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The amnestic syndrome of posterior cerebral artery infarction
BACKGROUND AND PURPOSE: Little is known about the character and underlying lesions of ischaemic amnesia. Episodic memory functions and brain lesions were therefore studied in 84 patients with acute ischaemic infarcts in the supply territory of the posterior cerebral artery. The aim was also to learn...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9541518/ https://www.ncbi.nlm.nih.gov/pubmed/35708171 http://dx.doi.org/10.1111/ene.15449 |
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author | Benke, Thomas Bodner, Thomas Wiesen, Daniel Karnath, Hans‐Otto |
author_facet | Benke, Thomas Bodner, Thomas Wiesen, Daniel Karnath, Hans‐Otto |
author_sort | Benke, Thomas |
collection | PubMed |
description | BACKGROUND AND PURPOSE: Little is known about the character and underlying lesions of ischaemic amnesia. Episodic memory functions and brain lesions were therefore studied in 84 patients with acute ischaemic infarcts in the supply territory of the posterior cerebral artery. The aim was also to learn how the neural memory systems are organized. METHODS: Standard neuropsychological tests were used to assess verbal and figural memory. Patients were split into memory‐impaired and memory‐intact groups. Lesions were demarcated, normalized and anatomically labelled, using standard mapping procedures. RESULTS: Of the 84 patients more than 80% had an amnestic syndrome, mostly with combined memory impairment, less often with figural or verbal memory impairment. Amnesia in subjects with left hemispheric lesions was more frequent and more severe, with significantly lower scores on the verbal memory test. Normal performance or figural amnesia were prevalent after right hemispheric lesions. However, no amnesia subtype was strictly tied to left‐ or right‐sided brain damage. Hippocampal and thalamic lesions were common, but 30% of lesions were extrahippocampal located in the ventral occipito‐temporal cortex and long occipital white matter tracts. Most amnestic patients lacked awareness for their memory impairment. CONCLUSIONS: Memory impairment is a key clinical manifestation of acute posterior cerebral artery stroke. Amnesia is more frequent and more severe after left stroke, suggesting a left hemisphere dominance of the two memory systems. Domain specific memory appears not to be strictly lateralized, since deficits in verbal and figural memory were found after lesions of both sides. Extrahippocampal lesions may also cause memory impairment. |
format | Online Article Text |
id | pubmed-9541518 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-95415182022-10-14 The amnestic syndrome of posterior cerebral artery infarction Benke, Thomas Bodner, Thomas Wiesen, Daniel Karnath, Hans‐Otto Eur J Neurol Stroke BACKGROUND AND PURPOSE: Little is known about the character and underlying lesions of ischaemic amnesia. Episodic memory functions and brain lesions were therefore studied in 84 patients with acute ischaemic infarcts in the supply territory of the posterior cerebral artery. The aim was also to learn how the neural memory systems are organized. METHODS: Standard neuropsychological tests were used to assess verbal and figural memory. Patients were split into memory‐impaired and memory‐intact groups. Lesions were demarcated, normalized and anatomically labelled, using standard mapping procedures. RESULTS: Of the 84 patients more than 80% had an amnestic syndrome, mostly with combined memory impairment, less often with figural or verbal memory impairment. Amnesia in subjects with left hemispheric lesions was more frequent and more severe, with significantly lower scores on the verbal memory test. Normal performance or figural amnesia were prevalent after right hemispheric lesions. However, no amnesia subtype was strictly tied to left‐ or right‐sided brain damage. Hippocampal and thalamic lesions were common, but 30% of lesions were extrahippocampal located in the ventral occipito‐temporal cortex and long occipital white matter tracts. Most amnestic patients lacked awareness for their memory impairment. CONCLUSIONS: Memory impairment is a key clinical manifestation of acute posterior cerebral artery stroke. Amnesia is more frequent and more severe after left stroke, suggesting a left hemisphere dominance of the two memory systems. Domain specific memory appears not to be strictly lateralized, since deficits in verbal and figural memory were found after lesions of both sides. Extrahippocampal lesions may also cause memory impairment. John Wiley and Sons Inc. 2022-07-14 2022-10 /pmc/articles/PMC9541518/ /pubmed/35708171 http://dx.doi.org/10.1111/ene.15449 Text en © 2022 The Authors. European Journal of Neurology published by John Wiley & Sons Ltd on behalf of European Academy of Neurology. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made. |
spellingShingle | Stroke Benke, Thomas Bodner, Thomas Wiesen, Daniel Karnath, Hans‐Otto The amnestic syndrome of posterior cerebral artery infarction |
title | The amnestic syndrome of posterior cerebral artery infarction |
title_full | The amnestic syndrome of posterior cerebral artery infarction |
title_fullStr | The amnestic syndrome of posterior cerebral artery infarction |
title_full_unstemmed | The amnestic syndrome of posterior cerebral artery infarction |
title_short | The amnestic syndrome of posterior cerebral artery infarction |
title_sort | amnestic syndrome of posterior cerebral artery infarction |
topic | Stroke |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9541518/ https://www.ncbi.nlm.nih.gov/pubmed/35708171 http://dx.doi.org/10.1111/ene.15449 |
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