What is schizophrenia? - Chapter 24

What are Bleuler's four A's?

About 100 years ago, Kraepelin described the clinical picture that is now known as the serious mental disorder schizophrenia. He called it dementia praecox: premature dementia. According to Kraeplin, the progressive course was particularly characteristic of the disorder, and he thought this would eventually result in a terminal type of dementia. He considered hallucinations to be an important symptom. Bleuler introduced the term schizophrenia and stated that delusions and hallucinations were not the core symptoms, but the factors that would later be classified under Bleuler's four A's:

1. Ambivalence (not being able to make choices).

2. Blunted Affect.

3. Autism (limitations in social intercourse).

4. Loosening of Association.

How is schizophrenia diagnosed?

Nowadays, Bleuler's four A's partly form the diagnostic criteria for schizophrenia and are subdivided into three categories: positive symptoms (hallucinations and delusions), negative symptoms (blunted affect, ambivalence, and autism), and disorganisation (loosening of association). The first psychotic episode usually arises in early adulthood (18-28 years). For diagnosis, the patient must meet two of the following criteria: negative symptoms, delusions, hallucinations, incoherent speech, severely chaotic or catatonic behaviour, deterioration in social functioning, and the symptoms must last at least 6 months. It is remarkable that cognitive impairments are not part of the diagnosis, while 70-80% of patients suffer from such impairments. 

Where does schizophrenia occur more often?

The incidence (not the prevalence) of schizophrenia is higher in urban areas and among migrants compared with the native people in rural areas. SES does not seem to be a risk factor. More men than women are affected by schizophrenia.  

What are the aetiology and neuropathology of schizophrenia?

The aetiology of schizophrenia

The aetiology is most likely to be found in a complex interaction between genes and environment. There is a genetic predisposition to schizophrenia and there are many possible contributing environmental factors: the father's age, pregnancy complications, birth complications, the season of birth, growing up in an urban environment, the use of cannabis, or exposure to trauma.

The neuropathology of schizophrenia

There are two structural brain abnormalities:

1. The smaller volume of the gray matter, especially in the superior temporal gyrus and medial temporal and limbic areas. The volume of the hippocampus gradually decreases and the ventricles gradually expand. It is important here to pay attention to the influence of medication: antipsychotics can increase the volume of the basal ganglia within six months.

2. The normal asymmetry of the hemispheres is not present.

When discussing functional abnormalities, the deviant DLPFC activity must not be overlooked. If there is a high task load, the limit is reached earlier (the patient gives up) and there is hypofrontality; with a low task load, patients get to the point where the most activation is, and then we speak of hyperfrontality. There are also functional activation patterns of the hippocampus for the storage and retrieval of information through structural and cellular changes. There is also a deviating activation of the amygdala: this is already active with neutral stimuli.

Available drugs

The classic antipsychotics (first generation) acted on dopamine receptors but induced many (motor) side effects. Moreover, they did not improve the negative symptoms. The atypical antipsychotics (first choice for treatment) have fewer side effects and also improve the negative symptoms by having more activity on serotonin and glutamate receptors. The cognitive impairments are not by definition undesirable side effects of antipsychotics.

What cognitive impairments can occur?

Disorders within the traditional function domains

There is no specific cognitive profile for schizophrenia. Patients score less well on all aspects of most neuropsychological tests compared with healthy controls, but not to such an extent that a distinction can be made between a schizophrenia patient and healthy control on the basis of test performance alone. Most likely, a generalized disorder (such as a lack of mental energy) is responsible for the overall impaired cognitive functioning. The regional deviations are related to the poor performance within the executive and memory domain.

Disorders within social cognition

Little research has been done into social cognition, but schizophrenia patients appear to have deficits in both lower-order processes (perception of basic emotions) and higher-order processes (interpretation of social information and ToM) (Couture, Penn & Roberts, 2006).

The course of cognitive impairment

Longitudinal studies show that patients already have minor abnormalities in general cognitive functioning prior to their first psychotic episode. For example, a meta-analysis by Woodberry, Giuliano and Seidman (2008) shows that the IQ score is consistently half an SD lower compared to healthy controls. The language skills of at-risk children are also less well developed (Hallet & Green, 1983) and there were already subtle developmental disorders in verbal reasoning, working memory and attention in the Dunedin cohort of premorbid schizophrenia patients in childhood (7-13 years) (Reichenberg and colleagues, 2010). In other cognitive domains, no clear differences between at-risk children and healthy children have been demonstrated. All subtle abnormalities reach a peak around the first psychotic episodes after which they stabilize. After the age of 65 years, the patient's cognitive deterioration may accelerate compared with normal age-related cognitive deterioration.  

The relationship between symptoms and cognitive impairments

There is virtually no causal relationship between cognitive impairment on the one hand and hallucinations and delusions on the other. Cognitive processes do contribute to the maintenance of positive symptoms. A disorder in the ToM contributes to paranoid delusions, but there are also schizophrenia patients with such disorders who do not develop delusions (Corrigan & Penn, 2001; Brüne, 2005). There are two specific cognitive processes that are associated with acute psychotic symptoms:

1. 'Source-monitoring bias': patients have more difficulty distinguishing their own thoughts and thoughts from others, even when these thoughts are written down. Patients with hallucinations also have more difficulty distinguishing their own voice from others' voices.

2. 'Jumping to conclusions': a style of thought defined as the inclination to draw conclusions when there is insufficient evidence available.

What other cognitive biases are there?

Other cognitive biases that contribute to the maintenance of the positive symptoms are the attentional bias and memory bias: more attention is devoted to stimuli that involve the delusional conviction, and these stimuli are also better remembered. Finally, patients with negative symptoms score slightly worse on neuropsychological tasks than patients with positive symptoms. Cognitive impairments also have an impact on the deteriorated social functioning, and problems at work (Corrigan & Penn, 2001). Green (1996) stated that the functional disorders interfered with each of the three social outcome measures: solving social problems, acquiring skills and functioning socially and socially. In this context, the functional disorders are 'rate-limiting factors (Mueser, 2000).