A functional magnetic resonance imaging study of the effect of sacral neuromodulation on brain responses in women with Fowler's syndrome
A functional magnetic resonance imaging study of the effect of sacral neuromodulation on brain responses in women with Fowler's syndrome
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DOI：
10.1111/j.1464-410x.2009.08819.x
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发表时间：
2010-02-01
影响因子：
4.5
通讯作者：
Griffiths, Derek
中科院分区：
文献类型：
--
作者：
Kavia, Rajesh;DasGupta, Ranan;Griffiths, Derek
目的：检测Fowler综合征（FS，一种表现为排尿和膀胱感觉受损的括约肌异常）的年轻女性患者的大脑对膀胱充盈的反应，用骶神经调节（SNM）进行治疗。患者和方法：6名女性，年龄18-39岁，FS患者在SNM治疗后和未治疗时（基线）立即进行功能性脑磁共振成像（fMRI）。在四个阶段收集数据：SNM后膀胱排空和充盈，以及基线时膀胱排空和充盈。在每次治疗中，在重复输注和抽取50 mL生理盐水的同时采集280次全脑扫描，使用按钮报告排尿欲望的变化。使用统计参数图分析数据。在基线时，膀胱排空，广泛反应（造影剂=输注-撤药）几乎完全是阴性的（“失活”），例如，在右侧膀胱，内脏感觉的位置。增加膀胱容量和/或SNM治疗减少失活并加强正常（阳性）反应，例如在上行脊髓传入神经的导水管周围灰质（PAG）末端。在基线时，有显着的相关性与最大尿道闭合pressure. CONCLUSION这些数据表明，大脑对膀胱充盈的反应是异常的FS。对这一点的最好解释是，原发性异常是尿道过度活动，产生异常强烈的抑制性传入信号，从而有效地阻断了骶骨水平的膀胱传入活动，并使PAG和更高的中枢失活，从而丧失了膀胱感觉和排尿能力。很明显，一个正常的抑制尿失禁的机制，涉及横纹尿道括约肌在FS中变得夸张，并阻止排尿。SNM似乎在骶骨水平起作用，通过阻断尿道传入的抑制作用。
OBJECTIVETo examine brain responses to bladder filling in young women with Fowler's syndrome (FS, a sphincter abnormality manifested by impaired voiding and bladder sensation), treated with sacral neuromodulation (SNM).PATIENTS AND METHODSSix women, aged 18-39 years with FS underwent functional brain magnetic resonance imaging (fMRI) immediately after SNM and when untreated (baseline). Data were collected at four sessions: after SNM with an empty and a full bladder, and at baseline with an empty and a full bladder. In each session, 280 whole-brain scans were acquired while repeatedly infusing and withdrawing 50 mL of saline, using push-buttons to report changing desire to void. Data were analysed using Statistical Parametric Mapping.RESULTSAt baseline with an empty bladder, extensive responses (contrast = infusion-withdrawal) were almost exclusively negative ('deactivations'), e.g. in the right insula, seat of visceral sensation. Increased bladder volume and/or SNM treatment reduced deactivations and strengthened normal (positive) responses, e.g. in the periaqueductal grey (PAG) terminus of ascending spinal afferents. At baseline, there was significant correlation of brain responses with maximum urethral closure pressure.CONCLUSIONThese data show that brain responses to bladder filling are abnormal in FS. The explanation for this that best explains the evidence is that the primary abnormality is an overactive urethra that generates abnormally strong inhibitory afferent signals, so effectively blocking bladder afferent activity at the sacral level and deactivating the PAG and higher centres, with consequent loss of bladder sensation and ability to void. Apparently, a normal mechanism for suppression of incontinence involving the striated urethral sphincter becomes exaggerated in FS and prevents voiding. SNM seems to act at the sacral level, by blocking inhibition by urethral afferents.