Models of schizophrenia
Interest in negative symptoms re-emerged in the 1970s, as exemplified by Strauss and Carpenter (1974) and Andreasen (1979a,b,c). The turning point came perhaps from the works of Crow who, in 1980, proposed a new typology for schizophrenia, which integrated clinical presentation, pathophysiology and treatment response in a single model (Crow 1980; Crow et al. 1981). Patients with type I schizophrenia presented clinically with positive symptoms such as delusions and hallucinations; Crow posited that the underlying pathophysiological mechanism for this subtype was a biochemical imbalance, such as an excess of dopamine D2receptors. Therefore, he hypothesized that the resulting clinical manifestations would be more likely to respond favourably to antipsychotic medication, to be characterized by exacerbations and remissions, and to have a more favourable outcome. Conversely, patients with type II schizophrenia, presenting with symptoms such as affective flattening and poverty of speech, were said to be manifestating an underlying structural/anatomical abnormality reflected by ventricular enlargement and cortical atrophy in neuroimaging studies. These symptoms therefore would tend to be poorly responsive to somatic treatment, follow a chronic course, and predict poor outcome.
Crow’s original model did not specify which of the various descriptors of type I vs. type II should be used in studies designed to disconfirm or verify the hypothesized dichotomy; that is, clinical presentation, pathophysiology or treatment response. Therefore the model was difficult to test. Andreasen developed two detailed standardized rating scales, the Scale for the Assessment of Negative Symptoms (SANS) (Andreasen 1983) and the Scale for the Assessment of Positive Symptoms (SAPS) (Andreasen 1984), for reliably assessing symptoms and exploring other aspects of the relationships between positive symptoms, negative symptoms and cognitive, psychosocial and neurobiological correlates of schizophrenia. One result from validation studies of these scales was Andreasen’s proposal of three subtypes of patients with schizophrenia: negative, positive and mixed (Andreasen & Olsen 1982). Both Crow (1980) and Andreasen et al. (1982) proposed that the negative symptoms of schizophrenia were indicators of a single ‘subtype’.
Dividing patients into mutually exclusive subgroups is firmly rooted in the ‘disease model’ in medicine. Symptomatology is the measure used to identify a category, and at this point the categories are referred to as ‘syndromes’ (literally, a running together), because they constitute an identifiable clinical pattern that makes sense in the context of observed relationships of the symptoms.
Once a specific pathophysiology or aetiology is identified, syndromes are elevated to the status of recognized diseases. In the ‘categorical approach’ it is assumed that the subtypes identified will differ from one another (and that this will eventually be discovered and documented) in terms of their pathophysiological mechanisms or aetiology, which may be reflected in differing responses to treatment, course of morbidity and underlying neurobiology.
The typology of schizophrenia proposed by Crow was inherently categorical, with subjects classified as either type I or II.
The expansion of this conceptualization by Andreasen to include a mixed type was also categorical. The research produced from the categorical approach was prolific throughout the 1980s, but eventually the need for a new type of explanatory model arose. Dividing patients into mutually exclusive groups based on positive and negative symptoms was eventually abandoned, for several reasons. First, most patients were of a ‘mixed’ subtype, and many fewer were purely ‘positive’ or ‘negative’ (Andreasen 1985). Secondly, longitudinal studies revealed that the symptoms of patients varied over time (Breier et al. 1987; Marneros et al. 1991).
One of the most difficult problems in the investigation and assessment of negative symptoms in schizophrenia involves the recognition that their measurement may be confounded by a variety of other factors. The four most commonly implicated factors are:
1 neuroleptic side-effects, such as akinesia;
2 depression, which has been reported to be present in schizophrenia in the early course of the illness (Knights & Hirsch 1981; Wassink et al. 1999), not to decrease in severity as the psychotic symptoms abate with medication (Knights & Hirsch 1981) and to be frequent during the residual phase (Siris 1991);
3 a response to positive symptoms, for example avoiding social interactions because of paranoia; and
4 environmental understimulation resulting from chronic institutionalization (Carpenter et al. 1985).
Carpenter and his group have been most active in their attempts to disentangle ‘primary’ and ‘secondary’ negative symptoms (Carpenter & Kirkpatrick 1988). Carpenter defines primary, or ‘deficit’, symptoms as enduring core-negative symptoms of schizophrenia such as anhedonia and blunted affect.
The secondary symptoms, however, are those negative symptoms that may be considered consequential to other symptoms or treatment of schizophrenia. Carpenter’s deficit symptoms include flattened affect, anhedonia, poverty of speech, curbing of interest and decrease in curiosity, lack of sense of purpose and diminished social drive. By definition, these symptoms must not be fully accounted for by depression, anxiety, medication effects or environmental deprivation. The non-deficit syndrome is defined by an absence of these deficit symptoms with the presence of any other schizophrenia symptoms, such as disorganized thought or hallucinations.
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