Deficit Syndrome Schizophrenia Research Articles

ROI-based analysis of diffusion indices in healthy subjects and subjects with deficit or non-deficit syndrome schizophrenia

We analyzed DTI data involving 22 healthy subjects (HC), 15 patients with deficit syndrome schizophrenia (DSZ), and 25 patients with non-deficit syndrome schizophrenia (NDSZ). We used a 1.5-T MRI scanner to collect diffusion-weighted images and T1 images, which were employed to correct distortions and deformations within the diffusion-weighted images. For 156 regions of interest (ROI), we calculated the average fractional anisotropy (FA), mean diffusion (MD), and radial diffusion (RD). Each ROI underwent a group-wise comparison using permutation F-test, followed by post hoc pairwise comparisons with Bonferroni correction. In general, we observed lower FA in both schizophrenia groups compared to HC (i.e., HC>(DSZ=NDSZ)), while MD and RD showed the opposite pattern. Notably, specific ROIs with reduced FA in schizophrenia patients included bilateral nucleus accumbens, left fusiform area, brain stem, anterior corpus callosum, left rostral and caudal anterior cingulate, right posterior cingulate, left thalamus, left hippocampus, left inferior temporal cortex, right superior temporal cortex, left pars triangularis and right lingual gyrus. Significantly, the right cuneus exhibited lower FA in the DSZ group compared to other groups ((HC=NDSZ)>DSZ), without affecting MD and RD. These results indicate that compromised neural integrity in the cuneus may contribute to the pathophysiological distinctions between DSZ and NDSZ.

Different Heschl's Gyrus Duplication Patterns in Deficit and Non-deficit Subtypes of Schizophrenia.

Deficit syndrome schizophrenia is a characteristic subtype defined by persistent negative symptoms and poor functional outcomes; however, the biological mechanisms underlying this specific subtype have not yet been elucidated in detail. The present magnetic resonance imaging study examined the prevalence of duplicated Heschl’s gyrus (HG), a potential neurodevelopmental marker, in schizophrenia patients with (N = 38) and without (N = 37) the deficit syndrome. The prevalence of the HG duplication pattern bilaterally was higher in the whole schizophrenia group than in 59 matched healthy controls. Furthermore, the prevalence of right HG duplication was significantly higher in the deficit schizophrenia group than in the non-deficit schizophrenia group. The HG pattern in schizophrenia was not associated with clinical variables, including illness duration, medication, and symptom severity, while right HG duplication correlated with higher scores for Proxy for the Deficit Syndrome. The present results suggest that the prominent neurodevelopmental pathology associated with gyral formation of HG may contribute to enduring negative symptomatology in schizophrenia.

Increased serum levels of apoptosis in deficit syndrome schizophrenia patients: a preliminary study

BackgroundSchizophrenia is a chronic and debilitating disorder, the etiology of which remains unclear. Apoptosis is a programmed cell death mechanism that might be implicated in neuropsychiatric disorders, including schizophrenia. In this study, we aimed to compare the serum levels of apoptosis among deficit schizophrenia (DS) syndrome patients, nondeficit schizophrenia (NDS) patients, and healthy controls (HCs).Patients and methodsAfter the inclusion and exclusion criteria were applied, 23 DS patients, 46 NDS patients, and 33 HCs were included in the study. The serum apoptosis levels were measured using a quantitative sandwich enzyme immunoassay with human monoclonal antibodies directed against DNA and histones.ResultsThere was a significant difference among the three groups in terms of the levels of apoptosis (F2,96=16.58; P<0.001). The serum apoptosis levels in the DS and NDS groups were significantly higher than those in the HC group. Furthermore, the serum apoptosis levels in the DS group were significantly higher than the levels in the NDS group.ConclusionThis study suggests that increased levels of apoptosis may be implicated in the pathophysiology of DS syndrome. However, further studies are needed to support the role of apoptosis in DS.

Comparison of Serum Vitamin D Levels Between Patients with Deficit and Non-deficit Schizophrenia

Aim: Vitamin D deficiency has been proposed to play role in a series of psychiatric disorders including schizophrenia, however there have not been any knowledge regarding relationship between vitamin D deficiency and deficit syndrome schizophrenia (DS). In this study, we aimed to evaluate the relationship between vitamin D deficiency and deficit syndrome by comparing serum vitamin D levels of deficit schizophrenia patients and non-deficit schizophrenia (NDS) patients. Materials and methods: Sixty-six patients who had diagnosis of schizophrenia were included. Twenty-six patients comprised the DS group, while forty patients comprised the NDS group. The severity of illness was assessed with Scale of Assessment of Negative Symptoms (SANS), Scale of Assessment of Positive Symptoms (SAPS), and Brief Psychiatry Rating Scale (BPRS). Vitamin D concentrations of both groups were measured by an electro chemiluminescence method. Results: The groups were similar regarding age and gender ( t= 1.32; p=0.18 and χ2=0.35; p=0.36 , respectively). The mean SANS score and BPRS was higher in DS group compared to NDS group (t= -3.86; p

Neuroimaging predictors of functional outcomes in schizophrenia at baseline and 6-month follow-up

PurposeStudies show that deficit syndrome schizophrenia patients, characterized by primary negative symptoms and poor functional outcome, have impairment in specific neural circuits. We assessed whether these same neural circuits are directly linked to functional outcomes across schizophrenia patients. MethodsT1- and diffusion-weighted MR images were obtained for schizophrenia (n=30) and matched healthy control participants (n=30). Negative symptoms and functional outcome were assessed at baseline and 6-month follow-up. Cortical thickness and tract-wise fractional anisotropy (FA) were compared between groups. To assess relationships of neuroimaging measures with functional outcome, principal component analysis (PCA) was performed on tract-wise FA values and components were entered into a multiple regression model for schizophrenia participants. ResultsConsistent with the literature, schizophrenia participants showed frontotemporal reductions in cortical thickness and tract-wise FA compared to controls. The top two components from PCA explained 71% of the variance in tract-wise FA values. The second component (associated with inferior longitudinal and arcuate fasciculus FA) was significantly correlated with functional outcome (baseline: β=0.54, p=0.03; follow-up: β=0.74, p=0.047); further analysis revealed this effect was mediated by negative symptoms. Post-hoc network analysis revealed increased cortical coupling between right inferior frontal and supramarginal gyri (connected by the arcuate fasciculus) in schizophrenia participants with poorer functional outcome. ConclusionsOur findings indicate that impairment in the same neural circuitry susceptible in deficit syndrome schizophrenia predicts functional outcome in a continuous manner in schizophrenia participants. This relationship was mediated by negative symptom burden. Our findings provide novel evidence for brain-based biomarkers of longitudinal functional outcome in people with schizophrenia.

Neurological soft signs might be endophenotype candidates for patients with deficit syndrome schizophrenia.

BackgroundSchizophrenia is a chronic, disabling, disorder that affects approximately 1% of the population. The nature of schizophrenia is heterogeneous, and unsuccessful efforts to subtype this disorder have been made. Deficit syndrome schizophrenia (DS) is a clinical diagnosis that has not been placed in main diagnostic manuals. In this study, we aimed to investigate and compare neurological soft signs (NSS) in DS patients, non-deficit schizophrenia (NDS) patients, and healthy controls (HCs). We suggest that NSS might be an endophenotype candidate for DS patients.MethodsSixty-six patients with schizophrenia and 30 HCs were enrolled in accordance with our inclusion and exclusion criteria. The patients were sub-typed as DS (n=24) and NDS (n=42) according to the Schedule for the Deficit Syndrome. The three groups were compared in terms of sociodemographic and clinical variables and total scores and subscores on the Physical and Neurological Examination for Soft Signs (PANESS). Following the comparison, a regression analysis was performed for predictability of total PANESS score and its subscales in the diagnosis of DS and NDS.ResultsThe groups were similar in terms of age, sex, and smoking status. The results of our study indicated that the total PANESS score was significantly higher in the DS group compared to the NDS and HC groups, and all PANESS subscales were significantly higher in the DS group than in the HC group. The diagnosis of DS was predicted significantly by total PANESS score (P<0.001, odds ratio =9.48, 95% confidence interval: 0.00–4.56); the synergy, graphesthesia, stereognosis, motor tasks, and ability to maintain posture subscales were found to be significant predictors.ConclusionThis study confirms that NSS were higher in patients with DS. In addition, we suggest that our results might support the notion of DS as a different and distinct type of schizophrenia. NSS might also be a promising candidate as an endophenotype for DS. However, large sampled, multicentric studies are needed to clarify the place of NSS as an endophenotype in DS.

Deficit Syndrome Schizophrenia: A Review about Biological Evidences.

Especially because of the lack of clinical homogeneity within schizophrenia patients, opinions claiming that there should be subtypes of schizophrenia have been existing since Kraepelin. Nevertheless, diagnostic validity of schizophrenia subtypes in leading classification systems have been controversial. It can be asserted that the biological proofs are the most important references to strengthen the validity of a classification system. The concept of “deficit syndrome schizophrenia” was introduced to identify a relatively homogeneous group within the schizophrenia patients, in terms of clinical signs and symptoms. This concept can be considered as a promising candidate for the attempts to identify subtypes of schizophrenia. In this review, the history of “deficit syndrome schizophrenia”, its clinical aspects and its diagnostic validity will be addressed shortly and then results of the biological studies about deficit syndrome schizophrenia will be evaluated, and by this way some information about the biological validity of this classification system will be presented.

Plasma cortisol levels and illness appraisal in deficit syndrome schizophrenia

Research investigating the association between negative symptoms and plasma cortisol levels in individuals with schizophrenia has produced inconsistent findings. This study investigated whether deficit syndrome schizophrenia (characterized by high levels of primary negative symptoms) is associated with comparatively high morning plasma cortisol levels, more negative appraisals about illness and higher levels of depression. Participants were 85 individuals diagnosed with schizophrenia and 85 individuals with no history of contact with psychiatric services matched for age and gender. All participants provided fasting 9.00a.m. plasma cortisol samples. There were no significant differences between the schizophrenia and control participants in plasma cortisol levels. The Proximal Deficit Syndrome method was used to identify individuals with deficit syndrome schizophrenia. Contrary to what had been hypothesized, participants with deficit syndrome schizophrenia had significantly lower plasma cortisol levels than both non-deficit syndrome participants and control participants. Participants with the deficit syndrome reported significantly less negative appraisals about illness (assessed by PBIQ) and lower levels of depression (assessed by BDI-II). Differences in cortisol levels continued to trend toward significance when levels of depression were controlled for. The patterns of illness-related appraisals and plasma cortisol levels raise the possibility that the deficit syndrome could be a form of adaptation syndrome.

Using negative feedback to guide behavior: Impairments on the first 4 cards of the Wisconsin Card Sorting Test predict negative symptoms of schizophrenia

Research has demonstrated that individuals with schizophrenia fail to appropriately use negative feedback to guide learning. These learning deficits are thought to arise from abnormalities in midbrain dopamine activity. Primary and enduring negative symptoms are also associated with abnormal dopamine activity and are expected to produce more severe deficits in learning when they present in individuals with schizophrenia. The current study examines this matter by comparing individuals with deficit syndrome schizophrenia, which is characterized by primary and enduring negative symptoms, to individuals with nondeficit syndrome schizophrenia and to normal controls in their use of positive feedback and negative feedback to guide learning on the first four cards of the WCST. Participants included 67 individuals with schizophrenia (15 deficit; 52 nondeficit syndrome) and 51 healthy controls. Accuracy data from the first 4 cards of the WCST and measures of global test performance were examined. Individuals with schizophrenia were significantly less accurate than controls in their performance on early (pre-shift) WCST trials, and this impairment was significantly greater in patients with deficit than nondeficit schizophrenia. Additionally, accuracy across the first 4 WCST cards significantly predicted the number of categories completed and percentage of perseverative errors across the entire test. These findings suggest that negative symptoms of schizophrenia are associated with difficulty using negative feedback to adaptively guide behavior, and are consistent with the notion that abnormal DA signaling contributes to the higher-order executive functioning impairments seen in schizophrenia with severe negative symptoms.

Hippocampal Volume Reduction Correlates With Apathy in Traumatic Brain Injury, But Not Schizophrenia

Apathy commonly accompanies both traumatic brain injury (TBI) and deficit syndrome schizophrenia (DSZ), despite unclear neurological bases. The authors examined differences in cortical thickness and subcortical/cerebellar regional volumes between adult TBI survivors, patients with DSZ, and healthy-control subjects by use of 3-D magnetic resonance imaging (MRI), and correlated imaging findings with clinical ratings of apathy and selected cognitive test scores. Imaging findings revealed specific areas of volume reduction in TBI survivors and areas of cortical thinning among patients with DSZ. The severity of apathy symptoms was similar across patient groups; however, severity of apathy was only correlated with imaging findings in TBI survivors.

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.

The failure of the schizophrenia concept and the argument for its replacement by hebephrenia: applying the medical model for disease recognition

The failure of the schizophrenia concept and the argument for its replacement by hebephrenia: applying the medical model for disease recognition

Olfactory function and schizophrenia: an update

Olfaction is a field of growing interest in schizophrenia research. This article reviews recent studies on olfactory functions in schizophrenia. The current literature provides additional insights into olfactory deficits, abnormalities, and olfactory hedonic dysfunction in schizophrenia. Recent findings reinforce particular associations with negative symptoms and deficit syndrome schizophrenia. Studies indicate that abnormalities in patients with schizophrenia extend to more peripheral olfactory structures and functions, including olfactory receptor neuron dysfunction. Olfactory identification ability was found to relate to prodromal disorganization symptoms in young high-risk patients. Further support for the notion of a genetic contribution to olfactory dysfunction in schizophrenia derives from studies reporting physiological olfactory dysfunction (olfactory event-related potentials) in unaffected relatives, and an odor-specific hyposmia, present in both patients with schizophrenia and family members. Further research is needed to improve our understanding of olfactory dysfunction in schizophrenia. Recent encouraging findings underscore that the olfactory system is a field of research that holds promise for advancing our understanding of the pathophysiology of schizophrenia and possibly as a useful endophenotypic marker of neurodevelopmental vulnerability.

Impaired facial affect labeling and discrimination in patients with deficit syndrome schizophrenia

Social and affective disturbances have long been thought to be core to schizophrenia. Deficits in accurately identifying and discriminating facial displays of emotion may be central components of the functional and social abnormalities seen in schizophrenia; however, their relationship with negative symptoms is less clear. The current study examined facial affect labeling and discrimination performance in a sample of 15 patients meeting criteria for deficit syndrome schizophrenia, 26 schizophrenia patients who do not meet criteria for the deficit syndrome, and 22 healthy controls. Results indicated that deficit schizophrenia patients displayed significantly greater facial affect labeling and discrimination difficulties than non-deficit patients and controls, as well as poorer performance on a basic visuoperceptual face processing task, suggesting that problems with facial affect processing may be mediated by a more general impairment in visuoperceptual processing. However, within this more generalized pattern of impairment, deficit syndrome patients were uniquely characterized by processing positive faces less accurately than negative faces. These findings suggest that abnormalities in processing facial emotion are associated with the negative symptoms of schizophrenia, with a unique deficit in the processing of positive emotions that stand out in the broader context of generalized impairment.

Periods of Recovery in Deficit Syndrome Schizophrenia: A 20-Year Multi-follow-up Longitudinal Study

Periods of recovery were examined in patients with and without deficit syndrome schizophrenia. Fifty-six patients with schizophrenia were studied, 39 of whom were divided into deficit and nondeficit syndrome schizophrenia subtypes using a proxy method. We also studied 39 nonpsychotic depressive comparison patients. Patients were evaluated as part of the Chicago Follow-up Study, which prospectively examined patients at regular intervals over a 20-year period. Using standardized instruments, patients were evaluated for the deficit syndrome, global recovery, rehospitalization, social dysfunction, occupational disability, and symptom presentation. Recovery was examined at 6 time points measured at 2-, 4.5-, 7.5-, 10-, 15-, and 20-year postindex hospitalization. Cumulatively, over the 20-year period, 13% of patients classified as meeting criteria for the deficit syndrome showed 1 or more 1-year periods of global recovery, in comparison to 63% of nondeficit schizophrenia patients and 77% of depressed patient controls. Results indicate that the deficit syndrome represents a persistently impaired subsample of schizophrenia patients, with continuous social, occupational, and symptom impairment. In contrast, nondeficit syndrome schizophrenia patients showed at least some periods of remission or recovery, with the likelihood of these periods increasing as they became older. Findings provide further support for the validity of the deficit syndrome concept and suggest that deficit status is characterized by a more persistently impaired course of illness and particularly poor long-term prognosis.

Automatic affective processing impairments in patients with deficit syndrome schizophrenia

Affective impairments were examined in patients with and without deficit syndrome schizophrenia. Two Emotional Stroop tasks designed to measure automatic processing of emotional information were administered to deficit ( n = 15) and non-deficit syndrome ( n = 26) schizophrenia patients classified according to the Schedule for the Deficit Syndrome, and matched non-patient control subjects ( n = 22). In comparison to non-deficit patients and controls, deficit syndrome patients demonstrated a lack of attention bias for positive information, and an elevated attentional lingering effect for negative information. These findings suggest that positive information fails to automatically capture attention of deficit syndrome patients, and that when negative information captures attention, it produces difficulty in disengagement Attentional abnormalities were significantly correlated with negative symptoms, such that more severe symptoms were associated with less attention bias for positive emotion and a greater lingering effect for negative information. Results are generally consistent with a mood-congruent processing abnormality and suggest that impaired automatic processing may be core to diminished emotional experience symptoms exhibited in deficit syndrome patients.

P.3.a.002 Deficits in reward sensitivity and reversal learning in chronic schizophrenia during decision-making tasks

Research has demonstrated that individuals with schizophrenia fail to appropriately use negative feedback to guide learning. These learning deficits are thought to arise from abnormalities in midbrain dopamine activity. Primary and enduring negative symptoms are also associated with abnormal dopamine activity and are expected to produce more severe deficits in learning when they present in individuals with schizophrenia. The current study examines this matter by comparing individuals with deficit syndrome schizophrenia, which is characterized by primary and enduring negative symptoms, to individuals with nondeficit syndrome schizophrenia and to normal controls in their use of positive feedback and negative feedback to guide learning on the first four cards of the WCST. Participants included 67 individuals with schizophrenia (15 deficit; 52 nondeficit syndrome) and 51 healthy controls. Accuracy data from the first 4 cards of the WCST and measures of global test performance were examined. Individuals with schizophrenia were significantly less accurate than controls in their performance on early (pre-shift) WCST trials, and this impairment was significantly greater in patients with deficit than nondeficit schizophrenia. Additionally, accuracy across the first 4 WCST cards significantly predicted the number of categories completed and percentage of perseverative errors across the entire test. These findings suggest that negative symptoms of schizophrenia are associated with difficulty using negative feedback to adaptively guide behavior, and are consistent with the notion that abnormal DA signaling contributes to the higher-order executive functioning impairments seen in schizophrenia with severe negative symptoms.

A brief smell identification test discriminates between deficit and non-deficit schizophrenia

Evidence is accumulating that smell identification deficits (SID) and social dysfunction in schizophrenia may share a common pathophysiology. While most schizophrenia studies utilize the lengthy 40-item University of Pennsylvania Smell Identification Test (UPSIT) to assess smell identification ability, a brief 12-item smell identification test (B-SIT) has recently been constructed as a culturally neutral substitute for the UPSIT. By selecting the 12 items of the UPSIT from which the B-SIT was originally derived, we constructed a proxy for the B-SIT and compared the performance of 83 patients with schizophrenia to 69 normal subjects. We examined select properties of the B-SIT proxy in relation to the UPSIT to determine its efficacy for use in psychiatric populations. We considered the sensitivity of the B-SIT proxy and evaluated a cutoff score for identifying deficit syndrome schizophrenia (DS). The UPSIT and B-SIT proxy were significantly related in the patients ( n=83, r=0.85, P=0.01) and in comparison subjects ( n=69, r=0.83, P=0.01), and both measures similarly distinguished DS from non-deficit syndrome (non-DS) patients. The results of this study support the utility of the B-SIT for schizophrenia research and highlight the robustness of the relationship between SID and social dysfunction in schizophrenia.

Neurocognitive, social, and emotional dysfunction in deficit syndrome schizophrenia

The deficit syndrome is a promising distinction within schizophrenia that requires further validation. This study examined the replicability of differences in clinical symptoms, neurocognitive functioning, affect perception, and social functioning previously reported among deficit ( n=15) and nondeficit syndrome ( n=30) schizophrenia patients classified according to the Schedule for the Deficit Syndrome (SDS; Psychiatry Res. 30 (1989) 119) and nonpatient controls ( n=41). Additionally, participants completed self-report affective trait measures of positive affectivity, negative affectivity, and social anhedonia to examine the deficit syndrome concept of diminished emotional range. We were able to replicate symptom profiles and neurocognitive and social functioning impairments in deficit vs. nondeficit patients, but did not find more severe affect perception impairment in deficit vs. nondeficit patients as previously reported. Regarding range of subjectively experienced emotion, deficit patients reported lower trait positive affectivity and marginally higher social anhedonia than nondeficit patients and controls, but also reported elevations in negative affectivity that were similar to nondeficit patients as compared to controls. While replication of patterns of impairment across multiple domains of functioning supports the validity of the deficit syndrome, results also suggest that SDS-defined deficit patients may be characterized by a relative reduction in the tendency or ability to experience positive emotions, rather than a pervasive diminution in the range of emotional experience.

Odor identification, eye tracking and deficit syndrome schizophrenia

Background: Deficit syndrome (DS) schizophrenia patients have smooth pursuit eye movement (SPEM) dysfunction. We examined if they also had smell identification deficits, since social affiliation is related to olfaction in other mammals. Methods: Sixty-seven patients had DS assessments: 31 patients had SPEM and 50 had Smell Identification Test (SIT) assessments, and 14 patients had both measurements. Results: DS patients had worse SPEM and SIT performance than the non-DS patients. Areas under the receiver-operator characteristic (ROC) curves for SIT and SPEM were both fairly accurate in identifying the DS. The odds ratio (OR) for the DS for impaired versus normal SPEM was 6.21 (95% confidence interval [CI]: 1.21, 32.25) and for microsmia versus normosmia was 10.4 (95% CI: 1.23, 88.18). Further analyses showed that the association of SIT with both SPEM and the DS could account for the SPEM-DS association. Conclusions: We found a strong association between the DS and SIT scores suggesting that the neural substrates of olfaction may be related to social affiliation in humans, as they are in other mammals. These data further support the notion that the DS defines a homogeneous subgroup of schizophrenia patients and further suggest that dysfunction in the neural circuitry of olfaction may contribute to its pathophysiology.