Sexual Dysfunction in Acquired Brain Injury (ABI)

Author(s): Parisa Zarreii, MD, Maria Humayun, D.O., and  Lawrence Horn, M.D.,

Originally published:11/10/2011

Last updated:03/13/2018

1. DISEASE/DISORDER:

Definition

Broadly, sexual dysfunction refers to disturbance in an individual’s subjective sense of pleasure and/or desire associated with sex or impairment in the objective performance of sexual activities. Sexual dysfunction can be further classified into four categories:

  • Sexual desire disorders
    • Sexual aversion
    • Hypoactive sexual desire
  • Sexual arousal disorders
    • Poor lubrication (women)
    • Erectile disorders
      • Men – penile
      • Women – clitoral
    • Orgasmic disorders
      • Anorgasmia
      • Ejaculatory disorders
        • Early ejaculation
        • Delayed ejaculation
        • Anejaculation
      • Sexual pain disorders
        • Dyspareunia
        • Vaginismus
        • Noncoital sexual pain disorder

Notably, the above conditions are only truly considered “disorders” when they create distress for the person experiencing the condition.

Etiology

Sexual dysfunction in ABI can be related to physical damage to specific brain regions or neural pathways, resultant alterations in the body’s neurochemical milieu, or endocrine disturbances. Behavioral and cognitive impairments, physical limitations, and medication effects may also compromise sexual performance in this population.

Epidemiology including risk factors and primary prevention

In the general population, 40%-50% of women and 20%-30% of men are believed to have at least one form of sexual dysfunction. In the TBI population there are high reported rates of sexual dysfunction (36-54%) after brain trauma. In a recent multicenter study, increased sexual dysfunction was correlated with female gender, older age, higher TBI severity, and decreased social participation. Studies in the stroke population (both men and women) indicate that the prevalence of sexual dysfunction ranges from 20% to 75%. In male stroke patients, the prevalence of post-stroke diminishment in libido ranges from 17-42%. Sexual dysfunction can arise from hormonal changes, medication side effects, fatigue, movement problems, spasticity, problems with self-esteem and other psychological factors, cognitive and communicative difficulties, and changes in relationships and social activities. Dependence in activities of daily living (ADLs) also increases the risk of sexual disorders. Comorbidities, especially diabetic dysautonomias, may further compromise sexual function.

Patho-anatomy/physiology

Because patients with acquired brain injury manifest numerous coexisting, interrelated impairments, it is frequently difficult to pinpoint a specific etiology of sexual dysfunction. Deficits can result from direct brain pathology or from downstream effects. The sexual response network requires intricate mechanisms of input (reception, perception and identification of sexually salient cues, signals and stimuli) and output (engagement of proper motor responses). Autonomic and somatic nerves participate in an elaborate network involving numerous spinal and supraspinal sites in the central nervous system. Some studies suggest that lesions in the right cerebral hemisphere cause more significant sexual dysfunction than those in the left hemisphere, but data are conflicting. Knowledge regarding neuroanatomical correlates of sexual responses has historically been extracted from animal research, and the functional neuroanatomy of human sexual behavior and control is incompletely understood.

Brain areas involved in sexual response:

  • Sexual desire/motivation: mediated primarily by subcortical structures (particularly the hypothalamus) as well as the amygdala. Stimulation of these structures can produce erection and a sense of pre-orgasmic pleasure.
    • The hypothalamus is rich in gonadal hormone receptors; it is interconnected with cortical and paralimbic cortex and the autonomic nervous system.
    • Hypothalamic sexual activity is not only influenced by gonadal hormones but is also expressed via regulation of pituitary gonadotropins.
    • Men and women with injury to the hypothalamic-pituitary system report significant decreases in sexual desire and function.
    • In children, lesions in the system may produce hormonal dysregulation resulting in precocious puberty or failure to achieve puberty.
    • Lesions in the medial and pre-optic hypothalamic nuclei eliminate sexual behaviors.
    • Stimulation of the hypothalamic dorsomedial nucleus results in ejaculation.
  • Sexual excitement: mediated primarily by cortical structures (frontal and parietal lobes) which control genital sensation and the motor aspects of the sexual response.
    • Dorsolateral lesions of the frontal area may lead to a paucity of sexual drive or the inability to fantasize.
    • Bilateral temporal lobe injury (Klüver-Bucy syndrome) may result in hypersexual behaviors.
    • Frontal lobes are involved in the maintenance of social propriety. Lesions of the orbitofrontal area may result in socially inappropriate behaviors (sometimes with sexual overtones).
  • Orgasm: Septal complex

Spinal involvement in sexual response:

  • Genital innervation is both somatic and autonomic.
    • During the excitement phase of sexual activity, somatic sensory afferents carrying tactile stimulation synapse in the sacral spinal cord to induce local sexual responses and also send sensory information to cortical regions to promote sexual excitation.
    • Erection is initiated and maintained via parasympathetic innervation via the pelvic nerves. Parasympathetic activity also causes clitoral erection, engorgement of the labia, and vaginal lubrication.
    • Sympathetic activity closes the bladder neck, preventing retrograde ejaculation (a common cause of male infertility). Sympathetic activity during orgasm results in contraction of pelvic structures including the uterus and pelvic floor muscles.

Neurochemical mediators of sexual response:

  • Dopamine: Promotes sexual behavior via the mesolimbic reward pathway
    • DopamineD1 and D2-like receptors in the paraventricular area, the medial pre-optic area, the spinal cord, and in the erectile tissue are involved in erection
    • Several agonists developed for the treatment of Parkinson’s disease are associated with increased libido
    • Apomorphine (general dopamine receptor agonist) has efficacy in treating erectile dysfunction
  • Serotonin: Most evidence indicates that 5-HT₁A receptor agonists inhibit sexual behavior while 5-HT₂ or 5-HT₃ receptors may exert a positive influence.

Other important chemical messengers include norepinephrine, nitric oxide, oxytocin, and gonadal hormones.

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

The frequency of sexual activity typically declines with advancing age: 50% of couples aged 60-65 engage in physical intimacy and this declines to 20% in those aged 78-83. Fertility also declines with advancing years.

It is difficult to draw many conclusions from the literature regarding trajectory and outcomes in sexual dysfunction in acquired brain injury because of the amount of heterogeneity inherent in the mechanisms of injury, the wide range of particular manifestations of sexual dysfunction in individual patients, the non-generalizability of findings due to different cultural customs and psychosocial expectations regarding sexuality, and the lack of utilization of a standardized or uniform assessment tool. In one study of patients with moderate to severe TBI, there was a small amount of improvement in sexual arousal from 6 to 12 months after injury; other measures of sexual function and satisfaction remained stable. A 2002 study by Choi-Kwon and Kim found decreased frequency of sexual intercourse in 65% of their sample 3 months after the stroke occurred, with only a slight improvement to 49% two years later. Other studies have noted return to sexual activity generally occurring between the third and sixth month following stroke. Individuals who sustain TBI prior to age 18 have higher biological parenthood rates post-injury than individuals injured as adults, but still in much lower proportion compared to age and gender matched individuals without brain injury.

Specific secondary or associated conditions and complications

Other comorbidities in central nervous disorders that impact sexual function include bowel and bladder dysfunction, spasticity, central pain, autonomic dysreflexia, heterotopic ossification, contractures and decubitus ulcers. In people with acquired brain disorders, perceptual, affective and behavioral changes may adversely affect the ability to engage in intimacy. Alcohol and substance abuse may also impair sexual performance. Medications that impact sexual performance negatively include adrenergic-blockers, selective serotonergic reuptake inhibitors, anti-psychotics, narcotics, benzodiazepines, and alpha agonists used for spasticity or for relaxation of the internal sphincter. Antipsychotics may increase the level of prolactin, which has an inhibitory effect on the male hypothalamic-pituitary-gonadal axis.

Anticonvulsants may lower levels of free gonadal hormones, and the hormones themselves, most notably estrogens, can lower seizure threshold. The use of anticonvulsants in women may compromise the effectiveness of hormonally-dependent birth control. Temporal lobe epileptics have significant sexual dysfunction, with 58% of men demonstrating hyposexuality or impotence and 40% of women showing reproductive dysfunction. The side of the temporal lobe focus may dictate the type of hormonal disorder; women with left temporal dysfunction may develop polycystic ovarian syndrome characterized by amenorrhea, obesity, hirsutism and infertility. These disorders are in large part hormonally based and relate to extra-hypothalamic control of the hypothalamic-pituitary axis. Gonadotropin deficiency occurs in 10%-15% of individuals after TBI, affecting libido and potentially fertility. Transient menstrual abnormalities occur in women with TBI, related to the general effects of trauma.

In acquired brain injury (traumatic or stroke), early tube-feeding should be considered as it can theoretically prevent worse sexual outcomes for patients. Iatrogenic dietary starvation of even just a few days can produce a state of leptin deficiency, which in turn can reduce gonadotropin secretion.

Comorbities in stroke can complicate sexual function. These include poststroke depression, use of antidepressants, diabetes with concomitant peripheral nerve or autonomic dysfunction, and coronary artery disease (CAD). There is a dramatic decline in sexual satisfaction in men and women after stroke. CAD may compromise erectile dysfunction, but the risk of myocardial infarction during sex is low. The metabolic demands of sexual intercourse are 3-5 METS, roughly equivalent to climbing a flight of stairs. However, it is also influenced by the duration of sexual activity. Diabetic dysautonomia also produces erectile dysfunction.

2. ESSENTIALS OF ASSESSMENT

History

Because sexuality can be a sensitive topic, it is important to maintain an open and non-judgmental approach. The history should progress from general medical and related issues, including current medications, to specific questions about desire, sexual orientation, prior sexual experience (including abuse), pain, sexual response, orgasm. Women should be queried about their menstrual cycle, and men for any change in libido, male pattern hair growth (change in need for shaving facial hair).

Physical examination

    • Communication: aphasia, dysarthria, dysprosodias, attention, memory
    • Range of motion
    • Motor control: weakness, ataxia, spasticity
    • Sensation: reduced, dysesthesias
    • Pelvic floor: genitalia, rectum, anal tone, bulbocavernosus, pelvic exam in females

Laboratory studies

  • Screening:
    • erythrocyte sedimentation rate (ESR)
    • complete blood count (CBC)
    • fasting glucose
    • lipids
    • Urine analysis
    • Liver function
    • Thyroid function studies
    • Renal function studies
    • Prolactin and testosterone (free and total, men and women)
  • More sophisticated testing
    • Pituitary hormones including provocative testing
    • Nocturnal penile tumescence
    • Provocative tests with intracorporeal injections (papaverine) and measurement with penile doppler
    • Somatosensory evoked responses
    • Electrodiagnosis: dorsal penile nerve conduction, BC, anal reflexes
    • MRI and vaginal photoplethysmography for objective measurement of sexual response in women
    • Genital sympathetic skin response

Supplemental Assessment Tools

Brain Injury Questionnaire of Sexuality (BIQS) – developed and validated specifically for TBI

The Brief Sexual Symptom Checklist – Helpful screening tool for clinical practice. Versions available for male and female patients.

3. REHABILITATION MANAGEMENT AND TREATMENTS

Available or current treatment guidelines

  • Techniques and treatments to improve erectile function
    • Phosphodiesterase type 5 inhibitors (sildenafil, tadalafil, vardenafil)
      • Effective in men with partial to full reflex erection response
      • Do not use within 48 hours of administration of any nitrate-containing medication; may cause severe, life-threatening hypotension
      • Side effects infrequent: headache, flushing, dyspepsia, visual changes (blue light)
      • Alcohol and full meals may impair effectiveness
    • Constrictor band
      • Monitor for skin breakdown
    • Vacuum pumps
      • Manual
      • Electric powered
      • Clitoral vacuum device for women (NuGyn Eros®)
    • Intracavernous injections of drugs
      • Papaverine, phentolamine, and prostaglandin E1, either as single drugs or in combination, are the drugs of choice.
      • Risk of priapism; person using these drugs should be reliable
    • Transurethral administration of vasoactive drugs
      • Prostaglandin E1 is available as a suppository
      • MUSE (alprostadil) is a prefilled, ready-to-use suppository, inserted with an applicator
        • May cause hypotension, especially if lesion above T6
        • Side effects infrequent: pain in penis, syncope, vertigo, hypotension, priapism
        • No need for injection
      • Topical agents
        • Nitroglycernin paste
        • Minoxidil
        • Prostaglandings
      • Low-intensity extracorporeal shockwave therapy (Li-ESWT): encourages angiogenesis in corpora cavernosa via microtrauma
      • Melanocortin receptor agonists: show some utility for ED and they have also been shown to increase vaginal blood volume
      • Penile prosthesis
        • Inflatable and semi-rigid designs available
        • Requires surgery
        • Quite costly
        • Do not typically provide a full-length erection or increase girth of penis
        • Complications can include rod malfunction, infection, and erosion.
        • Generally irreversible
      • Apomorphine (dopamine agonist): first CNS agent approved in Europe for erectile dysfunction. Undergoing trials for potential treatment of female sexual dysfunction.
  • Strategies and treatments to improve libido
    • Antidepressants
      • Trazodone and fenfluramine increase libido
      • Buproprion for libido (dopamine)
    • Opiate antagonists
    • Flibanserin: serotonin receptor 1A agonist/serotonin receptor 2A antagonist FDA approved for premenopausal female hypoactive sexual arousal disorder in 2015
    • “Natural” compounds:
      • Yohimbine (vascular problems) for impotence also may benefit physiologic response in women
        • Alpha blocker
      • Zestra® – Botanical massage oil with borage seed oil, evening primrose, extracts of angelica, coleus, forskolin, antioxidants and vitamin E. Double-blind, placebo-controlled RCT evidence of benefit in level of arousal, desire, genital sensation and sexual pleasure for women.
    • Hormonal agents
      • testosterone remains controversial in both sexes in absence of hypogonadism
      • human chorionic gonadotropin
        • trials in men with erectile dysfunction and low libido
      • Bremelanotide: Phase III success with increasing desire and arousal in premenopausal patients
      • Transcranial magnetic stimulation (TMS)
  • Sexual Behavior Disorders
    • Disinhibition
      • Behavioral therapy
      • Serotonin re-uptake blockers
      • Anticonvulsants
      • Cognitive therapies to address impulse control
    • Sexual offending disorders (6.5% of TBI patients) – must distinguish from disinhibition
      • May require hormonal therapy with estrogens
  • Techniques to enhance sexual satisfaction
    • Sex therapy: Typically done with partners
      • May include medication changes, behavioral and cognitive psychotherapeutic techniques.
      • May also employ various physical exercises
        • Kegel exercises
        • Start-stop techniques
        • “Squeeze technique” for premature ejaculation
      • Cabergoline has been studied for use in male delayed orgasm and anorgasmia
  • Treatment of sensorimotor disorders
    • Positioning
    • Sex toys
    • Alternative practices
    • Alteration in position to accommodate contractures or spasticity
      • May also be necessary to reduce cardiac work in CAD
  • Fertility:
    • Explore co-morbidities and medications
    • In TBI, likely hormonally-related

Patient & family education

  • Sexuality counseling incorporates the PLISSIT Model: Permission, Limited Information, Specific Suggestions, Intensive Therapy
  • A 2013 consensus document from the American Heart Association and the European Society of Cardiology recommends that stroke survivors and their partners be assessed regarding sexual function at the time of stroke and regularly in follow-up care.

4. CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE

Cutting edge concepts and practice

Voxel-based lesion-symptom mapping (VLSM) and advancements in functional connectivity neuroimaging techniques may help further elucidate neural correlates of sexual dysfunction

Stem cell therapy for erectile dysfunction: European Phase I trial showed promise for patients to regain spontaneous erections

Study in progress – “The Menopause Transition in Women with Traumatic Brain Injury”

5.GAPS IN THE EVIDENCE-BASED KNOWLEDGE

Gaps in the evidence-based knowledge

Studies inclusive of lesbian, gay, bisexual, transgender, and intersex (LGBTI) individuals who are currently not well-represented in the literature

High quality studies with larger and more diverse samples including women, younger stroke patients, mild TBI, patients with aphasia

Rigorous studies of specific treatment interventions to help guide clinical decision making

Effects of menopause in patients with history of TBI

REFERENCES

  1. Korpelainen JT, Nieminen P, Myllyla VV. Sexual functioning among stroke patients and their spouses. Stroke. 1999;30(4):715-719.
  2. Hibbard MR, Gordon WA, Flanagan S, Haddad L, Labinsky E. Sexual dysfunction after traumatic brain injury. NeuroRehabilitation. 2000;15(2):107-120.
  3. Masel B, DeWitt D. Traumatic brain injury: a disease process, not an event. J Neurotrauma. 2010;27:1529-1540.
  4. McCabe MP, Sharlip ID, Lewis R, et al. Incidence and prevalence of sexual dysfunction in women and men: A consensus statement from the fourth international consultation on sexual medicine 2015. The Journal of Sexual Medicine. 2016;13(2):144-152.
  5. Rees PM, Fowler CJ, Maas CP. Sexual dysfunction 2: Sexual function in men and women with neurological disorders. The Lancet. 2007;369(9560):512-25.
  6. Sander AM, Maestas KL, Nick TG, et al: Predictors of sexual functioning and satisfaction 1 year following traumatic brain injury: a TBI model systems multicenter study. J Head Trauma Rehabil 2013; 28: pp. 186-194
  7. Everaert K, de Waard WI, Van Hoof T, Kiekens C, Mulliez T, D’Herde C. 2010. Neuroanatomy and neurophysiology related to sexual dysfunction in male neurogenic patients with lesions to the spinal cord or peripheral nerves. Spinal Cord 48:182–191.
  8. DeLamater J: Sexual expression in later life: a review and synthesis. J Sex Res 2012; 49: pp. 125-141
  9. Chan JL, Mantzoros CS. Role of leptin in energy-deprivation states; normal human physiology and clinical imputations for hypothalamic amenorrhoea and anorexia nervosa. Lancet 2005; 366: 74-85.
  10. Dusenbury W, Palm Johansen P, Mosack V, Steinke EE. Determinants of sexual function and dysfunction in men and women with stroke: A systematic review. Int J Clin Pract. 2017;71(7):e12969
  11. Simpson GK, Sabaz M, Daher M. Prevalence, clinical features, and correlates of inappropriate sexual behavior after traumatic brain injury: A multicenter study. J Head Trauma Rehabil. 2013;28(3).
  12. Taylor B, Davis S. The extended PLISSIT model for addressing the sexual wellbeing of individuals with an acquired disability or chronic illness. Sex Disab. 2007;25(3):135-139.
  13. Strizzi J, Olabarrieta Landa L, Pappadis M, et al. Sexual functioning, desire, and satisfaction in women with TBI and healthy controls. Behavioural Neurology. 2015;2015:1-7.
  14. Georgiadis JR, Kringelbach ML. The human sexual response cycle: Brain imaging evidence linking sex to other pleasures. Prog Neurobiol. 2012;98(1):49-81.
  15. Hanks RA, Sander AM, Millis SR, Hammond FM, Maestas KL. Changes in sexual functioning from 6 to 12 months following traumatic brain injury: A prospective TBI model system multicenter study. J Head Trauma Rehabil. 2013;28(3):179-185.

Original Version of the Topic

Lawrence Horn, M.D. Sexual Dysfunction in Acquired Brain Injury (ABI). 06/07/2013

Author Disclosure

Parisa Zarreii, MD
Nothing to Disclose

Maria Humayun, D.O.
Nothing to Disclose

Lawrence Horn, M.D.
Nothing to Disclose

Related Articles