Objective: The research examined whether verbal learning and memory impairment previously observed 1 year after left hemisphere stroke endures over a longer period and whether stroke sufferers compensate for their impairments using working memory.
Methodology: Twenty-one persons with left hemisphere lesions; 20 with right hemisphere lesions only and 41 matched controls completed the Hopkins Verbal Learning Test-Revised (HVLT-R), a working memory test (Letter-Number Sequencing, LNS) and the Boston Naming Test (BNT).
Results: Persons with left hemisphere damage performed more poorly on HVLT-R than controls. They showed poorer immediate recall, delayed recall, recognition and learning, but intact retention, suggesting an encoding impairment. BNT and LNS scores predicted recall in this group. HVLT-R performance of persons with right hemisphere lesions only was comparable to controls. BNT (not LNS) predicted recall in these groups.
Conclusions: Persons with left hemisphere damage relied more on working memory and recruited diverse left hemisphere regions to compensate for their impaired encoding.
Implications: Tasks requiring verbal encoding and memory are effortful following left hemisphere stroke. This should be recognized and accommodated.
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http://dx.doi.org/10.3109/02699052.2014.888758 | DOI Listing |
Behav Brain Res
January 2025
Center for Child Health, Behavior and Development, Seattle Children's Research Institute, Seattle, WA, United States of America.
Background: Thalamocortical functional and structural connectivity alterations may contribute to clinical phenotype of Autism Spectrum Disorder. As previous studies focused mainly on thalamofrontal connections, we comprehensively investigated between-group differences of thalamic functional networks and white matter pathways projecting also to temporal, parietal, occipital lobes and their associations with core and co-occurring conditions of this population.
Methods: A total of 38 children (19 with Autism Spectrum Disorder) underwent magnetic resonance imaging and behavioral assessment.
Alzheimers Dement
December 2024
Department of Communication Sciences and Disorders, University of Wisconsin-Madison, Madison, WI, USA.
Background: Sensitive screening for early Alzheimer's disease (AD)-related cognitive decline are needed. Prior research links high beta-amyloid (Aβ) levels to reduced proper name (PN) retrieval in individuals without cognitive impairment. We examined whether language-related regional tau from PET associated with Logical Memory (LM) proper name recall, accounting for LM covariates.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Pittsburgh, Pittsburgh, PA, USA.
Background: Employing a custom 60-channel single-transmit/32-channel receive Tic-Tac-Toe (TTT) coil in 7T MRI imaging has enhanced the resolution and contrast for identifying White Matter Hyperintensities (WMHs), which are critical markers in Alzheimer's disease and related dementias (AD/ADRD).
Method: The method involves resecting the left hemisphere of the brain, excluding the cerebellum, followed by embalming in 10% formalin. 1.
Alzheimers Dement
December 2024
Texas A&M University Health, Bryan, TX, USA.
Background: Our studies show that the small non-coding RNA, mir20a-3p, is neuroprotective for stroke in the acute phase and also attenuates long term cognitive decline in middle-aged female rats. Cognitive decline due to vascular diseases, such as stroke, is associated with secondary neurodegeneration in cortex and limbic structures. In this study, we assessed the volume of white matter, ventricles and regional diffusion-weighted MR imaging measures to delineate pathological tissue characteristics from the postmortem brain of stroke rats.
View Article and Find Full Text PDFBackground: Classical literature has pointed at lateralization of the relationship between memory scores and cerebral hemisphere injury. Epilepsy studies have suggested an association between left hippocampal damage and verbal memory deficits, and between right hippocampal damage and visual memory deficits. We aimed to explore this concept in the context of tauopathy due to Alzheimer's disease.
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