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Disorders of Orgasm and Ejaculation in Men
Chris G. McMahon, MB, BS, FACSHP,* Carmita Abdo, MD,† Luca Incrocci, MD,‡Michael Perelman, PhD,§ David Rowland, PhD,¶ Marcel Waldinger, MD,#and Zhong Cheng Xin, MD**
* Australian Centre for Sexual Health, Sydney, Australia; † Psiquiatria, Sao Paulo, Brazil; ‡ Department of RadiationOncology, Daniel den Hoed Cancer Center, Rotterdam, The Netherlands; § New York, USA; ¶ Department of Psychiatry,Valparaiso University, Valparaiso, IN, USA; # Department of Psychiatry, Leyenburg Hospital, The Hague, TheNetherlands; ** Department of Urology, Peking University, Beijing, China
Summary of Committee. For the complete report please refer to Sexual Medicine: Sexual Dysfunctions in Men andWomen
, edited by T.F. Lue, R. Basson, R. Rosen, F. Giuliano, S. Khoury, F. Montorsi, Health Publications, Paris 2004.
A B S T R A C T
Ejaculatory/orgasmic disorders, common male sexual dysfunctions, include prema-
ture ejaculation, inhibited ejaculation, anejaculation, retrograde ejaculation and anorgasmia.
To provide recommendations/guidelines concerning state-of-the-art knowledge for man-
agement of ejaculation/orgasmic disorders in men.
An International Consultation in collaboration with the major urology and sexual medi-
cine associations assembled over 200 multidisciplinary experts from 60 countries into 17 commit-
tees. Committee members established speciﬁc objectives and scopes for various male and female
sexual medicine topics. The recommendations concerning state-of-the-art knowledge in the respec-
tive sexual medicine topic represent the opinion of experts from ﬁve continents developed in
a process over a 2-year period. Concerning the Disorders of Ejaculation/Orgasm in Men
Committee, there were nine experts from six countries.
Main Outcome Measure.
Expert opinion was based on grading of evidence-based medical litera-
ture, widespread internal committee discussion, public presentation and debate.
Premature ejaculation management is dependent upon etiology. When secondary to ED,
etiology-speciﬁc treatment is employed. When lifelong, initial pharmacotherapy (SSRI, topical
anesthesia, PDE5 inhibitors) is appropriate. When associated with psychogenic/relationship
factors, behavioral therapy is indicated. When acquired, pharmacotherapy and/or behavioral ther-
apies are preferred. Retrograde ejaculation, diagnosed with spermatozoa and fructose in centrifuged
post-ejaculatory voided urine, is managed by education, patient reassurance, pharmacotherapy or
bladder neck reconstruction. Men with anejaculation or anorgasmia have a biologic failure of emis-
sion and/or psychogenic inhibited ejaculation. Men with age-related penile hypoanesthesia should
be educated, reassured and be instructed in revised sexual techniques which maximize arousal.
More research is needed in understanding management of men with
Ejaculation; Premature Ejaculation; Retrograde Ejaculation; Inhibited Ejaculation;
Anejaculation; Selective Serotonon Re-Uptake Inhibitors; Psychotherapy
Conﬂicts of Interest.
Chris McMahon, Paid consultant and clinical trial investigator to Pﬁzer, Icos Lilly, Bayer, Glaxo-SmithKline, American Medical Systems, Johnson & Johnson.
Disorders of Orgasm and Ejaculation in Men
humans with different SSRIs. However, in thesestudies it is not obvious whether 5-HT2C and 5-
Ejaculatory dysfunction is one of the most HT1A receptors subtypes are also involved in
common sexual disorders in men, and extends
human ejaculation since SSRI treatment activates
from premature ejaculation, through inhibited
many different post-synaptic subtype receptors.
ejaculation to a complete inability to ejaculate,
Further studies with selective 5-HT2C and 5-
anejaculation, and includes retrograde ejaculation.
HT1A agonist and antagonists are required to
Orgasm and ejaculation constitute the ﬁnal
further unravel the neuropharmacological mecha-
phase of the sexual response cycle. There are three
basic mechanisms involved in normal ante-gradeejaculation—emission, ejection and orgasm .
Premature Ejaculation (PE)
Ejaculatory dysfunction can result from disruptionat any point in this cascade of events.
Ejaculation is a reﬂex comprising sensory
dimensional and multidimensional operational
receptors and areas, afferent pathways, cerebral
deﬁnitions of premature ejaculation. The lack of
sensory areas, cerebral motor centers, spinal
agreement as to what constitutes premature ejac-
motor centers and efferent pathways. The ejacu-
ulation has hampered basic and clinical research
latory reﬂex is predominantly controlled by a
into the etiology and management of this condi-
complex interplay between central serotonergic
tion. Quantitative measures of intercourse such as
the intravaginal ejaculatory latency time (IELT),
involvement of cholinergic, adrenergic, nitrergic,
the number of thrusts between penetration and
oxytocinergic and GABAergic neurons. Seminal
ejaculation, the extent of partner sexual satisfac-
emission and ejection are integrated into the
tion, and the patient’s assessment of his voluntary
complex pattern of copulatory behavior by several
control over ejaculation have been described. Each
forebrain structures including the medial preoptic
of the three criteria above has been operational-
area (MPOA) and the nucleus paragigantocellu-
ized, although not always with consistency .
laris (nPGi). Descending serotonergic pathways
Operationalization of PE using the quantiﬁable
from the nPGI to the lumbosacral motor nuclei
and objective number of intravaginal thrusts
tonically inhibit ejaculation. Disinhibition of the
between penetration and ejaculation has been
nPGI by the MPOA results in ejaculation. Several
reported by several authors [8–11], however these
brain areas are activated after ejaculation by
deﬁnitions were subjective, and not supported by
ascending ﬁbers from the spinal cord and may
normative data. Operationalization of PE using
have a possible role in satiety and the post-
the length of time between penetration and ejac-
ulation, the intravaginal ejaculatory latency time
Male rat studies demonstrate that serotonin and
(IELT), forms the basis of most current clinical
5-HT receptors are involved in the ejaculatory
studies on PE. There is considerable variance of
process. As far as is currently known, 5-HT2C and
the latencies used to identify men with PE with
5-HT1A receptors determine the speed of ejacu-
IELTs ranging from 1 to 7 minutes and none of
lation. Stimulation of 5-HT2C receptors with
the deﬁnitions offer any supportive rationale for
non-selective 5-HT2C agonists delays ejaculation
their proposed cut-off time or normative data
in male rats whereas stimulation of post-synaptic
[12–15]. The inability to control and defer ejacu-
5-HT1A receptors resulted in shorter ejaculation
lation until the female partner was sexually satis-
latency . Administration of selective serotonin
ﬁed on at least 50% of intercourse attempts was
re-uptake inhibitors (SSRIs) results in active
proposed as a deﬁnition of PE by Masters and
blockade of presynaptic membrane 5-HT trans-
Johnson . An inherent problem exists in deﬁn-
porters, and the resultant higher synaptic cleft
ing a man as dysfunctional based on the sexual
levels of 5-HT activate post-synaptic 5-HT2C and
responsivity of his partner, as only 30% of women
5-HT1A receptors and delay ejaculation [3,4].
achieve orgasm during sexual intercourse regard-
Waldinger et al. formulated the hypothesis that
less of the extent of their partner’s ejaculatory
men with premature ejaculation have hyposensi-
tivity of 5-HT2C and/or hypersensitivity of 5-
The lack of a reliable operational deﬁnition for
HT1A receptor [3,5,6]. The hypothesis that
PE has severely limited clinical research into the
activation of post-synaptic 5-HT receptors delays
understanding of PE as studies that fail to deﬁne
ejaculation is supported by numerous studies in
PE offer meaningless or difﬁcult to interpret
results. The lack of a universally accepted opera-
In many relationships premature ejaculation
tionalized deﬁnition makes comparison of differ-
causes few if any problems. In others, the couple
ent studies difﬁcult or impossible as experimental
may reach an accommodation of the problem
group subjects in one study may very well have
through various strategies—young men with a
been placed in the control group of a second study.
short refractory period may often experience a
The following multivariate deﬁnition of PE is
second and more controlled ejaculation during an
proposed: “Premature ejaculation is persistent or
episode of lovemaking. Frequently, however, pre-
recurrent ejaculation with minimal stimulation
mature ejaculation eventually leads to signiﬁcant
before, on, or shortly after penetration, and before
problems in the relationship with partners regard-
the person wishes it, over which the sufferer has
ing the man as selﬁsh and developing a pattern of
little or no voluntary control which causes the suf-
sexual avoidance. This only worsens the severity
ferer and/or his partner bother or distress.”
of the prematurity on the occasions when inter-
Premature ejaculation may be classiﬁed into
various subtypes based on the developmental
The cornerstones of behavioral treatment are
history and response characteristics. Acquired
the Seman’s “stop-start” maneuver and its modiﬁ-
PE and/or situational PE suggest a psychological
cation proposed by Masters and Johnson, the
etiology and behavioral therapy as the most
squeeze technique. Both are based on the theory
appropriate initial therapy and/or relationship
that premature ejaculation occurs because the man
counseling whereas lifelong and/or global PE
fails to pay sufﬁcient attention to pre-orgasmic
suggest a biogenic etiology and pharmacologic
levels of sexual tension [11,17]. As most men with
treatment as the most appropriate initial therapy.
premature ejaculation are aware of their anxiety
A signiﬁcant number of men with PE also report
and the sources of that anxiety tend to be relatively
having problems achieving and/or maintaining an
superﬁcial, treatment success with these behav-
erection, estimated as high as 30% .
ioral approaches is relatively good in the short
Historically, attempts to explain the etiology
of premature ejaculation have included a diverse
range of biogenic and psychological theories
Pharmacological modulation of ejaculatory
(Table 1). Most of these proposed etiologies are
threshold represents a novel and refreshing
not evidence based and are speculative at best. The
approach to the treatment of premature. The
lack of an operationalized deﬁnition for PE, and
introduction of the selective serotonin reuptake
the presence of methodological problems related
inhibitors (SSRIs) meant a revolutionary change in
to the inadequate deﬁnitions used, is a common
the approach to and treatment of premature ejac-
ﬂaw in the majority of these studies.
ulation. Selective serotonin reuptake inhibitorsencompass ﬁve compounds (citalopram, ﬂuoxe-
Treatment Of Premature Ejaculation
tine, ﬂuvoxamine, paroxetine and sertraline) witha similar pharmacological mechanism of action.
Men with premature ejaculation should be evalu-
Although the methodology of the initial drug
ated with a detailed medical and sexual history, a
treatment studies was rather poor, recent double
physical examination and appropriate investiga-
blind placebo-controlled studies demonstrated the
tions to establish the true presenting complaint
efﬁcacy of SSRIs and clomipramine in delaying
and identify obvious biological causes such as
ejaculation [20–24]. In spite of a development
genital or lower urinary tract infection (Figure 1).
towards more evidence based drug treatmentresearch, the majority of studies still lack adequate
Proposed etiologies of premature ejaculation
design and methodology . There are three
drug treatment strategies to treat premature
ejaculation: 1) daily treatment with serotonergic
antidepressants; 2) as-needed treatment with anti-
Ejaculatory control techniquesEvolutionary
depressants; and 3) topical local anaesthetics.
Examining daily treatment with serotonergic
antidepressants paroxetine, clomipramine, sertra-
line and ﬂuoxetine, a meta-analysis of drug treat-
ment studies demonstrates that paroxetine exerts
the strongest ejaculation delay . Ejaculation
delay usually occurs within 5–10 days but may
Disorders of Orgasm and Ejaculation in Men
occur earlier. Adverse effects are usually minor,
[32–34]. It is unlikely that phosphodiesterase
start in the ﬁrst week after intake, gradually dis-
inhibitors have a signiﬁcant role in the treatment
appear within 2–3 weeks and include fatigue,
of PE with the exception of men with acquired PE
yawning, mild nausea, loose stools or perspiration.
Diminished libido or mild erectile dysfunction areinfrequently reported.
Inhibited Ejaculation, Anejaculation
Administration of antidepressants as needed,
paroxetine, sertraline, ﬂuoxetine and clomipra-
The Diagnostic and Statistical Manual of Mental
mine 4–6 hours prior to intercourse, is efﬁcacious
Disorders deﬁnes inhibited ejaculation (IE) as
and well tolerated, is associated with less ejacula-
the persistent or recurrent difﬁculty, delay in, or
tory delay than daily treatment and may be com-
absence of attaining orgasm following sufﬁ-
bined with either an initial trial of daily treatment
cient sexual stimulation, which causes personal
or concomitant low dose daily treatment [26–28].
distress . Inhibited ejaculation or anejaculation
The use of topical local anesthetics such as lig-
can be classiﬁed as either a lifelong or acquired, or
nocaine and/or prilocaine as a cream, gel or spray
as global or situational. Any single or combination
is well established. They are moderately effective
of psychological or medical disease, surgical pro-
in retarding ejaculation, but do so at the price of
cedure or drug which interferes with either central
possibly causing signiﬁcant penile hypoanesthesia
control of ejaculation, the afferent or efferent
and possible transvaginal absorption, resulting in
nerve supply to the vas, bladder neck, pelvic ﬂoor
vaginal numbness and resultant female anorgasmia
or penis, can result in inhibited ejaculation, ane-
jaculation and anorgasmia (Table 2).
Several authors have reported their experience
Inhibited ejaculation, like other sexual dysfunc-
with sildenaﬁl citrate as a treatment for PE
tions, is more prevalent as men age . The pro-
Causes of inhibited ejaculation, anejaculation
Treatment of Inhibited Ejaculation, Anejaculation
Men with inhibited ejaculation, anejaculation
and/or anorgasmia should be evaluated with a
detailed medical and sexual history, a physical
examination and appropriate imaging and/or elec-
Transurethral resection of prostateBladder Neck Incision
trophysiological investigations to establish the true
presenting complaint, identify obvious biological
causes such as medication, diabetes mellitus or
recent pelvic surgery, and uncover sufﬁcient detail
to establish the optimal treatment plan. The exact
site of ejaculatory duct obstruction may be identi-
ﬁed by transrectal ultrasonography, vasography or
by percutaneous puncture of the seminal vesicles.
Four neurophysiological tests are routinely used—
pudendal somatosensory evoked potentials,
pudendal motor evoked potentials, sacral reﬂex arc
testing and sympathetic skin responses. Treatment
should be etiology speciﬁc and address the issue of
Tricyclic and SSRI antidepressantsPhenothiazine
infertility in men of a reproductive age.
Although multiple psychodynamic and behav-
ioral treatments for IE have been suggested,empirical evidence to support treatment efﬁcacy islacking [11,44–49]. Most reports are uncontrolled
gressive loss of the fast conducting peripheral
case reports with treatment ranging from a few
sensory axons which begins to be apparent in the
brief sessions of sex education to the nearly 2 years
third decade of life, and the dermal atrophy,
of multiple-modality treatment in more complex
myelin collagen inﬁltration and pacinian corpus-
cle degeneration observed in older men, may
There are multiple reports in the literature of
result in a degree of age-related degenerative
the use of a variety of drugs in the treatment of
penile hypoanesthesia and difﬁculty in achieving
inhibited ejaculation [50–59]. The drugs facilitate
ejaculation by either a central dopaminergic or
IE may be associated with cultural and religious
anti-serotoninergic mechanism of action. There
beliefs, concurrent psychopathology such as
are no published placebo controlled studies and
unconscious aggression and unexpressed anger,
most reports are anecdotal case reports/series that
insufﬁcient sexual arousal, preconditioning for
deal with the treatment of SSRI induced ejacula-
inhibited ejaculation due to a preference for mas-
tory dysfunction (Table 3). While medical treat-
turbation over partnered sex, fear of pregnancy or
ment may not always produce normal ejaculation,
sexually transmissible disease [11,37–41]. Apfel-
it may convert a patient with lack of emission into
baum observed that some males achieve erections
sufﬁcient for intercourse despite a relative absenceof subjective arousal and incorrectly regard them-
selves as ready for sex and capable of achievingorgasm . This same process is the likely cause
Men with premature ejaculation secondary to
of increased anecdotal clinical reports of inhibited
erectile dysfunction, other sexual dysfunction or
ejaculation in patients using pharmacologic treat-
genitourinary infection should receive appropriate
etiology speciﬁc treatment. Men with lifelong pre-
The ability to ejaculate is severely impaired by
mature ejaculation should be initially managed
spinal cord injury (SCI) and is dependent upon the
with pharmacotherapy. Men with signiﬁcant con-
level and completeness of SCI . Unlike erec-
tributing psychogenic or relationship factors may
tile capacity, the ability to ejaculate increases with
beneﬁt from concomitant behavioral therapy.
descending levels of spinal injury. Less than 5%
Recurrence of premature ejaculation is highly
of patients with complete upper motor neuron
likely to occur following withdrawal of treatment.
lesions retain the ability to ejaculate.
Men with acquired premature ejaculation can be
Disorders of Orgasm and Ejaculation in Men
Adjunctive drug therapy for SSRI-induced sexual dysfunction
treated with pharmacotherapy and/or behavioral
Chris G. McMahon, MD,
therapy according to patient/partner preference.
Australian Centre for Sexual Health, Suite 2–4, 1a
Restoration of ejaculatory control in men with
Berry Road, St. Leonards NSW Sydney, Australia 2065.
acquired premature ejaculation is likely to occur
following completion of treatment but is theexception in men with lifelong premature ejacula-
tion. Behavioral therapy may augment pharma-
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Comfort Care Measures Overview Vital signs – prn to evaluate “End-of-Life Vital Signs” for comfort, heart rate (tachycardia), respiration (apnea, rapid rate/tachypnea), temperature if warm to touch, secretions (gurgling or coarse crackles). Diet – Patient choice of time, quantity and type of food as tolerated. Family may provide food. Activity – as tolerated. Position
Fluorouracil 400mg/m2 bolus then 600mg/m2over 22 Hours d1, d2– Study (Mayo Regimen x 6 Cycles vs Xeloda)• Oxaliplatin infusion begun. 90 minutes breathing sensation, tingling in throat. • Increase Infusion Duration (2-6 Hours)– Delayed Cumulative Sensory Neuropathy• Comparable to Cisplatin• Impaired Sensation• Related to Cumulative Dose (800mg/m2)• Usually Reversible (75% Pa