Simulating lesion-dependent functional recovery mechanisms

Abstract Functional recovery after brain damage varies widely and depends on many factors, including lesion site and extent. When a neuronal system is damaged, recovery may occur by engaging residual (e.g., perilesional) components. When damage is extensive, recovery depends on the availability of o...

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Autores principales:	Noor Sajid, Emma Holmes, Thomas M. Hope, Zafeirios Fountas, Cathy J. Price, Karl J. Friston
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/a001e02149514f9ba1bda01fe334ff51
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spelling	oai:doaj.org-article:a001e02149514f9ba1bda01fe334ff512021-12-02T18:17:42ZSimulating lesion-dependent functional recovery mechanisms10.1038/s41598-021-87005-42045-2322https://doaj.org/article/a001e02149514f9ba1bda01fe334ff512021-04-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-87005-4https://doaj.org/toc/2045-2322Abstract Functional recovery after brain damage varies widely and depends on many factors, including lesion site and extent. When a neuronal system is damaged, recovery may occur by engaging residual (e.g., perilesional) components. When damage is extensive, recovery depends on the availability of other intact neural structures that can reproduce the same functional output (i.e., degeneracy). A system’s response to damage may occur rapidly, require learning or both. Here, we simulate functional recovery from four different types of lesions, using a generative model of word repetition that comprised a default premorbid system and a less used alternative system. The synthetic lesions (i) completely disengaged the premorbid system, leaving the alternative system intact, (ii) partially damaged both premorbid and alternative systems, and (iii) limited the experience-dependent plasticity of both. The results, across 1000 trials, demonstrate that (i) a complete disconnection of the premorbid system naturally invoked the engagement of the other, (ii) incomplete damage to both systems had a much more devastating long-term effect on model performance and (iii) the effect of reducing learning capacity within each system. These findings contribute to formal frameworks for interpreting the effect of different types of lesions.Noor SajidEmma HolmesThomas M. HopeZafeirios FountasCathy J. PriceKarl J. FristonNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-14 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Noor Sajid Emma Holmes Thomas M. Hope Zafeirios Fountas Cathy J. Price Karl J. Friston Simulating lesion-dependent functional recovery mechanisms
description	Abstract Functional recovery after brain damage varies widely and depends on many factors, including lesion site and extent. When a neuronal system is damaged, recovery may occur by engaging residual (e.g., perilesional) components. When damage is extensive, recovery depends on the availability of other intact neural structures that can reproduce the same functional output (i.e., degeneracy). A system’s response to damage may occur rapidly, require learning or both. Here, we simulate functional recovery from four different types of lesions, using a generative model of word repetition that comprised a default premorbid system and a less used alternative system. The synthetic lesions (i) completely disengaged the premorbid system, leaving the alternative system intact, (ii) partially damaged both premorbid and alternative systems, and (iii) limited the experience-dependent plasticity of both. The results, across 1000 trials, demonstrate that (i) a complete disconnection of the premorbid system naturally invoked the engagement of the other, (ii) incomplete damage to both systems had a much more devastating long-term effect on model performance and (iii) the effect of reducing learning capacity within each system. These findings contribute to formal frameworks for interpreting the effect of different types of lesions.
format	article
author	Noor Sajid Emma Holmes Thomas M. Hope Zafeirios Fountas Cathy J. Price Karl J. Friston
author_facet	Noor Sajid Emma Holmes Thomas M. Hope Zafeirios Fountas Cathy J. Price Karl J. Friston
author_sort	Noor Sajid
title	Simulating lesion-dependent functional recovery mechanisms
title_short	Simulating lesion-dependent functional recovery mechanisms
title_full	Simulating lesion-dependent functional recovery mechanisms
title_fullStr	Simulating lesion-dependent functional recovery mechanisms
title_full_unstemmed	Simulating lesion-dependent functional recovery mechanisms
title_sort	simulating lesion-dependent functional recovery mechanisms
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/a001e02149514f9ba1bda01fe334ff51
work_keys_str_mv	AT noorsajid simulatinglesiondependentfunctionalrecoverymechanisms AT emmaholmes simulatinglesiondependentfunctionalrecoverymechanisms AT thomasmhope simulatinglesiondependentfunctionalrecoverymechanisms AT zafeiriosfountas simulatinglesiondependentfunctionalrecoverymechanisms AT cathyjprice simulatinglesiondependentfunctionalrecoverymechanisms AT karljfriston simulatinglesiondependentfunctionalrecoverymechanisms
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Simulating lesion-dependent functional recovery mechanisms

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