Notice in Fig. 17.1, as bladder filling occurs EMG activity increases (increased somatic innervation to external sphincter) at the line annotated as “strong desire.” Once the patient is given the command, permission to void (line titled “void”), EMG activity diminishes, a detrusor contraction is generated and voiding ensues (Fig. 17.2).

In Fig. 17.2 there is increased EMG activity during an involuntary detrusor contraction. Ordinarily the sphincter complex relaxes resulting in EMG quieting prior to voiding. In some cases it is normal to see increased EMG activity during detrusor contraction. Contracting the external sphincter (Kegels) during episodes of urgency helps to suppress the detrusor contraction by decreasing parasympathetic activity to the bladder. Once this happens, the detrusor contraction abates and urgency is relieved. In Fig. 17.2, notice the increase in EMG activity during an involuntary detrusor contraction. This results in increased urethral resistance with preserved continence and the detrusor contraction is abated and filling continues until the next involuntary detrusor contraction at which point contraction of pelvic floor occurs again. In this scenario, sphincter contraction during detrusor contraction is a normal response, however, in other situations this process can represent pathology.

Figure 17.3a, b was taken during the voiding phase of an urodynamics study evaluating a 13-year-old female with persistent daytime and nighttime incontinence. She has a history of chronic constipation and holding her urine. The patient’s symptoms worsened with puberty. Patient is neurologically normal with no evidence of occult spinal dysraphism on exam.

During this study, once the patient was given permission to void there is evidence of increased EMG activity during voluntary detrusor contraction resulting in intermittency of urinary flow. Involuntary contraction of the external urethral sphincter during voiding in the absence of neurologic injury or disease is known as dysfunctional voiding. It has also been described as learned voiding dysfunction and by some as non-neurogenic, neurogenic bladder [3]. Dysfunctional voiding, as defined by the International Continence Society (ICS), is an intermittent and/or fluctuating flow rate due to involuntary intermittent contractions of the periurethral striated muscle during voiding, in neurologically normal subjects [4]. It can be difficult to diagnose using surface EMG electrodes because of other factors that can produce increased EMG activity on a tracing, including attempts at augmenting bladder contractions by abdominal straining, movement, guarding reflex, and wet electrodes. Using fluoroscopy has proven invaluable in the diagnosis because one can see a dilation of the urethra to the level of the striated sphincter (spinning top urethra) and/or intermittent contractions of the striated sphincter. Figure 17.3b is the fluoroscopic image taken at time of EMG activation. As indicated by notched arrows the patient’s bladder neck opens however there is minimal flow past EUS during this episode of sphincter activity (Fig. 17.3a, b).

The differences between the two studies are subtle but important. Once there is a conscious decision to void, the dominant reflex pathways are those responsible for bladder emptying. The fact that the patient’s EUS complex activates during a conscious void is pathologic. The other difference is in Fig. 17.2 where there is a conscious contraction on the pelvic floor resulting in increased EMG activity (an adaptive mechanism to prevent incontinence) whereas in Fig. 17.3 this is a learned, involuntary activation of pelvic floor. One way to determine if increased EMG activity is voluntary versus involuntary is to simply ask to patient during event while the study is in progress (Fig. 17.4).

In Fig. 17.4, rises in abdominal pressure (as noted by notched horizontal arrows) are associated with increases in EMG activity (diagonal arrows). This is due in part by the guarding reflex. Increases in abdominal pressure lead to increased EMG activity to maintain continence in patients with an intact reflex arc.

Neurological conditions, lesions, or trauma can cause disturbances in urinary storage and voiding resulting in bladder dysfunction. Detrusor sphincter dyssynergia (DSD) is defined by the ICS as “the impaired coordination between detrusor and sphincter during voiding due to a neurologic abnormality (i.e., detrusor contraction synchronous with contraction of the urethral and/or periurethral striated muscles)” [4]. Neurological conditions more commonly resulting in DSD include: SCI, MS, spinal dysraphism and transverse myelitis. In the absence of a neurological abnormality, impaired coordination of bladder contraction and sphincter relaxation is more appropriately referred to as dysfunctional voiding or pelvic floor hyperactivity.

As noted previously, during normal voluntary micturition, once the threshold bladder distention is reached, PMC activation increases inhibiting spinal guarding reflexes and transmits excitatory signals to the bladder. The EUS relaxes with synergistic contraction of the detrusor as noted in Fig. 17.1.

DSD occurs in the setting of neurological abnormalities between the PMC and sacral spinal cord (Onuf’s nucleus). This interruption is thought to result in failed inhibition of spinal guarding reflexes, and erroneous excitation of Onuf ’s nucleus causing external urethral sphincter contraction to occur during detrusor contraction (Fig. 17.5).