Research has yet to determine the exact cause of schizo phre nia. Researchers are increasingly turning to neurobiological explanations and away from psychodynamic explanations (Birtwistle & Baldwin 1998; Sharma & Murray 1993). Put simply, schizophrenia is more com monly viewed as an illness of neurological functioning than a disorder of the mind. In all probability the cause of schizophrenia lies in a complex interaction between multiple combinations of genetic and environmental factors—for example, exposure to infection during gestation or birth (Brown 2006; Venables et al 2007), which may interfere with normal brain development and function. This complex interplay results in the constellation of behaviours collectively known as the schizophrenias (Andreasen 1999; Geddes & Lawrie 1995; Levinson et al 1998; Munk-Jorgensen & Ewald 2001).

The fact that the brains of those with schizophrenia differ from those without the illness is now largely undisputed (Coffey 1998; Cotter & Pariante 2002). How or why these aberrations in brain biochemistry and anatomy affect the functioning of the brain remains a mystery, as does the reason that these abnormalities appear to remain dormant until late adolescence in most individuals (Cotter & Pariante 2002).

Biological theories

The three most commonly discussed biological causative factors are brain anatomy, genetics and brain biochemistry. It would be erroneous to consider these three factors as mutually exclusive. Far more likely is the existence of a relationship between the three; for example, some as-yet unidentified pattern of inheritance may predispose an individual to differences in anatomy or fluctuations in neurotransmitter biochemistry (Lewis & Murray 1987, cited in Coffey 1998).

Neuroanatomical abnormalities

Schizophrenia is often referred to as a neuropsychological disorder, which implies that the origins of the psychological disturbance lie in the neurological structure and function of the brain. Commonly, but not conclusively, modern imaging techniques reveal lower brain tissue volume and higher cerebrospinal volumes (Salokangas et al 2002). Precisely how or why these changes occur is unknown. It is commonly thought that either genetics or environmental factors during gestation are responsible for the brain abnormalities, with the effects remaining dormant until adolescence. In contrast to this commonly held notion, some research suggests that the brain changes occur as a result of the illness and may occur during or shortly after the first episode of psychosis (Lawrie et al 2002). Clearly, a great deal more research between abnormal brain anatomy and schizophrenia is required. Both Farrison (2000) and Coffey (1998) cite a number of literature reviews that suggest that it is still too early to state conclusively that neuroanatomy is the causative factor in schizophrenia.

Genetic predisposition

As with neuroanatomical explanations, genetic explanations are far from conclusive. What seems most likely is that an individual’s genetic make-up leaves them vulnerable to the development of the illness to some degree. In other words, we inherit a certain level of risk for developing the illness rather than inheriting the illness itself. What seems apparent, however, is the pattern whereby the person who is most at risk of developing schizophrenia is the person who shares the most genes with a person with the disorder. That is, a person with a family member with schizophrenia is at higher risk of developing the illness than a member of the general population.

The prevalence of schizophrenia is approximately 1%. This means that on average an individual has a 1 in 100 chance of developing the illness. It should be noted that this average figure has been shown to vary widely, depending on a range of environmental circumstances. A person is more likely to be diagnosed with schizophrenia, for example, if they grow up in an urban environment, belong to a lower socioeconomic group or were born in winter or spring (Haukka et al 2001; Munk-Jorgensen & Ewald 2001; Suvisaari, Haukka & Lonnqvist 2002; van Os 2000). Nevertheless, symptoms of schizophrenia tend to be found in individuals who have relatives with schizophrenia. Individuals are far more likely to show symptoms of schizophrenia if one or more parents have the disorder (Birtwistle & Baldwin 1998; Kety et al 1994). This pattern is also found if an identical twin has the disorder (Birtwistle & Baldwin 1998; Kety et al 1994) or if a fraternal twin or a non-twin sibling has the disorder (Birtwistle & Baldwin 1998). The probabilities associated with the above patterns fail to follow any known pattern of inheritance. As a result it is suggested that a number of genes across a number of chromosomes could contribute to vulnerability to the disorder (US DHHS 1999).

Biochemical theories

Biochemical theories share the belief that chemicals responsible for the transmission of nerve impulses across the synapse may be responsible for the development of schizophrenia. These chemicals are known as neurotransmitters. The most discussed theory relating to brain biochemistry involvement in schizophrenia relates to an abnormal amount or action of the neurotransmitter dopamine in the brain of the individual diagnosed with schizophrenia (Kapur & Seeman 2001; Rivas-Vazquez 2003). This theory is often referred to as the dopamine hypothesis, and despite the fact that it has been one of the most widely accepted theories for many years, it remains inconclusive.

In very simple terms, the theory is a mix of known facts and hypotheses. The first of these facts is that antipsychotic medications such as chlorpromazine and thioridazine act by blocking some of the dopamine receptor sites in the brain and therefore the amount of effective dopamine is reduced (Birtwistle & Baldwin 1998; Farrison 2000; O’Conner 1998). These medications also reduce symptoms such as hallucinations and paranoia.

A second fact is that certain substances, amphetamines in particular, increase the dopamine action and also mimic some of the symptoms of schizophrenia (Birtwistle & Baldwin 1998). Where the theory is reduced to hypothesis and supposition is in the area of symptoms, such as lack of social interest (commonly referred to as negative symptoms). Until recently the antipsychotic medications such as those mentioned previously have had an effect on symptoms such as delusional thinking and hallucinations (commonly referred to as positive symptoms). It seems that dopamine excesses may only be responsible for part of the constellation of features in schizophrenia, namely the positive symptoms.

It is recognised that serotonin, another commonly found neurotransmitter, may also be significant in the development of schizophrenia (Blin, Azorin & Bouhours 1996). A broad group of drugs collectively known as the atypical antipsychotics became increasingly popular in the early 1990s. Among this group are drugs such as clozapine, olanzepine and respiridone. These drugs block both serotonin and dopamine receptors and have been shown to be more effective in the treatment of many individuals suffering from schizophrenia and other schizophrenia-like psychoses. Whereas drugs such as the typical antipsychotic group almost exclusively target positive symptoms, the atypical antipsychotics are also effective against negative symptoms (Birtwistle & Baldwin 1998). They are named ‘atypical’ because they contrast with the more conventional drugs such as chlorpromazine and thioridazine in their action and pharmacology.

The stress-diathesis model

The stress-diathesis model seeks to bring much of what is known about the cause of schizophrenia together into one model of understanding. The basic assumption behind the stress-diathesis model is that individuals are exposed to stressful events in the course of their lives and that these events may precipitate symptoms in some people who have a predisposition to mental illnesses (Zubin & Spring 1977). Essential to this theory is the notion that some people are more vulnerable to mental illness than others. In the case of schizophrenia this vulnerability may be related to genetics, environmental factors, aberrations in brain anatomy or biochemistry or, more likely, a combination of all these things (van Heeringen 2000). Weisman (2005) expanded the understanding of the role of family as part of an individual’s environment by examining the literature in this area. She asserts that a sufferer’s family and home environment has the potential to affect the course of the illness. More specifically, in families that show high levels of expressed emotion, typified by excessive criticism, hostility or emotional over-involvement do less well than families with patterns of relating that are not high in expressed emotion. The importance of this model and its more contemporary redevelopment, known as the stress-vulnerability-protective factors model, to clinical practice is the fact that it suggests a range of appropriate actions, from targeting vulnerable but as yet asymptomatic individuals through to symptom reduction by medication (Kopelowicz, Liberman & Wallace 2003) and possibly family therapy and counselling (Weisman 2005). Despite the fact that the stress-diathesis model of schizophrenia has merit in that it integrates much of what is known, it still fails to bring us closer to a detailed understanding of schizophrenia (Hammen, Henry & Daley 2000).

Critical thinking challenge 15.1

How might the stress-diathesis model explain the high rates of mental illness among our society’s homeless population?

Diagnostic criteria

Diagnostic and Statistical Manual-IV-TR

The Diagnostic and Statistical Manual of Mental Disorders (4th edn, text rev.), DSM-IV-TR (American Psychiatric Association 2000), is a highly detailed listing of mental disorders and their corresponding diagnostic criteria. The benefit of the manual is that it allows clinicians to be consistent in their use of the term ‘schizophrenia’. Because mental illnesses have few if any laboratory tests or other diagnostic procedures that can either confirm or refute a diagnosis, the means available to make psychiatric diagnoses is through detailed history taking and skilled observation. The data gained from these processes are then measured against the diagnostic criteria stated in the DSM-IV-TR (APA 2000). In simple terms, the DSM-IV-TR describes the clinical presentation that needs to exist for a diagnosis of schizophrenia to be made. This allows for common and consistent understandings in diagnosing the disorder of schizophrenia.

Although the term ‘schizophrenia’ suggests a single illness, schizophrenia is more accurately viewed as a constellation of conditions, with a number of common features along with differences that allow subtypes to be recognised. These features and differences are described by the DSM-IV-TR (APA 2000) as follows: