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Sexual Dysfunction in Neurological Disorders
Acknowledgment
The authors wish to thank Anabelle Grenier-Genest PhD(c) and Geneviève Leblanc MA(c) for their help in preparing this chapter and Thomas Lefebvre for the figures.
Neurological disorders have many effects on sexual function that are often dismissed by rehabilitation professionals. They have been classified into primary, secondary, and tertiary impacts. Primary impacts refer to the direct effects of the neurological lesion on sexual function. Secondary impacts refer to their effects on other body functions involved in sexuality as well as the side effects of medications. Tertiary impacts refer to psychosocial aspects that reduce access to social contacts, thus interfering with sexual relationships.
This chapter explores these various aspects, starting with a review of the neural innervation of the male and female genitals, followed by a review of the primary, secondary, and tertiary impacts of neurological conditions on sexual function as well as a discussion of their treatment.
The Neurophysiology of Human Sexual Responses
The Neurophysiology of Male Sexual Responses
Erection
Erection is a reflex receiving excitatory and inhibitory influences from the brain ( ).
Reflexogenic erection arises from genital stimulation mediated by the spinal segments S2-S4 ( Fig. 46.1 ). Sensory fibers run through the dorsal penile nerve, synapse with the preganglionic pelvic nerves, run through the pelvic plexus, and synapse with the postganglionic cavernous nerves ( ). Nitric oxide (NO) release from the cavernous nerves and from the penile epithelium triggers a cascade of events, transforming GTP into cGMP, and resulting in relaxation of the smooth penile muscles and vasodilation of the penile arteries, leading to tumescence ( ). Sporadic stimulation of the perineal nerves during tumescence triggers contractions of the bulbospongiosus and ischiocavernosus muscles ( Fig. 46.2 ), increasing the internal penile pressure during erection and maximizing penile rigidity ( ).
Erection can also arise from psychogenic stimuli originating from the brain and feeding into the sacral pathway (facilitating or inhibiting reflex) or running through the thoracolumbar (TL) pathway exiting the T11-L2 segments and running down the paravertebral sympathetic chain that feeds into the pelvic plexus ( ).
Ejaculation
Ejaculation consists of emission and expulsion. Emission involves contractions of the internal reproductive organs, which release their content into the prostatic urethra and create the semen (see Fig. 46.1 ; ). Expulsion involves rhythmic contractions of the perineal muscles.
Emission is controlled by TL innervation, receiving inputs from the sacral pathway, which activates the sympathetic splanchnic nerves synapsing in the celiac and mesenteric ganglia with the hypogastric nerves innervating the internal reproductive organs (see Fig. 46.1 ). As semen is collected in the prostatic urethra (see Fig. 46.1 ), stimulation of urethral stretch receptors initiates expulsion controlled by the sacral spinal segments and mediated by the perineal nerves ( ).
These phases of ejaculation are orchestrated by a spinal generator of ejaculation (SGE), located in the L3-L4 spinal segments ( ), which coordinates the events from the sensory inputs of erection, to the intraspinal connections between the sacral and TL pathways, to emission and expulsion ( ).
Orgasm
Orgasm is characterized by cardiovascular responses (tachycardia, hypertension, hyperventilation), muscular contractions, and sympathetic discharge (sweating, shivering, red skin spots; ). Orgasm is suggested to be a nonpathological equivalent of autonomic dysreflexia (AD) normally submitted to supraspinal inhibition ( ). The neural control involves the sympathetic fibers (see Fig. 46.1 ) synapsing with the hypogastric nerves responsible for emission and suggested to also activate the overall sympathetic chain that stimulates the collective response of orgasm (hypertension, tachycardia, hyperventilation, and so on; ).
The Neurophysiology of Female Sexual Responses
Anatomy of the Female Genitalia
Recent ultrasonography and magnetic resonance imaging (MRI) reveal that the clitoris is composed not only of a glans ( Fig. 46.3 ) but is also prolonged by a short body attached to the suspensory ligament and extending into the vestibular bulbs (bulbospongiosus cavities; ) that shape the labia majora and the crura (ishiocavernous cavities) running laterally. The urethral opening is surrounded by erectile tissue, which, combined with the clitoris and the vaginal opening, forms the clitoro-urethro-vaginal complex involved in female orgasm ( ). The vestibular bulbs and crura surrounding the anterolateral vaginal wall support the existence of the G spot ( ), better known as the previously mentioned clitoro-urethro-vaginal complex ( Fig. 46.4 ; ).
Although these findings have been criticized by some authors ( ), others have suggested that the ultrasonographic and imaging findings of the female clitoral anatomy support the orgasms described by females, including clitoral, vaginal, urethral, and cervico-uterine orgasm. Multiple pathways from the genitals to the brain ( ) also support these possible expressions of female orgasm.
Arousal and Plateau Phase
The female sexual response has been classically described as consisting of four phases: arousal, plateau, orgasm, and resolution ( ) in addition to desire. Although this description is still useful for the assessment of females with neurological disorders, these several phases involve more complex interactions with motivational, emotional, experiential, and developmental factors ( ).
The arousal phase consists of clitoral erection, congestion of the labia majora and minora, and vaginal lubrication. These responses are controlled by reflexes (see Fig. 46.4 ) conveyed through the dorsal clitoral nerve synapsing in the sacral segments S2-S4 with the parasympathetic preganglionic pelvic nerve, running through the utero-vaginal plexus, and synapsing with the postganglionic cavernous nerves ( ).
Vaginal lubrication results from vasodilation and vasocongestion of the vaginal epithelium, triggering a pressure gradient that stimulates the transudation of plasma from the vaginal wall into its lumen ( ).
Sexual arousal also stimulates contractions of the uterine ligaments, resulting in anterior elevation of the uterus and functionally elongating the vagina (allowing stronger but painless thrusts). Bartholin gland (see Fig. 46.4 ) secretions provide a mucous lining that prevents irritation during intercourse ( ).
The plateau phase follows, with maximal congestion of the clitoral structure and contraction of the suspensory ligament embedding the clitoral glans under its prepuce (allowing stronger nonaversive stimulation). Maximal congestion of the vestibular bulbs stimulates the G spot (see Fig. 46.3 ), facilitating vaginal orgasm ( ).
Sexual arousal can also be activated by psychogenic stimuli feeding into the sacral pathway or synapsing with the TL pathway, traveling through the paravertebral sympathetic chain, and feeding into the utero-vaginal plexus.
Orgasm and Resolution
Orgasm is characterized by rhythmic contractions of perineal muscles perceived as clitoral, vulvar, vaginal, and anal pulsations and by various signs of autonomic discharge, including hypertension, tachycardia, hyperventilation, flushing, shivering, red skin spots, and the like ( ). Given the resemblance between these responses in males and females (see Figs. 46.1 and 46.4 ), the neural pathways governing climax in females is suggested to be identical to emission and ejaculation—that is, involving the concurrent activation of the hypogastric nerves and sympathetic chain ( ).
Following orgasm, the resolution phase clears out vasocongestion and brings cardiovascular and autonomic responses back to normal ( ).
Brain Regulation of Sexual Responses
Brain structures control sexual reflexes through excitatory or inhibitory influences ( , ; ) and modulate sexual desire and arousal ( ; ) as well as participating in the perceptual, cognitive-emotional, and rewarding effects of orgasm ( ).
The medial preoptic area (MPOA; ), the paraventricular nucleus (PVN), and the arcuate nucleus of the hypothalamus exert excitatory influences on sexual reflexes, whereas the nucleus paragigantocellularis (nPGI) exerts tonic inhibition (see Figs. 46.1 and 46.4 ). Excitatory inputs from the MPOA can be conveyed through connection with the PVN and the periaqueductal gray (PGA), both inhibiting the inhibitory nPGI ( ).
Sexual interest or desire ( ) and sexual arousal during manual stimulation of the genitals ( ; ) or visual erotic stimulation ( ; ; ) are associated with activity in the orbitofrontal cortex and insula, the frontal (motor) cortex, the parietal (sensory) cortex, the occipital (visual) cortex, and to some extent the temporal cortex. The basal ganglia, limbic system, and, in particular, the amygdala are also activated during manual stimulation of the genitals ( ; ; ) or in response to visual erotic stimulation ( ; ; ). In females, independent but overlapping cortical representations of the clitoris, vagina, cervix, and breast are found on the homunculus of the parietal lobe ( ). Generalized arousal, and that characterizing climax, is associated with activity in the thalamus, whereas visceral perception is associated with activity in the ventroposterior thalamus ( ). Cardiovascular activity and respiratory events ( ) are recorded in the brainstem and muscular spasms in the cerebellum. Cerebellar projections participate in the cardiovascular ( ) and motor aspects of orgasm ( ). Ventrolateral pontine area activity is partly responsible for climactic pelvic floor contractions ( ).
The emotional and phenomenological experiences of orgasm are associated with deactivation of the prefrontal, temporal, and entorhinal cortex and explain the hedonic and satiety experience of climax ( ; ). Similar deactivation of the amygdala but activity in limbic structures (PVN, MPOA, nucleus accumbens, hippocampus; ) explains the euphoric and emotional state of orgasm ( ). Further connections between limbic structures, the ventrotegmental area (VTA), and the mesodiencephalic zone containing dopamine neurons are held to be responsible for the rewarding effect of climax ( ).
Most brain areas, except for the brainstem and cerebellum, are deactivated at the very moment of orgasm ( ), suggesting a transient removal of supraspinal inhibition ( ).
The Impact of Neurological Conditions on Sexual Function
Spinal Cord Lesions
Of all neurological conditions, spinal cord lesions (SCLs) are the most studied with respect to sexual function ( ). The severity of the sexual deficits varies according to the level and completeness of the lesion, higher lesions being associated with better sexual reflexes ( Fig. 46.5 ) and lower lesions with major losses ( Fig. 46.6 ) ( ). Detailed assessment of remaining function despite the injury is recommended as a first step to treatment and may use the international standards of autonomic function as a guide ( ).
Primary Impacts of Spinal Cord Lesions on Male Sexual Function
Erection
Men with higher lesions generally maintain reflexogenic erections, but they have poor psychogenic erections unless the lesion is incomplete (see Fig. 46.5 ). Tetraplegic and paraplegic men whose lesions are above the sacral segments are capable of reflexogenic erection, the quality of which is superior for tetraplegic than paraplegic men ( ). Men with lower lesions (see Fig. 46.6 ) have sacral damage and lose reflexogenic erection unless the lesion is incomplete. In most cases they maintain psychogenic erections, but these are often of poor quality. The remaining potential with reflexogenic (genital) or psychogenic stimulation may or may not be of sufficient quality (e.g., duration, stability, rigidity) to complete intercourse ( ). In such cases, various treatment options are available (see section “Treatment Options for the Primary Impact of Neurologic Conditions on Sexual Function” later).
Ejaculation
Ejaculation requires preserved intraspinal connections between the sacral and TL pathways (see Fig. 46.5 ). Males with lesions above T10 maintain the potential for ejaculation ( ) but sometimes require vibrostimulation ( ), sometimes in association with additional midodrine ( ).
Males with lesions within the TL segments (i.e., T11-L2) or between the sacral and TL segments (i.e., L3-S1) lose the intraspinal connections necessary for emission. Lower thoracic lesions (T11-T12) have a better prognosis than upper lumbar lesions (L1-L2). Lower sacral lesions (e.g., conus terminalis) can present psychogenic emissions (see Fig. 46.6 ); however, they are generally dribbling and premature ( ).
Males with higher lesions (above T10) can experience anterograde and expulsive ejaculation but also retrograde ejaculation. Lower lesions damage the perineal muscles, leading to dribbling ejaculation ( ).
Orgasm
From 50% to 65% of males with SCLs report orgasm ( ), mostly during ejaculation, although often retrograde ejaculation ( ). Orgasm can be perceived in the absence of ejaculation ( ). In several cases, reports of orgasm in males (and females) with spinal cord injury (SCI) were recorded during functional magnetic resonance imaging (fMRI), documenting the activity in the sacral and TL spinal segments ( ). Orgasm intensity is sometimes attenuated ( ) but can also be heightened (or aversive) during AD ( ). In normal physiology, orgasm is accompanied by hypertension, tachycardia, hyperventilation, and autonomic discharge (piloerection, red spots on skin), which also characterizes AD. When hypertension exceeds 180 mm Hg or ejaculation is accompanied by headache, AD treatment is considered ( ).
Although orgasm is reported with psychogenic stimulation in lower lesions, ejaculation is more often lacking pleasurable sensations in such cases ( ).
Primary Impacts of Spinal Cord Lesions on Female Sexual Function
Arousal
Females with lesions above T10 maintain response to stimulation of the clitoris, vulva, vagina, G spot, and cervix, allowing clitoral erection, labial congestion, and vaginal lubrication ( ). Females with higher lesions ( Fig. 46.7 ) maintain vaginal lubrication with genital stimulation; females with lower lesions ( Fig. 46.8 ) show better vaginal lubrication with psychogenic lubrication ( ).
Orgasm
Orgasm can be achieved with clitoral, vaginal, or cervical stimulation (see Fig. 46.4 ) even with complete lesions but usually associated with higher levels of injury ( 2017; ). Reports of orgasm are supported by fMRI ( ) and positron emission tomography (PET) showing activity in the hypothalamus (PVN) and in the brainstem’s nucleus solitarius ( ). These findings suggest possible retrograde transmission of sympathetic activity during orgasm to these hypothalamic and brainstem nuclei as well as sympathetic plasticity in females with SCLs ( ). Orgasm, in contrast, is seldom achieved with psychogenic stimulation unless the lesion is incomplete, ruling out phantom as opposed to actual orgasm ( ). In general, females with lower motor neuron (LMN) lesions have greater difficulties achieving orgasm than females with upper motor neuron (UMN) lesions ( ).
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