ABSTRACT
Detrusor smooth muscle function has shown altered physiology in streptozotocin - or alloxan-induced diabetes mellitus animal models. Major physiologic alterations are changes in sensitivity and contractile forces. In most typical cases with diabetic cystopathy, cystometry shows a long curve with lack of sensation, often until bladder capacity is reached, with a low detrusor pressure. Pathophysiology of diabetic cystopathy has multifocal aspects. The typical cystometrogram finding of cauda equina injury is loss of detrusor contraction. Bladder biopsies from acontractile patients showed a derangement of the capillary bed of the muscle tissue, atrophy of the muscularis, and fibrotic replacement of the smooth muscle with attenuation of the lumen of the small arteries. Experimental data from animals indicate that somatic afferent input to the sacral spinal cord can modulate the guarding and bladder–bladder reflexes. Spinal cord injury produces bladder sphincter dyssynergia and inefficient bladder emptying by eliminating the brain mechanisms.
