Electromyography in urinary retention and obstructed voiding in women.

In 1988, it was proposed that an abnormality of the striated urethral sphincter was a cause of abnormal voiding or urinary retention in young women (1). The abnormality of the striated urethral sphincter was an electromyographic (EMG) activity detected using a concentric needle electrode, and was of a type that would generally be associated with a failure of relaxation. Also, many women had features of polycystic ovary syndrome, i.e. hirsutism and acne, with polycystic ovaries demonstrated by ultrasound. The EMG abnormality recorded from the striated urethral sphincter may have two components: complex repetitive discharges (CRD) and decelerating bursts (DB). The CRDs are observed to occur at about the same frequency as the background Ž ring motor units or alternatively as bursts of activity. Analysis of the complexes shows that the “jitter” between individual constituent potentials is so low that the activity is probably due to ephaptic transmission between muscle Ž bres (2, 3). The decelerating bursts result from a volley of CRDs in which the terminal components Ž re at a steadily decreasing rate. This produces a sound over the EMG recording apparatus that sounds somewhat like the activity found in myotonic conditions, but when heard in profusion, produced by many different complex generators, sounds like underwater recordings of whales (4). The basis for this type of activity is not fully understood but it denotes an excessive excitability of the muscle membrane as seen in other myotonic-like disorders associated with channelopathies (5). If the hypothesis is correct that a local striated muscle abnormality is the cause of impaired sphincter relaxation, various functional consequences would be expected. The repetitive Ž ring of complexes through ephaptic activity is thought to produce enlargement of muscle Ž bres by the effects of work hypertrophy and is seen, albeit uncommonly, in skeletal muscle in patients who may present with unilateral calf hypertrophy (2, 6). Working on the hypothesis that the CRDs might cause enlargement of the sphincter muscle, we estimated sphincter volume using ultrasound and have found the sphincter complex is signiŽ cantly larger in women with urinary retention and who have the EMG abnormality, compared to women with retention but without the EMG abnormality (where the cause of retention is unknown) (7). Furthermore, recordings of the maximum urethral closure pressure in the same two groups of women have shown that the mean MUCP in those with the EMG abnormality is signiŽ cantly higher than in those without (7). It is unlikely that the abnormal sphincter activity results in retention simply by obstruction; rather, it is likely to have a functional inhibitory effect on the micturition re ex. Experimental observations in the cat have shown that proprioceptive afferents from the striated urethral sphincter inhibit detrusor contraction (8, 9). This may be the underlying mechanism for retention in women. This being the case, the clinical manifestations of the EMG abnormality will depend on its secondary effect on the detrusor. It appears that in some women with the sphincter EMG abnormality