1 Integrative theories of schizophrenia and learning
A historical perspective
Paula M. Moran and Jenny L. Rouse
Schizophrenia is a disease, or more accurately a cluster of psychiatric symptoms, characterized by bizarre perceptual experiences in sufferers. It is surprisingly common, with a prevalence of 1 in a 100, meaning that that 1 person in a 100 will suffer from schizophrenia at some time during their life, rising to 3 in a 100 when all psychotic disorders are considered (Peraala et al., 2007). From the earliest incarnations of modern psychiatry and experimental psychology there have been attempts to understand and ascertain the origins of the symptoms of schizophrenia. This is partly because schizophrenia has always been a significant societal burden, particularly prior to the discovery of antipsychotic medication in the 1950s. However, a more likely reason is that an interest in the mind and behaviour is naturally accompanied by an interest in what happens when perceptual processes and behaviour go awry in such a dramatic fashion. To the student of human behaviour there is something inherently fascinating about extremes of behaviour and experience such as hallucinations and delusions. This fascination crystallized in the 19th century as the search for the origin of schizophrenia symptoms moved from the hands of religion into those of science.
In this chapter we will first show that the collaboration between learning theory and schizophrenia research goes back much earlier than is commonly acknowledged to the earliest days of both experimental psychology and psychiatry, in some cases foreshadowing the most recent advances in the field today. Second we will indicate how current theoretical approaches to schizophrenia continue to reflect the applications of learning theory.
What is schizophrenia?
Symptoms of schizophrenia are typically classified as positive (reality distortions such as hallucinations, delusions), negative (flattened affect, social withdrawal), or cognitive (working memory/executive problems, thought disorder). The class of symptoms that characterize schizophrenia most effectively are distortions in reality. Although there are certainly individual differences in the presentation of reality distortions, there are two principal symptom types: delusions and hallucinations.
Delusions can be defined as false beliefs that are at the least unlikely to be true, or may defy logic to such a degree they are impossible. Although an abundance of evidence is typically available to contradict the belief, delusions will remain relatively unaltered (Butler & Braff, 1991). Delusions of persecution are the most common form of delusion and these are culturally specific (Bentall, Corcoran, Howard, Blackwood, & Kinderman, 2001). An American is more likely to believe he/she is being spied on by the CIA than an individual in a village in India, where beliefs in magic may lead an individual to believe he or she is being persecuted by an evil spirit (Kulhara, Avasthi, & Sharma, 2000).
The other common group of reality distortions are hallucinations. Hallucinations are perceptual experiences in the absence of external stimulation (Silbersweig et al., 1995) and can occur in any sensory modality. Auditory hallucinations are commonly voices. The nature of these voices varies between patients, with some individuals reporting friendly and encouraging voices, although most are critical and angry.
Formal thought disorder is the general term used to describe disturbances in thinking. Thought disorder is considered an overt sign as it can be observed as confused speech that is difficult for the listener to understand. Specific disruptions include loosely connected thought patterns and a general lack of awareness of the listenerâs needs (Docherty, Hall, Gordinier, & Cutting, 2000). Thought disorder is prominent in both descriptions and conceptualizations of schizophrenia (Kerns & Berenbaum, 2002).
The final major group of symptoms can be loosely defined as disruptions in emotionality. Sometimes these disruptions can appear to be over-emotional responses such as inappropriate laughter. However, the majority of emotional disorder is impoverished, leading many to liken the symptoms to those seen in major depression (Winograd-Gurvich, Fitzgerald, Georgiou-Karistianis, Bradshaw, & White, 2006). Patients withdraw from society and appear emotionally detached. Many individuals will also show a reduction in their emotional responses, not smiling or producing necessary gestures to allow normal conversation.
All the symptoms above are considered cardinal to diagnosis of schizophrenia, though not all patients will show evidence of all the groups. Specific diagnosis is made according to one of two major classification systems: The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), or the International Classification of Diseases and Related Health Problems (ICD-10). It is notable that neither DSM-IV-TR nor ICD-10 include cognitive symptoms specifically, however this is likely to change in the forthcoming DSM-V and ICD-11 due to be published in 2013 (Keefe & Fenton, 2007). Given the complexity of the symptom profile and overlap with other disorders such as bipolar disorder, many have claimed that a single syndrome of schizophrenia does not exist and it is more accurate to consider the individual symptoms (Bentall, 2006).
It is important to note that there are demonstrated cultural differences not only in the manifestation of symptoms, but also in the diagnosis and clinical outcomes of schizophrenia. Patients in Western, developed countries show a higher frequency of depressive symptoms, thought insertion, and thought broadcasting and a less favourable progression and outcome than in developing countries (Sartorius et al., 1986). The specific cultural factors that contribute to these differences are not clear but may comprise social and kinship factors (Jablensky et al., 1992; Jablensky & Sartorious, 2008).
Biological theories of schizophrenia
A full treatment of the biological theories of schizophrenia are beyond the scope of this chapter but have been covered elsewhere in great detail (for recent comprehensive reviews see Van Os & Kapur, 2009; Keshavan, Tandon, Boutros, & Nasrallah, 2008). They can be considered under the rubrics of neurochemical, neurodevelopmental, and genetic hypotheses and most would agree that it is likely that abnormalities in all of these dimensions interact to produce the range of behavioural symptoms associated with the disease (Maynard, Sikich, Lieberman, & LaMantia, 2001; Wong & Van Tol, 2003).
There are a number of biological theories that have particular import for how the theoretical understanding of learning has been applied to understanding schizophrenia symptoms. The neurotransmitters dopamine and glutamate both have specific roles in learning and have been suggested to be abnormal in schizophrenia. The dopamine hypothesis of schizophrenia essentially suggests that overactivity in subcortical dopamine neural circuitry, including the ventral striatum, engenders the positive symptoms of schizophrenia while a later revision suggested that a consequent underactivity in meso-cortical regions gives rise to negative and cognitive symptoms (Toda & Abi-Dargham, 2007). This revision allowed the hypothesis to simultaneously explain hallucinations and delusions (overactivity in subcortical dopamine) and flat affect and executive dysfunction (underactivity in prefrontal dopamine) (Howes & Kapur, 2009). The glutamate hypothesis suggests that dysfunction in glutamatergic transmission in cortico-limbic brain regions is primarily responsible for the symptoms of schizophrenia, particularly the negative and cognitive symptoms (Coyle, 1996; Javitt, 2007; Belforte et al., 2010).
The role of dopamine in learning is complex and there are many hypotheses suggesting that dopamine and in particular the phasic signal mediates a number of aspects of the learning process; prediction error (a mismatch between actual and expected outcomes to stimuli that initiate learning) (Waelti, Dickinson, & Schultz, 2001), the gating of new information to the frontal cortex (Cohen, Braver, & Brown, 2002), and the assignation of incentive value to environmental stimuli (Berridge & Robinson, 1998). Glutamate plays an important role in long-term memory formation and there is strong evidence for modulatory actions on memory consolidation (for review see Riedel, Platt, & Micheau, 2003).
We will see how modern integrative theories of schizophrenia make explicit reference to these processes that are underpinned by dopamine and glutamate circuitry and hypothesized to be abnormally regulated in schizophrenia.
Applications of learning theory to schizophrenia: A long history
The first systematic attempts to describe schizophrenia in experimental terms was in the work of Kraepelin and Bleuler in the late 1800s and early 1900s, considered to be the founding fathers of modern Psychiatry. Emile Kraepelin (influenced by working closely with Alois Alzheimer who identified the first neuropathological hallmarks of what is now called Alzheimerâs Disease) suggested in 1896 that the disease was not a single psychotic entity but could be divided into âdementia praecoxâ and âmanic depressive insanityâ. He originally classified the disorder into three subtypes (catatonic, hebephrenic, and paranoid) but later added a fourth type (simple) and was one of the first to identify the progressive nature of the disease. It was Eugene Bleuler, a Swiss psychiatrist, who suggested the name âSchizophreniaâ in 1911, to denote a splitting of psychic functions, âschizâ meaning split and âphrenâ meaning mind. Bleuler proposed that the fundamental symptoms were incongruity of affect, ambivalences, autism, and loosening of associations (the Four As). The loosening of associations he described as follows:
Contradictory, competing, and more or less irrelevant responses can no longer be excluded.
⌠Schizophrenic patients themselves often complain about the confusion in their talk and thinking, saying that everything seems mixed up, the words do not come as they once did, thoughts rush in and are jumbled âŚ.
âThere are a million words,â one patient said, âI canât make sentences; everything is disconnected.â
Another patient made several attempts to speak and then gave up; the next day she complained her thoughts had been rushing through her mind so that she could say nothing.
(1911, p. 511)
While the Kraepelinian view is considered to be the most influential, it was Bleulerâs ideas that disordered thought processes in schizophrenia represent a loosening of associations that were crucial in the development of the idea that a disruption in learning might be of relevance to understanding the fragmented thinking and delusions that characterize schizophrenia. While documentary evidence is scarce, it is highly likely that psychiatrists such as Bleuler were influenced by the concurrent developments in experimental psychology in the late 19th and early 20th century, particularly the work of stimulus-response theorists Pavlov and Watson. In 1913 Watson published his behaviourist manifesto, marking a period in history when focus in Psychology began to shift away from the mind and towards behaviour. This is exemplified by a quote from Watson on mental illness âWhen the psychopathologist tries to tell me about a âschizâ ⌠I have the feeling that he doesnât know what he is talking about. And the reason I think he doesnât know what he is talking about is that he has always approached his patients from the point of view of the mindâ (Watson, 1924). In the early 20th century experimental psychology was dominated by stimulus-response learning theory with the work of Watson, Pavlov, Hull, Spence, and l...