Dynamical Signatures of Structural Connectivity Damage to a Model of the Brain Posed at Criticality
Synchronization of brain activity fluctuations is believed to represent communication between spatially distant neural processes. These interareal functional interactions develop in the background of a complex network of axonal connections linking cortical and subcortical neurons, termed the human &...
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2016
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_21580014_v6_n10_p759_Haimovici http://hdl.handle.net/20.500.12110/paper_21580014_v6_n10_p759_Haimovici |
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paper:paper_21580014_v6_n10_p759_Haimovici2023-06-08T16:34:24Z Dynamical Signatures of Structural Connectivity Damage to a Model of the Brain Posed at Criticality Anatomic connectivity brain injury dynamics functional connectivity modeling Article brain damage cingulate gyrus connectome middle cingulate cortex neuropathology pathological anatomy posterior cingulate priority journal structural connectome biological model brain brain injury computer simulation connectome diffusion tensor imaging human nerve cell network nerve tract pathophysiology physiology procedures statistics and numerical data Brain Brain Injuries Computer Simulation Connectome Diffusion Tensor Imaging Humans Models, Neurological Nerve Net Neural Pathways Synchronization of brain activity fluctuations is believed to represent communication between spatially distant neural processes. These interareal functional interactions develop in the background of a complex network of axonal connections linking cortical and subcortical neurons, termed the human "structural connectome." Theoretical considerations and experimental evidence support the view that the human brain can be modeled as a system operating at a critical point between ordered (subcritical) and disordered (supercritical) phases. Here, we explore the hypothesis that pathologies resulting from brain injury of different etiologies are related to this model of a critical brain. For this purpose, we investigate how damage to the integrity of the structural connectome impacts on the signatures of critical dynamics. Adopting a hybrid modeling approach combining an empirical weighted network of human structural connections with a conceptual model of critical dynamics, we show that lesions located at highly transited connections progressively displace the model toward the subcritical regime. The topological properties of the nodes and links are of less importance when considered independently of their weight in the network. We observe that damage to midline hubs such as the middle and posterior cingulate cortex is most crucial for the disruption of criticality in the model. However, a similar effect can be achieved by targeting less transited nodes and links whose connection weights add up to an equivalent amount. This implies that brain pathology does not necessarily arise due to insult targeted at well-connected areas and that intersubject variability could obscure lesions located at nonhub regions. Finally, we discuss the predictions of our model in the context of clinical studies of traumatic brain injury and neurodegenerative disorders. © 2016 Mary Ann Liebert, Inc. 2016 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_21580014_v6_n10_p759_Haimovici http://hdl.handle.net/20.500.12110/paper_21580014_v6_n10_p759_Haimovici |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
Anatomic connectivity brain injury dynamics functional connectivity modeling Article brain damage cingulate gyrus connectome middle cingulate cortex neuropathology pathological anatomy posterior cingulate priority journal structural connectome biological model brain brain injury computer simulation connectome diffusion tensor imaging human nerve cell network nerve tract pathophysiology physiology procedures statistics and numerical data Brain Brain Injuries Computer Simulation Connectome Diffusion Tensor Imaging Humans Models, Neurological Nerve Net Neural Pathways |
| spellingShingle |
Anatomic connectivity brain injury dynamics functional connectivity modeling Article brain damage cingulate gyrus connectome middle cingulate cortex neuropathology pathological anatomy posterior cingulate priority journal structural connectome biological model brain brain injury computer simulation connectome diffusion tensor imaging human nerve cell network nerve tract pathophysiology physiology procedures statistics and numerical data Brain Brain Injuries Computer Simulation Connectome Diffusion Tensor Imaging Humans Models, Neurological Nerve Net Neural Pathways Dynamical Signatures of Structural Connectivity Damage to a Model of the Brain Posed at Criticality |
| topic_facet |
Anatomic connectivity brain injury dynamics functional connectivity modeling Article brain damage cingulate gyrus connectome middle cingulate cortex neuropathology pathological anatomy posterior cingulate priority journal structural connectome biological model brain brain injury computer simulation connectome diffusion tensor imaging human nerve cell network nerve tract pathophysiology physiology procedures statistics and numerical data Brain Brain Injuries Computer Simulation Connectome Diffusion Tensor Imaging Humans Models, Neurological Nerve Net Neural Pathways |
| description |
Synchronization of brain activity fluctuations is believed to represent communication between spatially distant neural processes. These interareal functional interactions develop in the background of a complex network of axonal connections linking cortical and subcortical neurons, termed the human "structural connectome." Theoretical considerations and experimental evidence support the view that the human brain can be modeled as a system operating at a critical point between ordered (subcritical) and disordered (supercritical) phases. Here, we explore the hypothesis that pathologies resulting from brain injury of different etiologies are related to this model of a critical brain. For this purpose, we investigate how damage to the integrity of the structural connectome impacts on the signatures of critical dynamics. Adopting a hybrid modeling approach combining an empirical weighted network of human structural connections with a conceptual model of critical dynamics, we show that lesions located at highly transited connections progressively displace the model toward the subcritical regime. The topological properties of the nodes and links are of less importance when considered independently of their weight in the network. We observe that damage to midline hubs such as the middle and posterior cingulate cortex is most crucial for the disruption of criticality in the model. However, a similar effect can be achieved by targeting less transited nodes and links whose connection weights add up to an equivalent amount. This implies that brain pathology does not necessarily arise due to insult targeted at well-connected areas and that intersubject variability could obscure lesions located at nonhub regions. Finally, we discuss the predictions of our model in the context of clinical studies of traumatic brain injury and neurodegenerative disorders. © 2016 Mary Ann Liebert, Inc. |
| title |
Dynamical Signatures of Structural Connectivity Damage to a Model of the Brain Posed at Criticality |
| title_short |
Dynamical Signatures of Structural Connectivity Damage to a Model of the Brain Posed at Criticality |
| title_full |
Dynamical Signatures of Structural Connectivity Damage to a Model of the Brain Posed at Criticality |
| title_fullStr |
Dynamical Signatures of Structural Connectivity Damage to a Model of the Brain Posed at Criticality |
| title_full_unstemmed |
Dynamical Signatures of Structural Connectivity Damage to a Model of the Brain Posed at Criticality |
| title_sort |
dynamical signatures of structural connectivity damage to a model of the brain posed at criticality |
| publishDate |
2016 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_21580014_v6_n10_p759_Haimovici http://hdl.handle.net/20.500.12110/paper_21580014_v6_n10_p759_Haimovici |
| _version_ |
1768542713923239936 |