International Journal of Osteopathic Medicine 9 (2006) 66e71

www.elsevier.com/locate/ijosm

Case report

Manipulative treatment for idiopathic impotence in

a 24-year-old water polo player
William Thomas Crow*
Neuromusculoskeletal Residency Program, Department of Medical Education, Florida Hospital East Orlando Osteopathic Program,
7975 Lake Underhill Road, Suite 210, Orlando, FL 32822, USA
Received 7 July 2005; received in revised form 23 December 2005; accepted 11 January 2006

Abstract

This case report discusses the manipulative treatment of a 24-year-old water polo player for impotence and its potential causes.
2006 Elsevier Ltd. All rights reserved.

Keywords: Impotence; Impotence medicine; Osteopathy; Osteopathic manipulation; Manipulation; Erectile dysfunction

1. Case history postage stamps around the penis and if it is broken

A 24-year-old water polo player with no signicant
past medical history and no recent history of trauma
presented to an osteopathic manipulation specialist
with a six month history of impotence. In further discus-
sion with the patient he revealed that he had been kicked
and had been hit in the groin and testicles multiple times
during his water polo matches stating, that there was
a lot that went on under the water that the referees never
saw.
The patient denied loss of libido and stated that he
had no relationship diculties at the time his symp-
toms began. The patient had a negative home penile
tumescence study (no nocturnal erection) as determined
using a RigiScan home monitor (Timm Medical Tech-
nologies Inc., USA). Nocturnal erections are com-
monly evaluated by tests known as nocturnal penile
tumescence (NPT) studies. There are various forms of
NPT study, including: stamp test (pasting a roll of
* Tel.: 1 407 303 8683; fax: 1 407 303 8659.
E-mail address: thomas.crow.do@hosp.org
in the morning there was an erection during sleep)
and, snap gauges, strain gauges and electronic instru-
ments such as the RigiScan monitor.1 The patient
had failed several trials of erectile dysfunction medica-
tions, and his urologist informed him that surgical
evaluation was the next step.
1.1. Physical examination
On physical examination his weight was normal and
secondary sexual characteristics were normal. The neu-
rological exam showed normal pinprick and light touch
discrimination, vibration sense, deep tendon reexes
(DTRs), and perineal sensation was normal. The bulbo-
cavernosis and rectal tone were all normal, and the cre-
masteric reex was intact. On the osteopathic structural
exam there was increased paraspinal muscle tone at the
levels T11eL2. On manual examination of the pelvic
fascia and digital rectal exam multiple fascial restrictions
were noted, and the prostate was of normal size with
a smooth consistency without nodularity. The scrotal
contents were normal and the penis had no abnormal
curvature or obvious deformity.

1746-0689/$ - see front matter 2006 Elsevier Ltd. All rights reserved.
doi:10.1016/j.ijosm.2006.01.002
 W.T. Crow / International Journal of Osteopathic Medicine 9 (2006) 66e71
1.2. Laboratory data and imaging studies
The patients blood chemistries were normal. Testos-
terone and thyroid levels were both within normal
limits. An MRI study of the pelvis was unremarkable.
1.3. Osteopathic treatment
Given the multiple fascial restrictions in the pelvis
and perineum an ischiorectal fossa release, as well as
prostatic release and perineal release (all peformed inter-
rectally), was used to reduce fascial strain. To perform
the rst technique, the patient was placed supine with
knees exed and slightly abducted. The physician placed
one hand along the lateral wall of the ischiorectal fossa,
contacting the medial surface of the ischium and the
obturator internus muscle (Fig. 1).2
The physician then applied a slight force to achieve
a stretch of the obturator internus as well as the iliococ-
cygeus muscle of the levator ani. The neurovascular
bundle that is responsible for erection courses through
the lateral pelvic (endopelvic) fascia, which is connected
to the levator ani muscle.3 The physician also performed
a digital fascial release over the area of the prostate in
order to reduce restrictions in the Denonvilliers fascia
at the posterior apical portion of the prostate with the
intent of reducing tension on the same neurovascular
bundle. Stretching these structures in the pelvic dia-
phragm was performed with the intention of reducing
the palpable fascial restrictions, and reducing intercom-
partmental pressure on nervous tissue critical for erec-
tion. In addition, the somatic dysfunction identied at
the thoracolumbar region during the osteopathic struc-
tural examination was treated using high velocityelow
amplitude technique.
1.4. Follow up
The patient reported back to his osteopathic physi-
cian (the author) later that week stating that his impo-
tence had completely resolved.
Fig. 1. Adapted from Ligamentous Articular Strain: Osteopathic
Manipulative Techniques For the Body. Eastland Press German
Edition (used by permission).
67
2. Discussion
Erectile dysfunction can be dened as the inability to
achieve or maintain a penile erection sucient for satis-
factory sexual performance.4 Blunt trauma to the pelvic
or perineal region of the corpora cavernosa has long
been considered a risk factor for the subsequent devel-
opment of persistent erectile dysfunction.5e7 Munarriz
et al. report a 3% incidence of traumatic erectile dys-
function in a 9 year longitudinal study of impotent
men.8 Reporting data from the Massachusetts Male Ag-
ing Study, Feldman et al. estimate that there are 20 mil-
lion impotent men in the United States.9 Using the 3%
incidence of traumatic erectile dysfunction as reported
by Munarriz et al., this would suggest that as many as
600,000 American men may have become impotent as
a result of blunt pelvic and perineal injuries. Since
44% of the subjects in the Munarriz et al. study had
blunt trauma and impotence associated with sports-
related activities, an estimated 250,000 men have
become impotent secondary to falls and straddles onto
blunt and sharp non-penetrating objects, or secondary
to upward blunt forces from aimed body parts or
blunt objects during sports-related accidents. The most
common blunt injury was a fall onto a bicycle cross
bar.8
In most patients presenting with traumatic erectile
impairment the pathophysiology is multifactorial.
Abnormal psychological factors have been reported
previously even in patients with traumatic erectile
dysfunction.6,10 In the Munnariz et al. study of 131
patients, 4% had psychogenic impotence with normal
erectile hemodynamic studies. Abnormal neurological
factors have also been documented. The cavernous
autonomic eerent motor nerve passes in close prox-
imity to the prostatic and membranous urethra, which
in the patient described in this case report appears to
have been aected. The nding of virtually absent
erectile activity on nocturnal penile tumescence testing
in combination with minimal cavernous arterial insuf-
ciency and minimal focal corporeal veno-occlusive
dysfunction on pharmaco-cavernosometry strongly
suggests an associated autonomic nerve dysfunction.11
In this patients case, autonomic nerve dysfunction
was the most likely explanation for the patients
complaint.
St. Louis et al.12 report a case of impotence following
perineal trauma during a basketball game, with selective
internal pudendal arteriography demonstrating bilateral
total occlusion of the cavernous and dorsal penile ar-
teries. Levine et al. documented specic patterns of arte-
rial occlusive disease in the internal pudendal, common
penile dorsal and cavernous arteries following blunt pel-
vic or perineal traumatic episodes.6 This study was in
complete agreement with the arterial vasculopathic
ndings of the other investigations. The incidence of
68 W.T. Crow / International Journal of Osteopathic Medicine 9 (2006) 66e71
cavernous artery insuciency in patients with blunt
pelvic or perineal trauma was 70%.7,8
Impotence and penile sensory loss have been reported
in long distance amateur cyclists.The reported incidence
of bicycling related urogenital symptoms varies consider-
ably. The most common bicycling associated urogenital
problems are nerve entrapment syndromes presenting
as genitalia numbness, reported in 50e91% of cyclists,
followed by erectile dysfunction reported in 13e24%.
Direct nerve compression is cited as one possible cause,
and erectile function is often restored with rest.13
Schrader et al.14 report the ndings of a study investigat-
ing a bicycling police unit that was undertaken in
response to complaints of groin numbness. Seventeen
male cyclists were compared with 5 non-biking men.
Nocturnal erectile events were signicantly lower in the
cyclists than that were in non-cyclists. The greater dura-
tion the cyclist spent on the bike the more problems were
noted.
It is important to fully document the integrity of the
arterial and veno-occlusive hemodynamic involvements
in patients with traumatic impotence. This is especially
true in the evaluation of impotence in younger men
with a history of blunt pelvic or perineal trauma. Youn-
ger patients with impotence usually have absent or min-
imal exposure to systemic vascular risk factors, such as
diabetes, hypertension or hypercholesterolemia. They
are at the beginning of their sexual lives and have a nat-
ural desire to restore the impaired erectile function with-
out the need for chronic external or internal mechanical
devices, or chronic intracavernous injections of vasoac-
tive agents. The presence of traumatic corporeal veno-
occlusive dysfunction would unfavorably aect patient
prognosis in bypass surgery since there appears to be
no obvious long-term benet for surgical intervention
in the presence of veno-occlusive dysfunction.15,16
Munnariz et al. found that sports-related accidents
were the most prominent type (64%) of blunt impact
forces applied to the perineum leading to erectile dys-
function, including falls and straddles onto blunt objects
(most commonly a straddle fall onto a bicycle cross bar
in 38% of patients), falls and straddles onto sharp non-
penetrating objects (for example e the edge of a swim-
ming pool or the side of a snowmobile) and upward
blunt forces to the perineum from projectiles (hockey
pucks and baseballs), sticks or aimed body parts (kicks
from a foot, heel or knee) during contact sporting
events.8
The mean age of the individual at the time of the sus-
pected blunt pelvic or perineal injury was 34
12 years.
The youngest patient was 15 years old. There were 11
teenagers and 37% of the patients were 30 years old
or younger. Patients were generally healthy with few
vascular risk factors except for cigarette smoking
(42%). There was a mean delay of 5.9 years in the
subsequent evaluation for impotence, which was
signicantly shorter in patients with pelvic rather than
with perineal trauma. Injured patients claimed a signi-
cant decrease in frequency of intercourse and erectile
rigidity compared with the pre-morbid rigidity. Impact
injuries did not interfere with libido, ejaculation or
penile sensation. None of the 131 patients were pre-
sented for treatment of the acute traumatic episode.8
2.1. Physiology of erection
Erection is an integration of both neural and vascular
functions. An erection occurs when blood ow to the pe-
nis exceeds ow out of the penis. The cavernosal arteries
supply blood to the corpora cavernosa of the penis
(through the pudendal artery); the emissary veins
running through the tunica albuginea allow drainage.
During erection, relaxation of trabecular smooth muscle
results in increased blood ow to the corpora cavernosa
and expansion of the tissue. This distension causes me-
chanical compression of the emissary veins, which limits
blood drainage, and results in penile rigidity.19 Penile
blood ow is controlled by the parasympathetic (S2e
S4) and sympathetic (T12eL2) inputs to the pelvic
plexus, including the cavernous nerves that innervate
the cavernosal arteries and trabecular smooth
muscle.17,18
The somatic motor nerve supply arises from the
sacral spinal cord, whose bers join the pudendal nerve
innervating the bulbocavernosus and ischiocavernosus
muscles, active during ejaculation and climax.18
Three mechanisms trigger erections: psychogenic, re-
exogenic and centrally originated (nocturnal erections).
Psychogenic erections occur through stimulatory path-
ways (including sound, smell, sight and touch) that
travel from the spinal erection centers (T11eL2 and
S2eS4). Reexogenic erections are caused by direct gen-
ital stimulation. Nocturnal erections are seen during
Rapid Eye Movement sleep and are believed to be
caused by a relative decrease in sympathetic inhibition.18
Despite considerable recent experimentation in ani-
mal models and human volunteers, information on the
central pathways of erection remains cursory at best.
It is known that androgens play a predominantly mod-
ulating role by their eect on libido and sexual behavior.
Testosterone enhances sexual interest and the frequency
of sexual acts. It increases the frequency of nocturnal
erections but does not eect reexogenic or psychogenic
erections.19e21
2.2. Pathophysiology of erectile dysfunction
Numerous factors can disrupt the normal physiologic
mechanisms involved in erection. Most cases of erectile
dysfunction (ED) were thought to be psychologically
based, but it is now understood that most have an
organic cause.
 W.T. Crow / International Journal of Osteopathic Medicine 9 (2006) 66e71
There are three basic categories of ED:
(1) the failure to initiate the nerve impulse necessary to
generate erection, which can be psychogenic, endo-
crinologic, or neurogenic;
(2) a failure to ll (arteriogenic); and
(3) a failure to store (veno-occlusive).
Failure to initiate implies inhibition of the autonomic
response that allows parasympathetic and sympathetic
innervations of erectile tissue. Conditions that contrib-
ute to failure to initiate this nerve impulse include
psychological factors such as stress, anxiety, fear, and
aversion; and physical conditions such as lumbosacral
radiculopathy, multiple sclerosis, and spinal cord
injury.17
Failure to ll indicates an impaired arterial inow
leading to decreased perfusion pressure in the hypogas-
tric, pudendal, and cavernous arteries after autonomic
nerve activation. Arterial occlusion can be secondary
to either atherosclerotic disorders (secondary to diabetes
mellitus, heart disease, hypertension, cigarette smoking,
and low levels of high density lipoprotein cholesterol) or
trauma (pelvic fracture or blunt perineal trauma from
bicycling).8,17
Neurological causes can involve any nerve group,
either central or peripheral, leading to erectile dysfunc-
tion. Cerebral diseases can lead to decreased sexual
interest, possibly through over-inhibition of spinal
centers.19
The most important component of diagnosing erec-
tile dysfunction is obtaining a complete medical and sex-
ual history. It is important to distinguish the condition
from other sexual dysfunctions, such as premature ejac-
ulation and loss of libido. Several formalized sexual
questionnaires, such as the International Index of Erec-
tile Function (IIEF) and Erectile Dysfunction Inventory
of Treatment Satisfaction (EDITS), allow the clinician
to detect the presence and grade the severity of erectile
dysfunction.22 The circumstances surrounding erectile
dysfunction may be helpful in determining whether
a situational or non-organic factor is involved. Sudden
onset, maintenance of nocturnal erections, presence of
psychological problems and concurrent major life events
or relationship issues may be associated with non-
organic erectile dysfunction. Concurrent medical ill-
nesses and any medications the patient may be taking
should be reviewed. Erectile dysfunction is often a com-
ponent of generalized medical illness and may represent
the initial presentation of cardiovascular disease or dia-
betes. The history may also reveal certain reversible or
modiable risk factors, such as smoking or inadequate
diabetes control.23 The physical examination should fo-
cus on the vascular, neurological and endocrine systems.
Testes size should be noted and the penis shaft examined
to rule out a penile deformity such as Peyronies disease.
69
The aetiology of impotence can be delineated as pri-
marily a problem with libido, erection or ejaculation.
Risk factors for impotence include diabetes mellitus,
cardiovascular disease, smoking, depression, atheroscle-
rosis, hypertension, pelvic trauma or surgery, substance
abuse, medications, arthritis, allergies, renal failure,
endocrine abnormalities and ulcers.9 Psychogenic
impotence is dened as persistent inability to achieve
or maintain erection satisfactory for sexual performance
owing predominantly or exclusively to psychological or
interpersonal factors, with all other laboratory tests
being negative. A history of variably inconsistent erec-
tions that are present one day but absent the next day
is suggestive of a psychogenic cause.24
While there is no test available to exclude psycho-
genic impotence with 100% certainty and there is no
consensus on what constitutes an adequate evaluation
for impotence, this patient did not report problems
with libido, had no prior psychiatric history or relation-
ship diculties before his symptoms began, had a nega-
tive penile tumescence test, failed sildenal (Viagra)
therapy and resumed sexual behavior immediately after
successful treatment. This history collectively suggests
a non-psychogenic cause.
Normal Nocturnal Penile Tumescence and Rigidity
(NPTR) depends on both the integrity of the corticospi-
nal eerents to the penis and vascular responsiveness of
the penile tissues to those nerve signals. Unfortunately,
abnormal NPTR is of little value in determining the eti-
ology or classifying the severity of vascular impotence,
the most prevalent kind of end organ failure. Numerous
diagnostic tests have been employed to evaluate penile
hemodynamics. Insucient corporal veno-occlusion is
implicated in up to 50% of patients.25
2.3. Clinical evaluation of impotence
The evaluation of impotence begins with a sexual his-
tory and physical examination. The history and physical
examination have been reported to have a 95% sensitiv-
ity, but only a 50% specicity in determining the cause
of impotence.26
The history should include the rapidity of onset of an
erection, the presence or absence of spontaneous erec-
tions, and assessment of risk factors for impotence.
This historical information plus nocturnal penile tumes-
cence testing are often indicative of the cause of the
sexual dysfunction.
Men who had no sexual problems until one night
when they could not perform and thereafter become im-
potent usually have psychogenic impotence. Psycholog-
ical counseling is usually the preferred therapy in this
situation. Only radical prostatectomy or other overt
genital tract trauma causes a sudden loss of male sexual
function.27 In comparison, men suering from impo-
tence of any other cause complain that sexual function
70 W.T. Crow / International Journal of Osteopathic Medicine 9 (2006) 66e71
failed sporadically at rst, then more consistently. Com-
plete loss of nocturnal erections is present in men with
neurologic or vascular disease. Nonsustained erection
with detumescence (deation) after penetration is most
commonly due to anxiety.24,27
2.4. Risk factors for impotence
Prominent impotence risk factors that should be
asked about include a history of cigarette smoking,28
diabetes mellitus, hypertension, alcoholism, drug abuse,
obesity, and depression.9
2.4.1. Drugs
Many commonly prescribed medications disrupt
normal male sexual function including the following:
 spironolactone;
 sympathetic blockers such as clonidine, guanethi-
dine, or methyldopa;
 thiazide diuretics;
 most antidepressants;
 ketoconazole;
 cimetidine, but apparently not ranitidine or famoti-
dine; and
 alcohol, methadone, heroin and cocaine.29e32
2.4.2. Trauma
Less obvious, but of increasing importance is the as-
sociation of erectile dysfunction with bicycling and other
trauma to the perineum.
2.5. Physical examination when investigating
a complaint of impotence
In addition to the basic physical examination, the
evaluation of the impotent male should include the
following:
 Assessment of femoral and peripheral pulses as
a clue to the presence of vasculogenic impotence. If
pulses are normal, the presence of femoral bruits
implies possible pelvic blood occlusion.
 A check for visual eld defects, present in hypogona-
dal men with pituitary tumors.
 A breast examination to detect gynecomastia, often
present in Klinefelters syndrome.
 A search for penile strictures indicative of Peyronies
disease. Examination of the testicles looking for
atrophy, asymmetry or masses.
 Evaluation of the cremasteric reex, an index of the
integrity of the thoracolumbar erection center. This
is elicited by stroking the inner thighs and observing
ipsilateral contraction of the scrotum.
 Appropriate laboratory testing includes evaluation
of hormonal function.
 Nocturnal penile tumescence testing (NPT). Devices
such as the RigiScan monitor provide accurate,
reproducible information quantifying the number,
tumescence and rigidity of erectile episodes a man
experiences as he sleeps in the comfort of his own
bed.33 Impotent men with normal NPT are consid-
ered to have psychogenic impotence whereas those
with impaired NPT are considered to have organic
impotence usually due to vascular or neurologic dis-
ease. Testosterone decient hypogonadal men are
still capable of exhibiting some erectile activity dur-
ing NPT.
 Osteopathic exam to include the thoracolumbar
region and the pelvic oor and perineum with
appropriate treatment.
2.6. Further research
In treating the impotent patient, particularly those
with a history and physical examination consistent
with a musculoskeletal structural change in the pelvis
and perineal structures, osteopathic treatment, in com-
parison with other more invasive methods, may provide
a simple and cost eective method of addressing this
problem. Further study of osteopathic manipulation
of patients with impotence should be undertaken in
controlled clinical trials.
3. Conclusion
Idiopathic impotence in a 24-year-old water polo
player with no signicant past medical history is rare.
Adaptations to microtrauma include increased collagen
cross-linking and content, and muscular hypertrophy.1
The pelvic oor is especially susceptible to microtrauma
given its central location, and even more so in a water
polo player, whose intensive use of the pelvic girdle mus-
culature places additional strain on the region.
This case suggests that fascial restriction may play
a role in idiopathic impotence in patients with a history
of trauma, and may be a confounding factor for other
more directly explainable causes of impotence. The
ease with which pelvic myofascial release techniques
can be administered and the risk of nerve injury in
exploratory surgery provides a rationale for a trial of
pre-surgical myofascial treatment.
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