Microcavitation: the key to modeling blast traumatic brain injury?

Franck, Christian

doi:10.2217/cnc-2017-0011

Cited by 21 publications

(17 citation statements)

References 29 publications

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“…Recently, interest has grown in cavitation damage to biological materials including tissue (Mancia et al 2017, Pahk et al 2019) and surgical mesh (Bigelow et al 2019) given its relevance to therapeutic ultrasound and traumatic injuries. Cavitation is a potential source of neuron damage in blast traumatic brain injury (Goeller et al 2012, Estrada et al 2017, Franck 2017), and it has also been proposed as a useful context in which to study tissue damage incurred through high-strain-rate injuries (Estrada et al 2018). Laser surgery (Brujan and Vogel 2006) and therapeutic ultrasound (Brujan 2004) also motivate studies of controlled cavitation damage.…”

Section: Introductionmentioning

confidence: 99%

Modeling tissue-selective cavitation damage

Mancia¹,

Vlaisavljevich²,

Yousefi³

et al. 2019

Phys. Med. Biol.

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The destructive growth and collapse of cavitation bubbles are used for therapeutic purposes in focused ultrasound procedures and can contribute to tissue damage in traumatic injuries. Histotripsy is a focused ultrasound procedure that relies on controlled cavitation to homogenize soft tissue. Experimental studies of histotripsy cavitation have shown that the extent of ablation in different tissues depends on tissue mechanical properties and waveform parameters. Variable tissue susceptibility to the large stresses, strains, and strain rates developed by cavitation bubbles has been suggested as a basis for localized liver tumor treatments that spare large vessels and bile ducts. However, field quantities developed within microns of cavitation bubbles are too localized and transient to measure in experiments. Previous numerical studies have attempted to circumvent this challenge but made limited use of realistic tissue property data. In this study, numerical simulations are used to calculate stress, strain, and strain rate fields produced by bubble oscillation under histotripsy forcing in a variety of tissues with literature-sourced viscoelastic and acoustic properties. Strain field calculations are then used to predict a theoretical damage radius using tissue ultimate strain data. Simulation results support the hypothesis that differential tissue

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Section: Introductionmentioning

confidence: 99%

Modeling tissue-selective cavitation damage

Mancia¹,

Vlaisavljevich²,

Yousefi³

et al. 2019

Phys. Med. Biol.

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“…From the above equations, we can have a rough idea of how robust the cavitation can be. Thus, many researchers are now investigating the full mechanism of it during events like traumatic brain injury (TBI) 15 – 19 . In our previous study 17 , we reported that the cavitation bubble collapse can be strong enough to rupture sub-cellular structure, which has led us here to investigate the vulnerability of microtubule.…”

Section: Introductionmentioning

confidence: 99%

Damage and Failure of Axonal Microtubule under Extreme High Strain Rate: An In-Silico Molecular Dynamics Study

Adnan

2018

Sci Rep

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As a major cytoskeleton element of the axon, the breaking of microtubules (MTs) has been considered as a major cause of the axon degeneration. High strain rate loading is considered as one of the key factors in microtubule breaking. Due to the small size of microtubule, the real-time behavior of microtubule breaking is hard to capture. This study employs fully-atomistic molecular dynamics (MD) simulation to determine the failure modes of microtubule under different loadings conditions such as, unidirectional stretching, bending and hydrostatic expansion. For each loading conditions, MT is subjected to extreme high strain rate (108–109 s−1) loading. We argue that such level of high strain rate may be realized during cavitation bubble implosion. For each loading type, we have determined the critical energy for MT rupture. The associated rupture mechanisms are also discussed. We observed that the stretching has the lowest energy barrier to break the MT at the nanosecond time scale. Moreover, the breakage between the dimers starts at ~16% of total strain when stretched, which is much smaller compared to the reported strain-at-failure (50%) for lower strain rate loading. It suggests that MT fails at a significantly smaller strain states when loaded at higher strain rates.

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“…Dynamic cavitation in the brain is increasingly considered a potential damage mechanism for traumatic brain injury [16][17][18][19][20] . In this regard, one notable advance is in the characterization of cavitation properties for soft biomaterials under an impulsive force [21][22][23] .…”

Section: Mechanisms Of Cell Damage Due To Mechanical Impact: An In VImentioning

confidence: 99%

Mechanisms of cell damage due to mechanical impact: an in vitro investigation

Kang

Robitaille

Merrill

et al. 2020

Sci Rep

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The dynamic response of cells when subjected to mechanical impact has become increasingly relevant for accurate assessment of potential blunt injuries and elucidating underlying injury mechanisms. When exposed to mechanical impact, a biological system such as the human skin, brain, or liver is rapidly accelerated, which could result in blunt injuries. For this reason, an acceleration of greater than > 150 g is the most commonly used criteria for head injury. To understand the main mechanism(s) of blunt injury under such extreme dynamic threats, we have developed an innovative experimental method that applies a well-characterized and -controlled mechanical impact to live cells cultured in a custom-built in vitro setup compatible with live cell microscopy. Our studies using fibroblast cells as a model indicate that input acceleration ($${a}_{in}$$ain) alone, even when it is much greater than the typical injury criteria, e.g., $${a}_{in}>1{,}000$$ain>1,000 g, does not result in cell damage. On the contrary, we have observed a material-dependent critical pressure value above which a sudden decrease in cell population and cell membrane damage have been observed. We have unambiguously shown that (1) this critical pressure is associated with the onset of cavitation bubbles in a cell culture chamber and (2) the dynamics of cavitation bubbles in the chamber induces localized compressive/tensile pressure cycles, with an amplitude that is considerably greater than the acceleration-induced pressure, to cells. More importantly, the rate of pressure change with time for cavitation-induced pressure is significantly faster (more than ten times) than acceleration-induced pressure. Our in vitro study on the dynamic response of biological systems due to mechanical impact is a crucial step towards understanding potential mechanism(s) of blunt injury and implementing novel therapeutic strategies post-trauma.

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Microcavitation: the key to modeling blast traumatic brain injury?

Cited by 21 publications

References 29 publications

Modeling tissue-selective cavitation damage

Modeling tissue-selective cavitation damage

Damage and Failure of Axonal Microtubule under Extreme High Strain Rate: An In-Silico Molecular Dynamics Study

Mechanisms of cell damage due to mechanical impact: an in vitro investigation

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