Treatment of advanced Parkinson's disease by unilateral posterior GPi pallidotomy: 4-year results of a pilot study

Abstract

To assess the long‐term outcome following unilateral pallidotomy for advanced Parkinson's disease, we performed nonblinded Core Assessment Program for Intracerebral Transplantations protocol assessments in 10 of the original 15 patients in our pilot study for 4 years following surgery. Although Unified Parkinson's Disease Rating Scale motor examination scores returned to baseline levels at 3 and 4 years, most patients continued to show sustained improvements in contralateral tremor, akinesia, and drug‐induced dyskinesias. Contralateral tremor was absent at 4 years in all seven patients with preoperative tremor. Contralateral “off” arm movement times (averaged for three tasks) decreased by 37% at 1 year and by 30% at 4 years. Contralateral dyskinesia scores improved by 82% at 1 year and by 64% at 4 years. In contrast, after reaching speeds equal to the contralateral side at 1 year, ipsilateral “off” movement times increased by 13% over baseline levels at 4 years. Although most gait and postural stability measures showed modest initial improvement followed by a return to baseline values, “on” stand–walk–sit task performance declined significantly at 4 years. Despite the restriction of our surgeries to one side and the expected natural progression of Parkinson's disease, the results of patient self‐assessments suggest that 4 years after unilateral pallidotomy, most patients continue to experience a quality of life above preoperative levels.

Four year follow-up study after unilateral pallidotomy in advanced Parkinson's disease

“…These results are in accordance with two other reports on the long-term effects of UPVP. In the study by Baron et al, improvement in contralateral tremor, akinesia and drug-induced dyskinesias was present four years after surgery in a group of 10 out of the 15 initial patients [3]. Fine et al showed sustained effects on contralateral parkinsonian signs and dyskinesias in 17 patients evaluated at two-year follow-up, with some patients also being assessed at a longer follow-up period up to 64 months [8].…”

“…Some authors have presented their results at longer follow-up periods of two [14,16] and three years [24] but there are only three studies [3,7,8], involving only small numbers of pas Abstract Background Pallidotomy is widely accepted as a treatment for patients with Parkinson's disease (PD) who have disabling symptoms that are inadequately controlled with pharmacotherapy. There are, however, only a few studies, with a small number of patients, showing evidence after prolonged periods of time about the clinical outcome after pallidotomy.…”

Neuropsychiatric aspects of Parkinson’s disease: Recent advances

“…Several studies report reductions in anxiety and depression after pallidotomy that are unrelated to the improved motor function [76,78,136,137]. Short-(6 month) and long-term (4 years) follow-up in a carefully evaluated series suggested that pallidotomy has no consistent effects on depression or anxiety, but that a history of a previous or active affective disturbance at the time of surgery may be most closely associated with subsequent development of a mood disorder [12,138].…”

Effects of Transient Focal Inactivation of the Basal Ganglia in Parkinsonian Primates

“…Increased and abnormally patterned output in motor-related circuits of the basal ganglia to the thalamus may in part be responsible for the motor disturbances in Parkinson's disease (PD) (Albin et al, 1989;Bergman et al, 1990;DeLong, 1990;Wichmann and DeLong, 1996). Based on this premise and from previous experiences with pallidal ablative surgeries in patients with PD (Talairach et al, 1950;Guiot and Brion, 1953;Riechert and Wolff, 1953;Narabayashi and Okuma, 1954;Cooper and Bravo, 1958;Svennilson et al, 1960), the last decade has seen major advances in ablative and chronic stimulation techniques aimed at reducing basal ganglia output through interruption of neuronal activity in the internal pallidum (GPi) or the subthalamic nucleus (STN) (Laitinen et al, 1992;Benabid et al, 1994;Lozano et al, 1995;Krack et al, 1998;Baron et al, 1996Baron et al, , 2000Alvarez et al, 1999Alvarez et al, , 2000Fine et al 2000). Although the mechanisms by which electrical stimulation works in parkinsonian patients remain uncertain, the similarities between the effects of chronic stimulation and ablative lesions suggest that electrical stimulation may also serve to functionally inhibit the targeted nuclei.…”