Nonneurogenic Incontinence

Nonneurogenic incontinence has been associated with ectopic ureteral insertion and other congenital malfor­mations (see Chapter 105), urolithiasis (see Chapter 108), and neoplasia of the lower urinary tract. In mares, incontinence may develop after trauma to the external urethral sphincter from breeding accidents, dystocia, or repeated foaling. Iatrogenic trauma resulting from inadvertent insertion of a vaginal speculum into the urethra and bladder has also been reported as a cause of incontinence. Although rare, a few cases of estrogen-responsive incontinence resulting from low urethral sphincter tone have been reported in mares. Cystitis is a common feature of most micturition disorders and may cause frequent, involuntary detrusor contractions because of irritation of stretch receptors in the bladder wall, commonly referred to as urge incontinence. Primary bacterial cystitis is rare in horses.

Neurogenic Incontinence

Neurogenic incontinence implies dysfunction of the neural pathways associated with normal micturition. The latter is a reflux function that involves sacral parasympathetic (pelvic nerve), somatic (pudendal nerve), and lumbar sympathetic (hypogastric nerve) neurons under the central control of the brainstem and cerebral cortex. Neurogenic incontinence can be divided into upper (UMN) and lower (LMN) motor neuron deficits, depending on location of the lesion. Damage to the sacral spinal cord segments or to the pelvic and pudendal nerves results in detrusor and urethral sphincter atony with urinary retention and overflow incontinence (LMN bladder). Causes of LMN bladder paralysis in the horse include equine herpesvirus type 1 (EHV-1) encephalomyelopathy (see Chapter 90), cauda equine neuritis, sorghum toxicosis, equine protozoal myeloencephalitis (EPM), sacral vertebral trauma, and neoplasia. Additionally, epidural administration of alcohol in show horses has resulted in iatrogenic bladder paralysis.

With suprasacral spinal cord or brainstem lesions, urethral sphincter tone is exaggerated, and coordination of micturition is lost. The bladder usually is firmly distended and difficult to express (UMN bladder). Bladder function may return through the use of sacral spinal reflexes, but voiding is incomplete, which results in accumulation of large volumes of crystalloid sediment, termed sabulous urolithiasis. The weight of the sediment causes overstretching and atony of the detrusor muscle and eventually overflow incontinence, as with LMN bladder. Incontinence resulting from UMN dysfunction is rare in horses but may be associated with EHV-1 encephalomyelopathy, EPM, aberrant parasitic migration, or trauma. Occasionally, horses with primary disease processes that do not affect the sacral spinal segments (i.e., cervical stenotic myelopathy, equine degenerative myeloencephalopathy) develop signs similar to those of LMN bladder paralysis. This may occur if UMN bladder dysfunction goes unnoticed and has progressed to detrusor atony. Alternatively, it is possible that neurologic control of bladder function in the horse is not yet completely understood, especially with regard to the complexity of higher centers involved in the control of micturition.

Idiopathic Bladder Paralysis Syndrome

An idiopathic form of bladder paralysis characterized by urinary incontinence and sabulous urolithiasis, in the absence of overt neurologic deficits, has been described, affecting predominantly geldings. The cause remains elusive, although subtle neurologic disease or historical neurologic disease has been suspected. Furthermore, it has been speculated that incomplete bladder evacuation secondary to chronic lumbosacral pain and associated difficulty of attaining normal urination posture may be causative. In this scenario, sabulous urolithiasis develops as a consequence of incomplete bladder evacuation and causes myogenic bladder dysfunction through overstretching and irritation of the detrusor muscle.