Camilleri M, Fealey R D
Division of Gastroenterology, Mayo Foundation, Rochester, Minnesota 55905.
Dig Dis Sci. 1990 May;35(5):609-16. doi: 10.1007/BF01540409.
Gut dysmotility may result from disease of the extrinsic neural pathways supplying the gut. We report the results of studies on sweating, cardiovascular, and sudomotor reflexes in eight prospectively evaluated patients with apparently functional gastrointestinal disorders. There was no personal or family history of neurologic disease, except for one patient with known atony of the bladder. Motility of the esophagus, stomach, and small intestine were, respectively, abnormal in two, six, and seven patients and showed either uncoordination of contractions between segments or postcibal hypomotility. All had generalized or patchy anhidrosis; quantitative sudomotor axon reflex tests were also abnormal in four patients and borderline in one. Plasma levels of catecholamines were abnormal in one patient. All patients had evidence of sympathetic denervation: preganglionic in two patients, postganglionic in five patients, and mixed in one patient. Three patients also had abnormal heart-rate responses to deep breathing, suggesting parasympathetic dysfunction. No underlying cause for the autonomic dysfunction was identified in any of these patients despite extensive investigations. Thus, these data support the hypothesis that apparently functional gastrointestinal disorders may be due to idiopathic autonomic denervation.
肠道动力障碍可能源于供应肠道的外在神经通路疾病。我们报告了对8例经前瞻性评估的明显功能性胃肠疾病患者的出汗、心血管和汗腺运动反射研究结果。除1例已知膀胱无张力的患者外，均无神经疾病的个人或家族史。食管、胃和小肠的动力分别在2例、6例和7例患者中异常，表现为节段间收缩不协调或餐后运动减弱。所有患者均有全身性或斑片状无汗；4例患者的定量汗腺运动轴突反射试验也异常，1例为临界值。1例患者的血浆儿茶酚胺水平异常。所有患者均有交感神经去神经支配的证据：节前2例，节后5例，混合性1例。3例患者对深呼吸的心率反应也异常，提示副交感神经功能障碍。尽管进行了广泛的检查，但在这些患者中均未发现自主神经功能障碍的潜在原因。因此，这些数据支持以下假设，即明显功能性胃肠疾病可能是由于特发性自主神经去神经支配所致。
