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The Behavioral and Cognitive Executive Disorders of Stroke: The GREFEX Study
Many studies have highlighted the high prevalence of executive disorders in stroke. However, major uncertainties remain due to use of variable and non-validated methods. The objectives of this study were: 1) to characterize the executive disorder profile in stroke using a standardized battery, validated diagnosis criteria of executive disorders and validated framework for the interpretation of neuropsychological data and 2) examine the sensitivity of the harmonization standards protocol proposed by the National Institute of Neurological Disorders and Stroke and Canadian Stroke Network (NINDS-CSN) for the diagnosis of Vascular Cognitive Impairment.
237 patients (infarct: 57; cerebral hemorrhage: 54; ruptured aneurysm of the anterior communicating artery (ACoA): 80; cerebral venous thrombosis (CVT): 46) were examined by using the GREFEX battery. The patients' test results were interpreted with a validated framework derived from normative data from 780 controls.
Dysexecutive syndrome was observed in 88 (55.7%; 95%CI: 48-63.4) out of the 156 patients with full cognitive and behavioral data: 40 (45.5%) had combined behavioral and cognitive syndromes, 29 (33%) had a behavioral disorder alone and 19 (21.6%) had a cognitive syndrome alone. The dysexecutive profile was characterized by prominent impairments of initiation and generation in the cognitive domain and by hypoactivity with disinterest and anticipation loss in the behavioral domain. Cognitive impairment was more frequent (p = 0.014) in hemorrhage and behavioral disorders were more frequent (p = 0.004) in infarct and hemorrhage. The harmonization standards protocol underestimated (p = 0.007) executive disorders in CVT or ACoA.
This profile of executive disorders implies that the assessment should include both cognitive tests and a validated inventory for behavioral dysexecutive syndrome. Initial assessment may be performed with a short cognitive battery, such as the harmonization standards protocol. However, administration of a full cognitive battery is required in selected patients.
Journal Article
Handbook of emotion regulation
\"Reviewing the state of the science in a dynamic, thriving field, this influential handbook integrates knowledge from multiple psychological subdisciplines. Foremost experts address the neurobiological and cognitive bases of emotion regulation and examine how individuals develop and use regulatory strategies across the lifespan. The social context of emotion regulation is explored, as are personality processes and individual differences. Critical implications are discussed for psychopathology, psychosocial interventions, and health. Including helpful cross-referencing among chapters, the volume describes cutting-edge methods and identifies promising directions for future investigation. New to This Edition *Incorporates significant scientific advances and many new topics. *Greatly expanded coverage of clinical issues and applications. *Chapters on neural systems, delay of gratification, decision making, and health. *Chapters on adolescence, social baseline theory, and desire regulation, plus more\"-- Provided by publisher.
BOOK
Impairments of emotion and real-world complex behavior following childhood- or adult-onset damage to ventromedial prefrontal cortex
The behavioral syndrome resulting from damage to the ventromedial
prefrontal (VM) region presents major challenges for clinical assessment
and management, stemming from the absence of reliable neurologic or
psychometric markers, coupled with often debilitating impairments of
decision-making and behavior regulation. Damage to this region disrupts
neural circuitry critical for emotion, which in turn may contribute to
impairments in real-world competencies. Here we present findings from
patients with focal lesions in the VM region acquired either in childhood
or adulthood, and show that there is a relationship between emotional
dysfunction and impairments in real-world behavioral competencies. Emotion
was rated by participants' relatives on dimensions including
frustration tolerance, lability, anxiety, and blunted affect. Real-world
competencies were rated by the relatives on dimensions including judgment,
planning, and initiation, and were evaluated by clinician ratings in areas
including social, financial, and occupational function. VM damage resulted
in severe disruption of emotion, and this emotional dysfunction accounted
for a significant portion of impaired real-world competencies. The
long-term impairments associated with childhood-onset lesions were at
least as severe as those resulting from adult-onset damage. Greater focus
on the contribution of emotional dysfunction to the real-world
competencies of patients with damage in the VM region may sharpen their
neuropsychological assessment and facilitate rehabilitation efforts.
(JINS, 2006, 12, 224–235.)
Journal Article
Long-term neuropsychological outcomes following mild traumatic brain injury
Mild traumatic brain injury (MTBI) is common, yet few studies have
examined neuropsychological outcomes more than 1 year postinjury. Studies
of nonreferred individuals with MTBI or studies with appropriate control
groups are lacking, but necessary to draw conclusions regarding natural
recovery from MTBI. We examined the long-term neuropsychological outcomes
of a self-reported MTBI an average of 8 years postinjury in a nonreferred
community-dwelling sample of male veterans. This was a cross-sectional
cohort study derived from the Vietnam Experience Study. Three groups
matched on premorbid cognitive ability were examined, those who (1) had
not been injured in a MVA nor had a head injury (Normal Control;
n = 3214), (2) had been injured in a motor vehicle accident (MVA)
but did not have a head injury (MVA Control; n = 539), and (3)
had a head injury with altered consciousness (MTBI; n = 254). A
MANOVA found no group differences on a standard neuropsychological test
battery of 15 measures. Across 15 measures, the average neuropsychological
effect size of MTBI compared with either control group was −.03.
Subtle aspects of attention and working memory also were examined by
comparing groups on Paced Auditory Serial Addition Test (PASAT)
continuation rate and California Verbal Learning Test (CVLT) proactive
interference (PI). Compared with normal controls, the MTBI group evidenced
attention problems in their lower rate of continuation to completion on
the PASAT (odds ratio = 1.32, CI = 1.0–1.73) and in
excessive PI (odds ratio = 1.66, CI = 1.11–2.47). Unique to
the MTBI group, PASAT continuation problems were associated with
left-sided visual imperceptions and excessive PI was associated with
impaired tandem gait. These results show that MTBI can have adverse
long-term neuropsychological outcomes on subtle aspects of complex
attention and working memory. (JINS, 2005, 11,
228–236.)
Journal Article
Set shifting deficit in anorexia nervosa
Anorexia nervosa (AN) is a severe mental illness characterized in part
by rigid thinking and ritualized behaviors involving eating and weight.
Cognitive rigidity may play a role in the perpetuation of symptoms, and
may provide information as to important brain-based abnormalities.
Neuropsychological studies of patients with AN have shown cognitive
dysfunction, but few have focused on cognitive flexibility. This study
assessed set shifting in patients with AN, as a measure of cognitive
flexibility. In this study, 15 patients with AN were compared with 11
healthy controls using a neuropsychological battery including the
Wisconsin Card Sort Test (WCST). While patients with AN did not differ
from controls on 5 measures of neuropsychological function, they made
significantly more perseverative errors on the WCST, indicating a problem
in set shifting. This finding suggests that patients with AN have a
specific neurocognitive abnormality that may play a role in the
development and persistence of this disorder. (JINS, 2006,
12, 431–435.)
Journal Article
Cognitive impairment in schizophrenia: aetiology, pathophysiology, and treatment
Cognitive deficits are a core feature of schizophrenia, account for much of the impaired functioning associated with the disorder and are not responsive to existing treatments. In this review, we first describe the clinical presentation and natural history of these deficits. We then consider aetiological factors, highlighting how a range of similar genetic and environmental factors are associated with both cognitive function and schizophrenia. We then review the pathophysiological mechanisms thought to underlie cognitive symptoms, including the role of dopamine, cholinergic signalling and the balance between GABAergic interneurons and glutamatergic pyramidal cells. Finally, we review the clinical management of cognitive impairments and candidate novel treatments.
Journal Article
Cognitive dysfunction in psychiatric disorders: characteristics, causes and the quest for improved therapy
Key Points
Deficits in cognitive function — ranging from decreased attention and working memory to disrupted social cognition and language — are common in psychiatric disorders.
They severely compromise quality of life, yet are currently poorly treated.
Recent research has identified numerous interacting causes — genetic, epigenetic, developmental and environmental — that collectively disrupt the cerebral and cellular networks integrating and modulating cognition.
Several pharmacotherapeutic strategies for the restoration of cognition are under investigation but most drugs have only been evaluated in rodents, and there is limited positive feedback from the clinic.
The successful development of improved agents necessitates rigorous validation both in animals and in humans. In this regard, a broad palette of techniques, ranging from behavioural testing to brain imaging, is available for the exploration of innovative concepts and the characterization of new drugs.
Despite the key importance of pharmacotherapy, the relevance of alternative strategies should not be neglected. The association of both approaches may emerge to be particularly effective for realizing the goal of enhanced cognitive performance and, accordingly, improved quality of life in patients suffering from psychiatric disorders.
Studies of psychiatric disorders have traditionally focused on emotional symptoms, such as depression, anxiety and hallucinations, but poorly controlled cognitive deficits are also prominent and severely compromise quality of life. This article critically discusses our understanding of the nature and causes of cognitive impairment in psychiatric disorders, and reviews the opportunities and challenges in improving cognition in patients, including the development of more effective translational research approaches.
Studies of psychiatric disorders have traditionally focused on emotional symptoms such as depression, anxiety and hallucinations. However, poorly controlled cognitive deficits are equally prominent and severely compromise quality of life, including social and professional integration. Consequently, intensive efforts are being made to characterize the cellular and cerebral circuits underpinning cognitive function, define the nature and causes of cognitive impairment in psychiatric disorders and identify more effective treatments. Successful development will depend on rigorous validation in animal models as well as in patients, including measures of real-world cognitive functioning. This article critically discusses these issues, highlighting the challenges and opportunities for improving cognition in individuals suffering from psychiatric disorders.
Journal Article
Neurocognitive deficits in depression: a systematic review of cognitive impairment in the acute and remitted state
Previous research suggests a broad range of deficits in major depressive disorder. Our goal was to update the current assumptions and investigate the extent of cognitive impairment in depression in the acute and remitted state. A systematic review of the existing literature between 2009 and 2019 assessing the risk of bias within the included studies was performed. Of the 42 articles reviewed, an unclear risk of bias was shown overall. The risk of bias mainly concerned the sample selection, inadequate remedial measures, as well as the lack of blinding the assessors. In the acute phase, we found strong support for impairment in processing speed, learning, and memory. Follow-up studies and direct comparisons revealed less pronounced deficits in remission, however, deficits were still present in attention, learning and memory, and working memory. A positive correlation between the number of episodes and cognitive deficits as well as depression severity and cognitive deficits was reported. The results also demonstrate a resemblance between the cognitive profiles in bipolar disorder and depression. Comparisons of depression with schizophrenia led to unclear results, at times suggesting an overlap in cognitive performance. The main findings support the global deficit hypothesis and align with results from prior meta-analyses and reviews. Recommendations for future research are also presented.
Journal Article
Chromatographically isolated CD63⁺CD81⁺ extracellular vesicles from mesenchymal stromal cells rescue cognitive impairments after TBI
Extracellular vesicles (EVs) secreted by cells present an attractive strategy for developing new therapies, but progress in the field is limited by several issues: The quality of the EVs varies with the type and physiological status of the producer cells; protocols used to isolate the EVs are difficult to scale up; and assays for efficacy are difficult to develop. In the present report, we have addressed these issues by using human mesenchymal stem/stromal cells (MSCs) that produce EVs when incubated in a protein-free medium, preselecting the preparations of MSCs with a biomarker for their potency in modulating inflammation, incubating the cells in a chemically defined protein-free medium that provided a stable environment, isolating the EVs with a scalable chromatographic procedure, and developing an in vivo assay for efficacy of the cells in suppressing neuroinflammation after traumatic brain injury (TBI) in mice. In addition, we demonstrate that i.v. infusion of the isolated EVs shortly after induction of TBI rescued pattern separation and spatial learning impairments 1 mo later.
Journal Article