Sexual impairment is a commonly described consequence of traumatic brain injury. Indeed, many authors believe that sexual dysfunction is “more often the rule than the exception”. A brain trauma could involve all those brain regions activated during a normal sexual response. Nevertheless, sexual impairment in injured people seems to be related both to a direct effect of trauma on sexual pathway and to a situational change in the patient’s mood, the latter contributing to higher rates of sexual dysfunction after brain trauma (about 36-54%). Sexual dysfunctions after traumatic brain injury are more reported in men than in women, and mostly in severe rather than minor trauma.

Some investigators reported that sexual disorders do not correlate with cognitive impairment, length of post-traumatic amnesia or physical neurological disability caused by brain injury. Independent determinants of sexual outcome include a high sickness-impact profile, low-self-esteem, anxiety and depression, which are considered the most sensitive negative predictor.

Physiopathology and type of sexual disorders of post traumatic brain injury patients are closely dependent on the damaged brain area, although poor attention has been paid on understanding the specific nature or the impact of sexual dysfunction in these individuals. The most reported sexual dysfunctions in men after traumatic brain injury are erectile dysfunction (erectile dysfunction) and disorders of desire, mainly when anterior brain regions are damaged.

erectile dysfunction is considered to be due either to post traumatic brain injury depression or to damage of the hypothalamic-pituitary axis. Indeed, although many authors reported that head injured males experience erectile dysfunction when associated to depression, it has recently been found how erectile problems are often accompanied by signs and symptoms of cerebral damage and impaired libido.

Changes in sexual desire and behavior are by far the most common sexual problem after a brain injury. Since anterior brain regions are associated with emotional and behavioral impairment, prefrontal and lobar lesions might more frequently generate hyposexuality rather than hypersexuality. The latter is often reported as an intensified sexual experience after brain injury, an inappropriate sexual attention towards others, or a kind of sexual exhibitionism leading to sexually deviant criminal activities (i.e. rape or pedophilia). Many authors have reported that “the sexual activity of injured subjects is often a one-side act, done without regard for the partner”. Hypersexuality and alteration of sexual preference provide important clues for understanding the anatomy and physiology of human sexual behavior. Lesions in structures such as the amygdala, the hypothalamus, the temporal and frontal lobes have been described in association to these symptoms. In particular, lesions in the frontal lobe have been referred as an anatomical site producing true hypersexuality while the other structures are more related to changes of sexual preference.

Interestingly paraphilia has been described as occurring after brain damage, mostly of the frontal lobes and diencephalic structures. As Paraphilia rarely occurs after the age of 30, an acquired paraphilia onset in elderly people is often associated with focal brain injury. Many authors have tried to investigate the role of traumatic brain injury in sex offenders with inconclusive results related to complexity of this study. Lagevin has pointed out that 22.5% of sex offenders presented a previous traumatic brain injury, sometimes associated to lifestyle factors such as drug abuse or alcohol consumption. In some case brain injury is a direct result of an aberrant lifestyle. Moreover, sex offenders with a traumatic brain injury history might be distinguishable from those without it. Indeed, they showed a tendency to act out more with adults than with children and a polymorphous fashion of their sexual behavior.

On the contrary, hyposexuality is more related to the psychological aspect of sexuality. People with traumatic brain injury reported more frequently difficulties in sexual activity and relationship than in erectile function. Many patients report difficulties in positioning, body movement and decreased sensation, negatively impacting on their sexual activities and interest. These findings suggest a relationship among sexual satisfaction, level of dependence and degree of handicap leading to a negative body image and low self-esteem in sexual activities. Indeed, psychological factors could be the best predictor of hyposexuality in men after traumatic brain injury.

Moreover, severity of traumatic brain injury has been suggested as an important predictor of sexual disorders. However, since the global amount of brain tissue destroyed seems to be related to the awareness level, sexual dysfunctions are more often reported in patients with milder than severe injuries. Inconsistent results were found across studies on the effect of time post traumatic brain injury. Some authors have found a close relationship between length of time after traumatic brain injury and severity of sexual impairment, with shorter duration of time associated with better sexual function and satisfaction. Nevertheless, recent studies have pointed out how sexual difficulties could develop at any time post traumatic brain injury as well as at any age.

Lesions of the frontal and temporal lobe seem to lead more frequently to sexual problems than lesions of the posterior part of the brain. Disorder of ejaculation has also been reported in patients after a brain trauma with delayed ejaculation as the most frequent symptom (from 17% to 36%) and premature ejaculation with an incidence of 9%. Some authors have described cases of sexual hyperarousal and increased skin sensitivity of penis following minor traumatic brain injury in healthy persons, suggesting a secondary rather than primary (neurogenic) origin of premature ejaculation.

Hypotalamo-pituitary Trauma

Injury of pituitary gland is a frequent complication of head trauma and it is associated with high mortality rate during the acute phase. Serious and life-threatening adrenal crisis due to adrenocorticotropic deficiencies following traumatic brain injury is widely highlighted in many clinical studies. Occurrence of a fatal panhypopituitarism after traumatic brain injury is associated with severity of head trauma. Diffuse axonal injury, basal skull fracture and increased intracerebral pressure are the most frequent physiopathological mechanisms determining panhypopituitarism. Recovery between 6 and 12 months is almost always the rule, when hypopituitarism is quickly diagnosed and treated.

The prevalence of endocrine dysfunction after traumatic brain injury, due to anterior pituitary lesions, ranges from 15% to 68%. Both anterior and posterior parts of the gland could be damaged. Hemorrhage, necrosis and fibrosis in the context of pituitary gland are common complications of traumatic brain injury. Moreover, they are often associated with hypothalamopituitary impairment of the chronic traumatic brain injury phase.

Lesion of the anterior part of pituitary gland is associated with altered sexual desire related to Luteinizing Hormone, Follicle-Stimulating Hormone, Prolactin and Growth Hormone alterations. Luteinizing hormone and Follicle-stimulating hormone deficiency is associated with central hypogonadism, especially when trauma occurs during childhood. Central hypogonadism is also reported from 9 to 23% of men with low gonadotropin response or low testosterone levels after traumatic brain injury, while reduced Growth Hormone levels could influence sexuality through reduction of energy levels and general wellbeing.

Hyperprolactinemia is more associated with orgasm, libido and arousal disturbances in women rather than in men. The high levels of Prolactin hormone are thought to be a consequence of antidepressants and antipsychotic treatment rather than a direct effect of trauma.

Studies on the association of sexual dysfunction and anterior pituitary hormone impairment after traumatic brain injury need further investigations.

Lesions of the posterior part can cause a central diabetes insipidus due to depressed antidiuretic hormone blood level. Sexual dysfunctions following posterior pituitary trauma often occur with altered sexual arousal due to low oxytocin blood level, especially in women. Nevertheless, oxytocin has also inhibitory properties concerning postcoital satiety and male refractory period.

Deficiency in neuropeptidergic molecules as hypothalamic Orexin-A (i.e. Hypocretin-1) is sometimes associated with traumatic brain injury. Orexins are involved in regulation of sleep-wake cycle and low levels are often evidenced in patients in the subacute phase of moderate to severe traumatic brain injury. In these patients, levels of hypocretin-1 in the cerebrospinal fluid are comparable to those of narcoleptic patients. Reduced cerebrospinal fluid levels of Orexins are associated with hypersomnolence which may interfere with the normal sexual intercourse, behavior and arousal of posttraumatic patients.

Kluver-Bucy Syndrome

Kluver-Bucy Syndrome is one of the most common temporo-limbic syndromes caused by a bilateral damage of anterior temporal lobes. Kluver-Bucy Syndrome is quite frequent in post traumatic brain injury patients due to the injury of temporal and orbitofrontal areas with the bone of middle and anterior cranial fossae.

In 1939 Kluver and Bucy bilaterally removed the anterior temporal lobes in primates and noted six different neuropsychiatric symptoms, i.e. “Psychic blindness”, hypersexuality, altered emotional behavior, hyperorality, “hypermetamorphosis” and memory deficit, related to limbic cortex and amygdala involvement. They termed psychic blindness as the inability of animals to recognize emotional significance of the object, while they used hypermetamorphosis to indicate the tendency to react to every visual stimulus especially with the mouth. Indeed, their animals became tame with an excessive and sometimes life-threatening oral exploration of the environment.

In humans, Kluver-Bucy Syndrome is rare and described as typical in the post-traumatic remission phase and associated with favorable prognosis in the outcome of traumatic disturbances of consciousness in survivors of head trauma. Human Kluver-Bucy Syndrome is a more complex behavioral syndrome. Some authors attribute this complexity to the evolutionary advances of the human brain. Therefore, patients with Kluver-Bucy Syndrome didn’t show the full-blown syndrome but often other accompanying symptoms such as aphasia, amnesia, echopraxia, dementia and seizures. The presence of at least 3 of the 6 aforementioned main symptoms is mandatory for the diagnosis. Among humans, altered emotional behavior and hyperorality are the most common features, while hypersexuality is less common.

Alterations in emotional behavior in humans include apathy, lethargy and emotional unresponsiveness, whereas Kluver-Bucy Syndrome patients with aggressive and hypomaniac mood associated with hyperorality and hyperphagia have been reported.

Hypersexuality presented itself with a wide clinical spectrum varying form an inappropriate or obscene language in specific contexts to a dirty behavior acting with whatever person. The most reported symptoms are changes in sexual orientation, compulsive masturbation, inappropriate sexual remarks and gestures without care of situation.

Frequent causes of Kluver-Bucy Syndrome are infectious diseases such as herpes virus encephalitis, hypoxia, hepatic and metabolic impairment. Kluver-Bucy Syndrome is also observed in cases of pontine mielinolysis related to rapid correction of hyponatremia, or following temporal status epilepticus when associated with bilateral mesial temporal sclerosis. The latter could explain the easy response to carbamazepine treatment in these subjects. Kluver-Bucy Syndrome episodes are often reported in severe traumatic brain injury patients during recovery of awareness, especially when Magnetic Resonance Imaging shows a mesial and/or basal temporal lobe involvement.

Specific sides of the disease are still under debate. Although many authors have highlighted the role of the two amygdalae, recently someone has shown how the disruption of limbic circuitry associated with mediodorsal thalamic relay could develop Kluver-Bucy Syndrome. The complex pathways connecting the dorsomedial thalami with prefrontal or limbic areas are essential for memory and regulation of impulses and emotions. This cerebral circuitry involvement could explain the symptoms variability of Kluver-Bucy Syndrome in humans.

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