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Fetishism


BACKGROUND AND SIGNIFICANCE 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.


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