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Erectile Dysfunction (ED) BJUI Mini Reviews - June 2007 - Painful Ejaculation
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2 0 07 B J U I N T E R N A T I O N A L | 9 9 , 1 3 3 5 – 1 3 3 9 | doi:10.1111/j.1464-410X.2007.06664.x
1 3 3 5
Review Article
PAINFUL EJACULATION
ILIE
et al.
Painful ejaculation
Cristian P. Ilie, Dan L. Mischianu and
Richard J. Pemberton*
Departments of Urology, Central Clinical Emergency Military Hospital,
Bucharest, Romania, and *Sir Charles Gairdner Hospital, Perth, Western
Australia
Accepted for publication 6 October 2006
We reviewed previous publications on
post-orgasmic pain with reference to
prevalence, epidemiology and treatment
options, using the Ovid and PubMed
(updated May 2006) databases to
comprehensively search MEDLINE for
reports on post-orgasmic pain that
included peer-reviewed English-language
articles. Official proceedings of internationally
known scientific societies were also
assessed. Because of the heterogeneity
of the studies we did not apply metaanalytic
techniques to the data. The
incidence of post-orgasmic pain is 1–9.7%.
The ejaculatory pain is associated with
prostatitis, chronic pelvic pain syndrome,
benign prostatic hyperplasia, and
ejaculatory duct obstruction; it is also
described in patients after procedures
like radical prostatectomy. Aetiopathogenic
theories include those referring to bladder
neck closure and pudendal neuropathy.
The treatment options vary from self-care,
a ‘perineal hyperprotection programme’
to medication with the
α
-blocker,
topiramate, and even surgical procedures
like removing a section of the
sacrotuberous ligament, neurolysis of
the pudendal nerve or removing a section
of the sacrospinous ligament. This is
the first update of the subject, with
reference to prevalence, epidemiology
and treatment options. There is a need
for adequately powered, prospective
randomized trials on aetiology and
treatment options.
KEYWORDS
post-orgasmic pain, ejaculatory pain, man,
dysorgasmia, sexual dysfunction, male
INTRODUCTION
Ejaculatory pain or post-orgasmic pain
(dysorgasmia or orgasmalgia) represents a
component of sexual dysfunction that has
received little attention in published reports
[1]. This is the first review of the subject, with
reference to prevalence, epidemiology and
treatment options. It is a distressing problem
which compromises relationships and quality
of life, and is considered a serious problem for
88–91% of men who experience it [2–5].
Orgasm is defined as the combined
physiological changes and pleasure that
occurs coincident with ejaculation in men. It
has two phases, emission and ejaculation, as
Kaplan [6] described it almost 30 years ago.
After radical prostatectomy (RP), as the
ejaculatory apparatus (prostate, seminal
vesicles, ejaculatory ducts) are removed, the
patient cannot subsequently ejaculate and
therefore such patients have ‘dry orgasms’, as
Barnas
et al.
[7] defined them. Ejaculatory
pain would be a misnomer in these patients
and that is why the term ‘post-orgasmic pain’
is more appropriate.
There is a link between orgasmic function
(consistency, quality and satisfaction) and the
The first mini-review in this section
is a systematic literature review on
postorgasmic pain in the male.
The authors found a significant
incidence of this problem and have
suggested that studies are required
into aetiology and treatment.
The issue of saturation biopsy of
the prostate is discussed in the
second article, followed by papers
on basal cell carcinoma of the
prostate, and finally, a discussion
of screening for prostate cancer,
and particularly new efforts at
targeting special groups.
I L I E
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1 3 3 6
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2 0 07 B J U I N T E R N A T I O N A L
quality of the relationship in which the
individual is involved [8]. The resolution of
sexual dysfunction has been shown to
increase overall marital happiness [9]. Male
sexual dysfunction is an important factor in
marital problems and changes in orgasm
are associated with significant reductions of
emotional and physical satisfaction, which in
turn can lead to sexual-avoidance behaviour
and secondarily to discord in relationships
[10–12].
INCIDENCE
Painful ejaculation is a condition widely under
reported [13]. As with all surveys involving
sexual medicine, the studies are subject to
biases. They are characterized by difficulty
in calculating the true incidence of postorgasmic
pain. Their limitations are
represented by the varied response and
self-reporting bias. As many studies are
retrospective questionnaire-based analyses
there is also potential for recall bias. Most of
the questionnaires used in published studies
have not been validated.
According to Blanker
et al.
[14], pain during or
after ejaculation was reported by 1% of 1688
men in the Netherlands. In the recent largescale,
multinational survey of the ageing
male, a sensation of pain/discomfort with
ejaculation was noted in 6.7% of the sample
of men aged
≥
50 years [4]. In Olmsted
County, Minnesota, 1.5% of the 2115
respondents experienced pain [15]. An
analysis of urogenital pain by Lutz
et al.
[16]
showed a prevalence of
≈
1.4% in men aged
40–49, 60–69 and
>
70 years; the highest
prevalence of
≈
1.8% was in those aged
50–59 years. In the studies based in Lennox
and Addington counties (USA), 9.7% of
respondents, aged 20–74 years, reported
pain or discomfort in the perineum with
ejaculation [17]. During the creation of the
National Institute of Health (NIH) Chronic
Prostatitis (CrP) Symptom Index, the authors
found ejaculatory pain in 58% of patients
with prostatitis, vs 17% in patients with BPH
and 4% in controls [18].
In their study referring to patients with
chronic pelvic pain syndrome (CPPS),
Shoskes
et al.
[19] found that 24% of them
had ejaculatory pain regularly, half had it
intermittently and only 26% of them never
had it in a 3-month period. The authors stated
that when only assessing this symptom once
the true incidence would be underestimated.
Krieger
et al.
[20] found ejaculatory pain in
57% of men with confirmed bacterial
prostatitis NIH category II or IIIA CrP.
Barnas
et al.
[7] published data from a series
of 239 patients who had previously had RP;
this questionnaire-based study showed that
pain during orgasm (dysorgasmia) occurred in
14% of the patients, and that 22% of the
patients had no change in orgasm intensity
after RP, but 37% reported a complete
absence of orgasm, 37% had decreased
orgasm intensity and 4% reported more
intense orgasm than before RP. In those
respondents who had dysorgasmia, pain was
reported to occur always (with every orgasm)
in 33%, frequently in 13%, occasionally in
35%, and rarely in 19% [7]. Koeman
et al.
[1]
reported pain during orgasm in two of 18
(11%) men after RP and 14 of 17 (82%) used
words to describe the sensation of orgasm as
being diminished after surgery.
In a study of 818 patients surgically treated
for BPH, Goriunov and Davidov [21] reported
that 23% (118) had dysorgasmia after surgery.
In their study, Nickel
et al.
[22] interviewed
5096 men reporting LUTS suggestive of BPH
from Europe, Asia, Latin America, the Middle
East and Canada. There were 3700 sexually
active men who had an evaluable answer to
the Danish Prostate Symptom Score for
Sexual Symptoms questionnaire; 688 (18.6%)
of these reported pain/discomfort on
ejaculation and 609 (88%) considered it
was a problem. Patients with LUTS and
ejaculatory pain in this study were
characterized by the following: they were
slightly younger, had more severe LUTS and
greater bother severity, an extremely high
erectile dysfunction rate (72%) and reduced
ejaculation (75%), a higher prevalence of
UTI (12%) and a history of macroscopic
haematuria (5%) [22].
Fitzpatrick and Rosen [23], in their study of
2242 sexually active European men with LUTS,
found a prevalence of pain in 25.9% and a
strong association of ejaculatory symptoms
with the severity of LUTS. In patients with a
IPSS of
<
8 the prevalence was 15.4%, in those
with an IPSS of 8–19, 25.8% and in those
with an IPSS of
>
20, the prevalence was
34.2%. Ejaculatory pain after vasectomy is
uncommon and usually occurs within the
scrotum [24]. According to Johnson
et al.
[25] and Lawler
et al.
[26] ejaculatory duct
obstruction is associated with orgasmic pain.
LOCATION
Barnas
et al.
[7] reported that when given the
choice of penis, abdomen, rectum or ‘other’,
patients answered that the primary location
of pain at orgasm was in the penis (63%),
abdomen (9%), rectum (24%) and other areas
(4%). In another study of 98 patients, Barnas
et al.
[27] reported that pain was in the penis
(72%), testis (12%), rectum (8%), or abdomen
(4%).
DURATION
In one study Barnas
et al.
[27] reported that
most patients (52%) had pain for 1–5 min
after orgasm; the pain lasted
<
1 min in 32%,
but
>
5 min in 12%, and 4% of men had pain
for
>
15 min. In another study by the same
group [7], most patients (55%) had orgasmassociated
pain for
<
1 min; a third reported
pain for 1–5 min and pain for
>
5 min was
reported by 12%; only 2.5% of patients
complained of pain lasting
>
1 h.
Typically, as described by Antolak
et al.
[28],
pain began after ejaculation and the onset
varied from a few seconds to 2 days after
ejaculation. The duration of pain varied from
minutes to days, but most often lasted from 2
to 24 h. Pain varied from minor discomfort to
disabling pain, leading to the avoidance of
intercourse for months.
In their study of the 486 patients with
category III CrP, Shoskes
et al.
[19] found that
ejaculatory pain was associated with younger
age, poor mental and physical quality-of-life
scores, living alone, and having a lower
income. It was also associated with certain
sexual practices such as oral sex and
masturbation (
P
<
0.01). There was no
correlation with age at first intercourse or
with the number of sexual partners.
AETIOLOGY
The cause of dysorgasmia is not well
understood; there are several possibilities.
AFTER RP
Barnas
et al.
[7] referred to patients after RP
and postulated that the physiological bladder
neck closure that occurs during orgasm in
these men translates into spasm of the
vesico-urethral anastomosis, or dystonia
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1 3 3 7
of the pelvic floor musculature. The
muscle spasm concept is supported by the
amelioration of dysorgasmia using the
α
-blocker tamsulosin [27]. This phenomenon
was reported to be associated with penile and
testicular pain in men with CPP disorder [29].
EJACULATORY DUCT STONES
Ejaculatory pain can be caused by obstructive
stones in the ejaculatory duct, and the
surgical (open or laparoscopic) excision of the
affected seminal vesicle can be curative [30].
ANTIDEPRESSANT MEDICATION
Antidepressant-associated sexual dysfunction
is thought to be related to the serotonergic
system. Ferguson [31] described the
highest rates of sexual dysfunction with
antidepressants that act primarily on this
system including the selective serotonin
reuptake inhibitors, tricyclic antidepressants
such as clomipramine, and selective
noradrenaline reuptake inhibitors such as
venlafaxine. Painful ejaculation, a rarer sideeffect,
was described with imipramine,
desipramine, clomipramine, protriptyline,
amoxapine, fluoxetine, venlafaxine and
reboxetine [32–39].
Ejaculation represents the expulsion of semen
from the urethra by rhythmic contractions of
the urethral bulb and the striated perineal
musculature, propelling the seminal fluid
forward, in the act of ejaculation. It is
mediated by
α
1A-adrenoceptors and it is also
known, as Segraves [40] described, that
α
1Aadrenergic
antagonists can cause ejaculatory
problems. According to Demyttenaere and
Huygens [39], two hypothetical mechanisms
were previously proposed to explain painful
ejaculation. The first explanation, described by
Petrie [41], relies on a partial blockade of
peripheral sympathetic adrenergic receptors
like that observed during the administration
of tricyclic antidepressants, which could
interfere with coordinated contractions of the
smooth muscles involved in semen transport,
and thus induce painful spasms.
This theory does not explain why venlafaxine,
a dual-uptake inhibitor with very low
α
-
blockade, and reboxetine, can also induce
painful ejaculation, and why painful
ejaculation was described much more
frequently with the neuroleptic thioridazine
than with chlorpromazine, although their
α
1-
adrenoceptor inhibition is comparable
[34,38,39].
The second theory explains why painful
ejaculation has predominantly been described
with desipramine, imipramine, nortriptyline
and clomipramine (the metabolite
desmethylclomipramine is a powerful
noradrenaline reuptake inhibitor) and
amoxapine. It could also explain why painful
ejaculation has been described with the dualuptake
inhibitor venlafaxine and with
reboxetine. This theory states that
noradrenaline potentiation could interfere
with the ejaculatory mechanism, thereby
inducing painful spasticity. However, this
hypothesis cannot sufficiently explain the
development of painful ejaculation with
thioridazine [38,39].
PUDENDAL NEUROPATHY
Antolak
et al.
[28] consider that category
IIIB CrP/CPPS has the characteristics of a
compressive mononeuropathy of the
pudendal nerve and pain is the major
complaint. In their group of 47 men with
no prostatic inflammation, ejaculatory pain
occurred in 62% of potent men (including in
one both before and after RP). Ejaculatory
pain is rarely the chief complaint of men
with CPPS; most complain primarily of
penile, scrotal, perianal and coccygeal pain.
Neurophysiological tests can be used to
measure pudendal neuropathy caused by
perineal pressure [42]. Causes of CPPS
identified in this patient group include sitting,
repetitive climbing, and flexion exercises of
the hips (sit-ups and leg presses). Pelvic
movements during intercourse might be the
pathophysiological cause of ejaculatory pain.
Clinical and neurophysiological testing
suggests that these men have pudendal
neuropathy, defined variably as pudendal
nerve entrapment, pudendal canal syndrome,
or pudendal neuralgia [28,43,44].
Robert
et al.
[43] described the sites of trauma
to the pudendal nerve as a compression
between the sacrotuberous and sacrospinous
ligaments, impingement at the falciform
process of the sacrotuberous ligament, or
compression of the pudendal nerve as it
traverses the pudendal (Alcock) canal. (Fig. 1)
Myers [45] described the role of the obturator
internus muscle as a pelvic thruster; it is
active during intercourse and might pull on
the nerve, much like a ‘Chinese finger trap’,
causing post-ejaculatory pain. Shafik [44]
described microanatomical structures that
facilitate gliding of the pudendal nerve
between the layers of obturator fascia during
hip flexion, and he termed the problem the
‘pudendal canal syndrome’. Antolak
et al.
[28]
also discovered in their study that a femalesuperior
position or masturbation decreased
the occurrence of post-ejaculatory pain.
TREATMENT
Demyttenaere and Huygens [39] treated with
tamsulosin (0.4 mg, once daily) two men who
were complaining of urinary hesitancy and
painful ejaculation in association with
reboxetine treatment; 1 week later their
urinary complaints and the painful
ejaculation had completely disappeared.
Barnas
et al.
[27] published a prospective
study (not placebo-controlled); 98 patients
with orgasmic pain were interviewed and
given tamsulosin 0.4 mg orally for
≥
4 weeks.
Pain was evaluated using a visual analogue
scale before and after treatment. Patients
were separated into three groups based on
the cause (RP, radiation therapy, and other)
for statistical analysis; 76 of 98 (77%)
patients reported an improvement in the pain
and 12 (13%) noted complete resolution of
their pain. The visual analogue scale for pain
showed a statistically significant decrease in
pain for all groups in response to tamsulosin
treatment. The entire group had a mean
(range) decrease of 2.7 (5.8–3.1) points from
before to after treatment. As the authors
acknowledge, the limitations of the study
were the lack of a placebo arm, patient
selection bias (only patients presenting at a
sexual dysfunction clinic were assessed) and
the current uncertainty of the cause of their
orgasm-associated pain (evidence level 2b;
recommendation grade C).
FIG. 1.
Possible sites of trauma to the pudendal
nerve.
Pudendal Nerve S4
S3
Sacrospinous
ligament
S2
I L I E
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2 0 07 B J U I N T E R N A T I O N A L
Nickel
et al.
[46] published a double-blind
phase II trial of the use of tamsulosin in men
with CrP/CPPS disorder, in which 58 patients
aged
≤
55 years with a diagnosis of CPP were
treated with either tamsulosin or placebo in a
randomized fashion. At 45 days the treatment
effect (difference between treatment groups
in change from baseline) was
−
3.6 points
(
P
=
0.04) in favour of tamsulosin.
Perez
et al.
[47] reported a case of a 39-yearold
man with penile pain strongly related to
ejaculation; he was otherwise in good health.
The pain was refractory to conventional
analgesics and several neuropathic pain
therapies. Oral topiramate was titrated to
75 mg daily, and within a month the patient’s
pain score improved from 8/10 to 1/10.
Johnson
et al.
[25] and Lawler
et al.
[26]
described how orgasmic pain might be
secondary to ejaculatory duct obstruction,
and the relief of obstruction lead to
symptomatic recovery. This can be done either
by transurethral resection of the ejaculatory
duct or by balloon dilatation. The latter can be
achieved by retrograde catheterization,
cystoscopically, or by TRUS-guided seminal
vesicle puncture and catheterization. Johnson
et al.
reported that two of the four men who
complained of pain with ejaculation reported
resolution of the pain after transurethral
resection of the ejaculatory ducts.
Antolak
et al.
[28] described a sequential,
three-step treatment programme based on
self-care, and proceeded as necessary to
perineural injections and even surgical
intervention (Evidence level 2b;
recommendation grade C). For self-care, if
patients were not on analgesic therapy, they
received ketorolac 10 mg every 6 h for 5 days,
and amitriptyline at bedtime, increasing the
dose at 10-day intervals from 10 to 50 mg, as
tolerated. The ‘perineal hyperprotection’
programme included stopping activities
involving hip flexion, including cycling, situps
and leg presses. Sitting was discouraged;
standing and recumbency was encouraged.
For sitting, patients were instructed to make a
‘perineal suspension pad’ by cutting out the
central portion of a gardener’s kneeling pad.
This supports the ischial tuberosities and
elevates the perineum above seat cushions.
For injection therapy, using the technique
described by Bensignor
et al.
[48], perineural
injections into the pudendal nerve, with CT
guidance, were delivered using a mixture of
bupivacaine (1 mL) and triamcinolone (3 mL).
Depending on symptoms, injections were
given unilaterally or bilaterally. A series of
three injections were given at 2-week
intervals initially, but later at 6-week intervals
to permit the complete effect of long-acting
corticosteroids. The first two doses were
injected into the inter-ligamentous space
between the sacrospinous and sacrotuberous
ligaments. The third injection was into
Alcock’s canal. A positive response to local
anaesthetic might predict the likelihood of a
response to the corticosteroid, which is
usually noted after 10–20 days. The degree
and onset of relief were highly variable; men
with only short-term pain relief after
injections were offered surgical intervention.
For surgery, a transgluteal approach permits
the removal of a section of the sacrotuberous
ligament, neurolysis of the pudendal nerve,
removal of a section of the sacrospinous
ligament, fasciotomy of Alcock’s canal, and
nerve transposition anterior to the ischial
spine [28].
CONCLUSION
The incidence of post-orgasmic pain is
1–9.7%; in some groups of patients it can be
as high as 58%. It is considered a serious
problem for 88–91% of men who experience
it, and is a symptom that must not be ignored
by attending clinicians and researchers.
Published data are scarce and the present
review is the first update in the last 12 years.
CONFLICT OF INTEREST
None declared.
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Correspondence: Cristian P Ilie, Departments
of Urology, Central Clinical Emergency
Military Hospital, Bucharest, Romania.
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Abbreviations: RP, radical prostatectomy;
CPP(S), chronic pelvic pain (syndrome); NIH,
National Institute of Health; CrP, chronic
prostatitis.](http://www.urotoday.com/images/stories/bjui_june2007_cover.gif)
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