Schedule For The Deficit Syndrome Research Articles

The motivation and pleasure deficits but not expressivity affects social functioning through cognitive function in male patients with schizophrenia: A structural equation model.

This study aims to compare cognitive function and social functioning in male schizophrenia patients with deficit syndrome (DS) and non-DS, and to explore the associations among two different dimensions of negative symptoms (motivation and pleasure (MAP) and expressivity (EXP) deficits), cognitive function and social functioning base on a Structural Equation Model (SEM). The current study enrolled 161 male schizophrenia patients and 120 age- and education- matched healthy controls. The DS and non-DS group were categorized by the Chinese version of Schedule for the Deficit Syndrome (SDS). The psychotic and negative symptoms were evaluated by the Brief Psychiatric Rating Scale (BPRS) and the Brief Negative Symptoms Scale (BNSS). The Social functioning was measured by Scale of Social function in Psychosis Inpatients (SSPI). A battery of classical neurocognitive tests was used for assessing cognition including sustained vigilance/attention, cognitive flexibility, ideation fluency and visuospatial memory. Our study indicated that DS patients performed worser in cognitive function and social functioning than non-DS patients. The SEM model demonstrated that MAP significantly affected social functioning through direct influence and mediation of cognitive function. However, our results found that EXP had little influence on cognitive function and social function. Our findings provided evidence supporting that DS may represent as a subtype of schizophrenia, and the MAP factor play a pivotal role to influence the cognitive and social functioning in schizophrenia patients.

Risk factors of deficit and non-deficit schizophrenia: Results from a cross-sectional study

AimIt has been observed that deficit and non-deficit schizophrenia (SCZ-D and SCZ-ND) might be characterized by different risk factors. Therefore, the present study aimed to assess as to whether previously reported risk factors of schizophrenia are specifically associated with SCZ-D and SCZ-ND. MethodThis study was based on a cohort of 118 stable outpatients with schizophrenia. A diagnosis of SCZ-D was established using the Schedule for the Deficit Syndrome (SDS). Risk factors were recorded using structured interview, the Operational Criteria for Psychotic Illness (OPCRIT) checklist and the Traumatic Experience Checklist (TEC). The following risk factors were explored: male sex, a history of schizophrenia in first-degree relatives, seasonality of birth, birth weight <3000g, delivery by cesarean section, a history of childhood trauma (emotional abuse, emotional neglect, physical abuse and sexual abuse) as well as substance abuse (other than nicotine) and cigarette smoking at psychosis onset. ResultsIndividuals with SCZ-D were more likely to be males as well as reported higher rates of birth weight <3000g and any categories of childhood trauma. In turn, substance abuse (other than nicotine) at psychosis onset was significantly more frequent in patients with SCZ-ND. Binary logistic regression, controlling for multiple comparisons, revealed similar findings, except for the association with any categories of childhood trauma that appeared to be not significant. ConclusionOur findings partially replicate differential patterns of risk factors for SCZ-D (male sex and birth weight <3000g) and SCZ-ND (substance abuse at psychosis onset), likely attributable to the effects of timing of exposure.

Early versus late risk factors for deficit and nondeficit schizophrenia

AimWe examined whether timing of known risk factors for schizophrenia may influence the development of schizophrenia with primary negative symptoms. MethodThis cross-sectional single-centre study in England used a clinical cohort of 167 clozapine-treated schizophrenia patients. Deficit and nondeficit schizophrenia models were used as clinical proxies of patients with and without primary negative symptoms respectively. Patients were assessed using the Schedule for the Deficit Syndrome. We examined previously replicated risk factors (family history of psychosis, advanced paternal age, male gender, birth weight <3000g, summer birth, cannabis use, exposure to physical or sexual abuse and/or bullying) as well as other traumatic events for deficit and nondeficit schizophrenia. ResultsWe found a distinct risk factor pattern for the two groups. Compared to the nondeficit group, patients with deficit schizophrenia reported a significantly lower prevalence of cannabis use (p=0.005) at the time of first-episode psychosis (FEP), physical or sexual abuse (p=0.033) prior to FEP, less exposure to crime-related traumatic events (p=0.012) and significantly associated with summer birth (p=0.017). The groups did not differ in terms of family history of psychosis, advanced paternal age, male gender, or low birth weight. To account for multiple comparisons, a confirmatory analysis was performed using logistic regression which yielded similar results except that summer birth no longer reached statistical significance. ConclusionOur results suggest the timing of the insult may influence the symptom presentation, with insults later in life (cannabis or traumatic events) being associated with psychotic presentation and less with primary negative symptoms.

Early versus late risk factors for deficit and nondeficit schizophrenia.

We examined whether timing of known risk factors for schizophrenia may influence the development of schizophrenia with primary negative symptoms. This cross-sectional single-centre study in England used a clinical cohort of 167 clozapine-treated schizophrenia patients. Deficit and nondeficit schizophrenia models were used as clinical proxies of patients with and without primary negative symptoms respectively. Patients were assessed using the Schedule for the Deficit Syndrome. We examined previously replicated risk factors (family history of psychosis, advanced paternal age, male gender, birth weight <3000g, summer birth, cannabis use, exposure to physical or sexual abuse and/or bullying) as well as other traumatic events for deficit and nondeficit schizophrenia. We found a distinct risk factor pattern for the two groups. Compared to the nondeficit group, patients with deficit schizophrenia reported a significantly lower prevalence of cannabis use (p=0.005) at the time of first-episode psychosis (FEP), physical or sexual abuse (p=0.033) prior to FEP, less exposure to crime-related traumatic events (p=0.012) and significantly associated with summer birth (p=0.017). The groups did not differ in terms of family history of psychosis, advanced paternal age, male gender, or low birth weight. To account for multiple comparisons, a confirmatory analysis was performed using logistic regression which yielded similar results except that summer birth no longer reached statistical significance. Our results suggest the timing of the insult may influence the symptom presentation, with insults later in life (cannabis or traumatic events) being associated with psychotic presentation and less with primary negative symptoms.

White Matter Neurometabolic Signatures Support the Deficit and Nondeficit Distinction in Antipsychotic-Naïve First-Episode Psychosis Patients.

The deficit syndrome is thought to be a more homogenous clinical subgroup within the syndrome of schizophrenia that is characterized by enduring negative symptoms. It is hypothesized that distinct pathophysiological processes underlie the subtypes, where the deficit syndrome reflects an early onset nonprogressive developmental process, and the nondeficit form of the illness is characterized by attenuated neuroplasticity secondary to elevated glutamate levels. We used single-voxel magnetic resonance spectroscopy (PRESS; TE: 30 ms) to measure left frontal white matter neurometabolite levels in 61 antipsychotic-naïve first-episode psychosis patients (39 who did not display deficit features, 22 who did display deficit features, assessed with the Schedule for the Deficit Syndrome) and 59 healthy controls. Metabolite levels were quantified with the LCModel. We used a MANCOVA to determine neurometabolite differences between healthy controls, deficit syndrome patients, and nondeficit patients. We report a significant group difference when all metabolites were considered jointly (F[10,208] = 2.16; P = .02). Post hoc analyses showed that patients presenting without deficit features had higher glutamate levels than patients with deficit features and controls. Patients presenting without deficit features also had significantly higher myoinositol levels than controls; myoinositol levels were trend-level higher in patients presenting with deficit features compared to controls. Our data support the idea that the pathophysiology of patients presenting without deficit features may differ from those presenting with deficit features.

M117. ELUCIDATING ARCHITECTURE OF NEGATIVE SYNDROME IN SCHIZOPHRENIA

BackgroundThe conceptualization of negative symptoms has been refined in the past decades. Two-factor model comprising Motivation and Pleasure (MAP) and Emotional Expressivity (EE), five-factor model representing five domains of negative symptoms and second-order five-factor model incorporating the two-factor and five-factor models (Anhedonia, Asociality and Avolition regressed on MAP; Blunted Affect and Alogia regressed on EE) have been suggested as latent structure of negative symptoms. In most studies, the item “Lack of Normal Distress” in the Brief Negative Symptom Scale (BNSS) did not fit well in factor models. Nevertheless, the reported correlation and item-total correlation of Distress with other negative symptom domains and BNSS items were not negligible. Emotion deficit was also discussed as a part of negative symptoms conceptualization. As a single item may not be sufficient to represent an underlying construct that is potentially abstract and complex, the Schedule for the Deficit Syndrome (SDS) which comprises “Diminished Emotional Range” that is conceptually relevant to the BNSS Distress was employed. The study aimed to reexamine the conceptualization of negative symptoms by examining the model fit of several models when BNSS Distress and SDS Emotion (EMO) were included in the models using confirmatory factor analyses (CFA).MethodsTwo-hundred and seventy-four schizophrenia outpatients aged 21–65 were assessed on the BNSS and SDS. In the two-factor models, Restricted Affect, Diminished Emotional Range and Poverty of Speech in SDS and all items in BNSS Blunted Affect and Alogia subscales were regressed on EE, Curbing of Interests, Diminished Sense of Purpose and Diminished Social Drive in SDS and all items in BNSS Anhedonia, Asociality and Avolition subscales were regressed on MAP, without EMO, or with EMO regressed on either EE or MAP. Five-factor models and second-order five-factor models were examined, with or without EMO. Lastly, a six-factor model with EMO manifested by the sixth factor and second-order six-factor models in which EMO was regressed on either EE or MAP were tested. Root mean square error of approximation (RMSEA) <0.08, comparative fit index (CFI) >0.95, the Tucker-Lewis Index (TLI) >0.95, and weighted root-mean-square residual (WRMR) <1.0 indicate good model fit. CFAs were conducted using Mplus version 7.4.ResultsThe two-factor models did not yield adequate fit indices. Five-factor model and second-order five-factor model without EMO had good model fit; five-factor model: RMSEA=0.056 (0.044–0.068), CFI=0.996, TFI=0.995, WRMR=0.718; second-order five-factor model: RMSEA=0.049 (0.036–0.061), CFI=0.997, TFI=0.996, WRMR=0.758. When EMO was included as indicator in one of the factors in the five-factor models, only the model in which EMO was regressed on Alogia yielded adequate fit. Similarly, in the second-order five-factor models, adequate fit indices were observed only when EMO was regressed on Alogia and Blunted Affect. The six-factor model fitted the data well, RMSEA=0.053 (0.042–0.064), CFI=0.996, TFI=0.995, WRMR=0.711. Second-order six-factor model with EMO regressed on EE yielded better model fit than MAP, RMSEA=0.050 (0.039–0.061), CFI=0.996, TFI=0.995, WRMR=0.849.DiscussionIn line with previous studies, five-factor and second-order five-factor models without EMO fitted the data well. When EMO was included, a six-factor model and a second-order six-factor model in which the sixth factor was regressed on EE showed good model fit. Emotion, motivation and behavior are intertwined. Our results showed that diminished emotion may also be one of the components of negative symptoms, which had higher association with EE than MAP.

T89. THE RELIABILITY OF THE CORE NEGATIVE SYMPTOMS SCALE OF SCHIZOPHRENIA USING THE STANDARD FOR CLINICIANS’ INTERVIEW IN PSYCHIATRY (SCIP)

BackgroundRecent research on the negative symptoms of schizophrenia has produced reliable and validated scales such as the Scale for the Assessment of Negative Symptoms (SANS), the Schedule for the Deficit Syndrome, the Negative Symptoms Scale of Lewine, and others (1–3). More than 30 negative symptoms have been described, among these, avolition which is considered a core negative symptom (4). The DSM-5 recognizes five main negative symptoms: blunted affect, avolition, alogia, anhedonia and asociality (5). Other researchers consider attention impairment, poor self- care, and psychomotor retardation as negative symptoms (1, 6). There is a need to derive a short list of the core negative symptoms (CNS) of schizophrenia that are reliable and useful in clinical settings and clinical research.MethodsThe Standard for Clinicians’ Interview in Psychiatry (SCIP) is a new valid and reliable diagnostic interview that was tested in an international multisite study in three countries (USA, Canada and Egypt) between 2000 and 2012 (7–10). A total of 700 patients were interviewed at William R. Sharpe Jr. Hospital in Weston, West Virginia (670 patients) and Chestnut Ridge Center in Morgantown, West Virginia (30 patients). Mean patient age was 34, 59% male, 95% White and 34% had less than 12 years of education. The SCIP includes 8 items covering the main negative symptoms of schizophrenia: avolition, blunted affect, alogia, psychomotor retardation, poor self-care, anhedonia, attention impairment, and asociality.ResultsInter-rater reliability Kappa (k) and standard error (SE) were calculated for each of the main negative symptoms: avolition (k=0.74, SE=0.04), blunted affect (k=0.68, SE=0.05), alogia (k=0.62, SE=0.05), psychomotor retardation (k=0.72, SE=0.04), poor self-care (k=0.79, SE=0.06), anhedonia (k=0.87, SE=0.04), attention impairment (k=0.92, SE=0.12), asociality (k=0.74, SE=0.04).Cronbach’s alpha for internal consistency and the mean interitem correlation (MIC) of several models were calculated. Cronbach’s alpha and the MIC of the five-factor negative dimension (blunted affect, avolition, alogia, psychomotor retardation and poor self-care) were: alpha = 0.83, MIC=0.49. The item-rest correlations (IRCs) of each of the 5 negative symptoms were: blunted affect = 0.68, avolition = 0.57, alogia = 0.67, psychomotor retardation = 0.61 and poor self-care = 0.57. The high item-rest correlations of all five negative symptoms may indicate that they represent the Core Negative Symptoms (CNS) of schizophrenia.Adding anhedonia to the five-factor model to create a six-factor model resulted in a low item-rest correlation (IRC) of anhedonia (IRC=0.06) and a lower alpha (0.76).Similarly, adding attention impairment to the five-factor model to create a six-factor model resulted in a low item-rest correlation (IRC) of attention impairment (IRC=0.02) and a lower alpha (0.75). Similarly, adding asociality to the five-factor model to create a six-factor model resulted in a low item-rest correlation (IRC) of asociality (IRC=0.05) and a lower alpha (0.75). Finally, adding anhedonia, attention impairment and asociality to the five-factor model to create an eight-factor model resulted in low IRCs for anhedonia, attention impairment and asociality (IRCs are 0.12, 0.06, 0.10 respectively) and a lower alpha (0.67).DiscussionThe Core Negative Symptoms (CNS) Scale includes five negative items. Three items (avolition, psychomotor retardation and poor self-care) have good agreement (kappa >0.7) and two items (alogia and blunted affect) have fair agreement (kappa ranges from 0.5 to 0.7). Cronbach’s alpha was also high (0.83). The CNS scale can therefore be considered reliable at the dimensional level.

Characterization of deficit schizophrenia and reliability of the bidimensional model of its negative symptomatology

Background: Cumulative evidence has demonstrated important differences between deficit (DS) and non-deficit (NDS) schizophrenia, suggesting that DS may be a separate disease. However, most data come from the same research groups and more replication is needed to validate this hypothesis.Aims: Our study aimed to examine the distribution of DS, to compare their characteristics with NDS patients and to analyze the reliability of the two-factor structure of its negative symptomatology in a Spanish clinical sample.Methods: Sixty clinically stabilized patients with schizophrenia were evaluated. The Schedule for the Deficit Syndrome was used for DS/NDS categorization. Patient characteristics included age, gender, education, age at onset of psychosis, duration of illness, family history of psychosis, type of antipsychotic regimen, schizophrenia subtype and severity of the disease.Results: DS prevalence was 28.3%. Bivariate analysis revealed statistical differences between DS and NDS in terms of years of education and schizophrenia subtype. Factor analysis replicated the two-factor solution consisting of the ‘Expressive deficit’ and ‘Avolition–apathy’ domains reported in previous studies.Conclusions: Our results were consistent with the published data and indicated that the DS profile in the Spanish population is similar to that in other populations, which would corroborate the homogeneity of DS within the schizophrenia spectrum and contribute to the hypothesis that DS constitutes a separate disease.

Relationship between Alexithymia, Depression and the Negative Symptoms in Schizophrenia with and without Deficit Syndrome

The aim of this study was to compare schizophrenia patients with and without Deficit Syndrome (DS) with respect to alexithymia, depression and negative symptoms and to investigate the relationship between these variables. A total of 210 schizophrenia patients who joined the study were grouped on the basis of the Schedule for the Deficit Syndrome (SDS). Each patient was evaluated using the Positive and Negative Syndrome Scale (PANSS), the Calgary Depression Scale for Schizophrenia (CDSS), the Toronto Alexithymia Scale (TAS) and the UKU - Side Effect Rating Scale (UKU-SERS). The DS group had higher alexithymia scores that were not related to the negative symptoms. The prevalence of depression was significantly lower in the same group. Positive symptoms in the DS group were negatively correlated with the two TAS subscales of difficulty describing and identifying feelings. The negative symptoms scores of all the patients with and without DS correlated positively with the mean score on the TAS subscales. The severity of depressive and the negative symptoms predicted alexithymic symptoms. Lack of a correlation between the negative symptoms and alexithymic symptoms in DS suggested that the respective symptoms represented different independent phenomena in schizophrenia. A future study might explore the relationship between alexithymia and negative symptoms in association with cognitive functioning.

A positive take on schizophrenia negative symptom scales: Converting scores between the SANS, NSA and SDS

AimsTo provide quantitative conversions between commonly used scales for the assessment of negative symptoms in schizophrenia. MethodLinear regression analyses generated conversion equations between symptom scores from the Scale for the Assessment of Negative Symptoms (SANS), the Schedule for the Deficit Syndrome (SDS), the Positive and Negative Syndrome Scale (PANSS), or the Negative Symptoms Assessment (NSA) based on a cross sectional sample of 176 individuals with schizophrenia. Intraclass correlations assessed the rating conversion accuracy based on a separate sub-sample of 29 patients who took part in the initial study as well as an independent sample of 28 additional subjects with schizophrenia. ResultsBetween-scale negative symptom ratings were moderately to highly correlated (r = 0.73–0.91). Intraclass correlations between the original negative symptom rating scores and those obtained via using the conversion equations were in the range of 0.61–0.79. ConclusionsWhile there is a degree of non-overlap, several negative symptoms scores reflect measures of similar constructs and may be reliably converted between some scales. The conversion equations are provided at http://www.converteasy.org and may be used for meta- and mega-analyses that examine negative symptoms.

Clinical picture, pathogenesis and psychometric assessment of negative symptoms of schizophrenia.

Negative symptoms of schizophrenia constitute a serious diagnostic and therapeutic problem. They substantially account for the impairment of health, social functioning and quality of life whereas treatment is difficult. In this paper the development of the concept of schizophrenia and negative symptoms is presented. The models of positive and negative symptoms, introduced in the 1980's by Timothy Crow and Nancy Andreasen, and William Carpenter's concept of so-called deficit syndrome with the criteria of the division of negative symptoms into the primary and secondary, are discussed. Current views on the pathogenesis of negative symptoms are shown with reference to neuroimaging studies, neurotransmitter alterations, neuropsychological deficits, genetic, immunological and epidemiological studies. A subsection is devoted to the diagnostics tools for negative symptoms. Chronologically, they are divided into scales of the 1st and 2nd generation. The first generation includes: the Brief Psychiatric Rating Scale (BPRS), the Scale for the Assessment of Negative Symptoms (SANS), the Positive and Negative Syndrome Scale (PANSS), the Schedule for the Deficit Syndrome (SDS), and the Proxy for Deficit Syndrome. The second generation scales, developed as a result of the recommendation by American experts in 2006, include: the Brief Negative Syndrome Scale (BNSS) and the Clinical Assessment Interview for Negative Symptoms (CAINS), also the self-assessment scales: the Motivation and Pleasure Scale - Self Report (MAP-SR) and the Self-assessment of Negative Symptoms (SNS). The BNSS and the SNS scales, whose Polish versions were elaborated in the Department of Adult Psychiatry of Poznan University of Medical Sciences, are discussed in-depth.

Functional connectivity of the ventral tegmental area and avolition in schizophrenia: A resting state functional MRI study

IntroductionImpaired motivation is considered a fundamental aspect of the Avolition domain of negative symptoms. The ventral tegmental area (VTA) contains the highest number of DA neurons projecting to the brain areas involved in motivation-related processes.AimThe aim of our study was to investigate by functional MRI the resting-state functional connectivity (RS-FC) of the VTA in patients with schizophrenia and its relationships with real-life motivation and avolition.MethodThe RS-FC was investigated in 22 healthy controls (HC) and in 26 schizophrenia patients (SCZ) treated with second generation antipsychotics only and divided in high (HA = 13) and low avolition (LA = 13) subgroups. We used the Quality of Life Scale and the Schedule for the Deficit Syndrome to assess real-life motivation and avolition, respectively.ResultsHA, as compared to LA and HC, showed a reduced RS-FC of VTA with the right ventrolateral prefrontal cortex (R VLPFC), right posterior insula (R pINS) and right lateral occipital cortex (R LOC). The RS-FC for these regions was positively correlated with motivation in the whole sample and negatively correlated with avolition in schizophrenia patients.ConclusionOur findings demonstrate that motivational deficits in schizophrenia patients are linked to reduced functional connectivity in the DA circuit involved in retrieval of the outcome values of different actions to guide behavior. Further characterization of the factors modulating the functional connectivity in this circuit might foster the development of innovative treatments for avolition.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Deficit, but Not Nondeficit, Schizophrenia Is Characterized by Mucosa-Associated Activation of the Tryptophan Catabolite (TRYCAT) Pathway with Highly Specific Increases in IgA Responses Directed to Picolinic, Xanthurenic, and Quinolinic Acid.

Evidence suggests that activation of the tryptophan catabolite (TRYCAT) pathway is involved in the pathophysiology of schizophrenia. However, no previous study examined whether TRYCAT pathway activation is associated with deficit schizophrenia. We measured IgA responses to TRYCATs, namely quinolinic acid, picolinic acid, kynurenic acid, xanthurenic acid, and anthranilic acid and 3-OH-kynurenine, in 40 healthy controls and in schizophrenic patients with (n=40) and without (n=40) deficit, defined according to the Schedule for the Deficit Syndrome (SDS). Primary deficit schizophrenia is accompanied by an activated TRYCAT pathway as compared to controls and nondeficit schizophrenia. Participants with deficit schizophrenia show increased IgA responses to xanthurenic acid, picolinic acid, and quinolinic acid and relatively lowered IgA responses to kynurenic and anthranilic acids, as compared to patients with nondeficit schizophrenia. Both schizophrenia subgroups show increased IgA responses to 3-OH-kynurenine as compared to controls. The IgA responses to noxious TRYCATs, namely xanthurenic acid, picolinic acid, quinolinic acid, and 3-OH-kynurenine, but not protective TRYCATS, namely anthranilic acid and kunyrenic acid, are significantly higher in deficit schizophrenia than in controls. The negative symptoms of schizophrenia are significantly and positively associated with increased IgA responses directed against picolinic acid and inversely with anthranilic acid, whereas no significant associations between positive symptoms and IgA responses to TRYCATs were found. In conclusion, primary deficit schizophrenia is characterized by TRYCAT pathway activation and differs from nondeficit schizophrenia by a highly specific TRYCAT pattern suggesting increased excitotoxicity, cytotoxicity, and neurotoxicity, as well as inflammation and oxidative stress. The specific alterations in IgA responses to TRYCATs provide further insight for the biological delineation of deficit versus nondeficit schizophrenia.

Avolition in schizophrenia: associations with trait and state anhedonia

IntroductionCurrent research suggested that avolition in patients with schizophrenia (SCZ) is not due to a deficit of hedonic experience, but to a poor ability to translate pleasurable experiences into motivational states. In line with this hypothesis, several evidences showed a preserved hedonic experience, even in the presence of severe trait anhedonia and avolition in SCZ.ObjectivesTo test the hypothesis that memory dysfunction, generally found in SCZ, could lead to inaccurate representations of emotional experiences and interfere with translation of pleasurable experience in motivation.AimsThe present study was aimed to investigate the relationships between state and trait anhedonia, avolition and cognitive functioning in 35 SCZ.MethodsIn SCZ and matched healthy controls (HC) the Temporal experience of Pleasure (TEPS) and Chapman's scales were used to assess trait anhedonia. The MID task was used to assess in-the-moment hedonic experience. Avolition was measured by the Schedule for the Deficit Syndrome. MATRICS Consensus Cognitive Battery was used to assess cognition.ResultsSCZ did not differ from HC on TEPS or on MID task performance but reported higher scores for trait social anhedonia. Trait social anhedonia was associated with memory dysfunction and showed a correlation with avolition.ConclusionsOur results confirm the disjunction between state and trait anhedonia and demonstrate a relationship of the latter with memory impairment and avolition, suggesting that inaccurate representations of emotional experiences might impede their translation in motivation to act.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Negative Symptoms in Schizophrenia

Clinical heterogeneity is a confound common to all of schizophrenia research. Deficit schizophrenia has been proposed as a homogeneous disease entity within the schizophrenia syndrome. Utilizing the Schedule for the Deficit Syndrome (SDS) has allowed the definition of a subgroup dominated by persistent clusters of negative symptoms. While a number of studies have appeared over the years examining the electrophysiological correlates of the cluster of negative symptoms in schizophrenia, only a few studies have actually focused on the deficit syndrome (DS). PubMed as well as MEDLINE were searched for all reports indexed for "negative symptoms" or "deficit syndrome" and one of the following electrophysiology assessment tools: electroencephalography (EEG), evoked potentials (EPs), or polysomnography (PSG). While this line of research is evidently in its infancy, two significant trends emerge. First, spectral EEG studies link increased slow wave activity during wakefulness to the prevalence of negative symptoms. Secondly, sleep studies point to an association between decrease in slow wave sleep and prevalence of negative symptoms. Several studies also indicate a relationship of negative symptoms with reduced alpha activity. A host of other abnormalities--including sensory gating and P300 attenuation--are less consistently reported. Two studies specifically addressed electrophysiology of the DS. Both studies provided evidence suggesting that the DS may be a separate disease entity and not simply a severe form of schizophrenia.

2675 – Pattern recognition memory in first-episode treat-naive deficit and nondeficit schizophrenia patients

Objective To investigate the difference of visual pattern memory among first-episode treatment-naive patients with deficit and nondeficit schizophrenia. Methods 199 first-episode treatment-naive patients with schizophrenia, and 148 controls were recruited. Schedule for the Deficit Syndrome (SDS) was used to categorize the patients into deficit or nondeficit subtype. Pattern Recognition Memory (PRM) was used to test the immediate and delayed mode of visual pattern memory. Positive and Negative Symptom Scale PANSS was used to assess the degree of patients symptoms. Results The PRM immediate mode and delayed mode percent correct was significant lower and time latency was significant longer in two subtypes of patients. There were no significant difference in the performance of immediate mode of PRM between deficit and nondeficit patients[(86.49 ± 15.34) vs . (87.28 ± 16.00), P =0.960]. But the impairment was more severe in patients with deficit schizophrenia [percent correct (63.10 ± 19.17) vs . (70.69 ± 15.34), P vs . 3527.40 ± 3649.08 P =0.024] in the delayed mode. And PRM has no significant correlation with the negative symptoms of deficit schizophrenia. Conclusion There were significant difference in the performance of immediate and delayed mode of PRM between patients and controls. The difference between first-episode treatment-naive deficit schizophrenia and nondeficit schizophrenia was only in delayed mode of PRM, and has no correlation with the primary negative symptoms. The deficit schizophrenia is a subtype of schizophrenia with unique impairment of cognitive functions.

Olfactory processing, sex effects and heterogeneity in schizophrenia

IntroductionSmell identification deficits are associated with negative symptoms in schizophrenia, particularly in males. Far less information is known about the relationship of odor detection sensitivity (acuity) and negative symptoms in schizophrenia, and currently there is a dearth in sex-stratified research specifically examining odor sensitivity and smell identification. MethodsFifty-eight individuals with schizophrenia and 42 healthy comparison subjects were assessed on tests of odor sensitivity, smell identification and cognition. Negative symptoms were assessed with the Positive and Negative Syndrome Scale and the Schedule for the Deficit Syndrome. ResultsIn healthy males, increased odor detection sensitivity predicted better smell identification scores. In contrast, male schizophrenia patients showed a significant inverse relationship, in which increased odor sensitivity predicted lower smell identification scores. Odor sensitivity and smell identification were unrelated in both schizophrenia and healthy females. Olfactory processing was strongly linked to negative symptoms, but the relationships differed by sex. Emotional expression deficits were related to odor detection hypersensitivity in female patients, whereas smell identification deficits predicted these emotional deficits in male cases. ConclusionSex differences in olfactory functioning were identified in healthy subjects and in schizophrenia patients. Smell identification was related to negative symptoms in males with schizophrenia, whereas odor detection sensitivity predicted these features in females. Sex differences should be considered in future analyses that employ odor stimuli for neuropsychiatric research.

P03-344 - Tardive dyskinesia and deficit schizophrenia

IntroductionDespite comparable antipsychotic exposure, some patients experience involuntary movements yet others do not. Negative symptoms have been associated with tardive dyskinesia, but it is not certain that this is an association with primary negative symptoms.AimsTo determine whether patients with deficit schizophrenia (who have primary negative symptoms) are more likely to experience tardive dyskinesia than those with non-deficit schizophrenia.MethodsIn 2006 all the people with a clinical diagnosis of schizophrenia in Nithsdale, South West Scotland, were identified using the ‘key informant’ method. These patients were assessed using the Schedule for the Deficit Syndrome (SDS) and for the presence of dyskinesia using the Abnormal Involuntary Movements Scale (AIMS). Patients were also assessed for akathisia using the Barnes-Akathisia Scale and for extrapyramidal side effects using the Simpson and Angus rating scale.ResultsThere is a significant association between deficit and TD when controlling for age. Those with tardive dyskinesia are more likely to have deficit schizophrenia. The odds ratio is 3.08 (95% CI 1.28, 7.37), p = 0.012.ConclusionsOur findings support the proposal that the pathological process underlying deficit schizophrenia can predispose to the development of tardive dyskinesia.

Clinical significance of neurological soft signs in schizophrenia: Factor analysis of the Neurological Evaluation Scale

Background Nonlocalizing neurologic deficits detectable by clinical evaluation–“soft signs”–are a robust finding in patients diagnosed with schizophrenia, but their conceptual and neuroanatomical correlates remain unclear. The purpose of this study was to evaluate the organization of these deficits and their clinical correlates using the Neurological Evaluation Scale (NES). Methods Ninety-three male veterans with schizophrenia and schizoaffective disorder were evaluated using a detailed clinical assessment that included the NES, the Extrapyramidal Symptom Rating Scale, the Abnormal Involuntary Movement Scale (AIMS), the Barnes Akathisia Scale, the Positive and Negative Syndrome Scale, the Wisconsin Card Sorting Test (WCST), the Schedule for the Deficit Syndrome (SDS), and the Digit Symbol Substitution Task (DSST). Results Four factors explained 73% of the variance and had distinct clinical and neuropsychological correlates. Factor 1 reflected deficits involved with memory and sensory integration, and was associated with lower PANSS positive and higher AIMS scores. Factor 2 reflected impairments in motor control, and was associated with lower intelligence, more cognitive deficits, and deficit-syndrome schizophrenia. Factor 3 was related to lower intelligence and more perseverative errors on the WCST. Factor 4 was related to increasing age, more extrapyramidal symptoms, more perseverative errors, and worse scores on the DSST. Conclusions Neurologic deficits in schizophrenia have an intrinsic organization that appears to have clinical significance, highlighting the continued utility of the NES in studies of neurological deficits in schizophrenia patients. The theoretical underpinning of this organization remains unclear.

P50 gating in deficit and nondeficit schizophrenia

Dysfunctional auditory sensory processing has generally been found in schizophrenia and it has been suggested that these deficits might be related to clinical and psychosocial variables. The present study included P50 recordings using a simple-paired click auditory evoked potential paradigm in sixty patients with deficit schizophrenia (DS), sixty patients with nondeficit schizophrenia (NDS), and sixty comparison subjects. The Schedule for the Deficit Syndrome was used to categorize patients as DS or NDS. The two patient groups did not differ in clinical variables, except for higher negative dimension and lower community outcome scores in DS than in NDS patients. There were no differences in P50 ratios between deficit and nondeficit subgroups; compared with normal subjects both groups of schizophrenia patients showed impaired P50 ratios ( p < 0.0001). This ratio appears to be independent of positive and negative symptoms. However, impairment in P50 gating correlated with poorer community outcome. The data document the existence of early auditory sensory processing abnormalities in DS and NDS, and might suggest that common neuronal network abnormalities underlie both forms of schizophrenia. Deficient P50 gating may be associated with impaired functional outcome in schizophrenia.