Soldiers have been suffering severe concussions as a result of being near to explosions. If these same soldiers survive their tour of duty once they’re back home a refrain commonly heard by their families is, “this is not the same person, I don’t recognize my own son/daughter any more.”
So what happens to a human brain exposed to a massive pressure wave, which is the real physics involving blast pressure wave exposure?
I am citing from the following article:Medical Hypotheses
Volume 72, Issue 1, January 2009, Pages 76-83 the title is A thoracic mechanism of mild traumatic brain injury due to blast pressure waves authored by A.C.Courtney and M.W.Courtney
These authors have done some scary experiments. I’m not going into the gory details but were talking about blast injuries here. Even high powered bullets fired at a distance into an animals body creates concussions, what are more properly termed minor traumatic brain injuries (mTBI). The authors observations and speculations are crossing over into my territory. Hence my severe excitement reading their thoughts. I’ll quote the most pertinent parts.
“Remote injuries due to pressure waves caused by penetrating ballistic projectiles
Injuries due to ballistic pressure waves have been reported in both case studies and experiments. A Vietnam-era database of casualties includes observations of remote wounding due to pressure waves created by penetrating injuries, including two cases of remote lung injury, five cases of remote abdominal injury in which the peritoneum was not perforated, and at least one example of temporary nerve damage . Additional case studies also show indirect injuries , ,  and , including indirect neural injuries ,  and , due to pressure waves created by ballistic projectiles in soft tissues.
How far from the bullet path can remote effects of ballistic pressure waves be observed? Lai et al.  used a dog model to evaluate injury to vascular endothelial cells due to distant penetration (up to approximately 0.5 m) by military rifle bullets. The number of circulating endothelial cells (a systemic indicator of damage) increased with proximity of the penetration site (leg, abdomen or thorax). Locally, laceration of vascular intima was observed in the aorta, common carotid and middle cerebral arteries by electron microscopy. These results suggest that the ballistic pressure waves traveled to the brain via the large vessels and retained sufficient magnitude to cause endothelial damage to cerebral arteries.
Suneson et al.  recorded bursts of high frequency pressure waves of average magnitude about 150 kPa (22 psi) in the brain of anesthetized pigs shot in the thigh. In this model, a mean of 728 J of work was done by the projectile. Apneic periods lasting several seconds occurred following the injury. Histological observations were limited to ‘minor damage’ to the blood-brain and blood-nerve barriers. Goransson et al.  reported electroencephalogram (EEG) suppression and transient apnea in pigs similarly injured. In subsequent experiments  and  about 770 J of work was done by the projectile, and pressures in the range of 180–240 kPa (26–34 psi) were recorded in the brain. Microscopic damage in hippocampal and cerebellar neurons was also observed. The authors concluded that these effects were caused by pressure waves transmitted to the brain from the distant (0.5 m) point of origin.
Wang et al.  performed similar experiments in groups of dogs. In one experimental group, about 131 J of work was done by the ballistic projectile, and in the second, 740 J. Assays and electron microscopic examination showed neural damage in both groups compared with the uninjured control group; the damage in the 740 J group was more severe and detected earlier after injury. Observed damage was localized to neurons in the hippocampus. In the 740 J group, damage extended to the hypothalamus as well.
Like ballistic pressure waves, blast waves also cause focal internal injuries, including mTBI , , , , , ,  and . These injuries are similar to remote injuries caused by ballistic pressure waves, and may be caused by similar mechanisms. For example, in pigs exposed to blast waves, lung and intestinal injuries were observed . Moreover, EEG suppression, accompanied by transient apnea, was observed immediately after the blast and gradually returned to normal with 1–2 min.”
Here’s their most intriguing speculation:
“Are observed cerebral effects vagally mediated?
Some have suggested that CNS effects due to blast or ballistic pressure waves might not be due to direct exposure of brain tissue to the pressure wave, but might instead be mediated by the vagus nerve ,  and . Experimental results indicate that a vagally-mediated response is present, but that if the pressure wave reaches the brain with sufficient magnitude, it will cause damage. In human-sized pigs, periods of apnea were observed in intact animals when about 700 J of work was done on tissue behind body armor. Test subjects on which bilateral vagotomy had been performed did not exhibit apnea. However, vagotomy mitigated but did not eliminate EEG suppression 1 min after the ballistic impact. Both experimental groups showed evidence of lung contusions due to behind armor trauma.
A limitation of this study is that EEG records are reported at 1-min intervals, while important information may be contained in data from the first minute. In the ballistic pressure wave experiments by Goransson et al.  as well as the blast pressure wave experiments by Axelsson et al. , EEG changes that may be important indicators of neural effects were observed to occur “immediately” after the blast and were no longer present after 1 or 2 min.
Irwin et al.  also observed that rats exposed to blast experienced bradycardia and hypotension – effects that were mitigated in a group on which bilateral vagotomy had been performed. Respiratory and EEG data were not reported. Both experimental groups sustained severe blast lung injury. Cernak et al. reported similar results in rabbits exposed to a focused blast wave applied to the middle thoracic region. Vagotomy reduced but did not eliminate damage directly to brain cells .”
The results of these animal studies of ballistic and blast wave exposure suggest that the vagus nerve does play a role in the CNS response to pressure waves. In particular, apnea and bradycardia after exposure seem to be vagally-mediated responses. The resulting hypoxia may exacerbate the consequences of neural cell damage. However, the results of these experiments also indicate that brain cells can be damaged directly after exposure to pressure waves originating or focused at a distant location.
A potential limitation of the Cernak et al. blast wave experiment on rabbits is the inability to truly restrict the blast wave to the thoracic region (due to refraction of the blast wave at the edge of the shock tube). One is not certain of the magnitude of the external pressure wave applied to the rabbit’s head in these experiments.
Notice they have picked up on some strong observations. They use specific terms like apnea (cessation of breathing-upper brain stem/medulla-vagal) and vagal mediated response (brain stem rotation-cerebrovortex), more terms like bradycardia (medulla-vagal) and hypotension (medulla-vagal) Do you see why I’m jumping off my chair reading this? They are describing our working hypothesis which is: heart-brain axis pivoting point decoupling. Which is what we will be starting to examine in 2012 with our little mice who will share some of their mTBI secrets as we mimic these kind of concussive effects. When they cut the vagal things change, they are ‘mitigated’. So the crossover is here blast mTBI injuries are into our sphere of explanation too. The vagal response is all starting to get very coherent for me. So cool!