Cognitive profile of patients with Chiari 1 malformation

This paper presents literature review on cognitive impairments in patients with CM1, data on which began to be formed in the recent years. Data on the predominant deficit in the structure of executive functioning in patients with CM1 are presented. The genesis of cognitive deficits in patients with CM1 is most often considered in the context of cerebellar dysfunction and damage to the connections of the cerebellum with the prefrontal cortex, which leads to dysmetria of thinking and emotions. Data from other studies are presented that consider the role of additional factors of cognitive dysfunction in CM1, such as pain and emotional disorders.

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The claustrum-medial prefrontal cortex network controls attentional set-shifting

10.1101/2020.10.14.339259 ◽

2020 ◽

Author(s):

Leon Fodoulian ◽

Olivier Gschwend ◽

Chieko Huber ◽

Sophie Mutel ◽

Rodrigo F. Salazar ◽

...

Keyword(s):

Prefrontal Cortex ◽

Medial Prefrontal Cortex ◽

Cognitive Deficits ◽

Pyramidal Cells ◽

Excitatory Input ◽

Set Shifting ◽

Attentional Set ◽

Attentional Set Shifting ◽

Reciprocal Connections

SUMMARYIn various mental disorders, dysfunction of the prefrontal cortex contributes to cognitive deficits. Here we studied how the claustrum (CLA), a nucleus sharing reciprocal connections with the cortex, may participate in these cognitive impairments. We show that specific ensembles of CLA and of medial prefrontal cortex (mPFC) neurons are activated during a task requiring cognitive control such as attentional set-shifting, i.e. the ability to shift attention towards newly relevant stimulus-reward associations while disengaging from irrelevant ones. CLA neurons exert a direct excitatory input on mPFC pyramidal cells, and chemogenetic inhibition of CLA neurons suppresses the formation of specific mPFC assemblies during attentional set-shifting. Furthermore, impairing the recruitment of specific CLA assemblies through opto/chemogenetic manipulations prevents attentional set-shifting. In conclusion, we propose that the CLA controls the reorganization of mPFC ensembles to enable attentional set-shifting, emphasizing a potential role of the CLA-mPFC network in attentional dysfunctions.

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Role of trace amine‑associated receptor 1 in the medial prefrontal cortex in chronic social stress-induced cognitive deficits in mice

Pharmacological Research ◽

10.1016/j.phrs.2021.105571 ◽

2021 ◽

Vol 167 ◽

pp. 105571 ◽

Cited By ~ 1

Author(s):

Yue Zhang ◽

Ji-Tao Li ◽

Han Wang ◽

Wei-Pan Niu ◽

Chen-Chen Zhang ◽

...

Keyword(s):

Prefrontal Cortex ◽

Medial Prefrontal Cortex ◽

Cognitive Deficits ◽

Social Stress ◽

Chronic Social Stress ◽

Trace Amine

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Benefit of the doubt: a new view of the role of the prefrontal cortex in executive functioning and decision making

Frontiers in Neuroscience ◽

10.3389/fnins.2013.00086 ◽

2013 ◽

Vol 7 ◽

Cited By ~ 7

Author(s):

Erik Asp ◽

Kenneth Manzel ◽

Bryan Koestner ◽

Natalie L. Denburg ◽

Daniel Tranel

Keyword(s):

Decision Making ◽

Prefrontal Cortex ◽

Executive Functioning ◽

New View

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Microglial Activation Contributes to Cognitive Impairments in Rotenone-induced Mouse Parkinson’s Disease Model

10.21203/rs.3.rs-73528/v1 ◽

2020 ◽

Author(s):

Dongdong Zhang ◽

Sheng Li ◽

Liyan Hou ◽

Lu Jing ◽

Zhengzheng Ruan ◽

...

Keyword(s):

Lipid Peroxidation ◽

Cognitive Decline ◽

Passive Avoidance ◽

Cognitive Performance ◽

Cognitive Deficits ◽

Water Maze ◽

Microglial Activation ◽

Cognitive Impairments ◽

Synaptic Loss

Abstract BackgroundCognitive decline occurs frequently in Parkinson’s disease (PD), which greatly decreases the life quality of patients. However, the mechanisms remain to be investigated. Neuroinflammation mediated by over-activated microglia is a common pathological feature in multiple neurological disorders, including PD. This study is designed to explore the role of microglia in cognitive deficits by using rotenone-induced mouse PD model. Methods: To evaluate the role of microglia in rotenone-induced cognitive deficits, PLX3397, an inhibitor of colony-stimulating factor 1 receptor, and minocycline, a widely used antibiotic, were used to deplete or inactivate microglia, respectively. Cognitive performance of mice among groups was detected by morris water maze, objective recognition and passive avoidance tests. Neurodegeneration, synaptic loss, α-synuclein phosphorylation, glial activation and apoptosis were determined by immunohistochemistry, Western blot or immunofluorescence staining. The gene expressions of inflammatory factors and lipid peroxidation were further explored by using RT-PCR and ELISA kits, respectively. ResultsRotenone dose-dependently induced cognitive deficits in mice by showing decreased abilities of novel objective recognition, passive avoidance, as well as morris water maze performance compared with vehicle controls. Rotenone-induced cognitive decline was associated with neurodegeneration, synaptic loss, Ser129-phosphorylation of α-synuclein and microglial activation in the hippocampal and cortical regions of mice. Time course study revealed that rotenone-induced microglial activation preceded neurodegeneration. Interestingly, microglial depletion by PLX3397 or inactivation by minocycline significantly reduced neuronal damage and α-synuclein pathology as well as improved cognitive performance in rotenone-injected mice. Mechanistically, PLX3397 or minocycline attenuated rotenone-induced astroglial activation and production of cytotoxic factors in mice. Reduced lipid peroxidation was also observed in combined PLX3397 or minocycline and rotenone-treated mice compared with rotenone alone group. Finally, microglial depletion or inactivation was found to mitigate rotenone-induced neuronal apoptosis. ConclusionsTaken together, our findings suggested that microglial activation contributed to cognitive impairments in rotenone-induced mouse PD model via neuroinflammation, oxidative stress and apoptosis, providing novel insight for the immunopathogensis of cognitive deficits in PD.

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Factors Influencing AAC Usage by Individuals With Aphasia

Perspectives on Augmentative and Alternative Communication ◽

10.1044/aac19.3.70 ◽

2010 ◽

Vol 19 (3) ◽

pp. 70-78 ◽

Cited By ~ 10

Author(s):

Mary Purdy ◽

Aimee Dietz

Keyword(s):

Executive Functioning ◽

Training Program ◽

Cognitive Deficits ◽

Communicative Competence ◽

Cognitive Impairments ◽

Communication Training ◽

Factors Influencing ◽

Wide Range ◽

Attention Memory ◽

The Impact

Abstract Instructing individuals with aphasia in the usage of AAC strategies and devices is a challenging endeavor. Not only does this population present with a wide range of linguistic impairments, but many individuals also demonstrate cognitive deficits, which may adversely affect communication. This paper will summarize the wide variety of cognitive deficits demonstrated by individuals with aphasia, specifically attention, memory and executive functioning problems. In addition, we will review the impact of these cognitive impairments on communicative competence. Finally, we will discuss an intervention, the Multimodality Communication Training Program (MCTP), designed to address the cognitive impairments that influence AAC intervention.

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KCNA2 Autoimmunity in Progressive Cognitive Impairment: Case Series and Literature Review

Brain Sciences ◽

10.3390/brainsci11010089 ◽

2021 ◽

Vol 11 (1) ◽

pp. 89

Author(s):

Charles Timäus ◽

Philipp von Gottberg ◽

Sina Hirschel ◽

Claudia Lange ◽

Jens Wiltfang ◽

...

Keyword(s):

Cognitive Impairment ◽

Cognitive Deficits ◽

Cognitive Impairments ◽

Neuropsychiatric Symptoms ◽

Case Series ◽

Causal Link ◽

Current Evidence ◽

Progressive Dementia ◽

Systematic Assessment

Autoimmune dementia is a novel and expanding field which subsumes neuropsychiatric disorders with predominant cognitive impairments due to an underlying autoimmune etiology. Progressive dementias with atypical clinical presentation should trigger a thorough diagnostic approach including testing for neural surface and intracellular antibodies to avoid a delay in accurate diagnosis and initiating appropriate therapy. Here, we present two emerging cases of progressive dementia with co-existing serum autoantibodies against the KCNA2 (potassium voltage-gated channel subfamily A member 2) subunit. We found various cognitive deficits with dominant impairments in the memory domain, particularly in delayed recall. One patient presented a subacute onset of then-persisting cognitive deficits, while the other patient’s cognitive impairments progressed more chronically and fluctuated. Cognitive impairments coincided with additional neuropsychiatric symptoms. Both had a potential paraneoplastic background according to their medical history and diagnostic results. We discuss the potential role of KCNA2 autoantibodies in these patients and in general by reviewing the literature. The pathogenetic role of KCNA2 antibodies in cognitive impairment is not well delineated; clinical presentations are heterogeneous, and thus a causal link between antibodies remains questionable. Current evidence indicates an intracellular rather than extracellular epitope. We strongly suggest additional prospective studies to explore KCNA2 antibodies in specifically-defined cohorts of cognitively impaired patients via a systematic assessment of clinical, neuropsychological, neuroimaging, as well as laboratory and CSF (cerebrospinal fluid) parameters, and antibody studies to (1) determine the epitope’s location (intracellular vs. extracellular), (2) the mode of action, and (3) seek co-existing, novel pathogenetic autoantibodies in sera and CSF.

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Neurocognitive subtypes in patients with bipolar disorder and their unaffected siblings

Psychological Medicine ◽

10.1017/s003329171700143x ◽

2017 ◽

Vol 47 (16) ◽

pp. 2892-2905 ◽

Cited By ~ 29

Author(s):

M. Russo ◽

T. E. Van Rheenen ◽

M. Shanahan ◽

K. Mahon ◽

M. M. Perez-Rodriguez ◽

...

Keyword(s):

Bipolar Disorder ◽

Cognitive Deficits ◽

Verbal Memory ◽

Genetic Risk ◽

Cognitive Impairments ◽

Cognitive Profile ◽

Cluster Assignment ◽

Discrete Subgroups ◽

Cognitively Intact ◽

Substantial Heterogeneity

BackgroundOur previous work revealed substantial heterogeneity in the cognitive profile of bipolar disorder (BD) due to the presence of three underlying cognitive subgroups characterized as: globally impaired, selectively impaired, or cognitively intact. In an effort to determine whether these subgroups are differentially related to genetic risk for the illness, we investigated whether cognitive deficits were more pronounced in unaffected siblings (UAS) of BD probands within identified clusters.MethodsCluster analysis was used to identify cognitive clusters in BD (N = 60). UAS (N = 49) were classified into groups according to their proband sibling's cluster assignment; comparisons were made across all clusters and healthy controls (HCs; N = 71).ResultsThree cognitive clusters in BD emerged: a globally impaired (36.7%), a selectively impaired (30%), and a cognitively intact cluster (33.3%). UAS showed a qualitatively similar pattern to their BD siblings; UAS of the globally impaired BD cluster showed verbal memory and general cognitive impairments relative to HCs. In contrast, UAS of the other two clusters did not differ from HCs.ConclusionsThis study corroborates findings from prior work regarding the presence of cognitive heterogeneity in BD. UAS of subjects in the globally impaired BD cluster presented with a qualitatively similar cognitive profile to their siblings and performed worse than all other BD clusters and UAS groups. This suggests that inherited risk factors may be contributing to cognitive deficits more notably in one subgroup of patients with BD, pointing toward differential causes of cognitive deficits in discrete subgroups of patients with the disorder.

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Specificity of Cognitive Deficits in Psychosis; Initial Presentation and Course of Alterations among Different Diagnoses

European Psychiatry ◽

10.1016/s0924-9338(09)70489-4 ◽

2009 ◽

Vol 24 (S1) ◽

pp. 1-1

Author(s):

A. Zabala ◽

J.I. Eguiluz ◽

R. Segarra ◽

E. Elizagarate ◽

S. Enjuto ◽

...

Keyword(s):

Working Memory ◽

Executive Functioning ◽

Cognitive Deficits ◽

Memory Task ◽

First Episode Psychosis ◽

Cognitive Profile ◽

First Episode ◽

Episode Psychosis ◽

One Year

Objective:To describe possible differences in the initial cognitive profile between schizophrenia and non-schizophrenia first episode psychosis patients.Method:We assessed attention, working memory, and executive functioning in 57 first episode psychosis patients at baseline and at a one-year follow-up.Results:No significant differences were detected in the cognitive profile among schizophrenia (n=20) and non-schizophrenia (n=37) patients at baseline or at the one-year follow-up. For the overall group, significant reductions in the percentage of omission and commission errors for the sustained attention task (p< 0.001 and p=0.001 respectively), in the total time to complete the Stroop-I task (p< 0.001), in the percentage of omission errors for the working memory task (p=0.001), and in the percentage of perseverative errors for the WCST (p< 0.001) were detected, as well as a significant increase in the number of categories completed in the WCST (p< 0.001). The other cognitive variables analyzed remained stable (4 of the 10 variables tested). The pattern of change was similar for schizophrenia and non-schizophrenia patients in the areas of attention and working memory. For executive functioning, the non-schizophrenia group showed a more beneficial pattern of change.Conclusions:Our results indicate a lack of specificity of cognitive alterations related to the degree of affectation, at least during the first year after instauration of treatment. The course of cognitive deficits in first episode psychosis showed significant improvements over this period, being the patter of change in executive functioning slightly more beneficial for patients with a non-schizophrenia psychosis.

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Cognitive Deficits in Patients with Gambling Disorder

Counseling Psychology and Psychotherapy ◽

10.17759/cpp.2020280409 ◽

2020 ◽

Vol 28 (4) ◽

pp. 167-185

Author(s):

T.V. Agibalova ◽

O.D. Tuchina ◽

O.Zh. Buzik ◽

R.K. Potapova ◽

V.V. Potapov

Keyword(s):

Decision Making ◽

Executive Functioning ◽

Cognitive Deficits ◽

Gambling Disorder ◽

Cognitive Distortions ◽

Cognitive Impairments ◽

Cognitive Errors ◽

Risky Decision ◽

Psychotherapeutic Interventions ◽

Disorder Treatment

The paper provides a narrative review of cognitive deficits in patients with gambling disorder. We discuss several types of these deficits, namely, cognitive impairments due to deficits in executive functioning, impulsive and risky decision-making, gambling-related cognitive distortions, and cognitive errors in cognitive-behavioral terms. These deficits are reviewed from the perspective of their relevance for psychotherapy and the development of differentiated psychotherapeutic interventions for gambling disorder treatment.

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