Sunday, 21 October 2007

Schizophrenia

Schizophrenia

‘Schizophrenia’ = Skhizein (To split) and Phren (Mind) in Greek.

Schizophrenia is completely different to DID.
Schizophrenia is a loss of contact with reality – sufferers are not aware of the effects of their behaviour on others around them.

Speculations on the origins and development of schizophrenia range from entirely ‘genetic and biological’ through to ‘genetic predisposition and environment trigger’ to the ‘entirely environmental/social.’

Clinical Characteristics:

Catatonic Schizophrenia is one type of schizophrenia, there are several and all hold several features in common:
· Sufferers cognitive, social and emotional state suffers a general deterioration leading to difficulties and breakdowns in normal relationships including those at work and home;
· Onset occurs between 15-45 years.
· Equally common in males as females;
· Occurs 4-5 yrs earlier in males than females.
· Symptoms always appear before the age of 50 – usually in teens and early twenties for males and females respectively.;
· In most countries across the world the lifetime risk of acquiring schizophrenia is 1%.
· Symptoms last at least 6 months before they can be taken as symptoms of schizophrenia;
· Auditory hallucinations and visual delusions occur. Other symptoms include severe disturbances in thought and a loss of self understanding.
· Sufferers are unaware of the impact that they have on others around them and seem to live in their own distorted worlds.

A distinction exists between acute and chronic onset:
1. Chronic = Insidious change in an apparently normal young person who gradually starts to lose drive and motivation and drift away from friends. After months or even years of this deterioration, more obvious signs of disturbance, such as delusional ideas or hallucinations appear.
2. Acute = more obvious signs of stressful event are represented in very disturbed behaviour within a few days..


Sub types of schizophrenia include:
1. Paranoid schizophrenia:
Delusions and or hallucinations are the predominant characteristics. Negative symptoms such as flattening of affect and poverty of speech are less apparent than in other types.
2. Hebephrenic (AKA Disorganised) Schizophrenia
Disorganised behaviour and rambling incoherent speech;
Marked flattening, inappropriateness of affect.
3. Catatonic Schizophrenia
Psychomotor abnormality is the central characteristic;
Adoption of strange postures and flailing limbs;
Often show negativism where they resist all instruction or attempts to move them
4. Undifferentiated schizophrenia
Labelled where they have insufficient symptoms to fit into a sub type or excessive symptoms to fit into one single type.
5. Post Schizophrenic depression (Not in DSM-IV)
Criteria met in last 12 months for classification but not currently present;
Depressive symptoms are long and severe.
6. Residual Schizophrenia
Criteria met in past though not at the present time;
Have been many signs of negative symptoms throughout the previous 12 months.
7. Simple schizophrenia (Not in DSM-IV)
Minimum of 12 months progression development of social withdrawal, apathy, poverty of speech and marked decline scholastic / occupational performance.
General criteria must be met as well as specific criteria for each sub type.


Positive symptoms:
Symptom
Explanation
Example
Delusions
False beliefs that the sufferer thought to be true.
Persecution – having special knowledge or a belief that powers, thought or actions are being controlled by an external force.
Hallucinations
Imagined sensory perceptions.
Auditory – hearing imagined voices (And holding prolonged conversations with these voices)
Thought Disorder
Confused thinking that is evident in what they say and how they say it.
Incoherent speech – jumping from one subject to another with little or no logical connection. The grammar may be strange and only makes sense to the speaker. They may claim that thoughts are being broadcast or stolen from them or are being controlled or influenced by an alien, demon, or foreign power.
Bizarre Behaviour
Strange and inappropriate behaviour (Contravening social norms)
Undressing in public or making odd faces, body gestures and postures for no apparent purpose.

Negative Symptoms:
Symptom
Explanation
Example
Blunted Emotional Responses
No emotional involvement in or response to things in their immediate environment
Unchanging facial expression, gestures, or tone of voice regardless of whether the environment would require a happy or sad response, or an inappropriate response e.g. laughing at a funeral.
Loss of drive
Little interest or motivation to work or enjoy leisure activities
Inability to wash and feed to take decisions and being entirely passive.
Social Withdrawal
Difficulty making and keeping friends acquaintances or more intimate relationships
Negativity and passivity and a reluctance to engage in social interaction
Poverty of Thought
Considerable reduction in cognitive activity: Thinking limited to immediate concerns.
Limited amount of speech and may answer questions with ‘yes’ ‘no’ or ‘I don’t know’



Genetic Explanations for Schizophrenia:

Sample sizes and modestly positive results do not add up to certainty, however, a summary of evidence to this end includes:

Twin studies showing higher than expected probability that if one twin presents symptoms the other is likely to do so;
The closer the relative to the sufferer, the higher the probability that they might develop schizophrenia;
Adopted children who’s natural family contained a member who had developed schizophrenia were more at risk;
A child adopted by a family where a member later develops schizophrenia is no more likely to develop the illness itself.

Where biological changes do occur they could be the result of the schizophrenia rather than the cause, or linked in ways we have yet to discover.

The longitudinal Copenhagen High Risk Study (1962 - early 90’s) examined children who’s mothers were diagnosed as having schizophrenic symptoms and found them much more likely to develop the illness compared to those who did not. There was less than 1 in 10,000 chance (p<0.0001) that these findings could have occurred by chance.

However, this study cannot differentiate between the effects of genes and the effects of the environment.

Adoption studies provide some of the strongest evidence in support of the argument that genetics play a key role in the development of schizophrenia.


Below shows the evidence indicating strong genetic links between genetics and schizophrenia. However, it must be remembered that sample sizes are small and that circumstances of each study were not directly comparable. Also, there are issues to do with the fact that not all social groups are equally likely to be diagnosed with schizophrenia.

Evaluation:
· Research evidence is pretty persuasive for genetic linked risk factors;
· Degree of risk for relatives is never 100% - even with Mz Twins its less than 50%, therefore genetics cant be a complete explanation.
· Search for the relevant gene:
o Without knowing the exact gene it’s impossible to isolate the underlying mechanisms that lead from genetic risk to symptoms of the disorder. The search for the gene continues.

Biochemical explanations of schizophrenia

Dopamine is a brain chemical that increases the sensitivity of the brain cells that promote the individual’s awareness of events around her or him when in danger or aroused and when under stress. If, however, the individual’s level of brain activity is already highly aroused, then the effects of additional dopamine activity may trigger the onset of a psychotic state, such as schizophrenia. (Anti- psychotic drugs block the dopamine-2 (D2) receptors and reduce the severity of some psychotic symptoms.) Studies of other brain chemical (serotonin and noradrenalin) activity are also being extensively researched.

Neurons are individual nerve fibres that carry electrical/chemical ‘messages’. Many millions are densely packed into brain structures. There are tiny gaps between their endings and messages are carried across them by a neurotransmitter substance.
Neurons that have dopamine as their transmitter substance (Dopaminergic neurons) are overactive in individuals who exhibit schizophrenic symptoms. The dopamine hypothesis suggests that ‘excessive activity’ in the dopamine neurons leading to increased dopamine production and limited absorption of existing dopamine is associated with schizophrenia.

An interesting parallel exists with Parkinson’s Disease, where a dopamine increasing drug (L Dopa) seems to have the opposite effect.


Further support for the dopamine hypothesis comes from the post-mortems of patients with schizophrenia. These have revealed specific increase of dopamine in the left amygdale (Falkai et al. 1988) and increased dopamine receptor density in the caudate nucleus putamen (Owen et al. 1978)

Wong et al. (1986) shows in live patients using pet scans that the dopamine receptor density in the caudate nuclei is indeed greater in those with schizophrenia than in controls. This however is not supported in subsequent studies.

Evaluation of Dopamine Hypothesis:
1. Current available evidence supports some form of the dopamine hypothesis.
Drugs alleviate positive symptoms but are not so effective with negative symptoms.
2. Effects of different drugs on different sub types (Type I and II):
Amphetamines worsen positive symptoms (associated with acute schizophrenia) and lessen negative symptoms (Associated with chronic) while phenothiazines (Anti-psychotics) alleviate positive symptoms but aren’t as effective in lessening negative symptoms.
3. Cause or effect cant be established
4. Role of dopamine in other disorders:
Dopamine also implicated in mania and other disorders which have quite different symptoms. Main evidence in dopamine schizophrenia is the effectiveness of phenothiazines in alleviating symptoms.


Neuroanatomical explanations

Advances in brain scanning (neuro-imaging) technology are allowing cognitive and medical researchers to seek structural, organic abnormalities in the brains of people who exhibit behavioural disorders. Two such scanning technologies are Positron Emission Tomography (PET) and Magnetic Resonance Imaging (MRI).

PET scans are used in the diagnosis of problems in bodily organs, particularly the brain. The patient is injected with glucose that contains a tiny amount of radioactive substance — which emits positrons that can be detected by the scanner. As various brain centres use up the glucose their size, location, and connectivity to other brain centres can be recorded.

MRI is a complex diagnostic technique whereby a patient is surrounded by a cylinder that contains a strong magnet. Radio waves from the cylinder cause the atoms of the body to resonate. Each type of body tissue resonates at a different, known, frequency. Since these are known, a computer can build these resonances into a two-dimensional picture. It can ‘see through’ bone and can produce detailed images of just about all parts of the brain and body.

These technologies have shown abnormal brain structures in many patients exhibiting schizophrenic symptoms, for example, the differences in the density of receptor cells for dopamine in schizophrenia patients who were being treated with anti-psychotic drugs and those who were not.

Evidence for neuro-anatomical explanations:
Brown et al (1986) found decreased brain weight and enlarged ventricles, which are the cavities in the brain that hold cerebrospinal fluid.
Flaum et al. (1995) also found enlarged ventricles along with smaller thalamic hippocampal and superior temporal volumes.
Buchsbaum (1990) found abnormalities in the frontal hippocampus and the amygdale. As more MRI studies are being undertaken, more abnormalities are being identified.

The critical time period for the onset of schizophrenia is not usually before adolescence. Therefore if the brain abnormalities precede the onset of clinical symptoms this would confirm the view that schizophrenia is a developmental disorder. Weinberger (!988) claims that despite much research evidence remains inconclusive as to whether there are progressive structural brain changes prior to the initial onset of schizophrenia or whether they follow the onset of clinical symptoms.

Castner (1998) subjected monkeys to brain damaging x rays during fetal development and found that they showed no ill effects in childhood compared to the control group, but at puberty they developed symptoms of schizophrenia such as hallucinations. There are of course ethical issues associated with animal research of this kind.

Evaluation: The neuroanatomical explanation
· Conflicting findings about structural abnormalities.
While MRI studies appear to provide conclusive evidence of structural abnormalities they don’t always agree on the area of the brain that is affected.
Flaum (1995) found no abnormalities in the temporal lobe region,
while Woodruff et al. (1997) found quite significant reductions in the temporal lobe compared with control.
· Structural abnormalities as cause or effect?
Because most studies using MRI techniques have been carried out on people already
diagnosed with schizophrenia it is not clear whether structural abnormalities
predispose to schizophrenia or whether the onset of clinical symptoms cause
structural changes.
· Types of Study:
Prospective studies, which could have shed light on the direction of causality have been carried out only on animals and it is difficult to generalise findings to humans.

Pregnancy and birth factors as explanations for schizophrenia.

Viral illness may damage brain structure and functioning.
This increases if the pregnant woman contracts the illness.
E.g. Influenza, measles and chicken pox.

There is a significant correlation between being born in the winter and early spring and developing schizophrenia. This increases after epidemics of viral infections. (Torrey et al 1988; 1996)

In the southern hemisphere a high proportion of those diagnosed with schizophrenia were born July to September (I.e. Winter months.)

These facts support schizophrenia having a biological origin.
However, not all schizophrenia is associated with brain damage and not all can be linked to viral infection.

Mednick et all (1988) suggestion is that if the mother is infected during the pregnancy there is pre birth exposure to the influenza A virus. It is thought that the 25-30 week foetus is most vulnerable because of accelerated growth of the cerebral cortex at this time.

Its hypothesised that the viral infection enters the brain and gestates until it is activated by hormonal changes in puberty. Alternatively there may be a gradual degeneration of the brain which eventually becomes so severe that symptoms of schizophrenia emerge.

Torrey et all (1988) furthered support for the viral hypothesis comes from the observation that throughout its history peaks in schizophrenia diagnosis have corresponded with major flue epidemics

There are conflicting views as to whether abnormalities result from genetic defect or from birth complications leading to brain damage.

A longitudinal study by Dalman et al. (1999) found significant links between birth complications and later development of schizophrenia, with pre-eclampsia being the most significant risk factor.


Evaluation: Pregnancy and birth factor explanations.
· Methodological problems:
Evidence suggests some link between infection and schizophrenia; however, Torrey inferred causation while doing a correlation study.
Data was based on DSM-II rather than the tighter DSM-III diagnostic range.
· Genetic predisposition:
Torrey et al. (1988) claims the link between viral infection and schizophrenia only exists between those that have a genetic predisposition. Also MZ & DZ twins sharing the same uterus are exposed to same virus and therefore correlation should be 100% - is this the case?
· Birth complications as sole cause?
It’s unlikely that birth complications like pre-eclampsia could be the sole cause of schizophrenia, because this is a common problem and not all such infants go on to develop schizophrenia.

Diathesis-Stress explanations for Schizophrenia


While 51% of all schizophrenics in high EE families suffered a relapse, 49% didn’t.

Other triggers that herald the onset of an episode include momentous life events (Serious illness, Unexpected Bereavement etc.) or a combination of factors which could in isolation be dealt with. E.g. Unemployment, lowered sense of self worth, heavy drinking, marital problems, minor criminal activity, apprehension by the police and a magistrate courts appearance could all trigger an episode.


Schizophrenia did not always develop in those genetically vulnerable.

The Finnish adoption study undertaken by Tienari (1987) investigated environmental factors by assessing the quality of parenting through a battery of tests and interviews. All of the reported cases of schizophrenia occurred in families rated as ‘disturbed.’the high risk sample in healthy environments had occurrences well below the general populations rates. However, unfortunately, low risk children from disturbed envornments did not develop schizophrenia.

The Israeli High Risk Study (Marcus 1987) investigated environmental factorsby assessing the parents on hostility, inconsistency and over involvement.
All the reported cases of schizophrenia had poor parenting ratings. However, all the cases also showed signs of neurological abnormalities at the time of initial assessment (13 years previous) which raises the question of whether these abnormalities had influenced the parent child interaction.

These studies are ongoing and many of the children have not yet passed through the critical period for the onset of schizophrenia. However, the evidence so far strongly supports the diathesis-stress model.

Psychological explanations of Schizophrenia

1. Dysfunctional families:

This discredited theory claimed that families who were secretive, critical and punitive, created such anxieties and tensions that the child was predisposed to developing schizophrenia later. Such explanations are not supported by studies of schizophrenia sufferers and their families, and would not account for biological influences.

Several retrospective clinical studies identified the dysfunctional family, and breakdowns in communication between its various members, as the key cause of schizophrenia.

However, they simply assumed that the patterns of behaviour between family members that they observed would also have been found in the past. Nor were there any control groups of families who had similar patterns of behaviour, but no evidence of schizophrenia amongst their members.

It is hardly surprising that communication becomes strained and routines are disrupted when a family is trying to live and cope with the behaviour of a schizophrenic member. It seems highly likely that the dysfunctional behaviour observed in some families with a schizophrenic member is caused by having to live with someone who has lost contact with reality. Furthermore, more recent studies of dysfunctional families show that few people reared in such homes actually develop schizophrenia and most schizophrenia sufferers come from ‘normal’, well adjusted families.

2. Expressed Emotion (EE):

It was obvious that families may be involved in the progress of the condition, but they are unlikely to have been the cause of it. However, the environment the schizophrenia sufferer returns to after treatment influences the likelihood of successful recovery. Homes where face-to-face interaction is characterised by intense emotional concern or criticism are less conducive to recovery than homes with more emotionally stable interactions. Relapse rates are highest where contact is most fraught.

Brown (1972) showed that patients who returned from hospital to homes where there was a high level of emotionality (High levels of Emotion were Expressed — HEE) were more likely to have a relapse, and would have it sooner than those with LEE (Low levels of Emotion Expressed) families. The kinds of emotions that were expressed were high levels of concern for the sufferers, leading to doing everything for them, being highly critical of their attempts to help themselves, and being very ‘strung out’ generally. These families were characterised by people (mothers usually) rushing around and driving themselves to exhaustion, looking after each other, fussing constantly and being overly possessive. Vaughn and Leff (1976) found 51 per cent of schizophrenic relapses in HEE families, compared to 13 per cent in LEE homes. The more contact the sufferer had with HEE relatives, the higher the relapse rate.
The evidence for the effect of other family members and their emotional responses on recovery from schizophrenia is now well established (and the care package for schizophrenia recovery usually includes some education and support for other family members).

Evidence for the importance of expressed emotion has been found in studies across different cultures so there can be little doubt of its importance in explaining relapse. Unfortunately for the EE explanation, there are also high relapse rates amongst those recovering from schizophrenia who are not in contact with any former family members, so the expressed emotion hypothesis may not be entirely true.

Cognitive explanations for schizophrenia

Whilst not disputing schizophrenia’s genetic and biological origins, cognitive psychologists regard schizophrenia as a thought disorder. They are interested in studying whether there are abnormalities in the cognitive processes of those with schizophrenia, and of their close relatives.

For example, cognitive psychologists are trying to find out if there are similarities in memory function in individuals diagnosed as suffering from schizophrenia and their nearest relatives. Some similarities have been found, but the data available so far fail to explain why only some people with cognitive malfunctioning actually develop schizophrenia while others in the family do not.

Research into similarities and differences in cognitive functioning between schizophrenia and non-schizophrenia sufferers is in its infancy and no acceptable conclusions about the origins or causes of schizophrenia have been established yet.

Cognitive psychologists suggest that disturbed thinking processes are the cause rather than the consequence of schizophrenia.

It is suggested that people with schizophrenia cannot filter information in this way and they simply let in too much irrelevant information.

Explanations that relate underlying biological impairments to psychotic symptoms are often referred to as neuropsychological theories’.

One such hypothesis has been proposed by Hemsley (1993) who suggested that the central deficit in schizophrenia is a breakdown in the relationship between information that has already been stored in memory and new, incoming sensory information.

Hemsley suggests that this processing break down in schizophrenia and those schemas are not activated. As a result, people with schizophrenia are subjected to sensory overload and do not know which aspects of a situation to attend to and which to ignore.


Hemsley further suggests that internal thoughts are sometimes not recognized as arising from memory and so are attributed to an external source are - experienced as auditory hallucinations.

Frith’s model (1992) was an attempt to explain the onset and maintenance of sonic of the positive symptoms of schizophrenia. His idea is that people schizophrenia are cognitively impaired in that they are unable to distinguish between actions that are brougi about b external forces and those that are generated internally. He believes that most of the symptoms of schizophrenia can be explained in terms of deficits in three cognitive processes:

· Inability to generate willed action;
· Inability to monitor willed action;
· Inability to monitor the beliefs and intentions of others.

According to Frith, faulty operation of this mechanism is due to a functional disconnection between frontal areas of the brain concerned with action arid more posterior areas of the brain that control perception. He has produced some evidence for his ideas by detecting changes in cerebral blood flow in the brains of people with schizophrenia when engaged in specific cognitive tasks.

Cognitive psychologists are attempting to find evidence for genetic links by examining whether malfunctioning cognitive processing is a family trait.

Park et al. (1995) identified working memory deficits in people with schizophrenia arid in their first-degree non-schizophrenic relatives, a study that has been supported by Faraone et al. (1999), who also found impairments in auditory attention. Faraone and colleagues claim that these memory and attention impairments are a manifestation of the genetic predisposition to schizophrenia and are even bold enough to claim that these are the cause.
They admit they cannot explain why their relatives do not develop the illness, even though they have the predisposing genes.
They suggest that further work is needed to establish whether some people have a low ‘dose’ of the genes, or, alternatively, whether they have not been exposed to any environmental agents that may trigger the disorder. Cannon et al. (1994b), who also identified verbal memory and attention, but not visual memory deficits, in people with schizophrenia and their non- schizophrenic siblings, suggested that the mediating factors that determine the expression of these genes are birth complications.

References:

Falkai et al. (1988) & Owen et al. (1978) - Further support for the
dopamine hypothesis comes from the post-mortems of patients with schizophrenia. These have revealed specific increase of dopamine in the left amygdale and increased dopamine receptor density in the caudate nucleus putamen

Wong et al. (1986) - Shows in live patients using pet scans that
the dopamine receptor density in the caudate nuclei is indeed greater in those with schizophrenia than in controls. This however is not supported in subsequent studies.

Brown et al (1986) - Found decreased brain weight and enlarged
ventricles, which are the cavities in the brain that hold cerebrospinal fluid.

Flaum et al. (1995) - Also found enlarged ventricles along with
smaller thalamic hippocampal and superior temporal volumes.

Buchsbaum (1990) - Found abnormalities in the frontal
hippocampus and the amygdale. As more MRI studies are being undertaken, more abnormalities are being identified.

Castner (1998) - Subjected monkeys to brain damaging x rays
during fetal development and found that they showed no ill effects in childhood compared to the control group, but at puberty they developed symptoms of schizophrenia such as hallucinations. There are of course ethical issues associated with animal research of this kind.

Mednick et all (1988) - Suggestion is that if the mother is infected
during the pregnancy there is pre birth exposure to the influenza A virus. It is thought that the 25-30 week foetus is most vulnerable because of accelerated growth of the cerebral cortex at this time.

Torrey et all (1988) - Furthered support for the viral hypothesis
comes from the observation that throughout its history peaks in schizophrenia diagnosis have corresponded with major flue epidemics

Dalman et al. (1999) - Longitudinal study which found significant
links between birth complications and later development of schizophrenia, with pre-eclapsia being the most significant risk factor.
Tienari (1987) - The Finnish adoption study investigated
environmental factors by assessing the quality of parenting through a battery of tests and interviews.
Marcus (1987) - The Israeli High Risk Study investigated
environmental factors by assessing the parents on hostility, inconsistency and over involvement.

Brown (1972) - Showed that patients who returned from
hospital to homes where there was a high level of emotionality (High levels of Emotion were Expressed — HEE) were more likely to have a relapse, and would have it sooner than those with LEE (Low levels of Emotion Expressed) families.
Vaughn and Leff (1976) - Found 51 per cent of schizophrenic relapses
in HEE families, compared to 13 per cent in LEE homes. The more contact the sufferer had with HEE relatives, the higher the relapse
Hemsley (1993) - Suggested that the central deficit in
schizophrenia is a breakdown in the relationship between information that has already been stored in memory and new, incoming sensory information.

Park et al. (1995) - Identified working memory deficits in
people with schizophrenia arid in their first-degree non-schizophrenic relatives, a study that has been supported by Faraone et al. (1999)




Faraone et al. (1999) - Found impairments in auditory attention.
Faraone and colleagues claim that these memory and attention impairments are a manifestation of the genetic predisposition to schizophrenia and are even bold enough to claim that these are the cause.

Cannon et al. (1994b) - Identified verbal memory and attention, but
not visual memory deficits, in people with schizophrenia and their non- schizophrenic siblings, suggested that the mediating factors that determine the expression of these genes are birth complications.
Concepts to note:

Define these terms:

· bizarre behaviour
· blunted emotional responses
· delusions
· diathesis-stress explanations
· dissociative identity disorder
· dopamine
· dopamine hypothesis
· expressed emotion (EE)
· functional schizophrenia
· hallucinations
· loss of drive
· neurochemical theory
· neurons
· organic schizophrenia
· poverty of thought
· schizophrenia
· social withdrawal
· thought disorder

What did they do or say?

· Brown
· Faraone
· Kendler
· Park
· Vaughn and Leff

4 comments:

Olu said...

I love you!!!! I've got exam on schiphrenia in few days.

Got anything on Addiction?

Oscar said...

you are a beautiful beautiful person. thank you.

show.me.the.moni said...

WOW you are a life saver.

Kaiya Morton said...

This is brilliant! Really helped with my essays, and it summarises all the wordy books, in a simple manner. Thanks! :-)