Deficits In Aspects Research Articles

Reframing acute kidney injury as a pathophysiological continuum of disrupted renal excretory function.

Surrogate measures of glomerular filtration rate (GFR) continue to serve as pivotal determinants of the incidence, severity, and management of acute kidney injury (AKI), as well as the primary reference point underpinning knowledge of its pathophysiology. However, several clinically important deficits in aspects of renal excretory function during AKI other than GFR decline, including acid-base regulation, electrolyte and water balance, and urinary concentrating capacity, can evade detection when diagnostic criteria are built around purely GFR-based assessments. The use of putative markers of tubular injury to detect "sub-clinical" AKI has been proposed to expand the definition and diagnostic criteria for AKI, but their diagnostic performance is curtailed by ambiguity with respect to their biological meaning and context specificity. Efforts to devise new holistic assessments of overall renal functional compromise in AKI would foster the capacity to better personalize patient care by replacing biomarker threshold-based diagnostic criteria with a shift to assessment of compromise along a pathophysiological continuum. The term AKI refers to a syndrome of sudden renal deterioration, the severity of which is classified by precise diagnostic criteria that have unquestionable utility in patient management as well as blatant limitations. Particularly, the absence of an explicit pathophysiological definition of AKI curtails further scientific development and clinical handling, entrapping the field within its present narrow GFR-based view. A refreshed approach based on a more holistic consideration of renal functional impairment in AKI as the basis for a new diagnostic concept that reaches beyond the boundaries imposed by the current GFR threshold-based classification of AKI, capturing broader aspects of pathogenesis, could enhance AKI prevention strategies and improve AKI patient outcome and prognosis.

48 A Case of an Extremely Rare CNS C. Bantiana Infection with Cognitive Sequela in an Immunocompetent Patient

Objective:Central nervous system (CNS) infections with the dematiaceous fungus Cladophialophora bantiana (C. bantiana) are extremely rare, with approximately 120 confirmed cases reported as of 2016. C. bantiana is a highly neurotropic and thermotolerant fungus found in soil worldwide. The mode of entry into the CNS remains unknown, but inhalation of fungal spores or subcutaneous trauma have been suggested. Entry of fungal spores can cause cerebral phaeohyphomycosis with the main clinical manifestation of a brain abscess. Symptoms are non-specific and can include headache, fever, hemiparesis, aphasia, visual disturbances, and confusion. C. bantiana cerebral phaeohyphomycosis occurs in both immunocompetent and immunocompromised individuals, with a slightly higher prevalence in immunocompetent males for unknown reasons. Diagnosis is often delayed due to its nonspecific presentation and prevalence in individuals without pre-existing immunological disease. Prognosis is poor, with mortality rates of approximately 70% despite aggressive treatment. Treatment is not standardized but may include several anti-fungal agents and surgical intervention. Case reports documenting the variability seen with cerebral phaeohyphomycosis by C. bantiana can provide valuable insight into this emerging disease. C. bantiana’s neurotropic propensity also warrants cognitive investigation of the disease; however, there are currently limited descriptions of cognitive findings in published case reports of C. bantiana CNS infections.Participants and Methods:Here, we describe a case of a 35-year-old immunocompetent, college educated male with a CNS C. bantiana infection, presumably following a fall while biking in Costa Rica. First symptoms included left sided facial palsy, headache, and hand weakness, prompting extensive diagnostic workup, with diagnosis of C. bantiana infection confirmed 8 months after symptom onset. Initial treatment included anti-fungal agents and steroids, but his course of infection was complicated by infectious vasculitis with posterior circulation infarcts and obstructive hydrocephalus requiring ventriculoperitoneal shunt placement two years following the fungal infection diagnosis. The most recent brain MRI revealed encephalomalacia in global periventricular areas, two small masses, likely representing small fungal phlegmons, and enhancing lesions in the upper cervical spinal canal.Results:The patient reported cognitive changes following the infarcts and shunt placement including difficulties with spatial navigation, following directions, and articulating thoughts. Memory concerns and lapses in judgment were also reported. Results from a neuropsychological evaluation revealed high average baseline intellectual abilities with decrements in visuospatial processing, processing speed, executive functioning, and aspects of memory stemming from his executive dysfunction. At the time, his cognitive profile suggested parietal and frontosubcortical systems disruption meeting criteria for mild cognitive impairment. Two years later, the patient reported continuing cognitive difficulties prompting a follow-up neuropsychological evaluation. Results were similar to his first evaluation, revealing deficits in aspects of visuospatial processing, decreased verbal and visual learning, bradyphrenia and processing speed deficits, and difficulties with visual planning and organization. Minimal anxiety and depression, but increased apathy and executive dysfunction were endorsed on self-report measures.Conclusions:This case report highlights neurological sequela resulting from CNS infection with C. bantiana, -with a course complicated by subsequent strokes, hydrocephalus, and cognitive impairment-, and contributes additional insight into the relatively limited existing reports of an extremely rare but emerging disease.

A - 12 Investigating Relationships between Theory of Mind, Executive Functioning, and Adaptive Functioning in Non-Demented Older Adults.

Theory of mind (ToM) is a facet of social cognition that relies on the ability to infer the mental states of others and is a cognitive and emotional capacity that may become compromised in the context of neurodegeneration. This may put older adults at greater risk for financial exploitation or susceptibility to scams. We investigated relationships among executive functioning, financial capacity, and ToM in a sample of older adults who did not have a diagnosis of dementia. Participants were cognitively unimpaired or presented with subjective cognitive decline or mild cognitive impairment. As part of a comprehensive neuropsychological battery, participants completed the Reading the Mind in the Eyes Test (RMET), a measure of ToM in which participants view photos of the eye region of the face and select which social emotion they perceive to be depicted in each photo. Pearson correlations were calculated to test relationships among RMET performance and select measures of executive functioning (D-KEFS Trail Making Test 4, Letter Fluency) and basic financial skills (Financial Capacity Instrument, short form). Participants' (n = 72; M age = 75.36; M education = 15.676; 69% female) RMET performance was significantly associated with measures of executive functioning (r = 0.243, p = 0.041), mental flexibility (r = -0.283, p = 0.017), and financial skills (r = 0.291, p = 0.015). Capacity for ToM is linked with integrity of executive functioning skills and financial capacity in older adults with varying degrees of cognitive compromise. Older adults who demonstrate deficits in aspects of social cognition may be at risk for poor outcomes in key cognitive and adaptive skills in daily life.

Exposure to deltamethrin at the NOAEL causes ER stress and disruption of hippocampal neurogenesis in adult mice

In addition to age and traumatic brain injury, environmental exposure to pesticides is a potential risk factor for neurodegenerative diseases and cognitive impairments in humans. Deltamethrin is a type II pyrethroid insecticide widely used in agriculture and homes for pest control. Previously, we reported that repeated exposure of mice to 3 mg/kg deltamethrin for 30 or 60 days caused a marked increase in the endoplasmic reticulum (ER) stress and reduced adult hippocampal neurogenesis that was accompanied by impaired learning and memory. However, it is unknown whether an acute exposure to low doses of deltamethrin elicits similar effects. Here, we sought to characterize the dose-related effects of deltamethrin on ER stress and hippocampal neurogenesis at different time points following acute exposure. Following oral administration of 0, 0.3, 1, or 3 mg/kg deltamethrin, doses below, at, and above the acute NOAEL, mice were euthanized at 24 h, 48 h, 7 d, or 14 d to assess the acute and intermediate-term effects of deltamethrin on neural progenitor cells (NPCs). Deltamethrin at both 1 and 3 mg/kg elicited ER stress response and activation of apoptotic signaling. Data revealed that a dose as low as 1 mg/kg of deltamethrin, considered the acute NOAEL, produced a significant reduction in BrdU+ and Ki-67+ neural stem cells in the subgranular zone of the dentate gyrus of the hippocampus as early as 48 h after exposure. Furthermore, mice treated with 1 and 3 mg/kg deltamethrin exhibited a decreased number of immature neurons, determined by counting DCX-positive cells 7 days after exposure. These data establish that 0.3 mg/kg should be considered a NOAEL and that the previously established acute NOAEL of 1 mg/kg shows significant effects on ER stress and apoptotic pathways accompanied by deficits in aspects of adult hippocampal neurogenesis.

Series of virtual light therapy interventions for fatigue: a feasibility pilot study protocol for a series of personalised (N-of-1) trials

IntroductionFatigue is one of the most commonly recorded patient symptoms that can result in deficits in aspects of psychomotor functioning, cognition, work performance and mood. Research shows that bright light...

Changes in Loss Sensitivity During Treatment in Concurrent Disorders Inpatients: A Computational Model Approach to Assessing Risky Decision-Making.

BackgroundRecent studies have employed computational modeling to characterize deficits in aspects of decision-making not otherwise detected using traditional behavioral task outcomes. While prospect utility-based modeling has shown to differentiate decision-making patterns between users of different drugs, its relevance in the context of treatment has yet to be examined. This study investigated model-based decision-making as it relates to treatment outcome in inpatients with co-occurring mental health and substance use disorders.Methods50 patients (Mage = 38.5, SD = 11.4; 16F) completed the Cambridge Gambling Task (CGT) within 2 weeks of admission (baseline) and 6 months into treatment (follow-up), and 50 controls (Mage = 31.9, SD = 10.0; 25F) completed CGT under a single outpatient session. We evaluated 4 traditional CGT outputs and 5 decisional processes derived from the Cumulative Model. Psychiatric diagnoses and discharge data were retrieved from patient health records.ResultsGroups were similar in age, sex, and premorbid IQ. Differences in years of education were included as covariates across all group comparisons. All patients had ≥1 mental health diagnosis, with 80% having >1 substance use disorder. On the CGT, patients showed greater Deliberation Time and Delay Aversion than controls. Estimated model parameters revealed higher Delayed Reward Discounting, and lower Probability Distortion and Loss Sensitivity in patients relative to controls. From baseline to follow-up, patients (n = 24) showed a decrease in model-derived Loss Sensitivity and Color Choice Bias. Lastly, poorer Quality of Decision-Making and Choice Consistency, and greater Color Choice Bias independently predicted higher likelihood of treatment dropout, while none were significant in relation to treatment length of stay.ConclusionThis is the first study to assess a computational model of decision-making in the context of treatment for concurrent disorders. Patients were more impulsive and slower to deliberate choice than controls. While both traditional and computational outcomes predicted treatment adherence in patients, findings suggest computational methods are able to capture treatment-sensitive aspects of decision-making not accessible via traditional methods. Further research is needed to confirm findings as well as investigate the relationship between model-based decision-making and post-treatment outcomes.

Cystic fibrosis-related diabetes (CFRD) and cognitive function in adults with cystic fibrosis

BackgroundBeing able to function cognitively is imperative for successful achievement in school, working life, and disease self-management. Diabetes is known to cause changes in brain structure and long-term cognitive dysfunction. This work investigated cystic fibrosis-related diabetes (CFRD) as a mechanism for cognitive impairment in people with CF. It was hypothesised that cognition would be poorer in adults with CFRD than in those with CF without diabetes (CFND) or in healthy controls. MethodsCognitive performance was assessed using the Cambridge Neuropsychological Test Automated Battery which provides a comprehensive cognitive assessment with tests mapping onto specific brain regions. Demographic, clinical and self-reported health data were documented for all participants. CF specific clinical variables were recorded for the two CF groups. ResultsNinety-eight people with CF (49CFRD,49CFND) and 49 healthy controls were recruited. People with CF demonstrated deficits in aspects of verbal and spatial memory, processing speed and cognitive flexibility compared with healthy controls, with all areas of the brain implicated. Those with CFRD had additional difficulties with higher-level processes known collectively as ‘executive function’, which demand greater cognitive load and recruit the prefrontal cortex. Compared with healthy controls, those with CFND and CFRD had an estimated 20% and up to 40% reduction in processing speed respectively. ConclusionManaging CF requires higher order executive function. Impairments may be sufficient to interfere with self-care and the ability to perform everyday tasks efficiently. At which point in the CF disease trajectory these difficulties begin, and what may attenuate them, has yet to be determined.

Directing attention to event changes improves memory updating for older adults.

People use memory for observed actions to guide current perceptions. When actions change from one situation to the next, one must register the change to update memory. Research suggests that older adults may sometimes update memory for naturalistic action changes less effectively than younger adults. We examined whether this deficit reflects age differences in attention allocation by cuing attention to changed action features and testing memory for those features. Older (N = 47) and younger (N = 73) adults watched movies of an actor performing everyday activities on two fictive "days" in her life. Some activities began identically on both days (e.g., reaching for dessert) and ended with features that changed across days (e.g., cookie vs. brownie). Half of the changed activities included audio-visual cues on both days that signaled changed features, whereas the other half did not include cues. Memory updating was assessed through cued recall and two-alternative forced choice recognition (2AFC recognition) of recent action features. Cuing attention improved cued recall but not 2AFC recognition of recent action features for both older and younger adults. These recall benefits were associated with improved recollection that changes had earlier occurred. The present findings suggest that although older adults sometimes experience deficits in aspects of attention, using cues to guide their attention to features of everyday activities can enhance their event memory updating when the later memory test emphasizes recollection-based retrieval. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

Self-serving social strategies: A systematic review of social cognition in narcissism

Narcissistic Personality Disorder is characterised by inflated self-importance, an excessive need for admiration, and a lack of empathy. The interpersonal difficulties associated with narcissistic personality may be becoming more widespread given its increasing prevalence within the general population. This systematic review investigated the relationship between narcissistic personality traits and social cognition (i.e. theory of mind; emotion recognition; empathy; emotional intelligence) in clinical and non-clinical samples. Cognitive empathy (i.e. perspective taking) appears unlikely to be impaired, while affective empathy (relating to another’s emotion state) may be reduced in association with narcissism. Those with grandiose narcissism rate their empathic skills more highly than those with vulnerable narcissism, but concurrent administration of objective measures is rare, limiting insight into the validity of self-ratings. Rather than deficits in aspects of social cognition, the overall pattern could reflect motivation, or advantageous use of social cognitive skills to serve the self. Indeed, interpersonal strategies associated with narcissism (e.g. deception; manipulation) suggest the application of understanding another’s beliefs or desires in the context of low empathy. Further research should seek to explore performance on a wider range of emotion recognition and theory of mind tasks, and whether characteristics such as excessive jealousy and paranoia could reflect hyper-mentalizing.

Olfactory and Neuropsychological Functioning in Olfactory Reference Syndrome

Olfactory reference syndrome (ORS) is an underrecognized, understudied, and often severe psychiatric disorder characterized by a prominent and distressing or impairing preoccupation with a false belief of emitting an offensive body odor. As this condition has only recently been recognized in the International Classification of Diseases (the 11th Edition), no empirical evidence exists about the underlying features and etiology of the disorder. To examine the neuropsychological and olfactory functioning of individuals with ORS and address whether there is central nervous system or sensory dysfunction associated with the condition. In this preliminary investigation, 9 consecutive participants with ORS completed a structured clinical interview and neuropsychological and olfaction evaluations. A proportion of individuals with ORS displayed deficits in aspects of cognitive functioning (i.e., processing speed, executive functioning, recognition memory bias for ORS-related words), olfaction functioning (i.e., odor detection and discrimination), and emotional processing. Based on these preliminary findings of cognitive, olfaction, and emotional processing deficits in individuals with ORS, further neuropsychological and olfaction studies are needed that better characterize this understudied patient group and address this study's limitations.

A 9-year neuropsychological report of a patient with LGI1-associated limbic encephalitis

ABSTRACTIntroduction: Anti-leucine-rich glioma-inactivated 1 limbic encephalitis (LGI1-LE) is an autoimmune disorder associated with antibodies to voltage-gated potassium channels (VGKC). It is a non-paraneoplastic and partially reversible encephalitis that can be diagnosed via serological testing. Untreated LGI1-LE can be associated with neurocognitive as well as neuropsychiatric sequelae. Here we report the neuropsychological and clinical profile of a patient with LGI1-LE following three different treatment approaches: plasmapheresis (PA), intravenous immunoglobulin (IVIG), and corticosteroids (CO).Method: We investigated our patient with 10 neuropsychological evaluations obtained over a 9-year follow-up period. Multiple MRI scans, EEG recordings, neurological examinations, and serum tests were also obtained.Results: The neurocognitive profile of our patient was characterized by long-term memory impairment (verbal and visual-spatial), and deficits in aspects of executive functioning and language. Neuropsychiatric symptoms of depression and anxiety were noted intermittently.Conclusions: Non-specific treatment prior to diagnosis had marginal effects on neurocognitive profile, neuropsychiatric symptoms, or control of epileptic seizure. In contrast, specific treatments for LGI1-LE following diagnosis resulted in neurocognitive improvement and epileptic control. Among the three treatments, IVIG and CO had the most beneficial impact on neurocognitive status, likely due to the continuity of administration.

Asthenia in the psychopathological space of schizophrenia and schizophrenia spectrum disorders (The concept of asthenic deficit in aspect of the modern model of negative symptoms)

At the modern level of knowledge, classification of asthenic deficit as an independent psychopathological category and, in general terms, as the classification of asthenic symptomatic complexes of negative symptoms within schizophrenia and schizophrenia spectrum disorders is the subject of discussion. Studies of recent decades have shown that asthenia cannot be considered as a separate deficient monosyndrome, does not fit into the framework of negative disorders and is excluded from the block of scales of negative symptoms (SANS, PANSS, BNSS, CAINS). The authors suggest a working hypothesis that asthenia symptomatic complexes within schizophrenia are not comparable either in nature or in their psychopathological structure with primary deficiency disorders determined by the disease process. However, at the same time schizoasthenia, acting as a manifestation of the coenesthesiopathic hypochondriacal register, i.e. essentially in the space of positive disorders, is formed in close dependence on negative symptoms and is thus one of the markers of the already formed defect.

BEHAVIORAL VARIANT FTD CAUSED BY UBQLN2 P525S MUTATION, WITHOUT EVIDENCE OF MOTOR NEURON DISEASE

Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (FTD) represent extremes of a spectrum with significant overlap. Numerous gene mutations are known to cause these diseases in isolation or combination. Ubiquilin 2 (UBQLN2) mutations have recently been described and have been shown to cause either pure ALS or combination ALS/FTD. Presentation of a well characterized case of FTD caused by a UBQLN2 mutation without clinical or familial evidence of ALS. A 69-year-old right-handed man with a 2-year history of personality changes, unwelcomed familiarity, and increased gregariousness and embellishments with growing grandeur, at times delusional. There was “lack of filtering” and more childishness, playing with grandchildren “at their level”. Appetitive changes included a diet of Frappuccino's, jelly beans, and devil dogs. Lost $20 000 in a scam. Unable to maintain gainful employment as an information technology consultant. Past medical and psychiatric history: non-contributory. Family history: father passed from liver cancer at 53, mother from dementia at 83, sister with hypochotdriasis, and “bipolar” brother who passed in his 60s from pancreatic cancer. Examination: mild diffuse extrapyramidal syndrome without evidence of pyramidal or lower motor neuron disease. MoCA was 20/30, moderate deficits in attention/concentration with impact on memory, which was fully recovered with cues. Neuropsychological assessment revealed tangentiallity, impulsivity, and impersistence. There were deficits in aspects of learning, attention, and executive functions, with intact contextual memory, language, and visual spatial functions. MRI and FDG-PET scans showed focal frontal and anterior temporal atrophy and hypometabolism. Whole exome sequencing failed to reveal the better known genetic causes of FTD (MAPT, GRN, and C9orf72), but did show a known pathologic P525S mutation of the UBQLN2 gene. In addition, known risk or modifyier genes variants were also absent. Remains without clinical evidence of motor neuron disease 5 years following initial symptoms. To our knowledge, this is the first documented case of an isolated presentation of behavioral variant FTD without ALS, caused by a mutation in UBQLN2. Although still rare, this case further expands the spectrum of diseases caused by this mutation.

Learning and Memory in Adolescents With Critical Biventricular Congenital Heart Disease.

Although evidence exists of broadly defined memory impairment among adolescents with critical congenital heart disease (CHD), nuanced investigations of declarative memory in this at-risk population have not been conducted. This study had two primary aims: (1) to conduct a fine-grained analysis of a range of relevant learning and memory processes in adolescents with critical biventricular CHD, and (2) to identify risk, odds, and predictors of memory impairment. Data were combined from two single-center studies of neurodevelopmental outcomes in critical CHD. Two-hundred seven adolescents (M age =15.61±1.0 years) with critical CHD (139 with dextro-transposition of the great arteries and 68 with tetralogy of Fallot without an identified genetic condition), as well as 61 healthy referents (M age =15.27±1.1 years) completed a neuropsychological evaluation which included the Children's Memory Scale. Whereas visual-spatial memory deficits were found in both CHD subgroups, verbal memory abilities were relatively preserved. Adolescents with CHD demonstrated stronger memory for Stories than Word Pairs, t (203)=2.63, p=.009, and for Dot Locations than Faces, t(204)=-2.57, p=.01. CHD subgroup, socioeconomic status, sex, and seizure history were among the most frequent significant predictors of memory impairment. Seizure history, in particular, was associated with a 2 to 3 times greater odds of impaired performance on learning and memory tasks. Adolescents with critical biventricular CHD are at risk for deficits in aspects of declarative memory. Independent risk factors for worse outcome include history of seizures. (JINS, 2017, 23, 627-639).

Replicable in vivo physiological and behavioral phenotypes of the Shank3B null mutant mouse model of autism

BackgroundAutism spectrum disorder (ASD) is a clinically and biologically heterogeneous condition characterized by social, repetitive, and sensory behavioral abnormalities. No treatments are approved for the core diagnostic symptoms of ASD. To enable the earliest stages of therapeutic discovery and development for ASD, robust and reproducible behavioral phenotypes and biological markers are essential to establish in preclinical animal models. The goal of this study was to identify electroencephalographic (EEG) and behavioral phenotypes that are replicable between independent cohorts in a mouse model of ASD. The larger goal of our strategy is to empower the preclinical biomedical ASD research field by generating robust and reproducible behavioral and physiological phenotypes in animal models of ASD, for the characterization of mechanistic underpinnings of ASD-relevant phenotypes, and to ensure reliability for the discovery of novel therapeutics. Genetic disruption of the SHANK3 gene, a scaffolding protein involved in the stability of the postsynaptic density in excitatory synapses, is thought to be responsible for a relatively large number of cases of ASD. Therefore, we have thoroughly characterized the robustness of ASD-relevant behavioral phenotypes in two cohorts, and for the first time quantified translational EEG activity in Shank3B null mutant mice.MethodsIn vivo physiology and behavioral assays were conducted in two independently bred and tested full cohorts of Shank3B null mutant (Shank3B KO) and wildtype littermate control (WT) mice. EEG was recorded via wireless implanted telemeters for 7 days of baseline followed by 20 min of recording following pentylenetetrazol (PTZ) challenge. Behaviors relevant to the diagnostic and associated symptoms of ASD were tested on a battery of established behavioral tests. Assays were designed to reproduce and expand on the original behavioral characterization of Shank3B KO mice. Two or more corroborative tests were conducted within each behavioral domain, including social, repetitive, cognitive, anxiety-related, sensory, and motor categories of assays.ResultsRelative to WT mice, Shank3B KO mice displayed a dramatic resistance to PTZ seizure induction and an enhancement of gamma band oscillatory EEG activity indicative of enhanced inhibitory tone. These findings replicated in two separate cohorts. Behaviorally, Shank3B KO mice exhibited repetitive grooming, deficits in aspects of reciprocal social interactions and vocalizations, and reduced open field activity, as well as variable deficits in sensory responses, anxiety-related behaviors, learning and memory.ConclusionsRobust animal models and quantitative, replicable biomarkers of neural dysfunction are needed to decrease risk and enable successful drug discovery and development for ASD and other neurodevelopmental disorders. Complementary to the replicated behavioral phenotypes of the Shank3B mutant mouse is the new identification of a robust, translational in vivo neurophysiological phenotype. Our findings provide strong evidence for robustness and replicability of key translational phenotypes in Shank3B mutant mice and support the usefulness of this mouse model of ASD for therapeutic discovery.

The Role Of Sex As A Moderator Of Cognitive Outcome Following A Sport-related Concussion

Despite increasing research, results regarding sex as a moderator of outcome following a concussion are conflicting and management guidelines remain uncertain. PURPOSE: To determine if there is a gender difference in the long-term cognitive outcomes of athletes with a history of concussion (HOC). METHODS: 196 collegiate athletes (49 HOC women, HOC 49 men, 49 women matched controls, 49 men matched controls) completed a modified Cogstate test battery, to which a 2-back condition (N-back task) was added to increase our ability to detect persistent deficits in higher cognition. All participants were symptom-free at time of testing and those with a HOC were 6+ months from injury (24.0 ± 15.8 months, 1.44 ± 1.3 prior concussions). RESULTS: A significant interaction of error type × HOC × sex was observed. Specifically, HOC men exhibited a greater number of omission errors relative to HOC women (2.94 ± 2.5 vs. 0.31 ± 0.9, p<0.05). Moreover, irrespective of sex, HOC athletes exhibited a greater number of errors on the 1-back (2.30 ± 1.5 vs. 0.79 ± 0.9, p<0.01) and 2-back conditions (3.34 ± 2.6 vs. 1.46 ± 1.4, p<0.01), relative to controls. HOC athletes also exhibited decreased accuracy on the 1-back (95.45 ± 3.0% vs. 98.21± 2.2%, p<0.01) and 2-back conditions (93.98 ± 4.1% vs. 96.65 ± 3.3%, p<0.05). CONCLUSIONS: The current results suggest that beyond the acute phase of the injury, sex does not seem as a moderating variable of cognitive outcomes following concussion. Furthermore, the results reaffirm that concussive injuries can result in persistent deficits in aspects of higher cognition.

Executive Function in Children and Adolescents with Critical Cyanotic Congenital Heart Disease.

Children and adolescents with critical cyanotic congenital heart disease (CHD) are at risk for deficits in aspects of executive function (EF). The primary aim of this investigation was to compare EF outcomes in three groups of children/adolescents with severe CHD and controls (ages 10-19 years). Participants included 463 children/adolescents with CHD [dextro-transposition of the great arteries (TGA), n=139; tetralogy of Fallot (TOF), n=68; and, single-ventricle anatomy requiring Fontan procedure (SVF), n=145] and 111 controls, who underwent laboratory and informant-based evaluation of EF skills. Rates of EF impairment on D-KEFS measures were nearly twice as high for CHD groups (75-81%) than controls (43%). Distinct EF profiles were documented between CHD groups on D-KEFS tasks. Deficits in flexibility/problem-solving and verbally mediated EF skills were documented in all three CHD groups; visuo-spatially mediated EF abilities were impaired in TOF and SVF groups, but preserved in TGA. Parent, teacher, and self-report ratings on the BRIEF highlighted unique patterns of metacognitive and self-regulatory concerns across informants. CHD poses a serious threat to EF development. Greater severity of CHD is associated with worse EF outcomes. With increased understanding of the cognitive and self-regulatory vulnerabilities experienced by children and adolescents with CHD, it may be possible to identify risks early and provide individualized supports to promote optimal neurodevelopment.

Degradation of cognitive timing mechanisms in behavioural variant frontotemporal dementia

The current study examined motor timing in frontotemporal dementia (FTD), which manifests as progressive deterioration in social, behavioural and cognitive functions. Twenty-patients fulfilling consensus clinical criteria for behavioural variant FTD (bvFTD), 11 patients fulfilling consensus clinical criteria for semantic-variant primary progressive aphasia (svPPA), four patients fulfilling criteria for nonfluent/agrammatic primary progressive aphasia (naPPA), eight patients fulfilling criteria for Alzheimer׳s disease (AD), and 31 controls were assessed on both an externally- and self-paced finger-tapping task requiring maintenance of a regular, 1500ms beat over 50 taps. Grey and white matter correlates of deficits in motor timing were examined using voxel-based morphometry (VBM) and diffusion tensor imaging (DTI). bvFTD patients exhibited significant deficits in aspects of both externally- and self-paced tapping. Increased mean inter-response interval (faster than target tap time) in the self-paced task was associated with reduced grey matter volume in the cerebellum bilaterally, right middle temporal gyrus, and with increased axial diffusivity in the right superior longitudinal fasciculus, regions and tracts which have been suggested to be involved in a subcortical–cortical network of structures underlying timing abilities. This suggests that such structures can be affected in bvFTD, and that impaired motor timing may underlie some characteristics of the bvFTD phenotype.

Abnormal Neural Activation to Faces in the Parents of Children with Autism.

Parents of children with an autism spectrum disorder (ASD) show subtle deficits in aspects of social behavior and face processing, which resemble those seen in ASD, referred to as the "Broad Autism Phenotype " (BAP). While abnormal activation in ASD has been reported in several brain structures linked to social cognition, little is known regarding patterns in the BAP. We compared autism parents with control parents with no family history of ASD using 2 well-validated face-processing tasks. Results indicated increased activation in the autism parents to faces in the amygdala (AMY) and the fusiform gyrus (FG), 2 core face-processing regions. Exploratory analyses revealed hyper-activation of lateral occipital cortex (LOC) bilaterally in autism parents with aloof personality ("BAP+"). Findings suggest that abnormalities of the AMY and FG are related to underlying genetic liability for ASD, whereas abnormalities in the LOC and right FG are more specific to behavioral features of the BAP. Results extend our knowledge of neural circuitry underlying abnormal face processing beyond those previously reported in ASD to individuals with shared genetic liability for autism and a subset of genetically related individuals with the BAP.

Context-specific memory in children with ADHD

Objectives:Memory for where and when information is learned, or contextual aspects of memory, as opposed to fact or item memory, has been suggested to be more dependent on frontal brain and related executive control systems. Children with neurodevelopmental disorders involving frontal brain systems have been noted to have problems on contextual memory tasks. Children with attention deficit hyperactivity disorder (ADHD) have difficulties with forgetfulness and are known to have deficits in aspects of executive control with associated dysfunction in frontal brain systems; therefore, while their item memory is not typically impaired, they may have difficulty on tasks requiring contextual memory abilities. The goal of this study was to compare children with ADHD to typically developing children, on two different contextual memory tasks (source memory and memory for temporal recency) and to compare this with their respective performance on traditional fact/item memory tasks.Methods:Participants included 36 children with combined type ADHD and 36 typically developing controls ages 6–13 years, matched by age and gender. In addition to a measure of intellectual ability, children completed two different contextual memory tasks; one assessing recall for the source of new information and one assessing recall of the temporal context of information (recency). Incorporated into these tasks were standard measures of item/fact memory recall.Results:Results revealed that children with ADHD performed similarly to control participants on memory recognition tasks, but differed from controls on the contextual memory tasks. Children with ADHD outperformed control participants when recalling the source from which they had learned information, but performed more poorly than control on a task that required them to make a recency/temporal order judgment.Conclusion:The data suggest that while children with ADHD may have somewhat similar capacity to recognise new information, they differ in aspects of their performance on contextual aspects of memory. These differences are not uniform and mirror neuroscience findings supporting dissociable contextual memory systems. Potential theoretical explanations for the dissociations seen are discussed.