The effect of pallidotomy on movement in severe Parkinson's Disease.

Abstract

The effects of ablative and non-ablative pallidal surgery in Parkinson’s disease (PD) have been the subject of interest for many years. The techniques used have undergone dramatic change over this time. This study examines the effects of pallidal lesions on the clinical signs and the physiology of motor control in PD. A method for the kinematic analysis of rapid repetitive finger tapping (an “internally generated” movement) and a two stage sequential arm movement made in response to an auditory stimulus (an “externally generated” movement) was devised and validated in control subjects and in patients with PD. Consecutive patients undergoing pallidotomy for severe PD were studied pre-operatively and at 2-4 weeks, 3 months and 6 months post-operatively. In addition to kinematic assessments, clinical assessments of movement were performed using standardised rating scales. The spontaneous blink rate was measured pre- and post-operatively. In some patients, Bereitschaftspotentials (pre-movement cortical potentials) were recorded pre- and post-operatively, as patients performed a self-paced voluntary arm movement. The location of the pallidotomy lesions was established from post-operative CT head scans. The most dramatic clinical effect of pallidotomy was on drug-induced dyskinesias. Significant clinical improvements were also seen in limb bradykinesia, particularly on the side contralateral to the lesion. Kinematic analysis showed no improvement in rapid finger tapping after pallidotomy. Nor was there any improvement in the spontaneous blink rate or in the early component of the Bereitschaftspotential. However, both the speed and inter-onset latency of the two stage sequential arm movement improved post-operatively. It is concluded that the improvement in bradykinesia after pallidotomy is not due to an improvement in function of pallido-thalamo-mesial frontal circuits, which are particularly involved in the performance of internally generated movements. Rather, the abolition of pallidal activity by pallidotomy may allow more laterally placed motor circuits greater use of sensory cues to facilitate movement. Lesions almost always involved the posteroventral portion of the medial segment of the internal pallidum, the conventional site for pallidotomy in PD. However, many lesions also involved the ansa lenticularis, the lateral segment of the internal pallidum and the external pallidum. The potential relevance of these observations on an understanding of the pathogenesis of bradykinesia and dyskinesia in PD is discussed.