• “Overactive bladder” is a merely clinical diagnosis, comprising urgency, with or without urge incontinence (OAB-wet and OAB-dry), and either or both frequency and nocturia
• “Detrusor overactivity” (DO) is a urodynamic finding which may or may not underlay OAB, and has two types: phasic and terminal DO, the latter usually being of neurogenic origin
• “LUTS” comprise storage/OAB symptoms, voiding symptoms, and postmicturition symptoms. They equally affect men and women and are rather age- than gender-related
• In female OAB, antimuscarinics should be applied for 6–12 weeks before commencing invasive diagnostics. In the male, A1-receptor antagonists should first be tried alone, followed by a combination with antimuscarinics.
The symptomatic response of the lower urinary tract on different pathologies is rather uniform, the bladder therefore being referred to as an “unreliable witness”.
Urinary symptoms in male patients with an enlarged prostate have traditionally been thought to originate from the prostate rather than from the bladder, whilst same symptoms in women have generally been attributed to bladder dysfunction. Thus, medical treatment of men with urinary symptoms usually targets the prostate, ignoring the bladder as possible site of origin.
The term “Lower Urinary Tract Symptoms” (“LUTS”) was coined some 15 years ago to dissociate urinary symptoms from prostatic pathology. LUTS comprise voiding symptoms, postmicturition symptoms and storage symptoms which are also described by the term “overactive bladder” (OAB), as defined by the International Continence Society committee 2002 (Abrams et al., 2002) see also Chapters 1 and 2.
Urgency incontinence is the complaint of involuntary leakage accompanied by or immediately preceded by urgency. Urgency is the complaint of a sudden compelling desire to pass urine which is difficult to defer. Frequency is the complaint by the patient who considers that he/she voids too often by day. Nocturia is the complaint that the individual has to wake at night one or more times to void.
By contrast, detrusor overactivity (DO) is a merely urodynamic finding which may or may not underly OAB. It is characterized by involuntary detrusor contractions during the filling phase which may be spontaneous or provoked. The International Continence Society 2002 report describes two types:
• Phasic detrusor overactivity is defined by its characteristic waveform and may or may not lead to urinary incontinence
• Terminal detrusor overactivity is defined as a single involuntary detrusor contraction occurring at cystometric capacity, which cannot be suppressed, and causes incontinence.
Voiding symptoms may often be related to bladder outlet obstruction (BOO), as a result of benign prostatic obstruction (BPO), and are characterized by increased detrusor pressure and reduced urinary flow rate. BPO is regularly associated with benign prostatic enlargement (BPE), whereas the term benign prostatic hyperplasia (BPH) should be reserved for those cases in which hyperplastic tissue changes in the prostate are pathologically confirmed.
However, the relationship between voiding symptoms and urodynamic markers of prostatic conditions is as weak as is the relationship between OAB and DO (Chatelain, 2000).
6.2 Epidemiology of OAB
Voiding symptoms have been shown to be the most common LUTS in men, however, women also commonly present with voiding symptoms. On the other hand, four of the five most bothersome LUTS in men are storage (OAB) symptoms. Prostatic pathology and co-existing OAB symptoms are not always causally related, and many men with OAB symptoms do not have BOO. However, OAB symptoms are highly prevalent in men: according to two telephone interview-based prevalence studies, they affect 16% of men and women in Europe and the US, with a striking age-related increase in both sexes, starting around the age of 40. Milsom et al. found a prevalence of OAB of 42 % in men older than 75 years.
• The latest international population-based survey, the EPIC study, confirmed these findings, i.e. OAB was equally common in men (11%) and women (13%) and storage, voiding, and postmicturition symptoms showed a similar distribution in both sexes. These data demonstrate that storage symptoms are not sex specific and that the prostate is often not the underlying cause of LUTS in men. They rather infer that LUTS are age-related and prevalent in both male and female patients, with a similar distribution of storage and voiding symptoms. However, although men and women had the same prevalence of OAB overall (16.0% and 16.9%, respectively), men were shown to have a higher prevalence of “OAB dry” (13.4% as opposed to 7.6% in women) and women had a higher prevalence of “OAB wet” (9.3% as opposed to 2.6% in men)
6.3 Pathophysiology of OAB
In keeping with the clinical notion that LUTS, and in particular OAB, are only poorly correlated with distinctive urodynamical findings, the up-to-date prevailing theories regarding the development of OAB are based on intrinsic bladder dysfunctions of multiple origin. Four theories, not mutually exclusive, have been put forth to account for bladder OAB:
1. The neurogenic hypothesis: reduced peripheral or central inhibition increases activation of the micturition reflex and contractions associated with the overactive bladder. This mechanism is the key principle in cases of neurogenic detrusor overactivity.
2. The myogenic hypothesis: changes to the excitability and coupling of smooth muscle cells with other myocytes or interstitial cells leads to the generation of uninhibited contractions. For example, bladder hypertrophy due to outlet obstruction may lead to so-called patchy denervation (German et al., 1995; Charlton et al., 1999; Drake et al, 2000; Mills et al., 2000). Smooth muscle cells deprived of their innervation show an up-regulation of membrane receptors and may have a higher excitability.
3. The urotheliogenic hypothesis: changes in the sensitivity and coupling of the suburothelial myofibroblast network lead to an enhancement of spontaneous detrusor activity.
4. The modular autonomous hypothesis: structures within the bladder wall coordinate to drive spontaneous contractions, which become enhanced in pathology.
6.4 Implications for diagnostic work-up and management
This paradigm shift in the clinical understanding of LUTS, namely that the bladder is the central organ in the pathogenesis, has a direct bearing on the assessment and management of LUTS.
As presence of the OAB syndrome is established on the basis of patient history, frequent flow charts, and questionnaires, it is common practice to employ conservative management (lifestyle interventions) and oral pharmacotherapy (antimuscarinics) without a urodynamic diagnosis. Trials of conservative and/or drug therapy for 6 to 12 weeks are regarded as reasonable before commencing invasive diagnostics.
The relevance of urodynamical testing remains controversial: detrusor overactivity has been shown to occur in 60% of asymptomatic women undergoing ambulatory urodynamics (Heslington and Hilton, 1996), and in a study of over 500 men with LUTS, only 53 % were found to have BOO. (Figure 6.1)
• If bladder outlet obstruction is indicated by symptom assessment or uroflowmetry indicates bladder outlet obstruction, treatment should be commenced with an A1-receptor antagonist
• If the prostatic gland is significantly hypertrophied, additional use of 5α-reductase inhibitor is recommended
• If the patient's condition does not show adequate improvement, antimuscarinics should be added for treatment of overactive bladder symptoms no matter if bladder outlet obstruction is present or not
• Urodynamic measurements should be performed in those cases where there is no symptom improvement with A1-receptor antagonists, antimuscarinics, 5α-reductase inhibitors or combination therapy (Figure 6.2).
Abdel-Aziz KF, Lemack GE (2002) Overactive bladder in the male patient: bladder, outlet, or both? Curr Urol Rep 3: 445–51.Find this resource:
Abrams P (1994) New words for old: lower urinary tract symptoms for “prostatism” BMJ 308: 929–30.Find this resource:
Abrams P, Cardozo L, Fall M, Griffiths D, Rosier P, Ulmsten U, Van Kerrebroeck P, Victor A, Wein A (2003) The standardisation of terminology in lower urinary tract function: report from the standardisation sub-committee of the International Continence Society Urology 61: 37–49.Find this resource:
Brading AF (1997) A myogenic basis for the overactive bladder Urology 50: 57–67; discussion 68–73.Find this resource:
Brading AF, Turner WH (1994) The unstable bladder: towards a common mechanism Br J Urol 73: 3–8.Find this resource:
Chapple CR, Roehrborn CG (2006) A shifted paradigm for the further understanding, evaluation, and treatment of lower urinary tract symptoms in men: focus on the bladder Eur Urol 49: 651–8.Find this resource:
Chapple CR, Wein AJ, Abrams P, Dmochowski RR, Giuliano F, Kaplan SA, McVary KT, Roehrborn CG (2008) Lower urinary tract symptoms revisited: a broader clinical perspective Eur Urol 54: 563–9.Find this resource:
Eckhardt MD, van Venrooij GE, Boon TA (2001) Symptoms, prostate volume, and urodynamic findings in elderly male volunteers without and with LUTS and in patients with LUTS suggestive of benign prostatic hyperplasia Urology 58: 966–71.Find this resource:
de Groat WC (1997) A neurologic basis for the overactive bladder Urology 50: 36–52; discussion 53–6.Find this resource:
Drake MJ, Mills IW, Gillespie JI (2001) Model of peripheral autonomous modules and a myovesical plexus in normal and overactive bladder function Lancet 358: 401–3.Find this resource:
Hyman MJ, Groutz A, Blaivas JG (2001) Detrusor instability in men: correlation of lower urinary tract symptoms with urodynamic findings J Urol 166: 550–2; discussion 553.Find this resource:
Irwin DE, Milsom I, Hunskaar S, Reilly K, Kopp Z, Herschorn S, Coyne K, Kelleher C, Hampel C, Artibani W, Abrams P (2006) Population-based survey of urinary incontinence, overactive bladder, and other lower urinary tract symptoms in five countries: results of the EPIC study Eur Urol 50: 1306–14; discussion 1314–5.Find this resource:
Kanai A, Roppolo J, Ikeda Y, Zabbarova I, Tai C, Birder L, Griffiths D, de Groat W, Fry C (2007) Origin of spontaneous activity in neonatal and adult rat bladders and its enhancement by stretch and muscarinic agonists Am J Physiol Renal Physiol 292: F1065–72.Find this resource:
Milsom I, Abrams P, Cardozo L, Roberts RG, Thuroff J, Wein AJ (2001) How widespread are the symptoms of an overactive bladder and how are they managed? A population-based prevalence study BJU Int 87: 760–6.Find this resource:
Stewart WF, Van Rooyen JB, Cundiff GW, Abrams P, Herzog AR, Corey R, Hunt TL, Wein AJ (2003) Prevalence and burden of overactive bladder in the United States World J Urol 20: 327–36.Find this resource:
Temml C, Heidler S, Ponholzer A, Madersbacher S (2005) Prevalence of the overactive bladder syndrome by applying the International Continence Society definition Eur Urol 48: 622–7.Find this resource: