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Query: UMLS:C0036341 (schizophrenia)
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One hundred and eighty-seven patients suffering from DSM-III-R schizophrenia, schizoaffective, schizophreniform (psychotic group), unipolar, bipolar and other disorders were interviewed 5 years after discharge. Deficiencies were assessed by means of the Schedule for Deficit Syndrome (SDS) and the Scale for Assessment of Negative Symptoms (SANS). Binocular thresholds for discomfort to high luminances (TDHL) were assessed in 17 patients with a deficit syndrome. Results suggest that patients with psychotic disorders are in a high-risk group for deficit syndrome. Nevertheless, 9-28% and 9-30% of the 'nonpsychotic' group according to the SANS and the SDS, respectively, showed primary enduring negative symptoms. A positive correlation between the SANS total score and TDHL (r = 0.81) was found. These results suggest the nonspecificity of primary enduring negative syndromes. Furthermore preliminary data indicate a possible link between light sensitivity and the deficit syndrome, independently of diagnoses.
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PMID:The deficit syndrome in schizophrenic and nonschizophrenic patients: preliminary studies. 787 Nov 22

Plasma homovanillic acid (pHVA) was measured over a 13 hr-period in 16 DMS-III-R schizophrenic patients, all treated with neuroleptic drugs and in a stable clinical and therapeutic status for the preceeding 12 months. Patients were categorized into deficit (n = 9) and nondeficit (n = 7) forms of schizophrenia according to the Schedule for the Deficit Syndrome (SDS) criteria. As compared to the nondeficit group, deficit patients display significantly lower mean pHVA concentrations from 9 AM to 12 AM and a lack of diurnal variations. None of the demographic, clinical, and therapeutic variables can explain these biological differences. These data suggest a specific biochemical basis for the deficit syndrome of schizophrenia as defined by the SDS criteria, that is, primary, enduring, negative symptoms.
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PMID:A comparison of plasma homovanillic acid in the deficit and nondeficit subtypes of schizophrenia. 798 87

The negative symptoms of schizophrenia have generated a great interest leading some authors (Crow, Andreasen, Kay) to delineate schizophrenic subtypes based on their presence or absence. Carpenter et al. have recently proposed another subtype, the deficit syndrome, based on Kraepelin's clinical description. This differs from other proposed negative subtypes and refers to the presence or absence of prominent, enduring and primary negative symptoms. Primary negative symptoms have to be due to psychophrenia itself, in other words, independent of factors such as depression, anxiety, akinesia... Kirkpatrick et al. have proposed the Schedule for the Deficit Syndrome (SDS) to reliably identify this deficit syndrome. Some studies using this instrument have supported the validity of the deficit syndrome concept. Particularly, deficit patients have clinical, neuropsychological, neurological, eye-tracking and brain imaging impairments compared to nondeficit patients. We realized a french translation of SDS and used it to study a biological index (plasma homovanillic acid, pHVA) among deficit and nondeficit schizophrenic patients. Our data suggest a specific biochemical basis for the deficit syndrome, ie, significant lower mean pHVA levels with a lack of diurnal variation for deficit patients. The french version of SDS was validated by Kirkpatrick after english back translation. We present here our psychometric data regarding reliability (assessed by weighted and unweighted kappa coefficients) and cohesiveness of the construct (assessed by rank-order correlations of each negative symptoms with the other five, using Spearman's rho). These data are quite significant and in agreement with the SDS authors.
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PMID:[Schedule for evaluation of the deficit syndrome in schizophrenia: Schedule for Deficit Syndrome (SDS) (Kirkpatrick et al.). Importance pertinence of the SDS. Introduction of the French version]. 798 5

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.
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PMID:Depressive symptoms and the deficit syndrome of schizophrenia. 771 17

It is important to elaborate what we know about the symptomatic, syndromal, and functional course of schizophrenia in order to test models for this illness. The sample of schizophrenic patients from the Chestnut Lodge followup study was subtyped using classical (modified DSM-III-R) criteria and deficit/nondeficit (Schedule for the Deficit Syndrome) criteria. During the first 5 years of manifest illness, the subtype phenomenologies were moderately stable. Instability consisted of a drift toward disorganization (hebephrenia) and nonspecificity (undifferentiated) among the classical subtypes, and toward the deficit subtype within that categorization. Over the same time, positive symptoms were relatively stable, but negative symptoms became significantly worse. Such changes probably reflect "deterioration" because they were associated with poorer functional outcome an average of 15 years later. These data dovetail with other reports in the literature and suggest a hierarchy of symptomatic/syndromal progression in early manifest schizophrenia that may reflect active deterioration processes at work. We suggest that any theory of schizophrenic pathophysiology must account for these patterns of symptom course.
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PMID:Subtype progression and pathophysiologic deterioration in early schizophrenia. 845 14

Emerging evidence indicates that schizophrenia may in some cases be a neurodevelopmental disorder, resulting in part from the effects of prenatal exposures. Studies by our group have focused attention on the potential role of prenatal nutritional deficiency as a potential etiological factor. Therefore, we sought to examine the biological plausibility of prenatal nutritional deprivation in the etiopathogenesis of schizophrenia. We conducted a review of the pertinent literature. Four lines of evidence support prenatal nutritional deficiencies as a plausible set of risk factors for schizophrenia: a) their effects are not incompatible with the epidemiology of schizophrenia; b) they have adverse effects on brain development; c) general malnutrition results in neuropathological anomalies of brain regions implicated in schizophrenia; and d) prenatal malnutrition affects maternal systems critical to the developing fetal nervous system. There is sufficient evidence to warrant further studies of prenatal nutritional deficits as risk factors for schizophrenia. A strategy for testing these hypotheses is outlined.
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PMID:Neurobiological plausibility of prenatal nutritional deprivation as a risk factor for schizophrenia. 859 15

An autopsy case of malnutrition with spinal tract degeneration confined to the bilateral posterior columns is reported. The patient had schizophrenia in adolescence, and suffered from aplastic anemia in late middle age. Subsequently, he took little food due to delusions for 18 months until his death. He had malnutrition resulting in severe hypoproteinemia. He developed gait disturbance, loss of deep tendon reflexes and paresthesia of limbs. Neuropathological examination disclosed tract degeneration confined to the bilateral spinal posterior columns, in addition to the findings of aplastic anemia and hypoxic encephalopathy in the cerebrum. The myelin and axons were severely affected throughout the spinal cord; status spongiosus with many fatty-laden macrophages was seen in these lesions. Neurons in the posterior column nuclei were intact, while the dorsal roots and their ganglia were moderately affected. The unusual distribution and extension of the degeneration of the bilateral posterior columns in the poor nutritional state is discussed.
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PMID:Spinal tract degeneration confined to the bilateral posterior columns in malnutrition: report of an autopsy. 860 40

We report on a short overview of our work which has examined different definitions of negative syndromes across a broad spectrum of diagnoses. Primary enduring negative symptoms were assessed with the Schedule for Deficit Syndrome (SDS) and with the Scale for Assessment of Negative Symptoms (SANS) in schizophrenic and non-schizophrenic patients. Results suggested that patients with psychotic disorders are in a high-risk group for deficit syndrome. A further study included (in the deficit group) only neuroleptic-free patients without current depression or psychosis. The frequency of primary enduring negative symptoms (PENS) showed no significant difference between schizophrenic and depressive patients. Study three compared primary negative symptoms between schizophrenic and nonschizophrenic patients. There were no significant differences between both groups with regard to the SANS scores. The last study compared primary with secondary negative symptom complexes by means of the SANS. No significant differences could be found. The results suggest that PENS are not specific for schizophrenia. Moreover, further efforts are indicated to grasp "core" deficiencies in psychoses with help of new operationalized instruments.
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PMID:[Significance of primary negative symptoms in schizophrenic and other psychiatric patients]. 876 95

Since early descriptions of schizophrenia, heterogeneousness of clinical forms is one of the most typical figure of the disease. Nowadays authors perceived the necessity for patients to gather in groups in the most homogeneous way. First, different clinical effects have been noticed among schizophrenic patients with neuroleptics in function of their type or their dose. Then dichotomic concepts between positive and negative forms of schizophrenia succeeded one another. Several scales for negative symptoms of schizophrenia have been used to test the antideficit effect of different doses of neuroleptic agents. But these punctual evaluations cannot confirm primary nature of these symptoms, not derived from positive, depressive, anxious symptoms or secondary symptoms of neuroleptic treatment (as akinesia). Carpenter et al. defined the concept of deficit syndrome in schizophrenia, which can be evaluated with the SDS (Schedule for the Deficit Syndrome, Kirkpatrick et al., 1989). This classification of patients showed certain particularities: clinical, neurologic and biological ones, which seemed to confirm the initial hypothesis of homogeneousness of deficit syndrome in schizophrenia. The relevance of this concept forecasts a very promising future to research in the area of schizophrenia, with therapeutic and evolutive implications.
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PMID:[Deficit: the value and difficulty of defining the primary or secondary character of observed symptoms]. 876 36

Drug abuse is common in schizophrenia. Previous studies suggested patients with the deficit syndrome have a lower risk of drug abuse than do patients without deficit features. We distinguished deficit and nondeficit groups in the DSM-IV Field Trial dataset, and compared the two groups relative to current and lifetime (worst ever) severity of alcohol, cannabis, and other drugs of abuse. Deficit syndrome patients had a lower severity of current use of alcohol and other drugs, but the two groups did not differ significantly relative to cannabis use. Deficit patients also had less severe lifetime use of all three classes of drugs. These findings could not be attributed to differences between the deficit and nondeficit groups in demographics, severity of psychotic symptoms, chronicity of illness, or the quality of information available for the two groups. Deficit categorization and drug abuse were independently associated with poor level of function. Negative symptoms broadly defined were weaker predictors of drug abuse than was the deficit/nondeficit categorization. These findings further support the validity of the deficit syndrome of schizophrenia. Within schizophrenia, groups with relatively high or low risk for substance abuse can be identified.
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PMID:The deficit syndrome in the DSM-IV Field Trial: I. Alcohol and other drug abuse. 879 95


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