Deficit schizophrenia: an update

The authors provide a rationale for distinguishing the primary, enduring negative symptoms of schizophrenia (termed "deficit symptoms") from the more transient negative symptoms secondary to other factors. They argue that the former are more likely to provide a basis for meaningful subtyping of the schizophrenic syndrome, while the latter are more likely to respond to currently available treatments. They describe their experience in using clinical judgment based on longitudinal observations to identify deficit and nondeficit subtypes of schizophrenic patients and propose criteria for defining schizophrenia with the deficit syndrome.

This review examines the structural validity of negative symptoms focusing on 2 questions: (1) Do negative symptoms represent a domain separate from other symptoms in schizophrenia? and (2) Within negative symptoms, is there a structure that suggests multidimensionality? Results from exploratory and confirmatory factor analytic studies are examined to address these questions. Across studies and symptom instruments, negative symptoms appear to consistently emerge as a factor separate from other dimensions of the illness in schizophrenia. Whether 2-, 3-, or 5-factor models are identified, negative symptoms consistently load on a factor separate from positive symptoms, affective symptoms of depression or anxiety, and symptoms of disorganization. Focusing on negative symptoms themselves, factor analytic findings suggest that this construct is multidimensional with at least 2 factors (involving diminished expression and anhedonia-asociality). Although these factors were replicable, serious limitations were noted in this literature. Thus, 2- (or even 3- or 5-) factor models of negative symptoms should not be considered definitive, but rather all converge to support the general conclusion of the multidimensionality of negative symptoms. The later findings indicate the importance of employing assessments that provide adequate coverage of the broad domain of negative symptoms. Importantly, caution is noted in the interpretability of findings based on existing instruments, and implications for future assessment are discussed.

If schizophrenia is a clinical syndrome rather than a single disease, the identification of specific diseases within the syndrome would facilitate the advance of knowledge and the development of more specific treatments. We propose that deficit psychopathology (ie, enduring, idiopathic negative symptoms) defines a group of patients with a disease different from schizophrenia without deficit features, as the deficit and nondeficit groups differ in their signs and symptoms, course, biological correlates, treatment response, and etiologic factors. These differences cannot be attributed to more severe positive psychotic symptoms or a greater duration of illness in the deficit group. The alternative interpretation that patients with deficit schizophrenia are at the severe end of a single disease continuum is not supported by risk factor and biological features data, but there is a need for independent replication of these findings. We suggest a series of studies designed to falsify one of these hypotheses, ie, multiple diseases vs a single disease.