Point
3
Intro
Clinicians will rarely talk about the
deficits resulting from a lesion of the DSCT. Lesions in the
spinal cord usually damage other tracts that camouflage such
deficits. (One of these pathways lies right next to the DSCT
and we will talk about it next!). But if we think about the
information this tract is carrying we can see that such a
lesion would result in a loss of information regarding the
constant and changing lengths of muscle and tension on
muscles. This information is going to the cerebellum and we
are not really aware of it as we fish, ice skate, shoot
buckets, bike through the arboretum, or start our backswing
at the Ridge. This information tells the cerebellum about
how long each muscle is, how fast each muscle is moving and
how much tension is on each muscle. (#2 above) The
cerebellum then can compare this ascending
information regarding what the muscles are doing with
other information (the sources of which we will learn later)
regarding what higher motor centers want the muscles to do.
(#1 above) Then a correction can occur via pathways
that leave the cerebellum to influence motor performance
(#3 above). Whew!!
For our problem solving, let's equate a lesion of the DSCT with loss of unconscious proprioception and incoordination or ataxia. This incoordination deficit will be IPSILATERAL to the lesion because there is no crossing of information in the spinal cord. The DSCT is IPSI to the receptors. Also, the cerebellum influences (via several output pathways) the same or ipsilateral side of the body. Think about the dorsal column system. Is there crossing from the receptors to the fasc. gracilis and fasc. cuneatus in the spinal cord?? How about the pain and temperature pathways?