Subthalamic deep brain stimulation can improve gastric emptying in Parkinson's disease

Subthalamic deep brain stimulation can improve gastric emptying in Parkinson's disease
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DOI:
10.1093/brain/aws086
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发表时间:
2012-05-01
期刊:
影响因子:
14.5
通讯作者:
Yokosuka, Osamu
Yokosuka, Osamu
中科院分区:
医学1区
文献类型:
--
作者:
Arai, Eiji;Arai, Makoto;Yokosuka, Osamu

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丘脑深部电刺激丘脑底核可改善晚期帕金森病患者的运动功能,但其对自主神经功能的影响尚不清楚。本研究旨在探讨丘脑深部电刺激对胃排空的影响。16例帕金森病患者接受双侧丘脑底深部脑刺激。胃排空以C-13-乙酸盐呼气试验中(CO2)-C-13排泄的峰值时间(T-max)表示,并在术前和术后3个月分别给予和不给予100~150 mg左旋多巴/脱羧酶抑制剂,以及接受和不接受丘脑深部刺激。分析(CO2)-C-13排泄曲线的变化规律。为了评估与丘脑深部刺激对胃排空影响相关的潜在因素,我们还研究了胃排空、临床特征、左旋多巴等效剂量和血清Ghrelin水平之间的关系。未接受左旋多巴/脱羧酶抑制剂治疗的患者和接受左旋多巴/脱羧酶抑制剂治疗的患者胃排空高峰时间(T-max)分别为45.6±22.7min和42.5±13.6min(P=0.05),显示左旋多巴抵抗。术后(CO_2)-C_(13)排泄高峰时间(T-max)分别为44.0±17.5min和30.0±12.5min(P<0.001),说明丘脑深部刺激是有效的。同时,与无刺激的手术相比,(CO_2)-C_(13)排泄曲线的模式也有显著改善(P=0.002),尽管使用和不使用左旋多巴/脱羧酶抑制剂的差异不显著。术后运动功能障碍改善,左旋多巴当量剂量减少,但术前未使用左旋多巴/脱羧酶抑制剂和术后未使用左旋多巴/脱羧酶抑制剂及丘脑深部刺激时,(CO2)-C-13排泄峰值时间(T-max)与术前比较差异无统计学意义。在丘脑深部刺激试验中,术后Ghrelin水平的变化与T-max的变化之间几乎没有相关性(r=-0.20),而在丘脑深部刺激试验中,其他指标的变化与手术后的T-max之间没有相关性。这些结果表明,左旋多巴/脱羧酶抑制剂不影响胃排空,丘脑深部刺激可改善帕金森病患者的功能障碍,其机制可能是通过改变丘脑深部刺激后控制胃肠功能的神经系统来实现的。这是首次报道丘脑深部电刺激治疗帕金森氏病患者胃肠功能障碍的疗效。
It is established that deep brain stimulation of the subthalamic nucleus improves motor function in advanced Parkinson's disease, but its effects on autonomic function remain to be elucidated. The present study was undertaken to investigate the effects of subthalamic deep brain stimulation on gastric emptying. A total of 16 patients with Parkinson's disease who underwent bilateral subthalamic deep brain stimulation were enrolled. Gastric emptying was expressed as the peak time of (CO2)-C-13 excretion (T-max) in the C-13-acetate breath test and was assessed in patients with and without administration of 100-150 mg levodopa/decarboxylase inhibitor before surgery, and with and without subthalamic deep brain stimulation at 3 months post-surgery. The pattern of (CO2)-C-13 excretion curve was analysed. To evaluate potential factors related to the effect of subthalamic deep brain stimulation on gastric emptying, we also examined the association between gastric emptying, clinical characteristics, the equivalent dose of levodopa and serum ghrelin levels. The peak time of (CO2)-C-13 excretion (T-max) values for gastric emptying in patients without and with levodopa/decarboxylase inhibitor treatment were 45.6 +/- 22.7 min and 42.5 +/- 13.6 min, respectively (P = not significant), thus demonstrating levodopa resistance. The peak time of (CO2)-C-13 excretion (T-max) values without and with subthalamic deep brain stimulation after surgery were 44.0 +/- 17.5 min and 30.0 +/- 12.5 min (P < 0.001), respectively, which showed that subthalamic deep brain stimulation was effective. Simultaneously, the pattern of the (CO2)-C-13 excretion curve was also significantly improved relative to surgery with no stimulation (P = 0.002), although the difference with and without levodopa/decarboxylase inhibitor was not significant. The difference in peak time of (CO2)-C-13 excretion (T-max) values without levodopa/decarboxylase inhibitor before surgery and without levodopa/decarboxylase inhibitor and subthalamic deep brain stimulation after surgery was not significant, although motor dysfunction improved and the levodopa equivalent dose decreased after surgery. There was little association between changes in ghrelin levels (delta ghrelin) and changes in T-max values (delta T-max) in the subthalamic deep brain stimulation trial after surgery (r = -0.20), and no association between changes in other characteristics and delta T-max post-surgery in the subthalamic deep brain stimulation trial. These results showed that levodopa/decarboxylase inhibitor did not influence gastric emptying and that subthalamic deep brain stimulation can improve the dysfunction in patients with Parkinson's disease possibly by altering the neural system that controls gastrointestinal function after subthalamic deep brain stimulation. This is the first report to show the effectiveness of subthalamic deep brain stimulation on gastrointestinal dysfunction as a non-motor symptom in Parkinson's disease.