Psychopathology and neuropsychological impairments in deficit and nondeficit schizophrenia of Chinese origin
Introduction
Schizophrenia is characterized by marked clinical variance among patients in their symptoms, biological correlates, disease impact on function, and response to treatment. Present research has been hindered by extreme heterogeneity among patients (Maj, 1998, Tsuang et al., 2000). As a result, researchers have systematically parsed the symptomatology of schizophrenia into more homogeneous diagnostic categories, such as paranoid and non-paranoid subtypes or positive and negative subtypes. Deficit schizophrenia, proposed by Carpenter and colleagues (1988), is defined as a putative schizophrenia subtype, in which the primary negative symptoms are enduring, trait-like features throughout periods of clinical stability. Further, the primary negative symptoms are not attributable to depression, anxiety, paranoia, or medication side effects. The validity of the deficit/nondeficit schizophrenia classification has been supported by many studies indicating marked differences regarding (1) clinical signs and symptoms, (2) course of illness, (3) etiological vulnerability factors, (4) biological correlates, and (5) treatment response (Kirkpatrick et al., 2001). Longitudinal studies have demonstrated that the deficit subtype is a highly stable form of schizophrenia (Amador et al., 1999, Tek et al., 2001). Moreover, comparative studies have shown that the deficit subtype differs from the traditionally defined negative subtype in concept, treatment response and underlying neuropsychological correlates (Kirkpatrick et al., 1989, Kirkpatrick et al., 1993, Kopelowicz et al., 1997, Kopelowicz et al., 2000, Buchanan et al., 1998, Cohen and Docherty, 2004). Therefore, with respect to the exploration of the etiology and pathogenesis of schizophrenia, the implications of the deficit/nondeficit categorization are profound.
With regard to the clinical symptomatology, past studies from a number of countries consistently indicate that deficit patients have more severe anhedonia, less severe depression and anxiety, less suicidal ideation, less severe delusions and suspiciousness, and less substance abuse than nondeficit patients (Kirkpatrick and Buchanan, 1990, Kirkpatrick et al., 1996a, Kirkpatrick et al., 1996b, Earnst and Kring, 1999, Subotnik et al., 2000, Tiryaki et al., 2003, Galderisi et al., 2002, Arango et al., 2004). Furthermore, deficit schizophrenia has been shown to be characterized by poor premorbid functioning coupled with poor social and occupational functioning and quality of life after the onset (Fenton and McGlashan, 1994, Kirkpatrick et al., 1996a, Kirkpatrick et al., 1996b, Tek et al., 2001). Studies in the literature support the validity of the deficit/nondeficit categorization and, moreover, facilitate the identification of a subgroup of patients who appear to exhibit consistent clinical characteristics across independent studies.
In addition to the differences in symptomatology, individuals with deficit schizophrenia exhibit more severe neurological impairments and subsequently greater neurocognitive impairment, which likely contribute to their poorer social functioning (Kirkpatrick et al., 2001). Additionally, neuropsychological studies indicate that deficit schizophrenia patients show a significantly different profile from nondeficit patients when examining the dysfunction of separate brain regions. More specifically, several studies have shown that deficit patients performed significantly worse than nondeficit patients on executive function measures related to frontal lobe functioning (Putnam and Harvey, 2000, Bryson et al., 2001, Galderisi et al., 2002). Further, studies have found abnormalities among deficit schizophrenia patients in the sequencing of complex motor acts, visual attention/information processing tasks, and antisaccadic and eye tracking tasks, all of which are thought to derive from dysfunction in parietal and prefrontal areas (Thaker et al., 1989, Malaspina et al., 1994, Malaspina et al., 2002, Ross, 2000, Ross et al., 1996, Ross et al., 1997, Buchanan et al., 1997, Nkam et al., 2001). In contrast, when comparing the functioning of the temporal lobe between the two subgroups, most of above studies failed to find a significant difference.
To further verify the validity of the deficit/nondeficit categorization and better understand the differences between the two subtypes of schizophrenia, studies examining different geographical and racial samples should be conducted. In our previous work, we developed the Chinese version of the Schedule for the Deficit Syndrome (SDS, Kirkpatrick et al., 1989), the instrument used to classify deficit and nondeficit schizophrenia, and demonstrated that it had good reliability and validity (Wang et al., 2005). Therefore, it is valuable to compare Eastern and Western patients in their symptom profiles and brain functioning impairments on the basis of our reliability and validity research on the SDS-C. To date, there is a paucity of research examining the pathogenesis of deficit and nondeficit schizophrenia in mainland China. Thus, we attempt to use a convergence-of-evidence approach to investigate the symptoms and the underlying biological correlates of the deficit syndrome, including multiple measures such as psychopathological evaluation, neuropsychological assessments, neuroelectrophysiological assessment, and functional neuroanatomical imaging.
In the present study, we first examined the clinical characteristics and psychopathology of deficit and nondeficit schizophrenia in a Chinese sample. We hypothesized that the psychopathological characteristics of Chinese patients with the deficit syndrome would be consistent with the pattern that has emerged from past studies conducted in Western countries. Second, we compared the performances on the neuropsychological measures among the deficit, nondeficit and normal groups. We hypothesized that deficit patients would perform worse on the general ability measure and show a different cognitive function profile from the nondeficit sample, although both subgroups would show a poorer performance than the normal group. In particular, we hypothesized that neuropsychological indices of executive function and visuospatial abilities, which are related to frontal and parietal lobe functioning, would be more impaired in deficit schizophrenia than in nondeficit schizophrenia. However, the indices sensitive to temporal lobe dysfunction, such as the verbal and visual explicit memory measures, would be expected to show no significant differences between the two subtypes of schizophrenia.
Section snippets
Participants
Participants in the current study included 123 individuals diagnosed with schizophrenia who were recruited through the inpatient rehabilitation units of the Changsha Mental Rehabilitation Hospital and 103 healthy controls who were recruited from the local community. Although 129 schizophrenia patients were recruited, only those who completed all the study procedures were included in the data analysis of the current study. The final group consisted of 123 patients. All schizophrenia patients
Demographic characteristics
In the present study, 30 participants (24.4%) met the criteria for deficit syndrome schizophrenia, while 93 participants (75.6%) were classified as nondeficit. Demographic information of the sample and clinical characteristics for the deficit and nondeficit groups are presented in Table 1. There are no significant differences among the three groups with respect to age, education, or gender distribution. However, the three groups differed significantly in marital status (χ2 = 22.82, P < 0.001), with
Discussion
To date, the present study is the first to utilize Carpenter's categorization (Carpenter et al., 1988) of deficit schizophrenia in a Chinese sample to examine the differences in clinical symptoms and neuropsychological functions between deficit and nondeficit schizophrenia. Our results are consistent with findings in past studies regarding the psychopathological characteristics of deficit and nondeficit patients (Buchanan et al., 1990, Fenton and McGlashan, 1994, Kirkpatrick et al., 1996c, Roy
Acknowledgment
The authors thank Dr. Robert W. Buchanan for helping with the design of the study. Additionally, we thank Professor Lin Xu and Randy Patrick Auerbach for their suggestions and proofreading of an earlier version of the manuscript.
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