ArticlePDF AvailableLiterature Review

Post-SSRI Sexual Dysfunction: A Literature Review

Authors:
  • Harvard Medical School/MGH
  • Tulane University Medical Center

Abstract and Figures

Introduction: Selective serotonin reuptake inhibitors (SSRIs) are a widely used class of drug. Post-SSRI sexual dysfunction (PSSD) is a condition in which patients continue to have sexual side effects after discontinuation of SSRI use. The prevalence of persistent sexual side effects after discontinuing SSRIs is unknown. The recognition and study of PSSD will increase our knowledge base of this underreported and distressing condition. Aim: To provide coverage of the current literature on PSSD, update information on the pathophysiology of PSSD, and discuss potential management options. Methods: Comprehensive review of literature pertaining to PSSD. Main outcome measures: The symptoms, classification, pathophysiology, diagnostic considerations, and management of PSSD were reviewed. Results: Common PSSD symptoms include genital anesthesia, pleasure-less or weak orgasm, decreased sex drive, erectile dysfunction, and premature ejaculation. Different theories have been proposed to explain the pathophysiology of PSSD: epigenetic gene expression theory, cytochrome actions, dopamine-serotonin interactions, proopiomelanocortin and melanocortin effects, serotonin neurotoxicity, downregulation of 5-hydroxytryptamine receptor 1A, and hormonal changes in the central and peripheral nervous systems. The diagnosis of PSSD is achieved by excluding all other etiologies of sexual dysfunction. Treating PSSD is challenging, and many strategies have been suggested and tried, including serotonergic antagonists and dopaminergic agonists. There is still no definitive treatment for PSSD. Low-power laser irradiation and phototherapy have shown some promising results. Conclusion: PSSD is a debilitating condition that adversely affects quality of life. Further studies are warranted to investigate the prevalence, pathophysiology, and treatment of PSSD. Bala A, Nguyen HMT, Hellstrom WJG. Post-SSRI Sexual Dysfunction: A Literature Review. Sex Med Rev 2017;X:XXX-XXX.
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Post-SSRI Sexual Dysfunction: A Literature Review
Areeg Bala, MD, Hoang Minh Tue Nguyen, BA, and Wayne J. G. Hellstrom, MD, FACS
ABSTRACT
Introduction: Selective serotonin reuptake inhibitors (SSRIs) are a widely used class of drug. Post-SSRI sexual
dysfunction (PSSD) is a condition in which patients continue to have sexual side effects after discontinuation of
SSRI use. The prevalence of persistent sexual side effects after discontinuing SSRIs is unknown. The recognition
and study of PSSD will increase our knowledge base of this underreported and distressing condition.
Aim: To provide coverage of the current literature on PSSD, update information on the pathophysiology of
PSSD, and discuss potential management options.
Methods: Comprehensive review of literature pertaining to PSSD.
Main Outcome Measures: The symptoms, classication, pathophysiology, diagnostic considerations, and
management of PSSD were reviewed.
Results: Common PSSD symptoms include genital anesthesia, pleasure-less or weak orgasm, decreased sex drive,
erectile dysfunction, and premature ejaculation. Different theories have been proposed to explain the patho-
physiology of PSSD: epigenetic gene expression theory, cytochrome actions, dopamine-serotonin interactions,
proopiomelanocortin and melanocortin effects, serotonin neurotoxicity, downregulation of 5-hydroxytryptamine
receptor 1A, and hormonal changes in the central and peripheral nervous systems. The diagnosis of PSSD is
achieved by excluding all other etiologies of sexual dysfunction. Treating PSSD is challenging, and many stra-
tegies have been suggested and tried, including serotonergic antagonists and dopaminergic agonists. There is still
no denitive treatment for PSSD. Low-power laser irradiation and phototherapy have shown some promising
results.
Conclusion: PSSD is a debilitating condition that adversely affects quality of life. Further studies are warranted
to investigate the prevalence, pathophysiology, and treatment of PSSD. Bala A, Nguyen HMT, Hellstrom
WJG. Post-SSRI Sexual Dysfunction: A Literature Review. Sex Med Rev 2017;X:XXXeXXX.
Copyright 2017, International Society for Sexual Medicine. Published by Elsevier Inc. All rights reserved.
Key Words: Post-SSRI Sexual Dysfunction; Selective Serotonin Reuptake Inhibitors
INTRODUCTION
Selective serotonin reuptake inhibitors (SSRIs) are a widely
used class of drug that is prescribed for the management of
different disorders, including major depression, obsessive-
compulsive disorder, post-traumatic stress, generalized anxiety,
and social anxiety.
1
In addition, SSRIs are used to treat pre- and
postmenopausal syndromes, hot ashes, chronic pain, and
chronic fatigue syndromes.
2
In the United States, one in eight
people have used SSRIs in the past 10 years.
1
Occasionally,
SSRIs, because of the reversible sexual side effects, are prescribed
intentionally to treat cases of paraphilia and premature
ejaculation.
2
Post-SSRI sexual dysfunction (PSSD) is a condition
that arises after the use of SSRIs, in which patients continue to
have sexual side effects after the discontinuation of SSRIs. These
persistent side effects include decreased libido, genital anesthesia,
erectile dysfunction, delayed ejaculation, loss of lubrication in
women, and anorgasmia.
2
Bahrick
1
estimated that 1% to 10% of
patients with SSRI sexual side effects will experience resolution of
these side effects while still on medication, yet the remaining
cohort will still exhibit these side effects as long as SSRIs are used.
One post-market research study reported that 5% to 15% of
patients developed impairment of sexual function after the use of
SSRIs and serotonin-norepinephrine reuptake inhibitors.
3
The
prevalence of persistent sexual side effects after discontinuing
SSRIs is not well known.
1
With the wide use of SSRIs, psychi-
atrists and mental health practitioners must be well informed
about the medication side effects, because these drugs affect the
welfare of their patients. Sufciently informing the patients of
these potential side effects before initiating treatment and
Received June 2, 2017. Accepted July 4, 2017.
Department of Urology, Tulane University School of Medicine, New Orleans,
LA, USA
Copyright ª2017, International Society for Sexual Medicine. Published by
Elsevier Inc. All rights reserved.
http://dx.doi.org/10.1016/j.sxmr.2017.07.002
Sex Med Rev 2017;-:1e61
questioning for the occurrence of these effects while undergoing
treatment are of clinical importance.
2
Waldinger et al
4
proposed
that PSSD should be identied as a true syndrome in the liter-
ature, rather than as a side effect of SSRIs.
From 2006 to 2008, eight cases of treatment-emergent sexual
dysfunction persisting after SSRI discontinuation were reported,
leading to what Csoka et al
2
described as PSSD.
5e7
In 2012, the
database of the Netherlands Pharmacovigilance Centre (Lareb)
received 19 reports of persistent sexual dysfunction in patients who
had stopped using SSRIs for 2 months to 3 years previously and
had not yet regained normal sexual functioning.
8
In the reports, 13
patients were men and 6 were women. The SSRIs prescribed were
paroxetine, sertraline, venlafaxine, citalopram, uoxetine, uvox-
amine, and escitalopram.
8
Some patients reported multiple
symptoms of PSSD.
8
Hogan et al
9
reported 90 cases of PSSD
based on reports on RxISK.org, a portal for reporting adverse
events by patients or doctors or, ideally, patients and doctors;
RxISK is maintained by a group of high-prole medical experts
with international renown in early detection of drug side effects
and risk mitigation. Of the 90 cases, 75 were men and 15 were
women.
9
Ben-Sheetrit et al
10
conducted an internet survey of
sexual adverse effects in patients on antidepressants using a struc-
tured self-report questionnaire and well-dened case-denition
criteria; of 532 subjects, they found 183 possible cases, including
23 high-probability cases of PSSD. Several medications have
been associated with sexual dysfunction side effects after discon-
tinuation of use. The use of nasteride and dutasteride
(5a-reductase inhibitors) showed persistent erectile dysfunction in
some patients treated with these drugs.
11
Sexual dysfunction was
reported to persist longer than 3 months after discontinuation of
the a-reductase inhibitors in male rats, which can continue for
months and even years.
12
Moreover, isotretinoin was linked to
anejaculation and decreased fertility.
13
Drugs that increase sero-
tonin levels have been associated with similar sexual side effects;
tricyclic antidepressants such as clomipramine, amitriptyline,
imipramine, and doxepin showed the highest incidence of sexual
dysfunction symptoms.
14
However, a lack of sexual drive, decreased sexual desire, and
low libido are already established symptoms of depression.
15
Mathew and Weinman
16
stated that decreased arousal was pre-
sent in 40% to 50% of depressive patients, and 15% to 20% of
patients reported problems with orgasm and ejaculation. These
can superimpose the sexual dysfunction caused by SSRIs.
Although the PSSD literature is sparse, it continues to increase.
In this communication, we aim to provide an updated review of
the current literature on PSSD, possible pathogenesis, and the
latest management options.
METHODS
A literature review was performed on PubMed (www.ncbi.
nlm.nih.gov) using the search strings post-SSRI sexual dysfunc-
tion and persistent sexual dysfunction SSRI. We examined
74 articles and included 33 articles that were relevant to PSSD.
Articles that evaluated sexual dysfunction by SSRI instead of
PSSD were excluded. Based on reading the included results and
examining their references, we added peer-reviewed articles on
PSSD to our review (Figure 1).
CLINICAL PRESENTATION
Common PSSD symptoms include genital anesthesia
(decrease in sensation and numbness in the genital area),
pleasure-less or weak orgasm, decreased sex drive, erectile
dysfunction, and premature ejaculation (Table 1). In addition,
women can experience vaginal lubrication issues and nipple
insensitivity.
2
Of these symptoms, the most characteristic triad
consists of genital anesthesia, loss of libido, and erectile
dysfunction.
9
The symptoms of PSSD can start days or weeks
after beginning SSRIs and can persist after discontinuing SSRIs.
4
PSSD also can present after a single dose of an antidepressant.
2
Genital anesthesia, which is the most common symptom of
PSSD, can appear within 30 minutes of the rst dose of an
SSRI.
9
Hogan et al
9
reported additional PSSD symptoms,
including decreased penile size, smaller seminal volume, testic-
ular atrophy and pain, and irregular menstruation for women.
The symptoms of PSSD are very distressing to patients, which
negatively affect their lives.
10
Waldinger et al
4
classied PSSD into two categories based on
the onset of the symptoms: (i) PSSD that is characterized by early
onset, that is, sexual dysfunction occurring while SSRIs are being
used and persisting after discontinuing treatments, and (ii) PSSD
Figure 1. Literature review methodology. PSSD ¼sexual
dysfunction after selective serotonin reuptake inhibitor use;
SSRI ¼selective serotonin reuptake inhibitor.
Ta b l e 1 . Common symptoms of sexual dysfunction after selective
serotonin reuptake inhibitor use
Genital anesthesia
Decreased libido
Erectile dysfunction
Pleasure-less or weak orgasm
Premature ejaculation
Vaginal lubrication problems
Nipple insensitivity
Sex Med Rev 2017;-:1e6
2Bala et al
that occurs after the discontinuation of SSRIs as an aggravation
of SSRI-induced sexual side effects. In their case report,
Waldinger et al also reported continued anejaculation and erec-
tile dysfunction, despite improved penile sensitivity in their
patients, suggesting the involvement of a central pathway in
PSSD. Waldinger et al also reported other rare sexual side effects
that might start with SSRI treatment and continue after stopping
the medication; these include restless genital syndrome and
persistent genital arousal disorder. Persistent genital arousal dis-
order is a disorder in which genital arousal persists for hours or
days after the cessation of the sexual stimulation, despite the
experience of at least one orgasm.
17
Leiblum and Goldmeier
17
reported several cases of persistent genital arousal disorder that
was caused by antidepressant usage or withdrawal; SSRIs were
found to predispose to the vast majority of cases.
PATHOPHYSIOLOGY
Uncovering the exact cause of PSSD is challenging; however,
several etiologies have been proposed. Moreover, a combination
of these potential theories might be operational to the patho-
physiology of PSSD.
Epigenetic Change and Receptor Downregulation
Theory
Csoka and Szyf
18
observed that increased binding and stimu-
lation of 5-hydroxytryptamine receptor 1A (5HT1A) by seroto-
nin caused downregulation of these receptors and potentiated
serotonin transmission. Long-term usage of SSRIs is hypothesized
to cause persistent downregulation of 5HT1A (even after
discontinuation of SSRIs) by epigenetic changes in the form of
increased expression of methyl binding proteins MeCP2 and
MBD1. This leads to more production of HDAC2 mRNA and
lowers the production of histone H3 deacetylase.
18
These epige-
netic changes were observed in three areas of the brain: the frontal
cortex, the dentate gyrus of the hippocampus, and the caudate-
putamen. MDB1, MeCP2, and HDAC2 expression was noted
to be induced by uoxetine.
18
Popova and Amstislavskaya
19
indicated that this downregulation and desensitization of
5HT1A are involved in the regulation of sexual motivation, and
thus proposed this as a theory for PSSD.
Hormonal Theories
Different hormones are proposed to play a role in PSSD in
the central and peripheral nervous systems and cause neurochem-
ical changes, including an increase in serotonin and prolactin,
blockage of a
1
-adrenergic receptors, a decrease in dopamine,
testosterone, and oxytocin, and a decrease in nitric oxide synthesis.
2
Moreover, some neurochemical changes have been noticed in the
peripheral nervous system of patients with PSSD. This is note-
worthy because 95% of serotonin receptors are located outside the
brain. It was postulated that SSRIs cause PSSD by affecting
serotonin levels in peripheral nerves.
2
Ben-Sheetrit et al
10
postu-
lated that serotonergic neurotoxicity also might play a role in PSSD
in a similar mechanism to 3,4-methylenedioxymethamphetamine,
which stimulates the release and inhibits the uptake of serotonin.
3,4-Methylenedioxymethamphetamine causes persistent sexual
dysfunction long after its discontinuation, with axonal damage as
the proposed mechanism.
10
Ben-Sheetrit et al
10
suggested that
there might be a role for individual vulnerability to serotonin,
because most patients on SSRIs do not develop PSSD.
Damsa et al
20
pointed out the role of serotonin-dopamine inter-
action in causing PSSD. SSRIs cause inhibition of dopamine
transmission in the ventral tegmental area; dopamine is essential in
sexual arousal. In addition, serotonin regulates proopiomelano-
cortin neuron output and inhibits melanocortin MC4 receptors
through 5HT2C and 5HT2A action. Not only are proopiomela-
nocortin and melanocortin responsible for skin coloration, they
also play major roles in sexual behavior. As such, disturbances in
proopiomelanocortin and melanocortin caused by SSRIs can result
in persistent sexual dysfunction.
21
Furthermore, 5HT receptors
play a major role in the hypothalamic-pituitary-testicular axis, and
dysregulation of any of these receptors results in dysregulation of
the axis, which produces lower free testosterone levels.
7
Waldinger et al
4
postulated that PSSD is linked to transient
receptor potential ion channel transduction, which is responsible
for skin sensitivity to temperature, touch, taste, and smell.
Disturbances to these transient receptor potentials could mani-
fest as PSSD.
ANIMAL STUDIES
A few animal studies have been conducted to determine the
long-term effect of SSRIs on sexual function. In their research on
rats, Raap et al
22
found that treatment with uoxetine resulted in
persistent desensitization of 5HT1A, even after discontinuation
of the drug. Sukoff-Rizzo et al
23
noted that 5HT1A antagonists
treated and prevented the sexual dysfunction in rats that had
been administered uoxetine. Further studies suggested that
administering SSRIs in young rats resulted in persistent sexual
side effects into adulthood.
24,25
Gouvêa et al
26
administered
uoxetine in pregnant mice and observed an impairment of
sexual motivation in the adult offspring of these pregnant mice.
A systematic review of animal studies documented evidence of
persistent sexual behavioral changes in rats that had been exposed
to SSRIs at a young age.
27
DIAGNOSIS
Almost all patients who have used SSRIs develop some type of
sexual side effect.
18
The exact prevalence of PSSD is undeter-
mined owing to a paucity of studies. Ben-Sheetrit et al
10
cautioned that PSSD could be challenging to diagnose. For
example, a patient visits a doctor for a mental illness, where the
patient is prescribed an SSRI. The patient might experience a
Sex Med Rev 2017;-:1e6
Post-SSRI Sexual Dysfunction 3
sexual side effect(s) with administration of the SSRI. The patient
discontinues the medication because of these effects, but the
sexual dysfunction could persist, which leads to another visit to
the doctor. At this point, there will be confusion as to whether
the persistent sexual dysfunction is caused by the mental illness
or the SSRI. If the patient resumes the SSRI, the drug will be
blamed for the sexual side effects. Either way, conrming a PSSD
diagnosis is problematic.
10
Reisman
28
also suggested that the
overlapping between PSSD symptoms and the actual mental
illness symptoms renders the diagnosis of PSSD to be slightly
challenging. PSSD is diagnosed by reviewing all elements of a
patients clinical presentation, such as history of drug use, onset
of symptoms, and premorbid conditions. Furthermore,
excluding other possible causes of sexual dysfunction helps in
diagnosing PSSD. Some authorities have used genital anesthesia
as an indicator of the severity of sexual dysfunction caused by
SSRIs in PSSD.
10
According to Higgins et al,
29
a full detailed
evaluation is the rst step in evaluating PSSD to ensure that the
sexual side effects are indeed an outcome of SSRI use. This
evaluation ranges from physical assessment to a formal sexual
health inquiry. In general, the clinician should exclude con-
founding elements such as age, smoking, alcohol, and substance
abuse, because they are recognized to cause sexual dysfunction
symptoms. Similarly, the physicians must consider other diseases
that can affect sexual functions, such as diabetes, hypertension,
and depression.
29
MANAGEMENT AND PREVENTION
There is still no denitive treatment for PSSD. The treatments
described in the literature were meant for sexual dysfunction
induced by SSRI. Although there is no actual treatment for
PSSD, Waldinger et al
4
reported the effect of low-power laser
irradiation, or phototherapy, directed toward the scrotal skin and
the shaft of the penis in a male patient with PSSD and penile
anesthesia. Low-power laser irradiation improved the function of
transient receptor potentials, which is proposed as one of the
PSSD etiologies. In this patient, penile sensitivity improved by
40%. Nonetheless, despite the partial relief of penile anesthesia
and penile temperature sensitivity, low-power laser irradiation
failed to alleviate anejaculation and erectile dysfunction symp-
toms of PSSD in the same patient.
4
Hogan et al
9
suggested that
focusing on serotonergic and dopaminergic systems by adding
5HT1 agonists and 5HT2 and 5HT3 antagonists could
accomplish the management of PSSD. The drugs used were
buspirone, trazodone, and mirtazapine, respectively. The latter
two drugs can induce priapism and increase libido in normal
people, but has little to no effect in patients with PSSD. For the
dopamine agonists, pramipexole and cabergoline have been tried
for treatment of PSSD, with little benet reported.
9
However, a
5HT1A antagonist has been tested in rats and documented a
70% improvement in penile erection that had been impaired by
uoxetine use.
23
Montejo et al
7
reported on a Spanish
case-control study that evaluated a switch from SSRIs to a
dopaminergic antidepressant (amineptine) in patients with sexual
dysfunction and observed that 55% of these patients using SSRIs
had persistent sexual dysfunction 6 months after treatment
cessation, whereas only 4% of patients who had switched to
amineptine had these complaints at 6 months. Patients also
tried sildenal, vardenal, and other phosphodiesterase type 5
inhibitors and testosterone, but no improvement was docu-
mented.
9
An additional treatment option might be for patients to
switch to bupropion or nefazodone, antidepressants that are not
known to cause any sexual adverse effects.
29
Bupropion does not
have serotonergic activity and, hence, does not affect sexual
function in patients. In a placebo-controlled comparison study of
bupropion and sertraline treatment in patients, it was noted that
sexual dysfunction symptoms were present in sertraline-treated
patients; however, sexual desire and orgasm dysfunction were
reported much less in patients with bupropion. Overall, the
patients treated with bupropion reported satisfaction with their
sexual function.
30
Adjunct therapy with bupropion demon-
strated promising results in treating SSRI-related sexual
dysfunction.
29
Another double-blinded study conducted by
Clayton et al
31
with bupropion added as an adjunct drug to
SSRI-induced sexual dysfunction showed that bupropion was
a successful antidote. Patients treated with bupropion docu-
mented a recovery from their sexual dysfunction in desire and
frequency of sexual activity. This highlights the difculty of
managing patients with PSSD and the importance of PSSD
prevention.
Cognitive-behavioral therapy also has been used by psychia-
trists to help patients reach a better understanding of their
condition and cope better with their situation. Cognitive-
behavioral therapy is useful for dealing with the negative
thoughts that develop in many patients, such as sexual
inadequacy and low self-esteem.
29
Partners need to be involved
in this approach, because they are collaterally affected by PSSD.
Sex therapy and couples counseling should aim to educate the
partners that the sexual dysfunction is a side effect of the
medication and not a lack of interest. In addition, such behav-
ioral therapies can provide emotional and psychological support
for patients and partners.
29
These encouraging results suggest more research into the
management of PSSD could provide further breakthroughs.
With that in mind, it is crucial that all mental health practi-
tioners counsel their patients about PSSD before initiating
treatment.
4
Clinicians need to record baselines in these patients
and perform regular follow-ups for sexual function before, dur-
ing, and after SSRI administration.
10
Kashani et al
32
anecdotally
reported that saffron exhibited some benet in improving sexual
arousal and lubrication and might improve the sexual side effects
created by SSRI use. Physicians need to instruct patients to
report any loss of taste or smell, skin sensitivity, or genital
numbness, so that the physician can titrate the SSRI dose or
discontinue or change the medication. Whether a dose reduction
Sex Med Rev 2017;-:1e6
4Bala et al
will avert the possibility of PSSD is uncertain.
5
The patients
informed consent and the right to choose SSRIs as a treatment
option should be required before starting SSRIs.
10
CONCLUSION
PSSD is a persistent sexual dysfunction that occurs after
discontinuation of SSRI use. Commonly reported symptoms
include genital anesthesia, erectile dysfunction, pleasure-less
orgasm, decreased sex drive, decrease or absence of erection,
premature ejaculation, vaginal lubrication issues, and nipple
insensitivity in women. PSSD can result in patient non-
compliance to SSRIs.
7
Different theories have been proposed to
explain the pathophysiology of PSSD: epigenetic gene expression,
cytochrome actions, dopamine-serotonin interactions, proopio-
melanocortin and melanocortin effects, serotonin neurotoxicity,
downregulation of 5HT1A, and hormonal changes in the central
and peripheral nervous systems. Diagnosing PSSD is challenging
and should be done by reviewing the patients drug history, onset
of symptoms, and the patients sexual condition before starting
such a medication. Furthermore, excluding other comorbid dis-
eases and conditions that can cause PSSD is mandatory.
There is no denitive treatment for PSSD; however, there are
some proposed management options. Lowering SSRI dosage
could decrease the sexual side effects but weaken the drugs
initial treatment strategy. Adjunct therapy such as adding sil-
denal and bupropion did not show statistical benet.
Cognitive-behavioral therapy might help with PSSD. Buspirone,
trazodone, donepezil, ketamine, metformin, and mirtazapine
have been tested as PSSD treatments, with varying degrees of
success. Clinicians and mental health practitioners need to
counsel their patients about PSSD. All patients need to be
educated about the possibility of persistent impairment of sexual
dysfunction with SSRI usage. There are still many unknowns
about PSSD. It is important to investigate PSSD further to
elucidate its pathogenesis and to discover effective treatments for
PSSD.
Corresponding Author: Wayne J. G. Hellstrom, MD, FACS,
Department of Urology, Tulane University School of Medicine,
New Orleans, LA, USA; E-mail: whellst@tulane.edu
Conicts of Interest: The authors report no conicts of interest.
Funding: None.
STATEMENT OF AUTHORSHIP
Category 1
(a) Conception and Design
Areeg Bala; Wayne J. G. Hellstrom
(b) Acquisition of Data
Areeg Bala; Hoang Minh Tue Nguyen
(c) Analysis and Interpretation of Data
Areeg Bala; Hoang Minh Tue Nguyen
Category 2
(a) Drafting the Article
Areeg Bala
(b) Revising It for Intellectual Content
Hoang Minh Tue Nguyen; Wayne J. G. Hellstrom
Category 3
(a) Final Approval of the Completed Article
Areeg Bala; Hoang Minh Tue Nguyen; Wayne J. G. Hellstrom
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Sex Med Rev 2017;-:1e6
6Bala et al
... 24 Porém, várias teorias compreensivas foram propostas, principalmente relacionadas com alterações epigenéticas, inibição dos recetores serotoninérgicos e alterações nos eixos neuro-hormonais do sistema nervoso central provocadas pelo tratamento farmacológico com SSRIs. 25 De facto, são globalmente conhecidos os mecanismos pelos quais os SSRIs interferem negativamente na resposta sexual: aumento dos níveis de serotonina, diminuição dos níveis de dopamina, bloqueio dos recetores colinérgicos e α1 adrenérgicos, inibição da enzima óxido nítrico sintetase, elevação dos níveis de prolactina e diminuição dos níveis de oxitocina e testosterona. 17 Adicionalmente, também a neurotoxicidade provocada pelo aumento dos níveis de serotonina na fenda sináptica pode afetar áreas cerebrais importantes para a resposta sexual. ...
... 14,22 Também intervenções psicoterapêuticas foram propostas, particularmente a terapia cognitiva comportamental e a terapia de casal, com benefícios a nível psicológico, mas sem a reversibilidade ambicionada da PSSD. 25,26 Esta ausência de eficácia pode dever-se ao facto das estratégias terapêuticas desenvolvidas até ao momento se focarem sobretudo na tentativa de reversibilidade dos sintomas sexuais agudos em detrimento de se tentar reverter os mecanismos patofisiológicos responsáveis pela disfunção sexual persistente. 23 No entanto, tratamentos farmacológicos dirigidos para uma patofisiologia tão complexa que envolve teorias epigenéticas, citocromos, interações dopamina-serotonina, regulação de recetores serotoninérgicos bem como alterações hormonais centrais e periféricas, é ainda uma miragem científica sem substrato na literatura disponível. ...
... 23 No entanto, tratamentos farmacológicos dirigidos para uma patofisiologia tão complexa que envolve teorias epigenéticas, citocromos, interações dopamina-serotonina, regulação de recetores serotoninérgicos bem como alterações hormonais centrais e periféricas, é ainda uma miragem científica sem substrato na literatura disponível. 25 ...
... 24 Porém, várias teorias compreensivas foram propostas, principalmente relacionadas com alterações epigenéticas, inibição dos recetores serotoninérgicos e alterações nos eixos neuro-hormonais do sistema nervoso central provocadas pelo tratamento farmacológico com SSRIs. 25 De facto, são globalmente conhecidos os mecanismos pelos quais os SSRIs interferem negativamente na resposta sexual: aumento dos níveis de serotonina, diminuição dos níveis de dopamina, bloqueio dos recetores colinérgicos e α1 adrenérgicos, inibição da enzima óxido nítrico sintetase, elevação dos níveis de prolactina e diminuição dos níveis de oxitocina e testosterona. 17 Adicionalmente, também a neurotoxicidade provocada pelo aumento dos níveis de serotonina na fenda sináptica pode afetar áreas cerebrais importantes para a resposta sexual. ...
... 14,22 Também intervenções psicoterapêuticas foram propostas, particularmente a terapia cognitiva comportamental e a terapia de casal, com benefícios a nível psicológico, mas sem a reversibilidade ambicionada da PSSD. 25,26 Esta ausência de eficácia pode dever-se ao facto das estratégias terapêuticas desenvolvidas até ao momento se focarem sobretudo na tentativa de reversibilidade dos sintomas sexuais agudos em detrimento de se tentar reverter os mecanismos patofisiológicos responsáveis pela disfunção sexual persistente. 23 No entanto, tratamentos farmacológicos dirigidos para uma patofisiologia tão complexa que envolve teorias epigenéticas, citocromos, interações dopamina-serotonina, regulação de recetores serotoninérgicos bem como alterações hormonais centrais e periféricas, é ainda uma miragem científica sem substrato na literatura disponível. ...
... 23 No entanto, tratamentos farmacológicos dirigidos para uma patofisiologia tão complexa que envolve teorias epigenéticas, citocromos, interações dopamina-serotonina, regulação de recetores serotoninérgicos bem como alterações hormonais centrais e periféricas, é ainda uma miragem científica sem substrato na literatura disponível. 25 ...
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Os antidepressivos inibidores seletivos da recaptação da serotonina são psicofármacos frequentemente utilizados na prática clínica pelas especialidades de Medicina Geral e Familiar e de Psiquiatria no tratamento de perturbações depressivas e de ansiedade. As elevadas prescrições desta classe de antidepressivos resultam do seu concomitante perfil de eficácia, segurança e tolerabilidade.É clinicamente consensual que esta classe farmacológica pode interferir nas várias fases da resposta sexual durante o tratamento antidepressivo. No entanto, têm sido reportados cada vez mais casos na literatura em que a disfunção sexual não é reversível após a suspensão do fármaco, configurando uma nova entidade clínica persistente, cujo substrato patofisiológico se encontra presentemente sob intensa investigação científica. Rever a literatura recentemente publicada neste âmbito e consciencializar os clínicos para esta nova entidade revela-se uma prioridade com potenciais implicações, particularmente ao nível da abordagem de patologias psiquiátricas tão prevalentes na sociedade atual.
... Selective serotonin reuptake inhibitors (SSRIs) are commonly prescribed for managing different disorders, including depression (1). It has been reported that 1 in 8 people have utilized one of the SSRIs in the past 10 years. ...
... Men report issues of desire and orgasm especially. Sexual dysfunction may persist even after the discontinuation of SSRIs (1,4,8). In a study with 1022 participants, men have a higher incidence of sexual dysfunction (62.4%) than women (56.9%). ...
... Especially at the beginning of SSRI treatment, suicidal thoughts can increase. While most of these side effects improve over time, some can persist, especially sexual problems (Bala et al. 2018). In older adults, SSRI treatment can lead to severe hyponatraemia. ...
... However, one should keep in mind that especially in men, SSRI treatment may also be associated with erectile dysfunctioning, delayed ejaculation and inhibited orgasm which may increase non-compliance to treatment. Problems with erectile functioning can even persist after SSRI treatment has been terminated (Balon 2006;Bala et al. 2018). ...
Article
Objectives The current guidelines aim to evaluate the role of pharmacological agents in the treatment of patients with compulsive sexual behaviour disorder (CSBD). They are intended for use in clinical practice by clinicians who treat patients with CSBD. Methods An extensive literature search was conducted using the English-language-literature indexed on PubMed and Google Scholar without time limit, supplemented by other sources, including published reviews. Results Each treatment recommendation was evaluated with respect to the strength of evidence for its efficacy, safety, tolerability, and feasibility. Psychoeducation and psychotherapy are first-choice treatments and should always be conducted. The type of medication recommended depended mainly on the intensity of CSBD and comorbid sexual and psychiatric disorders. There are few randomised controlled trials. Although no medications carry formal indications for CSBD, selective-serotonin-reuptake-inhibitors and naltrexone currently constitute the most relevant pharmacological treatments for the treatment of CSBD. In cases of CSBD with comorbid paraphilic disorders, hormonal agents may be indicated, and one should refer to previously published guidelines on the treatment of adults with paraphilic disorders. Specific recommendations are also proposed in case of chemsex behaviour associated with CSBD. Conclusions An algorithm is proposed with different levels of treatment for different categories of patients with CSBD.
... Furthermore, a growing number of studies indicated that SSRI use may be associated with side effects such as an increased risk of developing type 2 diabetes (T2D) in adults [14], bleeding tendency [15], bone wound healing disorder [4], or sexual dysfunction after discontinuation of the SRI [16]. ...
Article
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Introduction Selective serotonin reuptake inhibitors (SSRIs) are a class of antidepressants used to treat depression, anxiety, panic states, and post-traumatic stress disorder (PTSD). Of particular importance is the drug treatment of SSRI, which correlates with an increased rate of dental implant loss. Literature suggests a higher risk of dental implant loss than patients not taking these medications. Presentation of the case We report a 46-year-old Caucasian female patient who presented for the extraction of teeth 36 and 46 followed by implant placement in regions 36 and 46. With good oral hygiene, the patient started taking an SSRI one year after the implantation. Thereafter, the titanium-zirconium and zirconium implants were lost. The loss of these implants in a short period of time is particularly striking. Discussion As the number of treatments for depression and also the number of dental implants are likely to continue to increase in the future, the combination of SSRIs and implantation will become more frequent. Given the two common treatments, the question arises whether SSRIs could be associated with dental implant loss in premenopausal Caucasian women. From an oral surgery perspective, the effects of SSRIs on bone formation are of particular concern, whilst the effects of SSRIs on the oral cavity have not been adequately studied due to the primary success of these drugs. In our case, as described in the literature, it can be assumed that the use of SSRIs after initial implantation may have a negative impact on the patient's bone remodelling. Therefore, the use of SSRIs may influence the most important factors for implant success. Conclusion As identifying conditions that put patients at higher risk of failure enables surgeons to make informed decisions and refine the treatment plan to optimize clinical outcomes, the aim of this case report is to highlight the association between SSRI use and the risk of dental implant failure. Clinicians should therefore be aware that SSRIs must be associated with adverse effects on bone and subsequent implant loss even in generally healthy patients.
... In fact, effects that are harmful to some could be beneficial to others. For example, a relatively common side effect of SSRIs is sexual dysfunction [23]. This is a negative effect of SSRIs for many people, but the very same phenomenon is a positive effect for people with premature ejaculation. ...
Article
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Background The way information about potential harms of trial intervention is shared within participant information leaflets (PILs) varies widely and can cause subjective ‘nocebo’ harms. This study aimed to develop principles to improve the composition of information about potential trial intervention benefits and harms within PILs so that variability and avoidable harms are reduced. Methods We conducted a two-round modified online Delphi survey, followed by a consensus meeting. For the first round of the survey, 27 statements were developed based on previous research and relevant guidance from the UK, the USA and the World Health Organization. Participants included members from each of the following stakeholder groups: patient and public representatives, research ethics committee members, industry representatives, medico-legal experts, psychologists and trial managers. Each participant was asked to rate their degree of agreement or disagreement with each statement on a 9-point Likert scale. In the second round, participants were invited to reappraise their ratings after reviewing the results of the first round. Finally, two members from each stakeholder group participated in a meeting to confirm those statements for which there was agreement. Results Two hundred and fifty participants completed round 1, and 201 participants completed round 2. In round 1, consensus was reached for 16 statements. In round 2, consensus was reached for an additional three statements. The consensus meeting confirmed the survey results and consolidated the statements. This process resulted in seven principles: (1) all potential harms of a given intervention should be listed, (2) all potential harms should be separated into serious and less serious, (3) it must be made explicit that not all potential harms are known, (4) all potential benefits should be listed, (5) all potential benefits and harms need to be compared with what would happen if the participant did not take part in the trial, (6) suitable visual representations should be added where appropriate and (7) information regarding potential benefits and harms should not be presented apart by one or more pages. Conclusions Our modified Delphi process successfully generated seven principles that can and should be used to guide how information is conveyed to patients in information leaflets regarding potential trial benefits and harms.
... Because of their significant curative effect and high safety profile, SSRIs have been front-line pharmacotherapies in the treatment of depression for a long time (Cipriani et al., 2018). Additionally, SSRIs can also be used as a medicine for premature ejaculation because of the reversible sexual side effects (Giuliano and Clement, 2012;Bala et al., 2018). ...
Article
Full-text available
Selective serotonin reuptake inhibitors (SSRIs) are widely used for a variety of diseases, and their impact on semen quality is unclear. We performed a systematic search in PubMed and Embase, and after a strict screening, we included 4 studies with a total of 222 male participants. In result, SSRIs reduced normal sperm morphology (95% CI [−16.29, −3.77], p = 0.002), sperm concentration (95%CI [−43.88, −4.18], p = 0.02), sperm motility (95%CI [−23.46, −0.47], p = 0.04) and sperm DNA fragmentation index (DFI) (95% CI [6.66,21.93], p = 0.0002), without a statistically significant effect on semen volume (95%CI [−0.75,0.65], p = 0.89). Moreover, the impact on both sperm morphology and sperm concentration were observed within the 3-month period of SSRIs use. In general, our meta-analysis showed that SSRIs have a negative effect on semen quality. More larger, randomized, well-controlled clinical studies should be conducted to support our conclusion.
Chapter
Mit über 2 Mrd. DDD stellen Arzneistoffe zur Behandlung der Depression, von Angststörungen, der bipolaren Störung und der Depression („Psychopharmaka“) eine der meist verordneten Arzneimittelgruppen dar. Dabei sind die seit vielen Jahren beobachteten Zuwächse vor allem auf steigende Verordnungen und Indikationsausweitungen von antidepressiven Arzneistoffen („Antidepressiva“) zurückzuführen sowie geringere Zunahmen bei den antipsychotischen Arzneistoffen („Antipsychotika“). Dagegen nehmen die Verordnungen von Arzneimitteln mit sedierender und anxiolytischer Wirkung („Tranquillantien“) seit langem kontinuierlich ab. Trend Im Durchschnitt haben die Verordnungen von Antidepressiva (Noradrenalin/Serotonin-Verstärker) in der letzten Dekade um mehr als 30 % zugenommen. Dies ist vor allem auf die zwei Arzneistoffgruppen der selektiven Serotonin-Rückaufnahme-Inhibitoren (SSRI) und der selektiven Serotonin-Noradrenalin-Rückaufnahme-Inhibitoren (SNRI) zurückzuführen, wohingegen die Verordnung der nichtselektiven Monoamin-Rückaufnahme-Inhibitoren (NSMRI, sog. trizyklischen oder heterozyklischen Antidepressiva) sich in den letzten 10 Jahren stetig rückläufig zeigte. Bei den Antipsychotika ist ein kontinuierlicher Verordnungsanstieg bei den sog. atypischen Antipsychotika (p-mGPCR-Antagonisten) wie Clozapin, Quetiapin, Risperidon und Amisulprid zu beobachten, der durch einen nur sehr moderaten Rückgang der Verschreibung klassisch hochpotenter Antipsychotika (D2R-mGPCR-Antagonisten) wie Haloperidol nicht kompensiert wird. Es handelt sich also vermutlich um Indikationsausweitungen oder einen Trend zur Verordnung höherer Dosierungen. Niedrigpotente Antipsychotika (D2R-mGPCR-Antagonisten) wie Melperon, Pipamperon und Promethazin wurden in gleichbleibendem Umfang verordnet. Die Verordnungen von Arzneimitteln zur Behandlung der Aufmerksamkeitsdefizit-/Hyperaktivitätsstörung (ADHS) sind seit starken Zuwächsen in den 2000er Jahren nunmehr seit 5 Jahren annähernd konstant.
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The multidimensionality and interpersonal dimension of human sexuality make the study of female sexual dysfunction (FSD) a challenge. The aspiration to pursue a patient-centered, holistic approach collides with the need to establish commonly accepted diagnostic criteria for different disturbances in sexual functioning, involving one or multiple phases of the sexual response cycle and pain associated with sexual activity. According to recently proposed classifications, which are continuously evolving, the most relevant FSDs include hypoactive sexual desire disorder, female arousal disorder, persistent genital arousal disorder, and female orgasm disorder. The present chapter aims to provide a clinical perspective on these disorders by reviewing the most recent evidence on the pathophysiology, definitions, prevalence, leading etiologies, diagnostic tools, and key therapeutic approaches. Sexual pain-related conditions will be reviewed in another chapter. It is evident that a gender bias still exists, with prominent biological etiologies of FSDs being neglected and understudied at the expense of psychodynamic and relational determinants. Moreover, classifications should serve to advocate the advancement of our knowledge of female sexual functioning. This process goes through the practical translation of the updated nosology in a language that is intelligible to primary healthcare providers all over the world, and ultimately, to women.
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Importance Case reports describe persistent erectile dysfunction (PED) associated with exposure to 5α-reductase inhibitors (5α-RIs). Clinical trial reports and the manufacturers’ full prescribing information (FPI) for finasteride and dutasteride state that risk of sexual adverse effects is not increased by longer duration of 5α-RI exposure and that sexual adverse effects of 5α-RIs resolve in men who discontinue exposure. Objective Our chief objective was to assess whether longer duration of 5α-RI exposure increases risk of PED, independent of age and other known risk factors. Men with shorter 5α-RI exposure served as a comparison control group for those with longer exposure. Design We used a single-group study design and classification tree analysis (CTA) to model PED (lasting ≥90 days after stopping 5α-RI). Covariates included subject attributes, diseases, and drug exposures associated with sexual dysfunction. Setting Our data source was the electronic medical record data repository for Northwestern Medicine. Subjects The analysis cohorts comprised all men exposed to finasteride or dutasteride or combination products containing one of these drugs, and the subgroup of men 16–42 years old and exposed to finasteride ≤1.25 mg/day. Main outcome and measures Our main outcome measure was diagnosis of PED beginning after first 5α-RI exposure, continuing for at least 90 days after stopping 5α-RI, and with contemporaneous treatment with a phosphodiesterase-5 inhibitor (PDE 5 I). Other outcome measures were erectile dysfunction (ED) and low libido. PED was determined by manual review of medical narratives for all subjects with ED. Risk of an adverse effect was expressed as number needed to harm (NNH). Results Among men with 5α-RI exposure, 167 of 11,909 (1.4%) developed PED (persistence median 1,348 days after stopping 5α-RI, interquartile range (IQR) 631.5–2320.5 days); the multivariable model predicting PED had four variables: prostate disease, duration of 5α-RI exposure, age, and nonsteroidal anti-inflammatory drug (NSAID) use. Of 530 men with new ED, 167 (31.5%) had new PED. Men without prostate disease who combined NSAID use with >208.5 days of 5α-RI exposure had 4.8-fold higher risk of PED than men with shorter exposure (NNH 59.8, all p < 0.002). Among men 16–42 years old and exposed to finasteride ≤1.25 mg/day, 34 of 4,284 (0.8%) developed PED (persistence median 1,534 days, IQR 651–2,351 days); the multivariable model predicting PED had one variable: duration of 5α-RI exposure. Of 103 young men with new ED, 34 (33%) had new PED. Young men with >205 days of finasteride exposure had 4.9-fold higher risk of PED (NNH 108.2, p < 0.004) than men with shorter exposure. Conclusion and relevance Risk of PED was higher in men with longer exposure to 5α-RIs. Among young men, longer exposure to finasteride posed a greater risk of PED than all other assessed risk factors.
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Background: There have been reports for over a decade linking serotonin reuptake inhibitors, finasteride and isotretinoin with enduring sexual dysfunction after treatment stops. Objective: To explore the clinical pictures linked to all 3 drugs. Methods: We have selected 120 reports to RxISK.org reporting the problem and mined these for data on age, gender, drug of use, and impact of the problem. Results: The data make it clear that the three drugs show extensive overlap in symptom profile, regardless of sex or country of origin. Conclusions: The availability of 120 reports from over 20 countries add to the case for the validity of the syndrome. This is severe and enduring condition can result in death. An understanding of its physiology and an approach to treatment are needed.
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Article
Introduction: Sexual dysfunctions are well-known side effects of selective serotonin reuptake inhibitor (SSRI) use. Altered libido, erectile dysfunction, vaginal dryness, ejaculatory disorders, and orgasmic problems are frequently reported by patients treated with SSRIs. Moreover, these antidepressant-emergent sexual dysfunctions do not always resolve after discontinuation of the medication and can persist indefinitely. These complaints are termed post-SSRI sexual dysfunctions (PSSD). Aim: To examine the existence of this clinical entity, possible theoretical mechanisms, possible risk factors, and possible treatment modalities. Methods: Through literature research and clinical experience, the available information about PSSD is reviewed. Main outcome measures: Summary of the current literature with insights into possible causes and management options. Results: There are some indications that antidepressant-emergent sexual dysfunctions do not always resolve after discontinuation of the medication and can persist indefinitely in some individuals. Although some or all sexual side effects that start with the use of SSRIs might continue after stopping the medication, other sexual complaints can develop. Decreased capacity to experience sexual pleasure is the most frequent characteristic of this syndrome. Conclusion: The research and understanding of PSSD remain limited and not well understood; however, the data support the existence of PSSD, which can have a substantial effect on the quality of life of these patients. More research is warranted to show the cause and possible mechanisms of PSSD that could lead to the correct diagnosis and treatment. Reisman Y. Sexual Consequences of Post-SSRI Syndrome. Sex Med Rev 2017;X:XXX-XXX.
Article
Background: Sexual dysfunction is a common adverse effect of selective serotonin reuptake inhibitors (SSRIs) and there is a concern that the sexual harms might persist after discontinuation of therapy. Objective: To assess whether the use of SSRIs in animals can lead to persistent sexual dysfunction. Methods: Systematic review of animal studies measuring sexual behaviour after end of treatment with SSRIs or serotonin norepinephrine reuptake inhibitors. Data sources: We searched PubMed and EMBASE. Results: We included 14 studies. The general quality of the studies was poor. Only four studies reported use of randomisation and none mentioned allocation concealment. All studies used placebo and were therefore blinded. For rats exposed to SSRIs compared with those exposed to placebo, we found a higher risk of no mounting behaviour (RR = 0.73; 95% CI = 0.62-0.86), no intromission behaviour (RR = 0.74; 95% CI = 0.60-0.92) and no ejaculation behaviour (RR = 0.49, 95% CI = 0.24-1.00). Conclusion: Our results showed substantial and lasting effects on sexual behaviour in rats after exposure to an SSRI early in life on important sexual outcomes.
Article
Objective: Neurophysiologic findings indicate an inhibition of dopaminergic neurotransmission by selective serotonin reuptake inhibitors (SSRIs). This article highlights the relationships between changes in dopaminergic neurotrans-mission induced by SSRIs and the occurrence of certain side effects such as hyperprolactinemia, extrapyramidal symptoms, sexual and cognitive dysfunction, galactorrhea, mammary hypertrophy, and, more rarely, gynecomastia. Data sources and selection: A systematic search of the literature in English, French, and German from 1980 to 2004 was performed in MEDLINE, EMBASE, and the Cochrane Library using the keywords SSRI, dopamine, serotonin, side effects, antidepressants, citalopram, escitalopram, sertraline, paroxetine, fluoxetine, fluvoxamine, and nefazodone. References cited in all trials were searched iteratively to identify missing studies. All studies concerning inhibition of dopaminergic neurotransmission by SSRIs and SSRI-related side effects were considered. We retained 62 significant articles debating the subject. Data extraction and synthesis: We critically reviewed the studies, depending on the methodologies (case reports, clinical reports, randomized studies), and assessed the pertinence of "dopamine-dependent" SSRI-related side effects. The analytic review of these articles suggests that some specific SSRI-related side effects be classified as dopamine-dependent. Conclusions: At a clinical level, it could be useful to underline dopamine-dependent characteristics of some SSRI-related side effects. This approach would allow clinicians the opportunity to search other dopamine-dependent side effects systematically. At a pharmacologic level, this approach could stimulate the development of molecules with a "corrective" function on dopamine-dependent side effects of SSRIs by facilitating dopaminergic neurotransmission.
Article
Emerging evidence suggests that sexual dysfunction emerging during treatment with selective serotonin reuptake inhibitors (SSRIs) and/ or serotonin-norepinephrine reuptake inhibitors (SNRIs) persists in some patients beyond drug discontinuation (post-SSRI sexual dysfunction [PSSD]). We sought to identify and characterize a series of such cases and explore possible explanatory factors and exposure-response relationship. Subjects who responded to an invitation in a forum dedicated to PSSD filled out a survey via online software. Case probability was defined according to the following 3 categories of increasing presumed likelihood of PSSD. Noncases did not meet the criteria for possible cases. Possible cases were subjects with normal pretreatment sexual function who first experienced sexual disturbances while using a single SSRI/SNRI, which did not resolve upon drug discontinuation for 1 month or longer as indicated by Arizona Sexual Experience Scale scores. High-probability cases were also younger than 50-year-olds; did not have confounding medical conditions, medications, or drug use; and had normal scores on the Hospital Anxiety and Depression Scale. Five hundred thirty-two (532) subjects completed the survey, among which 183 possible cases were identified, including 23 high-probability cases. Female sex, genital anesthesia, and depression predicted current sexual dysfunction severity, but dose/defined daily dose ratio and anxiety did not. Genital anesthesia did not correlate with depression or anxiety, but pleasureless orgasm was an independent predictor of both depression and case probability. Limitations of the study include retrospective design and selection and report biases that do not allow generalization or estimation of incidence. However, our findings add to previous reports and support the existence of PSSD, which may not be fully explained by alternative nonpharmacological factors related to sexual dys-function, including depression and anxiety.
Article
Treatment of paroxetine-induced penile anesthesia in Post SSRI Sexual Dysfunction (PSSD) by Low-power Laser Irradiation (LPLI) is unknown in medical literature. The aim of the current article is to report partial efficacy of LPLI for paroxetine-induced persistent penile anesthesia. We report on a male patient who presented with a history of reversible loss of smell, taste and skin sensitivity occurring within a week after start of 20mg/day paroxetine-hemihydrate for a depressive period. Concurrently, patient suffered from penile anesthesia, scrotum hypesthesia, anejaculation and erectile difficulties with normal sexual desire. During 2.5 years of paroxetine treatment and throughout 2 years after paroxetine discontinuation, genital and sexual complaints persisted. Penile anesthesia was treated by LPLI with single and multi diode pulsed laser probes. After 20 LPLI-treatment sessions of 15min each, patient reported partial return of penile touch and temperature sensation. Clinical improvement of glans penis sensitivity was reported to 20% and 40%, compared to pre-paroxetine treatment penile sensitivity during erect and flaccid states, respectively. However, anejaculation and erectile difficulties remained unchanged. Briefly, in the current patient with early onset of PSSD, LPLI treatment reduced paroxetine-induced penile anesthesia. It is hypothesized that SSRI treatment induces disturbances of transient receptor potential (TRP) ion channels of mechano-, thermo- and chemosensitive nerve endings and receptors resulting in the penile anesthesia in PSSD. It is further hypothesized that there are two types of PSSD, one of which occurs soon after the start of SSRI treatment. Copyright © 2014. Published by Elsevier B.V.
Article
Background: Cases reported in the literature suggest that in some individuals sexual dysfunction associated with selective serotonin reuptake inhibitors (SSRIS) may persist following the discontinuation of ssris. Aim: To find out how many reports of persistent sexual dysfunction associated with the use of ssris were received by the Netherlands Pharmacovigilance Centre, Lareb. Method: The database of the Netherlands Pharmacovigilance Centre Lareb was searched for reports of sexual dysfunction in patients who had been using SSRIS and whose sexual functioning had not returned to normal at the time of notification. Results: The database of the Netherlands Pharmacovigilance Centre Lareb contained 19 reports of persistent sexual dysfunction in patients who had stopped using ssris for two months up to three years and who had not regained normal sexual functioning. The sexual disorders that were reported most frequently were reduced libido, erectile dysfunction and delayed orgasm. It seems likely that these disorders were caused not only by pharmacological effects of ssris but also by psychological factors. Conclusion: Although it has previously been assumed that patients always regain normal sexual functioning shortly after discontinuation of ssris, emerging evidence suggests that this may not be the case.
Article
Objective: Saffron (Crocus sativus L.) has shown beneficial aphrodisiac effects in some animal and human studies. The aim of the present study was to assess the safety and efficacy of saffron on selective serotonin reuptake inhibitor-induced sexual dysfunction in women. Methods: This was a randomized double-blind placebo-controlled study. Thirty-eight women with major depression who were stabilized on fluoxetine 40 mg/day for a minimum of 6 weeks and had experienced subjective feeling of sexual dysfunction entered the study. The patients were randomly assigned to saffron (30 mg/daily) or placebo for 4 weeks. Measurement was performed at baseline, week 2, and week 4 using the Female Sexual Function Index (FSFI). Side effects were systematically recorded. Results: Thirty-four women had at least one post-baseline measurement and completed the study. Two-factor repeated measure analysis of variance showed significant effect of time × treatment interaction [Greenhouse-Geisser's corrected: F(1.580, 50.567) = 5.366, p = 0.012] and treatment for FSFI total score [F(1, 32) = 4.243, p = 0.048]. At the end of the fourth week, patients in the saffron group had experienced significantly more improvement in total FSFI (p < 0.001), arousal (p = 0.028), lubrication (p = 0.035), and pain (p = 0.016) domains of FSFI but not in desire (p = 0.196), satisfaction (p = 0.206), and orgasm (p = 0.354) domains. Frequency of side effects was similar between the two groups. Conclusions: It seems saffron may safely and effectively improve some of the fluoxetine-induced sexual problems including arousal, lubrication, and pain.