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Neurological causes of micturition disorders in small animals

It is important that animals do not develop complications, often due to incomplete bladder emptying

09 July 2020, at 8:00am

Disorders of micturition can be caused by diseases affecting the innervation of the bladder (neurogenic bladder) or by other systemic conditions (metabolic, hormonal, inflammatory) or localised conditions (urinary tract infections, stones, malformations) that affect the function of the bladder. In the case of neurogenic bladder, the clinician should try to distinguish between disorders of micturition due to an upper motor neuron (UMN) lesion or lower motor neuron (LMN) lesion of the nervous system, and then decide the pharmaceutical management accordingly.

Bladder dysfunctions

UMN bladder dysfunction

UMN bladder dysfunction is due to a lesion cranial to the L7 spinal cord segment (usually between the pons and L7). The most common cause is compression of the spinal cord (intervertebral disc herniation) that disrupts the pathways responsible for the detrusor reflex and the UMN pathways to the skeletal muscle of the urethral sphincter. In these cases, animals often develop incoordination of detrusor and sphincter function (“dyssynergia”).

Clinically the animals commonly show signs of severe UMN thoracolumbar spinal cord lesion, as non-ambulatory paraparesis (or paraplegia in some cases). The perineal reflex is often intact. Poor prognostic factors are the loss of nociception in the hind limbs and perineal area and the loss of perineal reflex.

Dogs diagnosed with thoracic arachnoid cyst/diverticu-lum or thoracic syringomyelia could develop UMN bladder dysfunction, despite being ambulatory. This is explained by the loss of supraspinal regulation of the bladder function, due to an intramedullary spinal lesion (different from an ex-tramedullary intervertebral disc compression) that affects the urinary pathways, located deeper in the spinal cord, before affecting the motor spinal pathways.

Clinical signs are caused by the inability to empty the bladder due to a reduced or absent detrusor reflex. The tone is generally increased, due to a lack of inhibition of the spinal cord. The urethral sphincter is spastic and on palpation the bladder is firm and very difficult to manually express. Bladder manipulation should be performed very carefully, as the risk of bladder rupture is increased. It is recommended to use a urinary catheter to empty the bladder (in addition to pharmacologic intervention, when needed).

In case of a reversible lesion, bladder function can be recovered within days or weeks. In general, as voluntary motor function of the limbs returns, so does voluntary control of micturition.

LMN bladder dysfunction

LMN bladder dysfunction is due to a lesion to the sacral segments of the spinal cord or to the sacral nerves of the cauda equina, which runs within the spinal canal. These signs might also be encountered with a lesion of the pelvic canal that involves the pelvic or lumbosacral plexus.

Clinical signs are due to an inability to empty the bladder due to an absent detrusor reflex, and the tone is generally decreased. On palpation, the bladder feels flaccid and difficult to palpate. The patient leaks urine (overflow incontinence) and increased abdominal pressure leads to urine outflow, therefore the bladder can easily be manually expressed. Urine scalding is a common complication, if patient cleanliness is not carefully maintained, together with urinary retention and urinary tract infections (UTIs). Manual expression of the bladder or the use of an indwelling catheter is recommended in these patients.

Clinical signs often involve reduced or absent perineal sensation and reflex, reduced or absent anal tone and possible involvement of the tail (paresis/paralysis/loss of nociception). If the lesion also affects the innervation to the pelvic limbs, the animal can show LMN signs, as paraparesis and reduced to absent spinal reflexes in the pelvic limbs.

Detrusor-urethral (sphincter) dyssynergia (DSD)

DSD is a micturition abnormality due to an abnormal coordination between the detrusor and the urethral sphincter muscles. The urethral muscles (external urethral sphincter) contract abnormally during detrusor contraction, resulting in abnormal interruption of urination. The causes are not clearly understood, but a lesion of the spinal pathways that inhibit the hypogastric (sympathetic) nerve function (and pudendal somatic nerve) during the voiding phase could cause DSD. Idiopathic DSD is described in middle-aged large-breed male dogs.

Detrusor atony

Atony of the detrusor muscle could be a complication of over-distension of the bladder, due to structural or functional causes that interfere with urine outflow. Frequent causes are obstruction of the urethra (calculi, neoplasia) or pain on urination, due to pelvic fractures and prolonged recumbency.
This over-distension causes the separation of the tight junction of the detrusor muscle fibres and the muscle becomes weak and ineffective.
The bladder is distended and has no tone, but there is no overflow of urine. Detrusor atony is caused by a lesion of the muscle, not by a neurological lesion.
Treatment aims at restoring the tight junctions of the detrusor muscle by keeping the bladder small. The use of an indwelling catheter is recommended for at least seven days and the use of parasympathetic drugs can help to increase detrusor contraction.

Treatment of disorders of micturition

Disorders of micturition can be treated surgically or medically. Surgical treatments are normally performed if medical treatments fail.

Medical treatment includes control of secondary complicating UTIs and management of the bladder and urethral dysfunctions. The detrusor muscle should never be stimulated to contract pharmacologically or expressed manually unless the bladder is easily manually expressed (the urethral sphincters are not contracted).

In cases of urinary retention, the bladder needs to be emptied regularly to avoid detrusor muscle over-distension. Residual urine volumes following intermittent catheterisation have been suggested to increase risk of UTIs.

If the urethral tone is increased, manual expression can be dangerous; therefore, aseptic urethral/bladder catheterisation is required by intermittent urinary catheterisation or by placement of an indwelling catheter.

The drugs most commonly used are:

  • Bethanecol chloride (2.5 to 25mg orally TID in dogs; 1.5 to 5mg orally TID in cats): used to stimulate detrusor muscle contraction. It should not be used alone in case of UMN bladder, as the urethral sphincter tone is normally increased
  • Diazepam (0.2mg/kg orally TID in dogs and cats): used to relax the external urethral sphincter (striated muscle) in patients with UMN bladder
  • Phenoxybenzamine hydrochloride (0.25 to 0.5mg/kg orally BID in dogs and cats): used to decrease the tone of the internal urethral sphincter (smooth muscle). Used mostly in UMN bladder
  • Prazosin (1mg/15kg BID, SID in dogs; 0.25mg/cat orally BID, SID) can decrease urethral sphincter tone. It can cause marked hypotension; therefore, it is recommended to start with half the calculated dose for the first few days. It can also be administered 30 minutes before bladder expression to release urethral sphincter tone. It can be used with dyssynergia

A new neuroprosthetic device (sacral nerves stimulator) has been tested for use in paraplegic dogs with urinary incontinence (UMN bladder). These devices are not effective in patients with LMN bladder injuries.


Prognosis is generally good if the underlying condition is treated and the patient receives the correct care. Ongoing chronic disorders of micturition have the potential of a less favourable or more guarded prognosis. In some cases, the animal might require lifelong medical treatment. It is very important that the animals do not develop complications, such as UTIs or bladder over-distension, often due to incomplete bladder emptying.

In cats, in cases of lesions of the cauda equina due to spinal trauma, intact sensation at the level of the perineum or the base of the tail is a favourable prognostic factor. Animals that do not recover nociception at the level of the perineum or the base of the tail within 30 days of the trauma have reduced chances of regaining bladder control.

Author Year Title
Carwardine D. R., Rose J. H., Harcourt-Brown T. R. and Granger N. 2016 Effectiveness of manual bladder expression in paraplegic dogs. American Journal of Veterinary Research, 78, 107-112
Coates, J. R. 2012 Tail, anal and bladder dysfunction. In: Platt, S. R. and Olby, N. (eds) BSAVA Manual of Canine and Feline Neurology, 4th ed. BSAVA, Quedgeley, pp. 368-387
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Granger, N., Chew, D., Fairhurst, P., Fawcett, J., Lacour, S., Craggs, M., Mosse, C., Donaldson, N. and Jeffery, N. 2012 Use of an implanted sacral nerve stimulator to restore urine voiding in chronically paraplegic dogs. Journal of Veterinary Internal Medicine, 27, 99-105
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Langfitt, E., Prittie, J. E., Buriko Y. and Calabro J. M. 2017 Disorders of micturition in small animal patients: clinical significance, etiologies, and management strategies. Journal of Veterinary Emergency and Critical Care, 27, 164–177
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Tatton, B., Jeffery, N. and Holmes M. 2009 Predicting recovery of urination control in cats after sacrocaudal injury: a prospective study. Journal of Small Animal Practice, 50, 593-596

Simona T. Radaelli, DVM, PhD, DipECVN, MRCVS, has worked in UK referral practices since 2005 and as a telemedicine specialist since 2019. She has also taught foundation and higher education students for seven years and lectured in several national and international congresses.

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