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Bilateral chronic subthalamic nucleus (STN) stimulation is a new and useful surgical method to improve parkinsonian disability. The improvement involves all the major parkinsonian signs.1Recently, Krack et al 2 reported that chronic stimulation of the STN also improved levodopa induced dyskinesias, although they explained this effect mainly by a decrease in the levodopa dosage. We report on a patient who presented a marked improvement of levodopa induced dyskinesias without decreasing the daily dosage of levodopa.
A 68 year old man was diagnosed with Parkinson’s disease at the age of 38, and started levodopa at the age of 43, with good initial effect. At the age of 56 he developed a peak of dose choreiform dyskinesias in the trunk and limbs and 2 years later he also had motor fluctuations of the wearing off type. Since 1993, the patient had severe generalised choreiform dyskinesias that were present for about 75% of the diurnal time. Presurgery treatment included benserazide/levodopa (50/200 mg five times a day), plus selegiline (10 mg/day). The motor score of the unified Parkinson’s disease rating scale (UPDRS) in the off condition was 51, and in the on condition, 37. The dyskinesia score (six body parts, each scored 0–4, maximum score 24)1 in the on condition was 15. The patient was operated on bilaterally in the STN according to the method of Limousin et al 1 with slight modifications, using neurophysiological recording (figure). Antiparkinsonian therapy was initially maintained. Three months after surgery, the motor score of the UPDRS in the off condition was 48, and in the on condition 36, when the stimulation was off; and improved to 37 and 22, respectively, when the stimulation was switched on. The patient had mild dyskinesias in the lower limbs for no more than 10% of the diurnal time. The dyskinesia score was assessed during the maximum motor response to a single morning dose of 50/200 mg benserazide/levodopa. Ten hours before this levodopa test, the stimulation was switched off, and the patient kept off levodopa. The dyskinesia score was 15 when the stimulation was off, and lessened immediately to 2 when the stimulation was switched on.
Unilateral STN stimulation induces hemiballism in healthy monkeys3 and improves all parkinsonian symptoms,1 including levodopa induced dyskinesias, in patients with Parkinson’s disease.2 Although the improvement of levodopa induced dyskinesias has been attributed by Krack et al 2 to the decrease of levodopa dosage, our patient showed a marked improvement after surgery despite the fact that the levodopa dose could not be decreased after optimising the antiparkinsonian therapy. The improvement of levodopa induced dyskinesias in our patient occurred both during activities of daily living and after a levodopa acute test. To minimise a possible maintained effect of the subthalamic STN stimulation, which hypothetically could have changed the dyskinesia threshold, the patient was in off drug and off stimulation conditions 10 hours before the levodopa acute test. Levodopa elicited a severe peak of dose dyskinesias that were relieved immediately when the STN stimulation was switched on. These data suggest that the effect of STN stimulation is different in healthy monkeys3 compared with parkinsonian patients with levodopa induced dyskinesias, and suggest that the improvement of levodopa induced dyskinesias could be related directly to the effect of STN stimulation.
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