There is a great deal of evidence that genetic factors contribute significantly to the disorder. Twin studies have shown that if one identical twin suffers from schizophrenia, there is a 40-60% chance of the other twin developing the disorder. If a non-identical twin has schizophrenia there is a 17% chance of the other twin developing the disorder. This means that there is a large genetic contribution to schizophrenia, but other, non-genetic factors must also be important Gottesman (1991).

The cognitive model explains schizophrenia in terms of diathesis-stress. This means that genetic abnormalities create a predisposition for the development of the disorder, but the disorder only develops in response to stress. These stressors may be biological (e.g., prenatal viral infection), psychosocial (e.g., living in an urban environment) or psychological (e.g., traumatic experiences). The more stressors accumulate, the greater the risk a susceptible person has of developing schizophrenia. Beck et al. (2009) also propose a mechanism to explain how these risk factors lead to the development of schizophrenia.

Neuroanatomical Abnormalities

Research into schizophrenia has shown that structural abnormalities of the brain are common in schizophrenia, these include:

• Enlargement of lateral ventricles
• Reduced brain volume
• Smaller frontal and temporal structures in the brain, especially the hippocampus (Davidson & Heinrichs (2003)
• Reduced densities in input layers of pyramidal cells in dorsolateral prefrontal cortex (Lewis et al. 2003)

Pyramidal cells are neurons that are involved in cognition, so if they are malformed it may explain why people with schizophrenia have difficulties with cognitive tasks (see below).

Functional Abnormalities

Studies that examine the functioning of the brains of people with schizophrenia have shown a number of differences in activity. Positron Emission Tomography (PET) has been used to scan the brains of people with schizophrenia while they take part in cognitive tasks. Compared with normal controls, the brains of schizophrenia patients show abnormal activation patterns in many brain regions in response to a task (Gur & Gur, 2005). One particular difficulty for schizophrenia is low frontal lobe activity when taking part in tasks that involve the frontal lobes.

Neurocognitive Deficits

Neurocognitive deficits are deficits in cognitive abilities because of poor brain function. Schizophrenia patients generally score poorly on all cognitive tasks, although there is individual variation in each persons profile of cognitive difficulty. The following are common areas of neurocognitive impairment in schizophrenia:

• General Intellectual Ability
• Verbal Memory
• Non-verbal Memory
• Recognition
• Executive Functions
• Motor Skills
• Language
• Attention
• Processing Speed

Beck et al. (2009) suggest that these neurological impairments occur because of a small hippocampus. The hippocampus may be small because of the pre- and postnatal environment; for example, prenatal exposure to viruses, traumatic childhood experiences, etc.

A small hippocampus means that schizophrenia patients have an exaggerated HPA response, which means that exposure to stress leads to the overproduction of cortisol. Excess cortisol leads to further reduction in the size of the hippocampus, which exaggerates the HPA response even more.

Crucially, in addition to its involvement in controlling the HPA response, the hippocampus also controls the mesolimbic dopamine pathway. The mesolimbic dopamine pathway is an area in the frontal lobes that is involved in reward (pleasure) and motivation; it has been found that blocking dopamine activity in this area reduces the hallucinationatory and delusional symptoms of schizophrenia.

According to Beck et al. (2009), low hippocampal volume leads to excessive dopamine activity in the mesolimbic pathway increases the load on cognitive resources that are already limited and sets the person on a pathway to psychosis.

The Pathway to Psychosis

Cognitive Insufficiency

A person with a predisposition to develop schizophrenia has limited cognitive resources due to the biological factors outlined above. However, as long as life is relatively stress-free they are able to compensate for this and their behaviour appears normal.

Cognitive Decompensation

When the load on the cognitive resources becomes too great, due to the accumulation of stress and brain damage caused by excess cortisol, they can no longer compensate for their deficits and there is a marked decline in information processing ability. The person experiences strange sensory experiences due to increased dopamine activity in the frontal lobes and delusions and hallucinations emerge. Delusions and hallucinations are not dismissed as such because the person's ability to test reality is impaired because of the strain on their cognitive resources.

Cognitive Failure

Eventually the demand on cognitive resources becomes so great that the person experiences a full blown psychotic episode.

Cognitive Explanation of the Symptoms of Schizophrenia

Delusions

According to Beck et al. (2009) delusions occur because of increased dopamine activity in the mesolimbic pathway (see above) and dysfunctional cognitive schemas.

Cognitive schemas are mental representations of oneself in relation to the world and other people; they influence how a person interprets their experiences of life.

In schizophrenia, dysfunctional cognitive schemas arise when a person experiences traumatic events, such as childhood abuse, this can lead to negative expectations and defeatist attitudes, such as 'I am inferior' and 'people are against me'. Memories of threat can lead to expectations of future threat.

Dysfunctional cognitive schemas may be inactive until increased dopamine activity makes them become 'hypersalient'. Hypersalient means that these schemas dominate the person's thinking.

Here are some examples of delusions and cognitive schemas that relate to them [adapted from Beck et al.(2009]:

Delusions of Persecution

• Beliefs of personal vulnerability
• Beliefs in others malicious intentions

Delusions of Influence

• Beliefs of the self as powerless
• Beliefs of others as powerful

Delusions of Grandeur

• Belief of the self as powerful (masking a real belief of the self as inadequate)

• Belief of others as unrewarding and inferior

Hallucinations

Hallucination are not always pathological. In fact, hallucinations are relatively common; for example, surveys of college students have found that between 30 & 70% have experienced hearing voices (Barrett, 1992). However, in patients with schizophrenia the crucial factor is the perception that the hallucinations are externally generated and are seen as beyond their control. This means that it is the attributions that patients make regarding their hallucinations that leads them to become psychotic symptoms.

There is a high incidence of childhood trauma in patients prone to hallucinations (Fowler, 2007). Beck et al. (2009) claim that childhood trauma can lead to a cognitive bias of the self as helpless and others as omnipotent (all powerful). Traumatic childhood events are often represented in hallucinations. For example, Beck et al. (2009) report of a patients who had hallucinations of a little girl crying and of voices calling him a “creep” and a “faggot”. Both of these hallucinations may have been childhood memories, since he had witnessed a young girl being sexually abused and had been bullied at school. This example also highlights the tendency of schizophrenia patients to externalise; that is to perceive internal thoughts as coming from outside.

Formal Thought Disorder

The cognitive model of schizophrenia explains formal thought disorder symptoms (e.g., derailment, incoherence, clanging, etc.) as occuring because of diminished cognitive resources, particularly those involved in the information processing of language. Having a normal conversation is quite a complex process, which requires choosing the appropriate words to say, monitoring what one is saying, observing non-verbal feedback, keeping in memory what the listener has said and dealing with the emotional stress of the social situation. All of these activities place demands on the patient's limited cognitive resources.

Choosing What To Say

Collins and Loftus' (1975) spreading activation model is a model of how conceptual information is organised in memory as interconnected nodes (see example below). If one node is activated, this activation can spread to connected nodes. For example, activation of the “rose” node could also activate “flower”, “got up”, people called “Rose”, words that rhyme with rose, and the Bette Midler song: “The Rose”. Normally, these associated concepts do not enter conscious awareness, however, Beck et al. (2009) suggest that schizophrenia patients with formal thought disorder have difficulty selecting the correct word. This accounts for symptoms such as 'clanging' (repeating rhyming words) and 'loosening of associations' (saying words that loosely relate to the intended word [e.g., 'apple' instead of 'red']) and 'neologisms' (putting related words together to form new words [e.g., 'dizziwhelmed'])

Limited Attentional Resources

Other aspects of formal thought disorder can be accounted for by limited attentional resources and poor allocation of resources. Studies have shown that schizophrenia patients have difficulty with 'sensory gating', this means that they are limited in their ability to filter out irrelevant external stimuli, which puts additional strain on their cognitive resources.

The cognitive model, therefore sees formal thought disorder as arising due to information overload from both internal (uncontrolled spreading activation) and external sources. This makes it difficult for the person to monitor what they are saying and leads to symptoms such as derailment, perseveration (repeating words), and echolalia (repeating back what the other person has just said).

negative symptoms

The negative symptoms of schizophrenia (e.g., asociality, anhedonia, avolition & alogia) have, for a long time, been thought of as entirely due to abnormalities in the structure of the brain. This view explains why negative symptoms do not usually respond to drug treatments. However, the cognitive model, while accepting that biological factors contribute strongly, suggests that negative symptoms are also affected by negative expectations and defeatist attitudes.

According to Beck et al. (2009), limited cognitive resources mean that the patient has experiences where they are less successful than others and where they fail to complete complex tasks. These failures lead to the development of negative expectations, such as “I won't succeed” and defeatist attitudes, such as “I am a failure” or “I can never succeed at anything”. These maladaptive beliefs also affect how those with schizophrenia interpret events around them and this leads to more negative experiences which consolidate the maladaptive beliefs.

Strong beliefs, such as that one can never succeed at anything, decrease motivation and mean that the patient no longer attempts to succeed. This lack of motivation manifests itself as negative symptoms.

One example of a negative symptom is “anhedonia”, the inability to experience pleasure. A study by DeVries & Delespaul (1989) involved sampling the experiences of schizophrenia patients and controls throughout the day. As expected, schizophrenia patients experienced fewer positive emotions and more negative emotions than controls. The traditional biological model explains these results as the inability of patients to actually experience pleasure; however, the cognitive model explains “anhedonia” as the patient not taking part in pleasurable activities due to a belief that they will not find them pleasurable.

Beck et al. (2009) asked one of their clients to create a list of activities that they used to find pleasurable but thought they would no longer be enjoyable. The client listed calling family, vacuuming house, taking baths, watching TV and praying and rated them all with an expectation of zero pleasure. When the client actually took part in the activities as a “behavioural experiment” and rated them in vivo, she experienced high pleasure when speaking to her mother on the phone, mild pleasure when vacuuming the house and moderate pleasure from watching TV and taking a bath. This shows that patients with anhedonia can experience pleasure and that the symptom arises due to low expectations of pleasure.

Other negative symptoms can be explained in a similar way: avolition occurs because of a low expectation of success (so why bother?); asociality because of low expectation of successful social relationships; and alogia due to an expectation of having difficulty speaking coherently.

Evaluation of the Cognitive Model of Schizophrenia

A major strength of the cognitive model of schizophrenia is that integrates known genetic, environmental (biological environment),  psychosocial and cognitive factors to create a truly holistic model of the disorder. Other theories tend to ignore influences outside their own discipline, whereas Beck et al. (2009) have attempted to provide a complete account of how schizophrenia develops.

A sound method for evaluating any theory of schizophrenia is to assess how well it incorporates the facts that researchers have established about the disorder. These have been conveniently collated by the Schizophrenia Research Forum here: http://www.schizophreniaforum.org/whatweknow/newssearch.asp?categoryID=24&type=all

The symptoms of the disorder vary from patient to patient

The cognitive model does explain why the symptoms of the disorder express themselves differently in each patient. Firstly, it takes into account that there will be differences in the biology of each patient because there are many biological routes to the structural abnormalities seen in schizophrenia patients. Moreover, individual variation in cognitive schemas, attitudes and beliefs allows for a wide range of symptoms among schizophrenia patients.

The incidence of schizophrenia varies in different parts of the world between 0.3 and 2.7% of the population

The cognitive model explains why there is so much variation in the incidence rates of schizophrenia around the world. Psychosocial factors such as living in an urban environment lead to higher stress levels than living in more rural environments. In the cognitive model, those with a predisposition to develop schizophrenia have an exaggerated stress response that leads to overproduction of cortisol, which damages the brain and diminishes cognitive resources. Stress factors also contribute to the maladaptive cognitive schemas that contribute to the disorder.

Men tend to develop schizophrenia in the late teens and early twenties, whereas women who tend to develop it in their late twenties and early thirties

The cognitive model does not explain why there are differences between males and females in the timing of the disorder.  The differences may be due to hormonal, behavioural or cultural differences between males and females. Nevertheless, at the moment no theory seems able to explain this difference conclusively.

The cognitive model can, however, account for the fact that schizophrenia is very rare in childhood. Since the cognitive model suggests that accumulated stress is a major factor in diminishing cognitive resources, it makes sense that the disorder develops later in life and not in childhood when life is usually less stressful.

If one identical twin has schizophrenia the other twin has a 50% chance of developing the disorder

Although twin studies have shown that schizophrenia is highly heritable, they have also shown that the disorder is not entirely inherited. The cognitive model gives a thorough account of how genetic predisposition interacts with stress and cognitive factors to lead to the development of the disorder. This means that some people with a genetic predisposition for schizophrenia will develop the disorder and others will not.

Cogntive Deficits are present in most, but not all schizophrenia patients

The biological basis of the cognitive model of schizophrenia is that cognitive insufficiency and stress lead to eventual cognitive decompensation, then failure. That is, when stress accumulates, the person can no longer compensate for insufficient cognitive resources and the symptoms of psychosis emerge. The cognitive model, therefore, gives a very good explanation of how cognitive deficits can lead to schizophrenia symptoms; however, the fact that not all schizophrenia patients have cognitive deficits (Minnesota Consensus Group, 2010) is problematic for the theory.

Further Reading

Beck, A. T., Rector, N. A., Stolar, N. & Grant, P. (2009). Schizophrenia: Cognitive Theory, Research and Therapy. London: The Guildford Press.