Interesting article, but there’s some things in it that are decidedly wrong, and others that are completely ridiculous. The idea that increasing intracranial pressure through trapped blood accumulation could somehow “cushion” the brain and reduce the impact force of the brain as it “sloshes” in side the skull was obviously dreamed up by someone that has no grounding in biomechanics whatsoever. First, many head “mild” injuries (the ones that don’t involve skull fracture or haematoma) occur because of rotation of the head, not linear impacts, and suppressing brain motion relative to the skull won’t do a thing to help that. Secondly, CSF is essentially water from a physical response standpoint–and if you have an object floating in water, increasing the pressure in the water doesn’t do a single thing cushion the object floating in it.
The other major issue that I can see is, based on the doctors and biologists I’ve talked to, the accumulation of tau protein associated with CTE can take a minimum of many months, and more generally several years, to occur after the head traumas that triggered it. Also, apparently once you hit a critical threshold level of tau buildup, it becomes self propagating, even if you don’t have any additional head trauma. So monitoring the increase in tau protein wouldn’t be a good way to decide when to hang up the cleats…you could quit when you were still at a “healthy” level, it could take a couple of years to accumulate more, hit the threshold, and you could still end up with early onset of dementia or other lasting brain injury.
The article also touches briefly on, but glosses over, an alternative diagnosis technique that does show promise…diffusion tensor imagine MRI. Although poorly understood, there’s some really promising research about using it to track the biomechanical insults that could lead to long term tau protein buildup.
This entire article sounds like the author took the researchers’ grant proposal and translated it into laymen terms. It also reads like a press release for UCLA’s patent-protected tau PET marker. I especially love how the author uses a PET image for Down syndrome as a substitute for how the missing tau results would look like.
Any device that constantly presses on the jugular vein is going to create more problems than it solves. Constant pressure/weak trauma leads to bruising, inflammatory responses, and ultimately thrombi, increasing the risk of pulmonary embolism. If the device extends to pressuring the carotid (which could easily happen when it’s constantly being jostled around), stroke is possible. In addition, the body self-regulates intercranial pressure. It’s likely that long term use of the device would decrease the amount of CSF produced by the choiroid, defeating the purpose of the device.
You are right, tau buildup is typically a chronic process that usually takes years to develop. While this might be useful in early retirement as a guide to early treatment, an annual/biannual test while playing isn’t likely to be very useful. The section covering clinical and neuropsych testing seems more promising as a early assessment for CTE risk.
My own expertise is in MRI, and I can tell you that the amount tau buildup required to see significant DTI-related changes is substantial and unlikely to be very useful for early diagnosis (or at least, not as sensitive/specific as tau-specific PET studies). In addition, the article talks about looking at changes in specific structures (the ones typically associated with AD/dementia patients). As a radiologist, I can tell you that those structure-specific size changes inform, but do not diagnose the disease. Brain scanning is typically performed to rule out other possibilities, but AD itself is primarily a clinical diagnosis. I’ve read many of those studies, and results are typically reported as something like “Overall, there was a 10% reduction in volume of the hippocampus over the 75 patients that were studied.” The specificity of that kind of finding on an individual patient basis is unreliable at best.
I don’t mean to sound so negative about the prospects in the article, but there’s a reason this stuff is so hard. The brain is the most complicated and hardest to measure organ in the body. Macroscopic scans just don’t do it justice, and microscopic tests are too invasive. We’ve got a long way to go. My own bias is that MRI-related improvements in technology will allow us to get to the microscopic/physiological level noninvasively before these other avenues pan out, but the more attention to the issue the better.
I’m a little confused here. Setting aside the implausibility of his suggested method of controlling brain movement relative to the skull, why wouldn’t that help? I was under the impression that the reason rotational movements were so bad is because the existing “cushioning” was bad at suppressing those movements, and so rotational movements tended to cause the brain to impact the skull. Is there something inherent in sudden rotation of the brain that causes damage even in the absence of contact?
by MJK :: Sat, 06/23/2012 – 6:59pm
Short answer: yes.
Brain tissue is “nearly incompressible” because it’s filled with fluid. It has a consistency kind of like pudding. That means that it is very resistant to pressure-induced changes in volume, and very succeptible to shear-induced changes in shape. When you subject a brain to pure linear motion, absent contact (and despite what you year, it takes a *lot* of linear motion to cause the brain to collide with the skull…the cushioning in the head is actually pretty good. Remember, we evolved from monkeys who were falling out of trees!), all you get in the tissue is a buildup of pressure–which causes very little actual deformation of the brain. While pressure can cause injury, you have to have either a lot of it, it has to last a long time, or you have to have negative pressure (“suction”), to injury things.
But when you rotate the brain, that creates shear loads in the tissues, which causes shear deformation of the tissue. Shear is believed to be far more damaging because a little bit of shear load causes a lot of shear deformation, which in turn can tear or damage the cells.
For a reasonabl analogy, imagine filling a bowl with pudding, right up to the brim, and put some stripes of food coloring or another kind of pudding across the top so you can see what’s going on. Put plastic wrap over it to keep it from sloshing. That’s your brain in the skull. Now slide the bowl back and forth–not much will happen. Then spin the bowl. The pudding inside will get all mixed up.