The relationship between fatigue and cognition has not been fully elucidated in children and adolescent survivors of brain tumours. The aim of the present study was to investigate the potential relationship between fatigue and cognitive impairments in these survivors, as this group is at risk for both types of deficits.

Survivors of paediatric brain tumours (n = 45) underwent a neuropsychological testing on average 4 years after diagnosis. Mean age at follow-up was 13.41 years. Cognition was assessed with neuropsychological tests, and fatigue with the Pediatric Quality of Life (PedsQL™) Multidimensional Fatigue Scale. Regression analysis, adjusted for cranial radiotherapy and age at diagnosis, was used to investigate the associations between cognitive variables and fatigue subscales. Cognitive variables associated with fatigue were subsequently exploratively assessed.

Significant associations were found for cognitive fatigue and measures of cognitive processing speed; Coding: p = .003, r = .583, 95% CI [9.61; 22.83] and Symbol Search: p = .001, r = .585, 95% CI [10.54; 24.87]. Slower processing speed was associated with poorer results for cognitive fatigue. Survivors with the largest decrease in processing speed from baseline to follow-up also experienced the most cognitive fatigue. Survivors expressed more cognitive fatigue compared to other types of fatigue.

The association between cognitive fatigue and cognitive processing speed in children and adolescents treated for brain tumours is in concordance with the results previously reported in adults. Some survivors experience fatigue without impairment in processing speed, indicating the need for comprehensive assessments. Moreover, the study supports that fatigue is a multidimensional concept which should be measured accordingly.

To evaluate the associations between cannabis use and neurocognitive functioning, including self-reported attention deficit hyperactivity disorder (ADHD) symptoms, in a large sample of emerging adults (ages 21–25) using a cross-sectional design. A secondary objective was to examine age of cannabis initiation as a moderator.

Participants were high-risk drinking emerging adults (n = 598) reporting past-month cannabis use in the following categories: 1) non-users (i.e., never or not in the past month; n = 276), 2) occasional users (i.e., monthly or weekly users; n = 201), and 3) daily users (n = 121). Categorical comparisons were conducted on working memory, attention, behavioral inhibition, delay and probability discounting, verbal intelligence, and ADHD symptoms. Complementary dimensional analyses examined cannabis severity in relation to neurocognition using regressions. Covariates were age, race, sex, income, years of education, tobacco use, and alcohol use.

Frequency of cannabis use was significantly associated with poorer working memory performance, more impulsive delay discounting, and greater endorsement of ADHD symptoms, but not other domains. Effect sizes were small and poorer performance was selectively present among daily, not occasional, cannabis users. Earlier age of initiation was not independently or interactively associated with neurocognitive performance.

Daily cannabis use was selectively adversely associated with aspects of memory, impulsivity, and subjective attentional functioning, but most cognitive indicators were not implicated, and evidence of amplification by earlier age of initiation was not observed. Ascertaining causal versus consequential roles of cannabis in neurocognitive functioning is an important priority.

Neurodegenerative diseases (NDDs), such as Alzheimer’s disease, frontotemporal dementia, dementia with Lewy bodies, and Huntington’s disease, inevitably lead to impairments in higher-order cognitive functions, including the perception of emotional cues and decision-making behavior. Such impairments are likely to cause risky daily life behavior, for instance, in traffic. Impaired recognition of emotional expressions, such as fear, is considered a marker of impaired experience of emotions. Lower fear experience can, in turn, be related to risk-taking behavior. The aim of our study was to investigate whether impaired emotion recognition in patients with NDD is indeed related to unsafe decision-making in risky everyday life situations, which has not been investigated yet.

Fifty-one patients with an NDD were included. Emotion recognition was measured with the Facial Expressions of Emotions: Stimuli and Test (FEEST). Risk-taking behavior was measured with driving simulator scenarios and the Action Selection Test (AST). Data from matched healthy controls were used: FEEST (n = 182), AST (n = 36), and driving simulator (n = 18).

Compared to healthy controls, patients showed significantly worse emotion recognition, particularly of anger, disgust, fear, and sadness. Furthermore, patients took significantly more risks in the driving simulator rides and the AST. Only poor recognition of fear was related to a higher amount of risky decisions in situations involving a direct danger.

To determine whether patients with an NDD are still fit to drive, it is crucial to assess their ability to make safe decisions. Measuring emotion recognition may be a valuable contribution to this judgment.

Neuropsychological assessment via videoconference could assist in bridging service access gaps due to geographical, mobility, or infection control barriers. We aimed to compare performances on neuropsychological measures across in-person and videoconference-based administrations in community-based survivors of stroke.

Participants were recruited through a stroke-specific database and community advertising. Stroke survivors were eligible if they had no upcoming neuropsychological assessment, concurrent neurological and/or major psychiatric diagnoses, and/or sensory, motor, or language impairment that would preclude standardised assessment. Thirteen neuropsychological measures were administered in-person and via videoconference in a randomised crossover design (2-week interval). Videoconference calls were established between two laptop computers, facilitated by Zoom. Repeated-measures t tests, intraclass correlation coefficients (ICCs), and Bland–Altman plots were used to compare performance across conditions.

Forty-eight participants (26 men; Mage = 64.6, SD = 10.1; Mtime since stroke = 5.2 years, SD = 4.0) completed both sessions on average 15.8 (SD = 9.7) days apart. For most measures, the participants did not perform systematically better in a particular condition, indicating agreement between administration methods. However, on the Hopkins Verbal Learning Test – Revised, participants performed poorer in the videoconference condition (Total Recall Mdifference = −2.11). ICC estimates ranged from .40 to .96 across measures.

This study provides preliminary evidence that in-person and videoconference assessment result in comparable scores for most neuropsychological tests evaluated in mildly impaired community-based survivors of stroke. This preliminary evidence supports teleneuropsychological assessment to address service gaps in stroke rehabilitation; however, further research is needed in more diverse stroke samples.

Patients with schizophrenia and individuals with schizotypy, a subclinical group at risk for schizophrenia, have been found to have impairments in cognitive control. The Dual Mechanisms of Cognitive Control (DMC) framework hypothesises that cognitive control can be divided into proactive and reactive control. However, it is unclear whether individuals with schizotypy have differential behavioural impairments and neural correlates underlying these two types of cognitive control.

Twenty-five individuals with schizotypy and 26 matched healthy controls (HCs) completed both reactive and proactive control tasks with electroencephalographic data recorded. The proportion of congruent and incongruent trials was manipulated in a classic colour-word Stroop task to induce proactive or reactive control. Proactive control was induced in a context with mostly incongruent (MI) trials and reactive control in a context with mostly congruent (MC) trials. Two event-related potential (ERP) components, medial frontal negativity (MFN, associated with conflict detection) and conflict sustained potential (conflict SP, associated with conflict resolution) were examined.

There was no significant difference between the two groups in terms of behavioural results. In terms of ERP results, in the MC context, HC exhibited significantly larger MFN (360–530 ms) and conflict SP (600–1000 ms) amplitudes than individuals with schizotypy. The two groups did not show any significant difference in MFN or conflict SP in the MI context.

The present findings provide initial evidence for dissociation of neural activation between proactive and reactive cognitive control in individuals with schizotypy. These findings help us understand cognitive control deficits in the schizophrenia spectrum.

Recent studies in Alzheimer’s disease (AD) have suggested that AD patients are not always able to rely on their feeling of familiarity to improve their memory decisions to the same extent as healthy participants. This underuse of familiarity in AD could result from a learned reinterpretation of fluency as a poor cue for memory that would prevent them to attribute a feeling of fluency to a previous encounter. The primary goal of this study was to determine whether AD patients could relearn the association between processing fluency and past exposure after being repeatedly exposed to situations where using this association improves the accuracy of their memory decisions.

Thirty-nine patients with probable AD were recruited and asked to complete several recognition tests. During these tests, participants were put either in a condition where the positive contingency between fluent processing and previous encounters with an item was systematically confirmed (intervention condition) or in a condition where there was no correlation between fluency and prior exposure (control condition). The efficacy of the intervention was evaluated at three time points (baseline, posttest, and 3-month follow-up).

Our results indicated that all AD patients do not benefit to the same extent from the training. Two variables appeared to influence the likelihood that participants increase and maintain their reliance on the fluency cues after the intervention: the ability to detect the fluency manipulation and the preservation of implicit metacognitive skills.

These findings indicate the importance of metacognition for inferential attribution processes in memory.

To compare cognitive phenotypes of participants with subjective cognitive decline (SCD) and amnestic mild cognitive impairment (aMCI), estimate progression to MCI/dementia by phenotype and assess classification error with machine learning.

Dataset consisted of 163 participants with SCD and 282 participants with aMCI from the Czech Brain Aging Study. Cognitive assessment included the Uniform Data Set battery and additional tests to ascertain executive function, language, immediate and delayed memory, visuospatial skills, and processing speed. Latent profile analyses were used to develop cognitive profiles, and Cox proportional hazards models were used to estimate risk of progression. Random forest machine learning algorithms reported cognitive phenotype classification error.

Latent profile analysis identified three phenotypes for SCD, with one phenotype performing worse across all domains but not progressing more quickly to MCI/dementia after controlling for age, sex, and education. Three aMCI phenotypes were characterized by mild deficits, memory and language impairment (dysnomic aMCI), and severe multi-domain aMCI (i.e., deficits across all domains). A dose–response relationship between baseline level of impairment and subsequent risk of progression to dementia was evident for aMCI profiles after controlling for age, sex, and education. Machine learning more easily classified participants with aMCI in comparison to SCD (8% vs. 21% misclassified).

Cognitive performance follows distinct patterns, especially within aMCI. The patterns map onto risk of progression to dementia.

In response to advancing clinical practice guidelines regarding concussion management, service members, like athletes, complete a baseline assessment prior to participating in high-risk activities. While several studies have established test stability in athletes, no investigation to date has examined the stability of baseline assessment scores in military cadets. The objective of this study was to assess the test–retest reliability of a baseline concussion test battery in cadets at U.S. Service Academies.

All cadets participating in the Concussion Assessment, Research, and Education (CARE) Consortium investigation completed a standard baseline battery that included memory, balance, symptom, and neurocognitive assessments. Annual baseline testing was completed during the first 3 years of the study. A two-way mixed-model analysis of variance (intraclass correlation coefficent (ICC)3,1) and Kappa statistics were used to assess the stability of the metrics at 1-year and 2-year time intervals.

ICC values for the 1-year test interval ranged from 0.28 to 0.67 and from 0.15 to 0.57 for the 2-year interval. Kappa values ranged from 0.16 to 0.21 for the 1-year interval and from 0.29 to 0.31 for the 2-year test interval. Across all measures, the observed effects were small, ranging from 0.01 to 0.44.

This investigation noted less than optimal reliability for the most common concussion baseline assessments. While none of the assessments met or exceeded the accepted clinical threshold, the effect sizes were relatively small suggesting an overlap in performance from year-to-year. As such, baseline assessments beyond the initial evaluation in cadets are not essential but could aid concussion diagnosis.

The purpose of this study was to examine whether self-efficacy predicted pediatric concussion symptom severity and explore whether affective mood states (e.g., depression) influenced this relationship.

Children (8–17 years) who were diagnosed with a concussion within 30 days of injury participated in the study (n = 105). Following a clinical assessment, participants and caregivers completed questionnaires that assessed overall concussion symptom severity and current depression symptoms. Participants also completed ratings capturing self-efficacy for managing concussion recovery.

Linear regression models revealed that greater levels of self-efficacy predicted lower parent- (R2 = 0.10, p = .001) and youth-rated (R2 = 0.23, p < .001) concussion symptom severity. Interestingly, depression symptoms moderated the relationship between self-efficacy and concussion symptom severity.

Findings provide initial support for a relationship between self-efficacy and concussion outcomes and highlight the influence of depressive symptoms. Interventions that optimize youth’s self-efficacy have the potential to increase treatment adherence, reduce concussion symptom severity, and improve recovery prognosis.

Alzheimer’s disease (AD) studies are increasingly targeting earlier (pre)clinical populations, in which the expected degree of observable cognitive decline over a certain time interval is reduced as compared to the dementia stage. Consequently, endpoints to capture early cognitive changes require refinement. We aimed to determine the sensitivity to decline of widely applied neuropsychological tests at different clinical stages of AD as outlined in the National Institute on Aging – Alzheimer’s Association (NIA-AA) research framework.

Amyloid-positive individuals (as determined by positron emission tomography or cerebrospinal fluid) with longitudinal neuropsychological assessments available were included from four well-defined study cohorts and subsequently classified among the NIA-AA stages. For each stage, we investigated the sensitivity to decline of 17 individual neuropsychological tests using linear mixed models.

1103 participants (age = 70.54 ± 8.7, 47% female) were included: n = 120 Stage 1, n = 206 Stage 2, n = 467 Stage 3 and n = 309 Stage 4. Neuropsychological tests were differentially sensitive to decline across stages. For example, Category Fluency captured significant 1-year decline as early as Stage 1 (β = −.58, p < .001). Word List Delayed Recall (β = −.22, p < .05) and Trail Making Test (β = 6.2, p < .05) became sensitive to 1-year decline in Stage 2, whereas the Mini-Mental State Examination did not capture 1-year decline until Stage 3 (β = −1.13, p < .001) and 4 (β = −2.23, p < .001).

We demonstrated that commonly used neuropsychological tests differ in their ability to capture decline depending on clinical stage within the AD continuum (preclinical to dementia). This implies that stage-specific cognitive endpoints are needed to accurately assess disease progression and increase the chance of successful treatment evaluation in AD.

To lay out the argument that exercise impacts neurobiological targets common to both mood and cognitive functioning, and thus more research should be conducted on its use as an alternative or adjunctive treatment for cognitive impairment in late-life depression (LLD).

This narrative review summarizes the literature on cognitive impairment in LLD, describes the structural and functional brain changes and neurochemical changes that are linked to both cognitive impairment and mood disruption, and explains how exercise targets these same neurobiological changes and can thus provide an alternative or adjunctive treatment for cognitive impairment in LLD.

Cognitive impairment is common in LLD and predicts recurrence of depression, poor response to antidepressant treatment, and overall disability. Traditional depression treatment with medication, psychotherapy, or both, is not effective in fully reversing cognitive impairment for most depressed older adults. Physical exercise is an ideal treatment candidate based on evidence that it 1) is an effective treatment for depression, 2) enhances cognitive functioning in normal aging and in other patient populations, and 3) targets many of the neurobiological mechanisms that underlie mood and cognitive functioning. Results of the limited existing clinical trials of exercise for cognitive impairment in depression are mixed but overall support this contention.

Although limited, existing evidence suggests exercise may be a viable alternative or adjunctive treatment to address cognitive impairment in LLD, and thus more research in this area is warranted. Moving forward, additional research is needed in large, diverse samples to translate the growing research findings into clinical practice.

The utility of informant-based measures of cognitive decline to accurately describe objective cognitive performance in Parkinson’s disease (PD) without dementia is uncertain. Due to the clinical relevance of this information, the purpose of this study was to examine the relationship between informant-based reports of patient cognitive decline via the Informant Questionnaire of Cognitive Decline in the Elderly (IQCODE) and objective cognition in non-demented PD controlling for cognitive status (i.e., mild cognitive impairment; PD-MCI and normal cognition; PD-NC).

One-hundred and thirty-nine non-demented PD participants (PD-MCI n = 38; PD-NC n = 101) were administered measures of language, executive function, attention, learning, delayed recall, visuospatial function, mood, and motor function. Each participant identified an informant to complete the IQCODE and a mood questionnaire.

Greater levels of informant-based responses of patient cognitive decline on the IQCODE were significantly associated with worse objective performance on measures of global cognition, attention, learning, delayed recall, and executive function in the overall sample, above and beyond covariates and cognitive status. However, the IQCODE was not significantly associated with language or visuospatial function.

Results indicate that informant responses, as measured by the IQCODE, may provide adequate information on a wide range of cognitive abilities in non-demented PD, including those with MCI and normal cognition. Findings have important clinical implications for the utility of the IQCODE in the identification of PD patients in need of further evaluation, monitoring, and treatment.

Depression is common in people living with HIV (PLWH) and can contribute to neurocognitive dysfunction. Depressive symptoms in PLWH are often measured by assessing only cognitive/affective symptoms. Latinx adults, however, often express depressive symptoms in a somatic/functional manner, which is not typically captured in assessments of depression among PLWH. Given the disproportionate burden of HIV that Latinx adults face, examining whether variations in expressed depressive symptoms differentially predict neurocognitive outcomes between Latinx and non-Hispanic white PLWH is essential.

This cross-sectional study included 140 PLWH (71% Latinx; 72% male; mean (M) age = 47.1 ± 8.5 years; M education = 12.6 ± 2.9 years) who completed a comprehensive neurocognitive battery, Wechsler Test of Adult Reading (WTAR), and Beck Depression Inventory-II (BDI-II). Neurocognitive performance was measured using demographically adjusted T-scores. BDI-II domain scores were computed for the Fast-Screen (cognitive/affective items) score (BDI-FS) and non-FS score (BDI-NFS; somatic/functional items).

Linear regressions revealed that the BDI-NFS significantly predicted global neurocognitive function and processing speed in the Latinx group (p < .05), such that higher physical/functional symptoms predicted worse performance. In the non-Hispanic white group, the cognitive/affective symptoms significantly predicted processing speed (p = .02), with more symptoms predicting better performance. Interaction terms of ethnicity and each BDI sub-score indicated that Latinx participants with higher cognitive/affective symptoms performed worse on executive functioning.

Depressive symptoms differentially predict neurocognitive performance in Latinx and non-Hispanic white PLWH. These differences should be considered when conducting research and intervention among the increasingly culturally and ethnically diverse population of PLWH.

The criteria for objective memory impairment in mild cognitive impairment (MCI) are vaguely defined. Aggregating the number of abnormal memory scores (NAMS) is one way to operationalise memory impairment, which we hypothesised would predict progression to Alzheimer’s disease (AD) dementia.

As part of the Australian Imaging, Biomarkers and Lifestyle Flagship Study of Ageing, 896 older adults who did not have dementia were administered a psychometric battery including three neuropsychological tests of memory, yielding 10 indices of memory. We calculated the number of memory scores corresponding to z ≤ −1.5 (i.e., NAMS) for each participant. Incident diagnosis of AD dementia was established by consensus of an expert panel after 3 years.

Of the 722 (80.6%) participants who were followed up, 54 (7.5%) developed AD dementia. There was a strong correlation between NAMS and probability of developing AD dementia (r = .91, p = .0003). Each abnormal memory score conferred an additional 9.8% risk of progressing to AD dementia. The area under the receiver operating characteristic curve for NAMS was 0.87 [95% confidence interval (CI) .81–.93, p < .01]. The odds ratio for NAMS was 1.67 (95% CI 1.40–2.01, p < .01) after correcting for age, sex, education, estimated intelligence quotient, subjective memory complaint, Mini-Mental State Exam (MMSE) score and apolipoprotein E ϵ4 status.

Aggregation of abnormal memory scores may be a useful way of operationalising objective memory impairment, predicting incident AD dementia and providing prognostic stratification for individuals with MCI.

Sleep deprivation is common among both college students and athletes and has been correlated with negative health outcomes, including worse cognition. As such, the current study sought to examine the relationship between sleep difficulties and self-reported symptoms and objective neuropsychological performance at baseline and post-concussion in collegiate athletes.

Seven hundred seventy-two collegiate athletes completed a comprehensive neuropsychological test battery at baseline and/or post-concussion. Athletes were separated into two groups based on the amount of sleep the night prior to testing. The sleep duration cutoffs for these group were empirically determined by sample mean and standard deviation (M = 7.07, SD = 1.29).

Compared with athletes getting sufficient sleep, those getting insufficient sleep the night prior to baseline reported significantly more overall symptoms and more symptoms from each of the five symptom clusters of the Post-Concussion Symptom Scale. However, there were no significant differences on objective performance indices. Secondly, there were no significant differences on any of the outcome measures, except for sleep symptoms and headache, between athletes getting insufficient sleep at baseline and those getting sufficient sleep post-concussion.

Overall, the effect of insufficient sleep at baseline can make an athlete appear similar to a concussed athlete with sufficient sleep. As such, athletes completing a baseline assessment following insufficient sleep could be underperforming cognitively and reporting elevated symptoms that would skew post-concussion comparisons. Therefore, there may need to be consideration of prior night’s sleep when determining whether a baseline can be used as a valid comparison.

Despite consensus that personality influences mild traumatic brain injury (mTBI) recovery, it has been underexamined. We evaluated the extent to which diverse personality and psychiatric symptom dimensions predict mTBI recovery.

This prospective cohort study involved psychological assessments of hospital patients with mTBI (n = 75; median = 2 days post-injury, range = 0–12 days) and orthopedic trauma controls (OTC; n = 79) who were used for comparison in mediation modeling. Chronic symptoms were evaluated at 3 months after mTBI (n = 50) using the Sport Concussion Assessment Tool (SCAT) symptom checklist. Linear regression analyses were used to identify the predominant predictors of chronic symptoms in mTBI. Modern mediation analyses tested the hypothesis that personality traits predict chronic symptoms through acute psychological response to injury.

In mTBI, trait psychoticism directly predicted chronic mTBI symptoms and was the strongest personality predictor overall. Furthermore, an internalizing personality dimension emphasizing negative affect/emotionality and detachment predicted chronic mTBI symptoms indirectly through enhancement of acute somatic complaints. In OTC, internalizing personality acted through the same mediator as in mTBI, whereas the effect of psychoticism was also mediated through acute somatic complaints. There was varying support for a moderated direct effect of personality traits at low levels of positive emotionality across models.

These causal models provide novel insights about the role of personality in mTBI symptom recovery, highlighting the complexity of how psychological processes may interact to affect recovery and revealing that some of these processes may be non-specific to brain injury.

Sleep quantity and quality are associated with executive function (EF) in experimental studies, and in individuals with sleep disorders. With advancing age, sleep quantity and quality decline, as does the ability to perform EF tasks, suggesting that sleep disruption may contribute to age-related EF declines. This cross-sectional cohort study tested the hypothesis that poorer sleep quality (i.e., the frequency and duration of awakenings) and/or quantity may partly account for age-related EF deficits.

Community-dwelling older adults (N = 184) completed actigraphic sleep monitoring then a range of EF tasks. Two EF factors were extracted using exploratory structural equation modeling. Sleep variables did not mediate the relationship between age and EF factors. Post hoc moderated mediation analyses were conducted to test whether cognitive reserve compensates for sleep-related EF deficits, using years of education as a proxy measure of cognitive reserve.

We found a significant interaction between cognitive reserve and the number and frequency of awakenings, explaining a small (approximately 3%), but significant amount of variance in EF. Specifically, in individuals with fewer than 11 years of education, greater sleep disturbance was associated with poorer EF, but sleep did not impact EF in those with more education. There was no association between age and sleep quantity.

This study highlights the role of cognitive reserve in the sleep–EF relationship, suggesting individuals with greater cognitive reserve may be able to counter the impact of disturbed sleep on EF. Therefore, improving sleep may confer some protection against EF deficits in vulnerable older adults.

Stress is a risk factor for numerous negative health outcomes, including cognitive impairment in late-life. The negative association between stress and cognition may be mediated by depressive symptoms, which separate studies have identified as both a consequence of perceived stress and a risk factor for cognitive decline. Pathways linking perceived stress, depressive symptoms, and cognition may be moderated by sociodemographics and psychosocial resources. The goal of this cross-sectional study was to identify modifying factors and enhance understanding of the mechanisms underlying the stress–cognition association in a racially and ethnically diverse sample of older adults.

A linear regression estimated the association between perceived stress and episodic memory in 578 older adults (Mage = 74.58) in the Washington Heights-Inwood Columbia Aging Project. Subsequent models tested whether depressive symptoms mediated the stress–memory relationship and whether sociodemographics (gender, race, and ethnicity) or perceived control moderated these pathways.

Independent of sociodemographics and chronic diseases, greater perceived stress was associated with worse episodic memory. This relationship was mediated by more depressive symptoms. Higher perceived control buffered the association between stress and depressive symptoms. There was no significant moderation by gender, race, or ethnicity.

Depressive symptoms may play a role in the negative association between perceived stress and cognition among older adults; however, longitudinal analyses and studies using experimental designs are needed. Perceived control is a modifiable psychological resource that may offset the negative impact of stress.

Friedreich’s ataxia (FRDA) is the most common hereditary ataxia. It is a neurodegenerative disorder, characterized by progressive ataxia. FRDA is also associated with cognitive impairments. To date, the evolution of cognitive functioning is unknown. Our aim was to investigate the changes in the cognitive functioning of FRDA patients over an average eight-year timeframe. In addition, we aimed to study the relationship between cognitive changes and clinical variables.

Twenty-nine FRDA patients who had been part of the sample of a previous study participated in the present study. The mean average time between the two assessments was 8.24 years. The participants completed an extensive battery of neuropsychological tests chosen to examine cognitive functioning in various cognitive domains: processing speed, attention, working memory, executive functions, verbal and visual memory, visuoperceptive and visuospatial skills, visuoconstructive functions and language.

At follow-up, cerebellar symptoms had worsened, and patients presented greater disability. Differences between baseline and follow-up were observed in motor and cognitive reaction times, several trials of the Stroop test, semantic fluency, and block designs. No other cognitive changes were observed. Deterioration in simple cognitive reactions times and block designs performance correlated with the progression of cerebellar symptoms.

Our study has demonstrated for the first time that patients with FRDA experience a significant decline over time in several cognitive domains. Specifically, after an eight-year period, FRDA patients worsened in processing speed, fluency, and visuoconstructive skills. This progression is unlikely to be due to greater motor or speech impairment.

The purpose of this study was to pilot safety and tolerability of a 1-week aerobic exercise program during the post-acute phase of concussion (14–25 days post-injury) by examining adherence, symptom response, and key functional outcomes (e.g., cognition, mood, sleep, postural stability, and neurocognitive performance) in young adults.

A randomized, non-blinded pilot clinical trial was performed to compare the effects of aerobic versus non-aerobic exercise (placebo) in concussion patients. The study enrolled three groups: 1) patients with concussion/mild traumatic brain injury (mTBI) randomized to an aerobic exercise intervention performed daily for 1-week, 2) patients with concussion/mTBI randomized to a non-aerobic (stretching and calisthenics) exercise program performed daily for 1-week, and 3) non-injured, no intervention reference group.

Mixed-model analysis of variance results indicated a significant decrease in symptom severity scores from pre- to post-intervention (mean difference = −7.44, 95% CI [−12.37, −2.20]) for both concussion groups. However, the pre- to post-change was not different between groups. Secondary outcomes all showed improvements by post-intervention, but no differences in trajectory between the groups. By three months post-injury, all outcomes in the concussion groups were within ranges of the non-injured reference group.

Results from this study indicate that the feasibility and tolerability of administering aerobic exercise via stationary cycling in the post-acute time frame following post-concussion (14–25 days) period are tentatively favorable. Aerobic exercise does not appear to negatively impact recovery trajectories of neurobehavioral outcomes; however, tolerability may be poorer for patients with high symptom burden.