Neurocognitive Symptoms Research Articles

Impaired health-related quality of life in long-COVID syndrome after mild to moderate COVID-19

A growing number of patients with SARS-CoV-2 infections experience long-lasting symptoms. Even patients who suffered from a mild acute infection show a variety of persisting and debilitating neurocognitive, respiratory, or cardiac symptoms (Long-Covid syndrome), consequently leading to limitations in everyday life. Because data on health-related quality of life (HRQoL) is scarce, we aimed to characterize the impact of Long-Covid symptoms after a mild or moderate acute infection on HRQoL. In this observational study, outpatients seeking counseling in the interdisciplinary Post-Covid consultation of the University Hospital Zurich with symptoms persisting for more than 4 weeks were included. Patients who received an alternative diagnosis or suffered from a severe acute Covid-19 infection were excluded. St. George’s Respiratory Questionnaire (SGRQ), Euroquol-5D-5L (EQ-5D-5L), and the Short form 36 (SF-36) were distributed to assess HRQoL. 112 patients were included, 86 (76.8%) were female, median (IQR) age was 43 (32.0, 52.5) years with 126 (91, 180) days of symptoms. Patients suffered frequently from fatigue (81%), concentration difficulties (60%), and dyspnea (60%). Patients mostly stated impairment in performing usual activities and having pain/discomfort or anxiety out of the EQ-5D-5L. EQ index value and SGRQ activity score component were significantly lower in females. SF-36 scores showed remarkably lower scores in the physical health domain compared to the Swiss general population before and during the COVID-19 pandemic. Long-Covid syndrome has a substantial impact on HRQoL. Long-term surveillance of patients must provide clarity on the duration of impairments in physical and mental health.Trial registration: The study is registered on www.ClinicalTrials.gov, NCT04793269.

On the relationship between neurocognitive measures and olfactory dysfunction in COVID-19 patients with and without anosmia

One of the predominant symptoms of the COVID-19 virus is the complete (anosmia) or partial (hyposmia) loss of smell. Anosmia may be a critical neurocognitive symptom because there is an empirically demonstrated association of anosmia with neurodegenerative diseases like Parkinson's disease, Alzheimer's disease, etc. The present study assessed the neurocognitive disorder patterns in recovered COVID-19 patients who either self-reported anosmia or its absence. Of the 60 adult participants (n = 32 males, n = 28 females; Mage = 20.78 years, range = 18–31 years), 15 reported COVID-19 induced anosmia, 15 reported COVID-19 without anosmia, and 30 reported not having contracted COVID-19. The participants were first administered a 10-item smell test, and analysis of variance revealed significantly better scores for the control group than the other two groups. Further, there was no significant difference in smell scores between the patients who self-reported anosmia or denied it. This statistical pattern was consistent across all neuropsychological tests: short- and long-term verbal memory, digit span, Trail Making, and a self-report 46-item neurocognitive scale. Regardless of the self-report of anosmia or denial, all thirty COVID-19 patients scored significantly poorer than the control group on all of the tests and neurocognitive scale. In summary, the self-report of anosmia appears to be unreliable, and the COVID-19 patients who were found to be anosmic on the initial objective smell test demonstrated poorer neuropsychological performance than controls.

The comorbidity of depression and neurocognitive disorder in persons with HIV infection: call for investigation and treatment.

Depression and neurocognitive disorder continue to be the major neuropsychiatric disorders affecting persons with HIV (PWH). The prevalence of major depressive disorder is two to fourfold higher among PWH than the general population (∼6.7%). Prevalence estimates of neurocognitive disorder among PWH range from 25 to over 47% - depending upon the definition used (which is currently evolving), the size of the test battery employed, and the demographic and HIV disease characteristics of the participants included, such as age range and sex distribution. Both major depressive disorder and neurocognitive disorder also result in substantial morbidity and premature mortality. However, though anticipated to be relatively common, the comorbidity of these two disorders in PWH has not been formally studied. This is partly due to the clinical overlap of the neurocognitive symptoms of these two disorders. Both also share neurobehavioral aspects - particularly apathy - as well as an increased risk for non-adherence to antiretroviral therapy. Shared pathophysiological mechanisms potentially explain these intersecting phenotypes, including neuroinflammatory, vascular, and microbiomic, as well as neuroendocrine/neurotransmitter dynamic mechanisms. Treatment of either disorder affects the other with respect to symptom reduction as well as medication toxicity. We present a unified model for the comorbidity based upon deficits in dopaminergic transmission that occur in both major depressive disorder and HIV-associated neurocognitive disorder. Specific treatments for the comorbidity that decrease neuroinflammation and/or restore associated deficits in dopaminergic transmission may be indicated and merit study.

Cognitive inhibition deficit in long COVID-19: An exploratory study.

An increasing number of research studies point toward the importance and prevalence of long-term neurocognitive symptoms following infection with COVID-19. Our objectives were to capture the prevalence of cognitive impairments from 1 to 16 months post-COVID-19 infection, assess the changes in neuropsychological functions over time, and identify factors that can predict long-term deficits in cognition. A cross-sectional research design was adopted to compare four sub-samples recruited over a 16-month timeframe (1-4, 5-8, 9-12, and 13-16 months). Phone interviews were conducted at least 6 weeks after being infected by COVID-19. Sociodemographic and clinical questionnaires were administered followed by standardized neurocognitive and psychological tests and health questionnaires screening cognitive symptoms, anxiety, depression, fatigue, and autonomy. Regarding general health questionnaires, 55.2% of the 134 participants had symptoms of psychiatric illness, while 21.6% of patients had moderate-to-severe anxiety or depression. Cognitive efficiency was diminished in 19.4% of our population. Executive dysfunction was screened in 56% of patients, and an impairment of cognitive flexibility and inhibition was revealed in 38.8%. Depression, hospital or intensive care unit (ICU) admission, and the duration of hospital or ICU stay were associated with an inhibition deficit. The duration elapsed from the initial infection, and the neurocognitive assessment was not associated with a decrease in inhibition deficit. The prevalence of cognitive impairments, other than inhibition deficit, tended to decrease during the study period. This study supports the extensive literature on the cognitive and neuropsychiatric sequelae of COVID-19 and highlights long-lasting inhibition deficits, while other cognitive functions seemed to improve over time. The severity of infection could interact as a catalyst in the complex interplay between depression and executive functions. The absence of a relation between inhibition deficits and sociodemographic or medical factors reinforces the need for cognitive screening in all COVID-19 patients. Future research should focus on inhibition deficits longitudinally to assess the progression of this impairment.

Low Vitamin D Levels Are Associated With Long COVID Syndrome in COVID-19 Survivors.

Long COVID is an emerging syndrome affecting 50% to 70% of COVID-19 survivors that still lacks predicting factors. Due to the extraskeletal effects of vitamin D, we retrospectively assessed the association between 25(OH) vitamin D levels and long COVID in COVID-19 survivors 6 months after hospitalization. Long COVID was defined according to NICE guidelines. Fifty long COVID and 50 non-long-COVID subjects matched on a 1:1 basis were enrolled from an outpatient clinic post-COVID cohort seen from August to November 2020. Therapies/comorbidities affecting calcium/vitamin D/bone metabolism, and/or admission to the intensive care unit during hospitalization were exclusion criteria. 25(OH) Vitamin D was measured at hospital admission and 6 months after discharge. We observed lower 25(OH) vitamin D levels, evaluated at follow-up, in subjects with long COVID than those without (20.1 vs 23.2 ng/mL, P = .03). Regarding the affected health areas evaluated in the entire cohort, we observed lower 25(OH) vitamin D levels in those with neurocognitive symptoms at follow-up (n = 7) than those without (n = 93) (14.6 vs 20.6 ng/mL, P = .042). In patients presenting vitamin D deficiency (<20 ng/mL), both at admission and at follow-up (n = 42), those affected by long COVID (n = 22) presented lower 25(OH) vitamin D levels at follow-up than those not affected (n = 20) (12.7 vs 15.2 ng/mL, P = .041). In multiple regression analyses, lower 25(OH) vitamin D levels at follow-up were the only variable significantly associated with long COVID in our cohort (P = .008, OR 1.09, CI 1.01-1.16). COVID-19 survivors with long COVID have lower 25(OH) vitamin D levels than matched patients without long COVID. Our data suggest that vitamin D levels should be evaluated in COVID-19 patients after hospital discharge. The role of vitamin D supplementation as a preventive strategy of COVID-19 sequelae should be tested in randomized controlled trials.

Missed meal boluses and poorer glycemic control impact on neurocognitive function may be associated with white matter integrity in adolescents with type 1 diabetes.

The notion that pediatric type 1 diabetes impacts brain function and structure early in life is of great concern. Neurological manifestations, including neurocognitive and behavioral symptoms, may be present from childhood, initially mild and undetectable in daily life. Despite intensive management and technological therapeutic interventions, most pediatric patients do not achieve glycemic control targets for HbA1c. One of the most common causes of such poor control and frequent transient hyperglycemic episodes may be lifestyle factors, including missed meal boluses. The aim of this study was to assess the association between specific neurocognitive accomplishments-learning and memory, inhibition ability learning, and verbal and semantic memory-during meals with and without bolusing, correlated to diffusion tensor imaging measurements of major related tracts, and glycemic control in adolescents with type 1 diabetes compared with their healthy siblings of similar age. This is a case-control study of 12- to 18-year-old patients with type 1 diabetes (N = 17, 8 male patients, diabetes duration of 6.53 ± 4.1 years) and their healthy siblings (N = 13). All were hospitalized for 30 h for continuous glucose monitoring and repeated neurocognitive tests as a function of a missed or appropriate pre-meal bolus. This situation was mimicked by controlled, patient blinded manipulation of lunch pre-meal bolus administration to enable capillary glucose level of <180 mg/dl and to >240 mg/d 2 hours after similar meals, at a similar time. The diabetes team randomly and blindly manipulated post-lunch glucose levels by subcutaneous injection of either rapid-acting insulin or 0.9% NaCl solution before lunch. A specific neurocognitive test battery was performed twice, after each manipulation, and its results were compared, along with additional neurocognitive tasks administered during hospitalization without insulin manipulation. Participants underwent brain imaging, including diffusion tensor imaging and tractography. A significant association was demonstrated between glycemic control and performance in the domains of executive functions, inhibition ability, learning and verbal memory, and semantic memory. Inhibition ability was specifically related to food management. Poorer glycemic control (>8.3%) was associated with a slower reaction time. These findings highlight the potential impairment of brain networks responsible for learning, memory, and controlled reactivity to food in adolescents with type 1 diabetes whose glycemic control is poor.

COVID-19 and Its Long-Term Neurological and Cognitive Implications: A Literature Review

Introduction: COVID-19 is an infectious disease resulting from severe acute respiratory syndrome. Individuals with prior COVID-19 infection have had neurological complaints of impaired attention, fatigue, and “brain fog”. This review seeks to summarize the associations between COVID-19 infection and the development of the neurocognitive elements of post-acute COVID syndrome (PACS) which is relevant to healthcare workers for the efficient treatment and management of the long-term effects of COVID. Methods: Literature that examines the neurocognitive complaints caused by COVID-19 infection, including brain fog, attention deficits, psychiatric impairment, and fatigue were selected. Google Scholar and PubMed were the primary databases used to obtain relevant literature. After preliminary searching, 21 articles were analyzed as part of this review. Results: The following symptoms of PACS were persistently reported by a large majority (approximately ⅓ to ½) of patients: breathlessness, cough, fatigue, and brain fog. PACS neurological symptoms were more prevalent in females than in males. Reported psychiatric symptoms from prior COVID-19 infection were ADHD, depression, and insomnia. Discussion: The causes of these neurocognitive symptoms were attributed to neuroinflammation of the choroid plexus, intracerebral hemorrhagic lesions, and hypoactivity in the anterior and posterior cingulate cortex. These possible pathways were confirmed with magnetic resonance imaging (MRI) findings, computed tomography (CT) scans, and positron emission tomography (PET) scans. Conclusion: This paper will add to the evidence regarding the association between COVID-19 and the development of neurocognitive PACS. It is hoped that future research will build on a clearer understanding of the etiology of neurocognitive issues associated with viral infection.

Abstract 63: Machine learning identifies experimental brain metastasis subtypes based on their influence on neural circuits

Abstract A high percentage of patients with brain metastases frequently develop neurocognitive symptoms, however understanding how brain metastasis co-opt the function of neuronal circuits beyond a mass effect remains unknown. We report a comprehensive multidimensional modelling of brain functional analysis in the context of brain metastasis. By testing different pre-clinical models of brain metastasis from various primary sources and oncogenic profiles we dissociated the heterogeneous impact on brain function that we detected from the homogeneous inter-model tumor size or glial response. In contrast we report a potential underlying molecular program responsible for impairing neuronal crosstalk in a model-specific manner. Additionally, measurement of various brain activity readouts matched with machine learning strategies confirmed model-specific alterations that could help to predict the presence and subtype of metastasis. Citation Format: Mariam Masmudi-Martín, A Sanchez-Aguilera, A Navas-Olive, P Baena, C Hernández-Oliver, S Martínez, M Lafarga, Renacer Red Nacional de Metástasis Cerebral, MZ Lin, L Menendez de la Prida, M Valiente. Machine learning identifies experimental brain metastasis subtypes based on their influence on neural circuits [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 63.

Temporal Network Analysis of Neurocognitive Functioning and Psychological Symptoms in Collegiate Athletes After Concussion.

Sport-related concussion (SRC) is associated with several post-injury consequences, including neurocognitive decrements and psychological distress. Yet, how these clinical markers interact with each other, the magnitude of their interrelationships, and how they may vary over time following SRC are not well understood. Network analysis has been proposed as a statistical and psychometric method to conceptualize and map the complex interplay of interactions between observed variables (e.g., neurocognitive functioning and psychological symptoms). For each collegiate athlete with SRC (n = 565), we constructed a temporal network as a weighted graph, with nodes, edges, and the set of weights associated with each edge at three time-points (baseline, 24-48 h post-injury, and asymptomatic), that graphically depicts the interrelated nature of neurocognitive functioning and symptoms of psychological distress throughout the recovery process. This graph shows that the inter-group relationships between neurocognitive functioning and symptoms of psychological distress were stronger at the 24-48 h time-point than at baseline or at the asymptomatic time-point. Further, all symptoms of psychological distress and neurocognitive functioning significantly improved from the 24-48 h time-point to asymptomatic status. The effect sizes of these changes ranged from 0.126 (small) to 0.616 (medium). This research suggests that significant improvements in symptoms of psychological distress appear necessary to drive related improvements in neurocognitive functioning and vice versa. Therefore, clinical interventions should consider the importance of managing psychological distress during the acute care of individuals with SRC to help ameliorate negative outcomes.

Neurological soft signs and schizophrenia.

Neurological soft signs (NSS) are likely to represent abnormal neurodevelopment and aberration in neural maturation and connectivity. They may not be unique to schizophrenia, but they appear to be a trait characteristic in psychosis and therefore could serve as an objective measure for the assessment of serious psychiatric disorder in the prodromal phase, at onset, and along the course of the disease. Evidence so far proposes that NSS are independent of antipsychotic treatment and therefore constitute a trait symptom, independent of the illness stage and medication. Somatomotor and somatosensory regions, spatial orientation, and visual processing areas, cerebellum, and basal ganglia are implicated as possible structural substrates of NSS. Several studies have examined the relationship between NSS and schizophrenia positive, negative symptoms and deficit syndrome; however, results have been so far ambiguous. Neurocognitive symptoms have been moderately related to NSS suggesting that neurocognitive deficits may contribute to the construct of NSS. Regardless of the fact that NSS are not unique to schizophrenia but extend across to the schizotypy continuum, they may help identify individuals at risk of developing schizophrenia later in life.

Cognition and Mental Health in Pediatric Patients Following COVID-19.

The global coronavirus pandemic has significantly impacted public health and has been a research subject since its emergence in 2019. The acute phase of the disease leads to pulmonary and non-pulmonary manifestations, which in some individuals may progress to long-lasting symptoms. In this article, we conducted a narrative review of the current literature to summarize current knowledge regarding long COVID syndrome in children, focusing on cognitive symptoms. The review included a search of three databases (PubMed, Embase, and Web of Science) using the key phrases "post COVID-19 cognitive pediatric", "long COVID pediatric", "mental health long COVID children", and "COVID-19 cognitive symptoms". A total of 102 studies were included. The review revealed that the main long-term cognitive symptoms following COVID-19 were memory and concentration deficits, sleep disturbances, and psychiatric states such as anxiety and stress. In addition to the direct physiological effects of a viral infection, there are psychological, behavioral, and social factors contributing to cognitive impairment, which should be addressed regarding the pediatric population. The high prevalence of neurocognitive symptoms in children following COVID-19 emphasizes the importance of understanding the mechanisms of nervous system involvement.

Association of Arts Event Attendance With Cognitive Function Among Older Adults Enrolled in the Health and Retirement Study.

Among the cognitively impaired, arts engagement is associated with improved neurocognitive symptoms. Less is known about arts engagement as a potentially modifiable lifestyle factor to prevent or slow cognitive decline. Our aim was to evaluate the association between arts event attendance and cognition. We used data from the 2014 and 2016 waves of the Health and Retirement Study to evaluate the association between arts event attendance and cognition using multivariable linear regressions. Arts event attendance in 2014 was our exposure of interest and included visiting an art museum or art gallery; attending an arts or crafts fair; attending a live performance (concert, play, or reading); and/or going to a movie theater. Cognitive function in 2016 measured on a 27-point scale by the Telephone Interview for Cognitive Status was our main outcome of interest. Of the 1,149 participants included in the final analysis, 70.7% attended an arts event. The mean baseline cognitive score was higher among those who attended art events (16.8 [standard deviation {SD}, ±3.8] vs 13.8 [SD, ±5.0]; p < .001). In our multivariable regressions, those who attended arts events in 2014 exhibited higher cognitive scores in 2016 after controlling for demographic, socioeconomic, health, and baseline cognitive covariates (β, 1.07 [95% confidence interval {CI}, 0.50-1.64]; p < .001). This association was primarily observed in those with lower baseline cognitive function (β, 1.19 [95% CI, 0.33-2.06]; p = .008). Arts event attendance may be associated with better cognitive function. Given concerns for residual confounding and reverse causality, this association warrants further study.

In utero methadone exposure permanently alters anatomical and functional connectivity: A preclinical evaluation.

The opioid epidemic is an ongoing public health crisis, and children born following prenatal opioid exposure (POE) have increased risk of long-term cognitive and behavioral sequelae. Clinical studies have identified reduced gray matter volume and abnormal white matter microstructure in children with POE but impacts on whole-brain functional brain connectivity (FC) have not been reported. To define effects of POE on whole brain FC and white matter injury in adult animals, we performed quantitative whole-brain structural and functional MRI. We used an established rat model of POE in which we have previously reported impaired executive function in adult rats analogous to persistent neurocognitive symptoms described in humans with POE. Pregnant Sprague-Dawley rat dams received continuous methadone (12 mg/kg/day) vs. saline infusion for 28 days via osmotic mini-pumps, exposing rats to pre- and postnatal opioid until weaning. At young adult age (P60), POE and saline exposed offspring underwent in vivo MRI included diffusion tensor imaging and functional MRI (fMRI). Results indicate that fractional anisotropy (FA) was decreased in adult animals with POE [n = 11] compared to animals that received saline [n = 9] in major white matter tracts, including the corpus callosum (p < 0.001) and external capsule (p < 0.01). This change in FA was concomitant with reduced axial diffusivity in the external capsule (p < 0.01) and increased radial diffusivity in the corpus callosum (p < 0.01). fMRI analyses reveal brainwide FC was diffusely lower in POE (p < 10-6; 10% of variance explained by group). Decreased connectivity in cortical-cortical and cortico-basal ganglia circuitry was particularly prominent with large effect sizes (Glass's Δ > 1). Taken together, these data confirm POE reduces brainwide functional connectivity as well as microstructural integrity of major white matter tracts. Altered neural circuitry, dysregulated network refinement, and diffuse network dysfunction have been implicated in executive function deficits that are common in children with POE. FC may serve as a translatable biomarker in children with POE.

Post COVID-19 condition after Wildtype, Delta, and Omicron SARS-CoV-2 infection and prior vaccination: Pooled analysis of two population-based cohorts.

Post COVID-19 condition (PCC) is an important complication of SARS-CoV-2 infection, affecting millions worldwide. This study aimed to evaluate the prevalence and severity of post COVID-19 condition (PCC) with novel SARS-CoV-2 variants and after prior vaccination. We used pooled data from 1350 SARS-CoV-2-infected individuals from two representative population-based cohorts in Switzerland, diagnosed between Aug 5, 2020, and Feb 25, 2022. We descriptively analysed the prevalence and severity of PCC, defined as the presence and frequency of PCC-related symptoms six months after infection, among vaccinated and non-vaccinated individuals infected with Wildtype, Delta, and Omicron SARS-CoV-2. We used multivariable logistic regression models to assess the association and estimate the risk reduction of PCC after infection with newer variants and prior vaccination. We further assessed associations with the severity of PCC using multinomial logistic regression. To identify groups of individuals with similar symptom patterns and evaluate differences in the presentation of PCC across variants, we performed exploratory hierarchical cluster analyses. We found strong evidence that vaccinated individuals infected with Omicron had reduced odds of developing PCC compared to non-vaccinated Wildtype-infected individuals (odds ratio 0.42, 95% confidence interval 0.24-0.68). The odds among non-vaccinated individuals were similar after infection with Delta or Omicron compared to Wildtype SARS-CoV-2. We found no differences in PCC prevalence with respect to the number of received vaccine doses or timing of last vaccination. The prevalence of PCC-related symptoms among vaccinated, Omicron-infected individuals was lower across severity levels. In cluster analyses, we identified four clusters of diverse systemic, neurocognitive, cardiorespiratory, and musculoskeletal symptoms, with similar patterns across variants. The risk of PCC appears to be lowered with infection by the Omicron variant and after prior vaccination. This evidence is crucial to guide future public health measures and vaccination strategies.

Representation of an Interdisciplinary Approach for Evaluation of Precision of a Neurocognitive Screening Bundle: A Proposal

Neurocognitive disorders encompass a range of conditions characterized by cognitive impairments, presenting significant challenges to individuals, families, and healthcare systems worldwide. Traditional paper-and-pencil assessments have limitations, including restricted access, limited frequency, and subjective interpretation. This research proposal aims to address these limitations by developing a reliable digital platform, a neurocognitive screening bundle, for year-round monitoring of neurocognitive symptom domains. The proposed research project adopts an interdisciplinary approach by integrating knowledge and expertise from the fields of neurology, psychology, cognitive neuroscience, and computer science. Neurology provides clinical context and expertise in understanding neurocognitive symptom domains, ensuring that the chosen screening bundle aligns with clinical needs. Psychology contributes insights into human behavior and cognitive processes, aiding in the selection, adaptation, or development of assessments targeting specific neurocognitive functions. Additionally, psychologists contribute expertise in data analysis and interpretation, enabling the identification of meaningful patterns within the collected data. Cognitive neuroscience offers a deeper understanding of the underlying neural mechanisms associated with neurocognitive symptom domains. By identifying the neural networks, brain regions, and cognitive processes involved in specific cognitive functions, cognitive neuroscientists bridge the gap between cognitive assessment and neurobiological underpinnings, aiding in the selection and interpretation of neurocognitive measures. Computer science plays a pivotal role in developing and evaluating the digital platform for neurocognitive screening. Computer scientists leverage their expertise in software development, data analysis, and machine learning to design algorithms for data processing, ensure data security and privacy, and develop user-friendly interfaces for assessments. By integrating technical skills with knowledge from other disciplines, computer scientists enhance the accuracy, reliability, and usability of the digital platform. This interdisciplinary research project aims to provide a comprehensive, accessible, and reliable tool for year-round monitoring of neurocognitive symptom domains, surpassing the limitations of traditional assessment methods. By leveraging the expertise from neurology, psychology, cognitive neuroscience, and computer science, this study aims to advance the field and improve clinical outcomes for individuals with neurocognitive disorders. The findings of this research project have the potential to revolutionize neurocognitive assessments, leading to more effective diagnosis and monitoring of these challenging conditions.

Patterns of acute stress disorder in a sample of blast-injured military service members: A latent profile analysis.

The primary aims of this study were to identify latent profiles of acute stress disorder (ASD) symptoms and to evaluate postconcussive symptom differences across the identified profiles as measured by the Acute Stress Disorder Scale and the Military Acute Concussion Evaluation, respectively. Participants (N = 315) in the current study were predominantly active-duty (75.0%), enlisted (97.8%) males (97.4%) serving in the U.S. Army (87.8%). Approximately, half of the sample reported being married or engaged (51.1%) and was on average 25.94 (SD = 6.31) years old. Participants were referred to the Air Force Theater Hospital, 332nd Air Expeditionary Wing, Joint Base Balad, Iraq, to be evaluated as part of routine clinical assessment for neurocognitive and psychological symptoms following exposure to a blast. A 3-profile solution was identified as the most parsimonious and best-fitting model based on statistical model fit indices. Blast injured service members in Profile 3 had greater ASD total and subscale severity compared to the other 2 subgroups, with effect size estimates largely differing by hyperarousal and reexperiencing symptoms. Furthermore, Profiles 2 and 3 were more likely to demonstrate postconcussive symptoms compared to Profile 1. Findings provide novel information on heterogenous ASD symptom profiles during the acute phase following a blast injury and highlight the relationship between psychological and physical symptoms. Classification of blast-injured service members may help identify at-risk individuals who would benefit from further clinical care and mitigate long-term psychological and neurocognitive issues. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Neurocognitive sequelae following COVID-19 infection in older adults with and without pre-infection neurocognitive impairment

In this case report,we describe the clinical characteristics of three older adults aged &gt;65years with cognitive difficulties prior to theirCOVID-19 infection who reported worsening of neurocognitive symptoms in the convalescent COVID-19 phase. Formal neuropsychological testingalong with neuroimaging were included with each patient. These patients described an initial worseningin cognitive functionafter recovering from the acute phase of COVID19. This case reportdescribes variable recoveryof cognitive abilities in the convalescent stage. The direct effectof the viral infection itselfon cognitive function are well documented. We hypothesize that the persistent inflammatory or immune response in the convalescent COVID-19 stage, more commonly referred to as the indirect mechanism, contributes to the clinical syndromeknown as the Post-Acute Sequelae of SARS-CoV-2 (PASC).

Neurocognitive and psychiatric symptoms following infection with COVID-19: Evidence from laboratory and population studies

ObjectiveThe objective of the current investigation was to examine associations between symptomatic COVID-19 history, neurocognitive function, and psychiatric symptoms using cognitive task performance, functional brain imaging, and a prospective population survey. MethodsStudy 1 was a laboratory study conducted between 3 May 2022 and 16 Nov 2022 involving 120 fully vaccinated community dwelling adults between 18 and 84 years of age (Mage = 31.96 (SD = 20.71), 63.3% female). In this cross-sectional study we examined the association between symptomatic COVID-19 infection history and performance on three computer tasks assessing cognitive function (Flanker interference, delay discounting and simple reaction time) and measured oxygen saturation within the prefrontal cortex using functional near infrared spectroscopy (fNIRS). Study 2 was a 2-wave population survey undertaken between 28 September 2021 and 21 March 2022, examining the prospective relationship between symptomatic COVID-19 and self-reported symptoms of cognitive dysfunction, depressive symptoms, anxiety symptoms, and agitation at 6-month follow up. The sample (N = 2,002, Mage = 37.0, SD = 10.4; 60.8% female) was collected using a quota process to ensure equal numbers of vaccinated and unvaccinated individuals. Structural equation modelling with latent variables was performed on the population-level data, evaluating the fit of the proposed mediational model of symptomatic COVID-19 to psychiatric symptoms through cognitive dysfunction. ResultsFindings from Study 1 revealed significant effects of symptomatic COVID-19 history on Flanker interference and delay discounting. Effects on flanker performance were significantly stronger among older adult women (effect: 9.603, SE = 4.452, t = 2.157, p = .033), and were accompanied by task-related changes cerebral oxygenation at the right superior frontal gyrus (F (1, 143.1) = 4.729, p = .031). Additionally, those with a symptomatic COVID-19 infection history showed evidence of amplified delay discounting (coefficient = 0.4554, SE = 0.2208, t = 2.0629, p = .041). In Study 2, baseline symptomatic COVID-19 history was associated with self-reported cognitive dysfunction and a latent variable reflecting psychiatric symptoms of anxiety, depression and agitation at follow-up. Mediational analyses revealed evidence of cognitive mediation of clinically significant psychiatric outcomes: depression (indirect effect = 0.077, SE = 0.026, p = .003) and generalized anxiety (indirect effect = 0.060, SE = 0.021, p = .004). ConclusionsConverging findings from laboratory and population survey data support the conclusion that symptomatic COVID-19 infection is associated with task-related, functional imaging and self-reported indices of cognitive dysfunction as well as psychiatric symptoms. In some cases, these findings appear to be more amplified among women than men, and among older women than younger.

VV-ECMO in severe COVID-19: multidimensional perspectives on the use of a complex treatment

VV-ECMO in severe COVID-19: multidimensional perspectives on the use of a complex treatment

Tolvaptan for the treatment of the syndrome of inappropriate antidiuresis (SIAD).

The syndrome of inappropriate antidiuresis (SIAD), the commonest cause of hyponatraemia, is associated with significant morbidity and mortality. Tolvaptan, an oral vasopressin V2-receptor antagonist, leads through aquaresis to an increase in serum sodium concentration and is the only medication licenced in Europe for the treatment of euvolaemic hyponatraemia. Randomised controlled trials have shown that tolvaptan is highly efficacious in correcting SIAD-related hyponatraemia. Real-world data have confirmed the marked efficacy of tolvaptan, but they have also reported a high risk of overly rapid sodium increase in patients with a very low baseline serum sodium. The lower the baseline serum sodium, the higher the tolvaptan-induced correction rate occurs. Therefore, a lower starting tolvaptan dose of 7.5 mg has been evaluated in small cohort studies, demonstrating its efficacy, but it still remains unclear as to whether it can reduce the risk of overcorrection. Most international guidelines, except for the European ones, recommend tolvaptan as second-line treatment for SIAD after fluid restriction. However, the risk of unduly rapid sodium correction in combination with its high cost have limited its routine use. Prospective controlled studies are warranted to evaluate whether tolvaptan-related sodium increase can improve patient-related clinical outcomes, such as mortality and length of hospital stay in the acute setting or neurocognitive symptoms and quality of life in the chronic setting. In addition, the potential role of a low tolvaptan starting dose needs to be further explored. Until then, tolvaptan should mainly be used as second-line treatment for SIAD, especially when there is a clinical need for prompt restoration of normonatraemia. Tolvaptan should be used with specialist input according to a structured clinical pathway, including rigorous monitoring of electrolyte and fluid balance and, if needed, implementation of appropriate measures to prevent, or when necessary reverse, overly rapid hyponatraemia correction.