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REMEMBER 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:
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.
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. |