The Overactive Bladder


Until the most recent definition of the International Continence Society (ICS), the term of bladder overactivity referred to urodynamic status. The bladder was considered as overactive when objectively shown to contract, spontaneously or on stimulation, during the filling phase of a cystometro-gram while the patient is attempting to inhibit micturition [2]. Furthermore, in the first standardization report, the threshold of 15cmH20 was necessary to conclude that an uninhibited bladder was related to detrusor overactivity [11]. The definition currently endorsed by the ICS is that of a symptom syndrome suggestive of lower urinary tract dysfunction characterized by urgency, with or without urge incontinence, usually with increased daytime frequency and nocturia, in the absence of local or metabolic factors explaining these symptoms [2]. This overactive bladder syndrome can also be described as urge syndrome or urgency-frequency syndrome.

Diagnosis of Overactive Bladder Clinical Parameters

The major role of cystometry in the diagnosis of overactive bladder (OAB) has recently been dissipated since overactive bladder is now taken to be a medical condition referring to the symptoms of frequency and urgency, with or without urge incontinence [2]. Thus the diagnosis of the OAB symptom complex is based upon the subjective perception of lower urinary tract dysfunction. However, as emphasized above, the OAB is a complex of symptoms that can be diagnosed as such only when there is no proven urinary tract infection or other obvious pathology.

Urgency is the complaint of a sudden compelling desire to pass urine that is difficult to defer [2]. Increased daytime frequency, or pollakiuria, is the complaint of voiding too often during the day [2]. Nocturia is having to get up one or more times at night to void [2]. Urge incontinence is characterized by a strong desire to void coupled with an involuntary loss of urine [2]. Since asking patients to record micturition and symptoms for a period of days provides invaluable information, measurement of lower urinary tract symptoms is based on a bladder diary. The bladder diary records the times of micturition and voided volumes, episodes of incontinence, pad usage and other information such as fluid intake, the degree of urgency and the degree of incontinence [2]. Validated questionnaires may also be useful for recording symptoms, their frequency, severity and bother, and the impact on quality of life [89, 168, 141].

Urodynamic Parameters [60]

Even if urodynamic testing is not yet required to define an OAB syndrome, it is often suggestive of urodynamically demonstrable detrusor overactivity. Detrusor overactivity is the urodynamic observation of involuntary detrusor contractions, whatever their amplitude, during the filling phase, which may be spontaneous or induced (Fig. 4).

The main interest of cystometry in patients suffering from OAB syndrome is to improve the diagnostic evaluation both by defining the underlying pathophysiology and by indicating treatment. However, there are controversial data concerning the correlation between OAB symptoms and urodynamic findings. Indeed, most authors do not recommend a filling and voiding study in the first-line treatment of OAB, but only in previously failed and complicated cases of OAB and prior invasive therapy.

Classification of Overactive Bladder

In some cases, detrusor overactivity may be further classified according to cause. Three main distinguishable types of detrusor overactivity are

Oab Electrical Stimulation
Fig. 4. Urodynamical characteristics of detrusor overactivity

usually considered [119]. The first is neurogenic detrusor overactivity (formerly detrusor hyperreflexia) in which there is a relevant neurological condition. Secondly, there is idiopathic detrusor overactivity (formerly detrusor instability) in which there is no defined cause. Finally, detrusor instability is related to bladder outlet obstruction or other conditions irrelevant for defining neurological causes.


The different forms of overactivity may result from neurogenic or myo-genic causes, or a combination of the two. These neurogenic and myogenic defects could be due to a wide variety of pathogenic conditions, which may be classified in 6 principal subtypes [119, 149].

1) Neurologic illness or injury, most commonly traumatic or medical spinal cord injury, demyelinating disease including multiple sclerosis, supraspinal disease such as stroke, Parkinson disease, tumor, degenerative disease or dementia. The neurogenic mechanism of OAB may be related to various changes in both peripheral and central neural pathways, such as a decreased peripheral or central inhibitory control, an enhancement of excitatory transmission in the micturition reflex pathway, an increased primary afferent input from the lower urinary tract, the emergence of bladder reflexes that are resistant to central inhibition, or some combination of these factors [50].

2) Bladder outlet obstruction, which alters sensory and motor aspects of micturitional reflexes and points to an abnormal activity pattern of the detrusor cells characterized by a spontaneous mechanical activity, a hy-persensitivity to acetylcholine with depressed responses to intrinsic nerve stimulation and increased sensitivity to direct electrical stimulation [Brad-ing 1997].

3) A hypersensitivity-induced overactivity due to the emergence of a aberrant voiding reflex mediated by unmyelinated capsaicin-sensitive C-afferents, which may be caused by neurogenic disease or factors not yet fully understood [109, 50].

4) Urethral weakness due to smooth sphincter deficiency and pelvic relaxation in middle-aged and elderly women [56].

5) Detrusor hyperactivity and impaired contractility in elderly patients [123].

6) So-called idiopathic bladder overactivity, which has no defined cause but may be due to an unknown combination of some of the above-mentioned factors [57, 124].

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