Some pathophysiological aspects of spasticity and the search for rational and successful therapy.
In spite of the different uses of the term "spasticity", hyperactivity of skeletal muscle stretch reflexes is the one common factor and we therefore need to know how this is produced by lesions within the central nervous system and what are its consequences to the initiation and execution of voluntary movement, not only initially but also chronically. The alpha motoneurone is directly responsible for the initiation of skeletal muscle contraction and final integration of excitatory and inhibitory nervous input normally takes place on its surface. In spasticity there is not only loss of descending direct excitatory and inhibitory control of motoneurones, but also loss of the control of spinal interneurones which would normally regulate (principally by inhibition) segmental spinal reflexes, including the stretch reflexes, especially those concerned with antigravity muscles. Gamma motoneurones may also have a reduction inhibitory control with consequent increase of muscle spindle sensitivity to stretch, and this may be further exaggerated by changes in the physical properties of affected muscles. The peripheral disorders of function are more accessible to study and to pharmacological and physical treatment, but with the increasing knowledge of inhibitory mechanisms and their pharmacology there is hope that some degree of influence may be possible within the central nervous system, by therapy with drugs that mimic or prolong the action of inhibitory transmitters.
D000818:Animals; D006801:Humans; D009046:Motor Neurons / Q000503:physiopathology; D009047:Motor Neurons, Gamma / Q000503:physiopathology; D009128:Muscle Spasticity / Q000503:physiopathology*; D009470:Muscle Spindles / Q000503:physiopathology; D012026:Reflex, Stretch; D014732:Vibration