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There are five types of schizophrenia, each based on the kind of symptoms the person has
at the time of assessment:
• Catatonic schizophrenia: The person with this type of schizophrenia primarily has
at least two of the following symptoms: difficulty moving, resistance to moving,
excessive movement, abnormal movements, and/or repeating what others say or
do.
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• Residual schizophrenia: While the full-blown characteristic positive symptoms of
schizophrenia (those that involve an excess of normal behavior, such as delusions,
paranoia, or heightened sensitivity) are absent, the sufferer has less severe forms
of the disorder or has only negative symptoms (symptoms characterized by a
decrease in function, such as withdrawal, disinterest, and not speaking).
•
• History of schizophrenia;
the term schizophrenia has only been in use since 1911. Soon before that, it was deemed
a separate mental illness in 1887 by Emil Kraepelin. Despite that relatively recent history,
it has been described throughout written history. Ancient Egyptian, Hindu, Chinese,
Greek, and Roman writings described symptoms similar to the positive symptoms of
schizophrenia. During medieval times, schizophrenia, like other illnesses, was often
viewed as evidence of the sufferer being possessed by spirits or evil powers.
Environmentally, the risks of developing schizophrenia can even occur before birth. For
example, the risk of schizophrenia is increased in individuals whose mother had one of
certain infections during pregnancy. Difficult life circumstances during childhood, like
the early loss of a parent, parental poverty, bullying, witnessing parental violence;
emotional, sexual, or physical abuse; physical or emotional neglect; and insecure
attachment have been associated with the development of this illness. Even factors like
how well represented an ethnic group is in a neighborhood can be a risk or protective
factor for developing schizophrenia. For example, some research indicates that ethnic
minorities may be more at risk for developing this disorder if there are fewer members of
the ethnic group to which the individual belongs in their neighborhood.
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What are schizophrenia symptoms and signs?
• Hearing, seeing, feeling, smelling, or tasting things that have no basis in reality
(hallucinations)
• Disorganized speech
• Disorganized behaviors
• Catatonic behaviors
• Lack of speech
• Lack of motivation
As is true with virtually any mental-health diagnosis, there is no one test that definitively
indicates that someone has schizophrenia. Therefore, health-care practitioners diagnose
this disorder by gathering comprehensive medical, family, and mental-health information.
Patients tend to benefit when the professional takes into account their client's entire life
and background. This includes but is not limited to the person's gender, sexual
orientation, cultural, religious and ethnic background, and socioeconomic status. The
practitioner will also either perform a physical examination or request that the
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individual's primary-care doctor perform one. The medical examination will usually
include lab tests to evaluate the person's general health and to explore whether or not the
individual has a medical condition that might produce psychological symptoms.
Diagnosing schizophrenia
The first step to schizophrenia treatment is getting a correct diagnosis. This isn’t always
easy, since the symptoms of schizophrenia can resemble those caused by other mental
and physical health problems. Furthermore, people with schizophrenia may believe
nothing is wrong with them and resist going to the doctor. Because of these issues, it is
best to see a psychiatrist with experience identifying and treating schizophrenia, rather
than a family doctor.
Click here for a list of clinics that specialize in the early diagnosis and treatment of
schizophrenia.
Source: Schizophrenia.com
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• Medical history and exam — Your doctor will ask about your personal and family
health history. He or she will also perform a complete physical examination to
check for medical issues that could be causing or contributing to the problem.
• Laboratory tests — While there are no laboratory tests that can diagnose
schizophrenia, simple blood and urine tests can rule out other medical causes of
symptoms. The doctor may also order brain imaging studies, such as an MRI or a
CT scan, in order to look for brain abnormalities associated with schizophrenia.
- The presence of two or more of the following symptoms for at least 30 days:
1. Hallucinations
2. Delusions
3. Disorganized speech
4. Disorganized or catatonic behavior
5. Negative symptoms (emotional flatness, apathy, lack of speech)
- Significant problems functioning at work or school, relating to other people, and taking
care of oneself.
- No other mental health disorder, medical issue, or substance abuse problem is causing
the symptoms.
Despite the widespread misconception that people with schizophrenia have no chance of
recovery or improvement, the reality is much more hopeful. Think of schizophrenia as
similar to a chronic medical condition like diabetes: although currently there is no cure, it
can be treated and managed with medication and supportive therapies. When
schizophrenia is stabilized with proper treatment, a person is:
Effective treatment also makes the challenges of schizophrenia less stressful and
frightening for both the individual with the disorder and his or her family members and
loved ones.
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Successful treatment for schizophrenia aims to relieve current symptoms, prevent future
psychotic episodes, and reintegrate the person into society. A treatment plan that
combines medication with supportive services and therapy is the most effective approach.
• 1 in 5 will get better within five years of their first episode of schizophrenia.
• 3 in 5 will get better, but will still have some symptoms. They will have times
when their symptoms get worse.
• 1 in 5 will continue to have troublesome symptoms.
There are two phases of schizophrenia treatment and recovery: one addresses the severe
symptoms of an acute psychotic episode and the other focuses on improving functioning
and preventing relapse during the maintenance or recovery phase of the illness.
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Please help improve this article by adding reliable references. Unsourced material may be
challenged and removed. (August 2009)
Contents
• 1 Introduction
• 2 Discussion
o 2.1 Evidence for the dopamine hypothesis
o 2.2 Evidence against the dopamine hypothesis
• 3 See also
• 4 References
• 5 External links
[edit] Introduction
Some researchers have suggested that dopamine systems in the mesolimbic pathway may
contribute to the 'positive symptoms' of schizophrenia (whereas problems with dopamine
function in the mesocortical pathway may be responsible for the 'negative symptoms',
such as avolition and alogia.)
[edit] Discussion
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Amphetamine, cocaine and similar drugs increase levels of dopamine in the brain and can
cause symptoms which resemble those present in psychosis, particularly after large doses
or prolonged use. This is often referred to as "amphetamine psychosis" or "cocaine
psychosis," but may produce experiences virtually indistinguishable from the positive
symptoms associated with schizophrenia. Similarly, those treated with dopamine
enhancing levodopa for Parkinson's disease can experience psychotic side effects
mimicking the symptoms of schizophrenia. Up to 75% of patients with schizophrenia
have increased signs and symptoms of their psychosis upon challenge with moderate
doses of methylphenidate or amphetamine or other dopamine-like compounds, all given
at doses at which control normal volunteers do not have any psychologically disturbing
effects.[2][3] Some functional neuroimaging studies have also shown that, after taking
amphetamine, patients diagnosed with schizophrenia show greater levels of dopamine
release (particularly in the striatum) than non-psychotic individuals. However, the acute
effects of dopamine stimulants include euphoria, alertness and over-confidence; these
symptoms are more reminiscent of mania than schizophrenia.[4]
Genetic evidence has suggested that there may be genes, or specific variants of genes,
that code for mechanisms involved in dopamine function, which may be more prevalent
in people experiencing psychosis or diagnosed with schizophrenia. Dopamine related
genes linked to psychosis in this way include COMT, DRD4, and AKT1.[7]
Further experiments, conducted as new methods were developed (particularly the ability
to use PET scanning to examine drug action in the brain of living patients) challenged the
view that the amount of dopamine blocking was correlated with clinical benefit. These
studies showed that some patients had over 90% of their D2 receptors blocked by
antipsychotic drugs, but showed little reduction in their psychoses. This primarily occurs
in patients who have had the psychosis for ten to thirty years. At least 90-95% of first-
episode patients, however, respond to antipsychotics at low doses and do so with D2
occupancy of 60-70%. The antipsychotic aripiprazole occupies over 90% of D2 receptors,
but this drug is both an agonist and an antagonist at D2 receptors.
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Furthermore, although dopamine-inhibiting medications modify dopamine levels within
minutes, the associated improvement in patient symptoms is usually not visible for at
least several days, suggesting that dopamine may be indirectly responsible for the illness.
[8]
Similarly, there is now evidence to suggest there may be a number of functional and
structural anomalies in the brains of some people diagnosed with schizophrenia, such as
changes in grey matter density in the frontal and temporal lobes.[1] It appears, therefore,
that there are multiple causes for psychosis and schizophrenia, including gene mutations
and anatomical lesions.
Other evidence suggests that social and environmental factors are important in explaining
how either schizophrenia, or specific episodes of psychosis, are triggered. This research
has led people[who?] to argue that a purely biological explanation, without reference to
social, cultural or environmental factors will never fully explain such phenomena. Such
cultural factors can become highly stressful to certain individuals, such as immigrants,
markedly altering their brain chemistry, including dopamine, and can be associated with
increased risk to psychotic episodes.[citation needed]
Psychiatrist David Healy has argued that drug companies have inappropriately promoted
the dopamine hypothesis of schizophrenia as a deliberate and calculated simplification
for the benefit of drug marketing.