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From the * Department of Surgery and Experimental
Research, Faculty of Medicine, Cairo University, Cairo, Egypt; and the
Department of Surgery, Faculty of Medicine,
Menoufia University, Shebin El-Kom, Egypt.
| Correspondence to: Dr Ahmed Shafik, 2 Talaat Harb St, Cairo 11121, Egypt (e-mail: shafik{at}ahmedshafik.com). |
| Received for publication March 10, 2005; accepted for publication July 14, 2005. |
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Abstract |
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Key words: Electromyography, erection, impotence, corpora cavernosa, action potentials, erectile dysfunction
The sexual sensory signals are mediated through the pudendal nerve and sacral plexus to the sacral segments of the spinal cord, and are then transmitted to the cerebrum (Lue et al, 1984; Lepor et al, 1985; Steers, 1990). Also, local reflexes integrated in the sacral and lumbar spinal cord may share in the sexual reaction (Bradley and Teague, 1977; Benson et al, 1980; Tabatabai et al, 1986).
The bulbocavernosus reflex exhibits the response of the cavernosus muscles or the external anal sphincter (EAS) to stimulation of the glans penis (GP) or clitoris (Ertekin and Ree, 1976; Siroky et al, 1979; Bird and Hanno, 1998). It is used as a diagnostic tool in the diagnosis of erectile disorders.
A previous study has demonstrated that the base loop of the EAS extends uninterrupted across the perineum to the bulb of the penis where it becomes continuous with the bulbocavernosus muscle (BCM) (Shafik, 1999). While lying over the bulb, the muscle bundles were arranged in 3 groups: 1 median and 2 lateral. The median fibers form the "retractor penis muscle," which is inserted into the corpora cavernosus, while the lateral fibers or the "compressor bulbae muscle" are inserted into the perineal membrane (Shafik, 1999). Upon glans stimulation, both the conjoined EAS and BCM contract synchronously with identical latency and action potentials (Shafik, 1999). The BCM is an integral part of the EAS and the muscle in its entirety is given the name "anogenital muscle" (Shafik, 1999) since it plays a dual and synchronous role in fecal control and sexual response.
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Materials and Methods |
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Methods
The response of the ICM to EAS stimulation or squeeze was studied. With the
subject lying supine, the knee and hip joints flexed and the thigh abducted, a
concentric electromyographic (EMG) needle electrode (type 13L49 Disa,
Copenhagen, Denmark) measuring 45 mm in length and 0.65 mm in diameter was
introduced into each of the ICM and EAS. For the ICM, the ischial ramus with
the overlying crus penis or clitoris was palpated, and the needle electrode
was inserted into the muscle on the medial aspect of the ramus to a depth of
0.5 cm. An identical needle electrode was introduced 1 to 1.25 cm deep into
the EAS and at a distance of 0.75 to 1 cm lateral to the anal orifice.
The EMG activity was displayed on the oscilloscope of a standard EMG apparatus (type MES, Medelec, Woking, United Kingdom). Films of the potentials were taken on light-sensitive paper (linagraph type 1895; Kodak, Rochester, NY) from which measurements of the latency of the reflex and motor unit action potentials were made. The EMG signals were, in addition, stored on an FM tape recorder (type 7758A; Hewlett-Packard, Waltham, Mass) for further analysis as required.
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Before performing the experiment, we tested all subjects for the normality of the myoelectric activity of the EAS and ICM by means of stimulating them with a needle electrode that had been introduced into each of the 2 muscles separately and then recording the motor unit action potentials with the recording needle electrode. All the subjects recorded normal EMG activity of the EAS and ICM.
Anesthetization of the EAS and ICM
To test whether the response of the ICM to EAS stimulation was a direct or
reflex action, the ICM was anesthetized by injecting 2 mL of 2% lidocaine into
the muscle around the electrode. The response of the anesthetized ICM to EAS
stimulation was recorded after 20 minutes from lidocaine injection, and 3
hours later when the anesthetic effect had dissipated. The test was repeated
after EAS anesthetization and after individual infiltration of the ICM and EAS
with normal saline. The aforementioned experiments were also performed on the
contralateral ICM.
To ensure reproducibility of the results, the recordings were repeated at least twice in the individual subject, and the mean value was calculated. The results were analyzed statistically using the Student's t test and values were given as the mean ± SD. Significance was ascribed to P < .05.
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Results |
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The ICM did not exhibit resting electrical activity (Figure 1). EAS stimulation by a repeated series of 10 electrical stimuli of 200 µs duration at a frequency of 0.2 Hz and intensities between 0 and 100 mA produced an increase in the EMG activity of the ICM to a mean amplitude of motor unit action potentials (AMUAPs) of 267.8 ± 42.7 µV (range, 186-336; Figure 1). Upon anal squeeze, the ICM showed an increase of the AMUAPs to a mean of 224.5 ± 45.3 µV (range, 164-295; Figure 2). Repeated and successive EAS stimulation did evoke the ICM response. The response was weaker in women than in men and in the multiparous than nulliparous women, although the difference was not significant (P > .05). The latency of the response measured from the start of EAS stimulation to the first deflection of the reflex muscle action potential complex recorded a mean of 17.4 ± 1.6 ms (range, 14-19) on EAS electrostimulation (Figure 1) and 17.7 ± 1.6 (range, 13-19) for anal squeeze (Figure 2).
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The aforementioned results were reproducible with no significant difference when the test was repeated in the individual subjects.
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Discussion |
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Role of the ICM in Corporeal Congestion and Erection
During sexual intercourse, BCM contraction was found to be associated with
synchronous contraction of the EAS
(Shafik, 1999). EAS
contraction presumably acts to prevent the leakage of flatus or fluid stools
at coitus that might lead to coitus interruptus. Meanwhile, the current study
has demonstrated that EAS contraction effected ICM contraction, which appears
to have a role in the erectile mechanism. The ICM, as it is directed forward
from its origin in the ischial tuberosity with upward inclination toward the
corpora cavernosa where it is inserted, functions on contraction to pull the
penis backward against the ischial tuberosity. The penile root consists of the
2 crura and the bulb. By pulling the penis backward, the ICM appears to fix
the penile shaft to its root against the ischial tuberosity. This action seems
to support and strengthen the penile shaft during vaginal penetration and
thrusting. Meanwhile the ICM, inserting in a "belt" form across
the proximal part of the 2 corpora cavernosa, presumably acts on contraction
as a constricting band that appears to compress the deep dorsal vein of the
penis. This seems to hamper the cavernosal venous return, and thus, augments
penile erection. Furthermore, studies have shown that ICM contractions were
associated with elevated intracavernous pressure and that ICP changes were
always in phase with changes in the ICM EMG
(Lavoisier et al, 1986).
Results of the study suggest involvement of the ICM in the process of penile
rigidity; the muscle produces suprasystolic intracavernous pressure, which
would result from pudendal motoneural activity
(Schmidt and Schmidt, 1993; Bernabe et al, 1999). The
studies have also shown that the GP erections were associated with
suprasystolic corpus spongiosum pressure (CSP) peaks concurrent with
bulbospongiosus (BS) muscle bursts
(Schmidt et al, 1995).
Measures of CSP and BS EMG activity were found to vary significantly with
glans erection intensity (Schmidt et al,
1995).
Role of the ICM in Penile Thrusting
ICM contraction seems to share in the mechanism of penile lifting to above
the horizontal level during erection. While flaccid, the penis points downward
(Figure 4) but on erotic
stimulation, is elevated upward to a near horizontal position of varying
degrees. This penile position seems to be effected jointly by the increased
arterial blood flow and the inhibited venous drainage that induces cavernous
tissue turgidity and tumescence. The resulting high intracorporeal pressure
stretches and elevates the penis to subhorizontal or horizontal level. The
elevation effect of the increased intracorporeal pressure on the flaccid penis
is similar to the stretch and elevation of an empty glove's finger on
inflation.
Originating from the ischial tuberosity and ramus, the ICM passes forward with an upward inclination and terminates at the sides and dorsum of the corpora cavernosa (Figure 4). It thus acts as a lever that probably comes into action after the penis is elevated horizontally by both the turgidity and increased intracorporeal pressure. While the penis is in the horizontal position, the lever action of the contracting ICM effects upward elevation of the penile shaft to above the horizontal level and acts to keep the penis in this position during penile thrusting at coitus (Figure 4).
The Anocavernosal Excitatory Reflex
The ICM contraction upon contraction of the EAS postulates a reflex
relation between the 2 actions. The constancy of this relation is evidenced by
its reproducibility, and its reflex nature is confirmed by its absence upon
anesthetization of either the EAS or the ICM, the 2 possible arms of the
reflex arc. We call this hitherto unrecognized reflex relation the
anocavernosal excitatory reflex. Lidocaine blocks C and A 
-fibers,
which are responsible for pain and reflex activity
(Yokoyami et al, 2000; Silva et al 2002). It appears
that, on EAS stimulation, impulses pass to the sacral spinal cord, which
eventually sends impulses to the ICM, effecting its contraction. Impulses are
apparently transmitted along the pudendal nerve. Anesthetization of the EAS or
ICM presumably blocks their innervation so that nerve impulses cannot be
transmitted from either the EAS to the spinal cord or from the spinal cord to
the ICM.
Diagnostic Role of the Anocavernosal Excitatory Reflex
The anocavernosal reflex may prove to be of diagnostic significance in
erectile dysfunction. Detectable changes in the latency or the MUAPs of the
reflex would indicate muscle or nerve damage from a disease of the spinal
cord, spinal nerve roots or peripheral nerves, or from a central lesion.
Further studies may prove that the anocavernosal excitatory reflex has the
potential of an effective investigative tool in the diagnosis of sexual
disorders.
On the other hand, the anocavernosal reflex seems to be more constant than the bulbocavernosus reflex, as the former is reproducible in the individual subject. The reported constancy of the bulbocavernosus reflex in normal subjects was questioned by investigators who found it inconstant and of variable latencies in the individual subject (Rattner et al, 1958; Lavoisier et al, 1989). The bulbocavernosus reflex is, however, currently used as a test to identify whether an erectile dysfunction is of neurogenic origin (Siroky et al, 1979; Ertekin et al, 1985). In this regard, the anocavernosal reflex could replace the bulbocavernosus one, a point that needs further study.
In conclusion, the ICM contracted on EAS contraction. This effect is suggested to be reflex and mediated through the anocavernosal excitatory reflex. ICM contraction seems to share in the erectile mechanism by elevating the penile shaft to above the horizontal level by means of its lever action. The reflex might prove of diagnostic significance in sexual function disorders, a point that needs further study.
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Acknowledgments |
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References |
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indicates electrostimulation.
