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Application
of pudendal evoked potentials in diagnosis of erectile dysfunction
Guang-You
ZHU, Yan SHEN Institute
of Forensic Sciences, Ministry of Justice, Shanghai 200063, China Asian J Androl 1999 Sep; 1: 145-150 Keywords:
AbstractAim: Extensive neurophysiological investigations were carried out in 100 healthysubjects and 84 patients with penile erectile dysfunction. Methods: Following examinations were performed, spinal and scalp somatosensory evoked potentials (SEPs) to stimulation of the dorsal nerve of penis, motor evoked potentials (MEPs) from bulbocavernosus (BC) in response to scalp and spinal root stimulation, and measurement of sacral reflex latency (SRL) from anal sphincter (AS). Results: In the healthy subjects, the mean sensory total conduction time (sensory TCT),as measured at the peak of the scalp P1 (P40) wave was 39.73 ms. The mean sensory central conduction time (sensory CCT=spinal-to-scalp conduction time) was 28.98 ms. The mean peripheral conduction time (PCP) was 9.40 ms. Transcranial brain stimulation was performed by using a magnetic stimulator during voluntary contraction of the examined muscle. Spinal root stimulation was performed at rest. Motor total conduction time (motor TCT) to BC muscles was 20.48 ms. Motor central conduction time (motor CCT) to sacral cord segments controlling BC muscles was 14.42 ms at rest. The mean SRL was 35.13 ms. Conclusion: Combined or isolated abnormalities of SEPs, MEPs, and SRL were found in patients with erectile dysfunction.1 Introduction Some
objective tools have recently been developed in order to differentiate
the nature of erectile dysfunction, i.e., nocturnal penile tumescence
(NPT)[1,2], electrically
induced bulbocavernosus(BC) reflex[3], penile blood pressure,
Doppler sonography, and plethysmography of penis[4,5]. These
new objective aids will probably reveal increasing cases of erectile dysfunction
due to organic causes, especially those of neurological origin. Recent
trends indeed, have shown that
erectile dysfunction is not uncommon in male patients with diseases
of the nervous system[6,7]. 2 Materials and methods 2.1
Subjects One
hundred adult healthy males (Han race, mean age=38 years old) without
any known neurological disorder and 84 patients (Han race) having erectile
dysfunction alone or in conjunction with various diseases, were investigated.
Of these patients, 31 cases developed erectile dysfunction after pelvic
fracture(mean age=31 years old),10 after spinal injury (mean age=42 years
old),16 with diabetes(mean age=50 years old) and 27 have a history of
masturbation more than 5 years(mean age=31 years old). 2.2
SEPs: stimulating and recording methods[8] The
dorsal nerves of the penis were stimulated via 2 ring electrodes, 1.5
cm apart, wrapped around the penile shaft, with the cathode placed proximally.
The response was bipolarly recorded at the spinal level (Th12-L1) and
from the scalp, roughly overlying the sensorimotor cortex for the genital
region (2 cm behind Cz, referred to Fz of the international 10-20 system).
The subject was asked to relaxedly lie down on a bed at a supine position.
Stimuli consisted of rectangular pulses 0.1 ms in duration, 3-4 times
above the subjective threshold and a 2.77/s repetition rate. The subjective
threshold was defined as the lowest perceivable intensity. The tracing
represented the final average of 250 artifact-free responses. This gave
reproducible SEPs in a reasonable time. The latency of the spinal response
was measured at the peak of the initial negative deflection(sensory peripheral
conduction time=sensory PCT). The latency of the scalp SEP was taken at
the first reliable positive peak(wave P40=sensory total conduction time=sensory
TCT). By subtracting the former from the latter, the sensory central conduction
time (sensory CCT) was obtained. 2.3
MEPs: stimulating and recording methods[8] Brain and sacral root stimulation was performed with simultaneous recording of the response in BC muscle with surface electrodes. Three different motor conduction times were determined: a motor total conduction time (motor TCT) which represents the transit time from brain to target muscle, a motor peripheral conduction time (motor PCT) which corresponds to the sacral roots to the target muscle transit time and, by subtracting the latter from the former,a motor central conduction time (motor CCT=brain to sacral roots conduction time) was obtained. Stimulation was performed via a magnetic stimulator (Cadwell MES-10) with a coil of 9 cm internal diameter applied in direct contact to the skin. The intensity of magnetic stimulation can be expressed as a percentage of the maximum (=2.5 Tesla). The stimulation was performed with the posterior edge of the coil applied 2 cm behind Cz. First,the stimulation intensity was progressively increased until an MEP could be recorded in the muscles with the subjects at rest. The transcranial stimulation was then repeated with the same intensity during a transient and moderate voluntary contraction of the examined muscles (facilitation procedure). Spinal root stimulation was performed with the center of the coil applied 5 cm laterally to the spine at the level of the right iliac crest. MEPs were recorded only at rest. Latencies were measured at the onset of the first steady deflection from the baseline. Both
SEPs and MEPs were obtained with a poststimulus analysis time of 100 ms and
50 ms, respectively, and a filtering bandpass of 10-500 Hz. They were
repeated several times and superimposed to facilitate discrimination of
stimulus locked from random activity. A relative negativity in grid 1
of the amplifier provoked an upward deflection. 2.4
SRL: stimulating and recording methods[8] 3 Results 3.1
Healthy subjects SEPs:
The cortical response had a w-shaped wave form. The mean latency
of the first positive peak (P1) measured as total sensory conduction time
(TCT) was 39.73 ms
(+3s=45.82 ms) (Table 1). Table
1.Somatosensory evoked potentials (SEPs) and motor evoked potentials (MEPs)
of 100 healthy adult males (latencies in ms)
A
spinal response of low voltage was recorded. This potential was seldom
well defined, being initially negative and predominantly monophasic. The
mean onset latency
of the spinal response measured as PCT was 9.40 ms (+3s=13.78 ms). The
CCT as measured from the onset of the spinal EP to the cortical P1 peak
was 28.98 ms (+3s=37.`47 ms). SRL:
SRL was recorded in AS. The mean latency for the first deflection was
35\^13 ms (+3s=45.69 ms)in the anal sphincter (Table 1). MEPs:
Brain stimulation was performed with facilitation and spinal stimulation
at rest. The scalp and spinal motor evoked potentials were recorded. In
the BC, the TCT and PCT
were 20.48 ms (+3s=27.11 ms) and 5.98 ms (+3s=10.84 ms), respectively.
The Mean CCT was 14.42 ms (+3s=22.10 ms) (Table 2).
The intensity of transcranial stimulation ranged between 60 %-90 % of
the stimulator's output
in the healthy subjects and 60%-100% of the output in the patients. 3.2
Patients We
briefly describe here the results of a few groups of patients with erectile
dysfunction. Abnormalities were defined when SEPs, MEPs or SRL were absent
or when latencies or conduction times were more than 3s from the control
mean, provided the height was in the range of the healthy male group. 3.3
Patients with pelvic fracture We
have investigated 31 cases of the patients having erectile dysfunction
after pelvic fracture. The results showed that 12 had abnormal pudendal
EPs. The rate of abnormality was 38.70%. (Table 2) Table
2.Pelvic fracture (latencies in ms, ?: absent, -: not tested).
3.4
Spinal damage patients There
were 10 patients in this group. The results showed that 5 had abnormal
pudendal EPs. The rate of abnormality was 50 %. (Table 3) Table
3. Spinal damage
(latencies in ms, ?: absent, -: not tested).
3.5
Diabetes patients We
have investigated 16 cases of diabetes patients. The results showed that
8 had abnormal pudendal
EPs. The rate of abnormality was 50%. (Table 4) Table
4. Diabetes patients (latencies in ms, ?: absent, -: not tested).
3.6
Masturbation patients We
have tested 27 patients with a history of 5 or more years of consistent masturbation.
Nine had abnormal pudendal EPs. The rate of the abnormality was 33.33%.
(Table 5) Table
5. Masturbation patients (latencies in ms, ?: absent, -: not tested).
4 Discussion 4.1
About healthy males Electrophysiological
techniques have opened new perspectives in the diagnosis of erectile dysfunction,
providing an objective way to test afferent and efferent somatic pathways
governing the erectile ability. In
agreement with other reports[9-11],we found that the pudendal
EPs in healthy subjects on stimulation of the penile are relatively easy
to elicit and demonstrate a consistent morphology and latency. SEP
examine the afferent pathways from the dorsal nerve of the penis to the
sensorimotor cortex. Although the role of this nerve is not well understood
in humans, its integrity is thought to be crucial in the maintenance of
erection, transmitting sensory impulses from the glans penis to the brain.
In agreement with the general results in the literature[8-10], we found
that the latency of scalp evoked potential (P1) was 39.73 ms (+3s=45.82
ms) and that of PCT was 9.40 ms (+3s=13.78 ms). Measurement
of SRL is useful in the evaluation of the spinal and peripheral somatic
innervation of the genito-urinary tract. The sacral reflex pathway consists
of the dorsal nerve of the penis, the S2-S4 cord segments, and the motor
branch of the pudendal nerve innervating the BC muscles, and anal and
urethral sphincters. SRL is also a useful index to examine the integrity
of parasympathetic nerves controlling penile erectile function. In the
present study the latencies of reflex responses in healthy male are 35.13
ms (+3s=45.69), which are the same as those previously reported[9-11]. Spinal
and transcranial magnetic stimulation is a complementary method used to
examine the central and peripheral motor pathways leading to the striated
muscles of the urogenital system. It is known that the motor pathway has
an important role in developing and maintaining the rigidity of penile
erection. In general, 80% of patients with spinal cord injury experience
erectile dysfunction. The
crucial problem is the duration of the erection: tumescence and rigidity
tend to fade away
quickly and the patient is unable to perform intercourse. This is thought
to be due to the injury of the central and/or peripheral motor pathway
leading to the striated muscles of the urogenital system. In our study
the MEPs in BC after transcranial stimulation have a latency of about
20.48 ms (+3s=27.11 ms) in the contracted state of pelvic floor muscles.
Spinal root stimulation provokes a response with a latency of about 5.98
ms (+3s=10.84 ms). These latencies are slightly shorter than those reported
previously[10]. The reason is perhaps due to the difference
in the intensity of the stimulation used. 4.2
About patients Abnormal SEPs, MEPS, and SRL were obtained in different ways and with variable frequencies due to varied locations of lesions in the peripheral and central nervous systems. Although
erectile dysfunction is known to occur in up to 50% of patients
with posterior urethral rupture after traumatic pelvic fracture[12],its
exact mechanism has remained unclear. The origin is usually assumed to
be neurovascular, without any differentiation between these 2 factors.
Recent advances in pudendal evoked potentials have permitted a more accurate
neurophysiologic evaluation of these injuries. Of our 31 patients with
a history of pelvic
fracture together with complete
or incomplete urethral disruption, 12 (38.70%) demonstrated distinct abnormal
pudendal evoked potentials. These results suggest that in these patients
the causes of the erectile dysfunction may be in part the injury
of pudendal nerves. In
many cases of spinal cord lesions, there is no difficulty in explaining
the cause of erectile dysfunction[13]. However, some patients
may suffer from erectile dysfunction alone or together with urinary incontinence,
especially those cases with mild cauda/conus traumatic lesions. The test
of the pudendal EPs in spinal lesions unmasked clinical and subclinical
involvement of the lower sacral and lower lumbar roots, respectively.
In the higher level of spinal cord involvement, SRL had no practical value
and was essentially normal, while both SEPs were more
important in showing the degree of involvement in the afferent spinal
tracts. In the present study we have investigated 10 patients, who developed
erectile dysfunction after spinal traumatic injuries with sensory disturbances
in the area of the pudendum and/or lower extremities. Six of them (50%)
showed abnormal pudendal EPs. In these patients, there was a high incidence
of the pudendal nerves injury. Different
types of erectile dysfunction were well documented in diabetes mellitus
and it was believed that most cases had autonomic and somatosensory neuropathy.
In our study we examined 10 cases of erectile dysfunction patients with
diabetes and found that 3 of them have abnormal pudendal Eps (Table 3). It
is thought that masturbation is a bad habits but not harmful to the health.
It is very interesting that we have encountered many young patients, who
complained of erectile dysfunction without any apparent causes except
a history of long continued masturbation. After careful examination we
found 9 of 27 cases (33.33%) having abnormal pudendal EPs. We do not quite
understand the relationship between erectile dysfunction and masturbation,
which seems to be worthy of further investigation. References [1]
Bradley WE, Timm GW, Gallagher JM, Johnson BK. New method for
continuous measurement of nocturnal penile tumescence and rigidity.
Urololgy 1985; 26: 4-9. Correspondence
to Prof. Guang-You ZHU.
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