Some aspects of the pathophysiology of spasticity and rigidity

Abstract

New discoveries in relution to the histology and electrophysiology of the muscle spindle show that the stretch reflexes are much more complex at the segmental level than was previously thought, and these must be taken into account in explaining various clinical hypertonias. Thus, the gamma‐1 fibers are believed particularly hyperactive in mild spasticity, while the gamma‐2 system may account for the large tonic stretch reflexes; in the “clasp‐knife” reactions sudden motoneuron inhibition occurs, while ordinarily, as stretch proceeds, more and more motoneurons are recruited. In some types of spasticity, alpha motoneuron hyperexcitability occurs and not the gamma, so that this type is resistant even to dorsal root section. Parkinsonian rigidity, characteristically mild and plastic, is relatively independent of the velocity of stretching, though the response of rigid muscles to fast stretch may be of the “cogwheel” type. Parkinsonian rigidity may be governed by gamma fibers and not maintained by the alpha system, which may account for the rapid and dramatic effect obtained with intramuscular procaine. Complex physiologic work on gamma systems of muscle spindles provides a working hypothesis to account for both spasticity and rigidity as well as for differential action of certain agents. Further work on the dual alpha and gamma systems is urgently needed, as is the development of methods for recording reflex action in man to quantitate spasticity and rigidity.