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SCHIZOPHRENIAs

Schizophrenia, also sometimes called split personality disorder, is a chronic, severe,


debilitating mental illness that affects about 1% of the population, corresponding to more
than 2 million people in the United States alone. Other statistics about schizophrenia
include that it affects men about one and a half times more commonly than women. It is
one of the psychotic mental disorders and is characterized by symptoms of thought,
behavior, and social problems. The thought problems associated with schizophrenia are
described as psychosis, in that the person's thinking is completely out of touch with
reality at times. For example, the sufferer may hear voices or see people that are in no
way present or feel like bugs are crawling on their skin when there are none. The
individual with this disorder may also have disorganized speech, disorganized behavior,
physically rigid or lax behavior (catatonia), significantly decreased behaviors or feelings,
as well as delusions, which are ideas about themselves or others that have no basis in
reality (for example, experience the paranoia of thinking others are plotting against them
when they are not).

What are the different types of schizophrenia?

There are five types of schizophrenia, each based on the kind of symptoms the person has
at the time of assessment:

• Paranoid schizophrenia: The individual is preoccupied with one or more delusions


or many auditory hallucinations but does not have symptoms of disorganized
schizophrenia.

• Disorganized schizophrenia: Prominent symptoms are disorganized speech and


behavior, as well as flat or inappropriate affect. The person does not have enough
symptoms to be characterized as catatonic schizophrenic.

• 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.

• Undifferentiated schizophrenia: This is characterized by episodes of two or more


of the following symptoms: delusions, hallucinations, disorganized speech or
behavior, catatonic behavior or negative symptoms, but the individual does not
qualify for a diagnosis of paranoid, disorganized, or catatonic type of
schizophrenia.

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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.

A number of accomplished individuals suffer from schizophrenia. The film A Beautiful


Mind depicts the life of John Nash, a noted scientist, and his struggles with paranoid
schizophrenia. The film The Soloist explores the challenges faced by Juilliard-trained
musician Nathaniel Ayers as a result of schizophrenia.

What are causes of schizophrenia? Is it hereditary?

One frequently asked question about schizophrenia is if it is hereditary. As with most


other mental disorders, schizophrenia is not directly passed from one generation to
another genetically, and there is no single cause for this illness. Rather, it is the result of a
complex group of genetic, psychological, and environmental factors. Genetically,
schizophrenia and bipolar disorder have much in common, in that the two disorders share
a number of the same risk genes. However, the fact is that both illnesses also have some
genetic factors that are unique.

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?

Symptoms of schizophrenia include the following:

Positive, more overtly psychotic symptoms

• Beliefs that have no basis in reality (delusions)

• Hearing, seeing, feeling, smelling, or tasting things that have no basis in reality
(hallucinations)

• Disorganized speech

• Disorganized behaviors

• Catatonic behaviors

Negative, potentially less overtly psychotic symptoms

• Inhibition of facial expressions

• Lack of speech

• Lack of motivation

How is schizophrenia diagnosed?

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.

In asking questions about mental-health symptoms, mental-health professionals are often


exploring if the individual suffers from hallucinations or delusions, depression and/or
manic symptoms, anxiety, substance abuse, as well as some personality disorders (for
example, schizotypal personality disorder) and developmental disorders (for example,
autism spectrum disorders). Since some of the symptoms of schizophrenia can also occur
in other mental illnesses, the mental-health screening is to determine if the individual
suffers from schizoaffective disorder or other psychotic disorder, bipolar disorder, an
anxiety disorder, or a substance abuse or personality disorder. Any disorder that is
associated with bizarre behavior, mood, or thinking, like borderline personality disorder
or another psychotic disorder, as well as dissociative identity disorder (DID), formally
known as multiple personality disorder (MPD) may be particularly challenging to
distinguish from schizophrenia. In order to assess the person's current emotional state,
health-care providers perform a mental-status examination as well.

In addition to providing treatment that is appropriate to the diagnosis, determining the


presence of mental illnesses that may co-occur (be comorbid) with schizophrenia is
important in improving the life of individuals with schizophrenia. For example, people
with schizophrenia are at increased risk of having a depressive or anxiety disorder and of
committing suicide.

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.

Find a Schizophrenia Specialist

Click here for a list of clinics that specialize in the early diagnosis and treatment of
schizophrenia.

Source: Schizophrenia.com

A diagnosis of schizophrenia is made based on a full psychiatric evaluation, medical


history, physical exam, and lab tests.

• Psychiatric evaluation — The doctor or psychiatrist will ask a series of questions


about you or your loved one’s symptoms, psychiatric history, and family history
of mental health problems.

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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.

Mental health professionals use the following criteria to diagnose


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.

- Continuous signs of schizophrenia for at least 6 months, with active symptoms


(hallucinations, delusions, etc.) for at least 1 month.

- No other mental health disorder, medical issue, or substance abuse problem is causing
the symptoms.

Treatment for schizophrenia

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:

• Less likely to have frequent or lengthy hospitalizations


• Less likely to require intensive support at home
• Less likely to abuse alcohol or drugs
• Less likely to commit suicide
• More likely to live and work independently
• More likely to enjoy satisfying relationships

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.

The Outlook for Schizophrenia

For every 5 people who develop schizophrenia:

• 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.

Source: Royal College of Psychiatrists

Stages of schizophrenia recovery

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.

• Acute phase — An acute episode of schizophrenia involves intense psychotic


symptoms such as hallucinations, delusions, paranoia, and confused thinking. The
aim of treatment in the acute phase is to get the psychotic symptoms under control
so the patient isn’t a danger to self or to others. Hospitalization may be required
during this time. Medication is the primary treatment. Given the right drug and
dose, schizophrenia medication can greatly reduce psychotic symptoms within six
weeks.
• Stabilization phase — Once the acute psychotic symptoms have been controlled,
most people go through a stabilization phase in which they continue to experience
bothersome, yet milder symptoms of schizophrenia. During this phase, patients
are particularly vulnerable to relapse. The aim of treatment in the stabilization
phase is to prevent relapse, reduce symptoms even more, and move the patient
forward into a more stable recovery phase.
• Maintenance phase — The long-term recovery phase of schizophrenia is known
as the maintenance phase of treatment. During the maintenance phase of
treatment, the goal is to sustain symptom remission or control, reduce the risk of
relapse and hospitalization, and teach skills for daily living. Maintenance
treatment typically involves medication, supportive therapy, family education and
counseling, and vocational and social rehabilitation.

Dopamine hypothesis of schizophrenia


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challenged and removed. (August 2009)

The dopamine hypothesis of schizophrenia or the dopamine hypothesis of psychosis


is a model attributing symptoms of schizophrenia (like psychoses) to a disturbed and
hyperactive dopaminergic signal transduction. The model draws evidence from the
observation that a large number of antipsychotics have dopamine-receptor antagonistic
effects. The theory, however, does not posit dopamine overabundance as a complete
explanation for schizophrenia.

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.)

Recent evidence on a variety of animal models of psychosis, such as sensitization of


animal behaviour by amphetamine, or phencyclidine (Angel Dust)[citation needed], or excess
steroids[citation needed], or by removing various genes (COMT, DBH, GPRK6, RGS9,
RIIbeta), or making brain lesions in newborn animals, or delivering animals abnormally
by Caesarian section, all induce a marked behavioural supersensitivity to dopamine and a
marked rise in the number of dopamine D2 receptors in the high-affinity state for
dopamine.[1] This latter work implies that there are multiple genes and neuronal pathways
that can lead to psychosis and that all these multiple psychosis pathways converge via the
high-affinity state of the D2 receptor, the common target for all antipsychotics, typical or
atypical.

[edit] Discussion

[edit] Evidence for the dopamine hypothesis

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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]

A group of drugs called the phenothiazines, including antipsychotics such as


chlorpromazine, has been found to antagonize dopamine binding (particularly at
receptors known as D2 dopamine receptors) and reduce positive psychotic symptoms.
This observation was subsequently extended to other antipsychotic drug classes, such as
butyrophenones including haloperidol. The link was strengthened by experiments in
1970s which suggested that the binding affinity of antipsychotic drugs for D2 dopamine
receptors seemed to be inversely proportional to their therapeutic dose. This correlation,
suggesting that receptor binding is causally related to therapeutic potency, was reported
by two laboratories in 1976.[5][6]

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]

Tobacco use is strongly associated with schizophrenia, likely through dopamine


modulation by nicotinic acetylcholine receptors.

[edit] Evidence against the dopamine hypothesis

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, a new generation of antipsychotic drugs (called the atypical antipsychotics)


were found to be just as effective as older typical antipsychotic drugs in controlling
psychosis, particularly the negative symptoms, despite the fact that they have lower
affinity for dopamine receptors than for various other neurotransmitter receptors.[9] More
recent work, however, has shown that atypical antipsychotic drugs such as clozapine and
quetiapine bind and unbind rapidly and repeatedly to the dopamine D2 receptor.[10]

The excitatory neurotransmitter glutamate is now also thought to be associated with


schizophrenia. Phencyclidine (also known as PCP or "Angel Dust") and ketamine, both
of which block glutamate (NMDA) receptors, are known to cause psychosis closely
resembling schizophrenia, further suggesting that psychosis and schizophrenia cannot
fully be explained in terms of dopamine function, but may also involve other
neurotransmitters.[11]

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.

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