Impaired Reaching and Grasping After Focal Inactivation of Globus Pallidus Pars Interna in the Monkey

Abstract

The purpose of this study was to test the hypothesis that the basal ganglia output from globus pallidus pars interna (GPi) contributes to inhibition of competing motor patterns to prevent them from interfering with a volitional movement. To test this hypothesis, the kinematics of a natural reach, grasp, and retrieval task were measured in the monkey before and after focal inactivation in GPi with the GABAAagonist muscimol. Two rhesus monkeys were trained to reach in a parasagittal plane to grasp a 1-cm cube of apple and retrieve it. Reflective markers were applied to the shoulder, elbow, wrist, and index finger. Movements were videotaped at 60 fields/s, digitized, and analyzed off-line. In each session the monkey performed 12–15 reaches before and 12–15 reaches after injection of 0.5 μl of 8.8 mM muscimol. Muscimol was injected into 22 separate locations in the “arm” area of GPi. Inactivation of the GPi with muscimol produced movement deficits in a reach-grasp-retrieve task that can be summarized as follows: 1) decreased peak wrist velocity during the reach to target; 2) decreased elbow and shoulder angular velocities, with elbow angular velocity relatively more impaired than shoulder angular velocity; resulting in 3) higher maximum vertical wrist and index finger positions at the apex of the reach; 4) prolonged latency from the end of the reach to the completion of grasp; and 5) less impairment of retrieval than reach, with inactivation at the majority of sites causing no impairment and some actually speeding up retrieval despite slow reaching. The results of this study show that reaching movements are impaired in a specific way after focal inactivation of GPi in previously normal monkeys. The slowing of the reach with normal (or fast) retrieval suggests that there is difficulty inhibiting the posture holding mechanisms that were active before the reach, but that assist the retrieval. The nature of the impairment supports the hypothesis that GPi lesions disrupt the ability to inhibit competing motor mechanisms to prevent them from interfering with desired voluntary movement.