BRAIN INJURY,

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A review of the effect of traumatic brain injury on the human sexual response
R O N IT A LO N I and SHLOMO KATZ

Beit Loewenstein Hospital, Raanana, Israel, Department of Psychology, Bar-Ilan University, Ramat-Gan, Israel (Received 20 October 1998; accepted 29 November 1998) A human sexual response format was used to describe possible sexual dysfunctions after TBI. Additional material was also included to qualify the information drawn from the above format. A number of possible conclusions were drawn, indicating that the causes and effects of sexual functioning after TBI are very confusing and that the literature does not clarify this confusion. One cannot accurately differentiate between primary and secondary sexual problems and, therefore, cannot evaluate the contribution of each problem to the presented sexual dysfunction.

Introd uctio n Professionals who work with persons after Traumatic Brain Injury (TBI) are aware of the fact that after the injury there may be significant sexual dysfunction [1]. As Zasler and Horn [2] state, neurological disability after TBI may result in sexual dysfunction at both a genital and a non-genital level. In order to deal adequately with the sexual dysfunction after TBI, it is important to understand the physiology of sexual dysfunctioning in general and, more specifically, how a head injury can disrupt the physiological determinants of sexuality. There are several papers published on the effect of brain damage on sexuality, but it is difficult to generalize from these papers. Some are based on case studies [3 9], while others on groups of patients who sustained injuries to various sites in the brain. The severity of injury of the various subjects was also different as was the duration of PTA. Thus, the data are not clearly organized, making it difficult to compare and obtain a clear picture of the effect of localization of injury on sexual function. In addition, most research studies are not based on large groups of patients, which also makes the generalization and application of localization, severity of injury, or duration of PTA problematic [1, 10 13]. Sexual dysfunction can be classified according to brain localization and function or according to stages of human sexual response. Literature focusing on overall brain function rarely relates to sexual function, and most of the data are derived from biological and mammal research [14, 15]. The literature based on sexual research provides limited information about the role of the brain in human sexual response. Masters and Johnson [16] did not refer at all to brain function, whereas Kaplan [17]
Correspondence to: Shlomo Katz, PhD, Department of Psychology, Bar-Ilan University, RamatGan, Israel.
Brain Injury ISSN 0269 9052 print/ISSN 1362 301X online 1999 Taylor & Francis Ltd http://www.tandf.co.uk/JNLS/bin.htm http://www.taylorandfrancis.com /JNLS/bin.htm

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referred to it, but concentrated mainly on the effect and role of the endocrine system the hypothalamus, hypophysis, and pituitary glands in sexual function. In general, TBI research is moving away from focusing on location of the injury toward evaluating function or dysfunction [18]. This approach appears to be justified for the field of sexuality because available literature on localization of TBI and sexual function is quite baffling. 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 [1, 19, 20]. 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 [14]. 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 emotional and relationship parameters to be considered, rendering the situation more difficult to evaluate. Thus, it would appear that perhaps using the human sexual response as a framework for discussing the impact of TBI on sexuality may be more valuable for the following reasons. No researchers have connected the result of emotional, cognitive, and physical sequelae of TBI with each phase of human sexual response with the exception of the desire phase [20, 21]. Furthermore, professionals dealing with sexual difficulties experienced by persons with TBI have paid very little attention to the effect of different disabilities on sexual response. The data concerning sym ptoms of inadequacy in each phase of the human sexual response exist and the prerequisites for adequate sexual response are clearly emphasized in the classical literature about sexuality. Hence, it may be theoretically true that these symptoms are the causes of the sexual inadequacy reported in the literature on both persons with TBI and their spouses. Integration of the existing data in the literature on TBI with the literature on sexual function will be performed. The `Human Sexual Response will be used as a framework for this discussion as it provides the reader with a clearer picture. In addition, it is easier to evaluate a person with the Human Sexual Response model than via the inconclusive data available on brain localization. In the following review, the discussion will be based on research which is directly associated with the subject of brain injury and sexuality. At the onset, it is important to distinguish between primary and secondary sexual dysfunction. Primary sexual dysfunction refers to a dysfunction that is organic in origin, caused directly by the injury [22]. The term `primary is used because it is part of the injury. For exam ple, an injury to the hypophysis can directly affect the endocrine system which, in turn, directly affects the hormone level that can cause sexual dysfunction of organic origin. It can then cause primary decreased libido and reduced desire, and/or primary impotence which can be detected by laboratory tests, such as hormone levels in blood tests, or Nocturnal Penile Tumescenece (NPT) in a sleep laboratory. Therefore, it is expected that all persons with the same injury will present almost the same primary, organic symptoms. Secondary sexual dysfunction refers to the delayed after-effect caused by the primary injury [22]. Usually it is an emotional reaction to the loss of the organ or the function. For example, after TBI a person may become hemiplegic with neuropsychological difficulties. The awareness of those losses can be accompanied by depression, performance anxiety, low desire, feelings of inadequacy as a male or a female, and difficulties in the initiation of an intimate relationship and can also affect erection and lubrication. All of these symptoms were not caused directly by the injury, but may be emotional reactions to the physical and neurological conse-

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quences. Each person presents different symptoms according to his/her own set of personal emotional reactions [22]. The decreased desire, erectile and lubrication dysfunctions in this case are defined as secondary symptoms. However, not all emotional reactions or symptoms will be automatically defined as secondary. There are emotional reactions that are the direct results of the injury in survivors of TBI [1]. However, one should also be aware of a difficulty that may arise when evaluating sexual function using the Human Sexual Response model. Decreased libido, lack of interest, inability to initiate, as well as other emotional factors may impede sexual function even when the person s sexual ability is intact [17]. It should be mentioned that the general population is also evaluated according to the above distinction. However, the difference between an able-bodied person and a person with TBI is that the latter may present a more complicated picture of primary and secondary symptoms and causes. The focus of this paper will be on attempting to differentiate between the primary/organic/direct effect of TBI on sexual function and secondary sexual dysfunction in order to provide a better and clearer picture of the issue. However, the scope of the review will be much broader and sexuality will be presented using a more holistic approach.

H um a n s exua l res p o ns e m od el Desire stage Desire is the first stage in the human sexual response model as defined by Kaplan [22]. There is no debate that this function is located solely in the brain and is associated with limbic areas as well as higher cortical functions. Thus, TBI can have a direct effect on desire. Table 1 presents the frequency of sexual dysfunction during the desire stage as described in the literature. (Frequency represents the number of times the problem is mentioned in the literature.) As can be seen from table 1, increased and decreased sexual desire with more evidence of low or diminished sexual drive and libido are most frequently described in the literature [20, 21, 23, 24]. Many authors correlate alteration in drive and libido with decreased frequency of sexual relationships and intercourse, considering changes in frequency as an indication of change in desire or libido [25 29]. In a conservative and traditional society, it is considered appropriate for males to initiate sexual or intimate relationships. Most persons with TBI are males, for whom the ability to initiate sexual encounters may be crucial to their masculine self-image. When the male partner s ability to initiate an intimate relationship is affected, the
Table 1. Frequency 28 14 13 7 3 2 Sexual sequelae after TBI desire phase

Sexual dysfunction Reduced libido Hyper sexuality + loss of control Increased libido Inability to initiate Altered sexual behaviour Low motivation

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frequency of intimate interaction will decrease. This does not appear to be the case if it is the female partner who sustained the TBI. Less frequently there is evidence of increased libido, which can be one of the causes of inappropriate sexual behaviour between the partners or in social environments. Hypersexuality is more of a threat to the family and the staff [1, 2, 5 8, 20, 21, 24 26, 28, 30 39]. Hypersexuality is widely dealt with in the literature, although most authors are aware that it is a rare phenomenon. Hypersexuality is a threat and can cause a great deal of distress and shame or embarrassm ent to both staff and family, as it leads to loss of control in sexual activity, to sexual promiscuity, and to inappropriate social sexual behaviour. Many times hypersexuality is not an indication of greater sexual needs, but rather a general loss of control in sexuality as in other areas of life [5, 9, 11, 22, 30, 33, 35 37, 39 42]. When this behaviour is exhibited while the person is in a relationship, hypersexuality can cause stress and shame. It usually consists of hedonistic behaviour with no awareness of the needs of the other person, leading to anger, withdrawal, and feelings of dislike. It is believed that desire is a prerequisite for every sexual activity and is responsible for the initiation of sexual and intimate contacts. Inability to initiate together with low motivation is frequently reported by authors [19, 20, 31, 39, 46]. It can affect the lyadic relationship simply by the reduction of intimacy occurrence and also by the deterioration of the male image for some of the more traditional spouses. The same losses can also alter the initiation of an intimate relationship in a social environment for single persons with TBI and may also be the cause of decreased frequency in sexual relationships. Although several authors [20, 21, 23, 24] noted the phenomenon of decreased libido and disinterest in sexual activity, most of them did not comment on whether this phenomenon is a primary result of TBI or a secondary one caused by the psychological or psychosocial sequelae of the injury. Griffith et al. [19] wrote that diffuse frontal injury with involvement of the neural and endocrine system is responsible for diminished sex drive. In addition, Griffith et al. [19] found that, although the primary factors are not as rare as was previously believed, the secondary emotional factors account for the great majority of sexual dysfunction. Garden [24] does not agree with Griffith et al. [19], since he found that medial temporal lesions account for hyposexuality, whereas bilateral temporal lesions with lesion of the limbic system cause hypersexuality. Zasler [39] in a literature review, found that the frontal temporal area, which is adjacent to the limbic structures in the right hemisphere, is responsible for arousal and sexual function. Lundberg [28] agrees with Zasler [39] and emphasizes that the basal hypothalamus and the adjacent areas of the temporal lobe regulate sexual desire. However, Rosenbaum and Hoggs [29] found a drastic reduction in sexual relations while finding no clear-cut relationship to the locus of injury.

Arousal stage The second phase of human sexual response is the arousal stage. Among other changes that take place during this phase are an increase in blood pressure and change in breathing rhythm, muscle tension, or skin sensitivity. Penile erection and vaginal lubrication are the most noticeable changes and most important for sexual function [16, 22]. Table 2 presents the frequencies of sexual dysfunction during the arousal stage.

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Table 2. Frequency 20 5 4 2 Sexual sequelae after TBI arousal phase

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Sexual dysfunction Impotence Loss of sensation Altered sexual arousal Dyspareunia

As can be seen from table 2, a high prevalence of erectile dysfunction (57%) after TBI is reported in the literature with a number of cases of loss of sensation and altered sexual arousal. The only dysfunction reported for females were two cases of Dyspareunia. There is no indication whether the authors identified erectile dysfunction as a primary dysfunction with organic causes or as a secondary one, which is a reaction to the emotional, neuropsychological, and cognitive losses of TBI [21, 34]. There are no reports of any systematic evaluation performed by the researchers to investigate the causes of sexual dysfunction. A few authors tried to measure the level of blood hormones, but did not find this parameter to be a sufficient explanation for altered erectile function [28, 47 49]. The NPT test was not mentioned as an assessment tool for evaluating survivors of TBI to determine whether the causes are primarily organic or secondary psychogenic, although this test is known to be most accurate for that purpose. Superficial sensation loss was found to be a cause for altered sexual arousal [1, 7, 8, 19, 20, 24, 27, 39, 44, 46, 51]. A number of possible reasons have been posited to explain the problems of impotence mentioned in the literature. The arousal process can be affected by communication problems in that both verbal and non-verbal communication can cause misunderstanding, stress, frustration, and withdrawal [1, 2, 45, 46, 50]. Lack of response by the partner due to miscom munication, anger, or other emotional or behavioural reasons previously discussed, as well as lack of response from the person with TBI because of altered ability for intimacy, may also have an effect on the arousal phase [25, 31, 43]. As a result of the impaired communication, feelings of mutual dislike can develop and, thus, affect arousal [30, 44]. Another possibility is anxiety and stress, which are known to inhibit sexual arousal [17, 39]. Zasler [39] explained that stress can alter sexual response by increasing prolactin levels, leading to an autom atic decrease in testosterone levels. Adequate testosterone levels are prerequisite for all male sexual responses including arousal. Survivors of TBI very often suffer from high levels of anxiety and stress which, for some, can cause erectile dysfunction or other changes in the arousal phase [2, 12, 32, 36, 50]. Distractibility in the sexual stimulation process caused by impulsivity, irritability, altered concentration, and impaired ability to fantasize were reported as additional causes of interference during the arousal process [12, 20, 30, 32 35, 41 44]. In order to `enjoy good sex, one must be able to suspend all distracting thoughts and lose oneself in the erotic experience [17, pp. 121]. Preoccupation and distraction were known as disrupting sexual responses by Masters and Johnson [16]. `Feelings of being physically unattractive or uncoordinated, and rejected by peers can also be the cause of erectile problems. Persons with TBI suffering physical disabilities may consequently be affected indirectly in their sexual function [2]. Social isolation and marked decrease in social relationships are experienced by

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Table 3. Sexual sequelae after TBI orgasm and ejaculation + other sexual dysfunction Frequency 1 5 3 5 Sexual dysfunction

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Unorgasma Unorgasma in the female partner Ejaculatory dysfunction Amenorrhea

both the persons with TBI and their family. They may feel rejected by their peers and, as a result, may develop arousal difficulties, such as inability to concentrate and positively receive the stimulation, which will automatically cause impotence in males or insufficient lubrication in females [5, 8, 12, 19, 20, 30 33, 38, 42, 44, 46, 48, 53, 54]. Orgasm stage The third stage of human sexual response is orgasm, followed by ejaculation in men. For many people, orgasm is the ultimate goal of sexual interaction. Loss of this ability may bring into question the purpose of initiation of sexual relationships for the survivors. The discussion about orgasm in the sexuality literature focuses solely on the genitals, with emphasis on womens unorgasm (see table 3). The role of the different parts of the brain is almost totally neglected. Kaplan [17, 22] refers to the septal region as the pleasure centre and Zasler and Horn [2] concur with this. Table 3 represents the frequency and type of dysfunction for the third stage of the human sexual response. Decreased frequency of achieving orgasm was reported by Zasler [39] in a descriptive paper. In another study, by Kreutzer and Zasler [1], 33% of male persons with TBI reported difficulty in achieving orgasm and 14% reported improved ability to do so. There is also a case report of unorgasm a in a woman who was cured by regular sex therapy, indicating that perhaps it was not a primary organic dysfunction [4]. Ejaculation stage Emission of semen is dependent on an intact hypogastric sympathetic nerve, whereas true ejaculation occurs secondarily to pudendal nerve activity and the resultant contraction of the pelvic floor musculature [6]. Although ejaculation is usually triggered by the central nervous system, it can still have a local function at the lower levels of the spinal cord. There is only one descriptive report on ejaculatory dysfunction in a male patient after TBI (see table 3) [34]. In general, men tend to combine ejaculation with orgasm, and inability to ejaculate can be experienced as unorgasm a as well. However, it is probably very rare, and it is still unclear whether the cause is organic or psychogenic in origin. Ejaculatory dysfunction can also cause fertility problems, which can become a major difficulty for the younger age group. As there is no one theoretical framework that can include all the existing sexualrelated conditions of TBI, a review of the literature regarding the effect of TBI on

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sexuality would not be complete without relating to other additional information on sexual-physical sequelae of TBI that do not fit into the above section. This additional information provides the reader with the feeling of the complexity of weaving the field of sexuality with the field of rehabilitation. A d d itiona l p hy s ica l s exua l a ffects of T B I The only defined primary sexual disorders may be hormonal, which can affect both men and women. As ejaculatory dysfunction is rarely considered to be a problem for persons with TBI, hormonal disruption may be the cause for infertility in both men and women. Horn and Zasler [6] believe that, since there is already a great deal of evidence to assume this is so, it is appropriate to check the hormone levels of persons with TBI routinely, as there is a wide gap between the drop in hormone levels and appearance of the first signs. The immediate signs or complaints which may indicate a drop in hormone levels are decreased libido, impotence, inability to ejaculate, and fertility problems in both males and females. Women may complain about amenorrhoea, oligomenorrhoea, and dysfunctional bleeding. Later consequences are the loss of secondary sexual characteristics such as hirsutism, worsening of acne, voice change, and obesity [17, 21]. The therapist s awareness is needed in this case as it is rare. When it does occur, careful evaluation is necessary and treatment is by hormone replacement therapy. Changes in hormone levels, when occurring early in children and prepubescents, can trigger puberty and may cause body image and self-confidence difficulties for those children and may lead to social withdrawal [2, 6]. In addition, hormonal changes may also affect the emotional state of the person with TBI, which in turn may also affect his/her sexual function and behaviour. For example, the loss of secondary sex characteristics as a result of hormonal changes may trigger negative emotional reactions, which may have a negative impact on the person s social relationships. As a result of these emotional changes the dyadic relationship might be altered and this combination might exacerbate the emotional, behavioural, and functional problems. Hormone levels can be affected not only by TBI, but also by medication, which can have a significant effect on the endocrine system and should be evaluated in detail [21]. Survivors after head injury take medications according to the severity of injury, duration of coma, and the symptoms presented in intensive care and afterwards. During the rehabilitation process, intake of medication should be reassessed to enable the person with TBI to maximally participate in therapeutic activities and to optimize his/her sexual functioning. The cooperation of the physician with the other members of the therapeutic team is critical at this stage of the process [21]. Current data concerning the effect of drugs on sexual function pertain mostly to males. There are hardly any data about the effect of drugs on the sexual functioning of females with TBI [55]. The medications that are commonly given to survivors of TBI are: antipsychotics, anticholinergics, antidepressants, anticonvulsants, and anti-spastics. Less common are H2-antihistamines, anti-inflammatory, anti-hypertensives and serotonergic agonists [19, 55, 56]. Anticholinergics and anti-spasticity drugs are prescribed for the survivors with TBI with hemiparesis, who suffer from spasticity or from reduced muscle tone (hypotonia). Anticonvulsant drugs are prescribed for those who suffered penetration

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TBI, had undergone brain surgery, have an abnormal EEG, and/or those who had brain haemorrhage and are at high risk for epilepsy. Antipsychotic drugs are given to survivors of TBI who exhibit severe agitation, psychosis, hallucinations, or depression. Antidepressants are for those in a state of depression or experiencing reaction depression. If the patient displays loss of appetite due to depression, anorexiants are prescribed. Antidepressants are usually sufficient. Non-steroidal anti-inflammatory drugs are for those survivors of TBI who suffer pain, resulting from bone fractures or inflammation of the joints that were injured during the trauma. Together with this medication, physicians prescribe H2-antihistamines to prevent ulcers. For older survivors of TBI who may develop hypertension, antihypertensive drugs with beta blockers are administered. Serotonergic agonists are prescribed rarely, and then only in cases of tumours or severe migraine. Boller and Frank [55] report no change in libido with the use of antidepressants, antipsychotics, anticonvulsants, and anticholinergic drugs. Zasler [21] differs, as he found that only antidepressants do not affect libido. The others, including antihypertensive drugs, H2-antihistamines and serotonergic agonists, were found to decrease libido, with the exception that serotonergic agonists increase libido in females. According to Boller and Frank [55] only tricyclic antidepressants and cholinergic blocking agents affect erection. Griffith et al. [19] added all antidepressants, major and minor tranquillizers, anticholinergic drugs, antihistamines and antipsychotic medications, such as Lithium, to the list of drugs in use that can cause organic impotence. Zasler [21] adds the following to the above list; anticonvulsants, a variety of antipsychotics, anti-spastics, anti-hypertensive drugs, and non-steroidal anti-inflammatory drugs with H2-antihistamines. While Boller and Frank [55] were uncertain whether most of these drugs have any effect on ejaculation, Zasler [21] reports that the antidepressants, antipsychotics, anticholinergics, and the antispasticity drugs, as well as the anti-hypertensive and anti-inflammatory ones, all inhibit or cause ejaculation. Boller and Frank [55] only agree concerning the antipsychotics and anticholinergic drugs. Delayed orgasm, only in women, was reported by Zasler [21] relating to antidepressant drugs. As more data are accumulated and with the growing awareness of the side effects of the various medications, it seems that every drug commonly used to treat survivors of TBI has an effect on sexual function. Therapists working with survivors after TBI have to be very careful when evaluating behaviours, emotional status, and function of persons with TBI, as they may be under heavy medication. Physicians as well should be very careful when prescribing drugs. They must inform the person with TBI about possible side effects in order to protect them from unanticipated failure, which can have a devastating effect on their sexual identity, self-esteem, body image, and self-confidence. The side effects can also impact the dyadic relationship and cause excess stress and distress for both partners. During this extremely crucial period of the rehabilitation process, the staff should be aware of all aspects of the life of the survivor of TBI and the possible disruptions caused as a result of the side effects of his/her medications. If the survivor with TBI is uncommunicative, the staff should alert the partner as to the side effect of the drugs which can have an effect on the dyadic intimate relationship.

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Pleasure is the ultimate purpose of any sexual encounter. It is not the organic sexual dysfunction that is crucial for giving or receiving pleasure, but rather the emotional, social, and dyadic states that will determine whether the person with TBI and his/ her partner will be able to receive pleasure and be satisfied. Satisfaction is also a subjective personal issue that depends on the person as an integration of cognitive, emotional, and behavioural states as well as the interaction of the person with significant others around him/her. Sexuality is the ultimate integration between body and soul. At present one still cannot accurately differentiate between primary or secondary sexual problems and, therefore, cannot evaluate the contribution of each problem to the presented sexual dysfunction. Professionals should be aware that the combination of personal loss, emotional reaction, and drastic changes and deterioration of the dyadic relationship may all cause sexual dysfunction. Further structured research that will utilize the most up-to-date evaluation techniques is needed to illuminate this process. It provides the reader with the feeling of the complexity of weaving the field of sexuality with the field of rehabilitation. The population having TBI is relatively young and has a long life expectancy. Therefore, more immediate practical solutions for the problems are needed, but are still not available. Many survivors of TBI are in the midst of their adolescence, trying to complete this complex stage and grow into adults looking forward to establishing a meaningful sexual relationship. This process requires close interaction with peers who appear in many cases to reject the survivor with TBI shortly after the injury. The adolescent survivor of TBI is also looking for meaning in his/her own life at the same time that his/her abilities are unknown. TBI challenges the survivors environment. That includes the family, primarily the partner, if there is one. Partners are expected to help and support survivors throughout the long and demanding rehabilitation process. In order for them to be able to do so, partners must be instructed and given support so that they can cooperate and participate in the enhancement of the well-being of the persons with TBI, themselves, and other family members they are responsible for, mainly their children. The literature provides very little information and few suggestions about practical intervention for dealing with sexual problems at the early stage of the rehabilitation process [57]. The proper intervention should focus on immediate needs, but with an outlook to the future. Intervention should provide meaning and hope for life, as many of these people will never be able to integrate fully or even partially into society. It is important to intervene as early as possible, so as to attempt to prevent future problems in the area of sexuality. Such an intervention programme should address the emotional, cognitive, behavioural, and functional sequelae of TBI in order to achieve its goals. The way to prevent the devastating sexual sequelae of TBI is apparently to break the vicious cycle and prevent it from being reinstated. It is important to provide persons with TBI with the appropriate skills to prevent them from encountering failure at a time when they must learn to cope with the sequelae of TBI. Thus, the prevention programme should attempt to eliminate traumas which could lead to a deterioration in sexual identity, self-esteem, self-confidence, and body image. In addition, preparation of survivors of TBI to deal with recent and future social, intimate, and sexual

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situations should be provided, as well as the provision of an appropriate framework for exercising practical skills for basic interactions and dyadic relationships. An example of this could be the use of a surrogate therapist.

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