5 Modelling of the Brain for Injury Simulation and Prevention
105
and newly developed sensors for deep brain functional detection are commonly
used. Unfortunately, these investigating modalities for human are not as specific
as histologic methods in animal studies. At present, how the brain mechanically
responds to impact during trauma and how these mechanical brain responses lead
to damage that showed up hours/days/weeks later remain largely unknown. To
summarise, the paucity of biomechanical responses and corresponding site-specific
injuries hinders the model advancements in two major aspects:
(i) The biofidelity of any existing models cannot be confirmed with high degree of
confidence.
(ii) Except some cortical contusion cases (e.g. [13, 79]), correlations between the
model-predicted biomechanical responses and diffuse types of injury can only
be conducted at the whole brain level (such as concussion or no concussion)
instead of region-specific correlations.
5.2.2 Lack of Proven Injury Mechanism
Intracranial strains, which are induced mostly by head rotation, seem to be a
plausible injury mechanism for correlations with TBI. By direct stretching of the
right optic nerve of an adult male guinea pig, Bain and Meaney [8] were able
to determine the strain-based threshold for morphological impairment of axon.
Several hypothesised injury mechanisms, such as CSDM, MPS, and BrIC, are
derived from the peak magnitudes of intracranial strains calculated from FE models.
Nevertheless, other experimental data appeared to suggest that strain is not the sole
culprit responsible for TBI. For example, Morrison et al. [70] reported an in vitro
model of TBI in which organotypic hippocampal slice cultures adhere to silicone
membranes and then stretched in an equi-biaxial manner at different loading rates.
Although the authors found positive correlations between cell damages and strains,
results also showed that not all brain regions were injured at the same rate and
injuries were not evenly distributed within the same region. Understanding that the
entire brain slice was subjected to the same mechanical stretches everywhere but
the damages were not evenly distributed, one must question what was the cause
for those tissues to be uninjured under the same mechanical stimuli? Additionally,
these results suggested that different substructure of the brain must possess different
injury thresholds. Such region-specific injury thresholds have been largely neglected
in literatures.
In recent Middle East conflicts, blast-induced TBI (bTBI) victims returned from
military theatres revealed that the primary blast overpressures did not produce
large head rotation. As such, intracranial strains were extremely small. In this
case, intracranial pressures and its gradients induced by blast waves, rather than
the magnitude of strain, are being investigated as the injury mechanism (e.g.
[48]). Other studies suggested that other parameters should be considered when
determining the risk of bTBI. For example, Zhu et al. [113] considered the effect
105
and newly developed sensors for deep brain functional detection are commonly
used. Unfortunately, these investigating modalities for human are not as specific
as histologic methods in animal studies. At present, how the brain mechanically
responds to impact during trauma and how these mechanical brain responses lead
to damage that showed up hours/days/weeks later remain largely unknown. To
summarise, the paucity of biomechanical responses and corresponding site-specific
injuries hinders the model advancements in two major aspects:
(i) The biofidelity of any existing models cannot be confirmed with high degree of
confidence.
(ii) Except some cortical contusion cases (e.g. [13, 79]), correlations between the
model-predicted biomechanical responses and diffuse types of injury can only
be conducted at the whole brain level (such as concussion or no concussion)
instead of region-specific correlations.
5.2.2 Lack of Proven Injury Mechanism
Intracranial strains, which are induced mostly by head rotation, seem to be a
plausible injury mechanism for correlations with TBI. By direct stretching of the
right optic nerve of an adult male guinea pig, Bain and Meaney [8] were able
to determine the strain-based threshold for morphological impairment of axon.
Several hypothesised injury mechanisms, such as CSDM, MPS, and BrIC, are
derived from the peak magnitudes of intracranial strains calculated from FE models.
Nevertheless, other experimental data appeared to suggest that strain is not the sole
culprit responsible for TBI. For example, Morrison et al. [70] reported an in vitro
model of TBI in which organotypic hippocampal slice cultures adhere to silicone
membranes and then stretched in an equi-biaxial manner at different loading rates.
Although the authors found positive correlations between cell damages and strains,
results also showed that not all brain regions were injured at the same rate and
injuries were not evenly distributed within the same region. Understanding that the
entire brain slice was subjected to the same mechanical stretches everywhere but
the damages were not evenly distributed, one must question what was the cause
for those tissues to be uninjured under the same mechanical stimuli? Additionally,
these results suggested that different substructure of the brain must possess different
injury thresholds. Such region-specific injury thresholds have been largely neglected
in literatures.
In recent Middle East conflicts, blast-induced TBI (bTBI) victims returned from
military theatres revealed that the primary blast overpressures did not produce
large head rotation. As such, intracranial strains were extremely small. In this
case, intracranial pressures and its gradients induced by blast waves, rather than
the magnitude of strain, are being investigated as the injury mechanism (e.g.
[48]). Other studies suggested that other parameters should be considered when
determining the risk of bTBI. For example, Zhu et al. [113] considered the effect