Competing models of the basis of limb apraxia were tested through analysis of joint coordination deficits in three apraxic subjects with lesions that included the left parietal lobe. Three-dimensional shoulder, elbow, wrist and hand trajectories were recorded for repetitive 'slicing' gestures made in a series of conditions in which contextual cues were introduced in a graded fashion. The apraxic subjects showed marked deficits in joint coordination across context conditions. Even when actually manipulating a tool and object, the apraxic subjects failed to show proper joint synchronization, failed to apportion their relative joint amplitudes properly, and failed to produce the correct phase relationships among pairs of arm angles. Thus, apraxic subjects not only have deficits in the spatial plan for the movement, but they also have deficits in translating those plans into the details of the angular motions at the joints, even when actually manipulating a tool and object. These data support a model of apraxia in which apraxia can result from either the destruction of visuo-kinaesthetic motor representations of learned movement, stored in posterior association cortex, or from a separation of these representations from premotor or motor areas.