Exp Brain Res (1998) 119:483±492  Springer-Verlag 1998 RESEARCH ARTICLE Helge Topka ´ Jürgen Konczak ´ Johannes Dichgans Coordination of multi-joint arm movements in cerebellar ataxia: Analysis of hand and angular kinematics Received: 28 October 1996 / Accepted: 30 September 1997 H. Topka ( ) ) ´ J. Konczak ´ J. Dichgans Department of Neurology, University of Tübingen, Hoppe-Seyler-Strasse 3, D-72076 Tübingen, Germany e-mail: topka@uni-tuebingen.de, Fax.: +49-7071-29-6507 Abstract Kinematic abnormalities of fast multijoint movements in cerebellar ataxia include abnormally in- creased curvature of hand trajectories and an increased hand path and are thought to originate from an impair- ment in generating appropriate levels of muscle torques to support normal coordination between shoulder and el- bow joints. Such a mechanism predicts that kinematic ab- normalities are pronounced when fast movements are per- formed and large muscular torques are required. Experi- mental evidence that systematically explores the effects of increasing movement velocities on movement kinemat- ics in cerebellar multijoint movements is limited and to some extent contradictory. We, therefore, investigated an- gular and hand kinematics of natural multijoint pointing movements in patients with cerebellar degenerative disor- ders and healthy controls. Subjects performed self-paced vertical pointing movements with their right arms at three different target velocities. Limb movements were record- ed in three-dimensional space using a two-camera infra- red tracking system. Differences between patients and healthy subjects were most prominent when the subjects performed fast movements. Peak hand acceleration and deceleration were similar to normals during slow and moderate velocity movements but were smaller for fast movements. While altering movement velocities had little or no effect on the length of the hand path and angular motion of elbow and shoulder joints in normal subjects, the patients exhibited overshooting motions (hypermetria) of the hand and at both joints as movement velocity in- creased. Hypermetria at one joint always accompanied hypermetria at the neighboring joint. Peak elbow angular deceleration was markedly delayed in patients compared with normals. Other temporal movement variables such as the relative timing of shoulder and elbow joint motion onsets were normal in patients. Kinematic abnormalities of multijoint arm movements in cerebellar ataxia include hypermetria at both the elbow and the shoulder joint and, as a consequence, irregular and enlarged paths of the hand, and they are marked with fast but not with slow movements. Our findings suggest that kinematic move- ment abnormalities that characterize cerebellar limb atax- ia are related to an impairment in scaling movement vari- ables such as joint acceleration and deceleration normally with movement speed. Most likely, increased hand paths and decomposition of movement during slow movements, as described earlier, result from compensatory mecha- nisms the patients may employ if maximum movement accuracy is required. Key words Cerebellar ataxia ´ Limb movement ´ Multijoint movement ´ Kinematics ´ Human Introduction Clinical signs of cerebellar limb ataxia include decreased resistance to passive manipulations, disordered voluntary movements with errors in trajectory, amplitude, and speed, and, frequently, action-induced static or kinetic tremor (Diener and Dichgans 1992; Diener et al. 1993; Gilman et al. 1981; Holmes 1917). Some basic cerebellar motor deficits such as the slowness and irregularity of movements have been identified in single-joint move- ments in both animal experiments (Flament and Hore 1986; Meyer-Lohmann et al. 1977) and human studies (Brown et al. 1990; Hallett and Massaquoi 1993; Hallett et al. 1975, 1991; Hore et al. 1991; Manto et al. 1995; Wild et al. 1996). Single-joint movements were shown to be dysmetric, most frequently overshooting the target. Other kinematic abnormalities included prolonged accel- eration times (Hallett and Massaquoi 1993), decreased peak joint acceleration and an increase in peak decelera- tion in relation to peak acceleration (Hore et al. 1991). Dysmetria of voluntary movements has been related to electromyographic (EMG) abnormalities such as a more gradual buildup and prolongation of agonist activity (Hal- lett et al. 1975; Hore et al. 1991) and a delayed onset of