Verbal Memory Deficits Research Articles

Disrupted functional connectivity of the habenula links psychomotor retardation and deficit of verbal fluency and working memory in late-life depression.

Functional abnormalities of the habenula in patients with depression have been demonstrated in an increasing number of studies, and the habenula is involved in cognitive processing. However, whether patients with late-life depression (LLD) exhibit disrupted habenular functional connectivity (FC) and whether habenular FC mediates the relationship between depressive symptoms and cognitive impairment remain unclear. Overall, 127 patients with LLD and 75 healthy controls were recruited. The static and dynamic FC between the habenula and the whole brain was compared between LLD patients and healthy controls, and the relationships of habenular FC with depressive symptoms and cognitive impairment were explored by correlation and mediation analyses. Compared with the controls, patients with LLD exhibited decreased static FC between the right habenula and bilateral inferior frontal gyrus (IFG); there was no significant difference in dynamic FC of the habenula between the two groups. Additionally, the decreased static FC between the right habenula and IFG was associated with more severe depressive symptoms (especially psychomotor retardation) and cognitive impairment (language, memory, and visuospatial skills). Last, static FC between the right habenula and left IFG partially mediated the relationship between depressive symptoms (especially psychomotor retardation) and cognitive impairment (verbal fluency and working memory). Patients with LLD exhibited decreased static FC between the habenula and IFG but intact dynamic FC of the habenula. This decreased static FC mediated the relationship between depressive symptoms and cognitive impairment.

Altered morphological characteristics and structural covariance connectivity associated with verbal working memory performance in ADHD children.

Deficits in verbal working memory (VWM) observed in attention deficit hyperactivity disorder (ADHD)children can persist into adulthood. Although previous studies have identified brain regions that are activated during VWM tasks, the neural mechanisms underlying the relationship between VWM deficits remain unclear. The objective of this study was to investigate the structural covariance network connectivity and brain morphology changes that are associated with VWM performance in ADHD children. For this study, we selected 26 ADHD children and 26 healthy control (HC) participants. Participants were instructed to perform a n-back VWM task and their accuracy and response times were subsequently recorded. This research utilized voxel-based morphometry to measure the grey matter (GM) volume, and conducted structural covariance connectivity network analysis to explore the changes of brain in ADHD. Voxel-based morphometry analysis showed that lower GM volume in the right cerebellum lobule VI and the left parahippocampal gryus in ADHD children. Moreover, a positive correlation was found between the GM volume in the right cerebellum lobule VI and the accuracy of 2-back VWM task with verbal, small reward, and delayed feedback (VSD). Structural covariance network analysis found decreased structural connectivity between right cerebellum lobule VI and right precentral gyrus, right postcentral gyrus, left paracentral lobule, right superior parietal gyrus, left hippocampus in ADHD children. The low GM volume and altered structural covariance connectivity in the right cerebellum lobule VI might potentially affect VWM performance in ADHD children. The innovation of this study lies in its more focused discussion on the morphological characteristics and structural covariance connectivity of verbal working memory deficits in ADHD children, and the innovative finding of a positive correlation between gray matter volume in the right cerebellum lobule VI and accuracy in completing the 2-back VWM task with verbal instructions, small reward, and delayed feedback(VSD). This expands upon previous research by elucidating the specific brain structures involved in verbal working memory deficits in ADHD children and highlights the potential importance of the cerebellum in this cognitive process. Overall, these innovative findings advance our understanding of the neural basis of ADHD and may have important implications for the development of targeted interventions for verbal working memory deficits.

The Spectrum of Cognitive Dysfunction in Amyotrophic Lateral Sclerosis: An Update.

Cognitive dysfunction is an important non-motor symptom in amyotrophic lateral sclerosis (ALS) that has a negative impact on survival and caregiver burden. It shows a wide spectrum ranging from subjective cognitive decline to frontotemporal dementia (FTD) and covers various cognitive domains, mainly executive/attention, language and verbal memory deficits. The frequency of cognitive impairment across the different ALS phenotypes ranges from 30% to 75%, with up to 45% fulfilling the criteria of FTD. Significant genetic, clinical, and pathological heterogeneity reflects deficits in various cognitive domains. Modern neuroimaging studies revealed frontotemporal degeneration and widespread involvement of limbic and white matter systems, with hypometabolism of the relevant areas. Morphological substrates are frontotemporal and hippocampal atrophy with synaptic loss, associated with TDP-43 and other co-pathologies, including tau deposition. Widespread functional disruptions of motor and extramotor networks, as well as of frontoparietal, frontostriatal and other connectivities, are markers for cognitive deficits in ALS. Cognitive reserve may moderate the effect of brain damage but is not protective against cognitive decline. The natural history of cognitive dysfunction in ALS and its relationship to FTD are not fully understood, although there is an overlap between the ALS variants and ALS-related frontotemporal syndromes, suggesting a differential vulnerability of motor and non-motor networks. An assessment of risks or the early detection of brain connectivity signatures before structural changes may be helpful in investigating the pathophysiological mechanisms of cognitive impairment in ALS, which might even serve as novel targets for effective disease-modifying therapies.

Brain volumetric changes in menopausal women and its association with cognitive function: a structured review.

The menopausal transition has been proposed to put women at risk for undesirable neurological symptoms, including cognitive decline. Previous studies suggest that alterations in the hormonal milieu modulate brain structures associated with cognitive function. This structured review provides an overview of the relevant studies that have utilized MRI to report volumetric differences in the brain following menopause, and its correlations with the evaluated cognitive functions. We performed an electronic literature search using Medline (Ovid) and Scopus to identify studies that assessed the influence of menopause on brain structure with MRI. Fourteen studies met the inclusion criteria. Brain volumetric differences have been reported most frequently in the frontal and temporal cortices as well as the hippocampus. These regions are important for higher cognitive tasks and memory. Additionally, the deficit in verbal and visuospatial memory in postmenopausal women has been associated with smaller regional brain volumes. Nevertheless, the limited number of eligible studies and cross-sectional study designs warrant further research to draw more robust conclusions.

Cognitive function and the longitudinal hippocampal axis in mesial temporal sclerosis

ObjectiveThe relationship of preoperative memory deficits in patients with mesial temporal lobe epilepsy (mTLE) and hippocampal sclerosis (HS) to the distribution of neuronal loss is uncertain. Building on the material specificity theory, we tested the hypothesis that visual memory deficits are associated with posterior hippocampal atrophy, whereas verbal memory deficits are associated with anterior hippocampal atrophy. MethodsWe studied 22 adults with mTLE and HS, calculating hippocampal head, body, and tail volumes, correcting for estimated total intracranial volume, using automated segmentation. Preoperative memory ability was evaluated with the Wechsler Memory Scale (WMS-II: logical memory, verbal paired associates, family pictures, and faces subtests). We correlated memory ability with hippocampal division volumes using SPSS 26.1 (repeated measures ANOVAs, one-way ANOVAs, Pearson r correlations) for statistical analysis. ResultsWe found a significant main effect of hippocampal subdivision, reporting volumetric differences between the head, body, and tail. Pairwise comparisons reported that the hippocampal head had significantly greater volume than both the body and tail (p < 0.001). For both left and right focus groups, the ipsilateral hippocampi were significantly smaller than the contralateral.Linear regression reported a left hippocampal model (head, body, and tail volumes) predicted performance on logical memory with the left hippocampal tail volume being the strongest predictor. A right hippocampal model (head, body, and tail volumes) predicted memory ability for family pictures and verbal paired associates at a trend level. ConclusionsIpsilateral hippocampal head and tail seem more vulnerable to injury than the body in both the left and right mTLE. Our study suggests there may be functional differences along the hippocampal longitudinal axis, particularly for the left hippocampal tail with verbal memory. Our findings are consistent with material-specific right-left differences in memory processing.

Post-stroke aggressive behavior in patients wıth first-ever ischemic stroke: underlying clinical and imaging factors.

Aggression is defined as a complex behavior consisting of a combination of sensory, emotional, cognitive and motor elements. We aimed to examine the relationships between post-stroke aggressive behavior (PSAB) and neuropsychological and neuroimaging findings. 380 patients in the stroke unit were classified as aggressive or non-aggressive based on symptoms elicited by the Neuropsychiatric Inventory (NPI) and aggression screening questionnaire. Aggressive behavior was detected in 42 (11.1%) of 380 patients who had a first ischemic stroke. Patients with PSAB were older than those without (338 patients) (66.98 + 13.68 vs. 62.61 + 13.06, P = 0.043). Hamilton depression and anxiety scales showed significantly higher rates of depression and anxiety in the PSAB group compared to the non-PSAB group (47.6% vs. 16.3% and 57.1% vs. 15.4%, respectively; P = 0.001). Lesion mapping analysis showed that lesions in patients with PSAB mostly included the lower parietal lobe and lateral frontal gyrus. Multiple regression analysis showed that gender (OR, 2.81; CI%, 1.24-6.39), lateral prefrontal infarction (OR, 6.43; CI%, 1.51-27.44), parietal infarction (OR, 2.98; CI%, 1.15-7.76), occipital infarction (OR, 2.84; CI%, 1.00-8.06), multiple infarcts (OR, 5.62; CI%, 2.27-13.93), anxiety (OR, 2.06; CI%, 0.89-4.81) and verbal memory deficit (OR, 4.21; CI%, 1.37-12.93) were significant independent predictors of PSAB. The presence of PSAB may be related to neuropsychiatric symptoms such as high anxiety and verbal memory impairment, and neuroanatomical location of the lesions.

Effect of transcutaneous cervical vagus nerve stimulation on declarative and working memory in patients with Posttraumatic Stress Disorder (PTSD): A pilot study

BackgroundPosttraumatic stress disorder (PTSD) is associated with changes in multiple neurophysiological systems, including verbal declarative memory deficits. Vagus Nerve Stimulation (VNS) has been shown in preliminary studies to enhance function when paired with cognitive and motor tasks. The purpose of this study was to analyze the effect of transcutaneous cervical VNS (tcVNS) on attention, declarative and working memory in PTSD patients. MethodsFifteen PTSD patients were randomly assigned to active tcVNS (N = 8) or sham (N = 7) stimulation in a double-blinded fashion. Memory assessment tests including paragraph recall and N-back tests were performed to assess declarative and working memory function when paired with active/sham tcVNS once per month in a longitudinal study during which patients self-administered tcVNS/sham twice daily. ResultsActive tcVNS stimulation resulted in a significant improvement in paragraph recall performance following pairing with paragraph encoding for PTSD patients at two months (p < 0.05). It resulted in a 91 % increase in paragraph recall performance within group (p = 0.03), while sham tcVNS exhibited no such trend in performance improvement. In the N-back study, positive deviations in accuracy, precision and recall measures on different day visits (7,34,64,94) of patients with respect to day 1 revealed a pattern of better performance of the active tcVNS population compared to sham VNS which did not reach statistical significance. LimitationsOur sample size was small. ConclusionsThese preliminary results suggest that tcVNS improves attention, declarative and working memory, which may improve quality of life and productivity for patients with PTSD. Future studies are required to confirm these results.

Brain-Cognition Associations in Older Patients With Remitted Major Depressive Disorder or Mild Cognitive Impairment: A Multivariate Analysis of Gray and White Matter Integrity

BackgroundAlmost half of older patients with major depressive disorder (MDD) present with cognitive impairment, and one-third meet diagnostic criteria for mild cognitive impairment (MCI). However, mechanisms linking MDD and MCI remain unclear. We investigated multivariate associations between brain structural alterations and cognition in 3 groups of older patients at risk for dementia, remitted MDD (rMDD), MCI, and rMDD+MCI, as well as cognitively healthy nondepressed control participants. MethodsWe analyzed magnetic resonance imaging data and cognitive domain scores in participants from the PACt-MD (Prevention of Alzheimer’s Disease With Cognitive Remediation Plus Transcranial Direct Current Stimulation in Mild Cognitive Impairment and Depression) study. Following quality control, we measured cortical thickness and subcortical volumes of selected regions from 283 T1-weighted scans and fractional anisotropy of white matter tracts from 226 diffusion-weighted scans. We assessed brain-cognition associations using partial least squares regressions in the whole sample and in each subgroup. ResultsIn the entire sample, atrophy in the medial temporal lobe and subregions of the motor and prefrontal cortex was associated with deficits in verbal and visuospatial memory, language skills, and, to a lesser extent, processing speed (p < .0001; multivariate r = 0.30, 0.34, 0.26, and 0.18, respectively). Widespread reduced white matter integrity was associated with deficits in executive functioning, working memory, and processing speed (p = .008; multivariate r = 0.21, 0.26, 0.35, respectively). Overall, associations remained significant in the MCI and rMDD+MCI groups, but not the rMDD or healthy control groups. ConclusionsWe confirm findings of brain-cognition associations previously reported in MCI and extend them to rMDD+MCI, but similar associations in rMDD are not supported. Early-onset and treated MDD might not contribute to structural alterations associated with cognitive impairment.

Multifocal hypometabolic correlates to deficits of verbal memory in mesial temporal lobe epilepsy

Background and ObjectivesNeuropsychological research on mesial temporal lobe epilepsy (MTLE) often highlights material-specific memory deficits, but a lesion-focused model may not accurately reflect the underlying networks that support episodic memory in these patients. Our study evaluated the pathophysiology behind verbal learning/memory deficits as revealed by hypometabolism quantified through 18-fluorodeoxyglucose positron emission tomography (FDG-PET). MethodsThis retrospective study included thirty presurgical patients with intractable unilateral MTLE who underwent interictal FDG-PET and verbal memory assessment (12 females, mean age: 38.73 years). Fluorodeoxyglucose-positron emission tomography mapping was performed with voxel-based mapping of glucose utilization to a database of age-matched controls to derive regional Z-scores. Neuropsychological outcome variables included scores on learning and recall trials of two distinct verbal memory measures validated for use in epilepsy research. Pearson’s correlations evaluated relationships between clinical variables and verbal memory. Linear regression was used to relate regional hypometabolism and verbal memory assessment. Post hoc analyses assessed areas of FDG-PET hypometabolism (threshold Z ≤ −1.645 below mean) where verbal memory was impaired. ResultsVerbal memory deficits correlated with hypometabolism in limbic structures ipsilateral to language dominance but also correlated with hypometabolism in networks involving the ipsilateral perisylvian cortex and contralateral limbic and nonlimbic structures. DiscussionWe conclude that traditional models of verbal memory may not adequately capture cognitive deficits in a broader sample of patients with MTLE. This study has important implications for epilepsy surgery protocols that use neuropsychological data and FDG-PET to draw conclusions about surgical risks.

Cognitive impairment in MOGAD is associated with ADEM-like episodes and deep grey matter atrophy (S40.006)

Cognitive impairment in MOGAD is associated with ADEM-like episodes and deep grey matter atrophy (S40.006)

Wernicke’s Encephalopathy Preceded by COVID-19 Infection: A Case Report (P2-7.006)

<h3>Objective:</h3> To describe a case of post-infectious encephalopathy following COVID-19 with MRI brain changes suggestive of Wernicke’s encephalopathy and a transient presence of anti-GAD65 autoantibodies in the cerebrospinal fluid (CSF). <h3>Background:</h3> Chronic malnutrition and alcoholism are known risk factors for developing Wernicke’s encephalopathy. However, it is not typically associated with thiamine deficiency resulting from acute starvation as in this case of severe respiratory syndrome due to coronavirus-2 (SARS-CoV-2). <h3>Design/Methods:</h3> NA <h3>Results:</h3> A 59 year-old female presented to the neurointensive care unit with subacute disorientation, decreased verbal fluency, memory deficits, gait dysfunction, confusion, and rapid weight loss that progressed to coma over two months following COVID-19 infection. Initial lumbar puncture (LP) one month following infection was notable for positive anti-GAD65 autoantibodies and elevated protein which was suggestive of post-infectious encephalitis. MRI brain at the time of initial evaluation was unremarkable for abnormalities and the patient’s symptoms continued to progress to include depressed mentation. Subsequent MRIs of the brain with and without contrast showed T2 FLAIR abnormalities in the periaqueductal grey, lateral walls of the third ventricle, splenium, and mammillary bodies. Repeat LP showed similar CSF profile and absence of anti-GAD65 autoantibodies. Electroencephalogram showed slowing with frequent generalized periodic discharges. Patient’s treatment course included high dose thiamine, methylprednisolone, intravenous immunoglobulin, and plasmapheresis without clinical improvement. The patient did not show meaningful cognitive recovery and was transitioned to comfort care. <h3>Conclusions:</h3> The patient’s progression to coma was suspected to be due to development of COVID-19 encephalopathy precipitating Wernicke’s encephalopathy in the setting of severely diminished oral intake. Because Wernicke’s encephalopathy is potentially reversible with thiamine administration, we propose that early empiric treatment should be considered in all patients suffering from persistent encephalopathy following COVID-19 infection. <b>Disclosure:</b> Dr. Volski has nothing to disclose. Dr. Wang has nothing to disclose. Dr. Chakrabarti Pulakanti has nothing to disclose. Dr. Dolla has nothing to disclose.

Teaching NeuroImages: Persistent anterograde amnesia due to sequential, bilateral vascular damage to the Papez circuit

A 62-year-old previously cognitively intact man presented to the emergency department with acute impairment of anterograde memory (ability to form new memories).1 Head CT did not show acute changes; however, amnesia persisted. MRI disclosed an acute infarct in the left posterior hippocampus and a nonacute lacunar stroke in the right anterior thalamus (figure). Memory testing showed severe deficits in verbal and visual memory, persisting after 2 months. Bilateral lesions located anywhere in the Papez circuit (hippocampal formations, mammillary bodies, anterior thalamic nuclei, cingulate and parahippocampal cortices, and their connections via fornix and mammillothalamic tracts) may be implicated in marked, persistent anterograde memory deficits.1,2 The hippocampus receives its blood supply from collateral branches of the posterior cerebral artery and the anterior choroidal artery.3 The anterior thalamus is supplied by the tuberothalamic artery.4

5607610 HETEROGENEITY IN COGNITIVE PRESENTATIONS AMONG CHILDREN AND ADOLESCENTS WITH SICKLE CELL DISEASE

Background: Children and adolescents with sickle cell disease (SCD) are at increased risk for central nervous system (CNS) sequelae. Deleterious effects on CNS functioning and cognition have been well-described in terms of global intellectual functioning and specific areas of cognitive weakness. Among school-aged youth with SCD, deficits are broadly observed across a range of abilities; however, less is known about the heterogeneity in presentations of cognitive deficits in SCD and associated implications. Aims: We aimed to determine rates of comorbid cognitive deficits across specific domains of functioning and examine disease-related correlates and functional outcomes of multiple co-occurring cognitive deficits. Methods: Participants (ages 7-16 years) with SCD completed the Wechsler Intelligence Scale for Children, Fifth Edition (WISC-V) and primary caregivers completed the Conners-3 to report on learning problems. WISC-V index scores were calculated for verbal comprehension, fluid reasoning, working memory, and processing speed. To investigate the heterogeneity of cognitive deficits, index scores were dichotomized and identified as a weakness if the standard score was ≤85 (i.e., 1 SD or more below the mean). Caregivers reported patient age and sex, while a review of the electronic health record was completed to verify SCD genotype and history of silent or overt cerebral infarct. Results: Ninety-one participants enrolled and completed a cognitive assessment. The mean age of participants was 10.43 years (SD=2.93) and the majority were female (59%), diagnosed with HbSS or HbS-beta0 thalassemia (75%), and had no evidence of silent or overt cerebral infarct (73%). While most participants demonstrated either no cognitive deficits or a deficit in only one domain of functioning (63%), a notable proportion of participants (37%) exhibited cognitive deficits across multiple (i.e., ≥2) domains. Nineteen percent of participants exhibited deficits in two domains of cognitive functioning, 11% had deficits in three domains, and 7% had deficits in four domains. In contrast, 17% of participants exhibited a cognitive deficit in only one domain. The most common comorbid deficits were observed for fluid reasoning and processing speed (18%) and working memory and processing speed (18%). Comorbid deficits in both verbal comprehension and working memory were the least common (9%). The number of domains ≥1 standard deviation below the mean was positively correlated with caregiver-rated learning problems (r=.38, p<.001). In a multiple linear regression controlling for age, sex, genotype, and stroke history, the number of domains of cognitive weakness significantly predicted caregiver-rated learning problems (b=4.29, p<.001). Conclusion: A high level of heterogeneity in cognitive deficits was observed in the current sample of youth with SCD. Among those with any cognitive deficits, it was more common for participants to have multiple areas of cognitive weakness than a single area of weakness. Deficits in processing speed showed high comorbidity with deficits in other areas, specifically in fluid reasoning and working memory. Having deficits across multiple areas of functioning was associated with increased learning problems. Additional research needs to examine the etiology of comorbid cognitive deficits, implications for disease self-management, and the extent to which cognitive interventions targeting multiple domains of weakness could enhance outcomes.

A clinical case of anosognosia in a CADASIL disease.

IntroductionCADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy) is a cerebrovascular disease, tht appears in 1.98/100,000. It´s caused by a mutation of the Notch3 gene and is characterized by accumulation of granular osmiophilic material in the middle layer of the small and median sized cerebral arteries.Sypmtoms are migraine, recurrent cerebral ischemic episodes, dementia, neuropsychiatric disorders (anosognosia, character disorders, apathy and cognitive impairment). It usually appears between 30-60 years, although there is an important variability. There is no curative treatment, only palliative.ObjectivesClinical review of anosognosia and its presence in CADASIL disease.MethodsClinical case and literatura review.ResultsWe presented the clinical case of a 68-year-old man, who was diagnosed with CADASIL after a stroke 3 years earlier. In his family, his brother was diagnosed also with CADASIL. The patient had previously presented disturbances in impulse control (hyperorality) and important executive failures. He currently presented anosognosia, deficits in verbal memory, spatial perception and executive functions, in addition to behavioral alterations and apathy. Due to these deficits he was prohibited from certain activities (driving, hunting).The patient was not aware of these deficits and becouse of his “no knowledge of his illness”, he disagreed with these prohibitions, so he showed rage and anger at the impotence of not understanding why certain actions are prohibited.In the consultation, mnesic errors and in naming objects were also objectified, for which it was recommended to carry out cognitive stimulation on a daily basis. In addition, he presented failures of sphincter incontinence, especially of urine and occasionally also of the anal sphincter. He had previously had episodes of myoclonus or fasciculations.A genetic study by massive sequencing confirmed the heterozygous presence of the pathogenic variant c.1819C&gt;T p.(Arg607Cys) in the NOTCH3 gene, a CADASIL disease.ConclusionsThe anosognosia that many patients with CADASIL disease present constitutes a problem because it contributes to the delay in consultation and, therefore, the delay in the adequate diagnostic approach, therapeutic possibilities and family genetic counseling. Due in part to anosognosia, CADASIL is considered an underdiagnosed entity. Due to the lack of awareness and the consequent lack of recognition of the deficit, these people are often seen as stubborn and difficult to deal with by people in their immediate environment.In addition, there is general difficulty in the rehabilitation process, since patients do not think the neccesity to be treated. This can generate frustration and despair both in their relatives and in the health personnel.For all these reasons, both in anosognosia and in CADASIL disease, adequate psychological support is needed for both those affected and their families.Disclosure of InterestNone Declared

The Role of the Cerebellum in Visual-Spatial Memory in Pediatric Posterior Fossa Tumor Survivors.

The cerebellum is involved in motor and non-motor functions. Cerebellar lesions can underlie the disruption of various executive functions. The violation of executive functions in cerebellar lesions is a serious problem, since children, after completing treatment, must return to school, finish their education, and get a profession. One of the important executive functions is working memory, which contributes to academic success. Deficits of verbal working memory in cerebellar tumors have been studied, in contrast to visual-spatial working memory. To assess this issue, 101 patients who survived cerebellar tumors and 100 healthy control subjects performed a visual-spatial working memory test. As a result, in children who survived cerebellar tumors, visual-spatial working memory is impaired compared to the control group. Moreover, with age, and hence the time since the end of treatment, the number of elements that children can retain in visual-spatial working memory increases, but still remains smaller compared to the control group. Our findings complement the idea of cerebellar involvement in visual-spatial working memory and suggest that it is disrupted by cerebellar lesions in children.

Dyslexia and dyscalculia: which neuropsychological processes distinguish the two developmental disorders?

ABSTRACT This study analyses the specific neuropsychological profiles of children with dyslexia and/or dyscalculia, in particular concerning phonological awareness, lexical access, working memory and numerical processing. Four groups were selected, through a screening process that used strict criteria, from 1568 7-10-year-old children: 90 with typical development, 61 with dyslexia, 13 with dyscalculia, and 14 with dyslexia + dyscalculia. Children with dyslexia show a deficit in phonological processing, lexical access, and verbal working memory, especially with alphabetic stimuli. Children with developmental dyscalculia show a deficit of phonological processing, verbal working memory with digits and visual-spatial working memory. They also show an impairment in spatial representation of numbers and in the automatic access to numerical semantics to a greater extent than those with double disturbance. Children with dyslexia + dyscalculia show a profile generally characterized by the summation of the deficits of the two disorders, although they have a lower deficit in access to numerical semantics and mental representation of numbers.

Impact of Cognitive Disturbances and Clinical Symptoms on Disability in Patients with Paranoid Schizophrenia: A Study of a Bulgarian Clinical Sample.

108 patients with schizophrenia were included (66 male and 42 female). Their average age was 38.86 ± 10.02 years and the disease duration was 12.80 ± 8.20 years, with mean disease onset of 24 years. Clinical symptoms were assessed with the PANSS, and cognitive performance was measured using a seven-item neurocognitive battery. The disability level of the subjects was assessed using the World Health Organization-Disability Assessment Schedule 2.0 (WHO-DAS 2.0). The relation between the variables studied was assessed using Spearman's rank correlation coefficient (rs) at a probability level of p < 0.05. An increase in symptom severity resulted in worsening of the "participation in society" (r = 0.56, p < 0.01), "life activities-household" (r = 0.55, p < 0.01), and "getting along with people" (r = 0.59, p < 0.01) WHO-DAS 2.0 domains. Positive symptoms (13.89 ± 3.48) correlated strongly with "getting along with people" (r = 0.55, p < 0.01), "life activities-household" (r = 0.58, p < 0.01), and "participation in society" (r = 0.62, p < 0.01), and negative symptoms (14.25 ± 4.16) with "participation in society" (r = 0.53, p < 0.01) and "life activities-household" (r = 0.48, p < 0.01). Symptoms of disorganization (15.67 ± 4.16) had the highest impact on "life activities-household" (r = 0.81, p < 0.01), "getting along with people" (r = 0.56, p < 0.05), and "participation in society" (r = 0.65, p < 0.01). Episodic memory (r = -0.28, p < 0.01) was remotely related to comprehension and communication. The information processing speed (rs = 0.38, p < 0.01), visual memory (rs = -0.30, p < 0.01), and focused executive functions showed moderate correlations with all domains on the WHO-DAS 2.0 scale (rs = 0.38, p < 0.01). Attention (rs = -0.33, p < 0.01) was moderately related to community activities. Semantic (rs = -0.29, p < 0.01) and literal (rs = -0.27, p < 0.01) verbal fluency demonstrated weak correlations with "cognition-understanding", "getting along with people", and "participation in society". Symptoms of disorganization and disturbed executive functions contribute most to disability in patients with schizophrenia through impairment of real-world functioning, especially in social interactions and communication. Severe clinical symptoms (negative and disorganization-related ones) as well as deficits in executive function, verbal memory, and verbal fluency cause the biggest problems in the functional domains of interaction with other people and participation in society.

Dynamic Amyloid and Metabolic Signatures of Delayed Recall Performance within the Clinical Spectrum of Alzheimer's Disease.

Associations between pathophysiological events and cognitive measures provide insights regarding brain networks affected during the clinical progression of Alzheimer's disease (AD). In this study, we assessed patients' scores in two delayed episodic memory tests, and investigated their associations with regional amyloid deposition and brain metabolism across the clinical spectrum of AD. We assessed the clinical, neuropsychological, structural, and positron emission tomography (PET) baseline measures of participants from the Alzheimer's Disease Neuroimaging Initiative. Subjects were classified as cognitively normal (CN), or with early (EMCI) or late (LMCI) mild cognitive impairment, or AD dementia. The memory outcome measures of interest were logical memory 30 min delayed recall (LM30) and Rey Auditory Verbal Learning Test 30 min delayed recall (RAVLT30). Voxel-based [18F]florbetapir and [18F]FDG uptake-ratio maps were constructed and correlations between PET images and cognitive scores were calculated. We found that EMCI individuals had LM30 scores negatively correlated with [18F]florbetapir uptake on the right parieto-occipital region. LMCI individuals had LM30 scores positively associated with left lateral temporal lobe [18F]FDG uptake, and RAVLT30 scores positively associated with [18F]FDG uptake in the left parietal lobe and in the right enthorhinal cortex. Additionally, LMCI individuals had LM30 scores negatively correlated with [18F]florbetapir uptake in the right frontal lobe. For the AD group, [18F]FDG uptake was positively correlated with LM30 in the left temporal lobe and with RAVLT30 in the right frontal lobe, and [18F]florbetapir uptake was negatively correlated with LM30 scores in the right parietal and left frontal lobes. The results show that the association between regional brain metabolism and the severity of episodic memory deficits is dependent on the clinical disease stage, suggesting a dynamic relationship between verbal episodic memory deficits, AD pathophysiology, and clinical disease stages.

The Effect of TNF-alpha rs1800629 Polymorphism on White Matter Structures and Memory Function in Patients With Schizophrenia: A Pilot Study.

This study investigated the effect of TNF-α rs1800629 polymorphism on white matter integrity and memory function in patients with schizophrenia. Fifty-five participants with schizophrenia were enrolled in this study. They were genotyped for TNF-α rs1800629 polymorphism and underwent diffusion tensor imaging. Memory function was assessed using the Rey-Kim memory test. Participants with schizophrenia were grouped into GG homozygotes and A-allele carriers. Compared to GG homozygotes, A-allele carriers had significantly lower scores for immediate and delayed recall and recognition of verbal memory and showed significantly lower fractional anisotropy in extensive brain regions. Lower total scores in immediate and delayed recall of verbal memory, immediate recall of visual memory, and figure copy of visual memory were significantly correlated with decreased mean fractional anisotropy in the white matter tracts of the corresponding brain regions. Our findings suggest that the A-allele, which is associated with higher levels of TNF-α expression, correlates with lower connectivity of the fronto-temporal white matter compared to that in GG homozygotes. Impaired fronto-temporal connectivity may be associated with genetic vulnerability to schizophrenia, leading to verbal and visual memory deficits in patients with schizophrenia.

Neurocognitive correlates of the varied domains of outcomes at 20 year follow-up of first-episode psychosis

Little is known about long-term outcomes of the first episode of psychosis (FEP) other than in the symptomatic domain. We hypothesised that cognitive impairment is associated with poorer multi-domain outcomes at a long-term follow-up of FEP patients. We followed-up 172 FEP patients for a mean of 20.3 years. Ten outcome dimensions were assessed (symptomatic, functional and personal recovery, social disadvantage, physical health, suicide attempts, number of episodes, current drug use, chlorpromazine equivalent doses (CPZ), and schizophrenia/schizoaffective disorder final diagnosis). Cognition was assessed at follow-up. Processing speed and verbal memory deficits showed significant associations with poor outcomes on symptomatic, social functioning, social disadvantage, higher number of episodes, and higher CPZ. Significant associations were found between visual memory impairments were significantly associated with low symptomatic and functional recovery, between attentional deficits and a final diagnosis of schizophrenia/schizoaffective disorder, and between social cognition deficits and poor personal recovery.Lower cognitive global scores were significantly associated with all outcome dimensions except for drug abuse and physical status. Using multiple outcome dimensions allowed for the inclusion of the patients’ perspective and other commonly neglected outcome measures. Taken together, cognitive impairment in FEP patients is strongly related to poor performance on several outcome dimensions beyond symptomatic remission.