of this is why lesioning the globus pallidus seems to reduce hemiballistic movements. the mechanism behind the effect of dopamine on patients' symptoms remains unknown. history the work of j.r. whittier, f.a. mettler, and m.b. carpenter in the mid-1900s helped scientists and clinicians form a more complete picture of hemiballismus. in their experiments, several lesions were made in the basal ganglia structures in monkeys and then they monitored the results. they noticed that the majority of the time, the monkeys did not have any unusual movements. however, when at least twenty percent of the subthalamic nucleus was damaged, abnormal movements were seen in the limbs opposite to the side of the brain that was damaged. this observation caused scientists to believe that hemiballismus outside the subthalamic nucleus did not occur. it was not until much later that this classical model began to expand to include other areas of the basal ganglia and even some cortical structures. they also noticed that unlike human patients, the unusual movements in the monkeys were mainly in the lower extremities. in about half of the monkeys, the hemiballismus continued until the monkey died. other scientists have also worked on this perplexing disorder and have found that the symptoms can be induced by injecting kainic acid or ibotenic acid into the subthalamic nucleus. i. hamada and m.r. delong found that by using these chemicals, they could destroy only four percent of the subthalamic nucleus and still see hemiballistic movements. however, the abnormal movements would usually disappear within four to five hours even though it did not appear as though the damaged tissue had healed. this suggests that the subthalamic nucleus is plastic enough to adapt to small amounts of damage in order to resume normal function.