Journal of clinical and experimental neuropsychology最新文献

Objective: To examine the role of administration setting (remote vs. in-person) on performance on four self-administered, smartphone-based neuropsychological measures delivered via the Mobile Toolbox (MTB) and MyCog Mobile (MCM) platforms.

Methods: Participants self-administered four cognitive tasks (i.e. Executive Function, Face Memory, Picture Memory, and Working Memory) on a smartphone either in the lab or remotely (in-person N = 292, remote N = 701). Robust methods were used to examine performance differences across in-person and remote samples while controlling for covariates.

Results: Remote testing was associated with higher Picture Memory Trial 1 scores (β = 1.114, p = 0.002) and lower Face Memory First Letter scores (β = -3.194, p < 0.001); the latter effect was moderated by education and version. Picture Memory Trial 2 showed only an indirect effect of setting through an interaction with age (β = 0.048, p < 0.001). No setting effects were found for Executive Function or Working Memory tasks. All observed setting effect sizes were small (partial η²≤.014). Perfect scores were more common remotely on memory tasks; however, sparse perfect scores for Trial 1 in the in-person group and ceiling effects on Trial 2 limit interpretation.

Conclusions: Performance on self-administered smartphone tasks was largely comparable across settings, with only small, subtest-specific differences in performance on memory tasks. These results support remote self-administration for research use while highlighting the need for design strategies that preserve score validity across settings.

Introduction: Rumination is a risk factor for the development of depression among adolescents. However, not all at-risk youth develop depression, suggesting the presence of factors that moderate risk patterns. Error-related negativity (ERN), an event-related potential indexing cognitive error processing, has been associated with both rumination and internalizing symptoms. However, it remains unknown whether ERN interacts with rumination to predict youth internalizing symptoms and if the interaction effects are specific to depression and anxiety symptoms. The current study examined the interplay of ERN and rumination in the 12-month prospective prediction of anxiety and depressive symptoms in a sample of youth.

Method: Participants included 60 youth (ages 9-16, 88% female) enrolled in a study on the intergenerational transmission of depression. At baseline, youth completed a self-report measure of rumination and a Flanker error monitoring task during electroencephalography to measure ERN. Youth completed self-report measures of depressive and anxiety symptoms at baseline and 12-month follow-up.

Results: Results revealed a two-way interaction between baseline child ERN and rumination in the prediction of 12-month depressive symptoms. Follow-up analysis indicated that greater baseline rumination predicted increases in depressive symptoms at 12-months for youth exhibiting a more enhanced ERN, but not for youth demonstrating a blunted ERN. This effect remained after covarying for child age, race, sex, and maternal depression history. Results revealed no significant interactive effect between child ERN and rumination in predicting 12-month anxiety symptoms.

Discussion: These findings highlight the unique interplay of rumination and neural error processing in the prospective prediction of youth depressive symptoms. If replicated, these results would suggest that rumination-targeted prevention programs may be particularly effective for reducing depressive symptoms among youth exhibiting an enhanced ERN.

Patients living with cancer often experience significant neuropsychological symptoms throughout their illness trajectories, stemming either from the cancer itself or from antineoplastic therapies. In many cases, these neuropsychological effects, including impacts on cognition, are the result of various comorbid symptoms patients with cancer frequently face. These comorbid symptoms include: 1) fatigue and sleep disturbance, 2) mood symptoms, 3) peripheral neuropathy and neuropathic pain, and 4) symptoms related to endocrine and nutritional dysfunction. This review discusses the putative pathophysiological mechanisms connecting each of these comorbid symptoms to cognitive dysfunction in patients with cancer, along with a review of recommendations for evaluating and managing these symptoms. The review highlights the influence of concomitant medication use on cognition with a survey of the most common medication classes that could have cognitive implications. Finally, this review concludes with a discussion of caregiver distress, a frequently neglected component of cancer care that may be especially pertinent in cases in which patient cognition is impaired.

Population-based incidence rates of childhood and adolescent cancers have increased over the past several decades, and the overall survival rate for childhood cancer exceeds 85% due to advances in treatment. There is a substantial burden of late effects in this growing and youthful survivorship population. In particular, neuropsychological late effects are common and life-altering sequelae of childhood cancer that adversely impact educational attainment, vocational attainment, and social integration. In this review article, we summarize the extant literature to describe neuropsychological late effects in survivors of childhood cancer, including underlying brain mechanisms and contributing individual, clinical, and socioenvironmental risk factors. We review existing guidelines for survivorship care and strategies for implementation of these guidelines via neuropsychological screening that are informed by developmental considerations. We end by identifying future directions for the field.

Introduction: Cancers of the central nervous system (CNS) include primary and metastatic tumors of varying cells of origin. These tumors may be benign or malignant, with incidence rates varying based on age, gender, and tumor type. While heterogeneous, all CNS tumors harbor risk of neurocognitive impairment, impairing patients' health-related quality of life (HRQoL).

Method: This narrative review was informed by a targeted literature search in PubMed and Scopus, focusing on studies reporting neurocognitive deficits in patients with gliomas, primary CNS lymphomas, and metastatic CNS tumors. Articles were selected based on clinical relevance, methodological quality, and their contribution to key themes in neurocognitive outcomes among patients with CNS tumor: impact of tumor type, location, and treatment modalities, including surgery, radiotherapy, chemotherapy, targeted therapy, and immunotherapy. The influence of adjunctive treatments such as corticosteroids and antiepileptics on neurocognitive function was also examined. Data synthesis included neurocognitive assessment measures, patient demographics, and potential modifiers such as brain plasticity and psychological distress. This approach was designed to support an integrative, expert-informed synthesis rather than a systematic or exhaustive review.

Results: Findings indicate that neurocognitive deficits are prevalent among CNS tumor patients, with impairments in memory, attention, processing speed, and executive function. Tumor location significantly influences the type and severity of deficits, with frontal and temporal lobe involvement being particularly detrimental. Treatment modalities contribute to neurocognitive decline, with radiotherapy having cumulative negative effects. Psychological distress and individual brain resilience further modulate outcomes, highlighting the need for individualized treatment strategies.

Conclusions: Neurocognitive impairment in CNS tumor patients results from both disease pathology and treatment effects. Understanding these mechanisms is crucial for developing targeted interventions, including cognitive rehabilitation and tailored treatment plans, to optimize patient outcomes. Improved management strategies incorporating neuroprotective approaches and psychological support are essential for enhancing long-term HRQoL in CNS tumor patients.

Cancer-Related Cognitive Impairment (CRCI) reflects changes in the cognitive performance of individuals diagnosed and treated for cancer. CRCI occurs in a significant percentage of cancer patients and cancer survivors, in both CNS and non-CNS cancer. However, research findings are mixed with regards to the prevalence, the domains affected, and the size of effects for the non-CNS cancer population. This may partly be due to cognitive effects being relatively subtle in this patient population. To improve the sensitivity of studies to detect CRCI, steps are being taken to establish larger samples, but these remain costly. In this narrative review, we describe methodological and statistical developments that may help to improve the sensitivity of our studies in detecting CRCI. We discuss several forms of supervised and unsupervised digital testing based on traditional tests commonly used in neuropsychological assessment, as well as newer paradigms such as Ecological Momentary Assessment and cognitive neuroscience-based tests. With digital tests, new types of behavioral data become available, which allows for more sophisticated data analyses. Additionally, we discuss several statistical approaches to the analysis of cognitive data that can be used to improve sensitivity, such as Item Response Theory, Bayesian mixed-effects models and Machine Learning (see Table 1). We close with several recommendations for the field, regarding the large number of digital test batteries that are becoming available, uncontrolled false positive rates, and inconsistent use of cognitive domains.[Table: see text].

Cancer and its treatments often result in cognitive impairment (CRCI), impacting the well-being of survivors. Chemotherapy and brain-targeted radiation therapy contribute significantly to central nervous system toxicity, which underlies these cognitive issues. Preclinical animal studies serve as pivotal tools in elucidating the cellular and molecular changes triggered by cancer therapies. This review assesses both clinical and preclinical evidence, offering insights into optimal preclinical study designs to deepen our understanding of the underlying injury mechanisms. Such understanding is crucial and adapted to precision medicine for advancing preventive and restorative interventions. Early interventions show promising outcomes, underscoring the importance of identifying predictive biomarkers for patient stratification.

Cancer is a significant global health concern and is one of the leading causes of death worldwide. Recent projections estimate about 2 million new diagnoses of cancer each year in the United States, with about 20 million new global cases. Despite the rising incidence of new cancer diagnoses, cancer-specific mortality is decreasing due to significant progress in prevention, treatment, and supportive care. This has led to increased attention in the field of cancer survivorship, which aims at improving quality of life and long-term symptom management in cancer survivors. Cognitive dysfunction is among the most prominent symptoms managed by patients with central nervous system and systemic cancer. While there has been significant progress in understanding cancer related cognitive dysfunction and related challenges faced by cancer survivors, future research is needed to identify risk factors and therapeutic options for these important symptoms. In this review, we provide an overview of cancer epidemiology, risk factors, and biology. We next discuss mechanisms and common side effects of cancer therapeutic modalities including surgery, radiation therapy, cytotoxic chemotherapy, molecular targeted therapy, hormone therapy, and immunotherapy. We end with a discussion of malignant and benign central nervous system tumors providing background into tumor types and treatment considerations. This review will provide background for the collection of articles included in this special issue.

Introduction: Cognitive difficulties are frequently reported after cancer treatments, such as chemotherapy or hormone therapy, and have a negative impact on patients' quality of life. Recently, some studies have shown that new cancer treatments, such as immunotherapy agents, can induce cognitive changes.

Method: This review presents the central neurological immune adverse events of immunotherapy treatments including Immune Checkpoint Inhibitors (ICI) and Chimeric Antigen Receptor (CAR) T-cell therapy. The physiopathological mechanisms and risk factors are developed and clinical studies on immunotherapy agents and cognition (among adult patients, using validated questionnaires and/or cognitive tests), psychological factors and quality of life were presented.

Results: Neurological toxicities are frequently observed with CAR-T cell therapies at acute stage, such as the immune effector cell-associated neurotoxicity syndrome (ICANS), inducing cognitive disorders such as disorientation and aphasia. However, few studies have accurately assessed the impact of immunotherapy on cognition. The methodology of these studies is heterogeneous and they mainly included nonspecific self-report questionnaires of cognitive complaints. Variable results have been obtained concerning the cognitive impact of ICI and CAR-T cell several months following immunotherapy: overall, while some studies reported cognitive difficulties (mainly processing speed and executive functions), the majority has not. Although anxiety and depression are frequently reported in patients treated with ICI or CAR-T cells, these symptoms tend to decrease after the start of immunotherapy. The current neurobiological investigations are too fragmentary to explain neurological symptoms and potential cognitive alteration, but neuroinflammation, vascular inflammation, brain blood barrier disruption, and immune cell brain infiltration would constitute common mechanisms relayed by CAR-T and to a lesser degree, ICI.

Conclusions: Acute neurological toxicities following CAR-T cell therapies are a major issue. Further studies are needed to better assess cognitive difficulties after the initiation of immunotherapy, in particular ICI, to better understand the physiopathology, including imaging studies, and risk factors.

Introduction: Cancer-related cognitive impairment (CRCI) is a multifaceted condition, influenced by numerous neurobiological mechanisms and individual risk factors. In the non-CNS oncology population, the concept has increasingly received attention over the last few decades. Neurotoxicity of cancer treatment modalities varies, with effects that are protocol- or agent-dependent that additionally interact with patient-specific characteristics (e.g. age, sex-specific endocrine mechanisms, metabolism, brain reserve, etc.), which differently impacts individual cognitive outcomes. Importantly, CRCI encompasses both patient-reported cognitive complaints and objectively measured cognitive impairments, which may not consistently align. Individually tailored neuropsychological follow-up in oncology is therefore important, which should encompass risk profiling, patient-reported, as well as objective cognitive assessments to support psychoeducation and the development of effective interventions.

Methods: This review summarizes the historical evolution of CRCI research, biophysiological mechanisms, the clinical presentation, and the array of international guidelines for research and clinical care.

Results: Current findings on interventions are reviewed, and innovative neuroscience-informed rehabilitation approaches are discussed.

Conclusion: While these more personalized interventions might hold promise for CRCI, further research is needed to determine their true efficacy, particularly considering the potential influence of practice effects. Additionally, in-depth, large-scale, transdiagnostic, and multimodal investigations are required to advance understanding of the mechanisms of toxicity, individual risk factors, and effective intervention strategies.