Jameson J S, Rogers J, Chia Y W, Misiewicz J J, Henry M M, Swash M
Department of Gastroenterology and Nutrition, Central Middlesex Hospital, London.
Gut. 1994 Mar;35(3):388-90. doi: 10.1136/gut.35.3.388.
The aim of this study was to define pelvic floor function in patients with multiple sclerosis and bowel dysfunction, either incontinence (MSI) or defecation difficulties without incontinence (MSC). Normal controls and patients with idiopathic neurogenic faecal incontinence without multiple sclerosis (FI, disease controls) were also studied. Thirty eight multiple sclerosis patients (20 incontinent, 18 incontinent) 73 normal controls, and 91 FI patients were studied. The FI group showed the characteristic combined sensorimotor deficit previously described in these patients of low resting and voluntary contraction and pressures, increased sensory threshold to mucosal stimulation, and increased pudendal nerve terminal motor latencies and fibre densities. MSI patients had significantly lower anal resting pressures (80 (30-140) cm H2O, median (range) v 98 (30-200), normal controls, p = 0.002) and both MSC and MSI patients had significantly lower anal maximum voluntary contraction pressures (65 (0-260) cm H2O, MSC and 25 (0-100), MSI v 120 (30-300), normal controls, p = < 0.0004) and higher external anal sphincter fibre densities (1.7 (1.1-2.6), MSC and 1.7 (1.1-2.4), MSI v 1.5 (1.1-1.75), normal controls, p < 0.006) compared with normal controls but pudendal nerve terminal motor latencies were similar and no sensory deficit was found. This contrasted with the idiopathic faecal incontinent patients who, in addition to significantly higher fibre densities (1.8 (1.1-3), p = 0.001) had increased pudendal latencies (2.5 (1.1-5.5) mS v 2.08 (1.4-2.6), p = 0.001) compared with normal controls. The idiopathic faecal incontinent group had significantly lower resting anal pressures (50 (10-160) cm H2O, p=0.02) than the MSI group. Comparison with the incontinent and continent multiple sclerosis groups showed that incontinence was associated with lower voluntary anal contraction pressures (25 (0-100) v 65 (0-260), p=0.03) but that there were no other differences between these two groups. Pelvic floor function is considerably disturbed in multiple sclerosis, showing muscular weakness with preservation of peripheral motor nerve conduction, providing indirect evidence that this is mainly a result of lesions within the central nervous system.
本研究的目的是明确多发性硬化症合并肠道功能障碍患者（包括大便失禁（MSI）或无失禁的排便困难（MSC））的盆底功能。还对正常对照组以及无多发性硬化症的特发性神经源性大便失禁患者（FI，疾病对照组）进行了研究。研究了38例多发性硬化症患者（20例大便失禁，18例大便失禁）、73例正常对照组和91例FI患者。FI组表现出先前在这些患者中描述的特征性感觉运动联合缺陷，即静息和自主收缩及压力较低、对黏膜刺激的感觉阈值增加、阴部神经终末运动潜伏期延长和纤维密度增加。MSI患者的肛管静息压力显著较低（80（30 - 140）cmH₂O，中位数（范围），与正常对照组98（30 - 200）相比，p = 0.002），MSC和MSI患者的肛管最大自主收缩压力均显著较低（65（0 - 260）cmH₂O，MSC组；25（0 - 100），MSI组，与正常对照组120（30 - 300）相比，p = < 0.0004），且肛管外括约肌纤维密度较高（1.7（1.1 - 2.6），MSC组；1.7（1.1 - 2.4），MSI组，与正常对照组1.5（1.1 - 1.75）相比，p < 0.006），但阴部神经终末运动潜伏期相似，未发现感觉缺陷。这与特发性大便失禁患者形成对比，后者除纤维密度显著更高（1.8（1.1 - 3），p = 0.001）外，与正常对照组相比，阴部潜伏期也延长（2.5（1.1 - 5.5）ms，与2.08（1.4 - 2.6）相比，p = 0.001）。特发性大便失禁组的肛管静息压力（50（10 - 160）cmH₂O，p = 0.02）显著低于MSI组。与大便失禁和大便正常的多发性硬化症组比较显示，失禁与较低的自主肛管收缩压力相关（25（0 - 100）与65（0 - 260），p = 0.03），但这两组之间无其他差异。多发性硬化症患者的盆底功能受到相当大的干扰，表现为肌肉无力但保留外周运动神经传导，这间接证明这主要是中枢神经系统内病变的结果。
