Swedish Headache Center, Seattle, WA 98104, USA.
Cephalalgia. 2010 Jun;30(6):648-54. doi: 10.1111/j.1468-2982.2009.01998.x. Epub 2010 Feb 11.
The aim of this study was to measure differences in occipital cortex excitability in migraineurs before and after administration of topiramate. We have previously demonstrated occipital cortex hyperexcitability in migraine using an objective technique of magnetic suppression of perceptual accuracy (MSPA). We hypothesized that a neuromodulator such as topiramate would demonstrate differences in MSPA in migraine compared with baseline. Ten migraine patients were recruited. To assess inhibitory function MSPA was measured using the following protocol. Timed transcranial magnetic stimulation were delivered at interstimulus intervals (ISI) varying from 40 to 190 ms (eight stimulations at each ISI) at 60% stimulus intensity. Subjects were asked to report letters projected at a fixed luminance on the screen. Visual suppression was calculated based on the number of errors the subjects made using automated analysis. This procedure was repeated at a minimum of two different dosages of topiramate when it was titrated for optimal migraine control. The interim dose was that at which an improvement in headache frequency was first observed, and the optimal dose was that at which the patient had a ≥ 50% reduction in headache frequency, or had reached a 100-mg dose. The mean [standard error (s.e.)] level of letters reported correct at baseline at 100-ms ISI was 91.6 (3.4) compared with 48.5 (6.0) (P = 0.001) at an optimal dose of topiramate. Dose ranged from 50 to 100 mg; the average dose was 75 mg. The interim dose for most patients was 50 mg; the mean (s.e.) percentage of letters reported correct at interim was 75.9 (6.2) compared with baseline (P = 0.01). Mean number of headaches at baseline was 27 per month, compared with eight headaches per month at interim dose and four headaches per month at optimal dose. There was no significant correlation between mean change in frequency of headache and mean change in inhibition from baseline to optimal dose (0.04, P = 0.89). Topiramate modulates occipital cortex excitability in chronic migraine possibly via mechanisms of cortical inhibition. Since there was not a strong correlation between the degree of inhibition and reduction of migraine frequency, it would appear that topiramate did have an independent effect on cortical excitability that was not dependent on reduction in migraine frequency.
这项研究的目的是测量偏头痛患者在服用托吡酯前后枕叶皮层兴奋性的差异。我们之前使用磁抑制知觉准确性的客观技术（MSPA）证明了偏头痛患者枕叶皮层兴奋性过高。我们假设，像托吡酯这样的神经调节剂在偏头痛患者中与基线相比，MSPA 会显示出差异。我们招募了 10 名偏头痛患者。为了评估抑制功能，我们使用以下方案测量 MSPA。在 60%的刺激强度下，以 40 到 190 毫秒的间隔（每个间隔 8 次刺激）施加定时经颅磁刺激。要求受试者报告在屏幕上以固定亮度显示的字母。根据受试者使用自动分析所犯的错误数量计算视觉抑制。当托吡酯被滴定用于最佳偏头痛控制时，在至少两个不同的托吡酯剂量下重复该过程。中间剂量是首次观察到头痛频率改善的剂量，最佳剂量是头痛频率降低≥50%的剂量，或达到 100mg 剂量的剂量。在最佳托吡酯剂量下，100ms ISI 时正确报告的字母平均[标准误差（s.e.）]水平为 91.6（3.4），而 48.5（6.0）（P=0.001）。剂量范围为 50 至 100mg；平均剂量为 75mg。大多数患者的中间剂量为 50mg；中间剂量时正确报告的字母平均（s.e.）百分比为 75.9（6.2），与基线相比（P=0.01）。基线时每月头痛平均次数为 27 次，中间剂量时每月头痛 8 次，最佳剂量时每月头痛 4 次。头痛频率的平均变化与从基线到最佳剂量的抑制平均变化之间没有显著相关性（0.04，P=0.89）。托吡酯可能通过皮质抑制机制调节慢性偏头痛患者的枕叶皮层兴奋性。由于抑制程度与偏头痛频率降低之间没有很强的相关性，因此托吡酯似乎对皮质兴奋性有独立的影响，而不依赖于偏头痛频率的降低。
