Direct effect of subthalamic nucleus stimulation on levodopa-induced peak-dose dyskinesia in patients with Parkinson's disease.
We examined the direct effect of deep brain stimulation of the subthalamic nucleus (STN-DBS) on levodopa-induced peak-dose dyskinesia in 45 patients with Parkinson's disease (PD) without reducing the levodopa dosage during the early period after surgery. In 8 patients (18%), the dyskinesia was quickly attenuated by bipolar stimulation in an experimental trial (5 min) with the contacts placed within the area above the STN. In contrast, bipolar stimulation using contacts placed within the STN itself tended to provoke or exacerbate the dyskinesia, indicating that dyskinesia could be inhibited by stimulation of the areas above the STN rather than the STN itself. In an attempt to control the cardinal symptoms of PD and dyskinesia at the same time, we employed bipolar stimulation with a longer interpolar distance as a therapeutic procedure (2 weeks), using contacts within the STN as a cathode and contacts within the area above the STN as an anode. Bilateral STN-DBS significantly attenuated the dyskinesia as evaluated by the dyskinesia severity rating scale (p < 0.05). In 24 patients (53%), almost complete control of the dyskinesia was observed. The contacts used as an anode in these patients were located more dorsally compared to those of the remaining patients, suggesting again that the dyskinesia was inhibited by stimulation of the areas above the STN rather than the STN itself. In the area above the STN, pallidothalamic, pallidosubthalamic and subthalamopallidal fibers are densely distributed. It appears that stimulation of these fibers may cause effects similar to thalamic or pallidal DBS and therefore inhibit peak-dose dyskinesia. Bipolar STN-DBS with contacts placed within the area above the STN as an anode appears to represent a useful option for controlling both the cardinal symptoms of PD and peak-dose dyskinesia at the same time.
Katayama
Yoichi
Y
Department of Neurological Surgery and Division of Applied System Neuroscience, Nihon University School of Medicine, Tokyo, Japan. ykatayam@med.nihon-u.ac.jp
Oshima
Hideki
H
Kano
Toshikazu
T
Kobayashi
Kazutaka
K
Fukaya
Chikashi
C
Yamamoto
Takamitsu
T
D000978:Antiparkinson Agents / Q000008:administration & dosage / Q000009:adverse effects*; D046690:Deep Brain Stimulation / Q000379:methods*; D004409:Dyskinesia, Drug-Induced / Q000628:therapy*; D006801:Humans; D007980:Levodopa / Q000008:administration & dosage / Q000009:adverse effects*; D010300:Parkinson Disease / Q000188:drug therapy* / Q000503:physiopathology; D012720:Severity of Illness Index; D020531:Subthalamic Nucleus / Q000503:physiopathology*; D016896:Treatment Outcome
D000978:Antiparkinson Agents; D007980:Levodopa