Gelber D A, Good D C, Laven L J, Verhulst S J
Division of Neurology, Southern Illinois University School of Medicine, Springfield 62794-9230.
Stroke. 1993 Mar;24(3):378-82. doi: 10.1161/01.str.24.3.378.
We prospectively studied bladder function in stroke patients to determine the mechanisms responsible for poststroke urinary incontinence.
Fifty-one patients with recent unilateral ischemic hemispheric stroke admitted to a neurorehabilitation unit were enrolled. The presence of urinary incontinence was correlated with infarct location, neurological deficits, and functional status. Urodynamic studies were performed on all incontinent patients.
Nineteen patients (37%) were incontinent. Incontinence was associated with large infarcts, aphasia, cognitive impairment, and functional disability (p < 0.05) but not with age, sex, side of stroke, or time from stroke to entry in the study. Urodynamic studies, performed on all 19 incontinent patients, revealed bladder hyperreflexia in 37%, normal studies in 37%, bladder hyporeflexia in 21%, and detrusor-sphincter dyssynergia in 5%. All of the patients with normal urodynamic studies were aphasic, demented, or severely functionally impaired. All of the patients with hyporeflexic bladders had underlying diabetes or were taking anticholinergic medications. Forty-six percent of incontinent patients treated with scheduled voiding alone were continent at discharge compared with 17% of patients treated pharmacologically.
There are three major mechanisms responsible for poststroke urinary incontinence: 1) disruption of the neuromicturition pathways, resulting in bladder hyperreflexia and urgency incontinence; 2) incontinence due to stroke-related cognitive and language deficits, with normal bladder function; and 3) concurrent neuropathy or medication use, resulting in bladder hyporeflexia and overflow incontinence. Urodynamic studies are of benefit in establishing the cause of incontinence. Scheduled voiding is a useful first-line treatment in many cases of incontinence.
我们对中风患者的膀胱功能进行了前瞻性研究,以确定中风后尿失禁的发病机制。
纳入51例近期因单侧缺血性半球中风入住神经康复科的患者。尿失禁的存在与梗死部位、神经功能缺损及功能状态相关。对所有尿失禁患者进行了尿动力学研究。
19例患者(37%)出现尿失禁。尿失禁与大面积梗死、失语症、认知障碍及功能残疾相关(p<0.05),但与年龄、性别、中风侧别或从中风到纳入研究的时间无关。对所有19例尿失禁患者进行的尿动力学研究显示,37%为膀胱反射亢进,37%研究结果正常,21%为膀胱反射减退,5%为逼尿肌-括约肌协同失调。所有尿动力学研究结果正常的患者均有失语症、痴呆或严重功能障碍。所有膀胱反射减退的患者均有潜在糖尿病或正在服用抗胆碱能药物。仅采用定时排尿治疗的尿失禁患者中,46%在出院时尿控良好,而药物治疗的患者这一比例为17%。
中风后尿失禁有三种主要机制:1)神经排尿通路中断,导致膀胱反射亢进和急迫性尿失禁;2)因中风相关的认知和语言缺陷导致的尿失禁,膀胱功能正常;3)并发神经病变或药物使用,导致膀胱反射减退和充溢性尿失禁。尿动力学研究有助于确定尿失禁的病因。在许多尿失禁病例中,定时排尿是一种有用的一线治疗方法。