Schizophrenia Basics
Schizophrenia is a type of mental illness. Schizophrenia causes problems with behaviour (the way people act), thinking, emotions, motivation and is linked to psychosis. People with schizophrenia are often thought to have 'lost touch with reality'.
The word schizophrenia comes from the Greek words σχίζω (schizo, break) and φρενός (frenos, mind) and means "shattered mind". Psychiatrist Emil Kraepelin
was the first person to separate schizophrenia from other types of
mental illness. He called it 'dementia praecox', and it was later
renamed 'schizophrenia'.
While people of many ages can have schizophrenia, most often it
starts in early adulthood. For many people, the symptoms of
schizophrenia will return throughout their life, although some people
will have only one or two episodes. The exact cause of schizophrenia is
not known, although many things are known to influence the condition.
Scientists have discovered that both life experiences and the biology
of the brain and body are important. Schizophrenia is partly genetic
(passed on within families) and can be triggered by trauma (disturbing experiences).
Schizophrenia is usually treated by the use of drugs which affect
the brain, and by training people to understand their thoughts and
behaviour with psychotherapy. About one out of every ten people with schizophrenia dies by suicide (killing self).
The famous mathematician John Forbes Nash had schizophrenia. John Forbes Nash was awarded the Nobel Prize in economics in 1994. He got the prize for his contributions to game theory. His life is protrayed in the film A Beautiful Mind.
Symptoms
- Hallucination: Seeing, hearing, tasting, smelling, and feeling things, which are not there.
- Delusions: Thoughts that do not make sense.
- Improper behavior: Person does things that do not make sense.
- Formal thought disorder:
Thoughts are confused and mixed up. This can cause a person to say
things that do not make sense, and to think in illogical ways.
(Simple "schizophrenia", also called "schizophrenic" autism,
negative schizophrenia(in other words, not schizophrenia),
"schizoidia", or "schizoid" personality disorder, is an autistic
disorder, has no schizophrenic symptoms, and is properly named neurotic
introversion)
Treatment
Drugs are usually given for Schizophrenia. But psychiatrists know that it cannot be healed by the drugs in use today. Drugs called anti-psychotics can suppress some of the positive symptoms. The negative symptoms cannot be cured.
Prognosis
Many people with schizophrenia can live good lives. Keeping taking
medicine is important to prevent relapses (symptoms suddenly
returning). About one-third of people with schizophrenia get totally
healed, about one-third improve a lot, and about one-third remain sick.
Schizophrenia for Advanced Level
Schizophrenia, from the Greek roots schizein (σχίζειν, "to split") and phrēn, phren- (φρήν, φρεν-, "mind"), is a psychiatric diagnosis that describes a mental illness characterized by impairments in the perception or expression of reality, most commonly manifesting 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,[1] with approximately 0.4–0.6%[2][3]
of the population affected. Diagnosis is based on the patient's
self-reported experiences and observed behavior. No laboratory test for
schizophrenia exists.[4]
Studies suggest that genetics, early environment, neurobiology and psychological
and social processes are important contributory factors. Current
psychiatric research is focused on the role of neurobiology, but a
clear organic cause has not been found. Due to the many possible
combinations of symptoms, there is debate about whether the diagnosis
represents a single disorder or a number of discrete syndromes. For
this reason, Eugen Bleuler termed the disease the schizophrenias (plural) when he coined the 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.
Increased dopaminergic activity in the mesolimbic pathway of the brain is a consistent finding. The mainstay of treatment is pharmacotherapy with antipsychotic
medications; these primarily work by suppressing dopamine activity.
Dosages of antipsychotics are generally lower than in the early decades
of their use. 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 hospital
stays are less frequent and for shorter periods than they were in
previous years.[5]
The disorder is primarily thought to affect cognition, but it also usually contributes to chronic problems with behavior and emotion. People diagnosed with schizophrenia are likely to be diagnosed with comorbid conditions, including clinical depression and anxiety disorders;[6] the lifetime prevalence of substance abuse is typically around 40%. Social problems, such as long-term unemployment, poverty and homelessness, are common and life expectancy
is decreased; the average life expectancy of people with the disorder
is 10 to 12 years less than those without, owing to increased physical
health problems and a high suicide rate.[7]
Signs and symptoms
A person experiencing schizophrenia may demonstrate symptoms such as disorganized thinking, auditory hallucinations, and delusions.
In severe cases, the person may be largely mute, remain motionless in
bizarre postures, or exhibit purposeless agitation; these are signs of catatonia.
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 schizophrenia-like psychosis of
shorter duration is termed a schizophreniform disorder.[4] No one sign is diagnostic of schizophrenia, and all can occur in other medical and psychiatric conditions.[4]
Social isolation commonly occurs and may be due to a number of factors. Impairment in social cognition
is associated with schizophrenia, as are the active symptoms of
paranoia from delusions and hallucinations, and the negative symptoms
of apathy and avolition. Many people diagnosed with schizophrenia avoid potentially stressful social situations that may exacerbate mental distress.[8]
Late adolescence and early adulthood are peak years for the onset of
schizophrenia. These are critical periods in a young adult's social and
vocational development, and they can be severely disrupted by disease
onset. To minimize the effect of 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, but may be present longer.[9] Those who go on to develop schizophrenia may experience the non-specific symptoms of social withdrawal, irritability and dysphoria in the prodromal period,[10] and transient or self-limiting psychotic symptoms in the prodromal phase before psychosis becomes apparent.[11]
Schneiderian classification
The psychiatrist Kurt Schneider
(1887–1967) listed the forms of psychotic symptoms that he thought
distinguished schizophrenia from other psychotic disorders. These are
called first-rank symptoms or Schneider's first-rank symptoms,
and they 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 that
comment on one's thoughts or actions or that have a conversation with
other hallucinated voices.[12] The reliability of first-rank symptoms has been questioned,[13] 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.[14] 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 or blunted affect and emotion, poverty of speech (alogia), anhedonia, and lack of motivation (avolition).
Despite the appearance of blunted affect, recent studies indicate that
there is often a normal or even heightened level of emotionality in
Schizophrenia especially in response to stressful or negative events.[15] A third symptom grouping, the disorganization syndrome,
is commonly described, and includes chaotic speech, thought, and
behaviour. There is evidence for a number of other symptom
classifications.[16]
Diagnosis
Diagnosis is based on the self-reported experiences of the person as
well as abnormalities in behavior reported by family members, friends
or co-workers, 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.[4]
An initial assessment includes a comprehensive history and physical
examination by a physician. Although there are no biological tests
which confirm schizophrenia, tests are carried out to exclude medical
illnesses which may rarely present with psychotic schizophrenia-like
symptoms.[4] These include blood tests measuring TSH to exclude hypo- or hyperthyroidism, basic electrolytes and serum calcium to rule out a metabolic disturbance, full blood count including ESR to rule out a systemic infection or chronic disease, and serology to exclude syphilis or HIV infection; two commonly ordered investigations are EEG to exclude epilepsy, and a CT scan of the head to exclude brain lesions. It is important to rule out a delirium
which can be distinguished by visual hallucinations, acute onset and
fluctuating level of consciousness and indicates an underlying medical
illness. There are several psychiatric illnesses which may present with
psychotic symptoms other than schizophrenia. These include bipolar disorder,[17] borderline personality disorder,[18] drug intoxication, brief drug-induced psychosis, and schizophreniform disorder.
Investigations are not generally repeated for relapse unless there is a specific medical indication. These may include serum blood sugar level (BSL) if olanzapine has been prescribed previously, liver function tests if chlorpromazine, or creatine phosphokinase (CPK) to exclude neuroleptic malignant syndrome.
Assessment and treatment are usually done on an outpatient basis;
admission to an inpatient facility is considered if there is a risk to
self or others.
The most widely used criteria for diagnosing schizophrenia are from the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, the current version being DSM-IV-TR, and the World Health Organization's International Statistical Classification of Diseases and Related Health Problems,
currently the ICD-10. The latter criteria are typically used in
European countries while the DSM criteria are used in the USA or the
rest of the world, as well as prevailing in research studies. The
ICD-10 criteria put more emphasis on Schneiderian first rank symptoms although, in practice, agreement between the two systems is high.[19] The WHO has developed the tool SCAN (Schedules for Clinical Assessment in Neuropsychiatry) which can be used for diagnosing a number of psychiatric conditions, including schizophrenia.
DSM IV-TR Criteria
To be diagnosed with schizophrenia, a person must display:[4]
- 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)
- 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 the diagnosis; thus schizophrenia cannot be diagnosed if symptoms of mood disorder or pervasive developmental disorder
are present, or 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 recognises a further 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)
Diagnostic issues and controversies
Schizophrenia as a diagnostic entity has been criticised as lacking in scientific validity or reliability,[20][21] 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[22][23] and often non-distressing delusional beliefs[24] amongst the general public.[23]
Another criticism is that the definitions used for criteria lack consistency;[25] this is particularly relevant to the evaluation of delusions and thought disorder.
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".[26]
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.[27]
More recent studies have found agreement between any two psychiatrists
when diagnosing schizophrenia tends to reach about 65% at best.[28]
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.[29]
In 2004 in Japan, the Japanese term for schizophrenia was changed from Seishin-Bunretsu-Byo (mind-split-disease) to Tōgō-shitchō-shō (integration disorder).[30]
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.[31]
Alternatively, other proponents have put forward using the presence of specific neurocognitive deficits to make a diagnosis. These 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.[32]
The diagnosis of schizophrenia has been used for political rather than therapeutic purposes; in the Soviet Union 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.[33] In 2000 there were similar concerns regarding detention and 'treatment' of practitioners of the Falun Gong movement by the Chinese government. This 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.[34]
Epidemiology
Schizophrenia occurs equally in males and females although typically
appears earlier in men with the peak ages of onset being 20–28 years
for males and 26–32 years for females.[1] Much rarer are instances of childhood-onset[35] and late- (middle age) or very-late-onset (old age) schizophrenia.[36] 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%.[3]
Despite the received wisdom that schizophrenia occurs at similar rates
throughout the world, its prevalence varies across the world,[37] within countries,[38] and at the local and neighbourhood level.[39] 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.[40] Schizophrenia is known to be 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.[41]
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 and environmental factors can act in combination to result in schizophrenia.[43]
Evidence suggests that the diagnosis of schizophrenia has a significant
heritable component but that onset is significantly influenced by
environmental factors or stressors.[44] The idea of an inherent vulnerability (or diathesis)
in some people, which can be unmasked by biological, psychological or
environmental stressors, is known as the stress-diathesis model.[45] The idea that biological, psychological and social factors are all important is known as the "biopsychosocial" model.
Genetic
Estimates of the heritability of schizophrenia tend to vary owing to the difficulty of separating the effects of genetics and the environment although twin studies have suggested a high level of heritability.[46] It is likely that schizophrenia is a condition of complex inheritance, with several genes possibly interacting to generate risk for schizophrenia or the separate components that can co-occur leading to a diagnosis.[47]
Recent work has suggested that genes that raise the risk for developing
schizophrenia are non-specific, and may also raise the risk of
developing other psychotic disorders such as bipolar disorder.[48][49]
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).[50] 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.[51]
Social
Living in an urban environment has been consistently found to be a risk factor for schizophrenia.[52][40] Social disadvantage has been found to be a risk factor, including poverty[53] and migration related to social adversity, racial discrimination, family dysfunction, unemployment or poor housing conditions.[54]
Childhood experiences of abuse or trauma have also been implicated as
risk factors for a diagnosis of schizophrenia later in life.[55][56]
Parenting is not held responsible for schizophrenia but unsupportive
dysfunctional relationships may contribute to an increased risk.[57][58]
Substance use
- See also: dual diagnosis
The relationship between schizophrenia and drug use is complex,
meaning that a clear causal connection between drug use and
schizophrenia has been difficult to distinguish. 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.[59] 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.[60] Schizophrenia can be triggered by heavy use of hallucinogenic or stimulant drugs.[61] One study suggests that cannabis
use can contribute to psychosis, though the researchers suspected
cannabis use was only a small component in a broad range of factors
that can cause psychosis.[62]
Psychological
A number of psychological mechanisms have been implicated in the development and maintenance of schizophrenia. Cognitive biases
that have been identified in those with a diagnosis or those at risk,
especially when under stress or in confusing situations, include
excessive attention to potential threats, jumping to conclusions,
making external attributions, impaired reasoning about social situations and mental states,
difficulty distinguishing inner speech from speech from an external
source, and difficulties with early visual processing and maintaining
concentration.[63][64][65][66] Some cognitive features may reflect global neurocognitive deficits in memory, attention, problem-solving, executive function or social cognition, while others may be related to particular issues and experiences.[67][57]
Despite a common appearance of "blunted affect", recent findings
indicate that many individuals diagnosed with schizophrenia are highly
emotionally responsive, particularly to stressful or negative stimuli,
and that such sensitivity may cause vulnerability to symptoms or to the
disorder.[68][69][70]
Some evidence suggests that the content of delusional beliefs and
psychotic experiences can reflect emotional causes of the disorder, and
that how a person interprets such experiences can influence
symptomology.[71][72][73][74] Further evidence for the role of psychological mechanisms comes from the effects of therapies on symptoms of schizophrenia.[75]
Neural
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.[76] These differences have been linked to the neurocognitive deficits often associated with schizophrenia.[77] The role of antipsychotic medication, which nearly all those studied had taken, in causing such abnormalities is also unclear.[78]
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, known as 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.[79]
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[80] and the discovery that the glutamate blocking drugs such as phencyclidine and ketamine can mimic the symptoms and cognitive problems associated with the condition.[81] 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.[82]
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.[83]
There have also been findings of differences in the size and
structure of certain brain areas in schizophrenia, starting with the
discovery of ventricular enlargement in those for whom negative symptoms were most prominent.[84]
However, this has not proven particularly reliable on the level of the
individual person, with considerable variation between patients. More
recent studies have shown various differences in brain structure
between people with and without diagnoses of schizophrenia.[85]
While brain structure changes have been found in people diagnosed with
schizophrenia who have never been treated with antipsychotic drugs[86] there is evidence that the medication itself might cause additional changes in the brain's structure.[87]
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.
Treatment and services
-
Molecule of chlorpromazine, which revolutionized treatment of schizophrenia in the 1950s.
The concept of a cure as such remains controversial, as there is no
consensus on the definition, although some criteria for the remission
of symptoms have recently been suggested.[88] The effectiveness of schizophrenia treatment is often assessed using standardized methods, one of the most common being the positive and negative syndrome scale (PANSS).[89]
Management of symptoms and improving function is thought to be more
achievable than a cure. Treatment was revolutionized in the mid 1950s
with the development and introduction of chlorpromazine.[90] A recovery model is increasingly adopted, emphasizing hope, empowerment and social inclusion.[91]
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.[5]
Following (or in lieu of) a hospital admission, support services
available can include drop-in centers, visits from members of a
community mental health team or Assertive Community Treatment team, supported employment[92] and patient-led support groups.
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.[93] The reasons for this effect are not clear, although cross-cultural studies are being conducted.
Medication
The mainstay of psychiatric treatment for schizophrenia is an antipsychotic medication.[94] These can reduce the "positive" symptoms of psychosis. Most antipsychotics take around 7–14 days to have their main effect.
Though expensive, the newer atypical antipsychotic drugs are usually preferred for initial treatment over the older typical antipsychotics; they are often better tolerated and associated with lower rates of tardive dyskinesia, although they are more likely to induce weight gain and obesity-related diseases.[95] Prolactin elevations have been reported in women with schizophrenia taking atypical antipsychotics.[96]It remains unclear whether the newer antipsychotics reduce the chances of developing neuroleptic malignant syndrome, a rare but serious and potentially fatal neurological disorder most often caused by an adverse reaction to neuroleptic or antipsychotic drugs.[97]
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.[98] Loss of glial cells was observed in monkeys[99] and signs of neuron death were detected in women[100].
Response of symptoms to medication is variable; "Treatment-resistant
schizophrenia" is a term used for the failure of symptoms to respond
satisfactorily to at least two different antipsychotics.[101] Patients in this category may be prescribed clozapine,[102] a medication of superior effectiveness but several potentially lethal side effects including agranulocytosis and myocarditis.[103] Clozapine may have the additional benefit of reducing propensity for substance abuse in schizophrenic patients. [104] 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. The United States of 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. Some
findings have found that in the longer-term some individuals may do
better not taking antipsychotics.[105] Despite the promising results of early pilot trials,[106] omega-3 fatty acids failed to improve schizophrenic symptoms, according to the most recent meta-analysis.[107]
Psychological and social interventions
Psychotherapy
is also widely recommended and used in the treatment of schizophrenia,
although services may often be confined to pharmacotherapy because of
reimbursement problems or lack of training.[108]
Cognitive behavioral therapy (CBT) is used to reduce symptoms and improve related issues such as self-esteem, social functioning, and insight. Although the results of early trials were inconclusive,[109] more recent reviews suggest that CBT can be an effective treatment for the psychotic symptoms of schizophrenia.[110] 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.[111]
A similar approach known as cognitive enhancement therapy, which
focuses on social cognition as well as neurocognition, has shown
efficacy.[112]
Family Therapy
or Education, which addresses the whole family system of an individual
with a diagnosis of schizophrenia, has been consistently found to be
beneficial, at least if the duration of intervention is longer-term.[113][114][115]
Aside from therapy, the impact of schizophrenia on families and the
burden on carers has been recognized, with the increasing availability
of self-help books on the subject.[116][117]
There is also some evidence for benefits from social skills training,
although there have also been significant negative findings.[118][119] Some studies have explored the possible benefits of music therapy and other creative therapies.[120][121][122]
The Soteria model is alternative to inpatient hospital treatment using a minimal medication approach. 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."[123]
Although research evidence is limited, a 2008 systematic review found
the programme equally as efffective as treatment with medication in
people diagnosed with first and second episode schizophrenia.[124]
Other
Electroconvulsive therapy is not considered a first line treatment
but may be prescribed in cases where other treatments have failed. It
is more effective where symptoms of catatonia are present,[125] and is recommended for use under NICE
guidelines in the UK for catatonia if previously effective, though
there is no recommendation for use for schizophrenia otherwise.[126] Psychosurgery has now become a rare procedure and is not a recommended treatment for schizophrenia.[127]
Service-user led movements have become integral to the recovery process in Europe and America; groups such as the Hearing Voices Network and the Paranoia Network
have developed a self-help approach that aims to provide support and
assistance outside 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. Partnerships between
hospitals and consumer-run groups are becoming more common, with
services working toward remediating social withdrawal, building social
skills and reducing rehospitalization.[128]
Prognosis
Numerous international studies have demonstrated favorable long-term
outcomes for around half of those diagnosed with schizophrenia, with
substantial variation between individuals and regions.[129]
One retrospective study found that about a third of people made a full
recovery, about a third showed improvement but not a full recovery, and
a third remained ill.[130]
A clinical study using strict recovery criteria (concurrent remission
of positive and negative symptoms and adequate social and vocational
functioning continuously for two years) found a recovery rate of 14%
within the first five years.[131]
A 5-year community study found that 62% showed overall improvement on a
composite measure of symptomatic, clinical and functional outcomes.[132]
Rates are not always comparable across studies because an exact
definition of what constitutes recovery has not been widely accepted,
although standardized criteria have been suggested.[88]
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),[133]
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.[134][135]
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.[136]
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.[137] 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.[138] [139]Another study suggested that 10% of persons with schizophrenia die by suicide.[140] Other identified factors include smoking, poor diet, little exercise and the negative health effects of psychiatric drugs.[7]
Violence
The relationship between violent acts and schizophrenia is a
contentious topic. Current research indicates that the percentage of
people with schizophrenia who commit violent acts is higher than the
percentage of people without any disorder, but lower than is found for
disorders such as alcoholism, and the difference is reduced or not
found in same-neighbourhood comparisons when related factors are taken
into account, notably sociodemographic variables and substance misuse.[141][142][143][144][145] Studies have indicated that 5% to 10% of those charged with murder in Western countries have a schizophrenia spectrum disorder.[146][147][148]
The occurrence of psychosis
in schizophrenia has sometimes been linked to a higher risk of violent
acts. Findings on the specific role of delusions or hallucinations have
been inconsistent, but have focused on delusional jealousy, perception
of threat and command hallucinations. It has been proposed that a
certain type of individual with schizophrenia may be most likely to
offend, characterized by a history of educational difficulties, low IQ,
conduct disorder, early-onset substance misuse and offending prior to
diagnosis.[146]
A consistent finding 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.[149][150] Another consistent finding is a link to substance misuse, particularly alcohol,[151]
among the minority who commit violent acts. Violence by or against
individuals with schizophrenia typically occurs in the context of
complex social interactions within a family setting,[152] and is also an issue in clinical services[153] and in the wider community.[154]
Screening and prevention
There are no reliable markers for the later development of
schizophrenia although research is being conducted into how well a
combination of genetic risk plus non-disabling psychosis-like
experience predicts later diagnosis.[155]
People who fulfil the 'ultra high-risk mental state' criteria, that
include a family history of schizophrenia plus the presence of
transient or self-limiting psychotic experiences, have a 20–40% chance
of being diagnosed with the condition after one year.[156]
The use of psychological treatments and medication has been found
effective in reducing the chances of people who fulfill the 'high-risk'
criteria from developing full-blown schizophrenia.[157]
However, the treatment of people who may never develop schizophrenia is
controversial, in light of the side-effects of antipsychotic
medication; particularly with respect to the potentially disfiguring tardive dyskinesia and the rare but potentially lethal neuroleptic malignant syndrome.[158]
The most widely used form of preventative health care for schizophrenia
takes the form of public education campaigns that provide information
on risk factors, early detection and treatment options.[159]
Popular views and misconceptions
Stigma has been identified as a major obstacle in the recovery of patients with schizophrenia.[160]
12.8% of a large, representative sample of Americans in a 1999 study
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.[161]
The perception of individuals with psychosis as violent has more than
doubled in prevalence since the 1950s, according to one meta-analysis.[162]
As public understanding of mental illness as a neurobiological disorder is yet developing, patients may be discouraged by friends or family members from taking prescribed medication.[163] Consumers' views on treatment and recovery may differ from those of mental health professionals.[91]
Alternative approaches
An approach broadly known as the anti-psychiatry movement, most active in the 1960s, opposes the orthodox medical view of schizophrenia as an illness.[164] Psychiatrist Thomas Szasz
argued that psychiatric patients are not ill, but rather individuals
with unconventional thoughts and behavior that make society
uncomfortable.[165]
He argues that society unjustly seeks to control them 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 construction,
created by society's concept of what constitutes normality and
abnormality. Szasz has never considered himself to be "anti-psychiatry"
in the sense of being against psychiatric treatment, but simply
believes that treatment 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 Colin Ross[166]
have argued that the symptoms of what is 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 notable 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 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.[167] In 1956, Palo Alto, Gregory Bateson and his colleagues Paul Watzlawick, Donald Jackson, and Jay Haley[168] articulated a theory of schizophrenia, related to Laing's work, as stemming from double bind
situations where a person receives different or contradictory messages.
Madness was therefore an expression of this distress and should be
valued as a cathartic and trans-formative experience. 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. Arieti's Interpretation of Schizophrenia won the 1975 scientific National Book Award in the United States.
The concept of schizophrenia as a result of civilization has been developed further by psychologist Julian Jaynes in his 1976 book The Origin of Consciousness in the Breakdown of the Bicameral Mind;
he proposed that until the beginning of historic times, schizophrenia
or a similar condition was the normal state of human consciousness.[169] 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. Researchers into shamanism have speculated that in some cultures schizophrenia or related conditions may predispose an individual to becoming a shaman;[170]
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.[171] Speculation 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.[172]
Psychiatrist Tim Crow has argued that schizophrenia may be the evolutionary price we pay for a left brain hemisphere specialization for language.[173]
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.
Alternative medical treatments
A branch of alternative medicine that deals with schizophrenia is known as orthomolecular psychiatry.
Orthomolecular psychiatry considers the schizophrenias to be a group of
disorders; management entails performing the appropriate diagnostic
tests and then providing the appropriate therapy.[174] Vitamin B-3 (Niacin) has been proposed as an effective treatment in some cases.[175] The body's adverse reactions to gluten are implicated in some alternative theories;
proponents of orthomolecular psychiatric thought claim that an adverse
reaction to gluten is involved in the etiology of some cases. This
theory—discussed by one author in three British journals in the 1970s[176]—is
unproven. A 2006 literature review suggests that gluten may be a factor
for patients with celiac disease and for a subset of patients afflicted
with schizophrenia, but that further study is needed to conclusively
confirm such a link.[177] Some researchers suggest that dietary and nutritional treatments may hold promise in the treatment of schizophrenia.[178]
History
Descriptions of schizophrenia-like symptoms date back to circa 2000 BC in the Book of Hearts—part of the ancient Egyptian Ebers Papyrus. However, study of the ancient Greek and Roman
literature shows 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.[179] Symptoms resembling schizophrenia were, however, reported in Arabic medical and psychological literature during the Middle Ages. In The Canon of Medicine, for example, Avicenna described a condition somewhat resembling schizophrenia which he called Junun Mufrit (severe madness), which he distinguished from other forms of madness (Junun) such as mania, rabies and manic depressive psychosis.[180]
Although a broad concept of madness has existed for thousands of years, 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 (early dementia—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,[181] and particularly a form of dementia, distinguished from other forms of dementia, such as Alzheimer's disease, which typically occur later in life.[182]
The word schizophrenia—which translates roughly as "splitting of the mind" and comes from the Greek roots schizein (σχίζειν, "to split") and phrēn, phren- (φρήν, φρεν-, "mind")[183]—was coined by Eugen 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.[184] 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
arises in part due to the meaning of Bleuler's term schizophrenia
(literally "split" or "shattered mind"). The first known misuse of the
term to mean "split personality" was in an article by the poet T. S. Eliot in 1933.[185]
In the first half of the twentieth century schizophrenia was
considered to be a hereditary defect, and sufferers were 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.[186][187] Along with other people labeled "mentally unfit", many diagnosed with schizophrenia were murdered in the Nazi "Action T4" program.[188]
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 America than in
Europe.[189] This was partly due to looser diagnostic criteria in the US, which used the DSM-II manual, contrasting with Europe and its ICD-9.
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.[190]
Cultural references
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 plenty of patience by the close
relatives of the patient. Other factual books have been written by
relatives on family members; Australian journalist Anne Deveson told the story of her son's battle with schizophrenia in Tell me I'm Here,[191] later made into a movie.
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 recounts his struggle into schizophrenia and his journey back to sanity.
References
- ^ a b 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. PMID 1790446. Retrieved on 2008-02-24.
- ^ Bhugra, D (2006). "The global prevalence of schizophrenia". PLoS Medicine 2 (5): 372-373. PMID 15916460. Retrieved on 2008-02-24.
- ^ a b 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. Retrieved on 2008-02-24.
- ^ a b c d e f
American Psychiatric Association (2004) Diagnostic and Statistical
Manual of Mental Disorders DSM-IV-TR (Text Revision). American
Psychiatric Association. ISBN 0890420246. DSM-IV & DSM-IV-TR Schizophrenia criteria
- ^ a b 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. Retrieved on 2008-02-24.
- ^
Sim K, Chua TH, Chan YH, Mahendran R, Chong SA. (2006) Psychiatric
comorbidity in first episode schizophrenia: a 2 year, longitudinal
outcome study. J Psychiatr Res, 40 (7), 656-63. PMID 16904688
- ^ a b Brown S; Inskip H, Barraclough B (2000). "Causes of the excess mortality of schizophrenia". Br J Psychiatry 177: 212-7. PMID 11040880. Retrieved on 2008-02-24.
- ^ 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. Retrieved on 2008-02-24.
- ^ 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. Retrieved on 2008-02-24.
- ^ Parnas J; Jorgensen A (1989). "Pre-morbid psychopathology in schizophrenia spectrum". British Journal of Psychiatry 115: 623-7. PMID 2611591. Retrieved on 2008-02-24.
- ^ 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. Retrieved on 2008-02-24.
- ^ Schneider, K. (1959) Clinical Psychopathology. New York: Grune and Stratton.
- ^ Bertelsen, A (2002). "Schizophrenia and Related Disorders: Experience with Current Diagnostic Systems". Psychopathology 35: 89-93. PMID 12145490. Retrieved on 2008-02-24.
- ^
Sims A (2002) Symptoms in the Mind: An Introduction to Descriptive
Psychopathology (3rd edition). Edinburgh: Elsevier Science Ltd. ISBN 0-7020-2627-1
- ^ Cohen & Docherty (2004). "Affective reactivity of speech and emotional experience in patients with schizophrenia". Schizophrenia Research 69 (1): 7-14. PMID 15145465. Retrieved on 2008-02-24.
- ^ Peralta
V; Cuesta MJ (2001). "How many and which are the psychopathological
dimensions in schizophrenia? Issues influencing their ascertainment". Schizophrenia Research 49 (3): 269-85. PMID 11356588. Retrieved on 2008-02-24.
- ^ Pope HG (1983). "Distinguishing bipolar disorder from schizophrenia in clinical practice: guidelines and case reports". Hospital and Community Psychiatry 34: 322-328. Retrieved on 2008-02-24.
- ^ McGlashan TH
(1987) Testing DSM-III symptom criteria for schizotypal and borderline
personality disorders. Archives of General Psychiatry, 44: 15–22.
- ^ 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. Retrieved on 2008-02-24.
- ^ Bentall RP (1992) Reconstructing Schizophrenia. London: Routledge. ISBN 0415075246
- ^ Boyle M (2002) Schizophrenia: A Scientific Delusion?. London: Routledge. ISBN 0415227186
- ^ 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. Retrieved on 2008-02-24.
- ^ a b Johns LC; van Os J (2001). "The continuity of psychotic experiences in the general population". Clinical Psychology Review 21 (8): 1125-41. PMID 11702510. Retrieved on 2008-02-24.
- ^ Peters
ER; Day S, McKenna J, Orbach G (2005). "Measuring delusional ideation:
the 21-item Peters et al. Delusions Inventory (PDI)". Schizophrenia Bulletin 30: 1005-22. PMID 15954204. Retrieved on 2008-02-24.
- ^ David AS (1999). "On the impossibility of defining delusions". Philosophy, Psychiatry and Psychology 6 (1): 17-20. Retrieved on 2008-02-24.
- ^ Tsuang MT; Stone WS, Faraone SV (2000). "Toward reformulating the diagnosis of schizophrenia". American Journal of Psychiatry 157 (7): 1041-1050. PMID 10873908. Retrieved on 2008-02-24.
- ^ Rosenhan D (1973). "On being sane in insane places". Science 179: 250-8. PMID 4683124. Retrieved on 2008-02-24.
- ^ 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. Retrieved on 2008-02-24.
- ^ Read J (2004) Does 'schizophrenia' exist? Reliability and validity. In Read J, Mosher LR, Bentall RP (eds) Models of Madness: Psychological, Social and Biological Approaches to Schizophrenia. ISBN 1-58391-906-6
- ^ Sato M (2004). "Renaming schizophrenia: a Japanese perspective". World Psychiatry 5 (1): 53-5. PMID 16757998. Retrieved on 2008-02-24.
- ^ Schizophrenia term use 'invalid'. BBC News Online, (9 October 2006). Retrieved on 2007-05-16.
- ^ Green MF (2001) Schizophrenia Revealed: From Neurons to Social Interactions. New York: W.W. Norton. ISBN 0393703347
- ^ Wilkinson G (1986). "Political dissent and "sluggish" schizophrenia in the Soviet Union". Br Med J (Clin Res Ed) 293 (6548): 641-2. PMID 3092963. Retrieved on 2008-02-24.
- ^ Lyons D (2001). "Soviet-style psychiatry is alive and well in the People's Republic". British Journal of Psychiatry 178: 380-381. PMID 11282823. Retrieved on 2008-02-24.
- ^ Kumra S; Shaw M, Merka P, Nakayama E, Augustin R (2001). "Childhood-onset schizophrenia: research update". Canadian Journal of Psychiatry 46 (10): 923-30. PMID 11816313. Retrieved on 2008-02-24.
- ^ Hassett A, Ames D, Chiu E (eds) (2005) Psychosis in the Elderly. London: Taylor and Francis. ISBN 18418439446
- ^ Jablensky
A; Sartorius N, Ernberg G, Anker M, Korten A, Cooper JE, Day R,
Bertelsen A (1992). "Schizophrenia: manifestations, incidence and
course in different cultures. A World Health Organization ten-country
study". Psychological Medicine Monograph Supplement 20: 1-97. PMID 1565705. Retrieved on 2008-02-24.
- ^ Kirkbride
JB; Fearon P, Morgan C, Dazzan P, Morgan K, Tarrant J, Lloyd T,
Holloway J, Hutchinson G, Leff JP, Mallett RM, Harrison GL, Murray RM,
Jones PB (2006). "Heterogeneity in incidence rates of schizophrenia and
other psychotic syndromes: findings From the 3-center ÆSOP study". Archives of General Psychiatry 63 (3): 250-258. PMID 16520429. Retrieved on 2008-02-24.
- ^ Kirkbride
JB; Fearon P, Morgan C, Dazzan P, Morgan K, Murray RM, Jones PB (2007).
"Neighbourhood variation in the incidence of psychotic disorders in
Southeast London". Social Psychiatry and Psychiatric Epidemiology 42 (6): 438-45. PMID 17473901. Retrieved on 2008-02-24.
- ^ a b Van Os J (2004). "Does the urban environment cause psychosis?". British Journal of Psychiatry 184 (4): 287-288. PMID 15056569. Retrieved on 2008-02-24.
- ^ 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. Retrieved on 2008-02-24.
- ^ Meyer-Lindenberg
A; Miletich RS, Kohn PD, Esposito G, Carson RE, Quarantelli M,
Weinberger DR, Berman KF (2002). "Reduced prefrontal activity predicts
exaggerated striatal dopaminergic function in schizophrenia". Nature Neuroscience 5: 267-71. PMID 11865311. Retrieved on 2008-02-24.
- ^ Harrison PJ; Owen MJ (2003). "Genes for schizophrenia? Recent findings and their pathophysiological implications". The Lancet 361 (9355): 417-9. PMID 12573388. Retrieved on 2008-02-24.
- ^ Day
R; Nielsen JA, Korten A, Ernberg G, Dube KC, Gebhart J, Jablensky A,
Leon C, Marsella A, Olatawura M, 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. Retrieved on 2008-02-24.
- ^ Corcoran
C; Walker E, Huot R, Mittal V, Tessner K, Kestler L, Malaspina D
(2003). "The stress cascade and schizophrenia: etiology and onset". Schizophrenia Bulletin 29 (4): 671-92. PMID 14989406. Retrieved on 2008-02-24.
- ^ O'Donovan MC; Williams NM, Owen MJ (2003). "Recent advances in the genetics of schizophrenia". Human Molecular Genetics 12 Spec No 2: R125-33. PMID 12952866. Retrieved on 2008-02-24.
- ^ Owen MJ; Craddock N, O'Donovan MC (2005). "Schizophrenia: genes at last?". Trends in Genetics 21 (9): 518-25. PMID 16009449. Retrieved on 2008-02-24.
- ^ Craddock
N; O'Donovan MC, Owen MJ (2006). "Genes for schizophrenia and bipolar
disorder? Implications for psychiatric nosology". Schizophrenia Bulletin 32 (1): 9-16. PMID 16319375. Retrieved on 2008-02-24.
- ^ Dalby JT; Morgan D, Lee M (1986). "Schizophrenia and mania in identical twin brothers". Journal of Nervous and Mental Disease 174: 304-308. PMID 3701318. Retrieved on 2008-02-24.
- ^ 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. Retrieved on 2008-02-24.
- ^ Brown AS (2006). "Prenatal infection as a risk factor for schizophrenia". Schizophrenia Bulletin 32 (2): 200-2. PMID 16469941. Retrieved on 2008-02-24.
- ^ van Os J; Krabbendam L, Myin-Germeys I, Delespaul P (2005). "The schizophrenia envirome". Current Opinion in Psychiatry 18 (2): 141-5. PMID 16639166. Retrieved on 2008-02-24.
- ^ Mueser KT & McGurk SR (2004). "Schizophrenia". The Lancet 363 (9426): 2063-72. PMID 15207959. Retrieved on 2008-02-24.
- ^ (2007) "Migration and schizophrenia". Current Opinion in Psychiatry 20 (2): 111-5. PMID 17278906. Retrieved on 2008-02-24.
- ^ 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. Retrieved on 2008-02-24.
- ^ Janssen;
Krabbendam L, Bak M, Hanssen M, Vollebergh W, de Graaf R, van Os J
(2004). "Childhood abuse as a risk factor for psychotic experiences". Acta Psychiatrica Scandinavica 109: 38-45. PMID 14674957. Retrieved on 2008-02-24.
- ^ a b Bentall
RP; Fernyhough C, Morrison AP, Lewis S, Corcoran R (2007). "Prospects
for a cognitive-developmental account of psychotic experiences". Br J Clin Psychol 46 (Pt 2): 155-73. PMID 17524210. Retrieved on 2008-02-26.
- ^ Subotnik,
KL; Goldstein, MJ, Nuechterlein, KH, Woo, SM and Mintz, J (2002). "Are
Communication Deviance and Expressed Emotion Related to Family History
of Psychiatric Disorders in Schizophrenia?". Schizophrenia Bulletin 28 (4): 719-29. PMID 12795501. Retrieved on 2008-02-24.
- ^ Gregg L; Barrowclough C, Haddock G (2007). "Reasons for increased substance use in psychosis". Clinical Psychology Review 27 (4): 494-510. PMID 17240501. Retrieved on 2008-02-24.
- ^ Laruelle
M; Abi-Dargham A, van Dyck CH, Gil R, D'Souza CD, Erdos J, McCance E,
Rosenblatt W, Fingado C, Zoghbi SS, Baldwin RM, Seibyl JP, Krystal JH,
Charney DS, Innis RB (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: 9235-40. PMID 8799184. Retrieved on 2008-02-24.
- ^ Mueser
KT; Yarnold PR, Levinson DF, Singh H, Bellack AS, Kee K, Morrison RL,
Yadalam KG (1990). "Prevalence of substance abuse in schizophrenia:
demographic and clinical correlates". Schizophrenic Bulletin 16 (1): 31-56. PMID 2333480. Retrieved on 2008-02-24.
- ^ 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. Retrieved on 2008-02-24.
- ^ Broome
MR; Woolley JB, Tabraham P, Johns LC, Bramon E, Murray GK, Pariante C,
McGuire PK, Murray RM (2005). "What causes the onset of psychosis?". Schizophrenia Research 79 (1): 23-34. PMID 16198238. Retrieved on 2008-02-26.
- ^ Lewis R (2004). "Should cognitive deficit be a diagnostic criterion for schizophrenia?". Journal of Psychiatry and Neuroscience 29 (2): 102-113. PMID 15069464. Retrieved on 2008-02-26.
- ^ Brune
M; Abdel-Hamid M, Lehmkamper C, Sonntag C (2007). "Mental state
attribution, neurocognitive functioning, and psychopathology: What
predicts poor social competence in schizophrenia best?". Schizophrenia Research 92 (1-2): 151-9. PMID 17346931. Retrieved on 2008-02-26.
- ^ Sitskoorn
MM; Aleman A, Ebisch SJH, Appels MCM, Khan RS (2004). "Cognitive
deficits in relatives of patients with schizophrenia: a meta-analysis".
Schizophrenia Research 71 (2): 285-295. PMID 15474899. Retrieved on 2008-02-26.
- ^ Kurtz MM (2005). "Neurocognitive impairment across the lifespan in schizophrenia: an update". Schizophrenia Research 74 (1): 15-26. PMID 15694750. Retrieved on 2008-02-26.
- ^ Cohen & Docherty (2004). "Affective reactivity of speech and emotional experience in patients with schizophrenia". Schizophrenia Research 69 (1): 7-14. PMID 15145465. Retrieved on 2008-02-26.
- ^ Horan
WP; Blanchard JJ (2003). "Emotional responses to psychosocial stress in
schizophrenia: the role of individual differences in affective traits
and coping". Schizophrenia Research 60 (2-3): 271-83. PMID 12591589. Retrieved on 2008-02-26.
- ^ Barrowclough
C; Tarrier N, Humphreys L, Ward J, Gregg L, Andrews B (2003).
"Self-esteem in schizophrenia: relationships between self-evaluation,
family attitudes, and symptomatology". J Abnorm Psychol 112 (1): 92-9. PMID 12653417. Retrieved on 2008-02-26.
- ^ Birchwood
M; Meaden A, Trower P, Gilbert P, Plaistow J (2000). "The power and
omnipotence of voices: subordination and entrapment by voices and
significant others". Psychol Med 30 (2): 337-44. PMID 10824654. Retrieved on 2008-02-26.
- ^ Smith
B; Fowler DG, Freeman D, Bebbington P, Bashforth H, Garety P, Dunn G,
Kuipers E (2006). "Emotion and psychosis: links between depression,
self-esteem, negative schematic beliefs and delusions and
hallucinations". Schizophrenia Research 86 (1-3): 181-8. PMID 16857346. Retrieved on 2008-02-26.
- ^ Beck, AT (2004). "A Cognitive Model of Schizophrenia". Journal of Cognitive Psychotherapy 18 (3): 281-88. Retrieved on 2007-05-16.
- ^ Bell V; Halligan PW, Ellis HD (2006). "Explaining delusions: a cognitive perspective". Trends in Cognitive Science 10 (5): 219-26. PMID 16600666. Retrieved on 2008-02-26.
- ^ Kuipers
E; Garety P, Fowler D, Freeman D, Dunn G, Bebbington P (2006).
"Cognitive, emotional, and social processes in psychosis: refining
cognitive behavioral therapy for persistent positive symptoms". Schizophrenia Bulletin 32 (Suppl 1): S24-31. PMID 16885206. Retrieved on 2008-02-26.
- ^ Green MF (2001) Schizophrenia Revealed: From Neurons to Social Interactions. New York: W.W. Norton. ISBN 0-393-70334-7
- ^ Green MF (2006). "Cognitive impairment and functional outcome in schizophrenia and bipolar disorder". Journal of Clinical Psychiatry 67 (Suppl 9): 3-8. PMID 16965182. Retrieved on 2008-02-26.
- ^ Dean CE (2006). "Typical neuroleptics and increased subcortical volumes". American Journal of Psychiatry 156 (11): 1843-4. PMID 10553769. Retrieved on 2008-02-26.
- ^ Jones HM; Pilowsky LS (2002). "Dopamine and antipsychotic drug action revisited". British Journal of Psychiatry 181: 271-275. PMID 12356650. Retrieved on 2008-02-26.
- ^ 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. Retrieved on 2008-02-26.
- ^ 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. Retrieved on 2008-02-26.
- ^ 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. Retrieved on 2008-02-26.
- ^ Tuominen HJ; Tiihonen J, Wahlbeck K (2005). "Glutamatergic drugs for schizophrenia: a systematic review and meta-analysis". Schizophrenia Research 72: 225-34. PMID 15560967. Retrieved on 2008-02-26.
- ^ Johnstone
EC; Crow TJ, Frith CD, Husband J, Kreel L (1976). "Cerebral ventricular
size and cognitive impairment in chronic schizophrenia". The Lancet 2 (7992): 924-6. PMID 62160. Retrieved on 2008-02-26.
- ^ 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. Retrieved on 2008-02-26.
- ^
Cahn W, Hulshoff Pol HE, Bongers M, Schnack HG, Mandl RC, Van Haren NE,
Durston S, Koning H, Van Der Linden JA, Kahn RS. (2002) Brain
morphology in antipsychotic-naïve schizophrenia: a study of multiple
brain structures. Br J Psychiatry Suppl, 43, s66-72. PMID 12271803
- ^
Molina V, Reig S, Sanz J, Palomo T, Benito C, Sánchez J, Sarramea F,
Pascau J, Desco M. (2005) Increase in gray matter and decrease in white
matter volumes in the cortex during treatment with atypical
neuroleptics in schizophrenia. Schizophr Res, 80(1), 61-71. 16150576
- ^ a b van Os J, Burns T, Cavallaro R, et al (2006). Standardized remission criteria in schizophrenia. Acta Psychiatrica Scandinavica, 113(2), 91–5. PMID 16423159
- ^ Kay SR, Fiszbein A, Opler LA (1987). The positive and negative syndrome scale (PANSS) for schizophrenia. Schizophrenia Bulletin, 13(2), 261–76. PMID 3616518
- ^ Turner T. (2007). "Unlocking psychosis". Brit J Med 334 (suppl): s7.
- ^ a b Bellack AS. (2006) Scientific and consumer models of recovery in schizophrenia: concordance, contrasts, and implications. Schizophrenia Bulletin. Jul;32(3):432-42. PMID 16461575
- ^ 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
- ^ 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
- ^ 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.
- ^
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
- ^
Dickson RA, Dalby JT, Williams R, Edwards AL. (1995) Risperidone
induced prolactin elevations in premenopausal women with schizophrenia.
American Journal of Psychiatry,152,1102-1103. PMID 7540803
- ^
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
- ^
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
- ^ Effect of Chronic Exposure to Antipsychotic Medication on Cell Numbers in the Parietal Cortex of Macaque Monkeys,
by Glenn T Konopaske, Karl-Anton Dorph-Petersen, Joseph N Pierri, Qiang
Wu, Allan R Sampson and David A Lewis, Neuropsychopharmacology, 2006,
1-8.
- ^ The influence of psychotropic drugs on cerebral cell female neurovulnerability to antipsychotics,
by Raphael M. Bonelli, Peter Hofmann, Andreas Aschoff, Gerald
Niederwieser, Clemens Heuberger, Gustaf Jirikowski and Hans-Peter
Kapfhammer, International Clinical Psychopharmacology 2005, 20:145-149
- ^ Meltzer HY (1997). "Treatment-resistant schizophrenia--the role of clozapine". Current Medical Research and Opinion 14 (1): 1–20. PMID 9524789.
- ^ Wahlbeck K, Cheine MV, Essali A (2007). "Clozapine versus typical neuroleptic medication for schizophrenia". The Cochrane Database of Systematic Reviews (2). John Wiley and Sons, Ltd.. doi:10.1002/14651858.CD000059. PMID 10796289. ISSN 1464-780X.
- ^ Haas
SJ, Hill R, Krum H (2007). "Clozapine-associated myocarditis: a review
of 116 cases of suspected myocarditis associated with the use of
clozapine in Australia during 1993–2003". Drug Safety 30: 47–57. PMID 17194170.
- ^ Lee
M, Dickson RA, Campbell M, Oliphant J, Gretton H, Dalby JT. (1998).
"Clozapine and substance abuse in patients with schizophrenia". Canadian Journal of Psychiatry 43: 855-856.
- ^ Harrow M,
Jobe TH. (2007) Factors involved in outcome and recovery in
schizophrenia patients not on antipsychotic medications: a 15-year
multifollow-up study. J Nerv Ment Dis. May;195(5):406-14. PMID 17502806
- ^ Peet
M, Brind J, Ramchand CN, Shah S, Vankar GK (2001). "Two double-blind
placebo-controlled pilot studies of eicosapentaenoic acid in the
treatment of schizophrenia". Schizophr. Res. 49 (3): 243–51. PMID 11356585.
- ^ Freeman
MP, Hibbeln JR, Wisner KL, Davis JM, Mischoulon D, Peet M, Keck PE,
Marangell LB, Richardson AJ, Lake J, Stoll AL (2006). "Omega-3 fatty
acids: evidence basis for treatment and future research in psychiatry".
The Journal of clinical psychiatry 67 (12): 1954–67. PMID 17194275.
- ^ 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.
- ^ Cormac I, Jones C, Campbell C (2002). Cognitive behaviour therapy for schizophrenia. Cochrane Database of systematic reviews, (1), CD000524. PMID 11869579
- ^
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
- ^ 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
- ^ 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
- ^ 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
- ^ Glynn SM, Cohen AN, Niv N (2007). New challenges in family interventions for schizophrenia. Expert Rev Neurother. Jan;7(1):33–43. PMID 17187495
- ^ Pharoah F, Mari J, Rathbone J, Wong W. (2006) Family intervention for schizophrenia Cochrane Database of Systematic Reviews, Issue 4
- ^ Jones, S., Hayward, P. (2004). Coping with Schizophrenia: A Guide for Patients, Families and Caregivers. Oxford, England: Oneworld Pub.. ISBN 1-85168-344-5.
- ^ Torrey, EF (2006). Surviving Schizophrenia: A Manual for Families, Consumers, and Providers (5th Edition). HarperCollins. ISBN 0-06-084259-8.
- ^ Kopelowicz A, Liberman RP, Zarate R (2006). Recent advances in social skills training for schizophrenia. Schizophrenia Bulletin. 2006 Oct;32 Suppl 1:S12–23. PMID 16885207
- ^ American Psychiatric Association (2004) Practice Guideline for the Treatment of Patients With Schizophrenia. Second Edition.
- ^ 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.
- ^ Ruddy R, Milnes D. (2005) Art therapy for schizophrenia or schizophrenia-like illnesses. Cochrane Database of Systematic Reviews, Issue 4
- ^ Ruddy RA, Dent-Brown K. (2007) Drama therapy for schizophrenia or schizophrenia-like illnesses. Cochrane Database of Systematic Reviews, Issue 1.
- ^ Mosher LR (1999) Soteria and Other Alternatives to Acute Psychiatric Hospitalization: A Personal and Professional Review. Journal of Nervous and Mental Disease, 187, 142–149. PMID 10086470
- ^
Calton T, Ferriter M, Huband N, Spandler H. A systematic review of the
Soteria paradigm for the treatment of people diagnosed with
schizophrenia. Schizophrenia Bulletin, 34 (1), 181-92. PMID 17573357
- ^ Greenhalgh J, Knight C, Hind D, Beverley C, Walters S (March 2005). "(abstract)
Clinical and cost-effectiveness of electroconvulsive therapy for
depressive illness, schizophrenia, catatonia and mania: systematic
reviews and economic modelling studies.". Health Technol Assess. 9 (9): 1-156. Retrieved on 2007-06-17.
- ^ National Institute for Health and Clinical Excellence (April 2003). The
clinical effectiveness and cost effectiveness of electroconvulsive
Therapy (ECT) for depressive illness, schizophrenia, catatonia and
mania. (English). National Institute for Health and Clinical Excellence. Retrieved on 2007-06-17.
- ^ Mashour GA, Walker EE, Martuza RL. (2005) Psychosurgery: past, present, and future. Brain Research: Brain Research Reviews, 48 (3), 409-19. PMID 15914249
- ^ 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
- ^ Harrison G,
Hopper K, Craig T, Laska E, Siegel C, Wanderling J, Dube KC, Ganev K,
Giel R, an der Heiden W, Holmberg SK, Janca A, Lee PW, León CA,
Malhotra S, Marsella AJ, Nakane Y, Sartorius N, Shen Y, Skoda C, Thara
R, Tsirkin SJ, Varma VK, Walsh D, Wiersma D. (2001) Recovery from
psychotic illness: a 15- and 25-year international follow-up study. Br J Psychiatry. Jun;178:506-17. PMID 11388966
- ^
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
- ^
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
- ^ Harvey, C.A., Jeffreys, S.E., McNaught, A.S., Blizard, R.A., King, M.B.(2007) The
Camden Schizophrenia Surveys III: Five-Year Outcome of a Sample of
Individuals From a Prevalence Survey and the Importance of Social
Relationships. International Journal of Social Psychiatry, Vol. 53, No. 4, 340-356
- ^
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
- ^ Davidson L, McGlashan TH. (1997) The varied outcomes of schizophrenia. Canadian Journal of Psychiatry, 42 (1), 34–43. PMID 9040921
- ^
Lieberman JA, Koreen AR, Chakos M, Sheitman B, Woerner M, Alvir JM,
Bilder R. (1996) Factors influencing treatment response and outcome of
first-episode schizophrenia: implications for understanding the
pathophysiology of schizophrenia. Journal of Clinical Psychiatry, 57 Suppl 9, 5–9. PMID 8823344
- ^ Bebbington PE, Kuipers E (1994). The predictive utility of expressed emotion in schizophrenia: an aggregate analysis. Psychological Medicine, 24, 707–718. PMID 7991753
- ^ Hannerz H, Borga P, Borritz M (2001). Life expectancies for individuals with psychiatric diagnoses. Public Health, 115 (5), 328–37. PMID 11593442
- ^
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
- ^ Williams R, Dalby JT. Eds. (1989). Depression in Schizophrenics. New York: Plenum Publishing.
- ^ Caldwell CB, Gottesman II. (1990). Schizophrenics kill themselves too: a review of risk factors for suicide. Schizophrenia Bulletin, 16(4), 571–89. PMID 2077636
- ^ Walsh E, Buchanan A, Fahy T (2002). Violence and schizophrenia: examining the evidence. British Journal of Psychiatry. 2002 Jun;180:490–5. PMID 12042226
- ^ 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.
- ^ 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
- ^ 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
- ^ Swanson JW,
Holzer CE, Ganju VK, Jono RT. (1990) Violence and Psychiatric Disorder
in the Community: Evidence From the Epidemiologic Catchment Area
Surveys Hosp Community Psychiatry 41:761-770, July 1990 PMID 2142118
- ^ a b 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.
- ^ 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
- ^ Fazel S, Grann M (2004). Psychiatric morbidity among homicide offenders: a Swedish population study. American Journal of Psychiatry, 161(11), 2129–31. PMID 15514419
- ^ 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
- ^
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
- ^ 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
- ^ 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.
- ^ 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
- ^ 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
- ^
Cannon TD, Cornblatt B, McGorry P. (2007) Editor's Introduction: The
Empirical Status of the Ultra High-Risk (Prodromal) Research Paradigm. Schizophrenia Bulletin, 33 (3), 661–4. PMID 17470445
- ^ Drake RJ, Lewis SW. (2005) Early detection of schizophrenia. Current Opinion in Psychiatry, 18 (2), 147–50. PMID 16639167
- ^ Van Os J, Delespaul P. (2005) Toward a world consensus on prevention of schizophrenia. Dialogues in Clinical Neuroscience, 7 (1), 53–67.
- ^
Haroun N, Dunn L, Haroun A, Cadenhead KS. (2006) Risk and protection in
prodromal schizophrenia: ethical implications for clinical practice and
future research. Schizophrenia Bulletin, 32 (1), 166–78. PMID 16207892. Full text
- ^ Hafner H, Maurer K, Ruhrmann S, et al. (2004) "Early detection and secondary prevention of psychosis: facts and visions". European Archives of Psychiatry and Clinical Neuroscience, 254 (2), 117–28. PMID 15146341
- ^ McGorry, Patrick (2003). "The Influence of Stigma on Preventive Efforts in Psychotic Disorders," in Schizophrenia (WPA Series in Evidence & Experience in Psychiatry), p. 292.
- ^ 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, 89(9):1339–45. PMID 10474550
- ^ Phelan, Jo
C., Link, Bruce G., Stueve, Ann, Pescosolido, Bernice A. (1997).
"Public Conceptions of Mental Illness in 1950 and 1996: What Is Mental
Illness and Is It to be Feared?," Journal of Health and Social Behavior, 41(2):188-207
- ^ American Psychiatric Association. Americans Still Cling to Myths About Mental Illness, Survey Finds. Psychiatric News. December 7, 2001 Volume 36 Number 23 Full text
- ^ Cooper D (1969) The Dialectics of Liberation. London: Penguin Books Ltd. ISBN 0140210296
- ^ Szasz T (1984) The Myth of Mental Illness: Foundations of a Theory of Personal Contact (revised edition. New York: Harper and Row. ISBN 0060911514
- ^ Colin, Ross (2004). Schizophrenia: Innovations in Diagnosis and Treatment. Haworth Press. ISBN 0789022699.
- ^ R.D. Laing's and Aaron Esterson. Sanity, Madness and the Family (1964)
- ^ Bateson, G.,
Jackson, D. D., Haley, J. & Weakland, J., 1956, Toward a theory of
schizophrenia. (in: 'Behavioral Science', vol.1, 251-264)
- ^ Jaynes J (1976) The Origin of Consciousness in the Breakdown of the Bicameral Mind. Houghton Mifflin. ISBN 0395207290
- ^ Polimeni J, Reiss JP (2002). How shamanism and group selection may reveal the origins of schizophrenia. Medical Hypothesis, 58(3), 244–8. PMID 12018978
- ^ 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.
- ^ Kurtz, Paul (1986). The Transcendental Temptation: A Critique of Religion and the Paranormal (Prometheus Books) ISBN 0-87975-645-4
- ^ Crow TJ (1997). Schizophrenia as failure of hemispheric dominance for language. Trends in Neurosciences, 20(8), 339–343. PMID 9246721
- ^ Pfeiffer, Carl C.. Nutrition and Mental Illness: An Orthomolecular Approach to Balancing Body Chemistry. Healing Art Press. ISBN 0-89281-226-5.
- ^ Hoffer and Walker, Orthomolecular Nutrition. Keats Publishing, 1978
- ^ Dohan FC (1970). Coeliac disease and schizophrenia. Lancet, 1970 April 25;1(7652):897–8. PMID 4191543
*Dohan FC (1973). Coeliac disease and schizophrenia. British Medical Journal, 3(5870): 51–52. PMID 4740433
* Dohan FC (1979). Celiac-type diets in schizophrenia. Am J Psychiatry, 1979 May;136(5):732–3. PMID 434265
- ^
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
- ^ Lakhan SE, Vieira KF (2008). "Nutritional therapies for mental disorders". Nutr J 7: 2. doi:10.1186/1475-2891-7-2. PMID 18208598.
- ^ 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
- ^
Hanafy A. Youssef, Fatma A. Youssef and T. R. Dening (1996), "Evidence
for the existence of schizophrenia in medieval Islamic society", History of Psychiatry 7: 55-62 [57].
- ^ Kraepelin E. (1907) Text book of psychiatry (7th ed) (trans. A.R. Diefendorf). London: Macmillan.
- ^ "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
- ^ Kuhn R; tr. Cahn CH (2004). "Eugen Bleuler's concepts of psychopathology". Hist Psychiatry 15 (3): 361–6. doi:10.1177/0957154X04044603. PMID 15386868.
- ^ 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
- ^ 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
- ^
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
- ^ 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
- ^ Lifton RJ. (2000) The Nazi Doctors: Medical Killing and the Psychology of Genocide. Basic Books. ISBN 0465049052
- ^ Wing JK (1971) International comparisons in the study of the functional psychoses. British Medical Bulletin, 27 (1), 77–81. PMID 4926366
- ^ Wilson M. (1993) DSM-III and the transformation of American psychiatry: a history. American Journal of Psychiatry, 150 (3), 399–410. PMID 8434655
- ^ Deveson, Anne (1991). Tell Me I'm Here. Penguin. ISBN 0-14-027257-7.
Further reading
- Bentall, R. (2003) Madness explained: Psychosis and Human Nature. London: Penguin Books Ltd. ISBN 0-7139-9249-2
- Dalby, J.T. (1997) Mental Disease in History: A selection of translated readings. New York: Peter Lang Publishing. ISBN 0-8204-3056-0
- 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
- 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 10818864
- Laing, R.D. (1999) The Divided Self: An Existential Study in Sanity and Madness. London: Penguin Books Ltd. ISBN 0-140-13537-5
- Lidz, Theodore, Stephen Fleck & Alice Cornelison, Schizophrenia and the Family. International Universities Press, 1965. ISBN 978-0823660018
- Noll, Richard (2007) The Encyclopedia of Schizophrenia and Other Psychotic Disorders, Third Edition ISBN 0-8160-6405-9
- Open
The Doors - information on global programme to fight stigma and
discrimination because of Schizophrenia. The World Psychiatric
Association (WPA)
- 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.
- Scientific American Magazine (January 2004 Issue) Decoding 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.)
- 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
- News, information and further description
- Critical approaches to schizophrenia
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