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Keywords:

  • ischaemic stroke;
  • sexual disorders;
  • stroke

Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. Disclosure of conflicts of interest
  9. References

Background and purpose

The present study sought to determine the impact of stroke on sexual function and well-being in a cohort of young ischaemic stroke patients and identify factors associated with impairment.

Methods

Over a 2-year period, all patients aged 60 or under with ischaemic stroke or transient ischaemic attack (n = 156) were included. Information on sexual function and well-being was obtained by means of a paper questionnaire mailed to participants 1 year after their stroke. Impaired sexual activity (ISA) was defined as a decline in sexual function and/or satisfaction. Psychological well-being was evaluated on the Hospital Anxiety and Depression Scale (HADS).

Results

The response rate was 67% (n = 104). Thirty of these responders (29%) reported ISA. Patients with ISA had a higher HADS score (19.7 vs. 11.2 in patients with no impairment; P < 0.001), anxiety score (10.0 vs. 6.3; P < 0.001) and depression score (8.7 vs. 4.8; P < 0.001) and were more likely to have left brain lesions (70% vs. 30%; P < 0.001) and use angiotensin-converting enzyme (ACE) inhibitors (73% vs. 31%; P < 0.001) and diuretics (50% vs. 19%; P = 0.003). In a stepwise logistic regression, depression (odds ratio 9.1, 95% confidence interval 2.45−33.46; P = 0.001) and ACE inhibitor use (odds ratio 6.0, 95% confidence interval 2.11−17.28; P = 0.001) were associated with ISA.

Conclusions

Impaired sexual activity was reported by almost one-third of younger patients 1 year after ischaemic stroke. Factors associated with post-stroke ISA may include specific medications and depression rather than the characteristics of the stroke per se.


Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. Disclosure of conflicts of interest
  9. References

Post-stroke impaired sexual activity (ISA) encompasses sexual dysfunction and/or impaired sexual satisfaction. The latter is defined as a decline in libido in both genders, erectile dysfunction and poor ejaculation in men and diminished lubrication and orgasm in women [1]. Although sexuality is considered to be an important part of quality of life, post-stroke ISA is poorly recognized by both patients (who do not usually ask for counseling) and stroke physicians (who may be unprepared for the diagnostic workup and treatment). Moreover, the scale that is commonly used for measuring functional outcome after stroke (i.e. the modified Rankin scale [2]) does not include an item specifically related to ISA in its grade 1 (‘persisting symptoms as a result of the stroke’). The few published studies on post-stroke sexual function show that ISA is not that uncommon in men and women, with a prevalence ranging from 17% to 42% [3-7]. Post-stroke ISA is thought to be caused by several etiologies and involves a complex interplay between psychological and organic factors [4, 8]. The factors reported to date include several specific characteristics of stroke (right hemisphere injury [9], thalamic lesions [10], motor impairment [6, 11]), previous hypertension, diabetes and cardiac disease [12], various psychosocial factors (the relationship with the spouse, the fear of a new stroke [3-6]) and depression [13]. Age is also reportedly an important factor in post-stroke ISA [1, 6]. Two-thirds of strokes occur in people aged 65 and over, in whom age-related changes in sexual function are frequent and are taken into account in their treatment [14]. However, young stroke patients (i.e. those aged 60 and under) have never been specifically evaluated in this respect. It was therefore decided to assess the prevalence of ISA after ischaemic stroke in young patients and determine factors associated with the development of ISA in this population.

Methods

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. Disclosure of conflicts of interest
  9. References

Study population

All under-60 patients admitted consecutively to our university medical center's neurology department with a diagnosis of ischaemic stroke or transient ischaemic attack (TIA) between January 2010 and December 2012 were eligible for inclusion in the study (n = 196). Patients with pre-existing sexual disorders (n = 10), major disability (modified Rankin scale score ≥4, n = 14) [2], severe aphasia (Boston Diagnostic Aphasia Examination score <3; n = 9) [15] or major cognitive disorders (Mini Mental State Examination score ≤ 17 out of 30, n = 7) [16] at the time of hospital discharge were excluded from the study. Six patients subsequently died, five were lost to follow-up and 41 patients did not return the questionnaire. Hence, the 104 remaining responders were included in our analysis. The present study's objectives and procedures were approved by the local institutional review board (Commission d'Evaluation Ethique des Recherches Non Interventionnelles, Amiens University Medical Center, Amiens, France).

Clinical data were prospectively collected for each patient according to a standardized protocol [17]. Computed tomography scans of the brain, an electrocardiogram, Doppler ultrasonography of the neck vessels, transthoracic echocardiography and standard laboratory tests were performed for all patients on admission. Specialized laboratory tests (optional coagulation screening tests, in particular) were performed in younger subjects. Holter electrocardiogram monitoring, transesophageal echocardiography, magnetic resonance imaging (MRI) and/or angiography were performed in selected patients. The following data on acute ischaemic stroke were collected: age, gender, living conditions before and after the ischaemic incident, the modified Rankin scale score [2] prior to hospitalization (according to an interview with the patient or, if necessary, the caregiver), previously identified stroke risk factors or those discovered during hospitalization [including hypertension (use of antihypertensive medications or systolic blood pressure >140 mmHg or diastolic blood pressure >90 mmHg prior to hospitalization), diabetes (use of insulin or oral antidiabetic therapies or fasting blood glucose >7 mM on two occasions during hospitalization), hypercholesterolemia (use of lipid-lowering medications or low density lipoprotein cholesterol >1 g/l), a history of myocardial infarction or angina, current smoking, frequent alcohol consumption (>3 alcoholic drinks per day), peripheral artery disease and overweight, defined as body mass index ≥25 kg/m2). The glomerular filtration rate (GFR) was estimated using the four-component Modification of Diet in Renal Disease equation, based on age, gender, race and serum creatinine concentration on admission. Chronic kidney disease (CKD) was defined as a GFR <60 ml/min/1.73 m2, in accordance with the National Kidney Foundation criteria [18]. The severity of neurological impairments caused by the index stroke at admission and at hospital discharge was assessed on the National Institutes of Health Stroke Scale (NIHSS) [19]. Subgroups of cerebral infarcts were defined according to the Oxford Community Stroke Project classification [20] and causes of ischaemic stroke were defined (according to the Trial of Org 10172 in Acute Stroke Treatment criteria) [21] as large-artery atherosclerosis, cardioembolism, small-vessel disease, other determined etiology and undetermined etiology.

Assessment of post-stroke sexual function

A follow-up questionnaire on sexual function, well-being and related information was mailed to all patients meeting the inclusion criteria 1 year after the stroke. The time interval of 1 year was chosen so that subjects had time to recover. The questionnaire was filled out by the patient or, if necessary, the caregiver. To optimize the response rate of the survey, additional telephone interviews were performed for non-responders. For the assessment of sexual function, the patient had to answer the question ‘Since your stroke, have you suffered from sexual impairment (a decline in libido, erectile dysfunction or poor ejaculation) or a lack of sexual satisfaction?’ and was invited to comment further on his/her sexual disorder (although this was not mandatory). Data on the current modified Rankin scale and current treatments (including antithrombotic agents, statins, antihypertensives and antidepressants) were also collected. The study questionnaire included the 14-item Hospital Anxiety and Depression Scale (HADS). To define a patient as being ‘anxious’ or ‘depressed’ or both, the generally accepted cut-off score of 10 (definite cases) for the anxiety (HADS-A) and depression (HADS-D) subscales was used [22].

Statistical analysis

Intergroup comparisons were performed by applying Student's t test to continuous clinical and radiological variables and the χ² test to categorical variables (except for the NIHSS score, to which the non-parametric Mann−Whitney test was applied). In a stepwise logistic regression analysis, the dependent variables were age, gender, type of stroke (ischaemic stroke or TIA), use or not of iv thrombolysis, main risk factors (hypertension, diabetes mellitus, hypercholesterolemia, ischaemic heart disease, smoking, alcohol consumption, peripheral artery disease, body mass index ≥ 25 kg/m2, previous stroke or TIA and CKD), clinical signs and NIHSS score at admission, NIHSS score at hospital discharge, type of ischaemic stroke, cause(s) of ischaemic stroke, brain MRI parameters (such as lesion side, lesion site and white matter abnormalities) and follow-up characteristics (time to follow-up, medications and HADS-A and HADS-D subscores). The threshold for statistical significance was set to P < 0.05. All statistical analyses were performed with spss software (SPSS Inc., Chicago, IL, USA).

Results

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. Disclosure of conflicts of interest
  9. References

The study population's disposition and the survey process are described in Fig. 1. Of the 156 patients who received the questionnaire, 104 replied (62 men and 42 women; 67%). Demographic data and vascular risk factors did not differ between responders and non-responders (data not shown). The mean ± SD age at the time of the stroke was 48.0 ± 9.4 years. Twenty of the responders (19%) lived alone and 84 (81%) lived with a partner. The family situation had changed after the stroke in only two cases (divorce, in both cases). The mean follow-up time was 13.1 ± 1.1 months.

image

Figure 1. Flow chart of the study population.

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Thirty responders (29%) reported ISA. The patients' characteristics as a function of the presence or absence of ISA are listed in Table 1. The eight male patients with ISA who commented further on their sexual disorder all reported erectile dysfunction. In a univariate analysis (and compared with patients in whom sexual activity was unimpaired), patients with ISA were more likely to have initial motor impairment (27% vs. 50%, respectively; P = 0.038), visual impairment (19% vs. 40%, respectively; P = 0.044), aphasia (28% vs. 50%, respectively; P = 0.043) and left brain lesions (30% vs. 70%, respectively; P < 0.001). However, the baseline NIHSS scores in the two groups did not differ significantly (3.4 vs. 4.0, respectively; P = 0.67). At the time of the follow-up interview, a comparison of patients in whom sexual activity was unimpaired and patients with ISA showed that the latter were more likely to be taking angiotensin-converting enzyme (ACE) inhibitors (31% vs. 73%, respectively; P < 0.001) and diuretics (19% vs. 50%, respectively; P = 0.003). A stepwise logistic regression identified the following independent factors for ISA: depression (odds ratio 9.1, 95% confidence interval 2.45–33.46; P = 0.001) and ACE inhibitors (odds ratio 6.0, 95% confidence interval 2.11–17.28; P = 0.001).

Table 1. Clinical and radiological characteristics of ischaemic stroke patients with and without impaired sexual activity (ISA)
 All patients (n = 104)ISA (n = 30)No ISA (n = 74) P
  1. Results are expressed as either the mean ± standard deviation (for age and baseline NIHSS score) or as the number of patients and percentage of patients in the group (n %).ACE, angiotensin-converting enzyme; ARB, angiotensin II receptor blocker; BMI, body mass index; CAD, coronary artery disease; HADS, hospital anxiety and depression scale; LACI, lacunar infarct; MMSE, mini mental state examination; MRI, magnetic resonance imaging; mRS, modified Rankin scale; NIHSS, National Institutes of Health Stroke Scale; OCSP, Oxford Community Stroke Project; PACI, partial anterior circulation infarct; PAD, peripheral artery disease; POCI, posterior circulation infarct; TACI, total anterior circulation infarct; TIA, transient ischaemic attack.*Missing data (n = 4).

Age (years)48.0 ± 9.448.7 ± 8.747.7 ± 9.70.61
Number (%) of males62 (60)17 (57)45 (61)0.83
mRS before hospitalization0.10 ± 0.340.2 ± 0.550.04 ± 0.200.13
Ischaemic stroke80 (77)26 (87)54 (73)0.20
Transient ischaemic attack23 (22)4 (13)19 (26)0.20
iv thrombolysis6 (6)2 (7)6 (8)1.00
Previous main risk factors
Hypertension35 (34)11 (37)24 (32)0.82
ACE inhibitors7 (7)2 (7)5 (7)1.00
Diuretics5 (5)1 (3)4 (5)1.00
Diabetes mellitus7 (7)2 (7)5 (7)1.00
Hypercholesterolemia29 (28)8 (27)21 (28)1.00
Active smoking45 (43)16 (53)29 (39)0.20
Alcohol consumption11 (11)5 (17)6 (8)0.29
CAD5 (5)1 (3)4 (5)1.00
Atrial fibrillation5 (5)05 (7)0.32
PAD4 (4)04 (5)0.32
Stroke/TIA4 (4)2 (7)2 (3)0.58
BMI ≥ 25 kg/m²53 (51)15 (50)38 (51)1.00
Chronic kidney disease7 (7)3 (10)4 (5)0.41
Initial clinical signs
Motor impairment35 (34)15 (50)20 (27)0.038
Sensory impairment21 (20)8 (27)13 (18)0.30
Visual impairment26 (25)12 (40)14 (19)0.044
Aphasia36 (35)15 (50)21 (28)0.043
MMSE score*27.7 ± 2.327.3 ± 3.028.0 ± 2.00.22
NIHSS score at admission3.6 ± 5.74.0 ± 5.03.4 ± 6.00.34
NIHSS score at hospital discharge1.8 ± 3.62.2 ± 4.01.7 ± 3.50.083
Transient ischaemic attack23 (22)4 (13)19 (26)0.20
Cerebral infarction80 (78)26 (87)54 (74)0.20
OCSP classification
PACI41 (39)13 (43)28 (38)0.66
TACI5 (5)1 (3)4 (5)1.00
LACI8 (8)4 (13)4 (5)0.22
POCI24 (23)8 (27)16 (22)0.61
Causes of ischaemic stroke
Atherosclerosis ≥ 50%7 (7)3 (10)4 (5)0.41
Cardioembolic13 (13)2 (7)11 (15)0.34
Lacunar8 (8)4 (13)4 (5)0.23
Undetermined54 (52)13 (43)41 (55)0.28
Other12 (12)5 (17)7 (9)0.32
Brain MRI parameters
Lesion side
Right lesion37 (36)6 (20)31 (42)0.043
Left lesion43 (41)21 (70)22 (30)<0.001
Lesion site
Posterior fossa19 (18)7 (23)12 (16)0.41
Thalamus8 (8)2 (7)6 (8)1.00
Posterior cortex19 (18)6 (20)13 (18)0.78
Anterior cortex27 (26)10 (33)17 (23)0.33
Deep structures31 (30)11 (37)20 (27)0.35
White matter abnormalities38 (37)12 (40)26 (35)0.66
Follow-up characteristics
Time to follow-up (months)13.1 ± 1.113.2 ± 1.213.0 ± 1.10.52
mRS1.5 ± 1.01.87 ± 0.821.35 ± 1.00.017
Treatment
Antiplatelet agents86 (83)24 (80)62 (84)0.77
Anticoagulants13 (13)4 (13)9 (12)1.00
Statins78 (75)24 (80)54 (73)0.62
Antidepressants14 (13)7 (23)7 (9)0.12
Antihypertensive therapy80 (77)26 (87)54 (73)0.20
Beta blockers14 (13)3 (10)11 (15)0.75
ACE inhibitors45 (43)22 (73)23 (31)<0.001
ARBs12 (12)3 (10)9 (12)1.00
Diuretics29 (28)15 (50)14 (19)0.003
Others23 (22)2 (7)21 (28)0.018
HADS13.6 ± 8.819.7 ± 7.711.2 ± 8.1<0.001
Anxiety34 (33)13 (43)11 (15)0.004
Anxiety subscore7.3 ± 4.810.0 ± 4.66.3 ± 4.4<0.001
Depression17 (16)12 (40)5 (7)<0.001
Depression subscore5.9 ± 4.68.7 ± 4.64.8 ± 4.1<0.001

Discussion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. Disclosure of conflicts of interest
  9. References

The present study of 104 young patients with ischaemic stroke revealed that 30% of these individuals suffered from self-reported ISA.

One of the study's most important findings is that ISA is not uncommon after ischaemic stroke or TIA. There are few literature data on the prevalence of post-stroke ISA [1], which may be as high as 40%, depending on the study population and the definition of sexual disorders used [3-7]. A few studies included patients with pre-existing sexual disorders [5] or did not take account of age as a potential cause of bias [6]. Furthermore, most of the literature studies had a short follow-up time (≤12 months); this may have led to overestimation of the prevalence of ISA, since sexual function usually improves during the first few months post-stroke [1]. Only Cheung et al. performed a similar study in a cohort of young Chinese patients. The researchers found a higher percentage of ISA and provided details of the patients' complaints but excluded patients with depression from their analyses, thus making it difficult to interpret the results [5].

Several clinical factors related to stroke or previous medical conditions are reportedly associated with post-stroke ISA. Surprisingly, sensory impairments and right brain lesions were not found to be associated with ISA in our study – even though both hemianesthesia and perceptual neglect interfere with erotic sensations [3, 23]. One possible explanation is that patients with right lesions would neglect their sexual activity. It was less surprising to find an association between motor impairments and ISA in our univariate analysis. It is well known that motor impairment can influence body positioning and movement during coitus [11]. However, given that most of our patients had few or no offputting impairments at the time of the questionnaire (i.e. drooling or incontinence), this association did not emerge in our stepwise logistic regression. Other clinical factors that might contribute to the development of ISA include hypertension, diabetes, heart failure, hypercholesterolemia and peripheral vascular disease [12]. None of these comorbidities appeared to be significantly associated with ISA in the present study, probably because our population was younger than those reported previously and so had fewer pre-morbid conditions. Our study is the first to have specifically evaluated the association between ISA and post-stroke medications. It was found that use of ACE inhibitors was significantly associated with ISA. Many antihypertensive drugs can worsen sexual function as a specific side effect; this is particularly the case for thiazide diuretics, ACE inhibitors and, to a lesser extent, beta-blockers [1, 24]. The Perindopril Protection Against Recurrent Stroke Study (PROGRESS) showed that antihypertensive therapy with a combination of perindopril (4 mg daily) and indapamide (2.5 mg daily) reduced stroke recurrence and the incidence of major vascular events and stroke-related dementia, regardless of the initial blood pressure. Since the publication of the PROGRESS results in 2001, this therapy has been part of guidelines-endorsed stroke prevention strategy in our neurology department. The high prevalence of ACE inhibitor use in our population may explain (at least in part) the high frequency of ISA observed 1 year after stroke. The fact that (i) four patients developed ISA 1 year after a TIA and (ii) erectile dysfunction was the main complaint reported by the patients who commented further on their sexual disorder reinforces the medication hypothesis. Lastly, our present results demonstrated a strong association between post-stroke depression and ISA. The tendency for stroke victims to develop depressive symptoms, anxiety and other mood disorders has been well documented [25, 26]. Depressive disorders may lead to sexual impairment. Conversely, one can speculate that post-stroke ISA can lead secondarily to depression.

The present study has several limitations. First, the number of patients who developed ISA was small and most of the patients with ISA had left brain lesions. One can hypothesize that ISA patients with right brain lesions are less aware of (or more indifferent to) this type of impairment. Secondly, a standardized, specific questionnaire was not used to assess ISA. Indeed, whilst a validated instrument to assess depression and anxiety was used, no specific validated scale was available to determine the prevalence of ISA after stroke. Furthermore, the diagnosis of ISA was based on self-reporting, and so some patients might not have wished to admit to sexual dysfunction, leading to underestimation of the latter's prevalence. The fact that patients often refrained from (optionally) giving additional information on ISA in the questionnaire suggests that this source of bias was present to some extent. Nevertheless, these potential effects are probably negligible, since the baseline clinical and radiological characteristics of the study population and the stated prevalence of ISA were similar to those observed in previous studies.

In conclusion, post-stroke ISA is frequent in young patients and should always be screened for. Our results evidence the predominant role of post-stroke depression in the development of ISA and also suggest that ISA might be related to the prescription of certain medications (e.g. ACE inhibitors) after the ischaemic incident. Our preliminary results require confirmation in larger, prospective studies.

Disclosure of conflicts of interest

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. Disclosure of conflicts of interest
  9. References

The authors declare no financial or other conflicts of interest.

References

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  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Acknowledgements
  8. Disclosure of conflicts of interest
  9. References
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