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Poor insight in schizophrenia: neurocognitive basis.  [cached]
Lele M,Joglekar A
Journal of Postgraduate Medicine , 1998,
Abstract: Poor insight in schizophrenia has been recently thought to be a reflection of prominent and enduring neurocognitive impairments. Reports supporting this theory have implicated prefrontal and parietal lobe functions, among other parameters. The results of other studies have negated the role of neuropsychological abnormalities in poor insight. The analogy between poor insight in schizophrenia and anosognosia in neurological illness as proposed by one set of workers has been elucidated in this review and it appears quite promising. However, the drawing of definite conclusions from all this work has been deferred by us, because of the need for more uniform and standardized methodologies for research on the subject. Nevertheless, attempts to improve the cognitive processes, which affect insight in schizophrenia, may be done to gain better treatment outcome in this disorder.
Monitoring the Mind: The Neurocognitive Correlates of Metamemory  [PDF]
Anne T. A. Do Lam, Nikolai Axmacher, Juergen Fell, Bernhard P. Staresina, Siegfried Gauggel, Tobias Wagner, Jan Olligs, Susanne Weis
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0030009
Abstract: Memory performance in everyday life is often far from perfect and therefore needs to be monitored and controlled by metamemory evaluations, such as judgments of learning (JOLs). JOLs support monitoring for goal-directed modification of learning. Behavioral studies suggested retrieval processes as providing a basis for JOLs. Previous functional imaging research on JOLs found a dissociation between processes underlying memory prediction, located in the medial prefrontal cortex (mPFC), and actual encoding success, located in the medial temporal lobe. However, JOL-specific neural correlates could not be identified unequivocally, since JOLs were given simultaneously with encoding. Here, we aimed to identify the neurocognitive basis of JOLs, i.e., the cognitive processes and neural correlates of JOL, separate from initial encoding. Using functional magnetic resonance imaging (fMRI), we implemented a face-name paired associative design. In general, we found that actual memory success was associated with increased brain activation of the hippocampi bilaterally, whereas predicted memory success was accompanied by increased activation in mPFC, orbital frontal and anterior cingulate cortices. Masking brain activation during predicted memory success with activation during retrieval success revealed BOLD increases of the mPFC. Our findings indicate that JOLs actually incorporate retrieval processes.
Characterization of Neurophysiologic and Neurocognitive Biomarkers for Use in Genomic and Clinical Outcome Studies of Schizophrenia  [PDF]
Gregory A. Light, Neal R. Swerdlow, Anthony J. Rissling, Allen Radant, Catherine A. Sugar, Joyce Sprock, Marlena Pela, Mark A. Geyer, David L. Braff
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0039434
Abstract: Background Endophenotypes are quantitative, laboratory-based measures representing intermediate links in the pathways between genetic variation and the clinical expression of a disorder. Ideal endophenotypes exhibit deficits in patients, are stable over time and across shifts in psychopathology, and are suitable for repeat testing. Unfortunately, many leading candidate endophenotypes in schizophrenia have not been fully characterized simultaneously in large cohorts of patients and controls across these properties. The objectives of this study were to characterize the extent to which widely-used neurophysiological and neurocognitive endophenotypes are: 1) associated with schizophrenia, 2) stable over time, independent of state-related changes, and 3) free of potential practice/maturation or differential attrition effects in schizophrenia patients (SZ) and nonpsychiatric comparison subjects (NCS). Stability of clinical and functional measures was also assessed. Methods Participants (SZ n = 341; NCS n = 205) completed a battery of neurophysiological (MMN, P3a, P50 and N100 indices, PPI, startle habituation, antisaccade), neurocognitive (WRAT-3 Reading, LNS-forward, LNS-reorder, WCST-64, CVLT-II). In addition, patients were rated on clinical symptom severity as well as functional capacity and status measures (GAF, UPSA, SOF). 223 subjects (SZ n = 163; NCS n = 58) returned for retesting after 1 year. Results Most neurophysiological and neurocognitive measures exhibited medium-to-large deficits in schizophrenia, moderate-to-substantial stability across the retest interval, and were independent of fluctuations in clinical status. Clinical symptoms and functional measures also exhibited substantial stability. A Longitudinal Endophenotype Ranking System (LERS) was created to rank neurophysiological and neurocognitive biomarkers according to their effect sizes across endophenotype criteria. Conclusions The majority of neurophysiological and neurocognitive measures exhibited deficits in patients, stability over a 1-year interval and did not demonstrate practice or time effects supporting their use as endophenotypes in neural substrate and genomic studies. These measures hold promise for informing the “gene-to-phene gap” in schizophrenia research.
Neurocognitive Correlates of Apathy and Anxiety in Parkinson's Disease  [PDF]
Yelena Bogdanova,Alice Cronin-Golomb
Parkinson's Disease , 2012, DOI: 10.1155/2012/793076
Abstract: Parkinson's disease (PD) is associated with various nonmotor symptoms including neuropsychiatric and cognitive dysfunction. We examined the relation between apathy, anxiety, side of onset of motor symptoms, and cognition in PD. We hypothesized that PD patients would show different neuropsychiatric and neurocognitive profiles depending on the side of onset. 22 nondemented PD patients (11 right-side onset (RPD) with predominant left-hemisphere pathology, and 11 LPD) and 22 matched healthy controls (NC) were administered rating scales assessing apathy and anxiety, and a series of neuropsychological tests. PD patients showed a higher anxiety level than NC. There was a significant association between apathy, anxiety, and disease duration. In LPD, apathy but not anxiety was associated with performance on nonverbally mediated executive function and visuospatial measures, whereas, in RPD, anxiety but not apathy correlated with performance on verbally mediated tasks. Our findings demonstrated a differential association of apathy and anxiety to cognition in PD. 1. Introduction Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the loss of nigrostriatal and mesocortical dopaminergic projections from the brain stem and limbic cortex to the basal ganglia and neocortex. The basal ganglia and related structures are critical structures in parallel frontal subcortical circuits involved in regulation of cognition, emotions, and behavioral activation [1–3]. While primarily characterized as a movement disorder, PD is associated with various nonmotor symptoms [4–6], including cognitive dysfunction [7–10] and neuropsychiatric symptoms, such as apathy [11–17] and anxiety [18–20]. Recent neuroimaging and neuropsychological findings raise the question of the role of apathy and anxiety in PD-related cognitive dysfunction, as these neuropsychiatric conditions reflect dysfunction in brain areas involved in PD. Typically, early motor signs of PD start on one side of the body, and side of onset remains a significant clinical and neuropathological factor in both clinical management and the study of PD. PD patients with symptoms starting on the right side of the body (RPD) have greater inferred left hemisphere pathology and those with left-side onset (LPD) have greater inferred right hemisphere pathology [21]. The motor symptoms of PD are associated with asymmetrical depletion of dopamine in the substantia nigra of the midbrain across the range of disease severity. These changes in the substantia nigra lead to asymmetrical dysregulation of the
Neurodevelopmental correlates in schizophrenia  [PDF]
Ivkovi? Maja,Damjanovi? Aleksandar,Paunovi? Vladimir R.
Srpski Arhiv za Celokupno Lekarstvo , 2003, DOI: 10.2298/sarh0308294i
Abstract: Contemporary aetiopathogenetic considerations, based on neuro-imaging genetic and developmental neurobiology studies, suggest neurodevelopmental origin of schizophrenia. Several lines of evidence including structural abnormalities on in vivo brain imaging, the excess of prenatal and obstetric complications and the association of congenital and minor physical anomalies with schizophrenia, strongly indicate the neurodevelopmental pathogenesis of schizophrenia. On the other hand, controversial concept of psychotic continuum suggests schizophrenia and depression sharing the same genetic contribution to the pathogenesis. If this would be the case, depression could also be considered as neuro developmental disorder. The aims of the study were to investigate the association between: a) pregnancy and birth complications (PBC), and b) minor physical anomalies (MPA) and schizophrenia or depression. Experimental groups consisted of 60 schizophrenic, 28 major depression patients and 30 healthy controls. All patients were diagnosed according to DSM-IV. Schizophrenic group was divided with regard to PANSS score into positive (n=32) and negative form (n=28) subgroups. PBC information were gathered from maternal recall while MPA were examined by using Waldrop scale for adults. The results showed that negative and positive schizophrenic subgroups had significantly more PBC than depressive group (p<0,05), as well than controls (p<0,001; p<0,05; respectively). There was no significant trend for more PBC in negative than in positive subgroup. All schizophrenic patients had higher rates of MPA than depressives (p<0,05). This trend for more MPA was not significant in comparison with healthy controls. These findings suggest that schizophrenia, especially its negative forms, could be considered as a member of the spectrum of neuro developmental disorders, which does not seem to be the case with depression. PBC and MPA could also be valuable in evaluation of risks for schizophrenia and possible predictive indicators of its development.
Study of Neurocognitive correlates of Schizotypy Personality Clusters in healthy individuals
Aguilera Ruíz,M. Carmen; Barrantes-Vidal,Neus; Guitart,Marc; Fa?anás,Lourdes;
The European Journal of Psychiatry , 2008, DOI: 10.4321/S0213-61632008000100003
Abstract: background and objectives: inconsistencies in the relationship between schizotypy dimensions and neurocognitive functions found in correlational studies may be clarified with the use of alternative methodological approaches. the aim of this study was to examine the existence of different profiles of schizotypal traits and their neurocognitive correlates in non-clinical subjects by means of cluster analysis. methods: we examined seventy six healthy adults from the general population with a comprehensive neurocognitive battery and a schizotypal personality self-report. results: four neurocognitive factors were extracted: visuospatial, semantic evocation, verbal memory, and set-shifting. a three cluster model yielded the following clusters: "lowschizotypy", "positive schizotypy", and "negative/disorganized schizotypy". the positive and negative/disorganized schizotypy clusters showed poorer performance on semantic evocation compared with the low schizotypy cluster. conclusions: we found different patterns of specific schizotypy features in a healthy adult community sample and these clusters presented differential performance in relation with the ability to evoke semantic information.
Study of Neurocognitive correlates of Schizotypy Personality Clusters in healthy individuals  [cached]
M. Carmen Aguilera Ruíz,Neus Barrantes-Vidal,Marc Guitart,Lourdes Fa?anás
The European Journal of Psychiatry , 2008,
Abstract: Background and Objectives: Inconsistencies in the relationship between schizotypy dimensions and neurocognitive functions found in correlational studies may be clarified with the use of alternative methodological approaches. The aim of this study was to examine the existence of different profiles of schizotypal traits and their neurocognitIve correlates in non-clinical subjects by means of cluster analysis. Methods: We examined seventy six healthy adults from the general population with a comprehensive neurocognitive battery and a schizotypal personality self-report. Results: Four neurocognitive factors were extracted: visuospatial, semantic evocation, verbal memory, and set-shifting. A three cluster model yielded the following clusters: "lowschizotypy", "positive schizotypy", and "negative/disorganized schizotypy". The positive and negative/disorganized schizotypy clusters showed poorer performance on semantic evocation compared with the low schizotypy cluster. Conclusions: We found different patterns of specific schizotypy features in a healthy adult community sample and these clusters presented differential performance in relation with the ability to evoke semantic information.
A Genetic Deconstruction of Neurocognitive Traits in Schizophrenia and Bipolar Disorder  [PDF]
Carla P. D. Fernandes, Andrea Christoforou, Sudheer Giddaluru, Kari M. Ersland, Srdjan Djurovic, Manuel Mattheisen, Astri J. Lundervold, Ivar Reinvang, Markus M. N?then, Marcella Rietschel, Roel A. Ophoff, Genetic Risk and Outcome of Psychosis (GROUP) , Albert Hofman, André G. Uitterlinden, Thomas Werge, Sven Cichon, Thomas Espeseth, Ole A. Andreassen, Vidar M. Steen, Stephanie Le Hellard
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0081052
Abstract: Background Impairments in cognitive functions are common in patients suffering from psychiatric disorders, such as schizophrenia and bipolar disorder. Cognitive traits have been proposed as useful for understanding the biological and genetic mechanisms implicated in cognitive function in healthy individuals and in the dysfunction observed in psychiatric disorders. Methods Sets of genes associated with a range of cognitive functions often impaired in schizophrenia and bipolar disorder were generated from a genome-wide association study (GWAS) on a sample comprising 670 healthy Norwegian adults who were phenotyped for a broad battery of cognitive tests. These gene sets were then tested for enrichment of association in GWASs of schizophrenia and bipolar disorder. The GWAS data was derived from three independent single-centre schizophrenia samples, three independent single-centre bipolar disorder samples, and the multi-centre schizophrenia and bipolar disorder samples from the Psychiatric Genomics Consortium. Results The strongest enrichments were observed for visuospatial attention and verbal abilities sets in bipolar disorder. Delayed verbal memory was also enriched in one sample of bipolar disorder. For schizophrenia, the strongest evidence of enrichment was observed for the sets of genes associated with performance in a colour-word interference test and for sets associated with memory learning slope. Conclusions Our results are consistent with the increasing evidence that cognitive functions share genetic factors with schizophrenia and bipolar disorder. Our data provides evidence that genetic studies using polygenic and pleiotropic models can be used to link specific cognitive functions with psychiatric disorders.
Anger under Control: Neural Correlates of Frustration as a Function of Trait Aggression  [PDF]
Christina M. Pawliczek, Birgit Derntl, Thilo Kellermann, Ruben C. Gur, Frank Schneider, Ute Habel
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0078503
Abstract: Antisocial behavior and aggression are prominent symptoms in several psychiatric disorders including antisocial personality disorder. An established precursor to aggression is a frustrating event, which can elicit anger or exasperation, thereby prompting aggressive responses. While some studies have investigated the neural correlates of frustration and aggression, examination of their relation to trait aggression in healthy populations are rare. Based on a screening of 550 males, we formed two extreme groups, one including individuals reporting high (n=21) and one reporting low (n=18) trait aggression. Using functional magnetic resonance imaging (fMRI) at 3T, all participants were put through a frustration task comprising unsolvable anagrams of German nouns. Despite similar behavioral performance, males with high trait aggression reported higher ratings of negative affect and anger after the frustration task. Moreover, they showed relatively decreased activation in the frontal brain regions and the dorsal anterior cingulate cortex (dACC) as well as relatively less amygdala activation in response to frustration. Our findings indicate distinct frontal and limbic processing mechanisms following frustration modulated by trait aggression. In response to a frustrating event, HA individuals show some of the personality characteristics and neural processing patterns observed in abnormally aggressive populations. Highlighting the impact of aggressive traits on the behavioral and neural responses to frustration in non-psychiatric extreme groups can facilitate further characterization of neural dysfunctions underlying psychiatric disorders that involve abnormal frustration processing and aggression.
A Genome-Wide Linkage Scan for Distinct Subsets of Schizophrenia Characterized by Age at Onset and Neurocognitive Deficits  [PDF]
Yin-Ju Lien, Po-Chang Hsiao, Chih-Min Liu, Stephen V. Faraone, Ming T. Tsuang, Hai-Gwo Hwu, Wei J. Chen
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0024103
Abstract: Background As schizophrenia is genetically and phenotypically heterogeneous, targeting genetically informative phenotypes may help identify greater linkage signals. The aim of the study is to evaluate the genetic linkage evidence for schizophrenia in subsets of families with earlier age at onset or greater neurocognitive deficits. Methods Patients with schizophrenia (n = 1,207) and their first-degree relatives (n = 1,035) from 557 families with schizophrenia were recruited from six data collection field research centers throughout Taiwan. Subjects completed a face-to-face semi-structured interview, the Continuous Performance Test (CPT), the Wisconsin Card Sorting Test, and were genotyped with 386 microsatellite markers across the genome. Results A maximum nonparametric logarithm of odds (LOD) score of 4.17 at 2q22.1 was found in 295 families ranked by increasing age at onset, which had significant increases in the maximum LOD score compared with those obtained in initial linkage analyses using all available families. Based on this subset, a further subsetting by false alarm rate on the undegraded and degraded CPT obtained further increase in the nested subset-based LOD on 2q22.1, with a score of 7.36 in 228 families and 7.71 in 243 families, respectively. Conclusion We found possible evidence of linkage on chromosome 2q22.1 in families of schizophrenia patients with more CPT false alarm rates nested within the families with younger age at onset. These results highlight the importance of incorporating genetically informative phenotypes in unraveling the complex genetics of schizophrenia.
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