Showing papers on "Executive dysfunction published in 2014"

Neurocognitive correlates of obesity and obesity-related behaviors in children and adolescents

Abstract: Childhood obesity rates have risen dramatically over the past few decades. Although obesity has been linked to poorer neurocognitive functioning in adults, much less is known about this relationship in children and adolescents. Therefore, we conducted a systematic review to examine the relationship between obesity and obesity-related behaviors with neurocognitive functioning in youth. We reviewed articles from 1976 to 2013 using PsycInfo, PubMed, Medline and Google Scholar. Search terms included cognitive function, neurocognitive function/performance, executive function, impulsivity, self-regulation, effortful control, cognitive control, inhibition, delayed gratification, memory, attention, language, motor, visuo-spatial, academic achievement, obesity, overweight, body mass index, waist-hip ratio, adiposity and body fat. Articles were excluded if participants had health problems known to affect cognitive functioning, the study used imaging as the only outcome measure, they were non-peer-reviewed dissertations, theses, review papers, commentaries, or they were non-English articles. Sixty-seven studies met inclusion criteria for this review. Overall, we found data that support a negative relationship between obesity and various aspects of neurocognitive functioning, such as executive functioning, attention, visuo-spatial performance, and motor skill. The existing literature is mixed on the effects among obesity, general cognitive functioning, language, learning, memory, and academic achievement. Executive dysfunction is associated with obesity-related behaviors, such as increased intake, disinhibited eating, and less physical activity. Physical activity is positively linked with motor skill. More longitudinal research is needed to determine the directionality of such relationships, to point towards crucial intervention time periods in the development of children, and to inform effective treatment programs.

The neuropathology of sport

Abstract: The benefits of regular exercise, physical fitness and sports participation on cardiovascular and brain health are undeniable. Physical activity reduces the risk for cardiovascular disease, type 2 diabetes, hypertension, obesity, and stroke, and produces beneficial effects on cholesterol levels, antioxidant systems, inflammation, and vascular function. Exercise also enhances psychological health, reduces age-related loss of brain volume, improves cognition, reduces the risk of developing dementia, and impedes neurodegeneration. Nonetheless, the play of sports is associated with risks, including a risk for mild TBI (mTBI) and, rarely, catastrophic traumatic injury and death. There is also growing awareness that repetitive mTBIs, such as concussion and subconcussion, can occasionally produce persistent cognitive, behavioral, and psychiatric problems as well as lead to the development of a neurodegeneration, chronic traumatic encephalopathy (CTE). In this review, we summarize the beneficial aspects of sports participation on psychological, emotional, physical and cognitive health, and specifically analyze some of the less common adverse neuropathological outcomes, including concussion, second-impact syndrome, juvenile head trauma syndrome, catastrophic sudden death, and CTE. CTE is a latent neurodegeneration clinically associated with behavioral changes, executive dysfunction and cognitive impairments, and pathologically characterized by frontal and temporal lobe atrophy, neuronal and axonal loss, and abnormal deposits of paired helical filament (PHF)-tau and 43 kDa TAR deoxyribonucleic acid (DNA)-binding protein (TDP-43). CTE often occurs as a sole diagnosis, but may be associated with other neurodegenerative disorders, including motor neuron disease (CTE-MND). Although the incidence and prevalence of CTE are not known, CTE has been reported most frequently in American football players and boxers. Other sports associated with CTE include ice hockey, professional wrestling, soccer, rugby, and baseball.

Military-related traumatic brain injury and neurodegeneration

Abstract: Mild traumatic brain injury (mTBI) includes concussion, subconcussion, and most exposures to explosive blast from improvised explosive devices. mTBI is the most common traumatic brain injury affecting military personnel; however, it is the most difficult to diagnose and the least well understood. It is also recognized that some mTBIs have persistent, and sometimes progressive, long-term debilitating effects. Increasing evidence suggests that a single traumatic brain injury can produce long-term gray and white matter atrophy, precipitate or accelerate age-related neurodegeneration, and increase the risk of developing Alzheimer's disease, Parkinson's disease, and motor neuron disease. In addition, repetitive mTBIs can provoke the development of a tauopathy, chronic traumatic encephalopathy. We found early changes of chronic traumatic encephalopathy in four young veterans of the Iraq and Afghanistan conflict who were exposed to explosive blast and in another young veteran who was repetitively concussed. Four of the five veterans with early-stage chronic traumatic encephalopathy were also diagnosed with posttraumatic stress disorder. Advanced chronic traumatic encephalopathy has been found in veterans who experienced repetitive neurotrauma while in service and in others who were accomplished athletes. Clinically, chronic traumatic encephalopathy is associated with behavioral changes, executive dysfunction, memory loss, and cognitive impairments that begin insidiously and progress slowly over decades. Pathologically, chronic traumatic encephalopathy produces atrophy of the frontal and temporal lobes, thalamus, and hypothalamus; septal abnormalities; and abnormal deposits of hyperphosphorylated tau as neurofibrillary tangles and disordered neurites throughout the brain. The incidence and prevalence of chronic traumatic encephalopathy and the genetic risk factors critical to its development are currently unknown. Chronic traumatic encephalopathy has clinical and pathological features that overlap with postconcussion syndrome and posttraumatic stress disorder, suggesting that the three disorders might share some biological underpinnings.

Assessment of executive functioning using the Behavior Rating Inventory of Executive Function (BRIEF).

Abstract: The Behavior Rating Inventory of Executive Function (BRIEF) was one of the first attempts to measure executive function via self- and informant reports of everyday functioning in the real-world environment and was the first published measure of these self-regulatory capabilities in children and adolescents (Gioia, Isquith, Guy & Kenworthy, 2000a) The impetus for the BRIEF arose among the authors in 1994 while trying to reconcile the often discrepant parent and teacher reports of children’s everyday functioning at home and in school with their performance on putative performance measures (ie, “tests”) of executive function At that time, there were few such performance measures of executive function developed for children and adolescents, no rating scales or structured observational methods for evaluating executive functions, and very few published articles on executive function in children (Bernstein & Waber, 2007)

Cognition in corticobasal syndrome and progressive supranuclear palsy: A review

Abstract: Corticobasal syndrome (CBS) and progressive supranuclear palsy (PSP) represent challenging neurodegenerative disorders for clinicians and nonclinical scientists alike. Although initially lumped together as "Parkinson's-Plus" syndromes, CBS and PSP are clinically and pathologically distinct from Parkinson's disease. It is now clear that behavioral and cognitive changes are common in both syndromes and affect impact quality of life and carer burden considerably. We briefly review the clinical, pathological, and neuroradiological features of each syndrome, followed by more detailed descriptions of the behavioral and cognitive deficits encountered in CBS and PSP. Clinically and pathologically heterogeneous, CBS is characterized by a wide range of cognitive and behavioral disturbances. impairments in executive function and memory are common, but nonspecific. In contrast, deficits in language and visuospatial abilities appear to be more distinctive features of CBS; the relevance of specific patterns of impairment to the underlying histopathology, or prognosis, remains to be fully elucidated. As in CBS, behavioral and cognitive changes are almost universal in PSP, with a wide range of reported deficits. Apathy is very common, often paradoxically accompanied by impulsivity. Executive dysfunction is prominent, but memory and visuospatial deficits also occur. An emerging field is the study of social cognition, which appears impaired in both syndromes. As therapeutic strategies for neurodegenerative pathologies emerge, more specific diagnostic tools in CBS and PSP will be required. Careful clinicopathological correlation, and the development of biomarkers for specific histopathologies, will be important milestones on the road to effective treatments.

Cognitive impairment in early‐stage non‐demented Parkinson's disease patients

Abstract: Objectives In Parkinson's disease (PD), Parkinson's disease dementia (PDD) and Parkinson's disease–mild cognitive impairment (PD-MCI) are common. PD-MCI is a risk factor for developing PDD. Knowledge of cognition in early-stages PD is essential in understanding and predicting the dementia process. Materials and Methods We describe the cognitive profile in early-stage PD patients with no prior clinical suspicion of cognitive impairment, depression or psychiatric disturbances, and investigate possible features distinguishing patients with cognitive deficits, defining a PD-MCI risk-profile. Single Photon Emission Computerized Tomography (SPECT) DaT-scan and neurological examination confirmed the diagnosis. Mini-mental state examination-, Addenbrooke's Cognitive Examination, Unified Parkinson's Disease Rating Scale scoring, Hoehn &Yahr/Activity of Daily Living staging and a neuropsychological test battery were applied. Mild cognitive impairment patients were identified according to modified criteria by Troster necessarily omitting subjective cognitive complaints. 80 patients, mean age 61.0 years (SD 6.6), mean duration of disease 3.4 years (SD 1.2) were included. 76 patients were neuropsychologically tested. Results 26 (34%) patients fulfilled modified PD-MCI criteria, 18 (69%) of these showed episodic memory deficits, 14 (54%) executive dysfunction, 13 (50%) language/praxis deficits, 12 (46%) visuospatial/constructional deficits and 9 (35%) attention/working memory deficits. Cognitive impairment was associated with higher Unified Parkinson's Disease Rating scale (UPDRS)-, bradykinesia- and rigidity scores and more symmetric distribution of symptoms, but not tremor scores. Patients with cognitive impairment were less educated. Other demographic and clinical variables were comparable. Conclusions 34% of early-stage PD patients without prior clinical suspicion of cognitive impairment exhibit cognitive impairment, which is associated to disease severity, especially bradykinesia, rigidity, axial symptoms and less asymmetry of motor symptoms, even at early disease stages and when cognitive symptoms are mild.

The caudate: a key node in the neuronal network imbalance of insomnia?

Abstract: Insomnia is prevalent, severe and partially heritable. Unfortunately, its neuronal correlates remain enigmatic, hampering the development of mechanistic models and rational treatments. Consistently reported impairments concern fragmented sleep, hyper-arousal and executive dysfunction. Because fronto-striatal networks could well play a role in sleep, arousal regulation and executive functioning, the present series of studies used an executive task to evaluate fronto-striatal functioning in disturbed sleep. Patients with insomnia showed reduced recruitment of the head of the left caudate nucleus during executive functioning, which was not secondary to altered performance or baseline perfusion. Individual differences in caudate recruitment were associated with hyper-arousal severity. Seed-based functional connectivity analysis suggested that attenuated input from a projecting orbitofrontal area with reduced grey matter density contributes to altered caudate recruitment in patients with insomnia. Attenuated caudate recruitment persisted after successful treatment of insomnia, warranting evaluation as a potential vulnerability trait. A similar selective reduction in caudate recruitment could be elicited in participants without sleep complaints by slow-wave sleep fragmentation, providing a model to facilitate investigation of the causes and consequences of insomnia.

Hypertension and Dementia

Abstract: The negative impact of hypertension on cognitive function was already hinted at in the 1960s in a study on psychomotor speed of air traffic controllers and pilots and has received extensive confirmation during the following decades.1 Thus, hypertension has been associated with a wide variety of cognitive deficits, including reduced abstract reasoning (executive dysfunction), impaired memory, attention deficit, and slowing of mental processing speed.1,2 Indeed, hypertension is a leading cause of vascular cognitive impairment, a term that includes all cognitive deficits attributable to vascular factors.3 The most extreme case of vascular cognitive impairment is vascular dementia, in which multiple cognitive domains are affected, with a negative impact on the activities of daily living. Increasing evidence also suggests that hypertension is a risk factor for Alzheimer disease (AD), highlighting its participation in all major causes of cognitive impairment.4,5 In the past 3 years (2011–2013), several articles published in Hypertension have provided new insight into the link between high blood pressure and dementia. These articles will be briefly discussed, highlighting their contribution to current concepts of pathobiology, prevention, and treatment of the end-organ damage to the brain inflicted by hypertension. Although it is well established that hypertension impairs cognition, one of the key issues still unsettled concerns the temporal relationships between blood pressure elevation and cognitive decline. On the one hand, cross-sectional studies indicated that individuals with dementia have lower blood pressure, challenging the involvement of hypertension.6 On the other hand, longitudinal studies, in which patient were followed for decades, revealed that individuals who develop dementia have a history of high blood pressure earlier in life.6,7 The effect is independent of other cardiovascular risk factors or comorbidities and is observed in both men and women. In this context, Joas et …

White matter integrity disruptions associated with cognitive impairments in type 2 diabetic patients.

Abstract: Type 2 diabetes mellitus (T2DM) is associated with a twofold increased risk of dementia and can affect many cognitive abilities, but its underlying cause is still unclear. In this study, we used a combination of a battery of neuropsychological tests and diffusion tensor imaging (DTI) to explore how T2DM affects white matter (WM) integrity and cognition in 38 T2DM patients and 34 age-, sex-, and education-matched normal control subjects. A battery of neuropsychological tests was used to assess a wide range of cognitive functions. Tract-based spatial statistics combined with region of interest-wise (ROI-wise) analysis of mean values of DTI metrics in ROIs was used to compare group differences of DTI metrics on WM skeletons to identify severely disrupted WM tracts in T2DM. We found that T2DM patients showed 1) various cognitive impairments, including executive function, spatial processing, attention, and working memory deficits; 2) widespread WM disruptions, especially in the whole corpus callosum, the left anterior limb of the internal capsule (ALIC.L), and external capsule (EC); and 3) a positive correlation between executive function and WM integrity in the ALIC.L and the left EC. In conclusion, T2DM patients show various cognitive impairments and widespread WM integrity disruptions, which we attribute to demyelination. Moreover, executive dysfunction closely correlates with WM abnormalities.

Executive function late effects in survivors of pediatric brain tumors and acute lymphoblastic leukemia.

Abstract: Background: Survivors of pediatric brain tumors (BT) and acute lymphoblastic leukemia (ALL) are at risk for neurocognitive late effects related to executive function. Procedure: Survivors of BT (48) and ALL (50) completed neurocognitive assessment. Executive function was compared to estimated IQ and population norms by diagnostic group. Results: Both BT and ALL demonstrated relative executive function weaknesses. As a group, BT survivors demonstrated weaker executive functioning than expected for age. Those BT survivors with deficits exhibited a profile suggestive of global executive dysfunction, while affected ALL survivors tended to demonstrate specific rapid naming deficits. Conclusion: Findings suggest that pediatric BT and ALL survivors may exhibit different profiles of executive function late effects, which may necessitate distinct intervention plans.

Multimodal Markers of Inflammation in the Subcortical Ischemic Vascular Disease Type of Vascular Cognitive Impairment

Abstract: Vascular cognitive impairment (VCI) is a heterogeneous disease that is caused by a wide variety of vascular factors.1 Pathological studies have shown that both large- and small-vessel damage occurs in patients with VCI.2,3 Large-vessel disease leads to strokes with a stepwise course as a result of multiple infarctions that result in concomitant loss of intellect. Small-vessel disease has several forms: it may either produce lacunes mainly in the basal ganglia without white matter damage or extensive changes in the white matter with or without lacunes (Table I in the online-only Data Supplement). The term subcortical ischemic vascular disease is often used for both lacunar state and white matter disease, but there may be different pathophysiologies involved, particularly when there is cerebral hypoperfusion, which has a major effect on the vulnerable deep white matter.4 Binswanger disease (BD) was first described in 1894 in patients with arteriolosclerotic demyelination.5 Patients with BD have a symptom complex that includes vascular risk factors, cognitive impairment, small stroke-like events, hyperreflexia, and imbalance (Table II in the online-only Data Supplement).6,7 Neuropsychological testing shows executive dysfunction, whereas difficulties with memory and language occur more commonly in Alzheimer disease (AD); overlap occurs in neuropsychological testing in BD and AD, making patterns of cognitive dysfunction only suggestive of diagnoses. The Montreal Cognitive Assessment, which includes tests of executive function, when compared with minimental status examination is more often abnormal in patients with BD, making it a better screening test.8 Clinical features alone may be insufficient to diagnose BD, and a multimodal approach with biomarkers may be helpful. The biomarkers that have been suggested include neuropsychological testing, brain imaging, and cerebrospinal fluid (CSF) studies. Routine MRI shows white matter hyperintensities (WMHs) on fluid-attenuated inversion recovery imaging, which are nonspecific and are …

Intrinsic Brain Abnormalities in Attention Deficit Hyperactivity Disorder: A Resting-State Functional MR Imaging Study

Abstract: We found that children and adolescents with attention deficit hyperactivity disorder (ADHD) have altered regional brain function and aberrant functional connectivity in large-scale networks that were associated with executive dysfunction, suggesting that the characteristics of the brain’s resting-state functional architecture are relevant to understanding relationships between neural substrate and executive function in ADHD.

Cognitive executive impairment and dopaminergic deficits in de novo Parkinson's disease

Abstract: Cognitive impairment in Parkinson's disease (PD) is common and does directly impact patients' everyday functioning. However, the underlying mechanisms of early cognitive decline are not known. This study explored the association between striatal dopaminergic deficits and cognitive impairment within a large cohort of early, drug-naive PD patients and tested the hypothesis that executive dysfunction in PD is associated with striatal dopaminergic depletion. A cross-sectional multicenter cohort of 339 PD patients and 158 healthy controls from the Parkinson's Progression Markers Initiative study was analyzed. Each individual underwent cerebral single-photon emission CT (SPECT) and a standardized neuropsychological assessment with tests of memory as well as visuospatial and executive function. SPECT imaging was performed with [123I]FP-CIT, and specific binding ratios in left and right putamen and caudate nucleus were calculated. The association between specific binding ratios, cognitive domain scores, and age was analyzed using Pearson's correlations, partial correlation, and conditional process analysis. A small, but significant, positive association between total striatal dopamine transporter binding and the attention/executive domain was found (r = 0.141; P = 0.009) in PD, but this was not significant after adjusting for age. However, in a moderated mediation model, we found that cognitive executive differences between controls and patients with PD were mediated by an age-moderated striatal dopaminergic deficit. Our findings support the hypothesis that nigrostriatal dopaminergic deficit is associated with executive impairment, but not to memory or visuospatial impairment, in early PD. © 2014 International Parkinson and Movement Disorder Society

Association Between Cerebellar Gray Matter Volumes, Gait Speed, and Information-Processing Ability in Older Adults Enrolled in the Health ABC Study

Abstract: Initial reports of the association between mobility impairment and cerebellum were made by Sir Gordon Holmes from observing World War I victims inflicted with gunshot wounds to the cerebellum whose gait he described as irregular, slow, and halting (1). These reports formed the foundation for understanding the role of the cerebellum in gait (reviewed in ref. 2). A combination of truncal instability, disequilibrium, slow gait speed with shortened stride length, increased gait variability, and a wide base of support constitute the hallmark of a cerebellar ataxic gait. Neural causes of age-associated slowing of gait, without other associated gait and balance changes, have primarily focused on cortical changes such as white matter disease and gray matter atrophy with aging. The role of the aging cerebellum in gait has not received similar attention in older adults. Research on nonmotor functions of the cerebellum is emerging (reviewed by ref. 3). The cerebellum plays an important role in cognitive and emotional processing (4). Cerebellar lesion studies demonstrate that deficits in executive function, attention, and spatial attention can emerge with damage to specific areas of the cerebellum without necessarily causing motor symptoms (5). Studies have explored cognitive functions of the cerebellum by demonstrating activation patterns associated with specific cognitive tasks in healthy populations using functional imaging (reviewed in ref. 6). Specifically, functional imaging studies reported distinct cerebellar regional activation for tasks requiring cognitive and motor functions (7,8). Executive dysfunction attributable to cerebellar pathology is evident on tasks that assess verbal fluency, planning, working memory, divided attention, and set shifting (9–11). Multiple cognitive functions rely on information-processing ability and attention, which are primarily frontal-subcortical functions (12). Information-processing ability is also associated with gait speed in older adults and is likely involved in sensory motor integration (13); both functions are also linked to prefrontal cortex (14–16). Signals transmitted from the prefrontal subcortical regions through the superior cerebellar peduncles to cerebellar regions may influence motor output of the cerebellum. Alternatively, cerebellar regions may have a specialized role for information processing that can influence downstream motor control and gait speed (13). It remains unknown which regions in the cerebellum are associated with information-processing ability and gait speed in older adults. Slow information processing reflects generalized slowing associated with aging that has important implications in mobility decline, cognitive decline, functional ability, and mortality in older adults (13,15). Understanding the role of the cerebellum in information processing and gait speed is therefore important in aging. Controlling for cortical measures could help to shed light on the de novo cerebellar influence on gait speed and information-processing ability. The aim of this study was to investigate the association between structural measures of cerebellar integrity, gait speed, and information-processing measures in community-dwelling older adults. We hypothesized that greater cerebellar gray matter volume (GMV) would be associated with faster gait and faster information processing, independent of the cortex. As cerebral GMV and small vessel disease are linked to gait speed (16), the above hypothesized associations would remain significant after controlling for cortical atrophy and small vessel disease severity. Furthermore, based on the topographic delineation of the cerebellum (6), the cognitive regions of the cerebellum would be more strongly associated with gait speed than the sensorimotor or vestibular cerebellar regions. Finally, if this association holds, then slower information processing would attenuate the strength of the association between cognitive cerebellum region and gait speed.

Neuroplasticity-based computerized cognitive remediation for treatment-resistant geriatric depression

Abstract: As well as substantial changes in mood, geriatric depression is also characterized by executive dysfunction (ED). Morimoto et al. show that some sufferers of geriatric depression do not respond to conventional drugs, and that ED in these patients can be alleviated with computerized cognitive remediation therapy.

Unawareness of Deficits in Huntington's Disease

Abstract: People with Huntington's disease (HD) may show reduced awareness of physical and mental changes in themselves. This article reviews the evidence for loss of awareness (anosognosia) in an attempt to elucidate its characteristics and possible underlying mechanisms. It is shown that defective awareness occurs across domains. People with HD may under-report the presence or severity of involuntary movements, under-estimate cognitive impairment and deny behavioural change. Nevertheless, awareness is not all or none. Moreover, it may be affected differentially for different symptom domains and emerge at different stages of disease, raising the possibility of distinct contributory mechanisms. Findings of an inverse relationship between insight and severity of disease suggest that cognitive impairment, in particular executive dysfunction, may be an important contributory factor. Evidence has accrued to support this argument. However, cognitive impairment cannot fully account for patients' lack of awareness of involuntary movements. Findings that patients accurately report consequences but not the experience of involuntary movements, and better acknowledge their presence when watching videotapes of themselves suggests that physiological factors play an important role. The putative role of denial as a coping mechanism is discussed. Recognition by clinicians of deficient self-awareness is crucial because of its implications for diagnosis and optimal clinical management of HD.

Preludes to brain failure: executive dysfunction and gait disturbances

Abstract: The progressive and insidious gait and cognitive decline seen in older individuals without overt disease may result from a combination of age-dependent neuronal changes that are often exacerbated by vascular pathomechanisms. Emerging evidence suggests that slow gait and executive dysfunction are early phenomena in this decline and may further evolve to the development of falls and dementia. These early manifestations can be seen as “brain failure” and their co-occurrence suggests that they may share a common underlying mechanism. The authors argue that brain cortical control of motor and gait performance; and high complex cognitive functions such as executive function, share the same brain networks. Due to its particular watershed vascularization, these brain networks are highly susceptible to microvascular damage and the effects of vascular risk factors. A unified approach for evaluating and treating these two features of aging will close the gap in our understanding of cognitive–motor interactions and ultimately alter the pathways to disability. Besides the standard treatment for cognitive and mobility decline, the authors suggest that treating reversible vascular risk factors and hypertension, especially when they represent early manifestations of brain damage, has the potential to be a complementary method to prevent loss of mobility and cognitive decline in older adults.

Internet addictive individuals share impulsivity and executive dysfunction with alcohol-dependent patients.

Abstract: Internet addiction disorder (IAD) should belong to a kind of behavioral addiction. Previous studies indicated that there are many similarities in the neurobiology of behavior and substance addictions. Up to date, although individuals with IAD have difficulty suppressing their excessive online behaviors in real life, little is known about the patho-physiological and cognitive mechanisms responsible for IAD. Neuropsychological test studies have contributed significantly to our understanding of the effect of IAD on the cognitive function. The purpose of the present study was to examine whether Internet addictive individuals share impulsivity and executive dysfunction with alcohol-dependent individuals. Participants include 22 Internet addictive individuals, 22 alcohol-dependent patients (AD) and 22 normal controls (NC). All participants were measured with BIS- 11, go/no-go task, WCST and Digit span task under the same experimental condition. Results showed that BIS-11 scores, false alarm rate, the total response errors, perseverative errors, failure to maintain set of IAD and AD group were significantly higher than that of NC group, and hit rate, percentage of conceptual level responses, the number of categories completed, forwards scores and backwards scores of IAD and AD group were significantly lower than that of NC group, however, no differences in above variables between IAD group and AD group were observed. These results revealed that the existence of impulsivity, deficiencies in executive function and working memory in an IAD and an AD sample, namely, Internet addictive individuals share impulsivity and executive dysfunction with alcohol-dependent patients.

Saccade deficits in amnestic mild cognitive impairment resemble mild Alzheimer's disease.

Abstract: Alzheimer’s disease (AD) is a disorder of progressive memory loss and executive dysfunction. Little is known about the progression from amnestic mild cognitive impairment (aMCI; isolated memory loss) to AD. Studies have found impairments in mild-stage AD and aMCI in specific tests of executive function. Here, we used objective saccade tasks to determine if they can effectively assess executive function deficits otherwise assessed by neuropsychological testing. To determine which executive function deficits the saccade tasks are most sensitive to, we also investigated the relationship between performance on saccade tasks and neuropsychological test scores. Twenty-two aMCI patients (63–90 years), 24 mild AD patients (61–87 years) and 76 healthy controls (60–85 years) performed a battery of neuropsychological tests, and two saccade tasks designed to probe sensory, motor and cognitive function. The prosaccade task requires a fast, automatic saccade toward an eccentric visual stimulus. The antisaccade task requires additional executive processing to inhibit the automatic prosaccade toward the stimulus, so that a voluntary saccade can be initiated to a location opposite the stimulus. Antisaccade performance was impaired similarly in aMCI and AD patients relative to controls; both groups were slower to initiate correct antisaccades and they made more direction errors (erroneous prosaccades), suggesting similar brain deficits. Scores on the Stroop task were inversely correlated with the percentage of short-latency direction errors in the antisaccade task for controls and aMCI patients, whereas other more global measures of executive function were not related to saccade measures in any subject group. Our results show that the antisaccade task is useful for detecting executive dysfunction in aMCI and AD, especially dysfunction in selective attention. Saccade tasks may therefore have potential to assess executive dysfunction when use of neuropsychological tests is not possible.

Neuropsychological and neurobehavioral outcome following childhood arterial ischemic stroke: attention deficits, emotional dysregulation, and executive dysfunction.

Abstract: Objectives. To investigate neuropsychological and neurobehavioral outcome in children with arterial ischemic stroke (AIS).Background. Childhood stroke can have consequences on motor, cognitive, and behavioral development. We present a cross-sectional study of neuropsychological and neurobehavioral outcome at least one year poststroke in a uniquely homogeneous sample of children who had experienced AIS.Method. Forty-nine children with AIS aged 6 to 18 years were recruited from a specialist clinic. Neuropsychological measures of intelligence, reading comprehension, attention, and executive function were administered. A triangulation of data collection included questionnaires completed by the children, their parents, and teachers, rating behavior, executive functions, and emotions.Key Findings. Focal neuropsychological vulnerabilities in attention (response inhibition and dual attention) and executive function were found, beyond general intellectual functioning, irrespective of hemispheric side of stroke. Di...

Apathy in Parkinson's disease: neurophysiological evidence of impaired incentive processing.

Abstract: Apathy is one of the most common and debilitating nonmotor manifestations of Parkinson's disease (PD) and is characterized by diminished motivation, decreased goal-directed behavior, and flattened affect. Despite its high prevalence, its underlying mechanisms are still poorly understood, having been associated with executive dysfunction, and impaired emotional processing and decision making. Apathy, as a syndrome, has recently been associated with reduced activation in the ventral striatum, suggesting that early- to middle-stage Parkinson's disease patients with this manifestation may have a compromised mesocorticolimbic dopaminergic pathway and impaired incentive processing. To test this hypothesis, we measured the amplitude of the feedback-related negativity, an event-related brain potential associated with performance outcome valence, following monetary gains and losses in human PD patients (12 women) and healthy controls (6 women) performing a gambling task. Early- to middle-stage PD patients presenting clinically meaningful symptoms of apathy were compared with nonapathetic PD patients and healthy controls. Patients with cognitive impairment, depression, and other psychiatric disturbances were excluded. Results showed that the amplitude of the feedback-related negativity, measured as the difference wave in the event-related brain potential between gains and losses, was significantly reduced in PD patients with apathy compared with nonapathetic patients and healthy controls. These findings indicate impaired incentive processing and suggest a compromised mesocorticolimbic pathway in cognitively intact PD patients with apathy.

Cognitive Factors Underpinning Poor Expressive Communication Skills After Traumatic Brain Injury: Theory of Mind or Executive Function?

Abstract: OBJECTIVE : The ability to see things from another's perspective, that is, have a theory of mind (ToM), is essential to effective communication. So too is the ability to regulate verbal output, that is, to exercise executive control. People with traumatic brain injuries (TBIs) have impaired communication abilities, but the extent to which this reflects ToM versus executive dysfunction is unclear. This study explored the relative contributions of executive abilities, specifically flexibility and inhibition and ToM abilities in language production post-TBI. METHOD: Twenty-five adults (18 males: mean age of 48.2 years, SD = 12.0 years) with moderate to severe TBI (posttraumatic amnesia = 69.2, SD = 54.6 days) and 28 noninjured adults (19 males: mean age 49.0, SD = 12.2 years) completed three sets of communication tasks with low executive demands, high flexibility, and high inhibition demands. Within each, parallel versions had low or high ToM requirements. RESULTS: For low executive and high flexibility tasks, scores on the high ToM versions were predicted by scores on the low ToM versions, suggesting that poor performance was explained by the executive demands the parallel tasks had in common. The exception was the high inhibition task. In this case, speakers with TBI had differential difficulty with the high ToM version, that is, they had specific difficulty inhibiting self-referential thoughts in order to cater for another's perspective. CONCLUSION: We found problems with inhibiting the self-perspective accords with descriptive accounts of the egocentric nature of some communication patterns following TBI, which points to potential targets for remediation.

The role of executive functions in the pragmatic skills of children age 4-5.

Abstract: Several studies suggest that pragmatic skills (PS) (i.e., social communication) deficits may be linked to executive dysfunction (i.e., cognitive processes required for the regulation of new and complex behaviors) in patients with frontal brain injuries. If impairment of executive functions (EF) causes PS deficits in otherwise healthy adults, could this mean that EF are necessary for the normal functioning of PS, even more so than cognitive maturation? If so, children with highly developed EF should exhibit higher levels of PS. This study aimed to examine the link between EF and PS among normally developing children. A secondary goal was to compare this relationship to that between intellectual quotient (IQ) and PS in order to determine which predictor explained the most variance. Participants were 70 French-speaking preschool children (3;10–5;7 years old). The PS coding system, an observational tool developed for this study, was used to codify the children's PS during a semi-structured conversation with a research assistant. Five types of EF processes were evaluated: self-control, inhibition, flexibility, working memory and planning. IQ was estimated by tallying the scores on a receptive vocabulary test and a visuoconstructive abilities test. The results of the test of differences between correlation coefficients suggest that EF contributed significantly more than IQ to the PS exhibited by preschoolers during conversation. More specifically, higher inhibition skills were correlated with a decrease in talkativeness and assertiveness. EF also appeared to foster quality of speech by promoting the ability to produce fluid utterances, free of unnecessary repetition or hesitation. Moreover, children with a high working memory capacity were more likely to formulate contingent answers and produce utterances that could be clearly understood by the interlocutor. Overall, these findings help us better understand how EF may assist children in everyday social interactions.