Clonus after human spinal cord injury cannot be attributed solely to recurrent muscle-tendon stretch.

Clonus, presented behaviorally as rhythmic distal joint oscillation, is a common pathology that occurs secondary to spinal cord injury (SCI) and other neurological disabilities. There are two predominant theories as to the underlying mechanism of clonus. The prevailing one is that clonus results from recurrent activation of stretch reflexes. An alternative hypothesis is that clonus results from the action of a central oscillator. We present evidence that the mechanism underlying clonus in individuals with SCI is not solely related to muscle stretch. We studied electromyography (EMG) of the soleus (SOL), medial gastrocnemius (MG), tibialis anterior (TA), medial and lateral hamstrings, vastus medialis, vastus lateralis, and rectus femoris from subjects with clinically complete and clinically incomplete SCI during stretch-induced ankle clonus, stepping, and non-weight-bearing standing. Clonic EMG of the SOL, MG, and TA occurred synchronously and were not consistently related to muscle-tendon stretch in any of the conditions studied. Further, EMG activity during stretch-induced ankle clonus, stepping, and non-weight-bearing standing had similar burst frequency, burst duration, silent period duration, and coactivation among muscles, indicating that clonic EMG patterns occurred over a wide range of kinematic and kinetic conditions, and thus proprioceptive inputs. These results suggest that the repetitive clonic bursts could not be attributable solely to immediate afferent feedback such as recurrent muscle stretch. However, these results support the theory that the interaction of central mechanisms and peripheral events may be responsible for clonus.