In these
studies, I examine the neurophysiologic properties of the spinal cord, both
caudal to (i.e. ‘below’) and rostral to (i.e. ‘above’) the injury locus. As shown here and here, a combination of stimulus-evoked
and mechanical reflexes have proven to be extremely accurate in predicting
whether or not a person with acute SCI that is neurologically-complete (i.e. unable to make voluntary
movements below the injury) will remain so, or will instead recover voluntary muscle contractions below the injury. This information has important implications regarding
rehabilitation, allocation of resources (e.g. structural modifications of the
home), and interpretation of novel treatment strategies.
More
recently, I’ve been studying changes in the autonomic nervous system, which is
responsible for control of blood pressure, heart-rate, bowel & bladder
function, and a host of other ‘involuntary’ actions in the body.
Another emphasis
has been on abnormal motor patterns (either spontaneous or evoked) that are
best explained by new growth and connections between nerve cells below the
injury (i.e. plasticity). Examples
include interlimb reflexes, and a central pattern generator (CPG) capable of producing stepping
movements in humans with limited (or no) input from supraspinal regions. A practical consequence of this finding
is that if you have a spinal cord injury and experience some form of
slow-motion and stepping-like rhythmic contractions in muscles of your legs or
abdomen – not the rapid contractions of clonus or spasticity – there’s a strong
chance you’ve got some situation sending pain signals to your spinal cord and
causing these movements, as reported in my most recent paper on this subject.
Finally, the cauda equina is the bundle of nerve roots found at the base
of the spinal cord, before they exit from more caudal levels. Roughly 15% of all human spinal cord
injuries involve the cauda equina, yet there is almost no research being done
in this country on this problem.
In theory, it should be easier to treat this injury, since the damaged
nerves are more like peripheral nerves (which we know can regenerate). Our lab has developed and characterized an animal model of cauda equina injury, with the eventual goal of translating
our repair strategy to humans with cauda equina injury. Two recent papers can be seen here and here.
