Upper spinal cord lesions, above T12 Such lesions result in a reflex neurogenic (spastic) bladder. In addition to multiple sclerosis and traumatic and compressive myelopathies, which are the most common causes, myelitis, neuromyelitis optica, spondylosis, dural arteriovenous fistula, syringomyelia, and tropical spastic paraparesis may cause a bladder disturbance of this type. If the cord lesion is of sudden onset, the detrusor muscle suffers the effects of spinal shock. At this stage, urine accumulates and distends the bladder to the point of overflow. This overflow incontinence is the result of vesicular pressure exceeding the opening pressure of the sphincter in an areflexic bladder. As the effects of spinal shock subside, the detrusor usually becomes reflexively overactive, and because the patient is unable to inhibit the detrusor and control the external sphincter, urgency, precipitant micturition, and incontinence result. Incomplete lesions result in varying degrees of urgency in voiding. With slowly evolving processes involving the upper cord, such as multiple sclerosis, the bladder spasticity and urgency worsen with time and incontinence becomes more frequent. In addition, initiation of voluntary micturition is impaired and bladder capacity is reduced. Bladder sensation depends on the extent of involvement of sensory tracts. Bulbocavernosus and anal reflexes are preserved. The cystometrogram shows uninhibited contractions of the detrusor muscle in response to small volumes of fluid. Most puzzling to the authors have been cases of cervical cord injury in which reflex activity of the sacral mechanism does not return; the bladder remains hypotonic.
Stretch injury of the bladder wall This occurs with anatomic obstruction at the bladder neck and occasionally with psyhcogenic retention of urine. Repeated overdistention of the bladder wall often results in varying degrees of decompensation of the detrusor muscle and permanent atonia or hypotonia, although the evidence for this mechanism is uncertain. The bladder wall becomes fibrotic and bladder capacity is greatly increased. Emptying contractions are inadequate, and there is a large residual volume even after the Credé maneuver (manual abdominal compression) and strong contraction of the abdominal muscles. As with motor and sensory paralyses, the patient is subject to cystitis, ureteral reflux, hydronephrosis and pyelonephritis, and calculus formation.
Nonpsychogenic urinary retention in women Fowler has described a disorder of bladder function in women, in which there is impaired relaxation of the periurethral striated muscle, as recorded by EMG. The complex repetitive discharges that are characteristic of the disorder are similar to, but distinctive from those seen in myotonia and cannot be voluntarily simulated. Fowler has theorized that the disorder is an efferent denervation of the detrusor muscle, which is coincident with the clinical observation that bladder distention in these patients is usually painless. This disorder has been seen in association with polycystic ovarian syndrome. Most young women with painless dilation of the bladder are diagnosed as having a psychogenic cause. The existence of a bona fide organic disorder may reduce stigma and facilitate treatment in some such patients. Some patients have been successfully treated with a sacral nerve stimulator.
Frontal lobe incontinence There is a supranuclear type of hyperactivity of the detrusor that results in precipitant voiding. If the lesions are extensive enough in the frontal lobes, the patient, because of an abulic or confused mental state, may additionally be unconcerned by the subsequent incontinence. The bladder itself and the associated sphincter functions are normal as would be seen in a precontinent child. These types of frontal lobe incontinence are considered in the description of abnormalities consequent to frontal lobe damage in Chap. 21.