Right thalamic lacunar infarction presenting with anomic aphasia

2015 ◽  
Vol 14 (2) ◽  
Author(s):  
Naveed Natanzi ◽  
Sogol Ashourpour ◽  
Pedram Goel ◽  
Patricia W. Nance
Keyword(s):  
Temporal Lobe ◽  
Cognitive Deficits ◽  
Medical Literature ◽  
Parietal Lobe ◽  
Speech Impairment ◽  
Subcortical Structures ◽  
Thalamic Infarction ◽  
Crossed Aphasia ◽  
Over Time

AbstractWe present two cases of thalamic infarction presentation with aphasia, which has rarely been documented in the literature. Of interest, the second case presented with a lesion in the non-dominant thalamus, which made the finding of speech impairment exceedingly rare. Anomic aphasia has been associated with lesions to the basal temporal lobe, anterior inferior temporal lobe, temporo-parieto-occipital junction and the inferior parietal lobe, but rarely in association with the thalamus. Thalamic strokes most often present with motor, sensory, and cognitive deficits; few reports in the medical literature associate aphasia with a thalamic infarction. Possible explanations include crossed aphasia, diaschisis, the hypometabolic theory, and the thalamus as a secondary language center. Our findings may hint to a relationship among language, higher cognitive function, subcortical structures, and interhemispheric connections that are yet to be understood completely. We postulate that an increasingly important role of subcortical neuronal structures in cognitive functions will be recognized as diagnostic imaging technology improves over time.

scholarly journals The role of cognitive functioning in the outcome of those at clinical high risk for developing psychosis

2012 ◽  
Vol 21 (4) ◽  
pp. 335-342 ◽  
Author(s):  
J. Addington ◽  
M. Barbato
Keyword(s):  
High Risk ◽  
Cognitive Functioning ◽  
Cognitive Deficits ◽  
Cognitive Abilities ◽  
Healthy Controls ◽  
Clinical High Risk ◽  
Cross Sectional ◽  
Cognitive Domains ◽  
Over Time

Although it is well established that cognitive impairment is a common feature of schizophrenia, only recently has cognitive functioning been prospectively studied in individuals at clinical high risk (CHR) for developing psychosis. To date, both cross-sectional and longitudinal studies have been conducted in the CHR population and in the context of later conversion to psychosis. A comprehensive review of the literature suggests that CHR individuals have general and specific baseline cognitive deficits compared to healthy controls. As a group, their cognitive course, tends to remain stable over time and in this way does not differ from healthy controls. For those who go on to develop a full-blown psychotic illness compared to those who do not convert, there appeared to be minimal differences at baseline with respect to cognition, although over time the converters may show deterioration in certain cognitive abilities compared to the non-converters. However, for many cognitive domains results are mixed, and may result from methodological limitations.

Spatiotemporal memory and rate of forgetting in acute schizophrenics

1988 ◽  
Vol 18 (4) ◽  
pp. 843-853 ◽  
Author(s):  
Mohammed A. Shoqeirat ◽  
Andrew R. Mayes
Keyword(s):  
Temporal Lobe ◽  
Cognitive Deficits ◽  
Medial Temporal Lobe ◽  
Parietal Lobe ◽  
Unknown Origin ◽  
Wisconsin Card Sorting Test ◽  
Type I ◽  
Card Sorting ◽  
Temporal Lobe Lesions ◽  
Sorting Test

SynopsisSome schizophrenics show anomalies in the frontal and temporal lobes. It is uncertain whether the cognitive deficits shown by Type I schizophrenics are caused directly by such anomalies, or by a deficit in the exertion of attentional effort. In this study, 16 acute schizophrenics, who broadly fitted the Type I characterization and their controls were given a battery of cognitive tests. The patients were impaired on effort-demanding tasks such as the Wisconsin Card Sorting Test, a verbal fluency test and the WAIS, which are susceptible in varying degrees to frontal, temporal and parietal lobe lesions. Patients were not disproportionately impaired, however, on a test of temporal memory and another of spatial memory, an impairment pattern that selectively reflects frontal and medial temporal lobe lesions respectively, nor were they impaired on a rate of forgetting task sensitive to medial temporal lobe lesions. These tasks were chosen not only because performance on them is selectively sensitive to frontotemporal lobe lesions, but also because it seems to depend on exerting minimum amounts of attentional effort. It is tentatively concluded that the cognitive deficits shown by Type I schizophrenics are caused by a problem in exerting attentional effort of unknown origin.

scholarly journals Longitudinal anatomic, functional, and molecular characterization of Pick disease phenotypes

Neurology ◽  
2020 ◽  
Vol 95 (24) ◽  
pp. e3190-e3202
Author(s):  
Jennifer L. Whitwell ◽  
Nirubol Tosakulwong ◽  
Christopher C. Schwarz ◽  
Matthew L. Senjem ◽  
Anthony J. Spychalla ◽  
...  
Keyword(s):  
Temporal Lobe ◽  
Parietal Lobe ◽  
Inferior Frontal Gyrus ◽  
Gray Matter Volume ◽  
Primary Progressive Aphasia ◽  
Progressive Aphasia ◽  
Primary Progressive ◽  
Β Amyloid ◽  
Pick Disease ◽  
Over Time

ObjectiveTo characterize longitudinal MRI and PET abnormalities in autopsy-confirmed Pick disease (PiD) and determine how patterns of neurodegeneration differ with respect to clinical syndrome.MethodsSeventeen patients with PiD were identified who had antemortem MRI (8 with behavioral variant frontotemporal dementia [bvFTD-PiD], 6 with nonfluent/agrammatic primary progressive aphasia [naPPA-PiD], 1 with semantic primary progressive aphasia, 1 with unclassified primary progressive aphasia, and 1 with corticobasal syndrome). Thirteen patients had serial MRI for a total of 56 MRIs, 7 had [18F]fluorodeoxyglucose PET, 4 had Pittsburgh compound B (PiB) PET, and 1 patient had [18F]flortaucipir PET. Cross-sectional and longitudinal comparisons of gray matter volume and metabolism were performed between bvFTD-PiD, naPPA-PiD, and controls. Cortical PiB summaries were calculated to determine β-amyloid positivity.ResultsThe bvFTD-PiD and naPPA-PiD groups showed different foci of volume loss and hypometabolism early in the disease, with bvFTD-PiD involving bilateral prefrontal and anterior temporal cortices and naPPA-PiD involving left inferior frontal gyrus, insula, and orbitofrontal cortex. However, patterns merged over time, with progressive spread into prefrontal and anterior temporal lobe in naPPA-PiD, and eventual involvement of posterior temporal lobe, motor cortex, and parietal lobe in both groups. Rates of frontotemporal atrophy were faster in bvFTD-PiD than naPPA-PiD. One patient was β-amyloid–positive on PET with low Alzheimer neuropathologic changes at autopsy. Flortaucipir PET showed elevated uptake in frontotemporal white matter.ConclusionPatterns of atrophy and hypometabolism differ in PiD according to presenting syndrome, although patterns of neurodegeneration appear to converge over time.

Identification of a Pathogenic PSEN1 Ala285Val Mutation Associated with Early-Onset Alzheimer’s Disease

2020 ◽  
Vol 17 (5) ◽  
pp. 438-445
Author(s):  
Van Giau Vo ◽  
Jung-Min Pyun ◽  
Eva Bagyinszky ◽  
Seong S.A. An ◽  
Sang Y. Kim
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Temporal Lobe ◽  
Early Onset ◽  
Parietal Lobe ◽  
Disease Diagnosis ◽  
Random Coil ◽  
Magnetic Resonance Imaging Scan ◽  
Preclinical Ad ◽  
Early Onset Alzheimer’S Disease

Background: Presenilin 1 (PSEN1) was suggested as the most common causative gene of early onset Alzheimer’s Disease (AD). Methods: Patient who presented progressive memory decline in her 40s was enrolled in this study. A broad battery of neuropsychological tests and neuroimaging was applied to make the diagnosis. Genetic tests were performed in the patient to evaluate possible mutations using whole exome sequencing. The pathogenic nature of missense mutation and its 3D protein structure prediction were performed by in silico prediction programs. Results: A pathogenic mutation in PSEN1 (NM_000021.3: c.1027T>C p.Ala285Val), which was found in a Korean EOAD patient. Magnetic resonance imaging scan showed mild left temporal lobe atrophy. Hypometabolism appeared through 18F-fludeoxyglucose Positron Emission Tomography (FDG-PET) scanning in bilateral temporal and parietal lobe, and 18F-Florbetaben-PET (FBB-PET) showed increased amyloid deposition in bilateral frontal, parietal, temporal lobe and hence presumed preclinical AD. Protein modeling showed that the p.Ala285Val is located in the random coil region and could result in extra stress in this region, resulting in the replacement of an alanine residue with a valine. This prediction was confirmed previous in vitro studies that the p.Trp165Cys resulted in an elevated Aβ42/Aβ40 ratio in both COS-1 and HEK293 cell lines compared that of wild-type control. Conclusion: Together, the clinical characteristics and the effect of the mutation would facilitate our understanding of PSEN1 in AD pathogenesis for the disease diagnosis and treatment. Future in vivo study is needed to evaluate the role of PSEN1 p.Ala285Val mutation in AD progression.

Raza, ciencia, sociedad

2015 ◽  
Vol 2 (4) ◽  
Author(s):  
Peter Wade
Keyword(s):  
Cultural Discourse ◽  
Human Biology ◽  
Science And Society ◽  
Race Science ◽  
And Behavior ◽  
Over Time

<p class="p1"><span class="s1"><strong>Resumen </strong></span>| En este trabajo quiero presentar una cronología convencional del concepto raza que marca un movimiento en el cual raza cambia de ser una idea basada en la cultura y el medio ambiente, a ser algo biológico, inflexible y determinante, para luego volver a ser una noción que habla de la cultura<span class="s2"><strong>.</strong></span>Resumo cómo la idea de raza ha cambiado a través del tiempo, mirando necesariamente el rol que ha desempeñado la ciencia, y enfocando los diferentes discursos de índole <em>natural-cultural </em>sobre los cuerpos, el medio ambiente y el comportamiento, en los cuales las dimensiones culturales y naturales siempre coexisten<span class="s2"><strong>.</strong></span>“La naturaleza” no puede ser entendida solamente como “la biología” y ni la naturaleza ni la biología necesariamente implican sólo el determinismo, la fijeza y la inmutabilidad Estar abiertos a la coexistencia de la cultura y la naturaleza y a la mutabilidad de la naturaleza nos permite ver mejor el ámbito de acción del pensamiento racial.</p><p class="p1"><strong><em>Race, Science and Society</em></strong></p><p class="p1"> </p><p class="p2"><span class="s1"><strong>Abstract </strong></span>| In this article I present and critique a standard chronology of race as, first, a concept rooted in culture and environment, and later in human biology and determinism, and finally back to culture alone<span class="s2"><strong><em>.</em></strong></span>I will outline changing understandings of race over time, with some attention to the role of science, broadly understood, and on the continuing but changing character of race as a natural-cultural discourse about organic bodies, environments and behavior, in which both cultural and natural dimensions always co-exist<span class="s2"><strong><em>.</em></strong></span>“Nature” is not to be understood simply as “biology,” and neither nature nor biology necessarily imply the fixity and determination that they are often assumed nowadays to involve<span class="s2"><strong><em>.</em></strong></span>Being open to the co-existence of culture and nature and the mutability of the latter allows us to better comprehend the whole range of action of racial thinking.</p>

Biopsychosocial Patterning of Multimorbidity and Its Consequences

2018 ◽  
pp. 220-236
Author(s):  
Elliot Friedman ◽  
Beth LeBreton ◽  
Lindsay Fuzzell ◽  
Elizabeth Wehrpsann
Keyword(s):  
Quality Of Life ◽  
Older Adults ◽  
Functional Outcomes ◽  
The United States ◽  
Chronic Medical Conditions ◽  
Quality Of Life Research ◽  
Increased Risk ◽  
Over Time

By many estimates the majority of adults over age 65 have two or more chronic medical conditions (multimorbidity) and are consequently at increased risk of adverse functional outcomes. Nonetheless, many older adults with multimorbidity are able to maintain high levels of function and retain good quality of life. Research presented here is designed to understand the influences that help ensure better functional outcomes in these older adults. This chapter presents findings that draw on data from the Midlife in the United States study. The independent and interactive contributions of diverse factors to multimorbidity and changes in multimorbidity over time are reviewed. The degree that multimorbidity increases risk of cognitive impairment and disability is examined. The role of inflammation as a mediator is considered. Multimorbidity is increasingly the norm for older adults, so better understanding of factors contributing to variability in multimorbidity-related outcomes can lead to improved quality of life.

Sign in / Sign up

Export Citation Format

Share Document