Oshima Hideki, Katayama Yoichi, Fukaya Chikashi, Kano Toshikazu, Kobayashi Kazutaka, Yamamoto Takamitsu, Suzuki Yutaka
Division of Applied System Neuroscience, Nihon University School of Medicine, Tokyo, Japan.
J Neurosurg. 2008 Jan;108(1):160-3. doi: 10.3171/JNS/2008/108/01/0160.
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.
剂量开始时运动功能恶化(BDMD)是帕金森病(PD)中左旋多巴药物治疗的一种并发症,推测是由左旋多巴的抑制作用引起的。文献中对BDMD的描述经验有限。作者报告了一例PD患者,在接受标准左旋多巴药物治疗时出现明显的BDMD。这位55岁女性有12年的PD病史和10年的左旋多巴治疗史。每次服用100mg左旋多巴后15至20分钟,症状会明显加重,持续约15分钟。在此期间,PD症状,尤其是震颤和僵硬,比剂末恶化时更明显地加重。通过丘脑底核(STN)刺激可以很好地控制BDMD,而左旋多巴药物治疗方案无需任何改变。这些观察结果表明,STN刺激通过直接作用抑制了BDMD。