Spasticity and the Human Pyramidal Tracts

After a long and tortuous history spanning over a century of clinicoanatomical and experimental observations, the concept of spasticity has assumed its current form as a velocity-dependent increase of tone in a group of passively stretched muscles. However, several gaps have remained in the understanding of spasticity as a clinical and experimental phenomenon. A long-standing controversy concerns the critical neural pathways that must be damaged for the production of spasticity. Two general explanations have been offered as a way out of this conundrum. The clinicoanatomical tradition (human) contends that spasticity is one of the four cardinal symptoms of pyramidal tract damage, whereas the experimental school (experimental animals) regards spasticity as a symptom of injury of extrapyramidal pathways, particularly the reticulospinal tracts. This review provides evidence that both claims are valid for different animal species. Thus, while spasticity (or its experimental equivalent) is a symptom of extrapyramidal injury in all mammals, including nonhuman primates, in humans it is a legitimate symptom of pyramidal tract lesion or dysfunction.