Premature ejaculation is not uncommon in the general population. In patient populations with cerebral disease, few comparative studies have been done. The condition may be associated with cerebral diseases including traumatic brain injury (TBI), cerebrovascular disease (CVD), Parkinson’s disease (PD), and epilepsy.

Surveys of sexual dysfunction after TBI have identified that between 17–36 % of males report a number of different post-injury ejaculatory problems, including PE [26, 27], with Meyer reporting a 9 % incidence of PE [28]. In contrast, de Morsier and Gronek [29] found that two of the 49 male patients (4 %) reported being premature ejaculators. In general, hyposexuality has a much higher incidence in this population than hypersexuality, although the latter can be seen occasionally [especially during the early stages after coming out of coma (the so-called posttraumatic amnestic state) and with bilateral temporal lobe lesions] [30]. Various authors attribute a particular sexual dysfunction to damage of different sites of the brain, or different sexual dysfunctions are connected to the same brain localization [31, 32]. It is also difficult to be precise about the exact location and severity of the injury at that particular site and its effect on sexual function. One cannot assume that, even when injury to a critical area is proven, the sexual dysfunction is definitely a result of that injury. There are always the neuroendocrine dysregulation, erectile dysfunction (ED), emotional, and relationship parameters to be considered, rendering the situation more difficult to evaluate [31, 33]. This differentiation is especially difficult since the issue of sexual function is usually raised at a later stage of the rehabilitation process. However, Simpson et al. [34] utilized a combination of medical, behavioral, and educative interventions to treat a case of PE. Successful treatment may indicate that PE may be due to psychogenic rather than organic causes.

Cerebrovascular accidents have generally been shown to alter sexuality in several ways, including decreased libido, ED, ejaculatory dysfunction, and decreased frequency of intercourse [35–37]. Ejaculatory dysfunction after stroke is common in men. Whereas most men were able to ejaculate before a stroke, only 29 % could do so afterwards in one study [38], and similar findings have been reported by others [39]. It seems that there is no good agreement regarding the incidence of sexual dysfunction as related to dominant vs. nondominant hemispheric involvement [35, 36], however Jung et al. noted that stroke lesions affecting the right cerebellum might be associated with ejaculation disorder [37]. Sexual dysfunction appearing after a stroke is a complex reaction with both organic and psychological factors. The main subjective reasons for diminished poststroke sexual activity are hemiparesis, spasticity, decreased libido, fear of a new stroke, ED, aphasia, associated comorbidities, drug-induced sexual dysfunction, as well as sensory deficits [36, 37]. It has been reported that sexual dysfunction correlated significantly with the presence of the sensory hemisyndrome [37, 40]. It is well known that tactile stimulations are extremely important in sexual arousal and orgasm during foreplay and intercourse. Therefore, it is obvious that the sensory hemisyndrome is related to problems with erection, ejaculation, and orgasm resulting in impaired libido and quality of sexual life [37]. Theoretically, elimination of all sensation from one half of the penis and scrotum may lead to delayed ejaculation in stroke patients showing pre-stroke PE and increased penile hypersensitivity. Whether cerebrovascular disease may emerge as a negative risk factor for PE in those patients with pre-stroke increased penile hypersensitivity remains to be determined. On the other hand, stroke patients may be susceptible to PE secondary to ED because patients with multiple brain lesions showed a significant decrease of erectile function compared with the patients with one lesion [37].

Sexual dysfunction is common even in young males with Parkinsonism. In comparison with age-matched controls, in whom the prevalence of ED was 37.5 %, the corresponding number in patients with PD was 60 % in one study [41]. Many men cannot ejaculate or reach orgasm, but PE has also been reported [42, 43]. In one study, Bronner et al. [43] diagnosed PE in 13 out of 32 patients (40.6 %). In contrast difficulties in reaching ejaculation was diagnosed in nine out of 33 patients (27.3 %) [43]. In another study, evaluation of young PD patients (<55 years of age at disease onset) revealed PE in 8 % of patients [44]. The mechanisms behind PE in PD are not well understood. In general, symptoms of PD are due to a progressive loss of nigral neurons causing striatal dopaminergic denervation. However, nigral degeneration is only a part of the underlying synucleinopathy, and clinical symptoms go far beyond motor Parkinsonism [45]. However, autonomic dysfunction, depression, and testosterone deficiency, are frequently seen [45–47]. Although antiparkinsonian dopaminergic medications such as levodopa may decrease the ejaculation latency [48, 49], previous studies found no correlation between medication regimen and sexual activity [42, 50]. The large number of possible combinations of antiparkinsonian medications makes systematic study of medication effects on sexual function difficult. The variability in the expression of symptoms such as PE and difficulty in reaching ejaculation might be explained by the specific topographical sequence of the pathology, depending on the extent and progression of the degenerative process at defined sites. A longitudinal study of the ejaculatory function from the onset of PD would be of value.

The relation between epilepsy and sexual function is more complicated. It is estimated that 38–71 % of men with epilepsy experience diverse sexual problems [51–53]. These problems include various types of sexual dysfunction (such as ED, PE, orgasmic dysfunction, and diminished sexual desire), deviant sexual behaviors, hypersexuality, and, most commonly, hyposexuality. These problems may be associated particularly with temporal lobe epilepsy [54–56]. In addition, sexual fantasies, arousal, intercourse, and orgasm can provoke an epileptic attack through several pathophysiological mechanisms [55–57]. For example, hyperventilation, commonly accompanying sexual activity, can provoke generalized epileptic seizures [57, 58]. Moreover, somatosensory auras presented as sensations in the genital organs like numbness, tingling, pain, and unpleasant feeling may be manifestations of epileptic seizure arising from a genital sensory cortical area [59–61]. These sensations involve discrete parts of the body contralateral to the ictal discharge. In one study, men with epilepsy have an approximately five-fold increase in risk of sexual dysfunction including diminished sexual interest and poor sexual performance [52]. The prevalence of the complaint of PE varies between 2 to 66.7 % [62–64]. The prevalence in the general population in the National Health and Social Life Survey study was 28.5 % for men between 18 and 59 years [65]. Although Nikoobakht et al. failed to detect a correlation between PE and seizure type, frequency of epileptic seizures, control of the disease, and the medication used [62], Daniele et al. noted that the incidence of PE was significantly higher in the group with right-temporal lobe epilepsy, as compared to left-temporal lobe epilepsy patients and to controls [66]. These findings can be analyzed in the same way as Suffren et al. explained why hypersexuality more often results from right-hemisphere than left-hemisphere lesions [67]. The authors noted that ictal orgasm more often occurs in patients with right-sided than left-sided seizure foci, with the symptom probably resulting from right-hemisphere activation. The left hemisphere may be specialized for increasing sexual tension, whereas the right hemisphere may be specialized for release of this tension (orgasm), the former being catabolic and the latter being anabolic. The mechanisms behind PE in epileptic patients are not well understood but are likely to be multifactorial, involving neurological, endocrine, iatrogenic, cognitive, psychiatric, and psychosocial factors [68]. For example, epileptiform discharges from the temporal lobe region may be transmitted through amygdala-hypothalamic pathways, disrupting the normal pulsatile secretion of gonadotropic hormones and the basal levels of dopamine secretion, resulting in hypogonadism and hyperprolactinemia [69]. Several antiepileptic medicines increase sex hormone-binding globulin (SHBG), including carbamazepine, phenytoin, valproate, and oxcarbazepine. The increase of SHBG could alter testosterone homeostasis [70].

Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system (CNS) with a predilection for white matter tracts in the cerebral hemispheres, optic nerves, brainstem, cerebellum, and spinal cord. The disease generally affects sexually active young adults in populations of the western world. Sexual dysfunction is a common complaint in men with MS and it affects more than 75 % of patients [71–73]. Male sexual dysfunction includes difficulty in achieving and/or maintaining an erection (ED), decrease or loss in libido, painful or uncomfortable genital sensations (burning, tingling, and numbness), and orgasmic and/or ejaculatory disorders. ED appears to be the most common form of sexual dysfunction documented in MS [73, 74]. PE research and management in MS have been minimal. The topic is underrecognized and undertreated. This is a less frequent complaint than ED among male MS patients with sexual dysfunction. The incidence of PE in patients with MS has been estimated between 0–45.2 % [72–75]. In their study, Tepavcevic et al. reported a 45.2 % incidence of PE among MS patients [73]. The authors noted statistically significantly lowered scores on sexual function (SeF), and sexual function satisfaction (SFS) subscales of the health-related quality of life (HRQoL) in patients with PE. On the other hand, Barak et al. failed to detect any case of PE among nine patients with PE [75]. This may be attributed to the fact that some patients with MS could not answer the question because they did not remember or they did not know exactly if sexual dysfunction began before, simultaneously, or after the other symptoms of MS [74]. Another explanation is that genital somatosensory evoked potential abnormalities are common in men with MS and sexual dysfunction. Decreased penile sensation has been reported in 53.8 % of cases in one study [72]. Theoretically this could explain the high incidence of delayed ejaculation and anejaculation rather than PE in patients with MS. Previous questionnaire surveys have quoted of 35–45 % of patients with MS reporting difficulty in achieving ejaculation [76, 77]. In one study [72], there were more complaints of difficulty with orgasm (53.8 %) and trouble of ejaculating (46.2 %) than of PE (7.6 %). In addition, it has been demonstrated that temperature and nociceptive (pain) signals from penile FNEs travel via small-diameter, thinly myelinated, or unmyelinated nerve fibers, whereas vibration, touch, and pressure utilize large-diameter, myelinated fibers [14]. These findings explain the low incidence of PE in MS because the nerves which are more heavily myelinated are more likely to be damaged by MS. The pudendal nerves enter the CNS at the most caudal aspect of the spinal cord. With the longest tract to the cortex, pudendal somatosensory tracts are the most likely to be damaged by MS. This has been borne out in the literature, with pudendal somatosensory evoked potential abnormalities frequently found in MS, even in early stages of the disease [78]. Sexual dysfunction may not only be due to lesions affecting the neural pathways involved in physiological function (primary dysfunction), but also results from general physical disabilities (secondary dysfunction) or psychological and emotional issues (tertiary dysfunction) [79]. The pathogenesis of PE in MS patients is not known. Explanations included: deficits in central serotonergic activity which are related to the rate of disability accumulation in relapsing-remitting MS and could be linked to the reported reduction of disease activity by serotonergic drugs [80], higher serum prolactin levels compared with healthy controls in MS [81], hypothalamo-pituitary gonadal dysfunction in some cases [82], and the increasing evidence that testosterone has a neuroprotective role and influences damage repair in the nervous system [83], secondary to ED, or psychological factors [84].

The annual incidence of spinal cord injury (SCI) in developed countries is estimated at 15–40 cases per million population [85]. Young adult sexually active men constitute roughly 82 % of these individuals [86]. The disruption to autonomic circuits and sensations following SCI can result in low sexual satisfaction and sexual dysfunction which are both well documented after SCI, and the resolution of these problems has been identified as a high priority [87–89]. These sexual problems include ED, decreased libido, orgasmic dysfunction and ejaculatory disorders [88, 89]. In general, the effect of SCI on sexual function is highly dependent on the site and extent of injury and the most commonly affected sexual responses are arousal and orgasm [90]. For example, individuals with upper motor neuron lesions (UMNL), and preserved S2–S5 roots, generally have preserved reflex genital arousal, as the reflexes mediating erection are located in the spinal cord. However, these individuals generally are unable to initiate genital arousal psychogenically. On the other hand, lower-level SCI (infraconal or cauda equina) tends to disrupt reflex vasocongestion, but can leave sympathetically mediated psychogenic arousal intact [91, 92].

Although men with SCIs are less likely than controls to achieve orgasm, orgasm is seen in 40–50 % of the patients [93, 94]. In these patients, latency to orgasm is not significantly different between controls and SCI subjects [91]. Men with incomplete SCIs are more likely to achieve orgasm and ejaculation than those with complete SCIs (Fig. 14.2). In contrast, men with complete lower motor neuron lesions (LMNL) affecting their sacral segments are significantly less likely than men with any other levels and degrees of SCI to achieve orgasm [93]. Although orgasm and ejaculation are generally associated during sexual activity, this is not always the case and ejaculation can occur without orgasm and vice versa in SCI. Subjects with complete LMN injuries affecting their sacral segments would be the least likely to achieve orgasm [92]. In SCI, presumably descending inhibitory pathways controlling ejaculation (and erection) were damaged, leaving descending facilitatory pathways functionally intact and unopposed leading to PE [95]. In general, patients with hyperesthesia in the genital region and patients with incomplete lesions of the conus region of the spinal cord may suffer from PE. In this context, Kuhr et al. reported six cases of acquired premature emission after thoracolumbar spinal cord trauma suggesting that spinal lesions may be a cause of premature emission [96]. These patients were sexually healthy before sustaining traumatic SCI. They demonstrated neurogenic bladder dysfunction on urodynamic evaluation and five of them required intermittent catheterization. Bulbocavernosus and anal reflexes were absent in all patients while perineal sensory deficits varied. Therefore, the authors were in doubt that bulbocavernosus muscle contraction and true ejaculation occurred although there was emission. Premature emission developed after a vertebral fracture with sacral cord damage in one case and after iatrogenic ischemic injury to the thoracic spinal cord also in one case. One patient was successfully treated with phenoxybenzamine before intercourse but the other declined treatment. Earlier and recent reports (table 14.3) of this association have been anecdotal [95, 97, 98], and SCI is generally found to lead instead to impairment of ejaculation. Ejaculation may be easily provoked by touching the glans penis or if the patients have thoughts about sexual contact [95, 97]. It may be induced spontaneously at the onset of micturition, in association with symptoms of urinary urgency or the sensation of bladder fullness. Spontaneous ejaculation also occurred occasionally during midstream micturition [97]. This complaint may occur many times per week and sometimes per day without any sexual desire, sexual excitation, or any provocative factors with preserved orgasm at every time ejaculation occurs [98]. This association is in need of further studies to disclose the exact pathophysiology.