The purpose of this review is to provide a comprehensive approach for assessing the upper extremity (UE) after stroke. First, common upper extremity impairments and how to assess them are briefly discussed. While multiple UE impairments are typically present after stroke, the severity of one impairment, paresis, is the primary determinant of UE functional loss. Second, UE function is operationally defined and a number of clinical measures are discussed. It is important to consider how impairment and loss of function affect UE activity outside of the clinical environment. Thus, this review also identifies accelerometry as an objective method for assessing UE activity in daily life. Finally, the role that each of these levels of assessment should play in clinical decision making is discussed in order to optimize the provision of stroke rehabilitation services.

Recent reports of functional impairment in the 'unaffected' limb of stroke patients have suggested that these deficits vary with the side of lesion. This not only supports the idea that the ipsilateral hemisphere contributes to arm movements, but also implies that such contributions are lateralized. We have previously suggested that the left and right hemispheres are specialized for controlling different features of movement. In reaching movements, the non-dominant arm appears better adapted for achieving accurate final positions and the dominant arm for specifying initial trajectory features, such as movement direction and peak acceleration. The purpose of this study was to determine whether different features of control could characterize ipsilesional motor deficits following stroke. Healthy control subjects and patients with either left- or right-hemisphere damage performed targeted single-joint elbow movements of different amplitudes in their ipsilateral hemispace. We predicted that left-hemisphere damage would produce deficits in specification of initial trajectory features, while right-hemisphere damage would produce deficits in final position accuracy. Consistent with our predictions, patients with left, but not right, hemisphere damage showed reduced modulation of acceleration amplitude. However, patients with right, but not left, hemisphere damage showed significantly larger errors in final position, which corresponded to reduced modulation of acceleration duration. Neither patient group differed from controls in terms of movement speed. Instead, the mechanisms by which speed was specified, through modulation of acceleration amplitude and modulation of acceleration duration, appeared to be differentially affected by left- and right-hemisphere damage. These findings support the idea that each hemisphere contributes differentially to the control of initial trajectory and final position, and that ipsilesional deficits following stroke reflect this lateralization in control.

Previous studies have demonstrated that following unilateral stroke, motor impairment occurs both contralateral, as well as ipsilateral, to the lesion. Although ipsilesional impairments can be functionally limiting, they can also provide important insight into the role of the ipsilateral hemisphere in controlling movement and the lateralization of specific motor control mechanisms, given that unilateral arm movements are thought to recruit processes in each hemisphere. The purpose of this study was to examine whether left and right hemisphere damage following stroke produces different ipsilesional deficits, and whether our dynamic dominance model of motor lateralization can predict such deficits. Specifically, the dynamic dominance model attributes control of multijoint dynamics to the left hemisphere, and control of steady-state position to the right hemisphere. Chronic stroke patients with either left or right hemisphere damage (LHD or RHD) used their ipsilesional arm, and the control subjects used either their left or right arm (LHC or RHC), to perform targeted reaching movements in different directions within the workspace ipsilateral to their reaching arm. We found that the LHD group showed deficits in controlling the arm's trajectory due to impaired multijoint coordination, but no deficits in achieving accurate final positions. In contrast, the RHD group showed deficits in final position accuracy but not in the ability to coordinate multiple joints during movement, thereby providing additional evidence for the hemisphere-specific nature of motor deficits. Furthermore, while both the LHD and RHD groups were functionally impaired to the same degree on the Jebsen Hand Function Test (JHFT), our results suggest that the underlying mechanisms for such impairment may be hemisphere-dependent.

The current study was designed to examine potential interlimb asymmetries in controlling movement extent. Subjects made repetitive single-joint elbow extension movements while the arm was supported on a horizontal, frictionless, air-jet system. Four targets of 10, 20, 35, and 45°e xcursions were randomly presented over the course of 150 trials. For both arms, peak tangential hand velocity scaled linearly with movement distance. There was no significant difference between either peak velocities or movement accuracies for the two arms. However, the mechanisms responsible for achieving these velocities and extents were quite distinct for each arm. For the dominant arm, peak tangential finger acceleration varied systematically with movement distance. In contrast, nondominant-arm peak tangential acceleration varied little across targets and, as such, was a poor predictor of movement distance. Instead the velocities of the nondominant arm were determined primarily by variation in the duration of the initial acceleration impulse, which corresponds to the time of peak velocity. These different strategies reflect previously identified mechanisms in controlling movement distance: pulse-height control and pulse-width control. The former is characterized by a variation in peak acceleration and has been associated with preplanning mechanisms. The latter occurs after peak acceleration and has been shown to depend on peripheral sensory feedback. Our findings indicate that the dominant-arm system controls movement extent largely through planning mechanisms that specify pulse-height control, whereas the nondominant system does so largely through feedback mediated pulse-width control.