We analyzed the features of neuronal activities, (a) firing rate, (b) firing pattern, and (c) response to passive joint movement, recorded from the globus pallidus internus (GPi) of patients with dystonia (DT) and Parkinson’s disease (PD). The spontaneous firing rate of GPi neurons in DT tended to be lower than that in PD. The reduced GPi activity resulted in disinhibition of thalamocortical pathways, which could cause DT as a form of hyperkinesia. However, identifying this reduced GPi activity is inconsistent with alleviation of DT in patients with pallidotomy. The pathology of DT, thus, cannot be explained solely by the reduced GPi activity. Quantitative examination of pauses and bursts from interspike intervals showed that pauses and bursts were significantly higher in DT than in PD. These abnormal firing patterns are conjectured to disrupt signaling along cerebello-thalamocortical pathways, impairing motor control and resulting in DT. Thus, abnormal firing patterns may represent temporal dysfunction. Changes in the GPi included enlargement of the receptive fields and an increased number of neurons exhibiting inhibitory reactions. DT symptoms may arise because of dysfunction of the mechanism inhibiting unrequired movements. The abnormal changes in the neurons in DT may underlie spatiotemporal dysfunction.