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Electrophysiological assessment of incontinence
97 Electrophysiological Assessment of Incontinence M. Swash and S. Snooks. The Sir Alan Parks Physiology Unit, St. Mark's Hospital, City Road, London ECIV 2PS.
Slowed conduction in the pudendal nerves has been demonstrated in patients with idiopathic (neurogenic) anorectal incontinence (Kiff and Swash,
1984).
We have used
two new methods, digitally directed pudendal nerve stimulation and transcutaneous spinal stimulation to measure the latency from the point of stimulation to the evoked muscle action potential (MVAP) in the striated urethral sphincter musculature (Snooks and Swash,
1984).
These methods have thus enabled motor conduction to be
assessed to both the external anal sphincter and urethral striated sphincter muscles in patients with double and urinary incontinence.
Thus allowing comparisons
to be made between control subjects and three groups of patients with; incontinence, double incontinence, and urinary incontinence.
faecal
In 20 normal subjects
the perineal nerve terminal latency following pudendal nerve stimulation, using an indwelling intra-urethral surface electrode mounted on a catheter for recording, was 2.4 ~ 0.2 ms.
In a group of 30 patients with
'idiopathic' double incontinence,
and 12 patients with stress (genuine) urinary incontinence, the perineal nerve terminal latencies were 4.2 ~ 1.3 ms and 3.9 ~ 0.8 ms respectively. both groups compared to control subjects).
(P < 0.01 for
In the 30 patients with double
incontinence and 12 with urinary incontinence the spinal nerve terminal latencies to the urethral striated sphincter muscle were 6.1 t 1.3 and 5.6 ~ 1.7 ms from LI and 4.9 ~ 0.8 ms and 4.5 ~ 1.2 ms from L4 respectively.
In 16 control subjects
the latency to the urethral striated sphincter muscles was 4.8 3 0.3 ms and 4.1 0.3 ms from LI and L4 respectively.
Significant differences from controls only
occurred in the double incontinent group (P < 0.01). These results indicate damage to the distal part of the innervation of the urethral sphincter musculature in double and urinary incontinence.
This distal
nerve lesion is similar to that which we have previously reported in the pudendal innervation of the external anal sphincter in patients with faecal incontinence.
REFERENCES Kiff E.S. and Swash M. Snooks S.J. and Swash M.
(1984). (1984).
Brit. J. Surg., 71,
614-616.
Brit. J. Urol., 56, 406-409.
Slowed conduction in the pudendal nerves has been demonstrated in patients with idiopathic (neurogenic) anorectal incontinence (Kiff and Swash,
1984).
We have used
two new methods, digitally directed pudendal nerve stimulation and transcutaneous spinal stimulation to measure the latency from the point of stimulation to the evoked muscle action potential (MVAP) in the striated urethral sphincter musculature (Snooks and Swash,
1984).
These methods have thus enabled motor conduction to be
assessed to both the external anal sphincter and urethral striated sphincter muscles in patients with double and urinary incontinence.
Thus allowing comparisons
to be made between control subjects and three groups of patients with; incontinence, double incontinence, and urinary incontinence.
faecal
In 20 normal subjects
the perineal nerve terminal latency following pudendal nerve stimulation, using an indwelling intra-urethral surface electrode mounted on a catheter for recording, was 2.4 ~ 0.2 ms.
In a group of 30 patients with
'idiopathic' double incontinence,
and 12 patients with stress (genuine) urinary incontinence, the perineal nerve terminal latencies were 4.2 ~ 1.3 ms and 3.9 ~ 0.8 ms respectively. both groups compared to control subjects).
(P < 0.01 for
In the 30 patients with double
incontinence and 12 with urinary incontinence the spinal nerve terminal latencies to the urethral striated sphincter muscle were 6.1 t 1.3 and 5.6 ~ 1.7 ms from LI and 4.9 ~ 0.8 ms and 4.5 ~ 1.2 ms from L4 respectively.
In 16 control subjects
the latency to the urethral striated sphincter muscles was 4.8 3 0.3 ms and 4.1 0.3 ms from LI and L4 respectively.
Significant differences from controls only
occurred in the double incontinent group (P < 0.01). These results indicate damage to the distal part of the innervation of the urethral sphincter musculature in double and urinary incontinence.
This distal
nerve lesion is similar to that which we have previously reported in the pudendal innervation of the external anal sphincter in patients with faecal incontinence.
REFERENCES Kiff E.S. and Swash M. Snooks S.J. and Swash M.
(1984). (1984).
Brit. J. Surg., 71,
614-616.
Brit. J. Urol., 56, 406-409.