Therapy Insight: Bladder Dysfunction Associated With Multiple Sclerosis

Vinay Kalsi; Clare J. Fowler


Nat Clin Pract Urol. 2005;2(10):492-501. 

In This Article

Neurological Control of the Bladder

Functional brain imaging studies are adding to our understanding of the contribution of higher centers and signal processing involved in bladder control, so that voiding can be achieved in a socially appropriate time and place. Such studies have shown that a complex of brain networks is involved in the two processes of bladder storage[10,11] and voiding,[12,13] but that the final result of these processes is either activation or inhibition of the pontine micturition center (PMC). Direct pathways from the PMC project to the sacral segments of the spinal cord (S2-S4) (Figure 1), and determine parasympathetic outflow to the detrusor and reciprocal activity of the motor neurons innervating the striated urethral sphincter.[14]

Whilst in the storage phase, detrusor pressure does not rise. This is because the bladder fills as a result of inhibition of parasympathetic innervation of the detrusor, and pressure within the urethra is maintained at a higher level than within the bladder by tonic firing of the motor units of the striated urethral sphincter and pelvic floor. At the initiation of micturition there is relaxation of the striated urethral sphincter and pelvic floor, followed by a coordinated contraction of the detrusor muscle. This synergistic activity between the sphincter and the detrusor is dependent on connections with the pontine region. A condition known as 'detrusor sphincter dyssynergia' (DSD) might arise if these connections are damaged or interrupted, resulting in sphincter contraction as the detrusor contracts.[15]

The most marked abnormality occurs as a consequence of disconnection of sacral segments from the PMC. This results in the emergence of a segmental reflex that causes detrusor contractions in response to bladder distension. Evidence from animal experiments and human studies show that, following any form of spinal cord lesion, unmyelinated C fibers that were formally quiescent (and therefore known as 'silent C fibers') become mechanosensitive and respond to bladder stretch.[16] Detrusor contractions are caused by this afferent activity, through synaptic activity in the sacral segment of the cord.[17] It is this process that is responsible for detrusor overactivity, the pathophysiology underlying the common complaints of urinary frequency, urgency and urgency incontinence, referred to collectively as overactive bladder syndrome.[18,19]

Abnormal urodynamic findings in patients with dysfunctional voiding symptoms and MS are common, as shown by a meta-analysis of 1,900 patients.[1] Table 1 summarizes the incidences of the major patterns of urodynamic dysfunction reported in patients with MS. Detrusor hyperreflexia, the most common urodynamic abnormality in MS, is now referred to as 'neurogenic detrusor overactivity', following recent changes in the nomenclature.[19] Since a relapsing and remitting, or more commonly progressive, clinical course is a characteristic of MS, the lower urinary tract symptoms might also worsen, and regular reviews of bladder status have been recommended.[20,21]

The worsening of bladder dysfunction with increasing spinal cord involvement in MS has been clinically demonstrated in a number of studies.[2,7,22] Imaging studies using MRI have reported a correlation between urologic complaints and spinal cord cross-sectional area, which is used as a marker for spinal cord atrophy,[23] yet there is little evidence for the association between urinary symptoms and brain MRI parameters.[24,25]

As the neurological condition progresses, the bladder dysfunction can become more difficult to treat. This can be attributed to worsening of detrusor overactivity, inefficient emptying of the bladder in the context of worsening paraparesis, recurrent urinary tract infections, spasticity, reduction in general mobility, and sometimes cognitive impairment. In contrast to urinary tract dysfunction following traumatic spinal cord injury, progressive neurological diseases rarely cause upper urinary tract involvement.[7,26] This is true even when longstanding MS has resulted in severe disability and spasticity. Although the reason behind this difference in action is unknown, the evidence implies that the focus of management should be on symptomatic relief. The pathophysiologic changes that occur in MS and their symptomatic consequences lead to detrusor overactivity and detrusor sphincter dyssynergia, resulting in incomplete bladder emptying.


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