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Abstract
The negative symptoms of schizophrenia, defined as the absence or diminution of normal behaviors and functions, have been recognized since Kraepelin Kraepelin et al.,(1919),Buchanan et al’s.,(2006) description of the ‘‘avolitional syndrome,’’ manifested as a‘‘weakening of those emotional activities which permanently form the mainsprings of volition, ’’and resulting in ‘‘emotional dullness, failure of mental activities, loss of mastery over volition, of endeavor, and of ability for independent action,’’ represents one of the most elegant descriptions of negative symptoms.
Also,Strauss et al.,(1974) separated the schizophrenic symptoms into 3 specific complexes (i.e., positive symptoms, negative symptoms, and disorders of relating) rekindled interest in the positive/negative classification of symptoms.
Other models using the positive /negative symptom dichotomy ensued, such as, type I and type II schizophrenia Crow et al., (1985) and positive and negative schizophrenia (Andreasen et al., 1982).
All these constructs were attempts to explain the heterogeneity of schizophrenia. Negative symptoms account for much of the long term morbidity and poor functional outcome of patients with schizophrenia (Kirkpatrick et al., 2001; Kurtz et al., 2005).
The development of a negative symptom treatment is a major challenge for the field. Negative symptoms, as broadly defined by measures as the Brief Psychiatric Rating Scale (BPRS) Overall et al., (1962) anergia factor, Scale for the Assessment of Negative Symptoms (SANS), Andreasen, (1984) or Positive and Negative Symptoms Scale (PANSS), Kay et al., (1987) has improved during conventional and second generation antipsychotic drug treatment (Marder et al., 1994; Tollefson et al., 1997).
However, in most of studies, this effect has been observed in the context of, and correlated with, concurrent improvement of positive, depressive, and/or extrapyramidal symptoms (Miller et al., 1994; Tollefson et al., 1997).
These are the major sources of secondary negative symptoms, and other sources of secondary symptoms are usually not even assessed. Thus, the use of negative symptoms broadly defined is unlikely to lead to the development of effective treatments for those negative symptoms, which persist during clinical stability and are associated with impaired role function performance (Carpenter, 2004).
There are 2 alternative approaches for defining negative symptoms in the context of clinical trials. The first approach is to restrict negative symptoms to primary, enduring negative symptoms or deficit symptoms that are highly correlated with impaired role function (Carpenter et al., 1988; Kirkpatrick et al., 2001).
Deficit symptoms are highly correlated with impaired role function (Kirkpatrick et al., 2001).