Papers documenting remote CNS wounding are relevant, because outdated (yet common references in these discussions) works such as HWFE, Bullet Penetration, and IWBA publications assert that temporary cavitation and tissue directly crushed tissue are the sole bullet wounding mechanisms. Remote wounding effects are necessary (but not sufficient) to support physiological incapacitation via “hydrostatic shock.” The data providing evidence for remote wounding effects contradicts supposedly “expert” opinions claiming that remote wounding does not exist. Science is based on supporting claims with published data rather than expert opinion. A long list of scientists and medical professionals have published data supporting remote wounding effects. In contrast, none of the (smaller) group making contrary claims have published work showing the lack of remote CNS wounding using detection techniques that would be sufficiently sensitive to see it in cases where it is expected from the shot placement and energy transfer.
Scientific discussion of incapacitation via of BPW is in terms of probability and averages rather than being an absolute predictor of outcomes in every case. This is consistent with standard practice in assessing the risk of injury and disease in the medical world. Thus the theory that “other factors being equal, bullets with higher ballistic pressure waves incapacitate more quickly, on average” or that “other factors being equal, a bullet creating a higher ballistic pressure wave is more likely to cause incapacitation in under five seconds” is analogous to the idea that “the probability of a broken bone increases with the height of the fall” or “the risk of a blast-induced traumatic brain injury increases with the blast wave pressure.” In contrast to the data-driven studies supporting the theory of more rapid incapacitation (on average), there is no published data contradicting the BPW theory as it predicts more rapid incapacitation. Rather than rehash the same tired opinions for the same handful of “experts”why not show some actual published data that might be capable of contradicting the theory either as applied to remote wounding effects or more rapid incapacitation?
Interested parties would do well to read the 2011 Neurosurgery paper and its citations as well as the 2007 Brain Injury paper and its citations. These papers appear in peer reviewed journals and if the citations did not support the claims they would be easy targets for peer-reviewed published replies in the same journals. However, if those posting criticism in internet forums attempted the same criticism in the peer-reviewed journals, I suspect the original authors, editors, and peer-reviewers would embarrass them with the reasoning and evidence presented in reply. Dialog in scientific journals is more limited to actual data and logic without the propensity to veer off into expert opinions and ad hominem attacks. What does it suggest when support for a theory can cite data from numerous scientific journals and opposition can only cite expert opinions from internet forums and a handful of outdated scholarly sources that also contain more opinion than relevant data?
The behind armor blunt trauma causing remote cerebral effects (depressed EEG, including flatlining and rapid death in some cases in human-sized pigs) occurs with pistol levels of energy transfer to the chest at 233, 386, 569, and 634 ft-lbs. As the energy applied to the chest is increased, the severity of EEG suppression and probability of death is increased. In the case of dogs shot in the thigh experiencing remote brain injuries, the energy transfer levels were 97 ft-lbs in the case of mild remote TBI and 546 ft-lbs for a more serious TBI. In the case of pigs shot in the thigh, 466 ft-lbs of energy and 570 ft-lbs of energy both produced transmission of significant pressure pulses to the brain and resulting damage. The study showing 33 cases of cerebrovascular damage (in 33 cases examined) in humans shot in the chest were with handguns with less than 500 ft-lbs of energy.
No one has claimed that hydrostatic shock/BPW is a reliable incapacitation mechanism at service handgun levels. However, nor is blood loss a reliable mechanism in the time span of most gun fights (less than 5 seconds). If the mechanism reduces the average time until incapacitation, then it is somewhat of a straw man fallacy to claim its absence in all cases except for truly instant incapacitation. Likewise, it is a fallacy to claim that absence of evidence of TBI in cases where sensitive detection techniques were not employed. Finally, when selecting ammunition, does it really matter whether the mechanism by which the BPW produces more rapid incapacitation is a remote CNS effect or a muculo-skeletal effect or a combination of both? Isn't knowing that increased BPW increases the probability of a positive outcome sufficient even if the mechanistic details are still under investigation?
Scientific discussion of incapacitation via of BPW is in terms of probability and averages rather than being an absolute predictor of outcomes in every case. This is consistent with standard practice in assessing the risk of injury and disease in the medical world. Thus the theory that “other factors being equal, bullets with higher ballistic pressure waves incapacitate more quickly, on average” or that “other factors being equal, a bullet creating a higher ballistic pressure wave is more likely to cause incapacitation in under five seconds” is analogous to the idea that “the probability of a broken bone increases with the height of the fall” or “the risk of a blast-induced traumatic brain injury increases with the blast wave pressure.” In contrast to the data-driven studies supporting the theory of more rapid incapacitation (on average), there is no published data contradicting the BPW theory as it predicts more rapid incapacitation. Rather than rehash the same tired opinions for the same handful of “experts”why not show some actual published data that might be capable of contradicting the theory either as applied to remote wounding effects or more rapid incapacitation?
Interested parties would do well to read the 2011 Neurosurgery paper and its citations as well as the 2007 Brain Injury paper and its citations. These papers appear in peer reviewed journals and if the citations did not support the claims they would be easy targets for peer-reviewed published replies in the same journals. However, if those posting criticism in internet forums attempted the same criticism in the peer-reviewed journals, I suspect the original authors, editors, and peer-reviewers would embarrass them with the reasoning and evidence presented in reply. Dialog in scientific journals is more limited to actual data and logic without the propensity to veer off into expert opinions and ad hominem attacks. What does it suggest when support for a theory can cite data from numerous scientific journals and opposition can only cite expert opinions from internet forums and a handful of outdated scholarly sources that also contain more opinion than relevant data?
The behind armor blunt trauma causing remote cerebral effects (depressed EEG, including flatlining and rapid death in some cases in human-sized pigs) occurs with pistol levels of energy transfer to the chest at 233, 386, 569, and 634 ft-lbs. As the energy applied to the chest is increased, the severity of EEG suppression and probability of death is increased. In the case of dogs shot in the thigh experiencing remote brain injuries, the energy transfer levels were 97 ft-lbs in the case of mild remote TBI and 546 ft-lbs for a more serious TBI. In the case of pigs shot in the thigh, 466 ft-lbs of energy and 570 ft-lbs of energy both produced transmission of significant pressure pulses to the brain and resulting damage. The study showing 33 cases of cerebrovascular damage (in 33 cases examined) in humans shot in the chest were with handguns with less than 500 ft-lbs of energy.
No one has claimed that hydrostatic shock/BPW is a reliable incapacitation mechanism at service handgun levels. However, nor is blood loss a reliable mechanism in the time span of most gun fights (less than 5 seconds). If the mechanism reduces the average time until incapacitation, then it is somewhat of a straw man fallacy to claim its absence in all cases except for truly instant incapacitation. Likewise, it is a fallacy to claim that absence of evidence of TBI in cases where sensitive detection techniques were not employed. Finally, when selecting ammunition, does it really matter whether the mechanism by which the BPW produces more rapid incapacitation is a remote CNS effect or a muculo-skeletal effect or a combination of both? Isn't knowing that increased BPW increases the probability of a positive outcome sufficient even if the mechanistic details are still under investigation?