Cognitive Deficits In Patients Research Articles

Cognıtıve functıons in idiopathic intracranial hypertensıon.

Cognitive problems in idiopathic intracranial hypertension (IIH) is generally overlooked in the presence of disabling headache and threat to visual function. The aim of this study was to search for cognitive deficits in patients with IIH using neuropsychologic tests in addition to P300 potential recordings to assess cognition related brain activity. Fifty IIH patients were examined using Montreal Cognitive Assessment Test, Stroop Test and Visual Aural Digit Span Test to measure different domains of cognition at the time of diagnosis. P300 potentials were recorded by using an oddball paradigm. Hospital Anxiety and Depression Scalewas used to determine anxiety and depression. Quality of life (QoL) was assessed by SF-36. The results were compared with fifty healthy controls with matching age, gender and body mass index. Neuropsychologic tests revealed wide cognitive impairment including attention, working memory, executive function, naming, language, delayed recall and orientation in IIH patients. In addition, quality of life was affected in the sub-parameters of general health perceptions, emotional role functioning, vitality, mental health and bodily pain. P300 potential latencies were long and the amplitudes were reduced indicating deficits in attention and working memory. Anxiety scores were high, and health-related QoL was low mainly involving vitality, emotional and mental health. Cognitive dysfunction was not correlated with the levels of anxiety and the correlation with headache severity was mild. A multidomain cognitive decline mainly involving attention and working memory was recorded in IIH patients. It was not correlated with anxiety and only a mild correlation with headache severity was present which may indicate a casual relationship between raised intracranial pressure and cognitive deficits. Screening is important as neuropsychological rehabilitation might be relevant in these patients.

The thalamic covariance network is associated with cognitive deficits in patients with cerebral small vascular disease.

Abnormalities in the gray matter structure of cerebral small vessel disease (CSVD) have been observed throughout the brain. However, whether cortico-cortical connections exist between regions of gray matter atrophy in patients with CSVD has not been fully elucidated. This question was tested by comparing the gray matter covariance networks in CSVD patients with and without cognitive impairment (CI). We performed multivariate modeling of the gray matter volume measurements of 61 patients with CI (CSVD-CI), 85 patients without CI (CSVD-NC), and 108 healthy controls using source-based morphological analysis (SBM) to obtain gray matter structural covariance networks at the population level. Then, correlations between structural covariance networks and cognitive functions were analyzed in CSVD patients. Finally, a support vector machine (SVM) classifier was used with the gray matter covariance network as a classification feature to identify CI among the CSVD population. The results of the analysis of all the subjects showed that compared with healthy controls, the expression of the thalamic covariance network, cerebellum covariance network, and calcarine cortex covariance network was reduced in patients with CSVD. Moreover, CSVD-CI patients showed a significant reduction in the expression of the thalamic covariance network, encompassing the thalamus and the parahippocampal gyrus, relative to CSVD-NC patients, which persisted after excluding CSVD patients with thalamic lacunes. In patients with CSVD, cognitive functions were positively correlated with measures of the thalamic covariance network. More than 80% of CSVD patients with CI were correctly identified by the SVM classifier. Our findings provide new evidence to explain the distribution state of gray matter reduction in CSVD patients, and the thalamic covariance network is the core region for early gray matter reduction during the development of CSVD disease, which is related to cognitive deficits. Reduced expression of thalamic covariance networks may provide a neuroimaging biomarker for the early identification of cognitive impairment in CSVD patients.

Cognitive Outcomes of Children With Sagittal Craniosynostosis Treated With Either Endoscopic or Open Calvarial Vault Surgery

Several studies have reported a higher incidence of neurodevelopmental delays and cognitive deficits in patients with single-suture craniosynostosis; however, there are few studies examining the associations of repair type with cognitive outcomes. To measure differences in neuropsychological outcomes between school-age children who were treated for sagittal craniosynostosis and unaffected controls and explore differences in cognitive function among children with sagittal craniosynostosis who were previously treated with either endoscopic strip craniectomy or open calvarial vault surgery. This cohort study was performed between 2018 and 2022. Eligible participants included patients aged 5 to 17 years who had previously been seen as infants or toddlers (<3 years) at 1 of 3 surgical centers for craniosynostosis repair with either endoscopic surgery or open calvarial vault surgery. A separate cohort of unaffected controls were included for comparison. Data analysis was conducted from November 2023 to February 2024. Open calvarial vault surgery or endoscopic repair for single-suture craniosynostosis. The primary outcome was the Differential Ability Scales-II (DAS-II) General Conceptual Ability (GCA) score, an index for overall intellectual ability. Secondary outcomes included DAS-II subscale scores (Verbal Ability, Nonverbal Reasoning, Spatial Ability, Working Memory, and Processing Speed), and Patient-Reported Outcomes Measurement Information System (PROMIS) cognitive function scores. A total of 81 patients with sagittal craniosynostosis (59 male [73%]; 22 female [27%]) and 141 controls (81 male [57%]; 60 female [43%]) were included. Of the 81 participants with sagittal craniosynostosis, 46 underwent endoscopic repair and 35 underwent open repair. Median (range) age at time of follow-up assessment was 7.7 (5.0-14.8) years for children with sagittal craniosynostosis and median age at assessment was 8.5 (7.7-10.5) years for controls. After controlling for age at assessment, sex, and socioeconomic status, there was no statistically significant or clinically meaningful difference in GCA scores between children who underwent endoscopic repair (adjusted mean score, 100; 95% CI, 96-104) and open repair (adjusted mean score, 103; 95% CI, 98-108) (P > .99). We found no significant difference in PROMIS scores between repair types (median [range] for endoscopic repair 54 [31-68] vs median [range] for open repair 50 [32-63]; P = .14). When comparing the treatment groups with the unaffected controls, differences in subscale scores for GCA and working memory were observed but were within normal range. In this cohort study, there were no statistically or clinically significant differences in cognitive outcomes among school-age children by and type of surgical procedure used to repair nonsyndromic sagittal craniosynostosis. These findings suggest primary care clinicians should be educated about different options for craniosynostosis surgery to ensure early referral of these patients so that all treatment options remain viable.

Uremic toxins and the brain in chronic kidney disease.

Chronic kidney disease (CKD) patients have an increased risk for cognitive impairment compared to the general population. The risk is much higher in CKD patients who progress to end-stage kidney disease (ESKD) and require hemodialysis or peritoneal dialysis. Multiple factors maycontribute to cognitive impairment in CKD patients and in patients on chronic dialysis. However, the observation that, after kidney transplantation, there is an improvement in several cognitive performance markers and that some structural and functional brain abnormalities mayimprove suggests that cognitive deficits in patients on dialysis may be at least partially reversible. Recent evidence supports the hypothesis that uremic toxins may disrupt the blood brain barrier and damage the brain cells. Such brain toxicity should prompt efforts to lower the burden of uremic toxins through dialytic and non-dialytic strategies.

Remote digital cognitive assessment reveals cognitive deficits related to hippocampal atrophy in autoimmune limbic encephalitis: a cross-sectional validation study

Autoimmune limbic encephalitis (ALE) is a neurological disease characterised by inflammation of the limbic regions of the brain, mediated by pathogenic autoantibodies. Because cognitive deficits persist following acute treatment of ALE, the accurate assessment of long-term cognitive outcomes is important for clinical assessments and trials. However, evaluating cognition is costly and an unmet need exists for validated digital methods. In this cross-sectional validation study, we investigated whether a remote digital platform could identify previously characterised cognitive impairments in patients with chronic ALE and whether digital metrics would correlate with standard neuropsychological assessment and hippocampal volume. Patients with ALE who had a chronic and stable presentation and received a clinical diagnosis of ALE were recruited for this study. The cognitive performance of 21 patients with ALE and 54 age-matched healthy controls - enrolled via the University of Oxford (UK) Cognitive Neurology Lab testing programme - was assessed with a battery of 12 cognitive tasks from the Cognitron online platform. The platform was optimised with National Institute for Health and Care Research (NIHR) support to be deliverable remotely to elderly and patient groups. The primary outcome measure was behavioural performance and corresponding neuroimaging and neuropsychological assessment metrics. Between February 15, 2021, and April 21, 2022, 21 patients with ALE (mean age 63.01 years, 14 males) and 54 healthy controls (mean age 65.56 years, 23 males) completed the digital cognitive assessment. Patients with ALE performed significantly worse in memory, visuospatial abilities, executive function, and language. No impairments in digit & spatial span, target detection (attention) and emotion discrimination were observed. The global score on the online cognitive tasks correlated significantly with the established Addenbrooke's Cognitive Examination III (ACE) pen-and-paper test. Deficits in visuospatial processing and language were identified in ALE compared to controls using remote digital testing but not using the ACE, highlighting higher sensitivity of computerised testing to residual cognitive impairment. Finally, the hippocampal volumes of patients with ALE and healthy controls correlated with online cognitive scores. These findings demonstrate that subtle cognitive deficits in patients with chronic ALE, who often show full recovery in measures of disability and dependence on daily activities, are detectable using a remote online platform, which also relates to hippocampal atrophy. Such methods may facilitate the characterisation of cognitive profiles in complex neurological diseases. Future longitudinal studies designed to assess the utility of such digital methods for further clinical characterisation are needed. The Wellcome Trust, Medical Research Council, National Institute for Health Research, Rhodes Scholarship, and the Berrow Foundation Scholarship.

Factors Associated with Cognitive Impairment in Patients with Persisting Sequelae of COVID-19

ObjectiveQuantify cognitive deficits in patients with postacute sequelae of COVID-19 (PASC) and identify key variables related to cognitive impairment in PASC. MethodPatients with polymerase chain reaction-confirmed COVID-19 underwent a comprehensive neuropsychological evaluation. The comparison group included patients without neurological disorders determined by the neuropsychologist to be cognitively intact. Cognitive impairment was defined as impairment (Composite T ≤35) in 1 of 6 cognitive domains. The PASC group was split into impaired or intact based on the above criteria. Multivariable logistic regression models assessed predictors including demographics, COVID-19 severity, clinical characteristics, and mood. ResultsThere were 210 patients with PASC, predominantly female (73.3%, P < .001), without other demographic differences when compared with 369 normal controls. Patients with PASC were more likely to have cognitive impairment (odds ratio 3.61; 95% confidence interval, 2.36-5.54; P < .001) compared with controls, with significantly lower scores in domains of memory, language, processing speed, visuospatial function, executive function (P < .001), and higher depressive (P = .004) and anxiety symptoms (P = .003). Patients with PASC who demonstrated cognitive impairment (n = 93) had higher body mass index compared with those with PASC without cognitive impairment (n = 117), without differences in other predictors. ConclusionPatients with PASC are almost 4 times more likely to evidence cognitive dysfunction compared with normal controls. Forty-four percent of patients with PASC demonstrated cognitive deficits about 7 months from infection. Estimated premorbid intelligence significantly correlated with impairment. Higher body mass index was the only metric shown to differentiate those with PASC and cognitive impairment from those with PASC who were cognitively intact.

Robotic assessment of sensorimotor and cognitive deficits in patients with temporal lobe epilepsy

ObjectiveIndividuals with temporal lobe epilepsy (TLE) frequently demonstrate impairments in executive function, working memory, and/or declarative memory. It is recommended that screening for cognitive impairment is undertaken in all people newly diagnosed with epilepsy. However, standard neuropsychological assessments are a limited resource and thus not available to all. Our study investigated the use of robotic technology (the Kinarm robot) for cognitive screening. Methods27 participants with TLE (17 left) underwent both a brief neuropsychological screening and a robotic (Kinarm) assessment. The degree of impairments and correlations between standardized scores from both approaches to assessments were analysed across different neurocognitive domains. Performance was compared between people with left and right TLE to look for laterality effects. Finally, the association between the duration of epilepsy and performance was assessed. ResultsAcross the 6 neurocognitive domains (attention, executive function, language, memory, motor and visuospatial) assessed by our neuropsychological screening, all showed scores that significantly correlated with Kinarm tasks assessing the same cognitive domains except language and memory that were not adequately assessed with Kinarm. Participants with right TLE performed worse on most tasks than those with left TLE, including both visuospatial (typically considered right hemisphere), and verbal memory and language tasks (typically considered left hemisphere). No correlations were found between the duration of epilepsy and either the neuropsychological screening or Kinarm assessment. SignificanceOur findings suggest that Kinarm may be a useful tool in screening for neurocognitive impairment in people with TLE. Further development may facilitate an easier and more rapid screening of cognition in people with epilepsy and distinguishing patterns of cognitive impairment.

Stakeholder Engagement to Identify Implementation Strategies to Overcome Barriers to Delivering Chronic Pain Treatments: A NIDILRR and VA TBI Model Systems Collaborative Project.

The purpose of this article is to illustrate the process of stakeholder-engaged intervention mapping approach to identify implementation strategies to overcome data-driven prioritized barriers to receiving chronic pain services for persons with traumatic brain injury (TBI). Community. Healthcare providers (n = 63) with 2 or more years' experience treating persons with TBI, interviewed between October 2020 and November 2021 provided data for identification of barriers. TBI, chronic pain, and qualitative research subject matter experts (SMEs) participated in the mapping approach. Participatory-based research design, using descriptive and intervention mapping approaches. Four barriers to accessing chronic pain treatment by persons with TBI which emerged from provider interviews were prioritized for intervention mapping: cognitive deficits of patients (67%); patient comorbidities (63%); mental health and/or substance abuse issues (59%); and patient participation (62%). SMEs used prioritized barriers to develop 4 primary objectives and implementation strategies designed to: (1) engage consumers to validate and identify strategies; (2) tailor pain treatment and delivery to overcome barriers; (3) develop and disseminate guidelines and best practices when delivering care to persons with TBI to support spread; and (4) increase awareness, skills, and readiness of workforce to deliver pain treatment to persons with TBI. SMEs used an evidence-based approach to develop a mapping matrix of the prioritized barriers, implementation objectives, and aligned implementation strategies to impact change. Implementation science is needed to facilitate knowledge translation into practice for this complex population to overcome barriers to care. Implementation strategies to address barriers to accessing chronic pain care for individuals with TBI were chosen through a participatory approach to engaging SMEs to support these rehabilitation implementation efforts. Future work includes gathering input from individuals with TBI and chronic pain and to move the intervention (implementation) mapping matrix forward to inform future implementation research, policy, and practice.

Dysfunction of the triple-network model is associated with cognitive impairment in patients with cerebral small vessel disease

PurposeThis study aimed to demonstrate the correlations between the altered functional connectivity patterns in the triple-network model and cognitive impairment in patients with cerebral small vascular disease (CSVD). MethodsResting-state functional magnetic resonance imaging data were obtained from 22 patients with CSVD and 20 healthy controls. The resting-state data were analyzed using independent component analysis and functional network connectivity (FNC) analysis to explore the functional alterations in the intrinsic triple-network model including the salience network (SN), default mode network (DMN), and central executive network (CEN), and their correlations with the cognitive deficits and clinical observations in the patients with CSVD. ResultsCompared to the healthy controls, the patients with CSVD exhibited increased connectivity patterns in the CEN-DMN and decreased connectivity patterns in the DMN-SN, CEN-SN, intra-SN, and intra-DMN. Significant negative correlations were detected between the intra-DMN connectivity pattern and the Montreal Cognitive Assessment (MoCA) total scores (r = −0.460, p = 0.048) and MoCA abstraction scores (r = −0.565, p = 0.012), and a positive correlation was determined between the intra-SN connectivity pattern and the MoCA abstraction scores (r = 0.491, p = 0.033). ConclusionsOur study findings suggest that the functional alterations in the triple-network model are associated with the cognitive deficits in patients with CSVD and shed light on the importance of the triple-network model in the pathogenesis of CSVD.

Постковидный синдром: от биологии к нейропсихологии

Background. Postcovid syndrome or Long COVID is a new term introduced into medical practice by WHO after the COVID -19 pandemic. Long COVID affects patients who have recovered from COVID -19. Objectives. The purpose of this work is to understand cognitive deficits caused by COVID-19 from the point of view of neuropsychology and pathophysiology. Data Sources. Literature search was conducted in the following electronic databases: Pubmed, Google.scholar and Scopus databases. 63 articles were selected. Keywords for the literature review included “neuropsychiatry/neuropsychology”, “pathophysiology”, “COVID-19”, “SARS-CoV-2”. Methods. Review and analysis of COVID-19 studies in terms of its relation to the appearance of cognitive deficits in patients. Results. The SARS-CoV-2 virus enters the human body and affects the structures of the brain. Some of the symptoms such as fatigue, shortness of breath, problems with concentration and memory, loss or change of taste and smell, pain in muscles and joints as well as sleep disorders are preserved in post-COVID period and may be explained by the peculiarity of the virus interaction with central nervous system. Neuropsychological analysis of observed disorders based on the theory of three functional blocks of the brain by A. R. Luria helps to identify the affected zones of the functional systems of higher mental functions (HMF). Neuropsychological assessment makes it possible to plan rehabilitation programme or cognitive training, and help doctor in choosing an adequate drug therapy to compensate for cognitive impairment. Conclusions. SARS-CoV-2 causes damage to brain structures such as the brainstem, limbic system, prefrontal cortex and olfactory tract, which explains the observed symptoms. Neuropsychological diagnostics makes it possible to identify the impaired component of the HMF in patients with post-COVID syndrome, to plan an adequate rehabilitation programme, as well as to choose drug therapy.

NLRP3-GSDMD-dependent IL-1β Secretion from Microglia Mediates Learning and Memory Impairment in a Chronic Intermittent Hypoxia-induced Mouse Model

Hypoxia/reoxygenation caused by chronic intermittent hypoxia (CIH) plays an important role in cognitive deficits in patients with obstructive sleep apnea. However, the precise underlying mechanism remains unclear. This study investigated whether the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is involved in CIH-induced spatial learning and memory impairment in mice, and the possible underlying upstream and downstream mechanisms. The C57BL/6 male mice were exposed to CIH (21% O2-6% O2, 4 min/cycle, 8 h/day) for 9 weeks to investigate the role of NLRP3 in CIH-induced spatial learning and memory impairment in mice. BV2 cells were exposed to intermittent hypoxia (21% O2-1% O2, 90 min/cycle) for 48 h to investigate the possible mechanisms in vitro. We found that: 1) inhibition of NLRP3 inflammasome activation improved CIH-induced spatial learning and memory impairment in mice. 2) CIH damaged hippocampal neurons but increased the number of microglia in mice hippocampi; CIH activated microglia-specific NLRP3 inflammasome, leading to upregulation of matured IL-1β and N-GSDMD. 3) intermittent hypoxia activated NLRP3 inflammasome via the ROS-NF-κB signaling pathway to promote the release of matured IL-1β from microglia in a GSDMD-dependent manner without pyroptosis. 4) The IL-1β released from microglia might impair the synaptic plasticity of hippocampal CA3-CA1 synapses by acting on IL-1 receptors in hippocampal neurons. Our findings reveal that ROS-NF-κB-NLRP3 inflammasome-GSDMD dependent IL-1β release from microglia may participate in CIH-induced spatial learning and memory impairment by acting on hippocampal neuronal IL-1 receptor, leading to synaptic plasticity impairment.

Imaging diagnosis and emotion recognition relationship in mild cognitive impairment

AbstractBackgroundRecent research has focused attention on social cognition impairment in Alzheimer Disease (AD). Specifically, emotion recognition can be evaluated with Reading the Mind in the Eyes Test (RMET). Some neuroanatomical changes could be related with social and cognitive deficits in patients. Therefore, future research combining cognitive indicators (RMET) with brain structure and function parameters (volumes, glucose metabolism, blood flow, amyloid deposits…) is required.MethodParticipants are patients from the Neurology Unit (Hospital Universitari i Politècnic La Fe). They were neuropsychologically evaluated, and CSF samples were obtained to determine some biomarkers (β‐amyloid‐42, β‐amyloid‐40, p‐Tau…). Also, brain imaging techniques (magnetic resonance (MR) and Positron Emission Tomography with [18F]Fluorodeoxyglucose (FDG‐PET/CT)) were applied to obtain brain structural and functional information, and to evaluate the relationship between them and emotion recognition evaluation (RMET). Imaging data were processed following SPM and CAT12 pipelines, a brain parcellation based on the Hammers atlas was used. Finally, 166 patients (with MR and/or FDG‐PET/CT) diagnosed with mild cognitive impairment (MCI) were included in the study.ResultThe correlation analysis between FDG‐PET/CT and RMET results showed significant correlations. Specifically, with prefrontal medial L and R (r = 0.36), posterior cingulate L and R (r = 0.34), parietal inferior L and R (r = 0.31), anterior cingulate L and R (r = 0.32), prefrontal lateral L and R (r = 0.32), insula R (r = 0.31) and basal ganglia R (r = 0.3). So, they are considered potential brain function biomarkers in MCI. Regarding the correlation analysis between MR (GM volumes (TIV‐corrected)) and RMET results, some significant correlations were observed. Specifically, with the straight gyrus L (r = 0.40), superior frontal gyrus L (r = 0.37), insula anterior inferior cortex R (r = 0.36), fusiform gyrus R (r = 0.36), anterior cingulate gyrus R (r = 0.36), insula anterior short gyrus L (r = 0.36), posterior and anterior cingulate gyrus L (r = 0.36, 0.35), and anterior orbital gyrus L (r = 0.35). So, they are considered potential brain structure biomarkers in MCI.ConclusionThe relationship between brain imaging parameters and emotion recognition impairment variables could provide important information for further biomarkers identification, as well as to identify potential physiopathological mechanisms involved in neurodegenerative development since early steps.

Unlocking cognition with pulsatile GnRH in Down Syndrome: implications for Alzheimer’s disease

AbstractBackgroundThere is currently no viable treatment for the cognitive and olfactory deficits of Trisomy 21 and Alzheimer’s disease.MethodPhysiological characterization and epigenetic, cellular, chemogenetic, and pharmacological interventions in male and female Ts65Dn mice (P9‐P360), a mouse model of Down syndrome, and 12‐month‐old THY::TAU22 male mice, a mouse model of Alzheimer’s disease, and their wild‐type littermates. Seven men with Down syndrome (20‐50 years of age) were enrolled in an open‐label pilot study to assess the effect of 6‐month pulsatile GnRH therapy on cognitive and olfactory function.ResultWe show in Ts65Dn mice that olfactory and cognitive neurological symptoms are closely related to a post‐pubertal decrease in hypothalamic and extra‐hypothalamic expression of a master molecule controlling reproduction ‐ gonadotropin‐releasing hormone (GnRH) ‐ and appear to be linked to an imbalance in a microRNA‐gene network known to regulate the maturation of GnRH neurons as well as to an alteration in hippocampal synaptic transmission. Restoring physiological GnRH levels abolishes olfactory and cognitive deficits in Ts65Dn and THY::TAU22 mice, while pulsatile GnRH treatment improves cognition and brain connectivity in adult T21 patients.ConclusionWe have discovered that GnRH plays a crucial role in olfaction and cognition, and pulsatile GnRH treatment holds promise for improving cognitive deficits in patients with Down syndrome. Such treatment could potentially also be beneficial for mobilizing cognitive reserve in pathological brain aging such as that found in Alzheimer’s disease.

A systematic review of drug interventions to enhance cognition in patients with primary central nervous system infections

AbstractBackgroundAlthough drug therapy is part of the clinical routine for individuals with central nervous system (CNS) infections, its efficacy with respect to cognitive impairments has not been systematically studied. We aimed to synthesize the evidence for optimal treatment decisions.MethodWe searched for experimental studies published in English prior to October 2021 in MEDLINE, Embase and Cochrane databases. We selected non‐randomized studies (NRS) and randomized control trials (RCT) of a drug efficacy versus placebo, another drug, or a combination of drugs. The certainty of the evidence was rated according to GRADE guidelines.ResultWe included eight RCTs and one NRS, involving a total of 805 patients (50.77% male patients; mean age 42.67±10.58; duration (in years) of primary CNS infections 4.69±3.16) with Lyme disease (LD), herpes simplex virus type 1 (HSV‐1), or Creutzfeldt–Jakob disease (CJD) studying the efficacy of antibiotics, antiviral, and non‐opioid analgesic drugs, respectively. The duration of the interventions varied, depending on the type of CNS infection and class of drug, with a range between four weeks in patients with LD treated with antibiotics and 18 weeks in patients with HSV‐1 treated with an antiviral drug. In patients with LD, antibiotics alone or in combination with other drugs enhanced certain cognitive domains relative to placebo. In patients with HSV‐1, the results were inconsistent. In patients with CJD, flupirtine maleate enhanced baseline cognitive scores. Of the available evidence, only one study had “low” risk of bias. An important limitation of the included studies was the lack of consistent reporting of adverse effects and safety parameters, which must be addressed in future work.ConclusionThere is not enough existing evidence of sufficient quality to support the use of antimicrobials and non‐opioid analgesics in combatting cognitive deficits in patients with LD, HSV‐1, or CJD. Future clinical trials enrolling participants at earlier stages of primary CNS infections, at the time of greatest inflammation, and which address the elements of biases found in the existing clinical trials, are warranted.

Attitude to the disease and quality of life in elderly patients with mild vascular dementia after the novel coronavirus infection

In order to study the types of attitude towards the disease and quality of life (QoL) in elderly patients with mild vascular dementia (MVD) living in the conditions of the psychoneurological institution Social Service House “Severnoye Izmailovo” in Moscow, there were 2 study groups: the patients with the clinical debut of the novel coronavirus infection (NCVI) of 6 months +/– 1 month with the recovery outcome (n=65; 33 men, 32 women) and those who did not have COVID-19 (hospital control group; n=67; 34 men, 33 women). The mean age of the studied patients was 73.05±3.48 years. The age and sex composition of the two groups was homogeneous (p&gt;0.05). Emotional disorders were investigated using the Cornell Scale for Depression in Dementia (CSDD); cognitive disorders – by means of the Montreal Cognitive Assessment (MoCA); QoL – by the Quality of Life in Alzheimer's Disease scale (QoL-AD): QoL self-assessment (QoL-AD-SR (self-rating)) and proxy QoL rating (QoL-AD-PR (proxy rating)); the type of attitude towards the disease – by the TATD scale (Wasserman L.I. et al., 2005). It was found that COVID-19 aggravates cognitive deficits in patients with MVD (according to MoCA 20.80±0.59 /21.40±0.78 points; p&lt;0.05) in the absence of depression (according to CSDD 1.52±0.50 / 1.52±0.84 points in the group of the patients after NCVI / hospital control group, respectively; p&gt;0.05). In the patients after COVID-19, a correlation was found between the proxy QoL rating and the severity of cognitive dysfunction according to the MoCA (R= – 0.28), while in the hospital control group – between the proxy QoL rating and the severity of depressive manifestations (R= – 0.33). The first group of the patients was characterized by a mixed type of attitude to the disease and intrapsychic maladaptation (the neurasthenic type ranked first at 16.03±8.29 / 9.34±5.03 points), while the second group had a diffuse type of attitude to the disease and interpsychic maladaptation (the sensitive type ranked first at 10.31±5.71 / 14.90±7.62 points by the TATD scale among the elderly patients with MVD who have / have not undergone NCVI; p&lt;0.05). The revealed patterns can contribute to the optimization of personalized models of medical and psychological rehabilitation of elderly patients with MVD living in closed-type care facilities.

IC3 protocol: a longitudinal observational study of cognition after stroke using novel digital health technology

IntroductionStroke is a major cause of death and disability worldwide, frequently resulting in persistent cognitive deficits among survivors. These deficits negatively impact recovery and therapy engagement, and their treatment is...

Dynamic brain activity states of memory impairment in stroke patients with varying motor outcomes.

The objective of this study was to characterize the alteration patterns of dynamic spatiotemporal activity in chronic subcortical stroke patients with varying motor outcomes, while investigating the imaging indicators relevant to the assessment of potential cognitive deficits in these patients. A total of 136 patients and 88 normal controls were included in the analysis of static and dynamic intrinsic brain activity, determined by amplitude of low-frequency fluctuations. The findings unveiled that subcortical stroke patients exhibited significantly aberrant temporal dynamics of intrinsic brain activity, involving regions within multiple brain networks. These spatiotemporal patterns were found to be contingent upon the side of the lesion. In addition, these aberrant metrics demonstrated potential in discerning cognitive deficits in stroke patients with memory impairment, with the dynamic indices exerting more influence than the static ones. The observe findings may indicate that subcortical stroke can trigger imbalances in the segregation and integration of spatiotemporal patterns across the entire brain with multi-domain networks, especially in patients with poor motor outcomes. It suggests that the temporal dynamics indices of intrinsic brain activity could serve as potential imaging indicators for assessing cognitive impairment in patients with chronic subcortical stroke, which may be associated with the motor outcomes.

53 Working Memory Network Load Engagement in Schizophrenia

Objective:Cognitive deficits in patients diagnosed with schizophrenia are a core feature of the disorder. There are currently no treatments for these cognitive deficits. Our aim was to examine and compare patterns of increased versus decreased activity in the central executive network (CEN), salience network (SN), and default mode network (DMN) between healthy controls (HCs) and patients diagnosed with schizophrenia (SZs) as well as to explore the influence of task load on these networks between HCs and SZs.Participants and Methods:Analyses focused on a secondary dataset comprising Blood Oxygen-Level Dependent (BOLD) data collected from 25 HCs and 27 SZs who completed a working memory (WM) task (N-back) with 5 load conditions while undergoing functional magnetic resonance imaging (fMRI). Region of interest (ROI) data were analyzed using linear mixed-effects models.Results:Group activation differences were found in the posterior salience network (pSN), default mode network (DMN), dorsal default mode network (dDMN), and ventral default mode network (vDMN) showing greater activity for SZs. Specifically, pSN, DMN, dDMN, and vDMN all showed increased activity in SZs compared to HCs. The curve of brain activity was consistent between HCs and SZs with the exception of the vDMN, where HCs show greater activation at modest mental workload (quadratic curve) and SZs showed greater brain activation at lower mental workload (linear). In the CEN, there were no group differences, and the response curve was the same for both groups.Conclusions:These group differences demonstrate network difference between HCs and SZs and could show value in treatments targeting cognitive deficits in SZs from a large-scale brain network connectivity perspective. Future studies are needed to confirm these results with larger sample size in order to examine potential subtleties of interactions between these networks.

68 Preliminary Evidence of a Therapeutic Effect of Electrical Neuromodulation on Cognitive Deficits in Patients with Mild Cognitive Impairment

Objective:Episodic memory functioning is distributed across two brain circuits, one of which courses through the dorsal anterior cingulate cortex (dACC). Thus, delivering non-invasive neuromodulation technology to the dACC may improve episodic memory functioning in patients with memory problems such as in amnestic mild cognitive impairment (aMCI). This preliminary study is a randomized, double-blinded, sham-controlled clinical trial to examine if high definition transcranial direct current stimulation (HD-tDCS) can be a viable treatment in aMCI.Participants and Methods:Eleven aMCI participants, of whom 9 had multidomain deficits, were randomized to receive 1 mA HD-tDCS (N=7) or sham (N=4) stimulation. HD-tDCS was applied over ten 20-minute sessions targeting the dACC. Neuropsychological measures of episodic memory, verbal fluency, and executive function were completed at baseline and after the last HD-tDCS session. Changes in composite scores for memory and language/executive function tests were compared between groups (one-tailed t-tests with a = 0.10 for significance). Clinically significant change, defined as &gt; 1 SD improvement on at least one test in the memory and non-memory domains, was compared between active and sham stimulation based on the frequency of participants in each.Results:No statistical or clinically significant change (N-1 X2; p = 0.62) was seen in episodic memory for the active HD-tDCS (MDiff = 4.4; SD = 17.1) or sham groups (MDiff = -0.5; SD = 9.7). However, the language and executive function composite showed statistically significant improvement (p = 0.04; MDiff = -15.3; SD = 18.4) for the active HD-tDCS group only (Sham MDiff = -5.8; SD = 10.7). Multiple participants (N=4) in the active group had clinically significant enhancement in language and executive functioning tests, while nobody in the sham group did (p = 0.04).Conclusions:HD-tDCS targeting the dACC had no direct benefit for episodic memory deficits in aMCI based on preliminary findings for this ongoing clinical trial. However, significant improvement in language and executive function skills occurred in response to HD-tDCS, suggesting HD-tDCS in this configuration has promising potential as an intervention for language and executive function deficits in MCI.

Prevalence, correlates and explanatory models of cognitive deficits in patients with schizophrenia-A cross sectional study.

Schizophrenia may cause significant impairment in social and economic aspects of a patient's life. Current evidence suggests that cognitive deficits may affect the functioning of a person with schizophrenia more than positive or negative symptoms. There is a lack of literature on explanatory models of cognitive deficits in schizophrenia that can influence help-seeking behavior. This study aimed to estimate the prevalence of cognitive deficits and assess their relationship with socio-demographic and clinical characteristics among patients with schizophrenia. We also planned to explore the explanatory models of cognitive deficits in these patients. Consecutive outpatients with schizophrenia who met eligibility criteria were recruited after obtaining informed consent. The Addenbrooke's Cognitive Examination Tamil version (ACE III) and Observable Social Cognition - A Rating Scale (OSCARS) and Positive and Negative Symptom Scale (PANSS) were used to assess cognitive functioning and symptom profile, respectively. Beliefs about illness were recorded using the modified Short Explanatory Model Interview (SEMI). Socio-demographic and treatment-related details were collected with a structured proforma. Statistical analysis was done using SPSS for Windows (version 16.0.1). One hundred and forty patients participated in the study. The prevalence of cognitive deficits was 75.7% using ACE-III scores, 19.3% on OSCARS, and 40% based on subjective reports. Though the majority (81.4%) of patients reported a medical explanatory model for cognitive impairment, a significant number of them (70.7%) also held non-medical models simultaneously. Cognitive deficits are prevalent in the majority of patients with schizophrenia. Poor test performance on cognitive testing was observed in those with a significant family history. Multiple contradictory explanatory models for the causation of cognitive deficits were reported.