Nondeficit Patients Research Articles

Family history and deficit form in schizophrenia

As no genetic study has been made in deficit patients, characterized by enduring and primary negative symptoms, the aim of the study was to test the involvement of a familial factor in deficit syndrome. The results in 71 schizophrenic patients showed less familial factors but a greater weight in heritage of schizophrenia in deficit than in nondeficit patients.

Drug abuse among deficit and nondeficit schizophrenic patients in the DSM-IV field trials

Drug abuse among deficit and nondeficit schizophrenic patients in the DSM-IV field trials

Depressive Symptoms and the Deficit Syndrome of Schizophrenia

One of the most influential ideas in schizophrenia research is that schizophrenia may be a syndrome with significant pathophysiological heterogeneity, rather than a single disease. Among patients with schizophrenia, presence or absence of the deficit syndrome has been suggested as a method for defining relatively homogeneous groups. The criteria for the deficit syndrome require the presence of negative symptoms that are judged primary to the illness, rather than to factors, such as depressive mood, that may resemble the negative symptoms of schizophrenia. To test one aspect of the validity of the primary/secondary judgment, we tested the relationship of depressive symptoms to the deficit/nondeficit categorization. Using independent clinician ratings, the depressive mood of deficit and nondeficit patients was compared at the time the categorization was made, and at an average follow-up of 2 1/2 years. Using patients' self ratings, deficit and nondeficit patients were compared at an average follow-up of 1 1/2 years. Deficit patients had significantly less severe depressive symptoms by clinicians' ratings both cross-sectionally and at follow-up, and less severe self-rated symptoms at follow-up. These differences were not due to confounding by age, race, sex, socioeconomic status, or chronicity. These results support the validity of the deficit/nondeficit categorization.

Case identification and stability of the deficit syndrome of schizophrenia

In certain situations, such as large epidemiological studies, it may be necessary to use proxy case-identification tools instead of “gold-standard” assessments. The deficit syndrome of schizophrenia requires a clinical assessment that may not be feasible in some study populations. Measures for the discrimination of deficit and nondeficit patients, based on the Brief Psychiatric Rating Scale (BPRS), were assessed in a group of 100 outpatients with chronic schizophrenia. A rationally based case-identification tool was validated, and its case-identification properties were found to be stable over time; consequently, this proxy measure may be of use in other data sets. The stability of the relationship between this BPRS measure and the deficit/nondeficit categorization supports the view that it is a valid categorization.

Structural abnormalities in deficit and nondeficit schizophrenia.

Previous studies have suggested the involvement of the frontal and parietal cortices and thalamus in a neural circuit underlying the production of primary enduring negative or deficit symptoms of schizophrenia. The purpose of this study was to examine whether structural changes in the proposed circuit are associated with the production of deficit symptoms. Magnetic resonance imaging was used to measure the volume of selected circuit brain regions (i.e., the prefrontal region and caudate) and noncircuit brain regions (i.e., the amygdala/hippocampus complex) in 17 deficit and 24 nondeficit schizophrenic outpatients and 30 normal comparison subjects. Right and left total prefrontal volumes discriminated deficit from nondeficit patients, with prefrontal volumes being smaller in nondeficit patients. There were no differences between the two schizophrenic subgroups in left caudate or right and left amygdala/hippocampus complex volumes. The right caudate was larger in deficit patients, but the difference between the two schizophrenic subgroups was not significant. There were no differences between deficit and normal subjects on any prefrontal region measure. Nondeficit patients had smaller total right and left prefrontal volumes than normal subjects. Both schizophrenic subgroups had larger left caudate volumes and smaller right and left amygdala/hippocampus complex volumes than the normal subjects. There was a trend for deficit patients to have larger right caudate volumes. These results suggest that structural changes in the prefrontal region are not responsible for deficit symptoms. The caudate, particularly the right caudate, may be associated with the production of these symptoms.

Deficit syndrome in older schizophrenic patients

Previous studies have reported that a proportion of younger schizophrenic patients have the “deficit syndrome,” with persistent “negative” symptoms not secondary to factors other than the disease process (e.g., depression). Yet, there is scant information on the deficit syndrome in older schizophrenic patients. We studied 46 schizophrenic patients over age 45. Seventeen met the criteria for the deficit syndrome as described by Carpenter et al. (1988), 20 were considered definite nondeficit patients, and 9 could not be classified. The deficit schizophrenic patients had a significantly higher total score on the Scale for the Assessment of Negative Symptoms but similar scores on scales for positive symptoms, depressive symptoms, and overall psychopathology as compared with nondeficit patients. The deficit patients also had a nonsignificantly greater impairment on the Halstead-Reitan Battery. One notable difference between our results and those of Carpenter et al. was in the prevalence of deficit syndrome. We found the prevalence (37%) to be significantly higher than that reported in younger patients (15%). Pending confirmation using larger sample sizes, the increased frequency of the deficit syndrome in our study could possibly be attributed to aging or a longer duration of illness in our subjects.

Clinical correlates of the deficit syndrome of schizophrenia

The authors propose using primary and enduring negative or deficit symptoms for dichotomizing schizophrenic patients into two groups, deficit and nondeficit. The validity of this approach was examined by comparing 17 deficit and 17 nondeficit patients for differences in premorbid adjustment and degree of neurological impairment. Deficit patients were characterized by poorer premorbid adjustment and greater neurological impairment. Neurological impairment was not related to premorbid adjustment in either group or in the total patient population. These findings support the utility of deficit symptoms for defining a more homogeneous subgroup of schizophrenia.

Anhedonia and the deficit syndrome of schizophrenia

Schizophrenic outpatients with and without the deficit syndrome were administered Chapman's “psychosis proneness” scales. As hypothesized, deficit syndrome patients had higher scores on Social Anhedonia and Physical Anhedonia, but did not differ from nondeficit patients on Perceptual Aberration, Magical Ideation, or Impulsive Nonconformity. The differences between the two groups were not related to race, gender, age, socioeconomic status of family of origin, or drug treatment. These results support the validity of the deficit syndrome, and suggest that the Social Anhedonia and Physical Anhedonia scales may be useful in future studies of schizophrenia.

Wisconsin card sort activated blood flow in dorsolateral frontal cortex in never medicated and previously medicated schizophrenics and normal controls

and to examine if altered function in these areas is related to dysfunction in subcortical areas, the metabolic activity of cortical and subcortical structures were examined in 11 neuroleptic free DSM-III schizophrenics, four deficit and seven non-deficit, and 12 normal controls using PET imaging with i8F-2-DG. All subjects were examined, at rest, on the NeuroPET, with eyes covered and ears plugged. Glucose utilization (mg glu/lOO gm tissue/minute) was significantly lower in the thalamus of deficit (8.1 + 0.8; mean 5 S.D.) compared to non-deficit patients (10.4 ? 0.7; mean + S.D., p < .Ol); there were no differences in any of the other subcortical areas. Glucose utilization was also lower in multiple regions of the frontal, parietal, and temporal cortices in the deficit patients. In contrast, there were no differences in these areas between the total schizophrenic group and the normal controls. The results suggest that deficit patients may be characterized by decreased thalamic and cortical metabolism, and raise the possibility that these areas mediate the production of deficit symptoms.