|Budget Amount *help
¥2,100,000 (Direct Cost : ¥2,100,000)
Fiscal Year 1993 : ¥500,000 (Direct Cost : ¥500,000)
Fiscal Year 1992 : ¥1,600,000 (Direct Cost : ¥1,600,000)
To evaluate the urinary disturbance of the patients with cerebrovascular dementia, we examined 100 patients with cerebrovascular disease. Forty-five patients(24 male and 21 female, mean 67.9 years old) were dementia and 55 patients(34 male and 21 female, mean 59.7 years old) were not dementia. 78% of the non-demented patients could void urine without using diapers or urethral catheter, but 40% of the demented patients used diapers and 20% of demented patients had urethral catheter. 83% of the demented patients complained urinary incontinence while 45% in non-demented patients. Brain lesions were examined using CT and/or MRI.88% (14/16) of the patients with large lesions had dementia and 93% (13/14) complained urinary incontinence. Correlation between brain lesions and lower urinary tract dysfunction were investigated. MRI demonstrated lesions in the frontal lobe, basal ganglia, internal capsule, cortex, brainstem etc., and patients who had lesions in the frontal lobe, basal ganglia and
internal capsule tended to have urinary incontinence. The degree of the dementia and lower urinary tract function was examined, but no correlation was found. After 3 months urological managements, 29% of the non-demented patients and 78% of the demented patients had urinary incontinence. No patient had urethral catheter in both groups. Patients with poor ADL tended to have urinary incontinence.
Electrical stimulation in the hippocampus could not produce reliable response to micturition reflex. Continuous electrical stimulation in the pontine micturition center(PMC) increased bladder capasity, but stimulation in the area dorsolateral to the PMC decreased bladder capacity. The mechanism of relaxation of the internal urethral sphincter during micturition and role of nitric oxide in vesicourethral function were examined. Electrical stimulation(0.3msec, 50Hz, 10-50muA,) in the PMC induced internal and external urethral sphincter relaxation as well as bladder contraction in decerebrate dogs and cats. Propranolol and atropine did not block the internal urethral sphincter relaxation evoked by PMC stimulation, but methylene blue inhibited this response. L-arginine increased bladder capacity and increased residual urine volume. Methylene blue blocked the effects of L-arginine. These results indicated that relaxation of the internal urethral sphincter during micturition was mediated a non-adrenergic and non-cholinergic mechanism, and that L-arginine - NO pathway was involved in this response. NO also may modulate bladder function. Less