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Task-induced brain activity in aphasic stroke patients: what is driving recovery?
The estimated prevalence of aphasia in the UK and the USA is 250 000 and 1 000 000, respectively. The commonest aetiology is stroke. The impairment may improve with behavioural therapy, and trials using cortical stimulation or pharmacotherapy are undergoing proof-of-principle investigation, but with...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4163030/ https://www.ncbi.nlm.nih.gov/pubmed/24974382 http://dx.doi.org/10.1093/brain/awu163 |
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author | Geranmayeh, Fatemeh Brownsett, Sonia L. E. Wise, Richard J. S. |
author_facet | Geranmayeh, Fatemeh Brownsett, Sonia L. E. Wise, Richard J. S. |
author_sort | Geranmayeh, Fatemeh |
collection | PubMed |
description | The estimated prevalence of aphasia in the UK and the USA is 250 000 and 1 000 000, respectively. The commonest aetiology is stroke. The impairment may improve with behavioural therapy, and trials using cortical stimulation or pharmacotherapy are undergoing proof-of-principle investigation, but with mixed results. Aphasia is a heterogeneous syndrome, and the simple classifications according to the Broca-Wernicke-Lichtheim model inadequately describe the diverse communication difficulties with which patients may present. Greater knowledge of how intact neural networks promote recovery after aphasic stroke, either spontaneously or in response to interventions, will result in clearer hypotheses about how to improve the treatment of aphasia. Twenty-five years ago, a pioneering study on healthy participants heralded the introduction of functional neuroimaging to the study of mechanisms of recovery from aphasia. Over the ensuing decades, such studies have been interpreted as supporting one of three hypotheses, which are not mutually exclusive. The first two predate the introduction of functional neuroimaging: that recovery is the consequence of the reconstitution of domain-specific language systems in tissue around the lesion (the ‘perilesional’ hypothesis), or by homotopic cortex in the contralateral hemisphere (the ‘laterality-shift’ hypothesis). The third is that loss of transcallosal inhibition to contralateral homotopic cortex hinders recovery (the ‘disinhibition’ hypothesis). These different hypotheses at times give conflicting views about rehabilitative intervention; for example, should one attempt to activate or inhibit a contralateral homotopic region with cortical stimulation techniques to promote recovery? This review proposes that although the functional imaging data are statistically valid in most cases, their interpretation has often favoured one explanation while ignoring plausible alternatives. In our view, this is particularly evident when recovery is attributed to activity in ‘language networks’ occupying sites not observed in healthy participants. In this review we will argue that much of the distribution of what has often been interpreted as language-specific activity, particularly in midline and contralateral cortical regions, is an upregulation of activity in intact domain-general systems for cognitive control and attention, responding in a task-dependent manner to the increased ‘effort’ when damaged downstream domain-specific language networks are impaired. We further propose that it is an inability fully to activate these systems that may result in sub optimal recovery in some patients. Interpretation of the data in terms of activity in domain-general networks affords insights into novel approaches to rehabilitation. |
format | Online Article Text |
id | pubmed-4163030 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-41630302014-09-15 Task-induced brain activity in aphasic stroke patients: what is driving recovery? Geranmayeh, Fatemeh Brownsett, Sonia L. E. Wise, Richard J. S. Brain Review Article The estimated prevalence of aphasia in the UK and the USA is 250 000 and 1 000 000, respectively. The commonest aetiology is stroke. The impairment may improve with behavioural therapy, and trials using cortical stimulation or pharmacotherapy are undergoing proof-of-principle investigation, but with mixed results. Aphasia is a heterogeneous syndrome, and the simple classifications according to the Broca-Wernicke-Lichtheim model inadequately describe the diverse communication difficulties with which patients may present. Greater knowledge of how intact neural networks promote recovery after aphasic stroke, either spontaneously or in response to interventions, will result in clearer hypotheses about how to improve the treatment of aphasia. Twenty-five years ago, a pioneering study on healthy participants heralded the introduction of functional neuroimaging to the study of mechanisms of recovery from aphasia. Over the ensuing decades, such studies have been interpreted as supporting one of three hypotheses, which are not mutually exclusive. The first two predate the introduction of functional neuroimaging: that recovery is the consequence of the reconstitution of domain-specific language systems in tissue around the lesion (the ‘perilesional’ hypothesis), or by homotopic cortex in the contralateral hemisphere (the ‘laterality-shift’ hypothesis). The third is that loss of transcallosal inhibition to contralateral homotopic cortex hinders recovery (the ‘disinhibition’ hypothesis). These different hypotheses at times give conflicting views about rehabilitative intervention; for example, should one attempt to activate or inhibit a contralateral homotopic region with cortical stimulation techniques to promote recovery? This review proposes that although the functional imaging data are statistically valid in most cases, their interpretation has often favoured one explanation while ignoring plausible alternatives. In our view, this is particularly evident when recovery is attributed to activity in ‘language networks’ occupying sites not observed in healthy participants. In this review we will argue that much of the distribution of what has often been interpreted as language-specific activity, particularly in midline and contralateral cortical regions, is an upregulation of activity in intact domain-general systems for cognitive control and attention, responding in a task-dependent manner to the increased ‘effort’ when damaged downstream domain-specific language networks are impaired. We further propose that it is an inability fully to activate these systems that may result in sub optimal recovery in some patients. Interpretation of the data in terms of activity in domain-general networks affords insights into novel approaches to rehabilitation. Oxford University Press 2014-10 2014-06-28 /pmc/articles/PMC4163030/ /pubmed/24974382 http://dx.doi.org/10.1093/brain/awu163 Text en © The Author (2014). Published by Oxford University Press on behalf of the Guarantors of Brain. http://creativecommons.org/licenses/by/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Geranmayeh, Fatemeh Brownsett, Sonia L. E. Wise, Richard J. S. Task-induced brain activity in aphasic stroke patients: what is driving recovery? |
title | Task-induced brain activity in aphasic stroke patients: what is driving recovery? |
title_full | Task-induced brain activity in aphasic stroke patients: what is driving recovery? |
title_fullStr | Task-induced brain activity in aphasic stroke patients: what is driving recovery? |
title_full_unstemmed | Task-induced brain activity in aphasic stroke patients: what is driving recovery? |
title_short | Task-induced brain activity in aphasic stroke patients: what is driving recovery? |
title_sort | task-induced brain activity in aphasic stroke patients: what is driving recovery? |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4163030/ https://www.ncbi.nlm.nih.gov/pubmed/24974382 http://dx.doi.org/10.1093/brain/awu163 |
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