Introduction. This study combines information from three lines of research. The first of these, which reached its height in the 1960s, is the identification of epileptiform EEG abnormalities in fetishists. The second, which began in the 1980s, is the elucidation of the inhibitory effects of serotonin on such epileptiform activity. The third, a product only of the 1990s, is the finding that drugs that enhance serotonergic transmission often decrease fetishistic behaviour. Because this pharmacological information is so new, most of the reports are anecdotal. A few small studies have appeared, but none have looked for electroencephalographic changes concomitantly with behavioural changes. In fact the early, electroencephalographic claims seem to have been ignored rather than subjected to any rigourous test. It is the purpose of this study to re-examine the claim of an increased incidence of abnormal EEG in fetishists, to assess the effect of the serotonin selective reuptake inhibitor fluoxetine on fetishistic sexual outlet, and to explore the possibility of a relationship between the electroencephalographic and pharmacological studies of fetishism.
Normality, Deviance, and Pathology. The word `normal' comes in two flavours. On the one hand there is the statistical sense, describing the frequency or prevalence of behaviours. On the other hand there is the moralistic sense, describing what some person or institution holds to be the ideal. It is not the intent of this proposal to define any deviant practice as unacceptable. Such decisions should be left to individuals. It is acknowledged, however, that uncontrollable, ego-dystonic sexual outlets are a significant cause of suffering and impact upon mental health. Fetishistic substitution of sexual object, in particular, can obstruct the formation of interpersonal sexual relationships and, in cases where it is associated with a high level of compulsion, can interfere with work and other daily activities. Even in the late nineteenth century, Krafft-Ebing [1939] wrote that testimonials of sexual deviants `reveal sufferings of the soul in comparison to which all the other afflictions dealt out by Fate appear as trifles'. The aim of this work is not to judge, but to afford every person a more complete choice and opportunity for self-determination of their own sexual behaviour.
History. Recent results promise the eventual elucidation of a biological basis for at least some sub-class of fetishism. Yet the existence of such a biological basis is not at all intuitive; indeed, fetishistic behaviour superficially seems purely psychic, a function of the personality and volition of the fetishist. This is an assumption that has long held sway. Freud [1928] incorporated fetishism into his theory of infantile sexuality and claimed that the fetish was a substitute for the mother's penis. Given this, he said, use of the fetish as a sexual vehicle preserves the fetishist from expressing homosexual desire. As early as 1886, however, Krafft-Ebing [1939] was claiming a more directly biological basis for fetishism. Krafft-Ebing regarded fetishism as a normal physiological capacity susceptible to a pathological accentuation, in which the fetishised object or quality assumes such prominence that it crowds out the sexual partner. Fetishism is perhaps best described as a perversion of the sexual releasing mechanism [Epstein 1987]. The fetish can be a particular object, such as a shoe or a coat, or a quality or attribute, such as curly hair or limb amputation. In this respect fetishistic deviance shades into the sexual quirks and preoccupations of everyday life. A fetish, it seems, is simply a very elaborate and specific `turn-on', and the boundary between the unusual and the firmly deviant is to some extent a function of the culture of the time and place.
Diagnosis. Nevertheless, fetishism in the extreme can be defined as a distinct character. DSM-III-R defines fetishism as a pattern of `recurrent, intense sexual urges and sexually arousing fantasies... involving the use of nonliving objects' that interferes with the capacity for reciprocal affectionate sexual activity. This interference is an important qualifier: someone who is excited by, say, a person in a latex body-suit is not necessarily a clinical fetishist, whereas in a fetishist the presence of the body-suit--with or without a partner--would be the sole determinant of ability to attain sexual arousal. DSM-III-R actually splits fetishism into two diagnostic categories. `Fetishism' (DSM-III-R 302.81) is excluded as a diagnosis in cases in which the fetish objects are all articles of female clothing which are worn. In this case the diagnosis of `transvestic fetishism' (DSM-III-R 302.30) is made. This latter category does not include all forms of cross-dressing, because it specifically excludes transsexualism and gender identity disorder as motivations and refers to these as distinct diagnoses. In fetishistic transvestism, the donning of a garment is not an attempt to identify oneself as a member of the morphologically opposite sex, but an attempt to possess more fully the fetish object, and by extension, the person with whom the object is more conventionally associated. Thus the symbolic mechanism of fetishistic transvestism is a sort of sympathetic magic by which the fetishist is allowed to possess a human partner without having to submit to her, an elaborate invention for the purpose of having one's cake and eating it too. It is not appropriate or productive to label all fringe or deviant sexual behaviour as pathological. But when such behaviour is or becomes ego-dystonic or a source of anguish for the individual or his loved ones, all possible steps should be taken to alleviate it.
Analogies to imprinting. Fetishistic predilections are often remarkably specific; the presence or absence of small details such as the pattern or style of a piece of clothing can make or break the erotic significance. Incidental properties such as wetness or dirtiness often are essential, also. Combined with this extreme specificity is the common early onset of fetishism: objects destined to become sexual fetishes often have extreme or unusual emotional valence from early childhood. This combination of specificity and early onset has occasioned analogies to the imprinting process in non-human animals [Kolársky & al. 1967, Wilson 1987]. Whether imprinting or any process akin to it occurs in humans, and, if so, how much we have in common with species that imprint in a time course of hours, is unclear. Certainly specificity and early onset are not by themselves sufficient to establish a primary biological basis for fetishism. For example, Freud explained these characteristics of the fetish by theorising that the fetishised object often was the last object seen before the traumatic first sight of the female genitals, and was therefore associated in the fetishist's mind with the last moment at which phalluses could be attributed to women.
Fetishism as anxiety release. Fetishism also can be viewed as a defence against anxiety and a mechanism for its release. Anxious persons are liable to discomfort with situations over which they have no control or predictive power. Epstein [1960] conjectured that the primary abnormality in fetishists is hyperæsthesia, and that fetishism arises as an attempt to control excessive stimulation. Interpersonal relationships probably are the most unpredictable of all circumstances, so it is natural to search for a substitute, inanimate sexual partner which can offer no back-talk. A lover has his or her own will which may conflict with the will of the fetishist. An object or quality, on the other hand, has no desires of its own and thus is more easily manipulated, possessed, and scripted into a stable sexual and emotional routine. Certainly anxiety is more common in fetishists than in the general population, but it is unclear what sort of causation is operating in this association. Fetishism may develop as a release for anxiety; alternatively, anxiety may be a consequence of the maladjustment caused by fetishistic preoccupations. The two states may well be mutually reinforcing. Pharmacological study has the potential to elucidate the relationship between fetishism and anxiety. For example, buspirone, a 5HT1A agonist, was effective against anxiety and cross-dressing in a fetishistic transvestite who reported that cross-dressing reduced anxiety, but alprazolam, a benzodiazepine anxiolytic, reduced his anxiety without having any effect on the cross-dressing [Fedoroff 1988, 1989].
Fetishism as an obsessive-compulsive behaviour. The routine is another salient aspect of fetishism. Several authors have observed that fetishism has some obsessive-compulsive character. Thus one increasingly finds references to `paraphilic obsession' [Perilstein & al. 1991], `sexual obsessions' [Stein & al. 1992], and `obsessive sexual thoughts' [Fedoroff 1992]. The fetish may appear in consciousness involuntarily. Epstein [1960] noted in his general clinical impression of a sample of fetishists `an imperative urge to perform certain motor acts', `occasional forced thinking', and `a general over-evaluation of the significance of symbols', and cited examples of these traits in several cases. Such observations are especially interesting in light of the successful fetishism therapies using serotonin selective reuptake inhibitors, a class of drugs that now constitute the treatment of choice for obsessive-compulsive disorder.
Association with epilepsy. Fetishism also has been associated with epilepsy. Krafft-Ebing [1939] reported three such cases. Epstein [1961] reported four cases of fetishism or fetishistic transvestism in which temporal EEG spike foci were detected. Of note is that only one of these four cases had manifested seizures. Hunter & al. [1963] reported a case in which a patient with long-standing transvestic fetishism developed temporal-lobe epilepsy, which was abolished, along with the fetishism, by lobectomy. Wålinder [1965] reported 12 `abnormal' EEGs--7 of them temporal and 5 extratemporal--collected during hyperventilation and photic stimulation in a sample of 26 transvestites. Hoenig and Kenna [1979] reported 10 temporal spike foci and 12 other EEG abnormalities in a sample of 46 transsexuals. Certainly the most spectacular case of epilepsy associated specifically with fetishism was that reported by Mitchell & al. [1954]. This patient had had a fetish for safety pins for as long as he could remember. During early childhood, contemplation of an actual or imagined safety pin would evoke a feeling described by the patient as `thought satisfaction'. At adolescence, this `thought satisfaction' developed into absence seizures. Subsequently motor automatisms developed. A temporal lobectomy at age 38 completely eliminated both the epilepsy and the desire for safety pins, and increased his motivation toward non-fetishistic sexual outlets. Research into the electrophysiological correlates of sexual deviance dwindled during the 1970s, probably because of cultural changes that enlarged the scope of behaviours and sexual practices tolerated by society. Unfortunately, this loss of interest prevented the undertaking of any sufficiently large, organised, well-controlled study that would have confirmed or denied all the stories about fetishism and epilepsy. As recently as 1986, the well-known sexologist John Money wrote,
The proportion of paraphiles who are also epileptics, and vice versa, has not yet been ascertained. Nor has the proportion of paraphiles with EEG abnormalities in the absence of clinical epilepsy.
[Money 1986, page 124].
Such reports suggest that epileptiform EEG activity, with or without actual seizures, is more common in fetishists than in the general population. If epileptiform spiking and fetishism are indeed linked, then it should be possible to demonstrate the reverse association. Gastaut and Collomb [1954] were the first to study sexual behaviour in epilepsy. Their main finding in temporal-lobe epilepsy was hyposexuality. Of 36 cases of temporal-lobe epilepsy, two thirds were judged to be hyposexual. This was not so with any other form of epilepsy. In addition to the hyposexuality, however, Gastaut and Collomb noted a small subpopulation of temporal-lobe epileptics with abnormalities of sexual outlet, which were more often part of interictal behaviour than associated with seizures. The finding of hyposexuality was confirmed by Blumer and Walker [1967] in 11 of 21 temporal-lobe epileptics who were candidates for surgery. Postoperative relief from seizures correlated with increase in sexuality in these 11. Taylor [1969] reported a high incidence of deviant sexuality in temporal-lobe epileptics scheduled for surgery, but his measures of sexual outlet are somewhat uncertain and he confounds homosexuality with pathological deviance. Shukla & al. [1979] again confirmed the finding of hyposexuality in the subset of their population of temporal-lobe epileptics who were sexually mature males, but they found no evidence of deviant sexuality. Bear and Fedio [1977] did not investigate sexual abnormalities specifically but did cite the prevalence of obsessional traits in temporal-lobe epileptics, the severity of which was uncorrelated with seizure frequency. Kolársky & al. [1967] studied 86 men who were patients at an epilepsy clinic and found a preponderance of early-onset lesions in the subgroup who had temporal-lobe localisations in conjunction with identified deviant sexuality. Of 49 temporal-lobe localisations, 17 were associated with deviant sexuality. 13 of these 17 deviants had an identified lesion onset before age 3, whereas only 7 of the subjects who were not identified as sexually deviant had an identified lesion onset before age 3. The investigators observed that the early onset of lesions fit with the establishment or seeding of fetishism very early in life, and conjectured that fetishism results from the abnormal overspecification of an innate sexual releasing mechanism by a process akin to imprinting.
The hypersexuality of Klüver-Bucy syndrome is well known in monkeys [Klüver & Bucy 1937] and in humans [Terzian & Dalle Ore 1955, Marlowe & al. 1975] in whom the temporal lobes have been resected. (Nonspecific hypersexuality has also been reported in temporal-lobe epilepsy [Van Reeth & al. 1958].) This suggests that temporal limbic structures may modulate and inhibit the release of sexual behaviour, perhaps via an amygdaloseptal route. The temporal lobe, implicated in end-stage visual processing, motivation, and memory, is a logical place to look for the biological mechanisms responsible for associating particular stimuli or classes of stimuli with complex affective and behavioural responses [Jones & Mishkin 1972]. The hypothesis of a sexual inhibitory mechanism resident in the temporal lobe fits well with current knowledge. Inactivation of such a mechanism, either by temporal lobectomy or by inhibitory stimulation arising from an epileptic focus, results in hypersexuality (constitutive release). Hyperactivation resulting from interictal epileptic activity results in hyposexuality (absence of release). Interference of interictal (or subictal) epileptiform activity with the correct formation of associations results in deviant sexuality (inappropriate modulation of release).
Serotonergic therapy. The serotonin selective reuptake inhibitors (SSRIs), which enhance serotonergic transmission by blocking uptake into the presynaptic terminal, have been reported to be effective at reducing behaviours associated with fetishism [Lorefice 1991, Kafka 1991, Kafka & Prentky 1992, Stein & al. 1992] and other paraphilias [Kafka 1991, Kafka & Prentky 1992, Stein & al. 1992]. SSRIs differ from other monoamine uptake inhibitors in that they block uptake of serotonin without significantly interfering with uptake of norepinephrin. SSRIs come in many chemical variations but they have a few characteristics in common. All of them contain a benzene ring separated from an amino group. The substituents on the benzene ring and amino group are important in establishing the selectivity of the SSRIs. In the case of fluoxetine, there is a trifluoromethyl group on the third carbon in the ring, and a methyl group on to the amine. Originally developed as antidepressants, the SSRIs also have proven effective in obsessive-compulsive disorder. In addition to fetishism, fluoxetine has been beneficial in other abnormalities of sexual outlet including compulsive voyeurism [Emmanuel & al. 1991], exhibitionism [Bianchi 1990, Perilstein & al. 1991], frotteurism [Perilstein & al. 1991], pedophilic obsession [Perilstein & al. 1991], and paraphilic coercive disorder [Kafka 1991]. Kafka [1991, 1992] evaluated various SSRIs in patients and found that these drugs were somewhat effective against the paraphilias but more effective against what he termed `sexual addictions'. Stein & al. [1992], opining that `Compulsivity and impulsivity may lie on a phenomenological and neurobiological spectrum', found that paraphiliacs improved less than sexual obsessives on various SSRIs.
Modulatory effects of serotonin. If serotonin is involved in regulating sexual behaviour, by what mechanism might this regulation proceed, how might abnormal serotonergic function cause it to go awry, and what pharmacologic manipulations might remedy such abnormal function? The answers to these questions are likely to involve serotonin's modulatory effects. The serotonergic system's widespread projections from the raphé nuclei [Törk 1990] allow it to modulate the activity of the entire brain. There is quite a bit of evidence for a modulatory action of serotonin on responses to excitatory transmitters, and some evidence for an anticonvulsant effect. The picture is complicated, though, by findings of opposite modulatory effects in various brain regions. In rat entorhinal cortical slices, Sizer & al. [1992] found that serotonin, while having no effect by itself on membrane potential, reduced the depolarisation in response to glutamate by up to half. However, the same investigators using the same method in neocortical slices found that serotonin augmented the response to glutamate. Reynolds & al. [1988] reported potentiation of NMDA response in rat neocortical slices. In cat neocortical slices, Nedergaard & al. [1986, 1986] found that serotonin potentiates response to NMDA, glutamate, and quisqualate. Eaton & al. [1989] recorded from the ventrobasal thalamus in vivo during iontophoretic application of serotonin with NMDA, quisqualate, and kainate, and found that serotonin increased the rate of firing in response to all these agonists. In the rat cerebellum, serotonin depresses response of Purkinje cells to glutamate and quisqualate [Gardette & al. 1987, Hicks & al. 1989]. In sum, serotonin certainly is a neuromodulator, but its pattern of modulation is heterogeneous, so the physiologic effects of systemic manipulations of serotonergic function are not readily predictable.
Anticonvulsant effect of serotonin. There is also some evidence for an anticonvulsant effect of serotonin, undoubtedly related to its modulatory actions. In the experiment of Sizer & al. mentioned above, serotonin reduced the amplitude of epileptiform bursts (especially the late afterdischarges) initiated by electrical stimulation of the underlying white matter in the presence of the GABA antagonist bicuculline. Pasini & al. prevented seizures induced by bicuculline injection into rat prepiriform cortex by injection of fluoxetine into the substantia nigra. Neuman & al. [1989] found that fluoxetine, imipramine, and the 5HT1A agonist 8-OH-DPAT all prevented the suppression of seizures by noxious stimulation in penicillin-induced epileptic foci in rats; they attributed this effect to suppression of raphé activity by activation of autoreceptors. Local administration of 8-OH-DPAT by microinjection, on the other hand, raises the threshold and shortens the duration of the afterdischarge in kindled hippocampal seizures in cats [Wada & al. 1992, 1993]. Leander [1992] reported that fluoxetine enhances the effect of anticonvulsants in mice subjected to electroshock. In genetically epilepsy-prone rats, which are deficient in both serotonin and norepinephrine [Dailey & al. 1992a], systemically administered carbamazepine and antiepilepserine increased levels of serotonin, but not norepinephrine, measured by microdialysis [Yan & al. 1992]. Conversely, pretreatment with the serotonin depletor p-chlorophenylalanine diminished the efficacy of these anticonvulsants. In another microdialysis study in genetically epilepsy-prone rats, Dailey & al. [1992b] found that fluoxetine delivered either systemically or in the dialysate increased serotonin levels and raised seizure threshold. The serotonergic agonist 5-methoxy-N,N-dimethyltryptamine suppressed photically induced myoclonus in LGN-kindled cats [Wada & al. 1992]. In sum, drugs that increase levels of serotonergic transmission in general have an anticonvulsant effect, though the result of Neuman & al. is an interesting anomaly possibly attributable to autoreceptor activation. (Similarly to Neuman & al., in a human, Grady & al. reported a seizure associated with combined fluoxetine and buspirone therapies for obsessive-compulsive disorder. Seizures were not a significant complaint during human trials of fluoxetine, though.) It is, admittedly, a long jump from a genetically epilepsy-prone rat to a human with temporal-lobe abnormalities, but these results are at least suggestive.
Is fetishism best viewed as a psychic or a biological phenomenon? Is it or can it be secondary to an anxiety disorder? Is it a disorder of imprinting? Is it an obsessive-compulsive trait, a disorder of impulse control, or an outlet created by a nonspecific hypersexuality? Is it related to temporal-lobe epilepsy and subictal or interictal epileptiform activity? What does it have to do with the serotonergic system? Research designs and analytic strategies that aim to explore the behavioural, pharmacological, and electroencephalographic nature of fetishism must consider these questions.