Nergårdh A, Naglo A S
Scand J Urol Nephrol. 1982;16(3):205-9. doi: 10.3109/00365598209179754.
The internal sphincter mechanism in the urinary bladder was investigated in three groups of children. Two groups had neurogenic bladder, one of them with and one without detrusor hyperactivity. The third group had no myelodysplasia and normal detrusor activity in the filling phase. In this group the sphincter contractions were sustained at high pressure level, with superimposed waves of substantial amplitude. Myelodysplasia of segments below L3 was associated with hyperactivity of the detrusor. The general sphincter pattern in this condition was the same as in the normal group, but the behavior of the sphincter was not synchronized with the pressure fluctuations in the bladder. In the children with low thoracic or high lumbar level of lesion ther was no detrusor hyperactivity. Their sphincter mechanism could be characterized as passive, with low mean pressure and low amplitude of superimposed waves. When detrusor hyperactivity is present, it seems to be the main factor in leakage from neurogenic bladder. In the absence of detrusor hyperactivity in neurogenic bladder, passivity of the internal urethral sphincter due to dissociation from the spinal centers is proposed as the explanation of incontinence.
对三组儿童的膀胱内括约肌机制进行了研究。两组患有神经源性膀胱,其中一组伴有逼尿肌活动亢进,另一组没有。第三组没有脊髓发育异常,充盈期逼尿肌活动正常。在这组中,括约肌收缩在高压水平持续,伴有幅度较大的叠加波。L3以下节段的脊髓发育异常与逼尿肌活动亢进有关。这种情况下的一般括约肌模式与正常组相同,但括约肌的行为与膀胱压力波动不同步。在胸段低位或腰段高位病变的儿童中,没有逼尿肌活动亢进。他们的括约肌机制可被描述为被动性,平均压力低,叠加波幅度小。当存在逼尿肌活动亢进时,它似乎是神经源性膀胱漏尿的主要因素。在神经源性膀胱不存在逼尿肌活动亢进的情况下,提出由于与脊髓中枢分离导致尿道内括约肌被动性是尿失禁的原因。