oily fish, flax seeds, hemp seeds, walnuts and canola oil) have recently been studied as a treatment for schizophrenia. One study found omega-3 supplements to be effective when used as a dietary supplement.

Psychological and social interventions

Psychotherapy may be used in the treatment of schizophrenia. It has been reported that, despite evidence and recommendations, treatment is often confined to pharmacotherapy alone because of reimbursement problems or lack of training. Electroconvulsive therapy may be used in countries where it is legal. It is not considered a first line treatment but may be prescribed in cases where other treatments have failed. Psychosurgery has now become a rare procedure and is not a recommended treatment for schizophrenia. Therapy which addresses the whole family system of an individual with a diagnosis of schizophrenia, including through psychological education, has also been found to have significant benefits.

Cognitive behavioral therapy may focus on the direct reduction of the symptoms, or on related aspects, such as issues of self-esteem, social functioning, and insight. Although the results of early trials with cognitive behavioral therapy (CBT) were inconclusive, more recent reviews suggest that CBT can be an effective treatment for the psychotic symptoms of schizophrenia. There have also been advances in social skills training.

Another approach is cognitive remediation therapy, a technique aimed at remediating the neurocognitive deficits sometimes present in schizophrenia. Based on techniques of neuropsychological rehabilitation, early evidence has shown it to be cognitively effective, with some improvements related to measurable changes in brain activation as measured by fMRI. A similar approach known as cognitive enhancement therapy, which focuses on social cognition as well as neurocognition, has shown efficacy. A recent randomised controlled trial found that music therapy significantly improved symptom scores in a group of patients diagnosed with schizophrenia. A notable early mention of the beneficial effect of music on mental illness was in 1621 by Robert Burton in The Anatomy of Melancholy.

Community and outpatient services

Support services available can include drop-in centers, visits from members of a 'community mental health team' or Assertive Community Treatment team, supported employment and patient-led support groups.

In recent years the importance of service-user led recovery based movements has grown substantially throughout Europe and America. Groups such as the Hearing Voices Network and more recently, the Paranoia Network, have developed a self-help approach that aims to provide support and assistance outside of the traditional medical model adopted by mainstream psychiatry. By avoiding framing personal experience in terms of criteria for mental illness or mental health, they aim to destigmatize the experience and encourage individual responsibility and a positive self-image. Peer-to-peer support is also developing a professional footing with partnerships between hospitals and consumer run groups becoming more common. These services work towards remediating social withdrawal, building social skills and reducing rehospitalization.

In many non-Western societies, schizophrenia may only be treated with more informal, community-led methods. The outcome for people diagnosed with schizophrenia in non-Western countries may actually be better than for people in the West. The reasons for this effect are not clear, although cross-cultural studies are being conducted.

Hospitalization may occur, with severe episodes of schizophrenia. This can be voluntary or (if mental health legislation allows it) involuntary (called civil or involuntary commitment). Long-term inpatient stays are now less common due to deinstitutionalization, although can still occur.

Prognosis

One retrospective study has shown that about a third of people make a full recovery, about a third show improvement but not a full recovery, and a third remain ill. A more recent study using stricter recovery criteria (i.e. concurrent remission of positive and negative symptoms and specific instances of adequate social / vocational functioning) reported a recovery rate of 13.7%. However, the exact definition of what constitutes recovery has not been widely defined, although criteria have recently been suggested to define a remission in symptoms. Therefore, this makes it difficult to give an exact estimate as recovery and remission rates are not always comparable across studies.

The World Health Organization conducted two long-term follow-up studies involving more than 2,000 people suffering from schizophrenia in different countries. These studies found patients have much better long-term outcomes in developing countries (India, Colombia and Nigeria) than in developed countries (USA, UK, Ireland, Denmark, Czech Republic, Slovakia, Japan, and Russia), despite the fact antipsychotic drugs are typically not widely available in poorer countries, raising questions about the effectiveness of such drug-based treatments.

Several factors are associated with a better prognosis: Being female, acute (vs. insidious) onset of symptoms, older age of first episode, predominantly positive (rather than negative) symptoms, presence of mood symptoms and good premorbid functioning. Most studies done on this subject, however, are correlational in nature, and a clear cause-and-effect relationship is difficult to establish. Evidence is also consistent that negative attitudes towards individuals with schizophrenia can have a significant adverse impact. In particular, critical comments, hostility, authoritarian and intrusive or controlling attitudes (termed high 'Expressed Emotion' or 'EE' by researchers) from family members have been found to correlate with a higher risk of relapse in schizophrenia across cultures.

Mortality

In a study of over 168,000 Swedish citizens undergoing psychiatric treatment, schizophrenia was associated with an average life expectancy of approximately 80–85% of that of the general population. Women with a diagnosis of schizophrenia were found to have a slightly better life expectancy than that of men, and as a whole, a diagnosis of schizophrenia was associated with a better life expectancy than substance abuse, personality disorder, heart attack and stroke. There is a high suicide rate associated with schizophrenia; a recent study showed that 30% of patients diagnosed with this condition had attempted suicide at least once during their lifetime. Another study suggested that 10% of persons with schizophrenia die by suicide.

Violence

The relationship between violent acts and the diagnosis of schizophrenia is a contentious topic. A national survey in the United States indicated that 61% of Americans judge individuals with schizophrenia as likely to commit an act of interpersonal violence, while 17% thought such an act would be committed by person described only as "troubled".

Research on violence indicates a moderately increased number of violent acts by a minority of individuals with a diagnosis of schizophrenia. An assessment verified by multiple sources indicated that 15% of individuals with schizophrenia had committed violent acts during the course of a year, which was statistically related to substance abuse, and to the relatively poor and violent neighbourhoods in which they resided. An assessment of individuals enrolled in a trial of antipsychotic medication indicated that 19% had committed violent acts in the preceding six months, with 15.5% being of a "minor" nature.

Population-attributable figures indicate that a small percentage (3% in the ECA study in America) of the overall violence of a given population is attributable to people with schizophrenia, and that the majority of this risk is attributable to substance misuse, young age, other correlated variables, and social and economic contexts, rather than schizophrenia per se. Studies suggest that 5–10% of those awaiting trial for murder in Western countries have a schizophrenia spectrum disorder, with lower figures for convictions, representing a tiny probability for a given individual with a diagnosis of schizophrenia. A consistent finding from this research is that individuals with a diagnosis of schizophrenia are often the victims of violent crime—at least 14 times more often than they are perpetrators, with 4.3% having been victims in a one-month period. Another consistent finding is a link to substance misuse, particularly alcohol, among the minority who commit violent acts.

The occurrence of psychosis in schizophrenia has also been linked to a higher risk of violent acts. Findings on the specific role of delusions or hallucinations are inconsistent, but have included a focus on delusional jealousy and perception of threat or command hallucinations. It has also been proposed that there is a type of individual with schizophrenia characterized by a history of educational difficulties, low IQ, conduct disorder, early-onset substance misuse and offending prior to diagnosis. Violence by or against individuals with schizophrenia typically occurs in the context of complex social interactions (including in atmosphere of mutually high "expressed emotion") within a family setting, as well as being an issue in healthcare settings and the wider community.

Alternative approaches

An approach broadly known as the anti-psychiatry movement, notably most active in the 1960s, has opposed the orthodox medical view of schizophrenia as an illness.

Psychiatrist Thomas Szasz has argued that psychiatric patients are not ill but are just individuals with unconventional thoughts and behavior that make society uncomfortable. He argues that society unjustly seeks to control such individuals by classifying their behavior as an illness and forcibly treating them as a method of social control. According to this view, "schizophrenia" does not actually exist but is merely a form of social constructionism, created by society's concept of what constitutes normality and abnormality. It is worth noting that Szasz has never considered himself to be "anti-psychiatry" in the sense of being against psychiatric treatment, but simply believes that it should be conducted between consenting adults, rather than imposed upon anyone against his or her will.

Similarly, psychiatrists R. D. Laing, Silvano Arieti, Theodore Lidz and presently Colin Ross have argued that the symptoms of what is normally called mental illness are comprehensible reactions to impossible demands that society and particularly family life places on some sensitive individuals. Laing, Arieti, Lidz and Ross were revolutionary in valuing the content of psychotic experience as worthy of interpretation, rather than considering it simply as a secondary but essentially meaningless marker of underlying psychological or neurological distress. Laing's work, co-authored with Aaron Esterson, Sanity, Madness and the Family (1964) described eleven case studies of people diagnosed with schizophrenia and argued that the content of their actions and statements was meaningful and logical in the context of their family and life situations. Arieti's Interpretation of Schizophrenia won the 1975 scientific National Book Award in the United States. In the books Schizophrenia and the Family and The Origin and Treatment of Schizophrenic Disorders Lidz and his colleagues explain their belief that parental behaviour can result in mental illness in children.

The Soteria model is an alternative treatment to institutionalization and early use of antipsychotics. It is described as a milieu-therapeutic recovery method, characterized by its founder as "the 24 hour a day application of interpersonal phenomenologic interventions by a nonprofessional staff, usually without neuroleptic drug treatment, in the context of a small, homelike, quiet, supportive, protective, and tolerant social environment." More recent adaptions of this model sometimes employ professional staff. The houses Soteria patients are admitted to are called Soteria houses, sometimes viewed as early intervention or crisis resolution services based on a supportive recovery model.

In the 1976 book The Origin of Consciousness in the Breakdown of the Bicameral Mind, psychologist Julian Jaynes proposed that until the beginning of historic times, schizophrenia or a similar condition was the normal state of human consciousness. This would take the form of a "bicameral mind" where a normal state of low affect, suitable for routine activities, would be interrupted in moments of crisis by "mysterious voices" giving instructions, which early people characterized as interventions from the gods. This theory was briefly controversial. Continuing research has failed to either further confirm or refute the thesis.

Psychiatrist Tim Crow argued in a 1997 paper that schizophrenia may be the evolutionary price we pay for a left brain hemisphere specialization for language. Since psychosis is associated with greater levels of right brain hemisphere activation and a reduction in the usual left brain hemisphere dominance, our language abilities may have evolved at the cost of causing schizophrenia when this system breaks down.

Researchers into shamanism have speculated that in some cultures schizophrenia or related conditions may predispose an individual to becoming a shaman. Certainly, the experience of having access to multiple realities is not uncommon in schizophrenia, and is a core experience in many shamanic traditions. Equally, the shaman may have the skill to bring on and direct some of the altered states of consciousness psychiatrists label as illness. Psychohistorians, on the other hand, accept the psychiatric diagnoses. However, unlike the current medical model of mental disorders they argue that poor parenting in tribal societies causes the shaman’s schizoid personalities. Speculations regarding primary and important religious figures as having schizophrenia abound. Commentators such as Paul Kurtz and others have endorsed the idea that major religious figures experienced psychosis, heard voices and displayed delusions of grandeur.

Alternative medicine tends to hold the view that schizophrenia is primarily caused by imbalances in the body's reserves and absorption of dietary minerals, vitamins, fats, and/or the presence of excessive levels of toxic heavy metals. The body's adverse reactions to gluten are also strongly implicated in some alternative theories (see gluten-free, casein-free diet). Although this theory is generally deemed to be unproven, it is worth noting that it was positively discussed in the Lancet in 1970, the British Medical Journal in 1973, and other publications. A recent literature by scientists at Johns Hopkins University confirms some of these findings. The branch of alternative medicine that deals with these views regarding the cause of schizophrenia, is known as orthomolecular psychiatry. Hoffer and Walker, in their book Orthomolecular Nutrition (Keats Publishing, 1978), argue that schizophrenia can be treated effectively with doses of Vitamin B-3 (Niacin).

An additional approach is suggested by the work of Richard Bandler who argues that "The usual difference between someone who hallucinates and someone who visualizes normally, is that the person who hallucinates doesn't know he's doing it or doesn't have any choice about it." (Time for a Change, p107). He suggests that because visualization is a sophisticated mental capability, schizophrenia is a skill, albeit an involuntary and dysfunctional one that is being used but not controlled. He therefore suggests that a significant route to treating schizophrenia might be to teach the missing skill — how to distinguish created reality from consensus external reality, to reduce its maladaptive impact, and ultimately how to exercise appropriate control over the vizualization or auditory process. Hypnotic approaches have been explored by the physician Milton H. Erickson as a means of facilitating this.

Accounts in literature

The book and film A Beautiful Mind chronicled the life of John Forbes Nash, a Nobel-Prize-winning mathematician who was diagnosed with schizophrenia. The Marathi film Devrai (Featuring Atul Kulkarni) is a presentation of a patient with schizophrenia. The film, set in the Konkan region of Maharashtra in Western India, shows the behavior, mentality, and struggle of the patient as well as his loved-ones. It also portrays the treatment of this mental illness using medication, dedication and lots of patience of the close relatives of the patient.

In Bulgakov's Master and Margarita the poet Ivan Bezdomnyj is institutionalized and diagnosed with schizophrenia after witnessing the devil (Woland) predict Berlioz's death. The book The Eden Express by Mark Vonnegut accounts his struggle into schizophrenia and his journey back to sanity.

Notes

1. ^ Castle E, Wessely S, Der G, Murray RM (1991). "The incidence of operationally defined schizophrenia in Camberwell 1965–84," British Journal of Psychiatry 159: 790–794.
2. Bhugra, D. (2005). The global prevalence of schizophrenia. PLoS Medicine, 2 (5), 372–373
3. ^ Goldner EM, Hsu L, Waraich P, Somers JM (2002). Prevalence and incidence studies of schizophrenic disorders: a systematic review of the literature. Canadian Journal of Psychiatry, 47(9), 833–43. PMID 12500753
4. Liddell & Scott (1980). Greek-English Lexicon, Abridged Edition. Oxford University Press, Oxford, UK. ISBN 0-19-910207-4.
5. Evans, K., McGrath, J., & Milns, R. (2003). Searching for schizophrenia in ancient Greek and Roman literature: a systematic review. Acta Psychiatrica Scandanavica, 107(5), 323–330. PMID 12752027
6. Kraepelin, E. (1907) Text book of psychiatry (7th ed) (trans. A.R. Diefendorf). London: Macmillan.
7. "Conditions in Occupational Therapy: effect on occupational performance." ed. Ruth A. Hansen and Ben Atchison (Baltimore: Lippincott Williams & Williams, 2000), 54–74. ISBN 0-683-30417-8
8. Stotz-Ingenlath G. (2000). Epistemological aspects of Eugen Bleuler's conception of schizophrenia in 1911. Medicine, Health Care, and Philosophy, 3(2), 153–9. PMID 11079343
9. Turner, T. (1999) 'Schizophrenia'. In G.E. Berrios and R. Porter (eds) A History of Clinical Psychiatry. London: Athlone Press. ISBN 0-485-24211-7
10. Allen GE. (1997). The social and economic origins of genetic determinism: a case history of the American Eugenics Movement, 1900–1940 and its lessons for today. Genetica, 99, 77–88. PMID 9463076
11. Read, J., Masson, J. (2004) Genetics, eugenics and mass murder. In J. Read, L.R. Mosher, R.P. Bentall (eds) Models of Madness: Psychological, Social and Biological Approaches to Schizophrenia. ISBN 1-58391-906-6
12. Wing JK (1971) International comparisons in the study of the functional psychoses. British Medical Bulletin, 27 (1), 77-81. PMID 4926366
13. Wilson M. (1993) DSM-III and the transformation of American psychiatry: a history. American Journal of Psychiatry, 150 (3), 399-410.
14. American Psychiatric Association (2000) Diagnostic and Statistical Manual of Mental Disorders, 4th Edition TR Washington, DC: American Psychiatric Association.
15. ^ Sadock & Sadock, p. 472
16. ^ Sadock & Sadock, pp. 490–491.
17. Freeman D, Garety PA, Kuipers E, Fowler D, Bebbington PE, Dunn G. (2007) Acting on persecutory delusions: the importance of safety seeking. Behaviour Research and Therapy, 45 (1), 89-99. PMID 16530161
18. Addington J, Cadenhead KS, Cannon TD, Cornblatt B, McGlashan TH, Perkins DO, Seidman LJ, Tsuang M, Walker EF, Woods SW, Heinssen R. (2007) North american prodrome longitudinal study: a collaborative multisite approach to prodromal schizophrenia research. Schizophrenia Bulletin, 33 (3), 665-72. PMID 17255119
19. Parnas J, Jorgensen A. (1989) Pre-morbid psychopathology in schizophrenia spectrum. British Journal of Psychiatry, 155, 623-7.
20. Amminger GP, Leicester S, Yung AR, Phillips LJ, Berger GE, Francey SM, Yuen HP, McGorry PD. (2006) Early-onset of symptoms predicts conversion to non-affective psychosis in ultra-high risk individuals. Schizophrenia Research, 84 (1), 67-76. PMID 16677803
21. Schneider, K. (1959) Clinical Psychopathology. New York: Grune and Stratton.
22. Bertelsen, A. (2002). Schizophrenia and Related Disorders: Experience with Current Diagnostic Systems. Psychopathology, 35, 89–93. PMID 12145490
23. Jakobsen KD, Frederiksen JN, Hansen T, Jansson LB, Parnas J, Werge T. (2005) Reliability of clinical ICD-10 schizophrenia diagnoses. Nordic Journal of Psychiatry, 59 (3), 209-12. PMID 16195122
24. BehaveNet® Clinical Capsule™: DSM-IV & DSM-IV-TR, Schizophrenia. Behavenet.com, Retrieved on 2007-05-17.
25. Pope H.G. (1983) Distinguishing bipolar disorder from schizophrenia in clinical practice: guidelines and case reports. Hospital and Community Psychiatry, 34: 322–328.
26. McGlashan T.H. (1987) Testing DSM-III symptom criteria for schizotypal and borderline personality disorders. Archives of General Psychiatry, 44: 15–22.
27. Bentall RP (1992) Reconstructing Schizophrenia. London: Routledge. ISBN 0415075246
28. Boyle M. (2002) Schizophrenia: A Scientific Delusion?. London: Routledge. ISBN 0415227186
29. Verdoux, H., & van Os, J. (2002). Psychotic symptoms in non-clinical populations and the continuum of psychosis. Schizophrenia Research, 54(1–2), 59–65. PMID 11853979
30. LC, van Os J. (2001). The continuity of psychotic experiences in the general population. Clinical Psychology Review, 21 (8),1125–41. PMID 11702510
31. E.R. Peters, S. Day, J. McKenna, G. Orbach (2005). Measuring delusional ideation: the 21-item Peters et al. Delusions Inventory (PDI). Schizophrenia Bulletin, 30, 1005–22. PMID 15954204
32. Johns LC, van Os J. (2001) The continuity of psychotic experiences in the general population. Clinical Psychology Review, 21 (8), 1125-41. PMID 11702510.
33. David, A.S. (1999) On the impossibility of defining delusions. Philosophy, Psychiatry and Psychology, 6 (1), 17-20
34. Tsuang, M. T., Stone, W. S., & Faraone, S. V. (2000). Toward reformulating the diagnosis of schizophrenia. American Journal of Psychiatry, 157(7), 1041–1050. PMID 10873908
35. Rosenhan, D (1973). On being sane in insane places. Science, 179, 250-8. PMID 4683124Full text as PDF
36. McGorry PD, Mihalopoulos C, Henry L, Dakis J, Jackson HJ, Flaum M, Harrigan S, McKenzie D, Kulkarni J, Karoly R. (1995). Spurious precision: procedural validity of diagnostic assessment in psychotic disorders. American Journal of Psychiatry, 152 (2), 220–3. PMID 7840355
37. Read, J. (2004) Does 'schizophrenia' exist? Reliability and validity. In J. Read, L.R. Mosher, R.P. Bentall (eds) Models of Madness: Psychological, Social and Biological Approaches to Schizophrenia. ISBN 1-58391-906-6
38. Sato, M. (2004). Renaming schizophrenia: a Japanese perspective. World Psychiatry, 5(1), 53–5. PMID 16757998
39. Schizophrenia term use 'invalid'. BBC News Online, (9 October 2006). Retrieved on 2007-05-16.
40. Green MF (2001) Schizophrenia Revealed: From Neurons to Social Interactions. New York: W.W. Norton. ISBN 0393703347
41. Wilkinson G. (1986) Political dissent and "sluggish" schizophrenia in the Soviet Union. Br Med J (Clin Res Ed), 293(6548), 641-2. PMID 3092963
42. Lyons, D. (2001). Soviet-style psychiatry is alive and well in the People's Republic. British Journal of Psychiatry, 178, 380-381. PMID 11282823
43. Sadock & Sadock, p. 473
44. Ustun TB, Rehm J, Chatterji S, Saxena S, Trotter R, Room R, Bickenbach J, and the WHO/NIH Joint Project CAR Study Group (1999). Multiple-informant ranking of the disabling effects of different health conditions in 14 countries. The Lancet, 354(9173), 111–115. PMID 10408486
45. Van Os J. (2004). Does the urban environment cause psychosis? British Journal of Psychiatry, 184 (4), 287–288. PMID 15056569
46. Meyer-Lindenberg A, Miletich RS, Kohn PD, et al (2002). Reduced prefrontal activity predicts exaggerated striatal dopaminergic function in schizophrenia. Nature Neuroscience, 5, 267–71. PMID 11865311
47. ^ Harrison PJ, Owen MJ. (2003). Genes for schizophrenia? Recent findings and their pathophysiological implications. Lancet, 361(9355), 417–9. PMID 12573388
48. Sadock & Sadock. p477
49. ^ Sadock & Sadock. p123
50. Day R, Nielsen JA, Korten A, Ernberg G, et al (1987). Stressful life events preceding the acute onset of schizophrenia: a cross-national study from the World Health Organization. Culture, Medicine and Psychiatry, 11 (2), 123–205. PMID 3595169
51. ^ Owen MJ, Craddock N, O'Donovan MC. (2005). Schizophrenia: genes at last? Trends in Genetics, 21(9), 518–25. PMID 16009449
52. Riley B, Kendler KS (2006). Molecular genetic studies of schizophrenia. Eur J Hum Genet, 14 (6), 669–80. PMID 16721403
53. van Os J, Krabbendam L, Myin-Germeys I, Delespaul P (2005) The schizophrenia envirome. Current Opinion in Psychiatry, 18 (2), 141-5.
54. Selten JP, Cantor-Graae E, Kahn RS. (2007) Migration and schizophrenia. Current Opininion in Psychiatry, 20 (2), 111-5. PMID 17278906
55. Schenkel LS, Spaulding WD, Dilillo D, Silverstein SM (2005). Histories of childhood maltreatment in schizophrenia: Relationships with premorbid functioning, symptomatology, and cognitive deficits. Schizophrenia Research, 76(2–3), 273–286. PMID 15949659
56. Janssen I, Krabbendam L, Bak M, Hanssen M, et al (2004). Childhood abuse as a risk factor for psychotic experiences. Acta Psychiatrica Scandinavica, 109, 38–45. PMID 14674957
57. Davies G, Welham J, Chant D, Torrey EF, McGrath J. (2003). A systematic review and meta-analysis of Northern Hemisphere season of birth studies in schizophrenia. Schizophrenia Bulletin, 29 (3), 587–93. PMID 14609251
58. Brown, A.S. (2006). Prenatal infection as a risk factor for schizophrenia. Schizophrenia Bulletin, 32 (2), 200–2. PMID 16469941
59. Gregg L, Barrowclough C, Haddock G. (2007) Reasons for increased substance use in psychosis. Clinical Psychology Review, 27 (4), 494-510. PMID 17240501
60. Laruelle, M., Abi-Dargham, A., Van-Dyck, C. H., et al (1996) Single photon emission computerized tomography imaging of amphetamine-induced dopamine release in drug-free schizophrenic subjects. Proceedings of the National Academy of Sciences of the USA, 93, 9235-9240. PMID 8799184.
61. Mueser KT, Yarnold PR, Levinson DF, et al (1990). Prevalence of substance abuse in schizophrenia: demographic and clinical correlates. Schizophrenic Bulletin, 16(1), 31–56. PMID 2333480
62. Arseneault L, Cannon M, Witton J, Murray RM (2004). Causal association between cannabis and psychosis: examination of the evidence. British Journal of Psychiatry, 184, 110-7. PMID 14754822 Full text
63. Johnstone EC, Crow TJ, Frith CD, Husband J, Kreel L. (1976). Cerebral ventricular size and cognitive impairment in chronic schizophrenia. Lancet, 30;2 (7992), 924–6. PMID 62160
64. Flashman LA, Green MF (2004). Review of cognition and brain structure in schizophrenia: profiles, longitudinal course, and effects of treatment. Psychiatric Clinics of North America, 27 (1), 1–18, vii. PMID 15062627
65. Green, M.F. (2001) Schizophrenia Revealed: From Neurons to Social Interactions. New York: W.W. Norton. ISBN 0-393-70334-7
66. Green MF. (2006) Cognitive impairment and functional outcome in schizophrenia and bipolar disorder. Journal of Clinical Psychiatry, 67, Suppl 9, 3-8. PMID 16965182
67. Jones HM, Pilowsky LS (2002) Dopamine and antipsychotic drug action revisited. British Journal of Psychiatry, 181, 271-275. PMID 12356650
68. Konradi C, Heckers S. (2003). Molecular aspects of glutamate dysregulation: implications for schizophrenia and its treatment. Pharmacology and Therapeutics, 97(2), 153–79. PMID 12559388
69. Lahti AC, Weiler MA, Tamara Michaelidis BA, Parwani A, Tamminga CA. (2001). Effects of ketamine in normal and schizophrenic volunteers. Neuropsychopharmacology, 25(4), 455–67. PMID 11557159
70. Coyle JT, Tsai G, Goff D. (2003). Converging evidence of NMDA receptor hypofunction in the pathophysiology of schizophrenia. Annals of the New York Academy of Sciences, 1003, 318–27. PMID 14684455
71. Tuominen HJ, Tiihonen J, Wahlbeck K. (2005). Glutamatergic drugs for schizophrenia: a systematic review and meta-analysis. Schizophr Res, 72:225–34. PMID 15560967
72. ^ van Os J, Burns T, Cavallaro R, et al (2006). Standardized remission criteria in schizophrenia. Acta Psychiatrica Scandinavica, 113(2), 91–5. PMID 16423159
73. Kay SR, Fiszbein A, Opler LA (1987). The positive and negative syndrome scale (PANSS) for schizophrenia. Schizophrenia Bulletin, 13(2), 261–76. PMID 3616518
74. Turner T. (2007). "Unlocking psychosis". Brit J Med. 334 (suppl): s7.
75. The Royal College of Psychiatrists & The British Psychological Society (2003). Schizophrenia. Full national clinical guideline on core interventions in primary and secondary care (PDF). London: Gaskell and the British Psychological Society. Retrieved on 2007-05-17.
76. Lieberman JA, Stroup TS, McEvoy JP, Swartz MS, Rosenheck RA, Perkins DO, Keefe RS, Davis SM, Davis CE, Lebowitz BD, Severe J, Hsiao JK, Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) Investigators. (2005). Effectiveness of antipsychotic drugs in patients with chronic schizophrenia. The New England Journal of Medicine, 353 (12), 1209–23. PMID 16172203
77. Ananth J, Parameswaran S, Gunatilake S, Burgoyne K, Sidhom T. (2004) Neuroleptic malignant syndrome and atypical antipsychotic drugs. Journal of Clinical Psychiatry, 65 (4), 464-70. PMID 15119907
78. Leucht S, Wahlbeck K, Hamann J, Kissling W (2003). New generation antipsychotics versus low-potency conventional antipsychotics: a systematic review and meta-analysis. The Lancet, 361(9369), 1581–9. PMID 12747876
79. Peet M, Stokes C (2005). Omega-3 fatty acids in the treatment of psychiatric disorders. Drugs, 65(8), 1051–9. PMID 15907142
80. Moran, M (2005). Psychosocial Treatment Often Missing From Schizophrenia Regimens. Psychiatr News November 18 2005, Volume 40, Number 22, page 24. Retrieved on 2007-05-17.
81. Sadock & Sadock, p. 1148
82. McFarlane WR, Dixon L, Lukens E, Lucksted A (2003). Family psychoeducation and schizophrenia: a review of the literature. J Marital Fam Ther. Apr;29(2):223–45. PMID 12728780
83. Glynn SM, Cohen AN, Niv N (2007). New challenges in family interventions for schizophrenia. Expert Rev Neurother. Jan;7(1):33–43. PMID 17187495
84. Cormac I, Jones C, Campbell C (2002). Cognitive behaviour therapy for schizophrenia. Cochrane Database of systematic reviews, (1), CD000524. PMID 11869579
85. Zimmermann G, Favrod J, Trieu VH, Pomini V (2005). The effect of cognitive behavioral treatment on the positive symptoms of schizophrenia spectrum disorders: a meta-analysis. Schizophrenia Research, 77, 1–9. PMID 16005380
86. Kopelowicz A, Liberman RP, Zarate R (2006). Recent advances in social skills training for schizophrenia. Schizophr Bull. 2006 Oct;32 Suppl 1:S12–23. PMID 16885207
87. Wykes T, Brammer M, Mellers J, et al (2002). Effects on the brain of a psychological treatment: cognitive remediation therapy: functional magnetic resonance imaging in schizophrenia. British Journal of Psychiatry, 181, 144–52. PMID 12151286
88. Hogarty GE, Flesher S, Ulrich R, Carter M, et al (2004). Cognitive enhancement therapy for schizophrenia: effects of a 2-year randomized trial on cognition and behavior. Arch Gen Psychiatry. Sep;61(9):866–76.PMID 15351765
89. Talwar N, Crawford MJ, Maratos A, Nur U, McDermott O, Procter S (2006). Music therapy for in-patients with schizophrenia: Exploratory randomised controlled trial. The British Journal of Psychiatry. Nov;189:405–9. PMID 17077429 Full text available. "Music therapy may provide a means of improving mental health among people with schizophrenia, but its effects in acute psychoses have not been explored."
90. Burton, R. The Anatomy of Melancholy. Project Gutenberg, Retrieved on 2007-05-17. Cf. especially subsection 3, on and after line 3480, "Music a Remedy".
91. McGurk, SR, Mueser KT, Feldman K, Wolfe R, Pascaris A (2007). Cognitive training for supported employment: 2–3 year outcomes of a randomized controlled trial. Am J Psychiatry. Mar;164(3):437–41. PMID 17329468
92. Goering P, Durbin J, Sheldon CT, Ochocka J, Nelson G, Krupa T. Who uses consumer-run self-help organizations? American Journal of Orthopsychiatry, 76 (3), 367-73. PMID 16981815
93. Kulhara P (1994). Outcome of schizophrenia: some transcultural observations with particular reference to developing countries. European Archives of Psychiatry and Clinical Neuroscience, 244(5), 227–35. PMID 7893767
94. Becker T, Kilian R. (2006) Psychiatric services for people with severe mental illness across western Europe: what can be generalized from current knowledge about differences in provision, costs and outcomes of mental health care? Acta Psychiatrica Scandinavica Supplement, 429, 9-16. PMID 16445476
95. Harding CM, Brooks GW, Ashikaga T, Strauss JS, Breier A (1987). The Vermont longitudinal study of persons with severe mental illness, II: Long-term outcome of subjects who retrospectively met DSM-III criteria for schizophrenia. American Journal of Psychiatry, 144(6), 727–35. PMID 3591992
96. Robinson DG, Woerner MG, McMeniman M, Mendelowitz A, Bilder RM (2004). Symptomatic and functional recovery from a first episode of schizophrenia or schizoaffective disorder. American Journal of Psychiatry, 161, 473–479. PMID 14992973
97. Hopper K, Wanderling J (2000). Revisiting the developed versus developing country distinction in course and outcome in schizophrenia: results from ISoS, the WHO collaborative followup project. International Study of Schizophrenia. Schizophrenia Bulletin, 26 (4), 835–46. PMID 11087016
98. Sadock & Sadock, p. 485
99. Bebbington PE, Kuipers E (1994). The predictive utility of expressed emotion in schizophrenia: an aggregate analysis. Psychological Medicine, 24, 707–718. PMID 7991753
100. Hannerz H, Borga P, Borritz M (2001). Life expectancies for individuals with psychiatric diagnoses. Public Health, 115 (5), 328–37. PMID 11593442
101. Radomsky ED, Haas GL, Mann JJ, Sweeney JA (1999). Suicidal behavior in patients with schizophrenia and other psychotic disorders. American Journal of Psychiatry, 156(10), 1590–5. PMID 10518171
102. Caldwell CB, Gottesman II. (1990). Schizophrenics kill themselves too: a review of risk factors for suicide. Schizophrenia Bulletin, 16(4), 571–89. PMID 2077636
103. Pescosolido BA, Monahan J, Link BG, Stueve A, Kikuzawa S (1999). The public's view of the competence, dangerousness, and need for legal coercion of persons with mental health problems. American Journal of Public Health. Sep;89(9):1339–45. PMID 10474550
104. ^ Walsh E, Buchanan A, Fahy T (2002). Violence and schizophrenia: examining the evidence. British Journal of Psychiatry. 2002 Jun;180:490–5. PMID 12042226
105. ^ Stuart, H (2003). Violence and mental illness: an overview. World Psychiatry. June; 2(2): 121–124. PMID 16946914 Full text, Retrieved on 2007-05-17.
106. Steadman HJ, Mulvey EP, Monahan J, et al (1998). Violence by people discharged from acute psychiatric inpatient facilities and by others in the same neighborhoods. Archives of General Psychiatry. May;55(5):393–401. PMID 9596041
107. Swanson JW, Swartz MS, Van Dorn RA, Elbogen EB, et al (2006). A national study of violent behavior in persons with schizophrenia. Archives of General Psychiatry. May;63(5):490–9. PMID 16651506
108. ^ Mullen PE (2006). Schizophrenia and violence: from correlations to preventive strategies. Advances in Psychiatric Treatment 12: 239–248. Full text available, Retrieved on 2007-05-17.
109. Simpson AI, McKenna B, Moskowitz A, Skipworth J, Barry-Walsh J (2004). Homicide and mental illness in New Zealand, 1970–2000. British Journal of Psychiatry, 185, 394–8. PMID 15516547
110. Fazel S, Grann M (2004). Psychiatric morbidity among homicide offenders: a Swedish population study. American Journal of Psychiatry, 161(11), 2129–31. PMID 15514419
111. Brekke JS, Prindle C, Bae SW, Long JD (2001). Risks for individuals with schizophrenia who are living in the community. Psychiatric Services. Oct;52(10):1358–66. PMID 11585953
112. Fitzgerald PB, de Castella AR, Filia KM, Filia SL, Benitez J, Kulkarni J (2005). Victimization of patients with schizophrenia and related disorders. Australia and New Zealand Journal of Psychiatry, 39(3), 169-74. (1), 187–9. PMID 15701066
113. Walsh E, Gilvarry C, Samele C, et al (2004). Predicting violence in schizophrenia: a prospective study. Schizophrenia Research, 67(2–3), 247-52. PMID 14984884
114. Solomon PL, Cavanaugh MM, Gelles RJ (2005). Family Violence among Adults with Severe Mental Illness. Trauma, Violence, & Abuse, Vol. 6, No. 1, 40–54. PMID 15574672Full text available.
115. Chou KR, Lu RB, Chang M (2001). Assaultive behavior by psychiatric in-patients and its related factors. Journal of Nursing Research. Dec;9(5):139–51. PMID 11779087
116. Logdberg B, Nilsson LL, Levander MT, Levander S (2004). Schizophrenia, neighbourhood, and crime. Acta Psychiatrica Scandinavica, 110(2) Page 92. PMID 15233709 Full text available, Retrieved on 2007-05-16
117. Cooper D. (1969) The Dialectics of Liberation. London: Penguin Books Ltd. ISBN 0140210296
118. Szasz T. (1984) The Myth of Mental Illness: Foundations of a Theory of Personal Contact (revised edition. New York: Harper and Row. ISBN 0060911514
119. Colin, Ross (2004). Schizophrenia: Innovations in Diagnosis and Treatment. Haworth Press. ISBN 0789022699.
120. Mosher, L. R. (1999). "Soteria and Other Alternatives to Acute Psychiatric Hospitalization: A Personal and Professional Review." Journal of Nervous and Mental Disease, 187, 142-149.
121. Luc Ciompi, MD, Switzerland: The Soteria-concept. Theoretical bases and practical 13-year experience with a milieu-therapeutic approach of acute schizophrenia
122. Janyes J (1976) The Origin of Consciousness in the Breakdown of the Bicameral Mind. Houghton Mifflin. ISBN 0395207290
123. Crow TJ (1997). Schizophrenia as failure of hemispheric dominance for language. Trends in Neurosciences, 20(8), 339–343. PMID 9246721
124. Polimeni J, Reiss JP (2002). How shamanism and group selection may reveal the origins of schizophrenia. Medical Hypothesis, 58(3), 244–8. PMID 12018978
125. DeMause, Lloyd, "The seven stages of historical personality" in The Emotional Life of Nations (Karnac, 2002). Available at primal-page.com, Retrieved on 2007-05-17.
126. Kurtz, Paul (1986). The Transcendental Temptation: A Critique of Religion and the Paranormal (Prometheus Books) ISBN 0-87975-645-4
127. Dohan FC (1970). Coeliac disease and schizophrenia. Lancet, 1970 April 25;1(7652):897-8. PMID 4191543
128. Dohan FC (1973). Coeliac disease and schizophrenia. British Medical Journal, 3(5870): 51–52. PMID 4740433
129. Dohan FC (1979). Celiac-type diets in schizophrenia. Am J Psychiatry, 1979 May;136(5):732-3. PMID 434265
130. Kalaydjian AE, Eaton W, Cascella N, Fasano A (2006). The gluten connection: the association between schizophrenia and celiac disease. Acta Psychiatr Scand. 2006 Feb;113(2):82–90. PMID 16423158

References

• Sadock BJ, Sadock VA (2003). Kaplan & Sadock's Synopsis of Psychiatry, Ninth Edition. Philadelphia, PA: Lippincott, Williams & Wilkins. ISBN 0-7817-3183-6.

Further reading

• Bentall, R. (2003) Madness explained: Psychosis and Human Nature. London: Penguin Books Ltd. ISBN 0-7139-9249-2
• Boyle, Mary, (1993), Schizophrenia: A Scientific Delusion, Routledge, ISBN 0-415-09700-2
• Deveson, Anne (1991), Tell Me I'm Here. Penguin. ISBN 0-14-027257-7
• Fallon, James H. et al. (2003) The Neuroanatomy of Schizophrenia: Circuitry and Neurotransmitter Systems. Clinical Neuroscience Research 3:77–107. Available at Elsevier article locater.
• Green, M.F. (2001) Schizophrenia Revealed: From Neurons to Social Interactions. New York: W.W. Norton. ISBN 0-393-70334-7
• Jones, S. and Hayward, P. (2004) Coping with Schizophrenia: A Guide for Patients, Families and Caregivers. ISBN 1-85168-344-5
• Keen, T. M. (1999) Schizophrenia: orthodoxy and heresies. A review of alternative possibilities. Journal of Psychiatric and Mental Health Nursing, 1999, 6, 415–424. PMID 10818864Full-text (PDF), Retrieved on 2007-05-17.
• Noll, Richard (2007) The Encyclopedia of Schizophrenia and Other Psychotic Disorders, Third Edition ISBN 0-8160-6405-9
• Read, J., Mosher, L.R., Bentall, R. (2004) Models of Madness: Psychological, Social and Biological Approaches to Schizophrenia. ISBN 1-58391-906-6. A critical approach to biological and genetic theories, and a review of social influences on schizophrenia.
• Shaner, A., Miller, G. F., & Mintz, J. (2004). Schizophrenia as one extreme of a sexually selected fitness indicator. Schizophrenia Research, 70(1), 101–109. PMID 15246469Full text (PDF), Retrieved on 2007-05-17.
• Szasz, T. (1976) Schizophrenia: The Sacred Symbol of Psychiatry. New York: Basic Books. ISBN 0-465-07222-4
• Tausk, V. : "Sexuality, War, and Schizophrenia: Collected Psychoanalytic Papers", Publisher: Transaction Publishers 1991, ISBN 0-88738-365-3 (On the Origin of the 'Influencing Machine' in Schizophrenia.)
• Torrey, E.F., M.D. (2006) Surviving Schizophrenia: A Manual for Families, Consumers, and Providers (5th Edition). Quill (HarperCollins Publishers) ISBN 0-06-084259-8
• Wiencke, Markus (2006) Schizophrenie als Ergebnis von Wechselwirkungen: Georg Simmels Individualitätskonzept in der Klinischen Psychologie. In David Kim (ed.), Georg Simmel in Translation: Interdisciplinary Border-Crossings in Culture and Modernity (pp. 123–155). Cambridge Scholars Press, Cambridge, ISBN 1-84718-060-5

External links

• Template:Dmoz
• Template:Dmoz — Support Groups
• Template:Dmoz — Articles and research

News, information and further description

• DSM V scholarly debates on schizophrenia
• NPR: the sight and sounds of schizophrenia
• National Mental Health Association fact sheet on schizophrenia
• Understanding Schizophrenia - A factsheet from the mental health charity Mind
• World Health Organisation data on schizophrenia from 'The World Health Report 2001. Mental Health: New Understanding, New Hope'
• National Institute of Mental Health (USA) Schizophrenia information
• The current World Health Organisation definition of Schizophrenia
• Schizophrenia in history
• Symptoms in Schizophrenia Film made in 1940 showing some of the symptoms of Schizophrenia.
• Open The Doors - information on global programme to fight stigma and discrimination because of Schizophrenia. The World Psychiatric Association (WPA)
• Scientific American Magazine (January 2004 Issue) Decoding Schizophrenia
• Symptoms, causes and treatment of schizophrenia

Critical approaches to schizophrenia

• Bola, John R., Ph.D.; & Mosher, Loren R., M.D. (2003). Treatment of Acute Psychosis Without Neuroleptics: Two-Year Outcomes From the Soteria Project. The Journal of Nervous and Mental Disease, (191: 219–229). Available as PDF.
• Leo, Jonathan Ph.D., & Jay Joseph, Psy. D. Schizophrenia: Medical students are taught it's all in the genes, but are they hearing the whole story?
• Mosher, Loren M.D. (Chief of the Center for Studies of Schizophrenia at the U.S. National Institute of Mental Health 1969–1980) Still Crazy After All These Years

Template:Link FA Template:Link FA

• Schizophrenia
• Disability
• Mental illness diagnosis by DSM and ICD