Journal of the Neurological Sciences 350 (2015) 7–13

Contents lists available at ScienceDirect

Journal of the Neurological Sciences

journal homepage: www.elsevier.com/locate/jns

Review article

Stroke and sexual dysfunction — A narrative review

Jong-Ho Park a,b, Bruce Ovbiagele b, Wuwei Feng b,⁎
a
Department of Neurology, Myongji Hospital, Goyang, South Korea
b
Department of Neurology, MUSC Stroke Center, Medical University of South Carolina, Charleston, SC, United States

a r t i c l e i n f o a b s t r a c t

Article history: Sexual function is an essential part of quality of life in adults. However, sexual dysfunction (SD) in stroke survi-
Received 5 October 2014 vors is a common but under-recognized complication after stroke. It is frequently neglected by patients and
Received in revised form 9 January 2015 clinicians. The etiology of post-stroke SD, which is multifactorial includes anatomical, physical and psychological
Accepted 1 February 2015
factors. Complete return of sexual function is an important target for functional recovery after stroke, so clinicians
Available online 7 February 2015
need to be aware of this issue and take a lead role in addressing this challenge in stroke survivors. Accurate diag-
Keywords:
nosis and prompt treatment of post-stroke SD should be routinely incorporated into comprehensive stroke reha-
Stroke bilitation. This narrative review article, outlines the anatomy and physiology of sexual function, discusses various
Sexual dysfunction factors contributing to post-stroke SD, and proposes directions for future research.
Complication © 2015 Elsevier B.V. All rights reserved.
Outcomes
Rehabilitation

Contents

1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8
2. Physiology of the sexual response cycle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8
3. Anatomical locations responsible for sexual dysfunction (Table 1) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8
3.1. Mesodiencephalolimbic system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8
3.2. Cerebral hemisphere, cortex and subcortex (Striatum) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8
3.3. Cerebellum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8
3.4. Anatomical locations responsible for hypersexuality . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9
4. Sexual dysfunction after stroke. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9
4.1. Factors contributing to post-stroke sexual dysfunction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10
4.1.1. Psychological factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10
4.1.2. Sociodemographic factors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10
4.1.3. Physical deficits . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10
4.1.4. Vascular risk factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10
4.1.5. Urogenic factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11
4.1.6. Autonomic dysfunction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11
4.1.7. Neuroendocrine dysfunction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11
4.1.8. Partner factor(s) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11
4.1.9. Medications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11
5. Return of sexual functionality after stroke . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11
6. Conclusions and future research . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12
Source of funding . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12
Disclosures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12
Acknowledgment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12

⁎ Corresponding author at: Department of Neurology and Neurosurgery, Medical University of South Carolina, Charleston, SC 29425, United States. Tel.: +1 843 792 3020.
E-mail address: feng@musc.edu (W. Feng).

http://dx.doi.org/10.1016/j.jns.2015.02.001
0022-510X/© 2015 Elsevier B.V. All rights reserved.
8 J.-H. Park et al. / Journal of the Neurological Sciences 350 (2015) 7–13
1. Introduction
Stroke is a leading cause of disability that can impair physical, lin-
guistic, cognitive and sexual function [1]. Of all post-stroke disabilities,
sexual dysfunction (SD) is considerably under-recognized. SD can pres-
ent as decreased libido, impotence or inability to ejaculate in males or
decreased libido, lack of vaginal lubrication, arousal problems or orgas-
mic dysfunction in females. Understandably stroke patients are often
embarrassed to discuss SD issues with their physicians. Patient reticence
and physician ignorance have arguably led to a relative neglect of post-
stroke SD, thereby limiting our ability to explore underlying mecha-
nisms and identify appropriate therapeutic strategies [2].
Normal sexual function relies on a complex network of central and
peripheral nervous system pathways involving autonomic (sym-
pathetic/parasympathetic), spinal, and somatic nervous systems [2].
However, little is known about the impact of stroke on sexual activity
or which specific psychological or organic factors contribute to SD
after stroke.
In this narrative review, we first outline the physiology and anatom-
ical correlations of sexual activity; secondly, we discuss the various fac-
tors contributing to post-stroke SD; and finally, we propose directions
for future research.
2. Physiology of the sexual response cycle
There are three ways that neurobiological systems are involved in
sexual response [2,3]: (1) physiologic input systems for inducing sexual
arousal, (2) spinal and mesodiencephalolimbic in mediating sexual
arousal, and (3) physiologic response in the genital region by sympa-
thetic/parasympathetic nervous system necessary for priming and exe-
cuting a sexual activity.
In males, the neurotransmitters and neuropeptides facilitating pe-
nile erections are oxytocin, dopamine, glutamic acid, opioid peptides,
hexarelin peptides, and pro-VGF peptides [4]. The paraventricular nu-
cleus (PVN) of the hypothalamus [4] is the most sensitive area for the
pro-erectile effect of oxytocin. It projects oxytocinergic neurons to
extra-hypothalamic brain areas (e.g., septum, hippocampus, amygdala,
ventral tegmental area, medulla oblongata and spinal cord). The PVN
is considered as a cardinal integration center between the central and
peripheral autonomic nervous systems [5]. During sexual arousal,
oxytocin-induced penile erection is mediated by Ca2+ influx into the
oxytocinergic neurons in PVN. This causes nitric oxide by activation of
nitric oxide-synthase. Nitric oxide in turn leads to the activation of
oxytocinergic neurons, which project to extra-hypothalamic brain
areas, thereby inducing penile erection and copulatory behavior [4,5].
Oxytocinergic pathways from PVN to extra-hypothalamic brain areas
that mediate penile erection are illustrated in Fig. 1. Furthermore, oxy-
tocin also activates mesolimbic dopaminergic neurons. Dopamine re-
leased in the nucleus accumbens (NAcc) in turn stimulates neural
pathways leading to the activation of incerto-hypothalamic dopaminer-
gic neurons in the PVN involved in erectile function [4].
On the contrary, little is known about precise mechanisms that me-
diate female sexual response.
Male genital apparatus is innervated mainly by pudendal nerves,
which contain the primary afferent sensory and motor pathways to
the penis, and by cavernous nerves, which contain the primary efferent
sympathetic and parasympathetic pathways [5]. Cavernous nerves are
innervated by hypogastric nerves, pelvic nerves, and paravertebral sym-
pathetic ganglia chain of the thoracic–lumbar tract (T11–L2) [5]. In
males, penile erection is mediated by pelvic parasympathetic activity
while ejaculation is controlled by thoracolumbar sympathetic system
[6]. In females, sexual stimulation increases blood flow to the vagina
resulting in lubrication and erection of the cavernous tissues and clito-
ris, which are innervated by the pudendal nerve [7]. Sexual function in
females proceeds in a more complex and circuitous manner than
males and is more vulnerable to psychosocial factors [8].
3. Anatomical locations responsible for sexual dysfunction (Table 1)
3.1. Mesodiencephalolimbic system
The thalamus may play a crucial role in penile erection. Jeon et al.
investigated the correlation of erectile dysfunction (ED) with stroke
lesion(s) in 44 ischemic stroke patients [9]. Thalamic lesions were
found to be more associated with ED compared to lesions in other lo-
cations. In an fMRI study, the thalamus was bilaterally activated dur-
ing erection in 10 out of 12 subjects [10]. In another study, eleven
healthy heterosexual young volunteers underwent positron emis-
sion tomography (PET) to measure increases in regional cerebral
blood flow (rCBF). During ejaculation, the mesodiencephalolimbic
system, including the ventral tegmental area, lateral central tegmen-
tal field, subparafascicular nucleus, and the medial/ventral thalamus
recorded the most intense activation [11]. However, another study
found no specific activation in the thalamus or hypothalamus to
the genital part of the primary somatosensory cortex during sexual
intercourse [12].
The NAcc is a part of the mesolimbic system and regulates dopamine-
driven pleasure and sexual activity [13]. Studies of NAcc relating to sex-
ual behavior have shown conflicting results. In a study with male rats,
bilateral NAcc lesions caused inability to have an erection and intromis-
sion [14], but other studies showed only minor impairment of sexual be-
havior or limited change after NAcc damage [15,16]. Moreover, increased
rCBF was not observed in NAcc in a human study [12].
The amygdala was found to be closely associated with ejaculation in
human studies [11,17]. Contrary to other limbic system studies, the amyg-
dala seems to have an inverse relationship between euphoric psycholog-
ical states and amygdala activation during human male ejaculation [11].
3.2. Cerebral hemisphere, cortex and subcortex (Striatum)
The right hemisphere is more likely to play a dominant role in acti-
vation/attention of libido and erectile functionality [18,19]. Sexual reac-
tion time is more impaired in right hemispheric stroke than left [19]. In a
PET study [12] to measure rCBF during various stages of sexual perfor-
mance, sexual stimulation of the penis increased rCBF in the posterior
insular and adjacent posterior part of the secondary somatosensory
cortex of the right hemisphere. In the neocortex, the activated regions
were primarily on the right side. The right hemisphere also dominates
in sensing emotional stimuli, as a result, right parietal lesions
frequently cause hemi-inattention [18] and increase susceptibility to
emotional disorders [20,21]. Patients with right hemispheric stroke
likely have difficulty in responding to erotic sensations because of
sensory and perceptual neglect [22]. Therefore, it is conceivable that
right parietal lesions are more closely associated with the development
of SD.
However, studies are not consistent regarding the laterality of
hemispheric lesion and SD. Monga et al. reported that females with
right-hemispheric lesions were more likely to experience a decline in
sexual function when compared to those with left-hemispheric lesions
[23]. Another study suggested that left hemispheric lesions play an
important role in post-stroke SD (diminished libido or satisfaction)
among male patients [24]. Post-stroke depression occurs more com-
monly with left hemispheric stroke and is closely related to SD, but
these studies failed to show a relationship between the lesion side and
SD [25–27].
3.3. Cerebellum
The cerebellum is involved with motor coordination, emotional pro-
cessing [28] and sexual arousal [17]. Large portions of cerebellum, in-
cluding deep cerebellar nuclei, vermis, and hemispheres are activated
during ejaculation, especially the left side [11]. Jung et al. showed that
right cerebellar lesions were associated with ejaculation disorder in a
 J.-H. Park et al. / Journal of the Neurological Sciences 350 (2015) 7–13 9

Fig. 1. Schematic representation of oxytocinergic neurons in the paraventricular nucleus (PVN) of the hypothalamus in males. Penile erection was mediated by Ca2+ influx into the
oxytocinergic neurons in PVN that are linked to extra-hypothalamic brain areas. Facilitatory neurotransmitters and neuropeptides that control penile erection are oxytocin, dopamine,
glutamic acid, opioid peptides, hexarelin peptides, and pro-VGF peptides. Nitric oxide-synthase-induced nitric oxide activates oxytocinergic neurons that project to extra-hypothalamic
brain areas and genital apparatus, thereby inducing penile erection.

survey of 109 post-stroke male patients [29]. Annoni et al. reported a

patient with a left cerebellar infarct who showed emotional blunting
and autonomic inability to react differentially to positive and negative Table 1
Relevant anatomical locations for sexual activation and function.
external stimuli [30]. The fastigial nucleus in cerebellum is closely con-
nected with hypothalamus, which is responsible for sympathetic/para- Anatomical locations Side Function(s)
sympathetic modulation [31]. prediction

Mesodiencephalolimbic area
Ventral tegmental area [11]⁎ Both Orgasm, ejaculation
3.4. Anatomical locations responsible for hypersexuality Lateral central tegmental Both Ejaculation
field⁎[11]
Subparafascicular nucleus⁎[11] Both Ejaculation
While hyposexuality is a common occurrence after a stroke,
Ventroposterior, midline, and Both Sexual arousal, erection,
hypersexuality can occur. Increased libido was reported in 10% of intralaminar thalamic nuclei⁎ sensory experience
192 stroke patients in one study [26]. Hypersexuality after stroke is [9–11]
commonly associated with temporal lobe lesions [32]. It can also de- Hypothalamus [12] Right Sexual arousal
velop after subthalamic or bilateral thalamic infarction [33,34]. Amygdala†[11,17] Left Ejaculation
Cerebral hemisphere [18–21,38] Right Activation/attention of libido
Frontolimbic structures may have an important role in sexual behav-
and erectile function,
ior as well. Hypersexuality may result from reactive hypermetabo- recognition
lism within the frontolimbic system (basal forebrain, temporal of emotional stimuli
lobes, anterior cingulate, and medial prefrontal cortices) and stria- Cerebral cortex and subcortex
Parietal cortex [11,19] Right Ejaculation, attention, reaction
tum ipsilateral to the stroke [33].
time
Posterior insula [12] Right Sexual arousal
Secondary somatosensory cortex Right Sexual arousal
4. Sexual dysfunction after stroke [12]
Inf. frontal gyrus [11] Right Ejaculation
As summarized in Table 2, post-stroke SD is quite common with a Inf. temporal cortex [11] Right Ejaculation
prevalence ranging from 20 to 75%. Majority of study subjects are Precuneus [11] Right Ejaculation
Sup. frontal gyrus (small portion) Left Ejaculation
males. However, SD can occur in either male or female stroke survivors [11]
[23–27,35–42]. Clinical presentations of SD for males include decreased Visual cortex [11] Both Ejaculation
sexual activity despite normal function, decreased libido, decreased fre- VL putamen [11] Both Ejaculation
quency of coitus, ED and ejaculatory dysfunction. In females, SD is gen- Claustrum [11] Both Ejaculation
Cerebellum‡[11,17,28–31] Left Sexual arousal, ejaculation,
erally exhibited as decreased libido, lack of vaginal lubrication, arousal
emotional processing,
problems and orgasmic dysfunction [23–27,35–40]. Of note, even in autonomic modulation
stroke patients with no or mild physical disability, nearly half experi-
VL: ventrolateral.
enced a decrease in libido, coital frequency, sexual arousal, orgasm ⁎ The strongest activation area.
and sexual satisfaction [39]. Occasionally, hypersexuality can occur as †
Deactivated structure.
‡
well [26,32–34]. Including deep cerebellar nuclei, vermis, and hemispheres.
10 J.-H. Park et al. / Journal of the Neurological Sciences 350 (2015) 7–13

Table 2
Summary from studies regarding sexual dysfunctions after stroke.

Studies Subjects (Mean) Predicting factor(s) Measures Prevalence (%)

(no) Age (y)

Korpelainen [26] 192 Pts, 59 Psychosocial factors (general attitude, ↓ Libido, coitus, EF/lubrication, 57
94 spouses fear, inability to discuss, unwillingness), orgasm, and SS
functional disability, spouse
Monga [23] 113 69-M, 68-F Fear for stroke recurrence ↓ Libido, coitus, EF/lubrication, 74 (M), 63 (F)
(78 M, 35 F) and orgasm
Kimura [24] 100 N/A Depression, Lt. hemisphere lesion ↓ Libido and EF 59 (M), 44 (W)
(75 M, 25 F)
Sjögren [25] 51 NA Psychogenic (performance orientation ↓ Libido, coitus, EF, and ejaculation 64 (M), 75 (F)
and sexual stigmatism)
Choi-Kwon [27] 70 NA Poststroke emotional incontinence ↓ Libido, coitus and EF 44 (↓ Libido), 49 (↓ Coitus),
20 (↓ EF)
Korpelainen [35] 50 32 to 65 Sensory hemisyndrome, spouse ↓ Libido, coitus, EF/lubrication, 28 at 2 months
(38 M, 12 F) ejaculation/orgasm, and SS 14 at 6 months
Sjögren [36] 110 NA ↓ Cutaneous sensibility, dependent ADL ↓ Coitus 75
Hawton [37] 50 M NA ↓ Prestroke sexual activity ↓ EF NA
Coslett [38] 26 M NA Rt. hemisphere lesion ↓ Libido and coitus 50
Cheung [39] 106 NA Unwillingness, belief in adverse effect ↓ Libido, coitus, SA, orgasm, 54 (↓ Libido), 44 (↓ Coitus),
(63 M, 43 F) of stroke on sexuality and SS 25 (F)/52 (M) (↓ SA),
20 (F)/46 (M) (↓ Orgasm), 29 (SS)
Giaquinto [40] 62 64 Fear, false belief of sexual life only to ↓ Libido, coitus, EF/lubrication, 57 (M), 25 (W)
(46 M, 16 F) healthy people, spouse and ejaculation
Forsberg-Wärleby [41] 67 spouses NA Sensorimotor symptom and low ability in ↓ Sexual life (at 1 year) NA
self-care, cognitive/emotional impairments
Stein [42] 38 55.1 – Changes in sexual functioning 47
questionnaire

M: male; F: female; EF: erectile function; SS: sexual satisfaction; SA: sexual arousal; ADL: activities of daily living; NA: not accessible.

4.1. Factors contributing to post-stroke sexual dysfunction
Post-stroke SD is thought to result from multiple factors, both
psychosocial (i.e. depression, anxiety, fear of stroke recurrence, loss of
self-esteem, role changes) and/or organic (i.e. stroke lesion, comorbidi-
ty and medications) [43]. Potential factors related to SDs after stroke are
summarized in Table 3 and reviewed as follows.
4.1.1. Psychological factors
Psychological factors may affect SD more than physical deficits.
Stroke survivors with no or mild physical impairment frequently expe-
rienced reduced sexual activity [36].
directly or indirectly. Many medications carry the adverse effect of fa-
tigue which can be a contributing factor as well.
4.1.2. Sociodemographic factors
Several studies have revealed that age or gender is not independent-
ly related to SD occurrence [24,26,27,40]. Additionally, there was no
clear correlation with marital status [26], marriage/partnership dura-
tion, or educational level [40]. It was suggested that an active sexual
life before stroke is a major determining factor for sexual activity after
stroke [37].

• Depression: Depression is very common after stroke. It is more likely

to contribute to SD than the stroke lesion itself [24,40]. In a study,
higher score of Hamilton Rating Scale for Depression after stroke
was an independent predictor of SD development for both male and
female (OR = 1.55) [24]. Korpelainen et al. also reported that post-
stroke SD is closely correlated with depression severity [26].
• Fear: Another important factor is fear of stroke occurrence during sex-
ual activity. Sexual intercourse may trigger an acute ischemic stroke
[44–46] or rupture of cerebral aneurysm [47] during or after sexual ac-
tivity, but the risk is very low [45] and unusual [46] as is the case in
myocardial infarction [48]. Ischemic stroke triggered by sexual inter-
course was reported in several young female patients presenting
with paroxysmal embolism (i.e. patent foramen ovale) [44–46]. Fear
can also be instigated by sexual partners. Giaquinto et al. evaluated
sexual changes one year after stroke with 62 patients, they found
that fear by patients' partners also played a substantial role in the re-
duction of sexual activity [40]. Many partners reported fear of relapse,
anguish, lack of excitation or even horror [40].
• Fatigue: It is a common issue that 30–39% of stroke survivors experi-
enced post-stroke fatigue [49–51]. It may result from a combination
of an organic brain lesion and psychosocial adjustment after stroke
[52,53]. Fatigue is a risk factor for activities of daily living (ADL) de-
pendence and higher case fatality [50]. Right hemispheric stroke is
particularly associated with fatigue [53,54]. There are few data on
post-stroke fatigue and SD, but fatigue may also contribute to SD
4.1.3. Physical deficits
Post-stroke physical deficits, such as, hemiparesis/hemiplegia and/
or spasticity may limit appropriate body position and movement, which
may contribute to SD. Stroke survivors with hemiparetic limb may expe-
rience challenges in embracing, stimulating and engaging in intercourse
[22]. Many negative symptoms from post-stroke spasticity—fatigue,
limb weakness, and loss of dexterity can also create a challenge for sexual
activities [55]. Drooling, pseudobulbar palsy, urinary/bowl incontinence,
and other unattractive features can cause intimacy issue [40]. Decreases
in intercourse frequency were positively correlated to the degree of phys-
ical impairment and levels of dependence in ADL [36].
4.1.4. Vascular risk factors
Vascular risk factors may affect sexual function via endothelial dys-
function and impaired smooth muscle cells in the genital organs. Diabe-
tes, hypertension, dyslipidemia, smoking and obesity are important
comorbid factors for ED in stroke patients [56]. ED is very common
among patients at high risk for cardiovascular disease [57]. In males,
dyslipidemia [high total cholesterol and low high-density lipoproteins
(HDL)] is associated with an increased risk of ED [58]. In pre-
menopausal females, dyslipidemia (especially, low HDL and high tri-
glyceride) is significantly associated with SD [59]. Hyperhomocysteine-
mia is a known risk factor for endothelial dysfunction, and is therefore, a
risk factor for ED as well [60]. Furthermore, ED and atherosclerosis share
 J.-H. Park et al. / Journal of the Neurological Sciences 350 (2015) 7–13 11

Table 3 serum testosterone levels were significantly lower in stroke patients

Potential non-lesion factors contributing to post-stroke sexual dysfunction. (vs. control). Both total and free testosterone levels were inversely asso-
Factors Features ciated with stroke severity and 6-month mortality at a significant level.
Psychological • May be independently linked to SD irrespective of
Total testosterone was also inversely correlated with infarct size.
Depression impairment
Fear • By organic brain lesion plus psychosocial stress 4.1.8. Partner factor(s)
Fatigue(?) • Right hemispheric stroke-prone Sexual activity is a mutual process between two adults. Post-stroke
Sociodemographic • Active sexual life prior to stroke is an important SD can also occur as a consequence of the dissatisfaction from partners
determining factor (or spouses) with regard to libido, sexual activity, and sexual satisfac-
• Questionable for age, gender, marriage, or tion [26,35]. Fear of relapse, anguish, lack of excitation, or even horror
education
(to face a naked disabled partner) may prevent a partner from engaging
Physical deficits • Depends on severity of physical impairment and in sexual activities [40]. Data suggest that spouses of stroke patients
Hemiparesis or level of dependence in ADL
with sensorimotor symptom and low ability in self-care or those with
hemiplegia ± spasticity
cognitive/emotional impairment are less satisfied with their leisure sit-
Vascular • May affect endothelial dysfunction and impair
uation, sexual life and partner relationship, particularly at 1 year after
Diabetes smooth muscle cells in genital organs
Hypertension stroke. There is a need for better psychological support of spouses/part-
Dyslipidemia ners, as well of patients, for better overall stroke recovery [41].
Smoking
Obesity 4.1.9. Medications
Hyperhomocysteinemia
Stroke survivors frequently take several medications to prevent re-
Urogenic • Severity correlated with age, male, stroke current strokes. Antihypertensive agents can inhibit erections by con-
Overactive bladder disability, and white matter hyperintensity
comitantly lowering of cavernosal artery pressure. For instance, beta
Autonomic dysfunction • Imbalance of sympathetic hyperactivity and para- blocker (i.e. metoprolol), calcium channel blocker (i.e. nifedipine),
sympathetic hypoactivity diuretics (i.e. hydrochlorothiazide) can reduce sexual desire and result
• Highly prevalent in right hemispheric stroke
in ED [22]. Antipsychotic drugs may affect prolactin levels and sub-
Neuroendocrine • Inverse relationship between testosterone level sequently influence sexual function. Antidepressants have been shown
dysfunction and infarct size and stroke outcome
to promote post-stroke recovery [71] and therefore widely prescribed.
Medications • Antihypertensive: beta blocker, calcium channel However, SD is a common side effect of antidepressants, especially
blocker, diuretics
with selective serotonin re-uptake inhibitors. The new agents, such as
• Antipsychotics
• Antidepressants: selective serotonin re-uptake bupropion and nefazodone are reported to be associated with the
inhibitors lowest risk for SD [72]. Other drugs, which potentially carry the adverse
• Others: phenytoin, ranitidine, cyclobenzaprine, effect of SD, include phenytoin, ranitidine, cyclobenzaprine, prome-
promethazine, meclizine thazine, and meclizine.
ADL: activities of daily living.
5. Return of sexual functionality after stroke

similar risk factors, so much so that ED can serve as an independent pre-
dictor of peripheral arterial disease [61].
4.1.5. Urogenic factors
Overactive bladder (OAB) is also a disturbing post-stroke complica-
tion that affects the daily life of stroke survivors. In a study of 141 stroke
patients with OAB, burden of OAB is correlated with advanced age, male,
and higher scores of modified Rankin Scale and white matter
hyperintensity [62]. OAB is significantly linked with SD (i.e. increased
ED, reduced sexual activity, or increased sexual dissatisfaction) [63].
4.1.6. Autonomic dysfunction
Post-stroke SD can be a consequence of imbalance of sympathetic
hyperactivity and parasympathetic hypoactivity [64,65]. High prevalent
of SD in patients with right-hemispheric stroke might be explained from
an autonomic dysfunction perspective. Sympathetic pathways tend to
be anti-erectile, whereas sacral parasympathetic pathways are pro-
erectile [66]. Stimulation of the right insular region increases the sym-
pathetic cardiovascular tone, while stimulation of the left insular region
activates parasympathetic activity [67].
4.1.7. Neuroendocrine dysfunction
Studies regarding sexual hormone levels in stroke survivors with SD
are scarce. Androgen is thought to play a major role in erectile function-
ality [68]. Halpern et al. showed that salivary testosterone levels
positively correlated with the numbers of sexual contacts [69]. Testos-
terone deficiency is associated with non-specific symptoms including
decline in libido, decreased muscle mass, decreased energy, and in-
creased depression. Jeppesen et al. studied the impact of sexual hor-
mone levels in males with ischemic stroke [70]. Mean total and free
The natural recovery trajectory of SDs is not currently well docu-
mented. Most studies were based on anecdotal personal interviews,
which make it difficult to determine an accurate prognosis. In an inter-
view with 50 males who suffered moderate to severe strokes, most of
them had encountered initial difficulties with sexual activities, and
two-thirds returned to sexual activity approximately seven weeks
after index event [37]. This was accomplished by assuming new sexual
position(s) to overcome the physical disabilities [37], but not everyone
can resume sexual intercourse [41]. In another study with 38 stroke pa-
tients, a majority (71%) identified SD as a “moderate to very important”
issue in overall stroke recovery [42]. Regarding recovery, it is important
to point out whether or not the couple resumes sexual activity after
stroke heavily depends on the frequency of sexual activity prior to
stroke [37]. Furthermore, fear was determined as a negative predictor
of sexual life because of perception of adverse effect of sexual activi-
ty [39]. In reality, the incidence of stroke during or after sexual inter-
course appears to be very low [45]. Generally sexual activity may
trigger a paradoxical embolism through preexisting patent foramen
ovale and cause stroke [44–46].
With regard to counseling, 81% report receiving insufficient in-
formation about post-stroke SD, and 60% express a preference for re-
ceiving sexual counseling from a physician. A significant proportion of
patients (26.5%) want to receive counseling prior to discharge from a
hospital or rehabilitation center. In another study, only 10% of patients
reported that their physician or psychologist discussed the sexual issues
with them during rehabilitation period [73]. Several factors, including
time limitations, workplace regulation and embarrassment, prevent
the healthcare professionals from discussing sex-related issues [74].
Since counseling on sexual issues is not yet a routine part of hospital dis-
charge or inpatient/outpatient rehabilitation plans, rehabilitation
12 J.-H. Park et al. / Journal of the Neurological Sciences 350 (2015) 7–13
guidelines should consider including guidance on counseling on sexual
adjustment for patients as well as their spouses [37]. Indeed, it has been
recommended that assessment of SD and sexual counseling by medical
experts should be integrated into comprehensive stroke rehabilitation
[43]. Post-stroke SD is a multifactorial medical issue. Periodic evaluation
and tailored treatment by a multidisciplinary team that includes a
stroke neurologist, neuropsychologist, and urologist would be ideal
[75].
6. Conclusions and future research
Post-stroke SD is likely more prevalent than expected. Post-stroke
SD can result from multiple factors. Psychosocial factors are important
contributing etiologies, since post-stroke SD can develop even in stroke
survivors with little or no physical impairment. However, there is a lack
of systematic and organized published data on post-stroke SD — most
published studies are based on surveys, questionnaires, or self-report.
Studies with objective and quantitative measurements are scarce,
thereby limiting the translation of these findings into clinical practice.
The natural course of recovery after post-stroke SD is poorly under-
stood. Clinically relevant post-stroke sexual adjustment assessment
tools should be developed and SD should be addressed in a multidisci-
plinary approach. Accurate diagnosis and implementation of SD man-
agement as part of comprehensive stroke rehabilitation protocol may
enhance the emotional and functional outcome in stroke survivors,
which could significantly improve quality of life. Proper identification
and timely treatment of vascular risk factors may also reduce the risk
of development of post-stroke SD.
There is an increasing trend of stroke in middle aged population [76].
Stroke survivors who experience stroke at a young age are frequently
left with significant disability that persists during their young adult
years and time of peak productivity. It is conceivable that post-stroke
SD is an unavoidable quality of life challenge that they may have to
face for a long time. This group of patients needs more attention, and fu-
ture studies should incorporate this age group.
Finally, most research of SD and stroke prognosis has focused on
male-related SD in both animal and human studies. Future studies
focusing on females and young adults deserve substantially more
attention.
Source of funding
None.
Disclosures
None.
Acknowledgment
We would like to thank Mr. James Sawers for his generous com-
ments to manuscript.
References
[1] Haacke C, Althaus A, Spottke A, Siebert U, Back T, Dodel R. Long-term outcome after
stroke: evaluating health-related quality of life using utility measurements. Stroke
2006;37:193–8.
[2] Pistoia F, Govoni S, Boselli C. Sex after stroke: a CNS only dysfunction? Pharmacol
Res 2006;54:11–8.
[3] Rowland DL. Neurobiology of sexual response in men and women. CNS Spectr 2006;
11(8 Suppl 9):6–12.
[4] Melis MR, Argiolas A. Central control of penile erection: a re-visitation of the role of
oxytocin and its interaction with dopamine and glutamic acid in male rats. Neurosci
Biobehav Rev 2011;35:939–55.
[5] Argiolas A, Melis MR. Central control of penile erection: role of the paraventricular
nucleus of the hypothalamus. Prog Neurobiol 2005;76:1–21.
[6] Kandeel FR, Koussa VK, Swerdloff RS. Male sexual function and its disorders: physi-
ology, pathophysiology, clinical investigation, and treatment. Endocr Rev 2001;22:
342–88.
[7] Levin RJ. Sexual arousal — its physiological roles in human reproduction. Annu Rev
Sex Res 2005;16:154–89.
[8] Basson R. Female sexual response: the role of drugs in the management of sexual
dysfunction. Obstet Gynecol 2001;98:350–3.
[9] Jeon SW, Yoo KH, Kim TH, Kim JI, Lee CH. Correlation of the erectile dysfunction with
lesions of cerebrovascular accidents. J Sex Med 2009;6:251–6.
[10] Park K, Seo JJ, Kang HK, Ryu SB, Kim HJ, Jeong GW. A new potential of blood oxygen-
ation level dependent (BOLD) functional MRI for evaluating cerebral centers of pe-
nile erection. Int J Impot Res 2001;13:73–81.
[11] Holstege G, Georgiadis JR, Paans AM, Meiners LC, van der Graaf FH, Reinders AA.
Brain activation during human male ejaculation. J Neurosci 2003;23:9185–93.
[12] Georgiadis JR, Holstege G. Human brain activation during sexual stimulation of the
penis. J Comp Neurol 2005;493:33–8.
[13] Wang CT, Huang RL, Tai MY, Tsai YF, Peng MT. Dopamine release in the nucleus ac-
cumbens during sexual behavior in prenatally stressed adult male rats. Neurosci Lett
1995;200:29–32.
[14] Kippin TE, Sotiropoulos V, Badih J, Pfaus JG. Opposing roles of the nucleus accumbens
and anterior lateral hypothalamic area in the control of sexual behaviour in the male
rat. Eur J Neurosci 2004;19:698–704.
[15] Everitt BJ. Sexual motivation: a neural and behavioural analysis of the mechanisms
underlying appetitive and copulatory responses of male rats. Neurosci Biobehav
Rev 1990;14:217–32.
[16] Liu YC, Sachs BD, Salamone JD. Sexual behavior in male rats after radiofrequency or
dopamine-depleting lesions in nucleus accumbens. Pharmacol Biochem Behav
1998;60:585–92.
[17] Redoute J, Stoleru S, Gregoire MC, Costes N, Cinotti L, Lavenne F, et al. Brain process-
ing of visual sexual stimuli in human males. Hum Brain Mapp 2000;11:162–77.
[18] Heilman KM, Van Den Abell T. Right hemisphere dominance for attention: the
mechanism underlying hemispheric asymmetries of inattention (neglect). Neurolo-
gy 1980;30:327–30.
[19] Howes D, Boller F. Simple reaction time: evidence for focal impairment from lesions
of the right hemisphere. Brain 1975;98:317–32.
[20] Heilman KM, Bowers D, Valenstein E, Watson RT. The right hemisphere: neuropsy-
chological functions. J Neurosurg 1986;64:693–704.
[21] Ley RG, Bryden MP. A dissociation of right and left hemispheric effects for recogniz-
ing emotional tone and verbal content. Brain Cogn 1982;1:3–9.
[22] Rees PM, Fowler CJ, Maas CP. Sexual function in men and women with neurological
disorders. Lancet 2007;369:512–25.
[23] Monga TN, Lawson JS, Inglis J. Sexual dysfunction in stroke patients. Arch Phys Med
Rehabil 1986;67:19–22.
[24] Kimura M, Murata Y, Shimoda K, Robinson RG. Sexual dysfunction following stroke.
Compr Psychiatry 2001;42:217–22.
[25] Sjögren K. Sexuality after stroke with hemiplegia II. With special regard to partner-
ship adjustment and to fulfilment. Scand J Rehabil Med 1983;15:63–9.
[26] Korpelainen JT, Nieminen P, Myllyla VV. Sexual functioning among stroke patients
and their spouses. Stroke 1999;30:715–9.
[27] Choi-Kwon S, Kim JS. Poststroke emotional incontinence and decreased sexual activ-
ity. Cerebrovasc Dis 2002;13:31–7.
[28] Middleton FA, Strick PL. Basal ganglia and cerebellar loops: motor and cognitive cir-
cuits. Brain Res Brain Res Rev 2000;31:236–50.
[29] Jung JH, Kam SC, Choi SM, Jae SU, Lee SH, Hyun JS. Sexual dysfunction in male stroke
patients: correlation between brain lesions and sexual function. Urology 2008;71:
99–103.
[30] Annoni JM, Ptak R, Caldara-Schnetzer AS, Khateb A, Pollermann BZ. Decoupling of
autonomic and cognitive emotional reactions after cerebellar stroke. Ann Neurol
2003;53:654–8.
[31] Haines DE, Dietrichs E, Mihailoff GA, McDonald EF. The cerebellar–hypothalamic
axis: basic circuits and clinical observations. Int Rev Neurobiol 1997;41:83–107.
[32] Monga TN, Monga M, Raina MS, Hardjasudarma M. Hypersexuality in stroke. Arch
Phys Med Rehabil 1986;67:415–7.
[33] Absher JR, Vogt BA, Clark DG, Flowers DL, Gorman DG, Keyes JW, et al. Hypersexual-
ity and hemiballism due to subthalamic infarction. Neuropsychiatry Neuropsychol
Behav Neurol 2000;13:220–9.
[34] Mutarelli EG, Omuro AM, Adoni T. Hypersexuality following bilateral thalamic in-
farction: case report. Arq Neuropsiquiatr 2006;64:146–8.
[35] Korpelainen JT, Kauhanen ML, Kemola H, Malinen U, Myllyla VV. Sexual dysfunction
in stroke patients. Acta Neurol Scand 1998;98:400–5.
[36] Sjögren K, Fugl-Meyer AR. Adjustment to life after stroke with special reference to
sexual intercourse and leisure. J Psychosom Res 1982;26:409–17.
[37] Hawton K. Sexual adjustment of men who have had strokes. J Psychosom Res 1984;
28:243–9.
[38] Coslett HB, Heilman KM. Male sexual function. Impairment after right hemisphere
stroke. Arch Neurol 1986;43:1036–9.
[39] Cheung RT. Sexual functioning in Chinese stroke patients with mild or no disability.
Cerebrovasc Dis 2002;14:122–8.
[40] Giaquinto S, Buzzelli S, Di Francesco L, Nolfe G. Evaluation of sexual changes after
stroke. J Clin Psychiatry 2003;64:302–7.
[41] Forsberg-Wärleby G, Moller A, Blomstrand C. Life satisfaction in spouses of patients
with stroke during the first year after stroke. J Rehabil Med 2004;36:4–11.
[42] Stein J, Hillinger M, Clancy C, Bishop L. Sexuality after stroke: patient counseling
preferences. Disabil Rehabil 2013;35:1842–7.
[43] Calabrò RS, Gervasi G, Bramanti P. Male sexual disorders following stroke: an over-
view. Int J Neurosci 2011;121:598–604.
 J.-H. Park et al. / Journal of the Neurological Sciences 350 (2015) 7–13
[44] Becker K, Skalabrin E, Hallam D, Gill E. Ischemic stroke during sexual inter-
course: a report of 4 cases in persons with patent foramen ovale. Arch Neurol
2004;61:1114–6.
[45] Velicu S, Biller J, Hacein-Bey L, Freihage JH, Leya F. Paradoxical embolism to the cen-
tral nervous system after sexual intercourse in a young woman with a complex atrial
septal abnormality. J Stroke Cerebrovasc Dis 2008;17:320–4.
[46] Calabrò RS, Pezzini A, Casella C, Bramanti P, Triolo O. Ischaemic stroke provoked by
sexual intercourse. J Clin Neurosci 2013;20:1316–7.
[47] Reynolds MR, Willie JT, Zipfel GJ, Dacey RG. Sexual intercourse and cerebral aneurys-
mal rupture: potential mechanisms and precipitants. J Neurosurg 2011;114:969–77.
[48] Möller J, Ahlbom A, Hulting J, Diderichsen F, de Faire U, Reuterwall C, et al. Sexual
activity as a trigger of myocardial infarction. A case-crossover analysis in the
Stockholm Heart Epidemiology Programme (SHEEP). Heart 2001;86:387–90.
[49] van der Werf SP, van den Broek HL, Anten HW, Bleijenberg G. Experience of severe
fatigue long after stroke and its relation to depressive symptoms and disease charac-
teristics. Eur Neurol 2001;45:28–33.
[50] Glader EL, Stegmayr B, Asplund K. Poststroke fatigue: a 2-year follow-up study of
stroke patients in Sweden. Stroke 2002;33:1327–33.
[51] Ingles JL, Eskes GA, Phillips SJ. Fatigue after stroke. Arch Phys Med Rehabil 1999;80:
173–8.
[52] Leegaard OF. Diffuse cerebral symptoms in convalescents from cerebral infarction
and myocardial infarction. Acta Neurol Scand 1983;67:348–55.
[53] Sisson RA. Life after a stroke: coping with change. Rehabil Nurs 1998;23:198–203.
[54] Sisson RA. Cognitive status as a predictor of right hemisphere stroke outcomes. J
Neurosci Nurs 1995;27:152–6.
[55] Soyuer F, Ozturk A. The effect of spasticity, sense and walking aids in falls of people
after chronic stroke. Disabil Rehabil 2007;29:679–87.
[56] Bener A, Al-Hamaq AO, Kamran S, Al-Ansari A. Prevalence of erectile dysfunction in
male stroke patients, and associated co-morbidities and risk factors. Int Urol Nephrol
2008;40:701–8.
[57] Roth A, Kalter-Leibovici O, Kerbis Y, Tenenbaum-Koren E, Chen J, Sobol T, et al. Prev-
alence and risk factors for erectile dysfunction in men with diabetes, hypertension,
or both diseases: a community survey among 1,412 Israeli men. Clin Cardiol 2003;
26:25–30.
[58] Vrentzos GE, Paraskevas KI, Mikhailidis DP. Dyslipidemia as a risk factor for erectile
dysfunction. Curr Med Chem 2007;14:1765–70.
[59] Esposito K, Ciotola M, Maiorino MI, Giugliano F, Autorino R, De Sio M, et al. Hyper-
lipidemia and sexual function in premenopausal women. J Sex Med 2009;6:
1696–703.
[60] Demir T, Comlekci A, Demir O, Gülcü A, Calýpkan S, Argun L, et al. Hyperhomocystei-
nemia: a novel risk factor for erectile dysfunction. Metabolism 2006;55:1564–8.
13
[61] Polonsky TS, Taillon LA, Sheth H, Min JK, Archer SL, Ward RP. The association be-
tween erectile dysfunction and peripheral arterial disease as determined by screen-
ing ankle-brachial index testing. Atherosclerosis 2009;207:440–4.
[62] Itoh Y, Yamada S, Konoeda F, Koizumi K, Nagata H, Oya M, et al. Burden of overactive
bladder symptom on quality of life in stroke patients. Neurourol Urodyn 2013;32:
428–34.
[63] Irwin DE, Milsom I, Reilly K, Hunskaar S, Kopp Z, Herschorn S, et al. Overactive blad-
der is associated with erectile dysfunction and reduced sexual quality of life in men. J
Sex Med 2008;5:2904–10.
[64] Korpelainen JT, Sotaniemi KA, Myllyla VV. Autonomic nervous system disorders in
stroke. Clin Auton Res 1999;9:325–33.
[65] Korpelainen JT, Sotaniemi KA, Suominen K, Tolonen U, Myllyla VV. Cardiovascular
autonomic reflexes in brain infarction. Stroke 1994;25:787–92.
[66] Giuliano F, Rampin O. Neural control of erection. Physiol Behav 2004;83:189–201.
[67] Oppenheimer SM, Gelb A, Girvin JP, Hachinski VC. Cardiovascular effects of human
insular cortex stimulation. Neurology 1992;42:1727–32.
[68] Rajfer J. Relationship between testosterone and erectile dysfunction. Rev Urol 2000;
2:122–8.
[69] Halpern CT, Udry JR, Suchindran C. Monthly measures of salivary testosterone pre-
dict sexual activity in adolescent males. Arch Sex Behav 1998;27:445–65.
[70] Jeppesen LL, Jorgensen HS, Nakayama H, Raaschou HO, Olsen TS, Winther K. De-
creased serum testosterone in men with acute ischemic stroke. Arterioscler Thromb
Vasc Biol 1996;16:749–54.
[71] Chollet F, Tardy J, Albucher JF, Thalamas C, Berard E, Lamy C, et al. Fluoxetine for
motor recovery after acute ischaemic stroke (FLAME): a randomised placebo-
controlled trial. Lancet Neurol 2011;10:123–30.
[72] Clayton AH, Pradko JF, Croft HA, Montano CB, Leadbetter RA, Bolden-Watson C, et al.
Prevalence of sexual dysfunction among newer antidepressants. J Clin Psychiatry
2002;63:357–66.
[73] Schmitz MA, Finkelstein M. Perspectives on poststroke sexual issues and rehabilita-
tion needs. Top Stroke Rehabil 2010;17:204–13.
[74] Dyer K, das Nair R. Why don't healthcare professionals talk about sex? A systematic
review of recent qualitative studies conducted in the United kingdom. J Sex Med
2013;10:2658–70.
[75] Calabrò RS, Bramanti P. Post-stroke sexual dysfunction: an overlooked and under-
addressed problem. Disabil Rehabil 2014;36:263–4.
[76] Kissela BM, Khoury JC, Alwell K, Moomaw CJ, Woo D, Adeoye O, et al. Age at stroke:
temporal trends in stroke incidence in a large, biracial population. Neurology 2012;
79:1781–7.