Women's Sexual Function and Dysfunction. Irwin Goldstein MD

Neurologic disorders: female neurosexology

P O Lundberg

Introduction

The mechanisms behind sexual dysfunction in women with neurologic disorders are of three different types. Firstly, the dysfunction may result from specific lesions to those parts of the nervous system that are directly involved in sexual physiology (see Chapters 4.1—4.4 of this book). Secondly, the dysfunction may result from lesions in the nervous system that impair cognition, movements, and communication (see Chapter 5.3). Thirdly, the dysfunction may refer to psychologic, social, and cultural issues (see Chapters 3.1—3.4). As we will see from the following, these mechanisms may work entirely differently in many well-known neurologic disorders.

Neurologic disorders may be congenital, leading to defect development of sexual anatomy and physiology. In such a case as well as in disorders starting before puberty, pubertal development may be retarded or missing. Defect anatomic development and hormone insufficiency may also lead to lack of organization of those parts of the nervous system involved in sexual physiology.

In evaluating a patient with a disease or a handicap, issues such as attraction and partner relationship have to be considered. The sexual prognosis is often highly dependent upon “sex before”, that is, how well the patient functioned sexually and how sexually experienced the patient was before the start of the disease or time of physical trauma.

Central and peripheral nervous system

From a neurologic point of view, female sexual physiology is largely dependent upon which sensory (afferent) mechanisms (Table 16.6.1) are actually stimulated in the women and what kinds of effects (efferent mechanisms) (Table 16.6.2) the sexual stimulation has in the body.1 This model is of essential importance for clinical understanding of the many different types of sexual symptoms summarized in the concept of female sexual dysfunction.

Our knowledge about what we could call “peripheral” sexual physiology is rather good. However, we know much less about what is actually going on in the brain, and where, during sexual arousal and activity. Here we have to rely on data from a limited number of patients with more or less precisely localized lesions of the brain. Now we also have a few studies with modern imaging techniques, such as positron-emission tomography (PET) and functional magnetic resonance imaging (fMRI) of the brain.2

Hypothalamo-pituitary disorders and malformations

In women with hypothalamo-pituitary disorders and malformations, amenorrhea and infertility are usually the problems that take the patient to the doctor (see Chapters 6.1 and 7.3). In women aged 20-60 years with morphologically verified hypothalamo-pituitary disorders,3 two-thirds noticed absence of, or a considerable and troublesome decrease in, sexual desire. This problem was much more common among women with hyperprolactinemia than among those with normal serum prolactin.4 Most of these women also had amenorrhea as well as problems with lubrication and/or orgasms.

Table 16.6.1. Stimulation of sexual arousal in women

Table 16.6.2. Sexual efferent mechanisms in women

Besides pituitary adenomas (Figs 16.6.1 and16.6.2), hormone- producing or nonfunctional, there is a large group of other types of tumors and pathologic processes in the hypothalamo-pituitary region also causing decrease in sexual desire, decreased lubrication, and anorgasmia. Among the tumors, craniopharyngiomas and meningiomas are the most important in women.

Congenital malformations of the pituitary, visualized as dystopia of the posterior pituitary and/or dysplasia of the sella turcica, the olfactogenital dysplasia with anosmia and the septo- optic dysplasia also with malformations of the optic nerves, all with hypogonadotropic hypogonadism, are easily diagnosed with modern computed tomography or magnetic resonance imaging.

There are a number of acquired hypothalamo-pituitary disorders, such as spontaneous pituitary apoplexy, pituitary bleeding during labor (Sheehan’s syndrome), sequela after traumatic hypothalamic bleeding, ruptured arterial aneurysm, and acute asphyxia. Spontaneously arrested infantile hydrocephalus, delayed radiation necrosis, meningo-encephalitis, sarcoidosis, and lymphocytic hypophysitis are further examples of hypogonadotropic hypogonadism with sexual dysfunction.5

Cerebellar disorders

In a number of families with cerebellar atrophy and ataxia, hypogonadism of the hypogonadotropic form, thus indicating hypothalamo-pituitary insufficiency, has been founds8 There is evidence of a hypothalamic gonadotropin-releasing hormone deficiency. This is in contrast to the hypergonadotropic hypogonadism indicating primary ovarian failure in, for example, mitochondrial disorders or sex-chromosome abnormalities. The women present with primary amenorrhea, lack of secondary sexual characteristics, and absence of sexual desire. The mechanism behind these syndromes is unknown.

Figure 16.6.1. A huge, prolactin-producing, invasively growing pituitary adenoma visualized by positron-emission tomography (PET) with 11C-L-methionine. "Before" indicates before treatment. The image to the right shows the result of 4-month treatment with the dopamine agonist carbergoline. Now only traces of the tumor remain. After further treatment, the tumor entirely disappeared.

Figure 16.6.2. High dopamine binding of the same tumor as in Fig. 16.6.1, visualized by PET with the dopamine agonist "C-L-raclopride, indicating that the tumor should be treated with dopamine agonists. Left horizontal, right sagittal image of the brain with tumor.

Traumatic brain injuries and encephalopathies

Disability and cognitive impairment occur rather often after traumatic brain injury. Sexual impairment is not rare, as a consequence of either the cerebral lesions or psychologic factors.Both decreased and increased sexual desire have been reported in women. Lesions of the frontal, temporal, and limbic cortex are the most important. Little is known about female sexual arousal after such injuries. However, in women, endocrine abnormalities are the most sensitive predictors of sexual dysfunction.10

Stroke

Because of the vascular anatomy, infarcts or bleedings in stroke patients are usually not localized to those parts of the brain directly involved in sexual physiology (see Chapter 7.3). Thus, the high frequency of sexual dysfunction and difficulty in desire, orgasm, and sexual activity in women who were sexually active before stroke can usually be explained in terms of coping.11,12 Orgasmic dysfunction is seen in three-quarters of the females.13 Decreased desire, sexual arousal, and satisfaction are related particularly to the presence of hemisensory symptoms.14

Sexual activity can provoke vascular catastrophes, such as subarachnoidal hemorrhage,15 or transitory ischemic attacks, such as transient global amnesia.16

Epilepsy

Epilepsy and sexuality have many interconnections. Sexual activity can provoke an epileptic fit. For example, hyperventilation during sexual encounters may in itself provoke an attack. Reflex mechanisms from the cortical area corresponding to the genitalia could also trigger a partial epileptic attack. Sexual fantasies as well as genital stimuli (masturbation or orgasm)17 are typical examples of triggering phenomena.

Sexual phenomena may be a part of an epileptic attack. Partial seizures generated from the genital sensory cortical area mentioned may result in sensations in the genital organs.18 Such sensations may be described as clitoral warmth, hot feelings in the vagina, and pleasant sensations of anal or vaginal constriction or of penetration, but also as attacks of actual genital pain. Most of the described cases have been associated with a parasagittal tumor involving the primary sensory cortex. Epileptic sensations of sexual excitement and orgasm also occur in patients with temporal lobe epilepsy.19

The sexual life of the epileptic patient may also be changed between attacks. Many female epilepsy patients20,21 report decreased sexual arousability, vaginismis, and dyspareunia. A diminution in genital vasocongestion in response to sexually arousing stimuli not accompanied by a decrease in self-perceived sexual arousal was observed in some women with temporal lobe epilepsy.22 In another study, epileptic female patients had a lower marriage rate than the general population. Married epileptic females have fewer children.23 Social and psychologic factors play an important role. Epileptic patients describe poorer psychologic health than healthy subjects. Paranoid delusions of being violated, abused, or seduced are another problem in epileptic women.

Antiepileptic drugs, especially phenytoin, phenobarbital, primidone, carbamazepine, and valproic acid, may cause hormonal changes,24 as well as decreased sexual desire and performance in women. Epileptic attacks are particularly common during the menstrual phase.25 Precocious puberty has been observed in a number of epileptic girls treated with carba- mazepine, clonazepam, or valproic acid. Some antiepileptic drugs (gabapentin, clonazepam, and valproic acid) may influence orgasmic capacity.

Narcolepsy-cataplexy syndrome

The narcolepsy-cataplexy syndrome is a distinct neurologic disorder, usually without a recognized neuropathology. The main components are irresistible but short episodes of sleep during daytime and short-lived attacks of loss of muscular tone often provoked by emotions. The patients often also have sleep paralysis, which means being awake without being able to move, and hyponagogic hallucinations. Anorgasmia is also a component of the syndrome, and sexual activity can sometimes provoke an attack of cataplexy.26 Drugs used to treat the sleep attack may interfere with sexual function.

Kleine-Levin syndrome

Kleine-Levin syndrome is a rare but very typical syndrome of unknown etiology with onset in adolescence. Periods of somnolence, hyperphagia, and hypersexuality with a time correlation to menstruation are the cardinal features.27 The sexual phenomenology is characterized by aggressiveness, sadomasochistic behavior, and delusions.

Parkinson’s disease and other movement disorders

Bladder, bowel, and sexual dysfunction is prominent in patients with Parkinson’s disease compared to controls of the same ages.28 The rate of sexual dysfunction was not increased with increasing handicap stage. About 80% of female Parkinson’s disease patients had less frequent sexual activity than before the disease.29 There was a decrease in both sexual interest and sexual drive in 71% and 62%, respectively, of these women. Vaginal dryness was noted in 38% and anorgasm also in 38%. Another study30 showed similar figures. When Parkinson’s disease women were compared with controls matched for age and marital status, the Parkinson’s disease women were less satisfied with their sexual relationships and partners, and they were also more depressed.31 In a further study,32 the partners of the Parkinson’s disease women were also questioned. Among these partners, a high level of sexual dysfunction was found. These observations show that, in Parkinson’s disease women, all the three different mechanisms behind sexual dysfunction (see above) have to be taken into account, and a multimodal therapeutic approach is needed. Treatment with dopaminergic drugs has resulted in increase of sexual desire in a number of women.

Multiple sclerosis

Changes in sexual function become very common during the evolution of the disease. In a recent study of 47 women with advanced multiple sclerosis, 60% reported decreased sexual desire; 36%, decreased lubrication; and 40%, diminished orgasmic capacity during the course of the disease. Sensory dysfunction in the genital area was experienced by 62% of the women, and 77% had weakness of the pelvic muscles.33 In a review of other studies, reduced interest was reported by 29-86% of female multiple sclerosis patients, reduced sensation by 43-62%, reduced orgasmic capacity by 24-58%, vaginal dryness by 12-40%, and dyspareunia by 6-40%.34

However, sexual dysfunction may also occur in early and mild cases of multiple sclerosis. Half of the women in one study of 25 females with multiple sclerosis aged 20-42 and with a low handicap score reported sexual problems. None of them had had sexual problems before the start of the disease.35 In this study, 25 women with migraine matched for age and parity served as controls. Here sexual problems were few and mild.

Sensory dysfunction seems to be the most important reason for sexual problems in multiple sclerosis women. Because of severe external dysesthesia, some patients reported that during a certain period they could not bear direct genital or nongenital contact with their partner. The dysesthesia was of maximum intensity from the beginning of an episode of neurologic symptoms, but resolved fairly rapidly, as is usual in multiple sclerosis.

Most multiple sclerosis patients report diminished sexual desire during the course of the disease. Some patients may experience a temporary decrease during an episode; in others, the problem continues. In certain cases, increased sexual desire has also been described. When this phenomenon is transitory and concurrent with an episode of new symptoms, there is reason to believe that the hypersexuality is the result of a distinct cerebral multiple sclerosis lesion, the localization of which is unknown. Another important symptom of sexual dysfunction in women with multiple sclerosis is deterioration of orgasmic capacity, intensity, and quality. In most cases, the orgasmic sensations are reduced, becoming shorter lasting, less intense, and/or less agreeable. These changes may be temporary. However, better orgasms have also been noticed. The orgasms may be more easily triggered, longer lasting, stronger, and more pleasant. Paroxysmal attacks of different types are common in multiple sclerosis. Attacks of pelvic pain are one type of such attacks.36

Sexual dysfunction correlates with bladder and bowel dysfunction (see Chapter 17. 4),33-35,37,38 but it correlates more mildly with motor and sensory dysfunction in the legs.33 The correlation is poor with disability scale, clinical course, and disease duration. Sexual dysfunction also correlates with lesions in the pons as detected by magnetic resonance imaging.39 Brainstem lesions seen on magnetic resonance imaging seem to be of particular importance for anorgasmia.40

Symptoms related to multiple sclerosis, such as fatigue, muscle contractures in the lower limbs, urinary disturbances and the use of aids to manage incontinence, and paroxysmal motor and sensory disturbances triggered by sexual intercourse, can indirectly exert a negative effect on sex life as well as social and physical changes. Depression and cognitive impairment play an important role.40,41

Neurophysiologic data, such as cortical evoked potentials of the dorsal nerve of the clitoris or pudendal nerve,39,42,43 as well as measurements of vibratory thresholds in the clitoris,44 imply that pudendal somatosensory innervation is necessary for one type of female sexual stimulation, that of the clitoris. To compensate for such a loss, more direct stimulation of the anterior vaginal wall (G-spot) is recommended (Table 16.6.1).

Amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis is a rapidly progressive motor disease leading to almost total paralysis of the whole body, including respiratory muscles. However, the patients do not have sensory or autonomic symptoms. Thus, the patients can usually control bladder and bowel functions, and sexual functions are possible. Patients with amyotrophic lateral sclerosis only late, or do not at all, lose their sexual desire. A recent study45 found sexuality to be an important issue for a high proportion of these patients, despite the fact that they were ventilated.

Diabetes mellitus

Studies of sexual function in women with diabetes mellitus have given conflicting results (see Chapters 7.3 and 17.1). In one early study, 35% of the diabetic women were reported to have had orgasmic dysfunction in the preceding year, as compared to 6% of the controls.46 In another study, the frequency of sexual dysfunction was around 25% both in insulin-treated diabetic women and in age-matched controls.47 A more recent, structured-interview study of 42 women with insulin-dependent diabetes, compared both with matched controls and results from the Sweden 1986 national sex survey study,48 found that 26% of the insulin-dependent diabetes mellitus women had decreased sexual desire, 22% had decreased vaginal lubrication, and 10% had decreased capacity to acquire orgasm. Several of the women reported more than one dysfunction. Overall, the figure for sexual dysfunction was 40%. Among the age-matched controls without diabetes or neurologic disease, only 7% reported some kind of sexual dysfunction.

When compared, type I diabetes was found to have little or no effect on women, while type II diabetes had a pervasively negative impact on sexual desire, lubrication, orgasmic capacity, sexual satisfaction, and sexual activity, and on the relationship with the sexual partner.49

Inadequate lubrication is described as the most important sexual problem in many studies.50 Diabetic women also often have dyspareunia from Candida infection. Loss of desire as a major problem has been reported in some other studies.51,52

Subjective sexual arousal as measured by vaginal lubrication was often found to be inadequate or to require prolonged stimulation in insulin-dependent diabetes mellitus women compared to controls.53 Two psychophysiologic studies in women with diabetes mellitus have been published. One of them found no difference from controls,54 but in the other, diabetic women experienced significantly less physiologic arousal to erotic stimuli than controls.55

Impaired subjective vulvar sensibility was noticed more often in women with insulin-dependent diabetes mellitus than in controls.48 The diabetic patients also had significantly higher vibration perception thresholds in the hands and clitoris than controls. Reduced foot perspiration, increased gustatory perspiration, constipation, and incontinence were also correlated with sexual dysfunction. This indicates that autonomic polyneuropathy is an important mechanism behind sexual dysfunction in diabetic women.

Tissue samples taken postmortem in 17 diabetic women showed evidence of both clitoral nerve degeneration and changes in blood vessels in the clitoris.56 A nondiabetic control group did not show any signs of neuropathy or vascular damage. However, so far, this study does not seem to have been replicated.

However, sexual problems in patients with diabetes mellitus may have many pathophysiologic mechanisms besides polyneuropathy. The metabolic process in itself, with variations in blood sugar, acidosis, and high-molecular-weight sugars, certainly plays a role. Vascular damage to small vessels as well as larger arteries may result in decreased blood flow to the clitoris and other cavernous tissues. However, other types of endocrine insufficiency, such as hypogonadism, are not considered to play an important role in either sexual desire or sexual arousal. Women with more diabetic complications have more sexual dysfunction.57 However, female sexual dysfunction may also precede other symptoms of insulin-dependent diabetes mellitus, and good glycemic control may restore normal sexual function at least in early cases.58

Peripheral poly- and mononeuropathies

Peripheral mononeuropathies of the pudendal nerve or branches of that nerve in particular are not uncommon in women. Solitary neurofibromas are one type.59 The pudendal nerve may also be involved in patients with hereditary motor and sensory neuropathies.60 Also in the polyneuropathy of primary systemic amyloidosis, changes of the pudendal as well as the autonomic pelvic nerves can lead to sexual dysfunction combined with bladder and bowel dysfunction.61 Autonomic polyneuropathy may also be a problem in malignant disorders, such as plasma cell dyscrasia.62 The nerve lesions often result in so much pain and dyspareunia that coitus becomes impossible or at least unpleasant.

Myopathies and encephalomyopathies

In some types of progressive muscular dystrophy, such as myotonic dystrophy,63,64 Becker’s myopathy, and ocular myopathy of the autosomal progressive external ophthalmoplegia type,65,66 and in Marinesco-Sjogren syndrome,67,68 secondary amenorrhea, in combination with disturbances of desire and sexual function, has been described. This is also the case in mitochondrial encephalomyopathies, such as myoclonus epilepsy with ragged red fibers and mitochondrial encephalo- myopathy with lactic acidosis and stroke syndromes.69 The hypogonadism in these cases is of a hypergonadotropic type, indicating primary ovarial failure, in contrast to the situation in hypothalamo-pituitary insufficiency (see above).

Headache

Women may have sudden severe headaches precipitated by sexual activity, occurring at the moment of orgasm or shortly after. Many of these attacks have a migraine-like appearance. The attacks are usually recurrent, and all symptoms disappear. This type of attack is called benign orgasmic headache in contrast to the malignant attacks resulting from subarachnoidal hemorrhage, as mentioned above.15 However, the attacks may be associated with a segmental reversible cerebral artery vasospasm.70 Beta-receptor blockers taken before sexual activity can prevent the attacks.

Sexual adverse reactions to psychopharmacologic drugs

Antidepressant drugs

Sexual dysfunction, decrease in libido in particular, is very often seen in women with depression. Many reports indicate that sexual desire may decrease during antidepressive treatment instead of being normalized, as would be expected in parallel to otherwise good therapeutic results. However, it is often difficult to decide what is caused by the disease itself and what by its pharmacologic treatment.

In contrast, anorgasmia is not a symptom of depression but instead a very typical adverse drug reaction to the antidepressant selective serotonin reuptake inhibitors. It is particularly common with fluoxetine, paroxetine, sertraline, and citalopram but less common with fluvoxamine. There are much fewer reports of anorgasmia in patients with the nonselective monoamine reuptake inhibitors, with the exception of clomipramine. Pharmacologically, this drug is rather close to the selective serotonin reuptake inhibitors. Among the other types of antidepressant drugs, mianserine, mirtazapine, and nefazodone have very few reports of anorgasmia, but venlafax- ine has rather many.71,72

Neuroleptic drugs

Neuroleptic drugs often cause sexual endocrine effects, such as amenorrhea, galactorrhea, and hyperprolactinemia. Decrease in sexual desire has been observed, but the number of reports of dysfunction of female sexual arousal and anorgasmia is rather low. However, one should remember that many patients treated with neuroleptic drugs have severe psychiatric disorders, making this group of patients difficult to evaluate.

Therapy and rehabilitation

For treatment of female sexual dysfunction in patients with neurologic disorders, the reader is referred to other chapters of this book and to European Federation of Neurologic Sciences’ Official Guidelines for Neurologists.73 Here more details about female neurosexology are to be found. The procedure of sexual rehabilitation in neurologic patients is described in the textbook on sexual rehabilitation.74

References

1. Lundberg PO. The peripheral innervation of the genital organs of women. Scand J Sexol 2001; 4: 213-25.

2. Whipple B. Where in the brain is a woman’s sexual response? Laboratory studies including brain imaging (fMRI and PET) during orgasm. Sex Relatsh Ther 2004; 19(Suppl 1): S57-8.

3. Hulter B, Lundberg PO. Sexual function in women with hypothalamo-pituitary disorders. Arch Sex Behav 1994; 23: 171-83.

4. Lundberg PO, Muhr C, Hulter B et al. Sexual libido in patients with hypothalamo-pituitary disorders. In Proceedings of the 7th World Congress of Sexology. Bombay: Indian Association of Sex Educators, 1986: 126-8.

5. Lundberg PO. Neurological disorders in andrology. In J Bain, ESE Hafez, eds. Diagnosis in Andrology. The Hague: Martinus Nijhoff, 1980: 195-213.

6. Neuhauser G, Opitz JM. Autosomal recessive syndrome of cerebellar ataxia and hypogonadotropic hypogonadism. Clin Genet

7. Berciano J, Amado JA, Freijanes Jetal. Familial cerebellar ataxia and hypogonadotropic hypogonadism: evidence for hypothalamic LHRH deficiency. J Neurol Neurosurg Psychiatry 1982; 45: 747-51.

8. Seminara SB, Acierno JS, Abdulwahid NA et al. Hypo- gonadotropic hypogonadism and cerebellar ataxia: detailed phenotypic characterization of a large, extended kindred.

9. Aloni R, Katz S. Sexual Difficulties After Traumatic Brain Injury and Ways to Deal with It. Springfield, IL: Thomas, 2003.

10. Hibbard MR, Gordon WA, Flanagan Setal. Sexual dysfunction after traumatic brain injury. NeuroRehabilitation 2000; 15: 107-20.

11. Boldrini P, Basaglia N, Calanca MC. Sexual changes in hemi- paretic patients. Arch Phys Med Rehabil 1991; 72: 202-7.

12. Sjogren K. Sexuality after stroke II, with special regard to partnership adjustment and to fulfillment. Scand J Rehab Med 1983; 15: 63-9.

13. Sjogren K, Damber J-E, Lilieqvist B. Sexuality after stroke I. Aspects of sexual function. Scand J Rehabil Med 1983; 15: 55-61.

14. Korpelainen JT, Kaulhanen M-L, Kemola H et al. Sexual dysfunction in stroke patients. Acta Neurol Scand 1998; 98: 400-5.

15. Lundberg PO, Osterman PO. The benign and malignant forms of orgasmic cephalgia. Headache 1974; 14: 164-5.

16. Monzani V, Rovellini A, Schinco G et al. Transient global amnesia or subarachnoidal haemorrhage? Eur J Emerg Med 2000; 7: 291-3.

17. Hoenig J, Hamilton CM. Epilepsy and sexual orgasm. Acta Psychiatr Neurol Scand 1960; 35: 448-56.

18. Calleja J, Carpizo R, Berciano J. Orgasmic epilepsy. Epilepsia 1988; 29: 635-9.

19. Rémillard GM, Andermann F, Testa GF et al. Sexual ictal manifestations predominate in women with temporal lobe epilepsy: a finding suggesting sexual dimorphism in the human brain. Neurology 1983;

20. Demerdash A, Shalaan M, Midani Aetal. Sexual behavior of a sample of females with epilepsy. Epilepsia 1991; 32: 82-5.

21. Morrell MJ, Guldner GT. Self-reported sexual function and sexual arousability in women with epilepsy. Epilepsia 1996; 37: 1204-10.

22. Morrell MJ, Sperling MR, Stecker M et al. Sexual dysfunction in partial epilepsy: a deficit in physiological arousal. Neurology 1994; 44: 243-7.

23. Dansky LV, Andermann E, Andermann F. Marriage and fertility in epileptic patients. Epilepsia 1980; 21: 261-71.

24. Isojarvi JIT. Serum steroid hormones and pituitary function in female epileptic patients during carbamazepine therapy. Epilepsy 1990; 31: 438-45.

25. Lundberg PO. Catamenial epilepsy: a review. Cephalalgia 1997; 17(Suppl 20): 42-5.

26. Roy A. Anorgasmia and cataplexy. Arch Sex Behav 1977; 6: 437-9.

27. Billiard M, Guilleminault C, Dement WC. A menstruation- linked periodic hypersomnia.  1975; 25: 436-43.

28. Sakakibara R, Shinotoh H, Uchiyama Tetal. Questionnaire- based assessment of pelvic organ dysfunction in Parkinson’s disease. Auton Neurosci 2001; 17: 76-85.

29. Koller WC, Vetere-Overfield B, Williamson Aetal. Sexual dysfunction in Parkinson’s disease. Clin Neuropharmacol 1990; 13: 461-3.

30. Wermuth L, Stenager E. Sexual problems in young patients with Parkinson’s disease.  1995; 91: 453-5.

31. Welsh M, Hung L, Waters CH. Sexuality in women with Parkinson’s disease. 1997; 12: 923-7.

32. Brown RG, Jahanshahi M, Quinn N et al. Sexual function in patients with Parkinson’s disease and their partners. J Neurol Neurosurg Psychiatry 1990; 53: 480-6.

33. Hulter B, Lundberg PO. Sexual function in women with advanced multiple sclerosis. J Neurol Neurosurg Psychiatry 1995; 59: 83-6.

34. Ghezzi A. Sexuality and multiple sclerosis. Scand J Sexol 1999; 2: 125-40.

35. Lundberg PO. Sexual dysfunction in female patients with multiple sclerosis. Int Rehab Med 1981; 3: 32-4.

36. Miro J, Garaa-Monco C, Leno  C et al. Pelvic pain: an undescribed paroxysmal manifestation of multiple sclerosis. Pain 1988; 32: 73-5.

37. Beck KP, Warren KG, Whitman P. Urodynamic studies in female patients with multiple sclerosis. Am J Obstet Gynecol 1981; 139: 273-6.

38. Hennessey A, Robertson NP, Swinger R et al. Urinary, faecal and sexual dysfunction in patients with multiple sclerosis. J Neurol 1999; 246: 1027-32.

39. Zivadinov R, Zorzon M, Locatelli Letal. Sexual function in multiple sclerosis: a MRI, neurophysiological and urodynamic study. 2003; 210: 73-6.

40. Barak Y, Achiron A, Elizur Aetal. Sexual dysfunction in relapsing-remitting multiple sclerosis: magnetic resonance imaging, clinical, and psychological correlates. J Psychiatr Neurosci 1996; 21: 255-8.

41. Foley FW, Sanders A. Sexuality, multiple sclerosis and women. International MS Support Foundation. www.imssf.org/sex3.shtml.

42. Yang CC, Bowen JR, Kraft GH et al. Cortical evoked potentials of the dorsal nerve of the clitoris and female sexual dysfunction in multiple sclerosis. Fowler C. Pudendal somatosensory evoked potentials in women with female sexual dysfunction and multiple sclerosis. Int J Impot Res 2002; 14(Suppl 3): S83.

44. Hulter B, Lundberg PO. Genital vibratory perception threshold (VPT) measurements in women with sexual dysfunction and/or sexual pain disorders. International Academy of Sex Research (IASR) 31st Annual Meeting: Ottawa, July 2005. Book of abstracts, 44.

45. Kaub-Wittemer D, von Steinbüchel N, Wasner M et al. Quality of life and psychosocial issues in ventilated patients with amyotrophic lateral sclerosis and their caregivers. J Pain Symptom Manage 2003;

46. Kolodny RC. Sexual dysfunction in diabetic females. Diabetes 1971; 20: 557-9.

47. Buus Jensen S. Diabetic sexual dysfunction: a comparative study of 160 insulin treated diabetic men and women and an age-matched control group. Arch Sex Behav 1981; 10: 493-504.

48. Hulter B, Berne C, Lundberg PO. Sexual function in women with insulin dependent diabetes mellitus. I. Correlation with neurological symptoms and signs. Scand J Sex 1998; 1: 43-50.

49. Schreiner-Engel P, Schiavi RC, Victorisz D et al. The differential impact of diabetes type on female sexuality. J Psychosom Res 1987; 31: 23-33.

50. Enzlin P, Mathieu C, Vanderschueren D et al. Diabetes mellitus and female sexuality: a review of 25 years’ research. Diabet Med 1998; 15: 809-15.

51. Campbell LV, Redelman MJ, Borkman M et al. Factors in sexual dysfunction in diabetic female volunteer subjects. Med J Aust 1989; 151: 550-2.

52. Newman AS, Bertelson AD. Sexual dysfunction in diabetic women. J Behav Med 1986; 9: 261-70.

53. Tyrer G, Steel JM, Ewing DJ et al. Sexual responsiveness in diabetic women. Diabetologia 1983; 24: 166-71.

54. Slob AK, Koster J, Radder JK et al. Sexuality and psychophysiological functioning in women with diabetes mellitus. J Sex Marital Ther 1990; 16: 59-69.

55. Wincze JP, Albert A, Bansal S. Sexual arousal in diabetic females: physiological and self-report measures. Arch Sex Behav 1993; 22: 587-601.

56. Zrustovâ M,57. Enzlin P, Mathieu C, Van Den Bruel Aetal. Sexual dysfunction in women with type 1 diabetes: a controlled study. Diabetes Care 2002; 25: 672-7.

58. Bultrini A, Carosa E, Colpi EM et al. Possible correlation between type 1 diabetes mellitus and female sexual dysfunction. J Sex Med 2004; 1: 337-40.

59. Tognetti F, Poppi M, Gaist G et al. Pudendal neuralgia due to solitary neurofibroma. J Neurosurg 1982; 56: 732-3.

60. Vodusek DB, Zidar J. Pudendal nerve involvement in patients with hereditary motor and sensory neuropathy. Acta Neurol Scand 1987; 76: 457-60.

61. Kelly JJ, Kyle R, O’Brian PC et al. The natural history of peripheral neuropathy in primary systemic amyloidosis. Ann Neurol 1979; 6: 1-7.

62. Takatsuki K, Sanada I. Plasma cell dyscrasia with polyneuropathy and endocrine disorder: clinical and laboratory features of 109 reported cases. Jpn J Clin Oncol 1983; 13: 543-55.

63. Marinkovic Z, Prelevic G, Würzburger M et al. Gonadal dysfunction in patients with myotonic dystrophy. Exp Clin Endocrinol 1990; 96: 37-44.

64. Olsson T, Olofsson B-O, Hagg E et al. Adrenocortical and gonadal abnormalities in dystrophia myotonica - a common enzyme defect? Eur J Intern Med 1996; 7: 29-33.

65. Lundberg PO. Observations on endocrine function in ocular myopathy. 66. Melberg A, Arnell H, Dahl N et al. Anticipation of autosomal progressive external ophthalmoplegia with hypogonadism. Muscle Nerve 1996; 19: 751-7.

67. Lundberg PO. Hereditary myopathy, oligophrenia, cataract, skeletal abnormalities and hypergonadotropic hypogonadism. Eur Neurol 1973; 10: 261-80.

68. Skre H, Bassoe HH, Berg K et al. Cerebellar ataxia and hypergonadotropic hypogonadism in two kindreds. Clin Genet 1976; 9: 661-7.

69. Chen CM, Huang CC. Gonadal dysfunction in mitochondrial encephalomyopathies. Eur Neurol 1995; 35: 281-6.

70. Valenca MM, Valenca LP, Bordini CA et al. Cerebral vasospasm and headache during sexual intercourse and masturbatory orgasms. Headache 2004; 44: 244-8.

71. Lundberg PO, Biriell C. Sexual dysfunction as a suspect adverse reaction to antidepressant drugs. Scand J Sexol 1998; 1: 97-105.

72. https://vigisearch.who-umc.org.

73. Lundberg PO, Ertekin C, Ghezzi Aetal. Neurosexology. Guidelines for neurologists. Eur J Neurol 2001; 8(Suppl 3): 1-24.

74. Fugl-Meyer A, Fugl-Meyer K, Lundberg PO. Sexual rehabilitation. In P Frommelt, H Grotzbach, eds. NeuroRehabilitation. Berlin: Blackwell, 1999: 370-88.