RyanM said:
I'm spotting several flaws in the methodology. Shooting cultured nerves is not very analogous to shooting a living thing. I notice that in the pig study where transducers were implanted in the brain, there was some minor blood-brain barrier damage, but in the pig study with no transducers, there was no observable gross damage to the brain whatsoever. That suggests that inserting the transducer is likely the primary cause of injury in that case. Kind of like that one drug study where they did spinal taps every month, and then concluded that the drug depletes cerebrospinal fluid.
Perhaps, but you need to take a wider view and consider all the literature in the field suggesting a pressure wave incapacitation mechanism. Such as
Wang Q,Wang Z, Zhu P, Jiang J: “Alterations of the Myelin Basic Protein and Ultrastructure in the Limbic System and the Early Stage of Trauma-Related Stress Disorder in Dogs. " The Journal of Trauma. 56(3):604-610; 2004.
Toth Z, Hollrigel G, Gorcs T, and Soltesz I: “Instantaneous Perturbation of Dentate Interneuronal Networks by a Pressure Wave Transient Delivered to the Neocortex.” The Journal of Neuroscience, 17(7);8106-8117; 1997.
Thompson HJ, Lif????z J, Marklund N, Grady MS, Graham DI, Hovda DA, McIntosh TK, “Lateral Fluid Percussion Brain Injury: A 15-Year Review and Evaluation”, Journal of Neurotrauma, 22(1):42-75 (2005).
Wang Q,Wang Z, Zhu P, Jiang J: “Alterations of the Myelin Basic Protein and Ultrastructure in the Limbic System and the Early Stage of Trauma-Related Stress Disorder in Dogs. " The Journal of Trauma. 56(3):604-610; 2004.
Knudsen SK, Oen EO: “Blast-induced neurotrauma in whales.” Neurosci Res. 46
(3): 377-386 (2003).
You also should consider the fact that Fackler's "Shockwave Myth" article contains serious flaws:
Fackler employs the straw man fallacy by referring to the pressure wave studied by Suneson et al. as “the sonic pressure wave.” The authors studied a “shock” wave and clearly stated that the wave includes both sub-sonic and super-sonic frequency components up to 250 kHz. By definition, sonic waves only include frequencies from 20 Hz - 20 kHz. The pressure wave under study has both sonic and super-sonic components. In addition, Fackler considers the “sonic pressure wave” to be limited to a very short (several microseconds) pulse that preceeds temporary cavitation. Suneson et al. are describing effects of pressure waves with a much longer duration.
Fackler creates a false dichotomy to divide effects beyond the permanent crush cavity into only the temporary cavity and the “sonic” pressure wave. Ballistic pressure waves have components both at frequencies below the sonic range (< 20 Hz), and at frequencies above the sonic range (> 20 kHz). The pressure wave consists of every force per unit area that can be detected by a high-speed pressure sensor.
Movement of tissue by cavitation is not distinct from the ballistic pressure wave. (One can consider temporary cavitation an effect of the inertial component of the pressure wave.) Consequently, ascribing the local neural injuries to the pressure wave is not unreasonable, though Fackler is correct to point out that in the local region, the pressure wave effects cannot be distinguished from temporary cavitation effects.
Suneson et al. also report regional and distant effects beyond the reach of the temporary cavity. Nerve damage is observed as far as 0.5m away from the wound channel. These regional and distant effects cannot be ascribed to temporary cavitation.
Fackler continues:
Fackler said:
Recently, eleven adult human-sized swine (90 kg) were shot in the proximal part of the hind leg with a projectile producing the damage profile of the Russian AK-74 Assault rifle bullet. This same projectile was used in another study in which five 90 kg swine were shot through the abdomen …No indication of any sort of “distant” damage was seen in the pigs’ behavior and no “distant” injuries were found at autopsy.
The methodology of Fackler’s pig experiments is significantly different from Suneson et al., who report that the neural damage is not easily observable, but rather depends upon examination with light and electron microscopy. The effects that Suneson et al. report “were evident a few minutes after the trauma and persisted even 48 hr after the extremity injury.” In Fackler’s experiments, autopsies were not performed until weeks or months later. With such great differences in experimental methodology, it is unfounded to assert that Fackler’s swine experiments contradict the conclusions of Suneson et al.
Fackler continues:
Fackler said:
A review of 1400 rifle wounds from Vietnam (wound Data and Munitions Effectiveness Team) should lay to rest the myth of “distant” injuries. In that study, there were no cases of bones being broken, or major vessels torn, that were not hit by the penetrating bullet.
It strains that boundaries of credulity that someone would refute modern observations (using new methods) of microscopic damage to nerve cells by referring to the absence of observations of broken bones or torn blood vessels in a Vietnam-era observations from trauma surgeons. The Vietnam-era study was not looking for distant nerve damage, and they did not employ the methods used by Suneson et al.
The results of Suneson et al. also find substantial agreement with later experiments in dogs conducted by an independent research group using a substantially similar methodology (see above references).
There are a number of additional papers in the peer-reviewed journals (see above references) studying the damage to the central nervous system caused by pressure wave effects. Since their focus is on long-term effects, this research does not reach definitive conclusions regarding whether these pressure wave effects contribute to rapid incapacitation of humans. However, there is a growing body of evidence that pressure waves near 30 PSI can cause CNS damage that would usually be undetected by a trauma surgeon or medical examiner, but can be quantified with advanced neurological techniques.
There is also well-established evidence that pressure waves near 30 PSI applied to the brain causes immediate incapacitation of laboratory animals. In a study applying a pressure wave directly to the brain via the lateral fluid percussion technique, Toth et al. report both instantaneous incapacitation and cellular damage:
Toth et al said:
The delivery of the pressure pulse was associated with brief (<120-200 sec), transient traumatic unconsciousness (as assessed by the duration of suppression of the righting reflex).
One reasonably wonders what relevance these live animal experiments using the lateral fluid percussion technique to induce a pressure wave injury in laboratory animals have for understanding neurological pressure wave effects in humans. A 15 year review and evaluation of this question concluded:
Thompson et al said:
We conclude that the lateral fluid percussion brain injury model is an appropriate tool to study the cellular and mechanistic aspects of human traumatic brain injury…
Consequently, there is significant support for the hypothesis of a pressure wave contribution to incapacitation not only in anecdotal observations and an anonymous experiment on goats, but also in well-established results of neurological experiments.
As of January 2006, there are published results showing that a pressure wave can cause rapid neurological incapacitation and/or damage in goats, dogs, swine, several species of laboratory rats, and even in whales. In many of these cases, detecting wounding requires advanced techniques such as electron microscopy, cellular analysis, EEG monitoring, and sophisticated chemical analysis. Consequently, the hypothesis that incapacitation only occurs from wounding that is easily detectable to the trauma surgeon or medical examiner has been disproven. This opens the door to consider support for pressure wave contributions to incapacitation by experiments observing incapacitation directly without concern for easily detectable wounding.
Michael Courtney
:banghead: 
