Point
4
Intro
REMEMBER MUSCLE SPINDLES ??
You have already
mastered most of the information illustrated in the diagram
to the right. The only addition is the presence of cortical
input to the gamma efferents. These efferents enable the
central nervous system to control the sensitivity of the
muscle spindles.
In addition to loss of the excitatory drive to the spinal neurons innervating muscle, and the resulting muscle weakness, interruption of LCST fibers also results in a loss of inhibitory input to the gamma motor neurons. The loss of inhibitory drive to these gamma efferents results in the following:
First, let's consider the chain fibers of
the muscle spindles.
- gamma efferents to the chain fibers increase their firing due to the loss of inhibition from the descending LCST.
- this increase in gamma efferent firing results in contraction of the ends of the chain fiber (detector of length).
- this shortening of the ends of the chain fiber results in an increase in the firing of the 1a and II fibers. The increase in action potentials over these fibers will in turn increase the firing of the ventral horn cells, which will in turn shorten the muscle fiber to a new length. Consider the biceps muscle in the arm (antigravity muscle). At this new shorter length, the muscle has increased tone (the muscle is more taut because the muscle fibers are firing more and resisting the pull of gravity).
The loss of descending inhibition from the gamma efferents that innervate the bag fibers results in shortening of the bag fiber. However, there is no increase in firing in the 1a when the muscle is at rest. I like to think of the situation as a "storing up" of action potentials until there is a sudden stretch. When there is lengthening of the muscle (stretch), there is a real barrage of 1a firing and an overzealous contraction. The physician evaluates muscle tone by (for example) extending the flexed arm of a hemiplegic. The increase (compared to normal) of muscle tone present in the biceps is referred to as "spasticity". This tone increase is rate dependent (more resistance the faster you try to stretch the muscle) and predominates in the flexors of the upper and the extensors of the lower limbs.
The physician evaluates muscle stretch reflexes, on the other hand, by tapping on a tendon. Following UMN lesions such reflexes are usually increased. The 1a barrage results in an overzealous response. However, keep in mind that this increase in muscle stretch reflex elicited by tapping a tendon is not considered to be a component of spasticity.
SPASTICITY is a very important term
in clinical neurology and refers to increased muscle tone
present when moving a limb. In addition LCST lesions
result in CLONUS. For example if the physician
suddenly flexes the foot at the ankle and holds it flexed,
there will be spasmodic alternation of contraction and
relaxation. Spasticity occurs primarily in the flexor
muscles in the upper extremity (biceps for instance) and
extensor muscles in the lower extremity (quadriceps). These
are antigravity muscles and appear to receive more LCST
input than their antagonists. There are other clinical
ramifications of losing the LCST control over the spinal
cord that you will learn from the clinicians. One I will
emphasize is the BABINSKI sign.
Stroking the ventral (plantar) surface of the lateral portion of the foot in a normal person results in the big toe going down (the plantar response is flexor). With lesions of the corticospinal or lateral corticospinal tract the big toe goes up when stroking the ventral surface of the foot (plantar response is extensor). This is called a Babinski sign.