The management of the unstable bladder poses a difficult problem. Patients present with a diversity of symptoms from disturbing frequency, nocturia and urgency to socially unacceptable incontinence. These symptoms result from uninhibited bladder contractions which the patient is unable to control and may even be unaware that they are occurring. Detrusor instability itself may occur as a consequence of overt neurological disease, or in the male, as a result of outflow tract obstruction (Turner-Warwick et al., 1973). However, the majority of patients belong to a primary (idiopathic) group in which the aetiology is unknown. A variety of operations to denervate the bladder have been designed in an attempt to control these uninhibited detrusor contractions but the results are disappointing. Recently, however, some success has been reported in the treatment of detrusor instability both by Torrens and Griffith (1974) using a more selective denervation technique and by Dunn, Smith and Ardran (1974) using prolonged bladder distension; but both of these are invasive techniques. Drugs remain the first line of treatment for primary detrusor instability. The commonly used drugs aim at modifying detrusor activity either by direct anticholinergic activity or by the stimulation of β adrenergic receptors. Although Moolgaoker et al.(1972) have reported good results from drug treatment, other workers have achieved only limited success, often with a high incidence of unacceptable side-effects in the therapeutic dose range (Brown, Arnold and Worth, 1973; Stanton, 1973) and this has also been our experience. Following a recent trial of bromocriptine (2 bromo-α-ergocriptine: C.B. 154. Sandoz)in males with benign prostatic hypertrophy it was suggested that this drug might also have a place in the treatment of the unstable bladder (Farrar and Pryor, 1976). This paper reports our preliminary experience with the use of bromocriptine in the treatment of patients with detrusor instability.
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Farrar et al. (1976) studied this question.
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