✓Beginning-of-dose motor deterioration (BDMD) is a complication of levodopa medications in Parkinson disease (PD) that is presumably caused by inhibitory effects of levodopa. Only limited experience of BDMD has been described in the literature. The authors report the case of a patient with PD who demonstrated a marked BDMD while being treated with standard levodopa medications. This 55-year-old woman had a 12-year history of PD and a 10-year history of levodopa treatment. Marked exacerbation of symptoms occurred 15 to 20 minutes after every dose of levodopa at 100 mg and lasted approximately 15 minutes. The PD symptoms, particularly tremor and rigidity, were exacerbated more markedly during this period than during the wearing-off deterioration. The BDMD could be controlled very well by subthalamic nucleus (STN) stimulation without any change in the regimen of levodopa medications. These observations suggest that the BDMD was inhibited by STN stimulation through a direct effect.
Hideki Oshima, Yoichi Katayama, Chikashi Fukaya, Toshikazu Kano, Kazutaka Kobayashi, Takamitsu Yamamoto and Yutaka Suzuki
Hideki Oshima, Yoichi Katayama, Takashi Morishita, Koichiro Sumi, Toshiharu Otaka, Kazutaka Kobayashi, Yutaka Suzuki, Chikashi Fukaya and Takamitsu Yamamoto
The objective of this study was to evaluate the efficacy of chronic subthalamic nucleus (STN) stimulation for alleviating pain related to Parkinson disease (PD).
Among 163 consecutive patients undergoing STN stimulation, 69 were identified as experiencing pain preoperatively that was related to their PD. All 69 patients suffering from pain were followed up prospectively for 12 months after surgery. All patients described the severity of their pain according to a visual analog scale (VAS) preoperatively and at 2 weeks, 6 months, and 12 months postoperatively. Pain unrelated to PD was not studied.
Several types of pain related to PD, the categories of which were based on a modification of 2 previous classifications (Ford and Honey), can occur in such patients: 1) musculoskeletal pain, 2) dystonic pain, 3) somatic pain exacerbated by PD, 4) radicular/peripheral neuropathic pain, and 5) central pain. The overall mean VAS score was significantly decreased postoperatively by 75% and 69% at 2 weeks and 6 months, respectively (p < 0.001). The mean VAS score at 12 months was also decreased by 80%, but 6 instances of pain (3 reports of somatic back pain and 3 reports of radicular/peripheral neuropathic pain) required additional spinal surgery to alleviate the pain severity. The results were analyzed using the Wilcoxon signed-rank test and demonstrated a significant reduction in VAS scores at all follow-up assessments (p < 0.001). Musculoskeletal pain and dystonic pain were well alleviated by STN stimulation. In contrast, somatic pain exacerbated by PD and peripheral neuropathic pain originating from lumbar spinal diseases, such as spondylosis deformans and/or canal stenosis, often deteriorated postoperatively despite attenuation of the patients' motor disability. Patients with central pain were poor responders.
This study found that STN stimulation produced significant improvement of overall pain related to PD in patients with advanced PD, and the efficacy continued for at least 1 year. The present results indicate that musculoskeletal pain and dystonic pain responded well to STN stimulation, but patients with back pain (somatic pain) and radicular/peripheral neuropathic pain originating from spinal disease have a potential risk for postoperative deterioration of their pain.