Schizophrenia

For other uses, see Schizophrenia (disambiguation).

Schizophrenia (/sktsfrni/ or /sktsfrini/) is a
mental disorder often characterized by abnormal social
behavior and failure to recognize what is real. Common symptoms include false beliefs, unclear or confused
thinking, auditory hallucinations, reduced social engagement and emotional expression, and inactivity. Diagnosis
is based on observed behavior and the persons reported
experiences.
Genetics and early environment, as well as psychological
and social processes, appear to be important contributory factors. Some recreational and prescription drugs
appear to cause or worsen symptoms. The many possible
combinations of symptoms have triggered debate about
whether the diagnosis represents a single disorder or a
number of separate syndromes. Despite the origin of the
term from the Greek roots skhizein (to split) and phrn
(mind), schizophrenia does not imply a split personal- Self-portrait of a person with schizophrenia, representing that inity, or "multiple personality disorder"a condition with dividuals perception of the distorted experience of reality in the
disorder
which it is often confused in public perception.[1] Rather,
the term means a splitting of mental functions, reecting the presentation of the illness.[2]

1 Symptoms

The mainstay of treatment is antipsychotic medication,

which primarily suppresses dopamine receptor activity.
Counseling, job training and social rehabilitation are also
important in treatment. In more serious caseswhere
there is risk to self or othersinvoluntary hospitalization
may be necessary, although hospital stays are now shorter
and less frequent than they once were.[3]

Individuals with schizophrenia may experience

hallucinations (most reported are hearing voices),
delusions (often bizarre or persecutory in nature),
and disorganized thinking and speech. The last may
range from loss of train of thought, to sentences only
loosely connected in meaning, to speech that is not
understandable known as word salad in severe cases.
Social withdrawal, sloppiness of dress and hygiene,
and loss of motivation and judgment are all common in schizophrenia.[8] There is often an observable
pattern of emotional diculty, for example lack of
responsiveness.[9] Impairment in social cognition is
associated with schizophrenia,[10] as are symptoms
of paranoia. Social isolation commonly occurs.[11]
Diculties in working and long-term memory, attention,
executive functioning, and speed of processing also
commonly occur.[4] In one uncommon subtype, the
person may be largely mute, remain motionless in
bizarre postures, or exhibit purposeless agitation, all
signs of catatonia.[12] About 30 to 50% of people with
schizophrenia fail to accept that they have an illness or
their recommended treatment.[13] Treatment may have
some eect on insight.[14] People with schizophrenia
often nd facial emotion perception to be dicult.[15]

Symptoms begin typically in young adulthood, and about

0.30.7% of people are aected during their lifetime.[4]
The disorder is thought to mainly aect the ability to
think, but it also usually contributes to chronic problems
with behavior and emotion. People with schizophrenia
are likely to have additional conditions, including major
depression and anxiety disorders; the lifetime occurrence
of substance use disorder is almost 50%.[5] Social problems, such as long-term unemployment, poverty, and
homelessness are common. The average life expectancy
of people with the disorder is ten to twenty ve years less
than the average life expectancy.[6] This is the result of
increased physical health problems and a higher suicide
rate (about 5%).[4][7]

1.1

Positive and negative

Schizophrenia is often described in terms of positive

and negative (or decit) symptoms.[16] Positive symptoms are those that most individuals do not normally
experience but are present in people with schizophrenia. They can include delusions, disordered thoughts
and speech, and tactile, auditory, visual, olfactory and
gustatory hallucinations, typically regarded as manifestations of psychosis.[17] Hallucinations are also typically
related to the content of the delusional theme.[18] Positive
symptoms generally respond well to medication.[18]

CAUSES

2.1 Genetic
Estimates of heritability vary because of the diculty in
separating the eects of genetics and the environment;[27]
averages of 0.80 have been given.[28] The greatest risk
for developing schizophrenia is having a rst-degree relative with the disease (risk is 6.5%); more than 40% of
monozygotic twins of those with schizophrenia are also
aected.[1] If one parent is aected the risk is about 13%
and if both are aected the risk is nearly 50%.[28]
It is likely that many genes are involved, each of small effect and unknown transmission and expression.[1] Many
possible candidates have been proposed, including specic copy number variations, NOTCH4, and histone protein loci.[29] A number of genome-wide associations such
as zinc nger protein 804A have also been linked.[30]
There appears to be overlap in the genetics of schizophrenia and bipolar disorder.[31] Evidence is emerging that the
genetic architecture of schizophrenia involved both common and rare risk variation.[32]

Negative symptoms are decits of normal emotional responses or of other thought processes, and respond less
well to medication.[8] They commonly include at expressions or little emotion, poverty of speech, inability to experience pleasure, lack of desire to form relationships,
and lack of motivation. Negative symptoms appear to
contribute more to poor quality of life, functional ability,
and the burden on others than do positive symptoms.[19]
People with greater negative symptoms often have a his- Assuming a hereditary basis, one question from
tory of poor adjustment before the onset of illness, and evolutionary psychology is why genes that increase the
response to medication is often limited.[8][20]
likelihood of psychosis evolved, assuming the condition
would have been maladaptive from an evolutionary
point of view. One idea is that genes are involved in
the evolution of language and human nature, but to
date such ideas remain little more than hypothetical in
1.2 Onset
nature.[33][34]
Late adolescence and early adulthood are peak periods
for the onset of schizophrenia,[4] critical years in a young
adults social and vocational development.[21] In 40% of
men and 23% of women diagnosed with schizophrenia, the condition manifested itself before the age of
19.[22] To minimize the developmental disruption associated with schizophrenia, much work has recently
been done to identify and treat the prodromal (pre-onset)
phase of the illness, which has been detected up to 30
months before the onset of symptoms.[21] Those who go
on to develop schizophrenia may experience transient or
self-limiting psychotic symptoms[23] and the non-specic
symptoms of social withdrawal, irritability, dysphoria,[24]
and clumsiness[25] during the prodromal phase.

2.2 Environment
Environmental factors associated with the development
of schizophrenia include the living environment, drug use
and prenatal stressors.[4] Parenting style seems to have no
major eect, although people with supportive parents do
better than those with critical or hostile parents.[1] Childhood trauma, separation from ones families, and being
bullied or abused increase the risk of psychosis.[35] Living in an urban environment during childhood or as an
adult has consistently been found to increase the risk of
schizophrenia by a factor of two,[1][4] even after taking
into account drug use, ethnic group, and size of social
group.[36] Other factors that play an important role include social isolation and immigration related to social
adversity, racial discrimination, family dysfunction, unemployment, and poor housing conditions.[1][37]

Causes
2.2.1 Substance use

Main article: Causes of schizophrenia

A combination of genetic and environmental factors play
a role in the development of schizophrenia.[1][4] People
with a family history of schizophrenia who have a transient psychosis have a 2040% chance of being diagnosed
one year later.[26]

About half of those with schizophrenia use drugs or alcohol excessively.[38] Amphetamine, cocaine, and to a lesser
extent alcohol, can result in psychosis that presents very
similarly to schizophrenia.[1][39] Although it is not generally believed to be a cause of the illness, people with
schizophrenia use nicotine at much greater rates than the
general population.[40]

3.2

Neurological

Alcohol abuse can occasionally cause the development

of a chronic substance-induced psychotic disorder via
a kindling mechanism.[41] Alcohol use is not associated
with an earlier onset of psychosis.[42]
A signicant proportion of people with schizophrenia use
cannabis to help cope with its symptoms.[38] Cannabis can
be a contributory factor in schizophrenia,[43][44][45] but
cannot cause it alone;[45] its use is neither necessary nor
sucient for development of any form of psychosis.[45]
Early exposure of the developing brain to cannabis increases the risk of schizophrenia,[43] although the size
of the increased risk is dicult to quantify;[43][44] only
a small proportion of early cannabis recreational users go
on to develop any schizoaective disorder in adult life,[44]
and the increased risk may require the presence of certain
genes within an individual[45] or may be related to preexisting psychopathology.[43] Higher dosage and greater
frequency of use are indicators of increased risk of
chronic psychoses.[44] Tetrahydrocannabinol (THC) and
cannabidiol (CBD) produce opposing eects; CBD has
antipsychotic and neuroprotective properties and counteracts negative eects of THC.[44]

3
may reect global neurocognitive decits such as memory loss, while others may be related to particular issues
and experiences.[49][50]
Despite a demonstrated appearance of blunted aect, recent ndings indicate that many individuals diagnosed
with schizophrenia are emotionally responsive, particularly to stressful or negative stimuli, and that such
sensitivity may cause vulnerability to symptoms or to
the disorder.[51][52] Some evidence suggests that the
content of delusional beliefs and psychotic experiences
can reect emotional causes of the disorder, and that
how a person interprets such experiences can inuence
symptomatology.[53][54][55] The use of safety behaviors
(acts such as gestures or the use of words in specic contexts) to avoid or neutralize imagined threats may actually contribute to the chronicity of delusions.[56] Further evidence for the role of psychological mechanisms
comes from the eects of psychotherapies on symptoms
of schizophrenia.[57]

3.2 Neurological

Other drugs may be used only as coping mechanisms by

individuals who have schizophrenia to deal with depression, anxiety, boredom, and loneliness.[38][46]
2.2.2

Developmental factors

Factors such as hypoxia and infection, or stress and malnutrition in the mother during fetal development, may result in a slight increase in the risk of schizophrenia later
in life.[4] People diagnosed with schizophrenia are more
likely to have been born in winter or spring (at least in the
northern hemisphere), which may be a result of increased Functional magnetic resonance imaging (fMRI) and other brain
rates of viral exposures in utero.[1] The increased risk is imaging technologies allow for the study of dierences in brain
about 5 to 8%.[47]
activity in people diagnosed with schizophrenia. The image

Mechanisms

Main article: Mechanisms of schizophrenia

A number of attempts have been made to explain the link
between altered brain function and schizophrenia.[4] One
of the most common is the dopamine hypothesis, which
attributes psychosis to the minds faulty interpretation of
the misring of dopaminergic neurons.[4]

3.1

Psychological

Many psychological mechanisms have been implicated

in the development and maintenance of schizophrenia.
Cognitive biases have been identied in those with the
diagnosis or those at risk, especially when under stress
or in confusing situations.[48] Some cognitive features

shows two levels of the brain, with areas that were more active in
healthy controls than in schizophrenia patients shown in orange,
during an fMRI study of working memory.

Schizophrenia is associated with subtle dierences in

brain structures, found in 40 to 50% of cases, and in brain
chemistry during acute psychotic states.[4] Studies using
neuropsychological tests and brain imaging technologies
such as fMRI and PET to examine functional dierences
in brain activity have shown that dierences seem to most
commonly occur in the frontal lobes, hippocampus and
temporal lobes.[58] Reductions in brain volume, smaller
than those found in Alzheimers disease, have been reported in areas of the frontal cortex and temporal lobes.
It is uncertain whether these volumetric changes are progressive or preexist prior to the onset of the disease.[25]
These dierences have been linked to the neurocognitive
decits often associated with schizophrenia.[59] Because
neural circuits are altered, it has alternatively been suggested that schizophrenia should be thought of as a collection of neurodevelopmental disorders.[60] There has been

4 DIAGNOSIS

debate on whether treatment with antipsychotics can itself cause reduction of brain volume.[61]
Particular attention has been paid to the function of
dopamine in the mesolimbic pathway of the brain. This
focus largely resulted from the accidental nding that
phenothiazine drugs, which block dopamine function,
could reduce psychotic symptoms. It is also supported
by the fact that amphetamines, which trigger the release
of dopamine, may exacerbate the psychotic symptoms
in schizophrenia.[62] The inuential dopamine hypothesis of schizophrenia proposed that excessive activation
of D2 receptors was the cause of (the positive symptoms of) schizophrenia. Although postulated for about
20 years based on the D2 blockade eect common to all
antipsychotics, it was not until the mid-1990s that PET
and SPET imaging studies provided supporting evidence.
The dopamine hypothesis is now thought to be simplistic,
partly because newer antipsychotic medication (atypical
antipsychotic medication) can be just as eective as older
medication (typical antipsychotic medication), but also
aects serotonin function and may have slightly less of a
dopamine blocking eect.[63]
Interest has also focused on the neurotransmitter
glutamate and the reduced function of the NMDA
glutamate receptor in schizophrenia, largely because
of the abnormally low levels of glutamate receptors
found in the postmortem brains of those diagnosed
with schizophrenia,[64] and the discovery that glutamateblocking drugs such as phencyclidine and ketamine can
mimic the symptoms and cognitive problems associated
with the condition.[65] Reduced glutamate function is
linked to poor performance on tests requiring frontal
lobe and hippocampal function, and glutamate can aect
dopamine function, both of which have been implicated
in schizophrenia, have suggested an important mediating
(and possibly causal) role of glutamate pathways in the
condition.[66] But positive symptoms fail to respond to
glutamatergic medication.[67]

John Nash, an American mathematician and joint winner of the

1994 Nobel Prize for Economics, who had schizophrenia. His
life was the subject of the 2001 Academy Award-winning lm A
Beautiful Mind.

4.1 Criteria

In 2013, the American Psychiatric Association released

the fth edition of the DSM (DSM-5). To be diagnosed
with schizophrenia, two diagnostic criteria have to be met
over much of the time of a period of at least one month,
with a signicant impact on social or occupational functioning for at least six months. The person had to be
suering from delusions, hallucinations or disorganized
speech. A second symptom could be negative symptoms
4 Diagnosis
or severely disorganized or catatonic behaviour.[69] The
denition of schizophrenia remained essentially the same
as that specied by the 2000 version of DSM (DSM-IVMain article: Diagnosis of schizophrenia
Schizophrenia is diagnosed based on criteria in ei- TR), but DSM-5 makes a number of changes.
ther the American Psychiatric Association's fth edi Subtype classications such as catatonic and
tion of the Diagnostic and Statistical Manual of Menparanoid schizophrenia are removed. These were
tal Disorders (DSM 5), or the World Health Organizaretained in previous revisions largely for reasons of
tion's International Statistical Classication of Diseases
tradition, but had subsequently proved to be of little
and Related Health Problems (ICD-10). These criteria
worth.[70]
use the self-reported experiences of the person and reported abnormalities in behavior, followed by a clinical
Catatonia is no longer so strongly associated with
assessment by a mental health professional. Symptoms
schizophrenia.[71]
associated with schizophrenia occur along a continuum
In describing a persons schizophrenia, it is recin the population and must reach a certain severity before
ommended that a better distinction be made bea diagnosis is made.[1] As of 2013 there is no objective
test.[68]
tween the current state of the condition and its

4.3

Dierential diagnosis
historical progress, to achieve a clearer overall
characterization.[70]

Special treatment of Schneiders rst-rank symptoms is no longer recommended.[70]

Schizoaective disorder is better dened to demarcate it more cleanly from schizophrenia.[70]

5
Undierentiated 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)

An assessment covering eight domains of

psychopathology such as whether hallucina- The ICD-10 denes two additional subtypes:[75]
tion or mania is experienced is recommended to
help clinical decision-making.[72]
Post-schizophrenic depression:
A depressive
episode arising in the aftermath of a schizophrenic
The ICD-10 criteria are typically used in European counillness where some low-level schizophrenic symptries, while the DSM criteria are used in the United States
toms may still be present. (ICD code F20.4)
and to varying degrees around the world, and are prevailing in research studies. The ICD-10 criteria put more
Simple schizophrenia: Insidious and progressive deemphasis on Schneiderian rst-rank symptoms. In pracvelopment of prominent negative symptoms with no
tice, agreement between the two systems is high.[73]
history of psychotic episodes. (ICD code F20.6)
If signs of disturbance are present for more than
a month but less than six months, the diagnosis of
schizophreniform disorder is applied. Psychotic symptoms lasting less than a month may be diagnosed as
brief psychotic disorder, and various conditions may be
classed as psychotic disorder not otherwise specied,
while schizoaective disorder is diagnosed if symptoms
of mood disorder are substantially present alongside psychotic symptoms. If the psychotic symptoms are the direct physiological result of a general medical condition
or a substance, then the diagnosis is one of a psychosis
secondary to that condition.[69] Schizophrenia is not diagnosed if symptoms of pervasive developmental disorder
are present unless prominent delusions or hallucinations
are also present.[69]

4.2

Subtypes

The DSM-5 work group proposed dropping the ve

sub-classications of schizophrenia included in DSM-IVTR:[74][75]

Sluggish schizophrenia is in the Russian version of the

ICD-10. Sluggish schizophrenia is in the category of
schizotypal disorder in section F21 of chapter V.[76]

4.3 Dierential diagnosis

See also: Dual diagnosis and Comparison of bipolar
disorder and schizophrenia
Psychotic symptoms may be present in several other mental disorders, including bipolar disorder,[77] borderline
personality disorder,[78] drug intoxication and druginduced psychosis. Delusions (non-bizarre) are also
present in delusional disorder, and social withdrawal in
social anxiety disorder, avoidant personality disorder and
schizotypal personality disorder. Schizotypal personality disorder has symptoms that are similar but less severe
than those of schizophrenia.[68] Schizophrenia occurs
along with obsessive-compulsive disorder (OCD) considerably more often than could be explained by chance, although it can be dicult to distinguish obsessions that
occur in OCD from the delusions of schizophrenia.[79]
A small number of people withdrawing from benzodiazepines experience a severe withdrawal syndrome which
may last a long time. It can resemble schizophrenia and
be misdiagnosed as such.[80]

Paranoid type: Delusions or auditory hallucinations

are present, but thought disorder, disorganized behavior, or aective attening are not. Delusions
are persecutory and/or grandiose, but in addition
to these, other themes such as jealousy, religiosity,
or somatization may also be present. (DSM code
295.3/ICD code F20.0)
A more general medical and neurological examination
Disorganized type: Named hebephrenic schizophre- may be needed to rule out medical illnesses which
nia in the ICD. Where thought disorder and at af- may rarely produce psychotic schizophrenia-like sympfect are present together. (DSM code 295.1/ICD toms, such as metabolic disturbance, systemic infection, syphilis, HIV infection, epilepsy, and brain lecode F20.1)
sions.
Stroke, multiple sclerosis, hyperthyroidism,
Catatonic type: The subject may be almost im- hypothyroidism and dementias such as Alzheimers dismobile or exhibit agitated, purposeless movement. ease, Huntingtons disease, frontotemporal dementia
Symptoms can include catatonic stupor and waxy and Lewy Body dementia may also be associated with
exibility. (DSM code 295.2/ICD code F20.2)
schizophrenia-like psychotic symptoms.[81] It may be

MANAGEMENT

necessary to rule out a delirium, which can be distinguished by visual hallucinations, acute onset and uctuating level of consciousness, and indicates an underlying
medical illness. Investigations are not generally repeated
for relapse unless there is a specic medical indication or
possible adverse eects from antipsychotic medication.
In children hallucinations must be separated from normal
childhood fantasies.[68]

Prevention

Prevention of schizophrenia is dicult as there are

no reliable markers for the later development of the
disease.[82] There is tentative evidence for the eectiveness of early interventions to prevent schizophrenia.[83]
While there is some evidence that early intervention in
those with a psychotic episode may improve short-term
outcomes, there is little benet from these measures after ve years.[4] Attempting to prevent schizophrenia in
the prodrome phase is of uncertain benet and therefore
as of 2009 is not recommended.[84] Cognitive behavioral
therapy may reduce the risk of psychosis in those at high
risk after a year[85] and is recommended by the National
Institute for Health and Care Excellence (NICE) in this Risperidone (trade name Risperdal) is a common atypical antipsychotic medication.
group.[86] Another preventative measure is to avoid drugs
that have been associated with development of the disorder, including cannabis, cocaine, and amphetamines.[1]
of relapse.[91][92] There is little evidence regarding eects
from their use beyond two or three years.[92]

Management

Main article: Management of schizophrenia

The choice of which antipsychotic to use is based on benets, risks, and costs.[4] It is debatable whether, as a class,
typical or atypical antipsychotics are better,[93][94] though
there is evidence of amisulpride, olanzapine, risperidone
and clozapine being the most eective medications.[95]
Typical antipsychotics have equal drop-out and symptom
relapse rates to atypicals when used at low to moderate
dosages.[96] There is a good response in 4050%, a partial
response in 3040%, and treatment resistance (failure of
symptoms to respond satisfactorily after six weeks to two
or three dierent antipsychotics) in 20% of people.[20]
Clozapine is an eective treatment for those who respond
poorly to other drugs (treatment-resistant or refractory schizophrenia),[97] but it has the potentially serious
side eect of agranulocytosis (lowered white blood cell
count) in less than 4% of people.[1][4][98]

The primary treatment of schizophrenia is antipsychotic

medications, often in combination with psychological
and social supports.[4] 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.[3] Community support services including drop-in centers, visits by members of a community mental health team, supported
employment[87] and support groups are common. Some
evidence indicates that regular exercise has a positive
eect on the physical and mental health of those with
Most people on antipsychotics have side eects. Peoschizophrenia.[88]
ple on typical antipsychotics tend to have a higher rate
of extrapyramidal side eects while some atypicals are
associated with considerable weight gain, diabetes and
6.1 Medication
risk of metabolic syndrome; this is most pronounced with
The rst-line psychiatric treatment for schizophrenia is olanzapine, while risperidone and quetiapine are also asantipsychotic medication,[89] which can reduce the posi- sociated with weight gain.[95] Risperidone has a simitive symptoms of psychosis in about 7 to 14 days. An- lar rate of extrapyramidal symptoms to haloperidol.[95]
tipsychotics, however, fail to signicantly improve the It remains unclear whether the newer antipsychotics renegative symptoms and cognitive dysfunction.[20][90] In duce the chances of developing neuroleptic malignant
those on antipsychotics, continued use decreases the risk syndrome or tardive dyskinesia, a rare but serious neu-

7
rological disorder.[99]

There is a higher than average suicide rate associated with

schizophrenia. This has been cited at 10%, but a more
recent analysis revises the estimate to 4.9%, most often occurring in the period following onset or rst hospital admission.[7][117] Several times more (20 to 40%)
attempt suicide at least once.[68][118] There are a variety
of risk factors, including male gender, depression, and a
high intelligence quotient.[118]

For people who are unwilling or unable to take medication regularly, long-acting depot preparations of antipsychotics may be used to achieve control.[100] They
reduce the risk of relapse to a greater degree than oral
medications.[91] When used in combination with psychosocial interventions they may improve long-term adherence to treatment.[100] The American Psychiatric Association suggests considering stopping antipsychotics in Schizophrenia and smoking have shown a strong associsome people if there are no symptoms for more than a ation in studies world-wide.[119][120] Use of cigarettes is
year.[92]
especially high in individuals diagnosed with schizophrenia, with estimates ranging from 80 to 90% being
regular smokers, as compared to 20% of the general
6.2 Psychosocial
population.[120] Those who smoke tend to smoke heavily, and additionally smoke cigarettes with high nicoA number of psychosocial interventions may be useful tine content.[121] Some evidence suggests that paranoid
in the treatment of schizophrenia including: family ther- schizophrenia may have a better prospect than other types
apy,[101] assertive community treatment, supported em- of schizophrenia for independent living and occupational
ployment, cognitive remediation,[102] skills training, to- functioning.[122]
ken economic interventions, and psychosocial interventions for substance use and weight management.[103] Family therapy or education, which addresses the whole family system of an individual, may reduce relapses and 8 Epidemiology
hospitalizations.[101] Evidence for the eectiveness of
cognitive-behavioral therapy (CBT) in either reducing
symptoms or preventing relapse is minimal.[104][105] Art
or drama therapy have not been well-researched.[106][107]

Prognosis

Main article: Prognosis of schizophrenia

Schizophrenia has great human and economic costs.[4] It
results in a decreased life expectancy by 1025 years.[6]
This is primarily because of its association with obesity,
poor diet, sedentary lifestyles, and smoking, with an
increased rate of suicide playing a lesser role.[4][6][108]
Antipsychotic medications may also increase the risk.[6]
These dierences in life expectancy increased between
the 1970s and 1990s.[109]
Schizophrenia is a major cause of disability, with
active psychosis ranked as the third-most-disabling
condition after quadriplegia and dementia and ahead
of paraplegia and blindness.[110] Approximately threefourths of people with schizophrenia have ongoing disability with relapses[20] and 16.7 million people globally are deemed to have moderate or severe disability
from the condition.[111] Some people do recover completely and others function well in society.[112] Most people with schizophrenia live independently with community support.[4] In people with a rst episode of psychosis
a good long-term outcome occurs in 42%, an intermediate outcome in 35% and a poor outcome in 27%.[113] Outcomes for schizophrenia appear better in the developing
than the developed world.[114] These conclusions, however, have been questioned.[115][116]

Disability-adjusted life years lost due to schizophrenia per

100,000 inhabitants in 2004.

Main article: Epidemiology of schizophrenia

Schizophrenia aects around 0.30.7% of people at
some point in their life,[4] or 24 million people worldwide as of 2011.[123] It occurs 1.4 times more frequently
in males than females and typically appears earlier in
men[1] the peak ages of onset are 25 years for males
and 27 years for females.[124] Onset in childhood is much
rarer,[125] as is onset in middle- or old age.[126] Despite the received wisdom that schizophrenia occurs at
similar rates worldwide, its frequency varies across the
world,[68][127] within countries,[128] and at the local and
neighborhood level.[129] It causes approximately 1% of
worldwide disability adjusted life years[1] and resulted
in 20,000 deaths in 2010.[130] The rate of schizophrenia
varies up to threefold depending on how it is dened.[4]
In 2000, the World Health Organization found the prevalence and incidence of schizophrenia to be roughly similar around the world, with age-standardized prevalence
per 100,000 ranging from 343 in Africa to 544 in Japan

HISTORY

and Oceania for men and from 378 in Africa to 527 in tia praecox disease concept at the end of the nineteenthSoutheastern Europe for women.[131]
century.[139]

History

Main article: History of schizophrenia

In the early 20th century, the psychiatrist Kurt Schneider
listed the forms of psychotic symptoms that he thought
distinguished schizophrenia from other psychotic disorders. These are called rst-rank symptoms or Schneiders
rst-rank symptoms. They include delusions of being
controlled by an external force; the belief that thoughts
are being inserted into or withdrawn from ones conscious
mind; the belief that ones thoughts are being broadcast to
other people; and hearing hallucinatory voices that comment on ones thoughts or actions or that have a conversation with other hallucinated voices.[132] Although they
have signicantly contributed to the current diagnostic
criteria, the specicity of rst-rank symptoms has been
questioned. A review of the diagnostic studies conducted
between 1970 and 2005 found that they allow neither
a reconrmation nor a rejection of Schneiders claims,
and suggested that rst-rank symptoms should be deemphasized in future revisions of diagnostic systems.[133]
The history of schizophrenia is complex and does not
lend itself easily to a linear narrative.[134] Accounts of
a schizophrenia-like syndrome are thought to be rare in
historical records before the 19th century, although reports of irrational, unintelligible, or uncontrolled behavior were common. A detailed case report in 1797 concerning James Tilly Matthews, and accounts by Phillipe
Pinel published in 1809, are often regarded as the earliest cases of the illness in the medical and psychiatric literature.[135] The Latinized term dementia praecox was rst used by German alienist Heinrich Schule
in 1886 and then in 1891 by Arnold Pick in a case report of a psychotic disorder (hebephrenia). In 1893
Emil Kraepelin borrowed the term from Schule and Pick
and in 1899 introduced a broad new distinction in the
classication of mental disorders between dementia praecox and mood disorder (termed manic depression and including both unipolar and bipolar depression).[136] Kraepelin believed that dementia praecox was probably caused
by a long-term, smouldering systemic or whole body
disease process that aected many organs and peripheral nerves in the body but which aected the brain after puberty in a nal decisive cascade.[137] His use of the
term praecox distinguished it from other forms of dementia such as Alzheimers disease which typically occur
later in life.[138] It is sometimes argued that the use of
the term dmence prcoce in 1852 by the French physician Bndict Morel constitutes the medical discovery
of schizophrenia. However this account ignores the fact
that there is little to connect Morels descriptive use of
the term and the independent development of the demen-

Molecule of chlorpromazine (trade name Thorazine), which revolutionized treatment of schizophrenia in the 1950s

The word schizophreniawhich translates roughly as

splitting of the mind and comes from the Greek roots
schizein (, to split) and phrn, phren- (,
-, mind)[140] was coined by Eugen Bleuler in
1908 and was intended to describe the separation of
function between personality, thinking, memory, and
perception. American and British interpretations of
Beuler led to the claim that he described its main symptoms as 4 A's: attened Aect, Autism, impaired Association of ideas and Ambivalence.[141][142] Bleuler realized
that the illness was not a dementia, as some of his patients
improved rather than deteriorated, and thus proposed the
term schizophrenia instead. Treatment was revolutionized in the mid-1950s with the development and introduction of chlorpromazine.[143]
In the early 1970s, the diagnostic criteria for schizophrenia were the subject of a number of controversies which
eventually led to the operational criteria used today. It
became clear after the 1971 US-UK Diagnostic Study
that schizophrenia was diagnosed to a far greater extent in America than in Europe.[144] This was partly due
to looser diagnostic criteria in the US, which used the
DSM-II manual, contrasting with Europe and its ICD9. David Rosenhans 1972 study, published in the journal Science under the title "On being sane in insane
places", concluded that the diagnosis of schizophrenia in
the US was often subjective and unreliable.[145] These
were some of the factors 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 in 1980.[146] The term schizophrenia is
commonly misunderstood to mean that aected persons
have a split personality. Although some people diag-

10.1

Violence

nosed 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 arises in part due
to the literal interpretation of Bleulers term schizophrenia (Bleuler originally associated Schizophrenia with dissociation and included split personality in his category
of Schizophrenia[147][148] ). Dissociative identity disorder
(having a split personality) was also often misdiagnosed
as Schizophrenia based on the loose criteria in the DSMII.[148][149] The rst known misuse of the term to mean
split personality was in an article by the poet T. S. Eliot
in 1933.[150] Other scholars have traced earlier roots.[151]

9
In the United States, the cost of schizophreniaincluding
direct costs (outpatient, inpatient, drugs, and long-term
care) and non-health care costs (law enforcement, reduced workplace productivity, and unemployment)was
estimated to be $62.7 billion in 2002.[155] The book and
lm A Beautiful Mind chronicles the life of John Forbes
Nash, a Nobel Prize-winning mathematician who was diagnosed with schizophrenia.

10.1 Violence

Individuals with severe mental illness including

schizophrenia are at a signicantly greater risk of
being victims of both violent and non-violent crime.[156]
10 Society and culture
Schizophrenia has been associated with a higher rate
of violent acts, although this is primarily due to higher
See also: List of people with schizophrenia and Religion rates of drug use.[157] Rates of homicide linked to
and schizophrenia
psychosis are similar to those linked to substance misuse,
In 2002 the term for schizophrenia in Japan was changed and parallel the overall rate in a region.[158] What role
schizophrenia has on violence independent of drug
misuse is controversial, but certain aspects of individual
histories or mental states may be factors.[159]
Media coverage relating to violent acts by individuals
with schizophrenia reinforces public perception of an association between schizophrenia and violence.[157] In a
large, representative sample from a 1999 study, 12.8%
of Americans believed that individuals with schizophrenia were very likely to do something violent against others, and 48.1% said that they were somewhat likely to.
Over 74% said that people with schizophrenia were either not very able or not able at all to make decisions
concerning their treatment, and 70.2% said the same of
money management decisions.[160] The perception of individuals with psychosis as violent has more than doubled
in prevalence since the 1950s, according to one metaanalysis.[161]

11 Research directions
See also: Animal models of schizophrenia

The term schizophrenia was coined by Eugen Bleuler.

from Seishin-Bunretsu-By
(mind-split-disease)
to Tg-shitch-sh
(integration disorder) to reduce stigma.[152] The new name was inspired by the
biopsychosocial model; it increased the percentage of patients who were informed of the diagnosis from 37 to 70%
over three years.[153] A similar change was made in South
Korea in 2012.[154]

Research has found a tentative benet in using

minocycline to treat schizophrenia.[162] Nidotherapy
or eorts to change the environment of people with
schizophrenia to improve their ability to function, is also
being studied; however, there is not enough evidence yet
to make conclusions about its eectiveness.[163] Negative
symptoms have proven a challenge to treat as they are
generally not made better by medication. Various agents
have been explored for possible benets in this area.[164]
There have been trials on drugs with anti-inammatory
activity, based on the premise that inammation might
play a role in the pathology of schizophrenia.[165]

10

12

12

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13

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14.2

Images

File:Artistic_view_of_how_the_world_feels_like_with_schizophrenia_-_journal.pmed.0020146.g001.jpg
Source:
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pmed.0020146.g001.jpg License: CC BY 2.5 Contributors: Plos Medicine Original artist: Craig Finn
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artist: ?
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artist: ?
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File:John_Forbes_Nash,_Jr._by_Peter_Badge.jpg Source:
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from English WP by User:Eleassar. Converted by User:AzaToth to a silver color.
File:Risperdal_tablets.jpg Source: http://upload.wikimedia.org/wikipedia/commons/2/22/Risperdal_tablets.jpg License: CC BY-SA 3.0
Contributors: Own work Original artist: Housed
File:Schizophrenia_2.ogg Source: http://upload.wikimedia.org/wikipedia/commons/1/19/Schizophrenia_2.ogg License: CC BY-SA 4.0
Contributors: Own work Original artist: Ex-nimh-researcher
File:Schizophrenia_fMRI_working_memory.jpg Source:
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fMRI_working_memory.jpg License: CC BY 2.5 Contributors: PLoS One. 2010 Aug 11;5(8):e12068. An event-related FMRI study of
phonological verbal working memory in schizophrenia.doi:10.1371/journal.pone.0012068.g002. PMID 20725639 Original artist: Kim J,
Matthews NL, Park S.
File:Schizophrenia_world_map_-_DALY_-_WHO2004.svg
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Schizophrenia_world_map_-_DALY_-_WHO2004.svg License: CC BY-SA 2.5 Contributors:
Vector map from BlankMap-World6, compact.svg by Canuckguy et al. Original artist: Lokal_Prol

14.3

Content license

File:Sound-icon.svg Source: http://upload.wikimedia.org/wikipedia/commons/4/47/Sound-icon.svg License:

Derivative work from Silsor's versio Original artist: Crystal SVG icon set

19

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File:Wikidata-logo.svg Source: http://upload.wikimedia.org/wikipedia/commons/f/ff/Wikidata-logo.svg License: Public domain Contributors: Own work Original artist: User:Planemad
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Contributors: This is a cropped version of Image:Wikinews-logo-en.png. Original artist: Vectorized by Simon 01:05, 2 August 2006 (UTC)
Updated by Time3000 17 April 2007 to use ocial Wikinews colours and appear correctly on dark backgrounds. Originally uploaded by
Simon.
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on original logo tossed together by Brion Vibber

14.3

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