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Sexual Disorders

Sexual Disorders

Dr B Green, MB, ChB, MRCPsych

Extract from Psychiatry in General Practice. (1994) Edited by Green
ISBN 0-7923-8851-8. Published by Kluwer Academic Publishers
(Updated December 2000) Previous Page

Classification Treatment Self assessment References Swaab references


Although the majority of sexual dysfunction probably has a physical basis it is fitting to mention some sexual disorders here because dysfunctions, whether mainly due to physical or psychological causes, can result in distress. For example, the individual with a sexual disorder may suffer related anxiety and sexual frustration which in turn leads to insomnia, and that insomnia may be the presenting complaint to the GP. The individual's close relationships may suffer and tension may build up in the family as a whole.

According to DSM-IV (the American Psychiatric Association's classification system) there are a dozen or so sexual disorders. All have to cause marked distress or interpersonal difficulty to rate as disorders. A brief overview follows:

1. Hypoactive sexual disorder
A persistently reduced sexual drive or libido, not attributable to depression where there is reduced desire, sexual activity and reduced sexual fantasy.

2. Sexual aversion disorder
An avoidance of or aversion to genital sexual contact

3. Female sexual arousal disorder
A failure of arousal and lubrication/swelling response.

4. Male erectile disorder
Inability to gain an erection or inability to maintain an erection once it has occurred.

5. Female orgasmic disorder
A lengthy delay or absence of orgasm following a satisfactory excitatory phase. The GP must take into account the patient's age, previous sexual experience and adequacy of sexual stimulation.

6. Male orgasmic disorder
A lengthy delay or absence of orgasm following normal excitation, erection and adequate stimulation.

7. Premature ejaculation
Ejaculation occurring with only minimal stimulation, either before penetration or soon afterwards, in either case ceratinly before the patient wishes it. Again the GP must take into account the patient's age, previous sexual experience, extent of sexual stimulation and 'novelty' of the sexual partner.

8. Dyspareunia (not due to general medical condition)
Recurrent pain associated with intercourse, but in women not due to vaginismus, poor lubrication, and in women and men not due to drugs or other physical causes

9. Vaginismus
An involuntary or persistent spasm of the muscles of the outer third of the vagina, again not attributable to physiological effects of physical causes. Vaginismus may be either lifelong or recent; generalised to all sexual encounters or specific to certain partners or situations.

10. Secondary sexual dysfunction
Dysfunction secondary to illness eg hypothyrodism, mental disorder eg depression, or drugs eg fluoextine.

11. Paraphilias
Exhibitionism (exposure of genitals to strangers). Fetishism (finding nonliving objects erotic eg women's underwear). Paedophilia. Frotteurism (fantasies, urges or behviour centred around rubbing self against non-consenting other). Sexual masochism and sadism. Transvestic festishism (cross-dressing for erotic pleasure). Voyeurism (fantasies, urges or behviour centred around watching non-consenting others undressing, or having sex).

12. Gender identity disorder
Strong and persistent identification of the self with another gender. Persistent dissatisfaction with own sex. Desire to participate in stereotyped games and pastimes of opposite sex. Preference for cross-dressing. May insist that they are wrong sex. May occur in children, adolescents and adults, (Green, 1985). Not concurrent with physical intersex condition. Aetiology was thought to involve aberrant psychological conditioning, but gender identity may be more defined by organic causes in the brain (as Swaab's work has suggested) , than the postnatal environment

Table One: Physical Causes of Male Erectile Disorder


Illness and disease


  • Alcoholism (neuropathy)
  • Diabetes mellitus
  • Arterial disease eg Leriche syndrome
  • Renal failure
  • Carcinomatosis
  • Neurosyphilis
  • Hypothalamo-pituitary dysfunction
  • Liver failure
  • Multiple sclerosis
  • and many others
  • Beta-blockers
  • Thiazide diuretics
  • Tricyclic antidepressants
  • Phenothiazines
  • Spironolactone
  • Cimetidine
  • Cannabis
  • Anti-epileptics


Table Two: Physical causes of dyspareunia that would need to be excluded



How common are sexual disorders?

The majority of adults can recall times in their lives when they were troubled with low desire or problems with orgasms. Arousal difficulties increase with age. Sexual dysfunction may arise in the most well-adjusted and satisfied of couples. In 100 educated young couples Frank et al (1978) found that 50% of men had difficulties with erection, ejaculation or orgasm sometimes and 75% of women had problems with arousal or orgasm sometimes.

Table Three: Estimated lifetime prevalence of sexual problems in young adults (at some time).

Possible physical treatments:


Premature ejaculation fluoxetine / clomipramine
Erectile difficulties Sildenafil (Viagra),intrapenile injections of papaverine and prostaglandin, inflatable prosthetic penile implants, suction devices, cockrings

Audit Points

As a doctor, estimate how often people come to see you with their sexual problems? Do you think that the majority of people who come to see you about their sexual difficulties can talk to you? What can you do to make it easier for people to talk to you about these issues?

What local resources are there to help doctors treat sexual disorders? If the resources seem scarce or have exceedingly long waiting times is there anything that can be done about this?

Self- Assessment MCQs

1. In terms of sexual function:

A women taking benzodiazepines may experience delayed orgasm
B men taking fluoxetine may experience delayed ejaculation
C sexual interest can be reduced by benperidol
D chlorpromazine may cause galactorrhoea in women
E libido can be reduced by digoxin therapy

2. Useful treatments for:

A erectile dysfunction include intrapenile injections of dobutamine
B premature ejaculation include the squeeze technique
C homosexuality include electric shock therapy
D vaginismus include the 'stop-start' technique
E premature ejaculation include fluoxetine


1. All true.
2. A=F, B=T, C=F, D=F, E=T.

Useful Addresses

Institute of Psychosexual Medicine, 11, Chandos Street, Cavendish Square, London, W1M 9DE. Tel: 0171-580-0631

Relate, Herbert Gray College, Little Church, Rugby, CV21 13AP. (Look in UK telephone directory for local address/telephone number).

References and further reading.

American Psychiatric Association, (1994). Diagnostic and Statistical Manual of Mental Disorders. Fourth Edition (DSM-IV). Washington, APA.

Bancroft, J. (1989) Human sexuality and its problems. 2nd Edition. Edinburgh, Churchill Livingstone.

Covington, S. (1991) Awakening your sexuality. San Francisco, Harper SanFrancisco.

Cranston-Cuebas, M A, Barlow, D H. (1990) Cognitive and affective contributions to sexual functioning. Annual Review of Sex Research. 1, 119-162.

Fisher, R, & Brown S. (1988) Getting Together. Boston, Houghton-Mifflin.

Frank, E, Anderson, C & Rubinstein D. (1978) Frequency of sexual dysfunction in 'normal' couples. The New England Journal of Medicine, 299, 111-115.

Green, R. (1985) Gender identity in childhood and later sexual orientation: follow-up of 78 males. American Journal of Psychiatry. 142, 339-341.

Haas, K & Haas, A, (1993) Understanding Human Sexuality, St. Louis, Mosby.

Kinsey A C, Pomeroy W B, Martin C E (1948) Sexual behaviour in the human male. Philadelphia, Saunders.

Kinsey A C, Pomeroy W B, Martin C E, Gebhard P H. (1953) Sexual behaviour in the human female, Philadelphia, Saunders.

Lipsius, S H. (1987) Prescribing sensate focus without proscribing intercourse. J-Sex-Marital-Ther. 13(2): 106-16

Masters W H, Johnson V E. (1970) Human sexual inadequacy. London, Churchill.

Mathers, N, et al. (1994) Assessment of training in psychosexual medicine. BMJ, 308, 969- 972.

Pollack-MH; Reiter-S; Hammerness-P (1992) Genitourinary and sexual adverse effects of psychotropic medication. Int-J-Psychiatry-Med. 1992; 22(4): 305-27.

Swaab References

Walbroehl-GS (1987) Sexuality in the handicapped. Am-Fam-Physician. 36(1): 129-33

Wyatt-GE; Peters-SD; Guthrie-D (1988) Kinsey revisited, Part I: Comparisons of the sexual socialization and sexual behavior of white women over 33 years. Arch-Sex-Behav.17(3): 201-39

Swaab References

Brain research, gender and sexual orientation.
Swaab DF; Gooren LJ; Hofman MA
Netherlands Institute for Brain Research, Amsterdam.
J Homosex, 1995, 28:3-4, 283-301
Recent brain research has revealed structural differences in the hypothalamus in relation to biological sex and sexual orientation. Differences in size and cell number of various nuclei in the hypothalamus for homosexual versus heterosexual men have recently been reported in two studies. We have found that a cluster of cells in the preoptic area of the human hypothalamus contains about twice as many cells in young adult men as in women. We have called this cluster the sexually dimorphic nucleus (SDN). The magnitude of the difference is the SDN depends on age. In other human research, two other hypothalamic nuclei (interstitial nuclei of the anterior hypothalamus [INAH] 2 and 3) and part of the bed nucleus of the stria terminalis (BST) have been reported to be sexually dimorphic in the human. Sexual differentiation to the human brain takes place much later than originally claimed. At birth the SDN contains only some 20% of the cells found at 2 to 4 years of age. The cell number rapidly increases in boys and girls at the same rate until 2 to 4 years of age. After that age period, a decrease in cell number takes place in girls, but not in boys. This causes the sexual differentiation of the SDN. This postnatal period of hypothalamic differentiation indicates that, in addition to genetic factors, a multitude of environmental and psychosocial factors may have profound influence on the sexual differentiation of the brain. No difference in SDN cell number was observed between homosexual and heterosexual men. This finding refutes Dörner's hypothesis that homosexual males have a "female" hypothalamus. However, in a sample of brains of homosexual men we did find that an area of the hypothalamus called the suprachiasmatic nucleus (SCN) contains twice as many cells as the SCN of a heterosexual group. A recent report by LeVay claims that another nucleus, INAH-3, is more than twice as large in heterosexual as in homosexual men, whereas Allen and Gorski found that the anterior commissure was larger in homosexual men than in heterosexual men or women. Preliminary research on male-to-female transsexuals is also discussed. The functional implications of these findings in determining adult sexual orientation are as yet far from clear.

Gender and sexual orientation in relation to hypothalamic structures.
Swaab DF; Gooren LJ; Hofman MA
Netherlands Institute for Brain Research, Amsterdam.
Horm Res, 1992, 38 Suppl 2:, 51-61
Animal experiments have provided evidence for the presence of sex differences from the synaptic level up to behaviour. Although sex differences in the human brain may have been presumed implicitly since the days of Aristotle, research on the presence of functional and structural sex differences of the human brain started only relatively recently. The most conspicuous sex difference in the mammalian brain was described by Gorski et al. [1978] in the preoptic area (POA) of the rat hypothalamus. We found that the volume of a putative homologue of this sexually dimorphic nucleus (SDN) in the adult human hypothalamus was more than twice as large in men as in women and contained about twice as many cells. Recently a similar sex difference and volume has been described for the human bed nucleus of the stria terminalis and 'interstitial nuclei of the hypothalamus' (INAH). Sexual differentiation of the hypothalamus was generally believed to take place between 4 and 7 months of gestation. A life span study on the SDN of more than 100 subjects revealed, however, that only after the age of 2-4 years postnatally sexual differentiation becomes manifest by a decrease in volume and cell number in the female SDN. If sexual differentiation of the brain indeed takes place postnatally, not only chemical and hormonal factors may influence this process but also social factors. A prominent theory on the development of sexual orientation is that it develops as a result of an interaction between the developing brain and sex hormones. According to Dörner's hypothesis, male homosexuals have a female differentiation of the hypothalamus. This hypothesis was not supported by our observations on the SDN. Neither the SDN volume nor the cell number in the hypothalamus of homosexual men differed from that of heterosexual men. However, a difference in SCN cell number was observed in relation to sexual orientation. The volume and cell number of the SCN of homosexual men was twice as large as that of a reference group. During development, the SCN volume and cell counts reach peak values around 13-16 months after birth. At this age the SCN contains about the same number of cells as the SCN of adult male homosexuals, whereas in the reference group the cell numbers subsequently decline to the adult value, which is about 35% of the peak value

Male-to-female transsexuals have female neuron numbers in a limbic nucleus.
Kruijver FP; Zhou JN; Pool CW; Hofman MA; Gooren LJ; Swaab DF
Graduate School Neurosciences Amsterdam, The Netherlands Institute for Brain Research.
J Clin Endocrinol Metab, 2000 May, 85:5, 2034-41
Transsexuals experience themselves as being of the opposite sex, despite having the biological characteristics of one sex. A crucial question resulting from a previous brain study in male-to-female transsexuals was whether the reported difference according to gender identity in the central part of the bed nucleus of the stria terminalis (BSTc) was based on a neuronal difference in the BSTc itself or just a reflection of a difference in vasoactive intestinal polypeptide innervation from the amygdala, which was used as a marker. Therefore, we determined in 42 subjects the number of somatostatin-expressing neurons in the BSTc in relation to sex, sexual orientation, gender identity, and past or present hormonal status. Regardless of sexual orientation, men had almost twice as many somatostatin neurons as women (P < 0.006). The number of neurons in the BSTc of male-to-female transsexuals was similar to that of the females (P = 0.83). In contrast, the neuron number of a female-to-male transsexual was found to be in the male range. Hormone treatment or sex hormone level variations in adulthood did not seem to have influenced BSTc neuron numbers. The present findings of somatostatin neuronal sex differences in the BSTc and its sex reversal in the transsexual brain clearly support the paradigm that in transsexuals sexual differentiation of the brain and genitals may go into opposite directions and point to a neurobiological basis of gender identity disorder.

Sexual differentiation of the human hypothalamus in relation to gender and sexual orientation.
Swaab DF; Hofman MA
Graduate School Neurosciences, Institute for Brain Research, Amsterdam, The Netherlands.
Trends Neurosci, 1995 Jun, 18:6, 264-70
Recently, sex differences in the structures of the human hypothalamus and adjacent brain structures have been observed that seem to be related to gender, to gender problems such as transsexuality, and to sexual orientation, that is, heterosexuality and homosexuality. Although these observations have yet to be confirmed, and their exact functional implications are far from clear, they open up a whole new field of physiological structural-functional relationships in human brain research that has so far focused mainly on such relationships in pathology.

Increased number of vasopressin neurons in the suprachiasmatic nucleus (SCN) of 'bisexual' adult male rats following perinatal treatment with the aromatase blocker ATD.
Swaab DF; Slob AK; Houtsmuller EJ; Brand T; Zhou JN
Netherlands Institute for Brain Research, Graduate School Neurosciences Amsterdam.
Brain Res Dev Brain Res, 1995 Apr, 85:2, 273-9
In an earlier article an enlarged subpopulation of vasopressin containing neurons was found in the suprachiasmatic nucleus (SCN) of homosexual men as compared to heterosexuals. The present study investigates the possibility that the number of vasopressin neurons in the SCN and sexual partner preference behavior in male rats are both influenced by sex hormones during brain development. For this purpose, we studied groups of adult male rats that had been treated either prenatally or pre- and postnatally with the aromatase inhibitor ATD (1,4,6-androstatriene-3,17-dione) which blocks the aromatization of testosterone to estradiol. Rats treated with ATD in both pre- and postnatal periods showed 'bisexual' partner preference behavior and appeared to have 59% more vasopressin-expressing neurons in the SCN than the controls. The prenatally treated rats did not differ from the controls. This observation supports the hypothesis that the increased number of vasopressin neurons found earlier in the SCN of adult homosexual men might reflect differences that took place in the interaction between sex hormones and the brain early in development.

The sexually dimorphic nucleus of the preoptic area in the human brain: a comparative morphometric study.
Hofman MA; Swaab DF
Netherlands Institute for Brain Research, Amsterdam, The Netherlands.
J Anat, 1989 Jun, 164:, 55-72
The sexually dimorphic nucleus of the preoptic area (SDN-POA) in the human hypothalamus is an ovoid, densely packed collection of large cells. The size, shape and cellular morphology of the SDN-POA was examined in relation to sex and age in adult human subjects. In this region the following parameters were measured: length of the rostrocaudal axis, maximum cross-sectional area, volume, numerical cell density, total number of cells, and the diameter of the cell nucleus. The SDN-POA was elongated in females and more spherical in males. The mean volume and total cell number were markedly sexually dimorphic: the volume of the SDN-POA was 2.2 times as large in males as in females and contained 2.1 times as many cells. No sex differences were observed in either cell density or mean diameter of the cell nuclei. Furthermore, multivariate regression analysis revealed that there are also sex-linked differences in the structural organisation of the human SDN-POA, finding expression in the way the morphometric parameters are interrelated. Of the parameters measured, only the volume and cell number of the SDN-POA showed a dramatic decrease with ageing. The reduction in cell number, however, was not constant throughout adulthood but was found to depend upon sex and age. In males, a major reduction in SDN-POA cell number was observed between the age of 50-60 years. In females, cell death was found to be more prominent than in males, especially among old people (t greater than 70 years), dropping to values which were only 10-15% of the cell number found in early childhood. In conclusion, the human SDN-POA has a sex-dependent pattern of ageing. Finally, the morphology of the SDN-POA was compared with that of other hypothalamic regions--the suprachiasmatic nucleus (SCN) and the paraventricular nucleus (PVN)--both in man and in rat. Species-specific differences in the dimensions of these nuclear regions are discussed in the light of their assumed functional significance.

A sexually dimorphic nucleus in the human brain.
Swaab DF; Fliers E
Science, 1985 May, 228:4703, 1112-5
A sexually dimorphic cell group is described in the preoptic area of the human hypothalamus. Morphometric analysis revealed that the volume of this nucleus is 2.5 +/- 0.6 times (mean +/- standard error of the mean) as large in men as in women, and contains 2.2 +/- 0.5 times as many cells. Between the ages of 10 and 93 years, the nucleus decreases greatly in volume and in cell number. Although no function has yet been established for this nucleus, it is located within an area that is essential for gonadotropin release and sexual behavior in other mammals.


Copyright Material
Priory Lodge Education Limited, 1995-2001.
First Published in June 1995
Version 1.2

Version 2.0 published December 2000


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