Kaplan et al. (1995) retrospectively analyzed the urodynamic findings of 115 male and 68 female diabetics with persistent voiding symptoms. Impaired detrusor contractility was defined by poorly sustained or weak detrusor contractions (<30 cmH₂O) and a catheterized urine flow rate of less than 12 ml/s. The results indicate that mean bladder capacity was 485 ± 89 ml with a mean first sensation of filling of 298 ± 67 ml. Of the 182 patients, 100 (55 %) had detrusor hyperreflexia, 42 (23 %) had impaired detrusor contractility, 20 (11 %) had indeterminate findings, 19 (10 %) had detrusor areflexia, and 1 (1 %) was normal. Surprisingly, the standard diabetic cystopathy is far less than detrusor overactivity. However, sacral cord signs correlated with either impaired detrusor contractility in 50 % or detrusor areflexia in 24 % of patients with diabetic cystopathy. These data suggest that classical diabetic cystopathy is not the most common urodynamic finding in patients with DM and voiding dysfunction, and in fact these patients may present with concomitant lesions, such as benign prostatic hyperplasia, and stress incontinence and make variable pathophysiological findings. The authors concluded that urodynamic studies in diagnosing voiding dysfunction in diabetics before initiation of therapy is important.

Impaired detrusor contractility may lead to incomplete bladder emptying and urinary retention. Yu et al. (2004) conducted a prospective study to compare voiding function between 176 female type 2 diabetic patients and 162 age-matched nondiabetic women, none of whom had ever sought treatment for voiding dysfunction. Diabetic patients were 5 times as likely to have unrecognized voiding difficulty, defined a maximal flow rate <12 ml/s or a post-void residual (PVR) urine volume ≥100 ml. Notably, 22 % had voiding difficulty and 14 % had high PVR levels ≥100 ml. Duration of diabetes of ≥20 years appeared to be an independent predictor.

Fifty-four diabetic patients, half men and half women, with lower urinary tract symptoms were involved in an urodynamic investigation by Kebapcı et al. (2007). Bladder dysfunction was present in 74 % of men characterized by impaired bladder sensation – volume at first desire to void > 150 ml, increased PVR ≥ 100 ml, increased bladder capacity ≥500 ml, and decreased bladder contractility on urodynamics. Bladder dysfunction was noted in 59 % of diabetic women including UAB in 44 %, detrusor overactivity 31 %, urge incontinence 13 %, and stress urinary incontinence 12 %. Prolongation of QTc on electrocardiogram, abnormal esophageal transit and gastric emptying times, microalbuminuria, and diabetic retinopathy were associated with an increased risk of PVR ≥ 100 ml. The authors also found that PVR ≥ 100 ml was associated with 21 and 4 times increased risk of recurrent UTI in men and in women, respectively. The establishment of UAB 8 years after the diagnosis of type 2 DM may be an important prognosticator for future serious diabetic bladder dysfunction.

Lee et al. (2009) studied urodynamic characteristics and bladder sensory function by intravesical current perception threshold testing at frequencies of 5 and 250 Hz in 86 diabetic women who had not sought treatment for diabetic bladder dysfunction. Among them, 30 (35 %) were classified as having detrusor underactivity, 12 (14 %) presented signs of detrusor overactivity, 11 (13 %) were referred to as having bladder outlet obstruction, and 33 (38 %) showed normal detrusor function. The detrusor underactivity group showed impaired emptying function and decreased sensation on cystometry and an increase in current perception threshold values associated with a decrease in bladder voiding efficiency on 5 and 250 Hz current perception threshold testing. The results support that impaired bladder sensation of Aδ and C fiber bladder afferent pathways may play a key role in diabetic bladder dysfunction.

Bansal et al. (2011) evaluated urodynamic study and sympathetic skin responses, motor and sensory nerve-conduction velocity studies in 52 diabetic men with lower urinary tract symptoms, and mean duration of DM of 11 years. Delayed first sensation of >250 ml was seen in 21 %, increased capacity of > 600 ml was noted in 25 %, and high PVR of more than one third of capacity in 65 %. Other abnormalities, such as detrusor overactivity (36 %), bladder outlet obstruction (29 %), and decreased compliance (33 %), were also common. Only 8 % of patients had normal bladder function on urodynamic evaluation. A large majority (81 %) had electrophysiologic evidence of autonomic dysfunction. The authors reported that electrophysiologic evidence of peripheral neuropathy was seen in 58 % of patients with diabetic bladder dysfunction. UAB with an elevated PVR highly correlates with neurologic abnormalities.

He et al. (2014) reported in 918 diabetic patients with impaired detrusor contractility (n = 787) or detrusor areflexia (n = 131) that the mean first sensation of filling was 238 ml, with a mean maximum cystometric capacity of 624 ml, mean maximum flow rate of 9.6 ml/s, mean detrusor pressure at maximum flow rate of 32 cmH₂O, and mean PVR of 323 ml. Thirty-eight of 131 patients with detrusor areflexia had impaired renal function and bilateral hydronephrosis.

In a prospective study of 181 women with type 2 DM and lower urinary tract dysfunction, Lin et al. (2012) demonstrated that the duration of DM relative to the urodynamic diagnoses of these women was longer in those with detrusor hyperactivity with impaired contractility and with poor voiding efficiency. Regression analysis indicated that age and recurrent urinary tract infections were the two independent factors associated with developing voiding dysfunction.

Diabetes is associated with a systemic inflammation, neuropathy, vascular complications, and metabolic syndrome, all of which have been linked to DM cystopathy (Yoshimura et al. 2005). The biology of DM cystopathy is multifactorial and can be a result of an alteration or aberrant function of the detrusor smooth muscle cell, the innervation or the neuronal component, or urothelium. Watanabe and Miyagawa (1999) suggested that there are three primary causes of UAB in diabetics:

Diabetic neuropathy is characterized by demyelinization, axonal degeneration, fiber loss, and defect in bladder Aδ and C afferent fibers. Diabetic cystopathy-affected specimens have shown focal axonal degeneration and decreased bladder wall cholinergic nerve fibers (Van Poppel et al. 1988). Furthermore, many associations have been linked between bladder dysfunction and peripheral nerve system dysfunction in diabetes, e.g., somatic pain sensation, motor and sensory nerve conduction velocities in the limbs, and sympathetic skin responses (sweating) (Yamaguchi et al. 2007).

The cause of diabetic neuropathy is multifocal, including altered metabolism of glucose and hyperglycemic activation of the polyol pathway causing direct neuronal damage. Ischemia, superoxide-induced free-radical formation, impaired axonal transport, and metabolic derangement of the Schwann cell result in segmental demyelination and impairment of nerve conduction (Yoshimura et al. 2005; Lee et al. 2009). Neuronal dysfunction may reflect a deficiency of axonal transport of nerve growth factor that may induce diabetic neuropathy (Sasaki et al. 2003).

UAB can be observed in many neurologic conditions, such as disturbed central nervous system function, peripheral neuropathy, and impaired bladder neurotransmission (Table 11.2), and this has been discussed in the recent comprehensive reviews (Miyazato et al. 2013; Andersson 2014).