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Impact-Induced Cortical Strain Concentrations at the Sulcal Base and Its Implications for Mild Traumatic Brain Injury
Author(s) -
Ashley Mazurkiewicz,
Sheng Jun Xu,
Hanspeter Frei,
Rohan Banton,
Thuvan Piehler,
Oren E. Petel
Publication year - 2021
Publication title -
journal of biomechanical engineering
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.546
H-Index - 126
eISSN - 1528-8951
pISSN - 0148-0731
DOI - 10.1115/1.4050283
Subject(s) - gyrification , internal capsule , strain (injury) , sulcus , neuroscience , traumatic brain injury , gyrus , cortex (anatomy) , central sulcus , biology , cerebral cortex , anatomy , psychology , medicine , motor cortex , white matter , radiology , psychiatry , magnetic resonance imaging , stimulation
This study investigated impact-induced strain fields within brain tissue surrogates having different cortical gyrification. Two elastomeric surrogates, one representative of a lissencephalic brain and the other of a gyrencephalic brain, were drop impacted in unison at four different heights and in two different orientations. Each surrogate contained a radiopaque speckle pattern that was used to calculate strain fields. Two different approaches, digital image correlation (DIC) and a particle tracking method, enabled comparisons of full-field and localized strain responses. The DIC results demonstrated increased localized deviations from the mean strain field in the surrogate with a gyrified cortex. Particle tracking algorithms, defining four-node quadrilateral elements, were used to investigate the differences in the strain response of three regions: the base of a sulcus, the adjacent gyrus, and the internal capsule of the surrogates. The results demonstrated that the strains in the cortex were concentrated at the sulcal base. This mechanical mechanism of increased strain is consistent with neurodegenerative markers observed in postmortem analyses, suggesting a potential mechanism of local damage due to strain amplification at the sulcal bases in gyrencephalic brains. This strain amplification mechanism may be responsible for cumulative neurodegeneration from repeated subconcussive impacts. The observed results suggest that lissencephalic animal models, such as rodents, would not have the same modes of injury present in a gyrencephalic brain, such as that of a human. As such, a shift toward representative mild traumatic brain injury animal models having gyrencephalic cortical structures should be strongly considered.

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