Neurocognitive Deficits In Patients Research Articles

Neurocognitive performance and cognitive biases in young adults with schizotypal traits

Recent research suggests that neurocognitive deficits in patients with schizophrenia may increase the risk of developing cognitive biases. As such, we set out to determine this predictive relationship as it pertains to the development of a first-episode psychosis. We hypothesized that poorer performance in processing speed would be associated with jumping to conclusions and an externalizing bias. Poorer performance in working memory would be associated with belief inflexibility and jumping to conclusions, and poorer performance in attention would be associated with attention to threat. We hypothesized that all cognitive biases would be associated with subsyndromal positive symptoms, and schizotypal traits would moderate these relationships. Undergraduate students (N = 130) completed the Schizotypal Personality Questionnaire, DAVOS Assessment of Cognitive Biases, Community Assessment of Psychic Experiences, and a computerized neuropsychological assessment battery. Processing speed had a small effect on externalizing bias, which in turn affected subsyndromal positive symptoms. There was no moderating effect of schizotypal traits on externalizing bias, but it was significantly associated with subsyndromal positive symptoms. Only the externalizing bias was associated with subsyndromal positive symptomatology, which might be explained by a restricted range and reduced variance in performance as a result of using a university student sample. This is one of few studies that sought to explain the mechanism responsible for the development of subsyndromal positive symptoms in a healthy sample using self-report measures.

Characterization of neurocognitive deficits in patients with post-COVID-19 syndrome: persistence, patients' complaints, and clinical predictors.

Cognitive symptoms persisting beyond 3 months following COVID-19 present a considerable disease burden. We aimed to establish a domain-specific cognitive profile of post-COVID-19 syndrome (PCS). We examined the deficits' persistence, relationships with subjective cognitive complaints, and clinical variables, to identify the most relevant cognitive deficits and their predictors. This cross-sectional study examined cognitive performance and patient-reported and clinical predictors of cognitive deficits in PCS patients (n = 282) and socio-demographically comparable healthy controls (n = 52). On the Oxford Cognitive Screen-Plus, the patient group scored significantly lower in delayed verbal memory, attention, and executive functioning than the healthy group. In each affected domain, 10 to 20% of patients performed more than 1.5 SD below the control mean. Delayed memory was particularly affected, with a small effect of hospitalization and age. Attention scores were predicted by hospitalization and fatigue. Thus, PCS is associated with long-term cognitive dysfunction, particularly in delayed memory, attention, and executive functioning. Memory deficits seem to be of particular relevance to patients' experience of subjective impairment. Hospitalization, fatigue, and age seem to predict cognitive deficits, while time since infection, depression, and pre-existing conditions do not.

ID: 209374 Temporal Lobe Epilepsy Patients Demonstrate Altered Age-Related Segregation Patterns in Brainstem Arousal Networks

Recurrent consciousness-impairing seizures are associated with widespread brain network changes and disabling neurocognitive deficits in patients with temporal lobe epilepsy (TLE) (Englot et al, 2020). We have shown altered functional connectivity in the brainstem ascending reticular acting system (ARAS) found in TLE patients (Englot et al, 2017) that may correlate with impairments in cognitive testing and may improve after surgical treatment (González et al, 2020). Studies of the ARAS network in control subjects have shown a significant age-related decrease in a within-network connectivity metric called segregation. Furthermore, patients with TLE have been shown to have clinical and radiological accelerated age-related changes. Thus, we sought to investigate any possible age-related ARAS network changes in TLE. Understanding how the ARAS is impacted may offer insight into how neurostimulation may improve its network dynamics.

Immune checkpoint inhibitor induced neurocognitive deficits in patients.

This scientific commentary refers to 'Neurological outcomes in immune checkpoint inhibitor-related neurotoxicity', by Farina et al. (https://doi.org/10.1093/braincomms/fcad169).

Music and neuro-cognitive deficits in depression.

BackgroundCognitive deficits are one of the core features of major depressive disorder (MDD) that play crucial role in functional recovery. Studies have explored cognitive deficits in MDD, however, given inconsistent results, especially in mild-moderate MDD. Recently, studies have explored music as cognitive ability in various clinical conditions. In MDD, large focus has been on evaluating emotion deficits and just a handful on music cognition. With growing evidence on use of music based intervention to target cognitive deficits, it is imperative to explore nature of music cognitive ability in MDD.AimTo examine musical and neuro-cognitive deficits in patients with mild-moderate MDD.MethodsPatients diagnosed with mild or moderate MDD (n = 19) and matched healthy controls (HC) (n = 18) were evaluated on selected tests from NIMHANS Neuropsychological test battery and Montreal battery for evaluation of amusia (MBEA).ResultsMDD group performed significantly lower than HC on working memory (p = 0.007), verbal learning (p = 0.02) and retention (p = 0.03). Three indices were computed for a comprehensive evaluation. Groups did not differ significantly in any of the indices- focused attention, executive function, learning and memory as well as on music cognition. Focused attention and memory index predicted music cognition in HC and the combined group (MDD + HC) (p < 0.01). Attention alone contributed to 62.1% of variance in music cognition. Similarly, music cognition significantly predicted focused attention (p < 0.01).ConclusionIndividuals with mild-moderate MDD show significant deficits in working memory, verbal learning and memory, however, not in music cognition. There exists a significant relationship between music cognition and attention, which could be implicated in use of music interventions to ameliorate cognitive deficits. Limitations of study include small sample size and heterogeneity. Future studies on larger cohort examining musical emotion perception and neurocognition is imperative to have deeper understanding of this debilitating condition.

Vitamin D Protects against Traumatic Brain Injury via Modulating TLR4/MyD88/NF-κB Pathway-Mediated Microglial Polarization and Neuroinflammation.

Vitamin D (VD) deficiency is associated with neuroinflammation and neurocognitive deficits in patients with traumatic brain injury (TBI). The present study was aimed at investigating the therapeutic effects of VD and the molecular mechanisms after TBI. After the intraperitoneal injection of VD (1 μg/kg), sensorimotor and cognitive function was assessed via a series of behavioral tests in TBI rats. Traumatic outcomes were investigated by brain edema, blood-brain barrier (BBB) disruption, and morphologic staining. In vitro, cellular viability and cytotoxicity in primary hippocampal neurons were detected via the MTT method and LDH release. Hippocampal oxidative stress-related enzymes and proinflammatory mediators and the serum concentration of VD were analyzed by ELISA. The expression of VDR, TLR4, MyD88, and NF-κB p65 was measured by Western blot. Furthermore, the levels of M1/M2 microglial markers were quantified using real-time PCR and Western blot. VD treatment significantly increased the serum level of VD and the hippocampal expression of VDR. VD not only effectively alleviated neurocognitive deficits, brain edema, and BBB disruption but also promoted hippocampal neuronal survival in vivo and in vitro. Moreover, VD therapy prevented excessive neuroinflammation and oxidative stress caused by TBI. Mechanically, the hippocampal expression of TLR4, MyD88, and nuclear NF-κB p65 was elevated in the TBI group but robustly restrained by VD treatment. Taken together, VD provides an important neuroprotection through modulating hippocampal microglial M2 polarization and neuroinflammation via the TLR4/MyD88/NF-κB pathway.

Altered white matter microstructure and neurocognitive function of HIV-infected patients with low nadir CD4.

Altered white matter microstructure has been reported repeatedly using diffusion tensor imaging (DTI) in HIV-associated neurocognitive disorders. However, the associations between neurocognitive deficits and impaired white matter remains obscure due to frequent physical and psychiatric comorbidities in the patients. Severe immune suppression, reflected by low nadir CD4 T-cell counts, is reported to be associated with the neurocognitive deficits in the patients. In the present study, we examined white matter integrity using DTI and tract-based spatial statistics (TBSS), and neurocognitive functions using a battery of tests, in 15 HIV-infected patients with low nadir CD4, 16 HIV-infected patients with high nadir CD4, and 33 age- and sex-matched healthy controls. As DTI measures, we analyzed fractional anisotropy (FA) and mean diffusivity (MD). In addition, we investigated the correlation between white matter impairments and neurocognitive deficits. Among the three participant groups, the patients with low nadir CD4 showed significantly lower performance in processing speed and motor skills, and had significantly increased MD in widespread regions of white matter in both hemispheres. In the patients with low nadir CD4, there was a significant negative correlation between motor skills and MD in the right motor tracts, as well as in the corpus callosum. In summary, this study may provide white matter correlates of neurocognitive deficits in HIV-infected patients with past severe immune suppression as legacy effects.

Tumor-related molecular determinants of neurocognitive deficits in patients with diffuse glioma.

Cognitive impairment is a common and debilitating symptom in patients with diffuse glioma, and is the result of multiple factors. We hypothesized that molecular tumor characteristics influence neurocognitive functioning (NCF), and aimed to identify tumor-related markers of NCF in diffuse glioma patients. We examined the relation between cognitive performance (executive function, memory, and psychomotor speed) and intratumoral expression levels of molecular markers in treatment-naive patients with diffuse glioma. We performed a single-center study in a consecutive cohort, through a two-step design: (1) hypothesis-free differential expression and gene set enrichment analysis to identify candidate oncogenetic markers for cognitive impairment. Nineteen molecular markers of interest were derived from this set of genes, as well as from prior knowledge; (2) correlation of cognitive performance to intratumoral expression levels of these nineteen molecular markers, measured with immunohistochemistry. From 708 included patients with immunohistochemical data, we performed an in-depth analysis of neuropsychological data in 197, and differential expression analysis in 65 patients. After correcting for tumor volume and location, we found significant associations between expression levels of CD3 and IDH-1 and psychomotor speed; between IDH-1, ATRX, NLGN3, BDNF, CK2Beta, EAAT1, GAT-3, SRF, and memory performance; and between IDH-1, P-STAT5b, NLGN3, CK2Beta, and executive functioning. P-STAT5b, CD163, CD3, and Semaphorin-3A were independently associated after further correction for histopathological grade. Molecular characteristics of glioma can be independent determinants of patients' cognitive functioning. This suggests that besides tumor volume, location, and histological grade, variations in glioma biology influence cognitive performance through mechanisms that include perturbation of neuronal communication. These results pave the way towards targeted cognition improving therapies in neuro-oncology.

Prof K C Dube Poster Award

BACKGROUNDRecent studies have shown altered N-Acetyl Aspartate (NAA) levels in the anterior cingulate cortex (ACC). Magnetic Resonance Spectroscopy (MRS) is a non-invasive method to examine the brain metabolites. In adult patients, most of the studies reported abnormalities in terms of decreased NAA levels in the ACC. Schizophrenia patients also show impaired performance on neurocognitive measures. These impairments are also seen in first episode patients.AIMS and OBJECTIVESThe purpose of the current study was to investigate the levels of NAA in the ACC along with neurocognitive deficits in patients of first episode schizophrenia, and if 6 weeks of usual treatment was able to produce any changes in the same.METHODOLOGY20 drug free or drug naïve patients of first episode schizophrenia and 10 healthy controls were taken. Single-voxel 1H-MRS was performed using the PRESS sequence with number of scans (NS) of 160, TR of 1500 ms and TE of 80 ms. Neurocognitive test was performed using Wisconsin Card Sorting test (WCST) and Montreal Cognitive Assessment (MoCA). Tests were repeated after 6 weeks of treatment. Statistical analysis was performed by SPSS 25.RESULTSThe peak height of NAA in the ACC and performance of the patients on the WCST and MoCA showed significant difference compared to healthy controls at baseline. The peak height of NAA in the ACC showed significant improvement after 6 weeks of treatment. Correlation studies showed significant positive correlation between MoCA total score and NAA height at baseline.DISCUSSION and CONCLUSIONThe study findings provide evidence in support of cognitive dysfunction in first episode schizophrenia, which is associated with neuronal loss, as evidenced by lower NAA peaks in the ACC in patients. The improvement in the metabolite levels after 6 weeks of antipsychotic treatment demonstrates neuroplastic effects of drug therapy.

Transdiagnostic neurocognitive deficits in patients with type 2 diabetes mellitus, major depressive disorder, bipolar disorder, and schizophrenia: A 1-year follow-up study

BackgroundNeurocognition impairments are critical factors in patients with major depressive disorder (MDD), bipolar disorder (BD), and schizophrenia (SZ), and also in those with somatic diseases such as type 2 diabetes mellitus (T2DM). Intriguingly, these severe mental illnesses are associated with an increased co-occurrence of diabetes (direct comorbidity). This study sought to investigate the neurocognition and social functioning across T2DM, MDD, BD, and SZ using a transdiagnostic and longitudinal approach. MethodsA total of 165 participants, including 30 with SZ, 42 with BD, 35 with MDD, 30 with T2DM, and 28 healthy controls (HC), were assessed twice at a 1-year interval using a comprehensive, integrated test battery on neuropsychological and social functioning. ResultsCommon neurocognitive impairments in somatic and psychiatric disorders were identified, including deficits in short-term memory and cognitive reserve (p < 0.01, η²p=0.08–0.31). Social functioning impairments were observed in almost all the disorders (p < 0.0001; η²p=0.29–0.49). Transdiagnostic deficits remained stable across the 1-year follow-up (p < 0.001; η²p=0.13–0.43) and could accurately differentiate individuals with somatic and psychiatric disorders (χ² = 48.0, p < 0.0001). LimitationsThe initial sample size was small, and high experimental mortality was observed after follow-up for one year. ConclusionsThis longitudinal study provides evidence of some possible overlap in neurocognition deficits across somatic and psychiatric diagnostic categories, such as T2DM, MDD, BD, and SZ, which have high comorbidity. This overlap may be a result of shared genetic and environmental etiological factors. The findings open promising avenues for research on transdiagnostic phenotypes of neurocognition in these disorders, in addition to their biological bases.

Impaired test performance yet spared neurocognitive functioning in individuals with obsessive-compulsive disorder: the role of performance mediators

ABSTRACT Introduction Although most studies report neurocognitive deficits in patients with obsessive-compulsive disorder (OCD), important exceptions exist, highlighting the possible role of mediators (e.g., poor motivation). This study investigated neurocognitive functioning and potential influences affecting performance in OCD. Methods Forty-three participants (13 OCD patients, 30 healthy controls) were assessed using a battery of neurocognitive tests. During the assessment, the examiner completed the Impact on Performance Scale (IPS) which measures variables that may impact neurocognitive performance. Results Pooled neurocognitive performance was lower in OCD patients versus healthy controls at a moderate effect size. Patients performed more poorly on the IPS, particularly the Well-Being During Assessment subscale. Performance differences across the two groups were attenuated to a non-significant small-to-medium effect when the IPS was entered as a covariate. A total of 34% of patients showed scores greater than one standard deviation below the mean compared to 9.63% in healthy individuals. Yet, when a conservative impairment criterion (≥2 standard deviations below the mean) was applied, less than 10% of patients displayed deficits. Conclusions Neurocognitive impairment in OCD is likely exaggerated. In addition to considering important mediators researchers should report the percentage of participants displaying performance deficits rather than mean group differences alone; the latter obscures the high percentage of patients without impairment and thus may unduly foster stigma in this population.

Neurocognitive deficits in patients suffering from glioma in speech-relevant areas of the left hemisphere

ObjectivePatients with brain tumors frequently present neurocognitive deficits. Aiming at better understanding the impact of tumor localization on neurocognitive processes, we evaluated neurocognitive function prior to glioma surgery within one of four specific regions in the left speech-dominant hemisphere. MethodsBetween 04/2011 and 12/2019, 43 patients undergoing neurocognitive evaluation prior to awake surgery for gliomas (WHO grade I: 2; II: 6; III: 23; IV: 11) in the inferior frontal gyrus (IFG; n = 20), the anterior temporal lobe (ATL; n = 6), the posterior superior temporal region/supramarginal gyrus (pST/SMG; n = 7) or the posterior middle temporal gyrus (pMTG; n = 10) of the language dominant left hemisphere were prospectively included in the study. Cognitive performances were analyzed regarding an influence of patient characteristics and tumor localization. ResultsSevere impairment in at least one neurocognitive domain was found in 36 (83.7%) patients. Anxiety and depression were observed most frequently, followed by verbal memory impairments. Verbal memory was more strongly affected in patients with ATL or pST/SMG tumors compared to IFG tumors (p = 0.004 and p = 0.013, resp.). Overall, patients suffering from tumors in the ATL were most frequently and severely impaired. ConclusionPatients suffering from gliomas involving different regions within the language dominant hemisphere frequently present impairments in neurocognitive domains also other than language. Considering individual functions at risk may help in better advising patients prior to treatment and in tailoring the individual therapeutic strategy to preserve patients' quality of life.

Ketamine Alters Functional Gamma and Theta Resting-State Connectivity in Healthy Humans: Implications for Schizophrenia Treatment Targeting the Glutamate System.

Disturbed functional connectivity is assumed to cause neurocognitive deficits in patients suffering from schizophrenia. A Glutamate N-methyl-D-aspartate receptor (NMDAR) dysfunction has been suggested as a possible mechanism underlying altered connectivity in schizophrenia, especially in the gamma- and theta-frequency range. The present study aimed to investigate the effects of the NMDAR-antagonist ketamine on resting-state power, functional connectivity, and schizophrenia-like psychopathological changes in healthy volunteers. In a placebo-controlled crossover design, 25 healthy subjects were recorded using resting-state 64-channel-electroencephalography (EEG) (eyes closed). The imaginary coherence-based Multivariate Interaction Measure (MIM) was used to measure gamma and theta connectivity across 80 cortical regions. The network-based statistic was applied to identify involved networks under ketamine. Psychopathology was assessed with the Positive and Negative Syndrome Scale (PANSS) and the 5-Dimensional Altered States of Consciousness Rating Scale (5D-ASC). Ketamine caused an increase in all PANSS (p < 0.001) as well as 5D-ASC scores (p < 0.01). Significant increases in resting-state gamma and theta power were observed under ketamine compared to placebo (p < 0.05). The source-space analysis revealed two distinct networks with an increased mean functional gamma- or theta-band connectivity during the ketamine session. The gamma-network consisted of midline regions, the cuneus, the precuneus, and the bilateral posterior cingulate cortices, while the theta-band network involved the Heschl gyrus, midline regions, the insula, and the middle cingulate cortex. The current source density (CSD) within the gamma-band correlated negatively with the PANSS negative symptom score, and the activity within the gamma-band network correlated negatively with the subjective changed meaning of percepts subscale of the 5D-ASC. These results are in line with resting-state patterns seen in people who have schizophrenia and argue for a crucial role of the glutamate system in mediating dysfunctional gamma- and theta-band-connectivity in schizophrenia. Resting-state networks could serve as biomarkers for the response to glutamatergic drugs or drug development efforts within the glutamate system.

Persistent COVID-19-associated neurocognitive symptoms in non-hospitalized patients

As cases of coronavirus disease 2019 (COVID-19) mount worldwide, attention is needed on potential long-term neurologic impacts for the majority of patients who experience mild to moderate illness managed as outpatients. To date, there has not been discussion of persistent neurocognitive deficits in patients with milder COVID-19. We present two cases of non-hospitalized patients recovering from COVID-19 with persistent neurocognitive symptoms. Commonly used cognitive screens were normal, while more detailed testing revealed working memory and executive functioning deficits. An observational cohort study of individuals recovering from COVID-19 (14 or more days following symptom onset) identified that among the first 100 individuals enrolled, 14 were non-hospitalized patients reporting persistent cognitive issues. These 14 participants had a median age of 39 years (interquartile range: 35–56), and cognitive symptoms were present for at least a median of 98 days (interquartile range: 71–120 following acute COVID-19 symptoms); no participants with follow-up evaluation reported symptom resolution. We discuss potential mechanisms to be explored in future studies, including direct viral effects, indirect consequences of immune activation, and immune dysregulation causing auto-antibody production.

Нормативная оценка когнитивных функций по шкале «Краткая оценка когнитивных функций у пациентов с шизофренией» (BACS) в томской популяции: конституциональные факторы вариативности

The article provides arguments in favor of developing ideas about cognitive functions and their implementation not only in the practice of scientific knowledge, but also in everyday life. The relevance of the study is due to the priority links with psychosocial functions and cognitive management of public life. The aim of the study was to provide a normative assessment of cognitive functions using the Brief Assessment of Cognitive Functions in Patients with Schizophrenia (BACS) scale in the Tomsk population of healthy individuals. Our objectives were to determine the nature and severity of cognitive functions in the representation of the BACS scale in a group of healthy individuals in the study of the normative indicators variability in different populations; to determine the influence of constitutional factors (gender, age) on the variability of cognitive functions (CF) indicators; to carry out a comparative analysis with the data obtained from other normative indicators studies; to determine the variability of CF indicators in the covariance-dispersion representation; to determine the co-variability of CF indicators in the covariance-dispersion representation. The sample consisted of 161 people without mental disorders living in Tomsk. The age ranged from 20 to 69 years old. The markers of the state of cognitive functions are the assessments of the BACS scale. The BACS scale meets the requirements for rapid assessment of the cognitive functions state and includes tasks for evaluation of planning and control functions, speech fluency, working memory, and motor skills. This study keeps developing ideas about cognitive indicators of the Russian population norm. The article examines the gender and age influence on the scale assessments. Statistically significant decrease with age in male and female subpopulations for all tests is shown. The most significant decrease is noted for test scores “Symbol Coding” and “Tower of London”. Comparative analysis of the state of cognitive functions shows that in the Tomsk population “Token Motor" and "Verbal Fluency" indicators were higher and other test indicators were significantly lower than those of the Moscow sample. The variability of the scale values is found to be due to such constitutional factors as age and gender. According to ANOVA data, gender and age significantly influences the mean scores of test performance. Based on the calculations of the covariance-dispersion matrix, it is shown that cognitive functions are highly connected in the male subpopulation. Comparison of empirical data from different study groups shows that the BACS reveals high validity with respect to measurable attributes and sensitivity to regional variability in CF indices. The scores can be used as normative for the Tomsk population when studying neu-rocognitive deficits in patients with schizophrenia.

P.568 Trihexyphenidyl in combination with antipsychotic therapy does not affect the severity of neurocognitive deficits in patients with schizophrenia

Every state in the United States has established laws that allow an unharmed newborn to be relinquished to personnel in a safe haven, such as hospital emergency departments, without legal penalty to the parents. These Safe Haven, Baby Moses, or Safe Surrender laws are in place so that mothers in crisis can safely and legally relinquish their babies at a designated location where they can be protected and given medical care until a permanent home can be found. It is important for health care professionals to know about and understand their state’s law and how to respond should an infant be surrendered at their facility. No articles were found in the peer-reviewed literature that describe a method to evaluate nurse competency during infant relinquishment at a Safe Haven location. This article will describe commonalities and differences among these Safe Haven Laws, responsibilities of the hospital and staff receiving a relinquished infant, and 1 hospital’s experience when running an infant relinquishment drill in their emergency department.

Influence of clinical and therapeutic indicators on the severity of neurocognitive deficits in patients with schizophrenia

Aim. To assess the association of clinical and therapeutic parameters with the severity of the neurocognitive deficits in patients with schizophrenia. Materials and methods. We examined 118 patients with schizophrenia, aged 34 [29; 41] years, and with a disease duration of 10 [4; 16] years. 33 patients (28%) received conventional antipsychotic drugs (CAD), and 85 (72%) patients received atypical antipsychotic drugs (AAD). As concomitant therapy, 58 people (49.1%) took trihexyphenidyl, 60 people did not take it (50.9%). Assessment of cognitive functions was carried out for all patients using the Brief Assessment of Cognition in Schizophrenia (BACS), and clinical psychopathological symptomatology was evaluated using the Positive and Negative Syndrome Scale (PANSS). Statistical analysis of the data was performed using the Kruskal-Wallis test ANOVA with the multiple comparison procedure, the Pearson’s chi-squared test, and K-means cluster analysis. Results. Neurocognitive deficits formed three clusters of disturbances that differ in clinical severity: 1) mild, 2) moderate, 3) severe. According to the subscale of positive PANSS symptoms, patients with mild neurocognitive deficits had a lower average total score compared to patients with severe neurocognitive deficits ( p = 0.011), who, in turn, received significantly longer antipsychotic therapy compared with patients with moderate ( p = 0.014) and mild ( p = 0.01) neurocognitive deficits. Herewith, the duration of CAD treatment did not differ between clusters; consequently, the obtained results on antipsychotics as a whole were obtained due to AAD ( p = 0.005 and p = 0.001, respectively). Trihexyphenidyl did not affect the severity of neurocognitive deficits. Conclusion. The severity of positive symptoms of schizophrenia was lower in patients with mild neurocognitive deficits. The most pronounced neurocognitive deficits are observed in patients receiving AAD.

Isolated agenesis of the corpus callosum and normal general intelligence development during postnatal life: a case report and review of the literature

BackgroundAgenesis of the corpus callosum can occur isolated or as part of a complex congenital syndrome. Patients with isolated agenesis of the corpus callosum may present with severe intellectual disability, although a proportion of affected individuals develop normal intelligence. However, even in patients with no apparent deficits, subtle neuropsychological alterations may occur as the cognitive demand increases with age. Hence, patients with this deffect require a strict follow-up during their postnatal life. Thus, physicians require a better knowledge of the cognitive features of agenesis of the corpus callosum to improve their approach to this cerebral malformation. Here, we report an illustrative case of a school-age child with isolated agenesis of the corpus callosum and normal intelligence. We also provide a literature review about the postnatal screening of neurocognitive deficits in patients with agenesis of the corpus callosum.Case presentationAn 8-year-old Hispanic boy with total agenesis of the corpus callosum attended for medical follow-up. The defect was identified during the neonatal period by cranial ultrasonography and brain computed tomography scan. However, he did not present any craniofacial or non-cerebral malformation suggestive of a congenital syndrome. Furthermore, he showed no neuropsychiatric disorder or intellectual disability during his early childhood. At the age of 4, he was subjected to a control brain magnetic resonance imaging that showed total agenesis of the corpus callosum and colpocephaly. At his arrival, a neurological examination was normal with no signs of intracranial hypertension. His intelligence quotient was unaltered and he scored normal in the Mini-Mental State Examination test. The literature reviewed here suggested that patients with agenesis of the corpus callosum require a strict neurocognitive follow-up during postnatal life, as they may present neuropsychological deficits during adolescence, when development of the corpus callosum is completed and there is maximum reliance on this structure. Thus, our patient was scheduled for future annual neurocognitive testing.ConclusionsIsolated agenesis of the corpus callosum is not innocuous, and patients with this defect require a strict neurocognitive follow-up. We provide an informative reference tool useful for the postnatal neuropsychological screening of patients with isolated agenesis of the corpus callosum.

Relationship of metabolic syndrome and neurocognitive deficits in patients with schizophrenia

This study aimed to evaluate the association of the metabolic syndrome (MS) and its components with neurocognition among patients with schizophrenia. 121 patients with schizophrenia from an outpatient service of two psychiatric centers were assessed on a neurocognitive battery and by metabolic measures. More than half (56.2%) of the patients fulfilled the consensus criteria for MS. After controlling/adjusting for various covariates (age, education in years, duration of illness, age of onset, Positive and Negative Symptom scale score and presence of smoking status), it was found that compared to patients without MS, those with MS had significantly poorer performance “in the cognitive domains” of cognitive processing and selective attention (Stroop effect percentile; p value 0.002; effect size-0.45) and auditory and verbal memory (AVLT; p value <0.001; effect size 0.68). Patients with a higher number of abnormal parameters of MS had poorer functioning in the domains of cognitive processing and selective attention, auditory and verbal memory, and executive tasks. To conclude, this two center study suggests that MS has a negative impact on neurocognition in patients with schizophrenia. There is a need to identify and monitor metabolic abnormalities among patients with schizophrenia to minimize the negative effect of metabolic parameters on neurocognition.

The Stereotype Threat Effect

Abstract. Neurocognitive deficits in patients with mental disorders are partially due to secondary influences. “Stereotype threat” denotes the phenomenon that performance is compromised when a participant is confronted with a devaluing stereotype. The present study examined the impact of stereotype threat on neuropsychological performance in schizophrenia. Seventy-seven participants with a self-reported diagnosis of schizophrenia were randomly assigned to either an experimental condition involving stereotype threat activation or a control condition in an online study. Participants completed memory and attention tests as well as questionnaires on motivation, self-efficacy expectations, cognitive complaints, and self-stigmatization. Contrary to our prediction, the two groups showed no significant differences regarding neuropsychological performance and self-report measures. Limitations, such as a possibly too weak threat cue, are discussed and recommendations for future studies are outlined.