• Genetic
  • Biochemical
  • Neuroanatomical
  • Viral Infection
  • Evolutionary Theories


  • Schizophrenogenic family
  • Expressed Emotion
  • Social Drift Hypothesis


  • Psychodynamic
  • Behavioural
  • Cognitive





Schizophrenia is a group of psychotic disorders that are characterised by a loss of contact with reality.

“…a serious mental disorder that is characterised by severe disruptions in psychological functioning. Schizophrenics may experience a variety of disturbing and frightening symptoms…”

Cardwell, 1996.

Estimates of its prevalence vary between 0.2% and 2.0% of the population and as such schizophrenia affects approximately between one in every five hundred and one in every fifty of the population. The symptoms exhibited vary somewhat, but typically include cognitive, perceptual, emotional and motor disturbances as well as dysfunction in forming and maintaining social relationships.

According to the DSMmd IV – 94 (Diagnostic and Statistical Manual of mental disorders Volume 4, 1994), the criteria for schizophrenia include:

  • Two or more of the following symptoms, each of which must have been present for a significant period of time over a 1 -month period: delusions, hallucinations disorganised speech, grossly disorganised or catatonic (rigid) behaviour and negative symptoms (lack of emotion, lack of motivation, speaking very little or uninformatively).

Only one symptom is needed if the delusions are bizarre or the hallucinations consist of a voice commenting on the individual’s behaviour

  • Continuous signs of disturbance over a period of at least 6 months.

  • Social and/or occupational dysfunction.

There are two major symptom categories, characterised by positive and negative symptoms.

  • TYPE ONE (functional acute) symptoms are those that are present in schizophrenics but normally absent in the general population, Symptoms include delusions, hallucinations, persecution complex and paranoia and bizarre forms of behaviour. This is known as PARANOID SCHIZOPHRENIA.

  • TYPE TWO (organic chronic) negative symptoms include those that are present in the general population but absent in schizophrenics. Symptoms include an absence of emotion and motivation, language deficits, general apathy, and an avoidance of social situations. This is known as CATATONIC SCHIZOPHRENIA.

According to DSMmd, IV – 94 there are THREE main types of schizophrenia:

  • Paranoid schizophrenia: this type involves delusions of various kinds, paranoia, persecution complex and some hallucinations

  • Disorganised schizophrenia: this type involves some delusions and hallucinations, incoherent disorganised speech and behaviour, and large mood swings

  • Catatonic schizophrenia: the main feature is almost total immobility for hours at a time, with the patient simply staring blankly.


About one-third of patients have a single episode or a few brief episodes and then recover fully.

A further one-third have occasional episodes of the disorder throughout their lives and, in between these, they are able to function reasonably effectively. When there is absence of symptoms they may be classified as in remission, but there is some dispute over when it is most appropriate to apply this label.

The remaining third deteriorate over a series of episodes, each of which becomes progressively more incapacitating.

Those patients for whom schizophrenia comes on suddenly tend to have a better prognosis, and the same is true for patients where positive symptoms predominate. Although it can emerge later in life, the onset of schizophrenia for men is usually in the late teens or early twenties and for women onset is usually in the late twenties.

AETIOLOGIES (Explanation of Cause)

There are two main categories of aetiology for schizophrenia. These are biological explanations and social psychological explanations.

Biological Explanations:

  • Genetic Factors
  • Biochemical
  • Neurological
  • Evolutionary
  • Viral/infection


There are three main sources of evidence in offering a genetic aetiology for schizophrenia. These are Twin studies, Family studies and Adoption studies.


Twin studies offer perhaps the best means of establishing genetic links, by comparing the difference in concordance rates for MZ and DZ twins. Both share the same environment, but only the MZ twins have identical genetic make-up. Many studies have been conducted and they all show a much higher concordance rate in MZ than in DZ twins.

Gottesman and Shields (1982) used the Maudsley twin register and found 58 per cent (seven out of twelve MZ twin pairs reared apart) were concordant for schizophrenia.

+ Environment factored out of the equation

–  Concordance not 100%

If the genetic hypothesis is correct, then the offspring of a non-affected discordant MZ twin should still be high-risk. Fischer (1971) found that 9.4 per cent of such offspring developed schizophrenia, which is a much higher incidence than in the general population (approximately I per cent).


+ There is strong evidence of genetic factors in schizophrenia from the studies of twins.

+ MZ Twins exhibit a greater scale up in risk, than do DZ twins

+ Concordance rates for MZ twins show a significant increase in risk, compared to controls

+ A wide range of evidence to support the genetic hypothesis

– It is difficult to isolate environmental contributory factors as they are often brought up in the same environment. There are even issues with MZ twins reared separately. Some critics (e.g., Kamin, 1977) have suggested that some of the reared apart twins in Shields’ study had not always spent the whole of their childhood apart and some were raised by relatives and even went to the same school.

– No study has revealed more than 58% concordance and so therefore the disorder cannot be purely genetic

– There are other convincing biological explanations


Family history studies have been conducted since the 1900s in an attempt to identify a genetic link with schizophrenia.

Kendler et al (1985) have shown that first-degree relatives of those with schizophrenia are 18 times more at risk than the general population.

+ Again a clear scale up in risk

– Family studies have specific methodological limitations. In this study, Kendler and colleagues used mainly interview data, although they did check with hospital records for confirmation of psychotic diagnosis in relatives.

A study on 109 sibling pairs in the UK diagnosed with schizophrenia was conducted by Cardno et al (1998) to try to ascertain whether they shared the same schizophrenic symptoms, which might be expected if the behaviour was environmentally learned. The expression of symptoms was so different between the siblings that they concluded the study offered no support for shared environmental factors contributing to the cause of schizophrenia. However, they were also sceptical about genetic links.

Finally, Gottesman and Bertelsen (1989) reported some convincing findings on importance of genetic factors. One of their findings was that their participants had a 17% chance of being schizophrenic if they had a parent who was an identical twin and had schizophrenia. This could be due to either heredity or environment. However, they also studied participants with a parent who was an identical twin and did not have schizophrenia, but whose identical twin did. These participants also had a 17% chance of being schizophrenic.  Genes passed on by parents seems to be the most important factor.

+ The evidence reported by Gottesman indicates clearly that schizophrenia runs in families. Furthermore, as predicted by the genetic hypothesis, the concordance rate is much higher between relatives having high genetic similarity. However, the fact that family members who are more similar genetically tend to spend more time together means that environmental factors are also indicated in this evidence.

–  Family studies are generally inconclusive because they are conducted retrospectively, in that they are comparing a cross section of people who have already been diagnosed. A prospective (longitudinal) study can provide more reliable data and a number of large scale projects have been undertaken in different parts of the world.


Conducted in order to isolate environment from genetics and therefore a valuable for of research for psychologists. However there are relatively few MZ twins with a family history of schizophrenia who have been raised separately.

The Finnish Adoption study, which Tienari began in 1969, identified adopted-away offspring of biological mothers who had been diagnosed with schizophrenia (112 index cases), plus a matched control group of 135 adopted-away offspring of mothers who had not been diagnosed with any mental disorder. Adoptees ranged from 5 to 7 years at the start of the study and all had been separated from their mother before the age of 4. The study reported that 7 per cent of the index adoptees developed schizophrenia, compared to 1.5 per cent of the controls (Tienari et al 1987).

The Danish Adoption Study, reported by Kety et al (1994), taking a national sample from across Denmark, found high rates of diagnosis for chronic schizophrenia in adoptees whose biological parents had the same diagnosis, even though they had been adopted by ‘healthy’ parents.

+ The data they have provided so far, however, indicate a strong genetic link for schizophrenia.

+ Twin, adoption and family studies continue to provide reliable evidence that the degree of risk increases with the degree of genetic relatedness

– A major problem in these longitudinal studies, however, is that diagnostic criteria for schizophrenia are continually being updated and changed.

– No twin study has yet shown 100 per cent concordance in MZ twins, which would provide the most conclusive evidence for genetic links alone.


Research into schizophrenia has also focused on neurochemical abnormalities. Convincing evidence has come from research on dopamine receptors.

Interest in dopamine arose when it was found that phenothiazines serve to inhibit dopamine activity

L-dopa (a synthetic dopamine-releasing drug) can induce symptoms resembling paranoid (acute) -schizophrenia in non-psychotic people.

Studies on amphetamines have provided further support for the dopamine hypothesis. The symptoms of amphetamine psychosis are similar to paranoid schizophrenia and one of the actions of amphetamines is the release of dopamine at central synapses.

Amphetamines have also been shown to worsen the symptoms of schizophrenia. (van Kammen, Docherty, & Bunney, 1982).

In a study by Randrup and Munkvan (1966), behaviour similar to that found in those suffering from schizophrenia was induced in rats by administering amphetamines and the effects were then reversed by neuroleptic drugs.

Further support comes from post mortems of patients with schizophrenia, which have revealed a specific increase of dopamine in the left amygdala (Falkai et al 1988) and increased dopamine receptor density in the caudate nucleus putamen (Owen et al 1978).

PET scan research conducted by Wong et al (1986) revealed that dopamine receptor density in the caudate nuclei is indeed greater in those with schizophrenia than in controls.

Unfortunately, neither post mortems nor PET scans can reveal whether increased dopamine activity causes schizophrenia, or whether schizophrenia interferes with dopamine metabolism.

Problems with the dopamine hypothesis

As Barlow and Durand (1995) pointed out, there are some problems with the dopamine hypothesis.

  • Neuroleptic drugs block dopamine fairly rapidly, but generally fail to reduce the symptoms of schizophrenia for days or weeks thereafter. This is puzzling if high levels of dopamine are responsible for maintaining the symptoms.

  • Only between 50% and 60% of patients respond to anti-psychotic drug treatment

  • The evidence on the relationship between schizophrenia and dopamine levels is mostly correlational in nature. As a result, we do not know whether the changed dopamine activity in schizophrenics occurs before or after the onset of the disorder. If it occurs after, then clearly dopamine plays no part in causing schizophrenic symptoms.

  • Excessive dopamine activity seems to be associated with type one schizophrenia but not organic-chronic type two schizophrenia (Davison & Neale, 1996).


As more MRI studies are being undertaken, more abnormalities are being identified. Magnetic resonance imaging (MRI) has been a tremendous breakthrough because it provides a picture of the brain. MRI studies show quite definite structural abnormalities in the brains of many patients with schizophrenia.

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

  • Velakoulis et al (1999) found smaller hippocampal volumes which are present from the onset of the illness and

  • Kwon et at (1999) report a reduction by 28 per cent of the volume of grey matter (so-called because of its pinkish-grey colour) in the left planum temporale.

  • Flaum et al. (1995) also found enlarged ventricles, along with smaller thalamic, hippocampal and superior temporal volumes.

  • Buchsbaum (1990) found abnormalities in the frontal and prefrontal cortex, the basal ganglia, the hippocampus and the amygdala.

  • Young et al (1991), using MRI, found a number of structural brain differences between people diagnosed with schizophrenia and controls, particularly in the asymmetry of the brain. For example, in controls the amygdala was smaller on the left than the right, but in the schizophrenia group, asymmetry was absent.

  • Finally Pahl, Swayze, and Andreasen (1990) reviewed almost 50 studies, the great majority of which found abnormally large lateral ventricles (liquid-filled cavities) in the brains of schizophrenics.

Evaluation of Neoroanatomical Explanations

– Structural abnormalities have been found more often in those with negative/chronic symptoms, rather than positive/acute symptoms, lending support to the belief that there are two types of schizophrenia.

– Furthermore, Weinberger (1988) claims that, despite the wealth of research, the evidence is still inconclusive as to whether there are progressive structural brain changes prior to the initial onset of schizophrenia. This means that the causal direction of the hypothesis is still in question -whether structural abnormalities predispose to schizophrenia, or whether the onset of clinical symptoms cause structural changes.

+ A study on teenage monkeys by Castner et al (1998) may shed some light on this debate. They subjected the monkeys to brain damaging X-rays during fetal development and found that they showed no ill effects during childhood, compared to the control group, but at puberty they developed symptoms of schizophrenia, such as hallucinations.

– It is difficult, however, to link behaviour in monkeys to symptoms of schizophrenia that have been identified in humans and there are, of course, ethical issues associated with animal research of this kind.


In essence the evolutionary view is that schizophrenia is at least in part genetic and the gene for schizophrenia must offer some advantage in order to explain why it has remained in the gene pool.

One possibility is the group-splitting hypothesis (Stevens & Price, 1996). The personality characteristics of the schizophrenic enable one subgroup to split off from a main group, a valuable function at times when the main group has become too large to be optimum.

A second explanation has been advanced in relation to the origin of language. Crow (2000) has suggested that schizophrenia is the price that humans pay for language. He points out that schizophrenia involves a breakdown in the brain’s internal linguistic controls. Schizophrenics often believe they are hearing voices and/or may use atypical language.

Evaluation of the evolutionary approach

  • There is a lack of supporting evidence for the ‘group splitting hypothesis’.

  • Evolutionary explanations which point to language as a key component in schizophrenia, ignore that schizophrenia type symptoms have been induced in laboratory animals. There seems to be a more clearly demonstrated link with type one schizophrenia than there is with type two.


A number of viral infections, such as measles, scarlet fever, polio, diphtheria and pneumonia and, in particular, the virus Influenza A, have been suggested as an explanation (Torrey et al 1988, Torrey et al 1996).

Influenza A is most prevalent in the winter and could explain the high proportion of winter births in those diagnosed with schizophrenia. The suggestion is that if the mother is infected during pregnancy there is pre-birth exposure to the Influenza A virus. It is thought that the 25- to 30 week foetus is most vulnerable because of accelerated growth in the cerebral cortex at this time (Mednick et al, 1988) I

t is 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.

Further support for the viral hypothesis comes from the observation that, throughout history, peaks in schizophrenia diagnosis have corresponded with major flu epidemics (Torrey et al 1988).


  • It is worth noting, however, that these are correlational data and so caution should be observed when attempting to infer causation.

  • The data are also based on DSM-II diagnostic criteria for schizophrenia, which included a broader diagnostic range of patients than DSM III onwards.








It is probable that several social, psychological or environmental factors contribute to the development of schizophrenia.


In the 1950s and 1960s it was thought that people suffering from schizophrenia were from dysfunctional families. There was even a strong belief that schizophrenia was caused by a dysfunction of communication within the family.

The term ‘schizophrenogenic families’ (Fromm Reichmann 1948) was used to describe families with

  • high emotional tension

  • many secrets

  • close alliances &

  • conspiracies.

An associated suggestion was the double-bind situation, where children are given conflicting messages from parents who express care, yet at the same time appear critical (Bateson et al, 1956). It was thought that this led to confusion, self doubt and eventual withdrawal. The double-bind theory accounts in part for the confused thinking of schizophrenic patients. However, it suffers from the serious problem that there is very little evidence supporting it.

The families of schizophrenics tend to have inadequate interpersonal communication. Mischler and Waxler (1968) found that mothers talking to their schizophrenic daughters were rather aloof and unresponsive. However, the same mothers behaved in a much more normal and responsive way when talking to their normal daughters. Thus, the presence of a schizophrenic patient in the family may cause poor communication patterns rather than the other way around. (Direction of Causality problem Schroeder and Costa 1984)


  • This theory went into decline because of a failure to replicate findings across studies.

  • Another reason for the loss of interest in it in the 1970s was the convincing evidence appearing for a genetic predisposition in schizophrenia.

  • Also many other convincing biological theories were being developed

  • The main problem, however, was that families were studied retrospectively, long after the person’s mentaI disorder may have affected the family system. Living with someone who is suffering from schizophrenia is difficult and distressing for the whole family. Routines are disrupted, often with one parent having to give up paid employment to care for the person. As families struggle to cope with schizophrenia, to suggest that they have caused the disorder is at least unhelpful and at most highly destructive.


Not an aetiology, but rather an assessment of the conditions under which relapse is most likely to occur in schizophrenics in remission

By the mid-1970s, psychologists had become more interested in the part the family might play in the course, rather than the cause, of schizophrenia. Brown (1972) showed that patients with schizophrenia who returned to homes where a high level of emotion was expressed (high EE) – such as hostility, criticism, over-involvement and over-concern showed a greater tendency to relapse than those returning to low-EE homes.

Vaughn and Leff (1976) working at the Medical Research Council in London found similar results, with

51 per cent relapse in those in high-EE homes and only 13 percent relapse in low-EE homes.

Vaughn and Leff included in the study the amount of Lime spent in face-to-face contact with relatives after discharge and found that relapse rates increased as face-to-face contact increased with high-EE relatives.

So well accepted has this model become, that treatment programmes for schizophrenia usually include education and training for family members in controlling levels of EE.


However, despite the widely held acceptance of the EE model, it is not without its critics.

  • First, many patients with schizophrenia are either estranged from their families or have minimal contact, and yet there is no evidence that such people are less prone to relapse (Goldstein 1988).

  • Added to this, it has been suggested that high EE may well develop as a response to the burdens of living with schizophrenia.

  • The direction of causality is not clear in studies of expressed emotion. One possibility is that expressed emotion within the family causes relapse.

  • Another possibility is that individuals who are in poor psychological shape are more likely to provoke expressed emotion from members of their family.


  • Freud was mainly interested in neuroses, such as anxiety and depression.

  • He assumed that neuroses occurred as a result of severe conflicts and traumatic experiences.

  • Information about these conflicts and traumas is stored in the unconscious mind, and treatment involves trying to resolve these internal conflicts.

  • Freud argued that conflicts and traumas are also of importance in schizophrenia.

  • However, an important difference is that schizophrenics have regressed or returned to an earlier stage of psychosexual development

  • More specifically, they have regressed to a state of primary narcissism (or great self-interest).

  • In this state, the ego or rational part of the mind has not separated from the id or sexual instinct.

  • The importance of this is that the ego is involved in reality testing and responding appropriately to the external world.

  • Schizophrenics have a loss of contact with reality because their ego is no longer functioning properly.


The psychodynamic approach to schizophrenia is limited for several reasons.

  • First, it is very speculative, and is not supported by much evidence.

  • Later psychodynamic theorists tended to be unconvinced about the involvement of sexual impulses, preferring to emphasise the role of aggression in schizophrenia.

  • Third, the notion that adult schizophrenics resemble infants in many ways is not very sensible.

  • Fourth, the psychodynamic approach ignores the role of genetic factors in the development of schizophrenia.

  • Implications for the treatment of Schizophrenia are at best misguided and at worst dangerous


According to the behavioural approach, learning plays a key role in causing schizophrenia.

Early experience of punishment may lead children to retreat into a rewarding inner world.  (operant conditioning)

This causes others to label them as “odd” or “peculiar”.

According to Scheff’s (1966) labelling theory, individuals who have been labelled in this way may continue to act in ways that conform to the label.

Their bizarre behaviour may be rewarded with attention and sympathy for behaving bizarrely – a process known as secondary gain.

This bizarre behaviour becomes more and more exaggerated, and eventually is labelled as schizophrenia.


+ The fact that schizophrenics often respond to reinforcement when used in therapy provides modest support for the behavioural approach.

+ For example, schizophrenics have learned to make their own beds and to comb their hair when rewarded for doing so ( Token economy – Ayllon & Azrin, 1968).

However, the behavioural approach

–  ignores the genetic and other evidence and

–  it trivialises a very serious disorder


Cognitive psychologists examine the cognitive functioning of people with schizophrenia, bearing in mind that schizophrenia is a ‘thought’ disorder.

The cognitive view accepts that there are almost certainly physiological abnormalities associated with schizophrenia and that these are transcribed into cognitive malfunctioning.

Park et al (1995) identified working memory deficits in people with schizophrenia and 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.

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.

Attentional mechanisms have been studied in relation to ‘eye-tracking’ dysfunctions (ETD) and these have been identified in people with schizophrenia (e.g. Levy et al 1993). Dysfunctions are detected by a procedure of following a moving target in a horizontal plane whereby the colour changes randomly and the participant must count the number of changes.

A study by Kinney et al. (1999) has identified an ETD in people with schizophrenia and also in their nonschizophrenic relatives. They suggest that this is a genetic defect.

Cognitive impairments thought to have a genetic origin have, however, been implicated in a number of different mental disorders, for example Attention Deficit Hyperactivity Disorder.


+ Takes into account the possibility that there are both genetic and cognitive factors  working in tandem to produce schizophrenia

– As an explanation for schizophrenia, this is a new area of research and as yet it is not possible to evaluate the validity of such a link.


  • Social factors are emphasised by the social causation hypothesis.

  • This hypothesis was designed to explain why it is that schizophrenics tend to belong to the lower social classes. According to this hypothesis, members of the lower social classes have more stressful lives than middle-class people, and this makes them more vulnerable to schizophrenia.

  • The key issue here is whether belonging to the lower social classes makes individuals likely to develop schizophrenia, or whether developing schizophrenia leads to reduced social status, as in the social drift hypothesis.

  • There is some evidence that being in the lower social classes can precede the onset of schizophrenia. Turner and Wagonfeld (1967) found that the fathers of schizophrenics tended to belong to the lower social classes.

– Social factors alone cannot explain schizophrenia


  • Since the 1980s the diathesis-stress model has been applied to schizophrenia.

  • The reasoning behind this theory is that those individuals who develop schizophrenia may be genetically predisposed.

  • In addition they are also extremely sensitive to psychosocial elements in their environment.

  • Therefore, stressful events in the environment, such as major life events, traumatic experiences, or dysfunctional families, may act as a ‘trigger’ in a high-risk individual.

  • Support for the ‘diathesis-stress’ model also comes from prospective longitudinal studies.

  • As research gathered further evidence for genetic factors, it was also becoming clear that schizophrenia did not always develop in those thought to be genetically vulnerable.

  • This led researchers back to the environment in the search for precipitating factors.

  • Day et al. (1987) carried out a study in several countries. They found that schizophrenics tended to have experienced a high number of stressful life events in the few weeks before the onset of schizophrenia.


+ The diathesis-stress model proposes that a complete explanation of any mental disorder is likely to involve both a predisposition to the disorder and a stressor which triggers the appearance of the symptoms.

+ This can be seen to apply to schizophrenia where there is clear evidence of a genetic link, yet we have seen that not everyone who inherits the genetic component (as in identical twins) becomes schizophrenic.

+ We can explain this in terms of the psychological factors that trigger the disorder, such as troubled families or stressful life events.

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