Schizophrenia has long been characterized by significant variability in symptoms, course of illness, and clinical profiles. In an attempt to reduce the heterogeneity of this complex disorder, researchers have tried to identify homogeneous subtypes that will facilitate the identification of links between symptoms and putative neurobiological mechanisms. Among these, deficit schizophrenia (DS)1–2
has been found to be a distinct subtype within the diagnosis of schizophrenia, with DS patients differing from nondeficit schizophrenia with regard to risk factors, symptom profiles, neuropsychological functioning, family history, course of illness, treatment response, and structural and functional neurobiology.3–13
DS has been shown to have solid long-term diagnostic stability,14–15
with a prevalence of 15% among first-episode patients and up to 32% among chronic patients.5, 16
Although some of the data are consistent with the view of DS as representing the severe end of a single continuum of schizophrenia, a large body of literature on risk factors and biological features is inconsistent with this view, supporting the hypothesis of a separate disease.5
While research findings support the concept of DS as a distinct subtype of schizophrenia, it has not been determined that the symptoms of DS represent a single, cohesive domain of psychopathology, as the factorial structure of DS has not been investigated. In fact, there is some evidence pointing to the possibility that the symptoms making up DS may be independent of each other. Kelley et al. found 2 factors (diminished motivation and affective flattening) in a study of negative symptoms among 93 neuroleptic-free males with schizophrenia.17
Sayers et al. used exploratory and confirmatory factor analyses to identify the factor structure of negative symptoms as assessed by the Scale for the Assessment of Negative Symptoms within a large sample of schizophrenia patients (N
They found 3 factors: diminished expression, inattention/alogia, and social amotivation. However, there was a high interfactor correlation (r
= .83) between the diminished expression and inattention/alogia factors.
Thus, the aim of this study is to investigate the factor structure of DS. Based on a review of the 6 symptoms of the Schedule for the Deficit Syndrome2
and previous factor-analytic studies of negative symptoms,17–18
we tested the hypothesis that DS may have 2 distinct factors: a factor relating to volition and a second factor relating to affect. Our belief is that clear delineation of specific areas of psychopathology will facilitate the discovery of links between symptoms and putative neurobiological mechanisms, possibly indicating that these phenomena are separate targets for treatment studies.