At the RIRC Lab

Okay, this is basic stuff but until I just saw it, I didn’t really get it.

There’s a post-doc showing us preserved specimens of a human brain and spinal cord, a rat brain and cord, and a mouse brain and cord.

  • The human brain is like a medium sized cantaloupe.
  • The rat brain is like a fattish raspberry.
  • The mouse brain is like a medium sized peanut.
  • The mouse cord is a bit of thin spaghetti, about an inch and a half long.
  • The rat cord is worm thickness, maybe twice as long as the mouse cord.
  • The human cord looks like a tangly fat mess of variably thick strands . . . the center is the cord itself, still surrounded in dura, and there are these things like flaps that hold the dorsal root ganglia.  It’s as long as my forearm.  You can see why they call the caudal equina that — it does look like a horse’s tail.

I’m kind of freaked out, for two reasons.  One is just the idea that this thing in front of me used to be somebody’s central nervous system.  The other is that this makes it real, how big the problems are that come with trying to ramp up from what works in mice to what works in us.   The guy is saying that size isn’t everything, because physiologically there’s so much that’s the same between these species.

Here are the names of the other stations we can visit here:

fMRI, electron microscope, 3-D imaging, Histology, and two-photon microscope . . . not much time left!

Talking with Robert Gramer at the fMRI station.  Only 34% of injuries are complete, and most research has been done on completes, and what they know is that only 40% of normal activation is there.  The brain recruits available capacity for other things.

So, what happens with incompletes?  Specifically, do ASIA Ds have changed patterns of activation?  Yes, they actually use even more brain activation in the usual areas when using their legs.  They did a study of ASIA C and Ds who could walk more than 10 meters with assistance, and looked at ASIA impairment scale and gait velocity.   They used fMRI, sent patients on their backs into the doughnut and showed them a cartoon of a foot moving to tell them when to move their foot, which was sticking out.  These were chronics, injured 2 years to more than 20 years.

What they saw on their screens was that people with incomplete injuries were activating big sections of their brains that the AB controls didn’t need . . . even using the right side of the brain to move the right foot, which isn’t the normal pattern.  The motor planning area was lit up too, because incompletes have to use it a lot more than AB people do; it takes concentration for incompletes to do what is automated in non-injured brains.  The activation patterns got stronger over time — meaning that the longer-term chronics were using more of their brains than the shorter term ones.

Then they showed that faster gait correlates with higher activation of the part of the brain that has to do with concentration and high cognitive functioning.

Why does this matter?  Because the old studies that were based on completes meant that eventual therapies would need to address both brain inactivity and cord inactivity . . . but this one means that in the case of incompletes, it will be a one-step event, because the brain is already functioning even better than normal when it comes to movement.

Here’s the interesting thing.  All this was meant as a pretest.  It was followed by having the same subjects visualize themselves doing motor tasks, 30 minutes a day, 3 days a week, for 8 weeks, listening to headphones giving them vivid imagery of themselves doing tasks (picking up something with their toes e.g.), and compared to those who didn’t do visualization, their brains were more activated.

And that’s your brain geekout for the day.  Time for lunch, and then almost everybody is leaving.

It’s been fun, and challenging, and hopeful.

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