Cognitive processes underlying verbal and design fluency, and their neural correlates in patients with Alzheimer’s disease (AD) and behavioural variant Frontotemporal Dementia (bvFTD) remain unclear. We hypothesised that verbal and design fluency may be associated with distinct neuropsychological processes in AD and FTD, showing different patterns of impairment and neural basis.

We enrolled 142 participants including patients with AD (n = 80, mean age = 74.71), bvFTD (n = 34, mean age = 68.18), and healthy controls (HCs) (n = 28, mean age = 71.14), that underwent cognitive assessment and 18F-fluorodeoxyglucose positron emission tomography imaging.

Semantic and phonemic fluency showed the largest effect sizes between groups, showing lower scores in bvFTD than AD and HCs, and lower scores in AD than HC. Both AD and bvFTD showed a lower number of unique designs in design fluency in comparison to HC. Semantic fluency was correlated with left frontotemporal lobe in AD, and with left frontal, caudate, and thalamus in bvFTD. Percentage of unique designs in design fluency was associated with the metabolism of the bilateral fronto-temporo-parietal cortex in AD, and the bilateral frontal cortex with right predominance in bvFTD. Repetitions in AD were correlated with bilateral frontal, temporal, and parietal lobes, and with left prefrontal cortex in bvFTD.

Our findings demonstrate differential underlying cognitive processes in verbal and design fluency in AD and bvFTD. While memory and executive functioning associated with fronto-temporo-parietal regions were key in AD, attention and executive functions correlated with the frontal cortex and played a more significant role in bvFTD during fluency tasks.

The current study aims to examine the prevalence rates and the relationship of symptoms of depression, anxiety, and comorbid depression/anxiety with neurocognitive performance in college athletes at baseline. We hypothesized a priori that the mood disturbance groups would perform worse than healthy controls, with the comorbid group performing worst overall.

Eight hundred and thirty-one (M = 620, F = 211) collegiate athletes completed a comprehensive neuropsychological test battery at baseline which included self-report measures of anxiety and depression. Athletes were separated into four groups [Healthy Control (HC) (n = 578), Depressive Symptoms Only (n = 137), Anxiety Symptoms Only (n = 54), and Comorbid Depressive/Anxiety Symptoms (n = 62)] based on their anxiety and depression scores. Athletes’ neurocognitive functioning was analyzed via Z score composites of Attention/Processing Speed and Memory.

One-way analysis of variance revealed that, compared to HC athletes, the comorbid group performed significantly worse on measures of Attention/Processing Speed but not Memory. However, those in the depressive symptoms only and anxiety symptoms only groups were not significantly different from one another or the HC group on neurocognitive outcomes. Chi-square analyses revealed that a significantly greater proportion of athletes in all three affective groups were neurocognitively impaired compared to the HC group.

These results demonstrate that collegiate athletes with comorbid depressive/anxiety symptoms should be identified, as their poorer cognitive performance at baseline could complicate post-concussion interpretation. Thus, assessing for mood disturbance at baseline is essential to obtain an accurate measurement of baseline functioning. Further, given the negative health outcomes associated with affective symptomatology, especially comorbidities, it is important to provide care as appropriate.

Neuropsychological testing reveals a pattern of impairment among patients with obsessive-compulsive disorder (OCD) which implicates the orbitofrontal region. Studies of neuropsychological function in OCD differ regarding performance deficits on classical tests of frontal executive function. In some studies, OCD patients did not demonstrate impaired performance on tests of executive function. However, other researchers have documented performance deficits among OCD patients on measures of executive function. Patients with OCD also exhibit performance deficits on tests of visual/spatial memory and verbal memory. Again, in some studies, OCD patients did not demonstrate impaired performance on tests of memory function. How can we account for the conflicting findings? One possibility is that performance deficits on tests of cognitive function are associated with comorbid conditions. In prior work, we observed that OCD patients who did poorly on executive function tasks obtained high scores on a measure of schizotypal personality. A second possibility is that executive function deficits among patients with OCD are associated with comorbid depressive symptoms.

In the present study, a comprehensive neuropsychological test battery was administered to patients with OCD and matched healthy control subjects. We also administered dimensional measures of schizotypal personality and depression to patients with OCD and controls. We conducted analyses of covariance (ANCOVA), with scores on measures of schizotypal personality and depression used as covariates.

OCD patients demonstrated performance deficits on measures of delayed memory, response inhibition, alternation learning, and obtained significantly higher scores on measures of disinhibition, impulsivity, and temporolimbic symptoms; however, OCD patients did not exhibit impaired performance on tests of executive function and verbal fluency, and did not report a significantly greater number of dysexecutive symptoms, when coexistent depressive and schizotypal symptoms were taken into account.

Findings are consistent with the contention that dysfunction of an orbitofrontal-limbic network underlies OCD.

To characterize adults with comorbid attention-deficit/hyperactivity-disorder (ADHD) and borderline personality disorder (BPD) with regard to ADHD symptoms, psychopathology, cognitive functioning and psychosocial factors.

A between-group design compared a group of individuals diagnosed with ADHD (n = 40) with a group diagnosed with BPD and who also met the criteria for ADHD (ADHD + BPD) (n = 20).

Significant differences were observed for both childhood and current impulsivity symptoms, whereby ADHD + BPD exhibited increased impulsivity; no differences on self-report and cognitive measures of impulsivity were reported. The ADHD + BPD group scored significantly higher on measures of depression, anxiety and numerous other axis I and II conditions. The ADHD + BPD group scored significantly lower on most measures of intellectual functioning and attention, however largely not on those relating to response inhibition. Furthermore, group differences were observed for psychosocial factors, including education, substance use and criminal record.

Comorbid ADHD and BPD is characterized by more symptoms of impulsivity, additional psychopathology, comparatively lower intellectual and attentional functioning and increased psychosocial difficulties.

Emerging data suggest that recovery from mild traumatic brain injury (mTBI) takes longer than previously thought. This paper examines trajectories for cognitive recovery up to 48 months post-mTBI, presenting these visually using a Sankey diagram and growth curve analysis.

This sample (n = 301) represents adults (≥16 years) from a population-based Brain Injury Outcomes in the New Zealand Community study over a 4-year follow-up on the CNS-Vital Signs neuropsychological test. Data were collected within 2 weeks of injury, and then at 1, 6, 12 and 48 months post-injury.

Significant improvement in cognitive functioning was seen up to 6 months post-injury. Using growth curve modelling, we found significant improvements in overall neurocognition from baseline to 6 months, on average participants improved one point per month (0.9; 95% CI 0.42–1.39) p < 0.001. No change in neurocognition was found within the time periods 6–12 months or 12–48 months. The Sankey highlighted that at each time point, a small proportion of participants remained unchanged or declined. Proportionally, few show any improvement after the first 6 months.

Most individuals remained stable or improved over time to 6 months post-injury. Summary statistics are informative regarding overall trends, but can mask differing trajectories for recovery. The Sankey diagram indicates that not all improve, as well as the potential impact of individuals moving in and out of the study. The Sankey diagram also indicated the level of functioning of those most likely to withdraw, allowing targeting of retention strategies.

The logopenic variant of primary progressive aphasia (lvPPA) has disparate pathological and anatomical features when compared to the semantic (svPPA) and non-fluent (nfvPPA) variants of PPA. As such, there is increasing need for measures that improve diagnostic accuracy particularly when etiology-specific treatments become available. In the current study, we used meta-analytic methods to establish the neuropsychological profile of lvPPA and compare it to recent findings in svPPA and nfvPPA.

We extracted neuropsychological data from 51 publications representing 663 lvPPA patients and 1379 controls. We calculated Hedges’ g effect sizes for nine domains of neuropsychological functioning in lvPPA and assessed the influence of demographic, disease, and task characteristics on effect size magnitude. Results obtained in lvPPA were compared to findings in svPPA and nfvPPA.

In lvPPA, the magnitude of deficits in attention, math, visuospatial memory, and executive functioning were as prominent as language deficits. Within the language domain, lvPPA patients demonstrated greater naming than repetition deficits. Compared to svPPA and nfvPPA, lvPPA patients demonstrated greater neuropsychological deficits overall and greater impairment on attention, math, and visual set-shifting tests.

Tests of attention, delayed visuospatial memory, visual set-shifting, and math distinguish lvPPA from svPPA and nfvPPA likely reflecting the posterior temporoparietal atrophy observed early in the course of lvPPA. These findings support the inclusion of these measures in the clinical neuropsychological assessment of lvPPA and underscore the need for additional clinicopathological and longitudinal studies of arithmetic and visuospatial memory across the PPA variants.

Neuropsychological investigations can help untangle the aetiological and phenomenological heterogeneity of schizophrenia but have scarcely been employed in the context of treatment-resistant (TR) schizophrenia. No population-based study has examined neuropsychological function in the first-episode of TR psychosis.

We report baseline neuropsychological findings from a longitudinal, population-based study of first-episode psychosis, which followed up cases from index admission to 10 years. At the 10-year follow up patients were classified as treatment responsive or TR after reconstructing their entire case histories. Of 145 cases with neuropsychological data at baseline, 113 were classified as treatment responsive, and 32 as TR at the 10-year follow-up.

Compared with 257 community controls, both case groups showed baseline deficits in three composite neuropsychological scores, derived from principal component analysis: verbal intelligence and fluency, visuospatial ability and executive function, and verbal memory and learning (p values⩽0.001). Compared with treatment responders, TR cases showed deficits in verbal intelligence and fluency, both in the extended psychosis sample (t = −2.32; p = 0.022) and in the schizophrenia diagnostic subgroup (t = −2.49; p = 0.017). Similar relative deficits in the TR cases emerged in sub-/sensitivity analyses excluding patients with delayed-onset treatment resistance (p values<0.01–0.001) and those born outside the UK (p values<0.05).

Verbal intelligence and fluency are impaired in patients with TR psychosis compared with those who respond to treatment. This differential is already detectable – at a group level – at the first illness episode, supporting the conceptualisation of TR psychosis as a severe, pathogenically distinct variant, embedded in aberrant neurodevelopmental processes.

Delirium is an acute, severe deterioration in mental functioning. Inattention is the core feature, yet there are few objective methods for assessing attentional deficits in delirium. We previously developed a novel, graded test for objectively detecting inattention in delirium, implemented on a computerized device (Edinburgh Delirium Test Box (EDTB)). Although the EDTB is effective, tests on universally available devices have potential for greater impact. Here we assessed feasibility and validity of the DelApp, a smartphone application based on the EDTB.

This was a preliminary case-control study in hospital inpatients (aged 60–96 years) with delirium (N = 50), dementia (N = 52), or no cognitive impairment (N = 54) who performed the DelApp assessment, which comprises an arousal assessment followed by counting of lights presented serially. Delirium was assessed using the Confusion Assessment Method and Delirium Rating Scale-Revised-98 (DRS-R98), and cognition with conventional tests of attention (e.g. digit span) and the short Orientation-Memory-Concentration Test (OMCT).

DelApp scores (maximum score = 10) were lower in delirium (scores (median(IQR)): 6 (4–7)) compared to dementia (10 (9–10)) and control groups (10 (10–10), p-values < 0.001). Receiver operating characteristic (ROC) analyses revealed excellent accuracy of the DelApp for discriminating delirium from dementia (AUC = 0.93), and delirium from controls (AUC = 0.99, p-values < 0.001). DelApp and DRS-R98 severity scores were moderately well correlated (Kendall's tau = −0.60, p < 0.001). OMCT scores did not differ between delirium and dementia.

The DelApp test showed good performance, supporting the utility of objectively measuring attention in delirium assessment. This study provides evidence of the feasibility of using a smartphone test for attentional assessment in hospital inpatients with possible delirium, with potential applications in research and clinical practice.

An association between metabolic syndrome (MetS) and disturbances in neurocognitive function has been identified in Caucasians but the nature and extent of impaired cognition in Asian MetS patients, who may be at greater risk of degenerative cognitive decline, remains unspecified.

A cross-sectional study was conducted at the National University Hospital of Singapore. Participants were recruited from a diabetes clinic at the National University Hospital. Fifty-three patients who met MetS criteria and 44 clinical controls were recruited. All participants were 55 years and above and community ambulant. Neurocognitive function was assessed using the Cambridge Neuropsychological Test Automated Battery (CANTAB). CANTAB performances between MetS and control groups were examined with analysis of variance (ANOVA) and the relative contributions of vascular risk, and intrademographic factors on CANTAB scores were dilineated with stepwise regression analyses.

Participants with MetS consistently performed significantly worse than controls across all CANTAB subtests. Education and Chinese race were found to be potential protective factors.

Executive and memory impairment is present in Asian patients with midlife MetS who may be particularly vulnerable to the detrimental impact of MetS in midlife.

Our previous work identified deficits in interference processing and learning/memory in past suicide attempters who were currently depressed and medication-free. In this study, we extend this work to an independent sample studied at various stages of illness and treatment (mild symptoms, on average) to determine if these deficits in past suicide attempters are evident during a less severe clinical state.

A total of 80 individuals with a past history of major depression and suicide attempt were compared with 81 individuals with a history of major depression and no lifetime suicide attempts on a battery of neurocognitive measures assessing attention, memory, abstract/contingent learning, working memory, language fluency and impulse control.

Past attempters performed more poorly in attention, memory and working memory domains, but also in an estimate of pre-morbid intelligence. After correction for this estimate, tests that had previously distinguished past attempters – a computerized Stroop task and the Buschke Selective Reminding Test – remained significantly worse in attempters. In a secondary analysis, similar differences were found among those with the lowest levels of depression (Hamilton Depression Rating Scale score <10), suggesting that these deficits may be trait markers independent of current symptomatology.

Deficits in interference processing and learning/memory constitute an enduring defect in information processing that may contribute to poor adaptation, other higher-order cognitive impairments and risk for suicidal behavior.