scholarly journals Hippocampal network abnormalities explain amnesia after VGKCC-Ab related autoimmune limbic encephalitis

2019 ◽  
Vol 90 (9) ◽  
pp. 965-974 ◽  
Author(s):  
Clare Loane ◽  
Georgios P D Argyropoulos ◽  
Adriana Roca-Fernández ◽  
Carmen Lage ◽  
Fintan Sheerin ◽  
...  

ObjectiveLimbic encephalitis associated with antibodies to components of the voltage-gated potassium channel complex (VGKCC-Ab-LE) often leads to hippocampal atrophy and persistent memory impairment. Its long-term impact on regions beyond the hippocampus, and the relationship between brain damage and cognitive outcome, are poorly understood. We investigated the nature of structural and functional brain abnormalities following VGKCC-Ab-LE and its role in residual memory impairment.MethodA cross-sectional group study was conducted. Twenty-four VGKCC-Ab-LE patients (20 male, 4 female; mean (SD) age 63.86 (11.31) years) were recruited post-acutely along with age- and sex-matched healthy controls for neuropsychological assessment, structural MRI and resting-state functional MRI (rs-fMRI). Structural abnormalities were determined using volumetry and voxel-based morphometry; rs-fMRI data were analysed to investigate hippocampal functional connectivity (FC). Associations of memory performance with neuroimaging measures were examined.ResultsPatients showed selective memory impairment. Structural analyses revealed focal hippocampal atrophy within the medial temporal lobes, correlative atrophy in the mediodorsal thalamus, and additional volume reduction in the posteromedial cortex. There was no association between regional volumes and memory performance. Instead, patients demonstrated reduced posteromedial cortico-hippocampal and inter-hippocampal FC, which correlated with memory scores (r = 0.553; r = 0.582, respectively). The latter declined as a function of time since the acute illness (r = -0.531).ConclusionVGKCC-Ab-LE results in persistent isolated memory impairment. Patients have hippocampal atrophy with further reduced mediodorsal thalamic and posteromedial cortical volumes. Crucially, reduced FC of remaining hippocampal tissue correlates more closely with memory function than does regional atrophy.

Brain ◽  
2021 ◽  
Author(s):  
David Berron ◽  
Jacob W Vogel ◽  
Philip S Insel ◽  
Joana B Pereira ◽  
Long Xie ◽  
...  

Abstract In Alzheimer’s disease, postmortem studies have shown that the first cortical site where neurofibrillary tangles appear is the transentorhinal region, a subregion within the medial temporal lobe that largely overlaps with area 35, and the entorhinal cortex. Here we used tau-PET imaging to investigate the sequence of tau pathology progression within the human medial temporal lobe and across regions in the posterior-medial system. Our objective was to study how medial temporal tau is related to functional connectivity, regional atrophy, and memory performance. We included 215 β-amyloid negative cognitively unimpaired, 81 β-amyloid positive cognitively unimpaired and 87 β-amyloid positive individuals with mild cognitive impairment, who each underwent [18]F-RO948 tau and [18]F-flutemetamol amyloid PET imaging, structural T1-MRI and memory assessments as part of the Swedish BioFINDER-2 study. First, event-based modelling revealed that the entorhinal cortex and area 35 show the earliest signs of tau accumulation followed by the anterior and posterior hippocampus, area 36 and the parahippocampal cortex. In later stages, tau accumulation became abnormal in neocortical temporal and finally parietal brain regions. Second, in cognitively unimpaired individuals, increased tau load was related to local atrophy in the entorhinal cortex, area 35 and the anterior hippocampus and tau load in several anterior medial temporal lobe subregions was associated with distant atrophy of the posterior hippocampus. Tau load, but not atrophy, in these regions was associated with lower memory performance. Further, tau-related reductions in functional connectivity in critical networks between the medial temporal lobe and regions in the posterior-medial system were associated with this early memory impairment. Finally, in patients with mild cognitive impairment, the association of tau load in the hippocampus with memory performance was partially mediated by posterior hippocampal atrophy. In summary, our findings highlight the progression of tau pathology across medial temporal lobe subregions and its disease-stage specific association with memory performance. While tau pathology might affect memory performance in cognitively unimpaired individuals via reduced functional connectivity in critical medial temporal lobe-cortical networks, memory impairment in mild cognitively impaired patients is associated with posterior hippocampal atrophy.


2010 ◽  
Vol 16 (9) ◽  
pp. 1083-1090 ◽  
Author(s):  
VM Anderson ◽  
LK Fisniku ◽  
Z. Khaleeli ◽  
MM Summers ◽  
SA Penny ◽  
...  

Background: In multiple sclerosis (MS), demyelination and neuroaxonal damage are seen in the hippocampus, and MRI has revealed hippocampal atrophy. Objectives: To investigate and compare hippocampal volume loss in patients with relapsing—remitting MS (RRMS) and primary progressive MS (PPMS) using manual volumetry, and explore its association with memory dysfunction. Methods: Hippocampi were manually delineated on volumetric MRI of 34 patients with RRMS, 23 patients with PPMS and 18 controls. Patients underwent neuropsychological tests of verbal and visuospatial recall memory. Linear regression was used to compare hippocampal volumes between subject groups, and to assess the association with memory function. Results: Hippocampal volumes were smaller in MS patients compared with controls, and were similar in patients with RRMS and PPMS. The mean decrease in hippocampal volume in MS patients was 317 mm3 (9.4%; 95% CI 86 to 549; p = 0.008) on the right and 284 mm3 (8.9%; 95% CI 61 to 508; p = 0.013) on the left. A borderline association of hippocampal volume with memory performance was observed only in patients with PPMS. Conclusion: Hippocampal atrophy occurs in patients with RRMS and PPMS. Factors additional to hippocampal atrophy may impact on memory performance.


2008 ◽  
Vol 38 (9) ◽  
pp. 1319-1330 ◽  
Author(s):  
G. Bedi ◽  
J. Redman

BackgroundAlthough there have been several reports linking ecstasy use with lowered cognitive function, much previous research suffers from substantial methodological limitations. The present study aimed to examine associations between ecstasy use and higher-level cognitive functions, using a larger sample size than most previous research and better controlling for a range of potential confounds.MethodA cross-sectional cohort design assessed 45 currently abstinent ecstasy polydrug users (EP), 48 cannabis polydrug users (CP) and 40 legal drug users (LD). Standardized neuropsychological tests were used to measure attention, verbal, visual and working memory and executive function. Prospective memory function was also assessed.ResultsIt was not possible to discriminate between groups on the basis of the cognitive functions assessed. Regression analyses showed an inverse association between lifetime dose of ecstasy and verbal memory performance. A combination of drug-use variables, including measures of ecstasy use, contributed to prediction of attention/working memory. However, individual associations were small, explaining 1–6% of variance in cognitive scores.ConclusionsAlthough the results suggest that heavy use of ecstasy is associated with some lowering of higher-level cognitive functions, they do not indicate a clinical picture of substantial cognitive dysfunction.


2008 ◽  
Vol 29 (17) ◽  
pp. 2125-2132 ◽  
Author(s):  
S. Knecht ◽  
C. Oelschlager ◽  
T. Duning ◽  
H. Lohmann ◽  
J. Albers ◽  
...  

2001 ◽  
Vol 31 (3) ◽  
pp. 441-449 ◽  
Author(s):  
A. F. JORM ◽  
H. CHRISTENSEN ◽  
A. E. KORTEN ◽  
P. A. JACOMB ◽  
A. S. HENDERSON

Background. There is considerable dispute about the validity of memory complaints. While some studies find that complaints are an early indicator of dementia or cognitive decline, there are also many studies showing that complaints are more closely associated with negative affect (depression, anxiety and neuroticism). The present paper used three-wave longitudinal data to test three hypotheses: (1) that memory complaints reflect an evaluation of present and past memory performance; (2) that memory complaints predict future memory performance; and (3) that memory complaints predict current and future negative affect.Methods. A longitudinal study was carried out with a community sample of people aged 70 and over. Participants were assessed for memory complaints, memory performance and negative affect at three waves separated by 3·6 years and 4·0 years. There were 331 persons with data on all relevant variables. The data were analysed using structural equation modelling.Results. Significant paths in the structural model were found from memory performance to future memory complaints, as well as from memory complaints to future memory performance, supporting hypotheses 1 and 2. Memory complaints were associated with current negative affect, but did not predict future negative affect.Conclusions. Memory complaints do reflect perceptions of past memory performance and are also an early manifestation of memory impairment. However, current negative affect (anxiety and depression symptoms) shows the greatest association with memory complaints.


2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Christophe Lancon ◽  
Daniel Dassa ◽  
Jessica Fernandez ◽  
Raphaelle Richieri ◽  
Romain Padovani ◽  
...  

Objective. The aim of this study is to assess the relationships of cardiovascular risk factors with verbal learning and memory in patients with schizophrenia. Methods and Design. cross-sectional study. Inclusion Criteria. Diagnosis of schizophrenia according to the DSM-IV-TR criteria. Data Collection. Sociodemographic information, clinical characteristics, anthropometric measurements, blood tests, and episodic memory using the California Verbal Learning Test (CVLT). Analysis. A multivariate analysis using multiple linear regressions was performed to determine variables that are potentially associated with verbal learning and memory. Results. One hundred and sixty-eight outpatients participated in our study. An association was found between the metabolic syndrome (MetS) and memory impairment on measures of verbal learning, and short- and long-term memory. Among the different components of MeTS, hypertriglycerides, abdominal obesity, and low HDL cholesterol were the only factors associated with memory impairment. Alcohol dependence or abuse was associated with a higher rate of forgetting. Conclusion. Our findings suggest that MetS and alcohol use may be linked with memory impairment in schizophrenia. These findings provide important insights into the interdependencies of cardiovascular risk factors and cognitive disorders and support novel strategies for treating and preventing cognitive disorders in patients with schizophrenia.


2002 ◽  
Vol 14 (4) ◽  
pp. 186-191 ◽  
Author(s):  
Wim J. Riedel ◽  
Sjacko Sobczak ◽  
Nancy Nicolson ◽  
Adriaan Honig

Objective:In the present paper the association of stress-induced cortisol with memory impairment is discussedMethods:An experiment is described in which an attempt is made to block stress-induced cortisol by lowering 5-HT neurotransmission by means of acute tryptophan depletion (ATD). Forty-five healthy control subjects participated in the experiment.Results:Stress-induced peak cortisol and immediate memory performance were negatively associated. ATD tended to block stress-induced cortisol response. ATD also blocked the association between peak cortisol response and memory impairment.Conclusions:Stress-induced cortisol and its association with memory impairment is mediated at least partially by serotonin.


Author(s):  
Siddharth Ramanan ◽  
David Foxe ◽  
Hashim El-Omar ◽  
Rebekah M. Ahmed ◽  
John R. Hodges ◽  
...  

ABSTRACTLogopenic Progressive Aphasia is a rare language disorder characterised by repetition and naming difficulties, reflecting the progressive degeneration of left-lateralized peri-sylvian temporal and inferior parietal regions. Mounting evidence suggests that cognitive impairments in this syndrome extend beyond the language domain to include episodic encoding and retrieval disturbances. To date, it remains unknown whether autobiographical memories from across the lifespan are also subject to decline, yet this information is critical to arrive at a comprehensive understanding of the Logopenic syndrome. The objective of this study was to provide the first in depth examination of autobiographical memory function in Logopenic Progressive Aphasia using the Autobiographical Interview, a validated semi-structured interview which assesses recollection of the past under free and probed recall conditions. Autobiographical memory performance in 10 well-characterised Logopenic Progressive Aphasia patients was contrasted with that of 18 typical amnestic Alzheimer’s disease and 16 healthy Control participants. Relative to Controls, Logopenic Progressive Aphasia cases showed marked impairment in the free recall of episodic details, scoring comparably to disease-matched cases of Alzheimer’s disease. This impairment was evident across all time periods and persisted even when formal structured probing was provided. Importantly, controlling for overall level of language disruption failed to ameliorate the autobiographical memory impairment in the Logopenic Progressive Aphasia group, suggesting a genuine amnesia spanning recent and remote memories. Whole-brain voxel-based morphometry analyses revealed that total episodic information retrieved in Logopenic Progressive Aphasia was associated with decreased grey matter intensity predominantly in a bilateral posterior parietal network. Taken together, our findings reveal for the first time the presence of marked remote and recent autobiographical memory impairments in Logopenic Progressive Aphasia, that cannot be explained solely due to their language difficulties or disease staging. Our findings hold important clinical implications for the accurate characterization of Logopenic Progressive Aphasia, and suggest that episodic memory difficulties should be considered as one of the core clinical features of this syndrome.


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