Abstract
Objective: This study aimed to evaluate the direct anti-dyskinesia effect of deep brain stimulation (DBS) of subthalamic nucleus (STN) on levodopa-induced on-dyskinesia in Parkinson's disease (PD) patients during the early period after surgery without reducing the levodopa dosage.Methods: We retrospectively reviewed PD patients who underwent STN-DBS from January 2017 to October 2019 and enrolled patients with levodopa-induced on-dyskinesia before surgery and without a history of thalamotomy or pallidotomy. The Unified Dyskinesia Rating Scale (UDysRS) parts I+III+IV and the Unified Parkinson's Disease Rating Scale part III (UPDRS-III) were monitored prior to surgery, and at the 3-month follow-up, the location of active contacts was calculated by postoperative CT–MRI image fusion to identify stimulation sites with good anti-dyskinesia effect.Results: There were 41 patients enrolled. The postoperative levodopa equivalent daily dose (LEDD) (823.1 ± 201.5 mg/day) was not significantly changed from baseline (844.6 ± 266.1 mg/day, P = 0.348), while the UDysRS on-dyskinesia subscores significantly decreased from 24 (10–58) to 0 (0–18) [median (range)] after STN stimulation (P < 0.0001). The levodopa-induced on-dyskinesia recurred in stimulation-off/medication-on state in all the 41 patients and disappeared in 39 patients when DBS stimulation was switched on at 3 months of follow-up. The active contacts which correspond to good effect for dyskinesia were located above the STN, and the mean coordinate was 13.05 ± 1.24 mm lateral, −0.13 ± 1.16 mm posterior, and 0.72 ± 0.78 mm superior to the midcommissural point.Conclusions: High-frequency electrical stimulation of the area above the STN can directly suppress levodopa-induced on-dyskinesia.
Highlights
Dyskinesia is one of the most troublesome symptoms of advanced Parkinson’s disease (PD), often induced by long-term dopaminergic treatment
The Deep brain stimulation (DBS) strategies could be different for on-dyskinesia and off-dystonia: stimulating the sensorimotor region could significantly improve cardinal parkinsonian symptoms [16] and significantly improve off-dystonia [6, 17], while stimulating subthalamic nucleus (STN) itself could not suppress on-dyskinesia [11] and even induce dyskinesia [18,19,20]; this study only focuses on levodopa-induced on-dyskinesia
The Unified Dyskinesia Rating Scale (UDysRS) on-dyskinesia subscores significantly reduced after STN-DBS stimulation [from baseline 24 [10–58] to 0 (0–18), median, P < 0.0001; Figure 1B); 36/41 (87.8%) patients scored 0 on Unified Parkinson’s Disease Rating Scale (UPDRS)-IV item 32, and only 5 patients (P27, P28, P30, P38, P40) continued to experience persistent dyskinesia, and their dyskinesia was observed in four experimental conditions with stimulation and medication on and off subdivided into the following (Table 1): 1 patient (P27) presented with stimulation-induced dyskinesia (SID), 2 patients (P28, P30) presented with unilateral levodopainduced on-dyskinesia, and the remaining 2 patients (P38, P40) experienced abnormal involuntary movements after DBS surgery despite medication withdrawal and cessation of DBS stimulation, which may be induced by a microlesion in the STN due to surgery [21]
Summary
Dyskinesia is one of the most troublesome symptoms of advanced Parkinson’s disease (PD), often induced by long-term dopaminergic treatment (levodopa-induced dyskinesia, LID). Deep brain stimulation (DBS) of subthalamic nucleus (STN) could reduce the required levodopa dosage for symptom control [3, 4], and the majority of researchers opine that the antidyskinesia effect of STN stimulation is mainly due to the significant postoperative reduction of levodopa medication [5,6,7,8], which is an indirect inhibition. Kim et al found that LID was reduced following STN-DBS in PD regardless of whether the levodopa dosage was reduced [9], and by developing a multiple regression model to predict postoperative dyskinesia scores, Mossner et al found that STN-DBS improved dyskinesia beyond levodopa reduction [10]. We switch on the stimulation within 3 days after DBS implantation without levodopa dosage reduction till the first follow-up at 3 months postoperatively, which provides an opportunity to evaluate the direct anti-dyskinesia effect of STN-DBS
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