Temporal lobe seizures and hypersexuality. Dopaminergic effects.

Proc. 7th Synip. World Soc. Stereotactic and Functional Neurosurgery, Sao Paulo 1977 Appl. Neurophysiol. 41: 13-28 (1978)

Temporal Lobe Seizures and Hypersexuality Dopaminergic Effects

O rlando J. A ndy and Sudha V elamati Neurosurgery Center for Seizure and Behavioral Disorders, Department of Neurosurgery, University of Mississippi Medical Center, Jackson, Miss.

Key Words. Hypersexuality • Limbic • Seizures • Dopaminergic • Neurotrans mitters • Amphetamine • Haloperidol • Cat • Temporal lobe • Apomorphine Abstract. Postictal hypersexuality was induced in 9 male adult cats by repeated stimulation and discharges in limbic and basai ganglia structures.

The dopaminergic activity was either increased or decreased by the administration of apomorphine, d-amphetamine, phenoxybenzamine and haloperido) in varying amounts and combinations. Haloperidol, a blocker of dopamine transmission, appeared to attenuate or abolish seizure in duced hypersexuality. Amphetamine and phenoxybenzamine were thought to compensate for the haloperidol effects by tilting the catechol amine balance in favor of increased dopamine activity. These findings tended to support the assumption that increased dopaminergic activity fa cilitates the development of seizure induced hypersexuality. The actual onset day of seizure-induced hypersexuality appeared to depend upon at taining a specific seizure duration. Progressively increasing seizure dura tions were first accompanied by increasing sexual drive. The hypersexual ity was subsequently attentuated or abolished by further prolongation of the seizures. The sexuality related to the evolution of limbic seizures was previously described as the ‘hypersexual growth and decay curve’ [1]. The drug effects on hypersexuality may, in part, be due to their effects upon the seizure durations. Introduction

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Hypersexuality has been related to temporal lobe lesions in both ani mals [8, 11-13, 19] and man [2, 3, 5, 10, 17]. Temporal lobe seizures, on

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the other hand, have been associated with decreased sexuality in both ani mals [9] and man [2, 6, 21]. In the cat, it was demonstrated that temporal lobe or limbic system seizures may induce hypersexuality in the early stages of seizure development and decreased sexuality in the late stage [1]. It has also been noted that hyposexuality occurs following lesions of the basal ganglia [14] and that increased sexuality occurs with administra tion of L-dopa [7]. The primary objective of this study was to evaluate the effects of ac centuating dopaminergic activity upon limbic and basal ganglia seizure in duced hypersexuality. Material and Methods


Animals. 9 adult male domestic cats were used. 8 exhibited no spontaneous hy persexuality and 1 (S19) had 4 + spontaneous hypersexuality before being utilized in the study. Electrode insertion. Chronic animals were prepared under general anesthesia. Bi polar electrodes with 1 mm bare tips 1.5 mm apart were stereotactically inserted into various parts of the limbic and basal ganglia systems. The structures included were the amygdala, hippocampus, septum, caudate nucleus, globus pallidus, gyrus proreus, cingulate gyrus, putamen, piriform cortex, fornix, thalamus, hypothalamus and preoptic area. Electrical stimulation and recording. There were over 5,000 electrical stimula tions, Over 1,300 seizures were evoked, each longer than 10 sec duration. The num ber of stimulations and seizures between animals varied from 257 to 1,087 and 47 to 360, respectively. Each stimulation consisted of a constant current of 60 Hz, 1 msec pulse for 15 sec. The threshold for inducing seizures was established for each subject. A series of 2-10 stimulations per structure was utilized on each day of stim ulation. The stimulus strength was begun at threshold or just below and progressive ly increased with a 3-min interval between stimulations. A daily session consisted of stimulating 2-4 structures in a fixed sequence. Bipolar electroencephalographic re cordings were made from both stimulated and nonstimulated structures. Behavior. The subjects were allowed to move freely in a 3.5 X 1.5 X 1.5 ft chamber with a transparent front window. The behavior of the animal was evaluat ed before, during, and after the applied stimulations and drugs. Tactile stimulation and exposure to female and male cats were evaluated before and after drug admin istration, induced electrical stimulations and after-discharges. Postictal hypersexual behavior was tested in both familiar and nonfamiliar territory [4, 15, 16]. The hy persexual drive was arbitrarily rated from 1+ to 5+ as follows: 1+ vocalization and approach; 2+ biting; 3 + mounting; 4+ pelvic thrust; 5+ intromission. Atten tion was also given to the speed of sexual attack, the frequency of pelvic thrust, the persistence and duration of the behavior. Drugs. Drugs were given individually or in varying combinations to increase the dopaminergic activity or to alter the catecholamine balance in favor of dopamine,

Feline Limbic Seizures and Hypersexuality

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amphetamine, phenoxybenzamine, apomorphine and haloperidol. Varying drugs were administered inlraperitoneally on varying days in each animal with no duplica tion in the schedule. Following drug injection, each subject was observed for 1530 min before seizures were induced. Histology. The animals were sacrificed with a general anesthetic, and the brains were perfused with 10°/o formalin, serially sectioned to 75 nm thickness and stained. The electrode placements were histologically localized.

Results Characteristics of the Hypersexual Drive The hypersexual drive was indiscriminant and disregarded territoriali ty. It also occurred with the experimenter’s coat sleeve. Pelvic thrust of ten was present even without pelvic body contact. The hypersexual drive was so strong that it was difficult to displace a mounting cat (fig. 1, 2). Merely seeing a male cat or female cat excited the hypersexual response. Body contact also induced the response, and during the disappearance of the response the visual stimulus dissipated before that of body contact. Hypersexuality only occurred after the termination of a seizure (postictal) and in some instances between the electrically induced seizures (interjetai or preictal). No hypersexuality occurred during the applied 15-min electri cal stimulation and the actual discharge.


Onset of Hypersexual Drive Hypersexuality was present before electrical stimulation and drug ad ministration in 1 subject (SI9) and in the remaining subjects it developed on the 7th through the 46th stimulation day. Subjects receiving amphet amine, phenoxybenzamine or apomorphine developed hypersexuality within the 7th through the 15th stimulation day, whereas the 1 subject re ceiving haloperidol developed hypersexuality on the 46th day. In no in stance did drug alone induce the hypersexual drive. Amphetamine (0.33 mg/kg) was given in S4 on days 4 and 6 and the hypersexual onset was on day 8. Amphetamine (1.0 mg/kg) was given in S20 on days 1 through 15, and the hypersexual onset was on day 15. In S14, amphetamine (1 mg/kg) was given on days 2 through 15, and hyper sexuality developed on day 15. In S5, amphetamine (0.33 mg/kg) was given on days 4 and 6 and phenoxybenzamine (1 mg/kg) on days 9 through 13, and the hypersexual onset was on day 13. Apomorphine (1 mg/kg) in S9 was given on days 4, 5, 9, 10, and 11, and the hypersex-

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Fig. 1. Postictal mounting with thrusting activity and biting the leather collar around the neck of a male cat. Fig. 2. The biting of the strap and the copulatory drive were so intense that at tempts to forcefully disrupt postictal mounting were not successful.


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ual onset was on day 13; in S10 it was given on days 7, 8, 9, 12, 13, and 14, and the hypersexual onset was on day 15. In S12 it was given on days 6,7, 8, 10, 12, and 13, and the hypersexual onset was on day 13. Amphet amine (1 mg/kg) and phenoxybenzamine (1 mg/kg) in S20 was given on day 6 and haloperidol (1 mg/kg) was given on day 7; the hypersexual drive onset was on day 7. In S17 haloperidol (0.5 mg/kg) was given on days 1 through 20; amphetamine (1 mg/kg) on days 21 through 33; am phetamine (1 mg/kg) plus haloperidol (1 mg/kg) on days 34 through 43; and amphetamine (1 mg/kg) plus phenoxybenzamine (1 mg/kg) on days 44 through 45; and haloperidol (0.5 mg/kg) on the day 46, and hypersex uality first appeared on day 46. The postictal sexual drive during the early days of onset was relatively short, lasting only 10-30 min. With the increasing number of stimulation days, there was an increasing duration of the postictal hypersexuality last ing for several hours. In some subjects the hypersexual behavior persisted over a 24-hour period from one stimulation session to the next with a de creasing intensity before the next stimulation. Amphetamine Influence on Hypersexuality In S9, amphetamine (0.33 mg/kg) was given daily for 4 days, and dur ing that time the postictal hypersexuality was 3 + and the average seizure duration was 98.6 sec. Increasing the amphetamine to 1 mg/kg daily for 4 days resulted in prolonging the average seizure duration to 167 sec and

200

-

R(A,GP) Stim. 48 Seiz. 5

A m phe- 1j tam ine 1 0 0 o f 3 4 1 2 Daily stim ulation sessions

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Amphetamine 0 6

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Fig. 3. Postictal hypersexuality occurred following an excessively long limbicbasal ganglia seizure (over 200 sec) elicited from the simultaneous stimulation of the amygdala-hippocampus-globus pallidus complex. Stimulations of the septum-fornix and the cingulate gyrus in this subject (S4) did not elicit postictal hypersexuality.

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300 ■ A m phetam ine 0.33 m g/kg RC -

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Days 1

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Phenoxybenzamine 1.0 mg/kg

Hypersexual * 1

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Fig. 4. Limbic system seizures elicited daily in conjunction with administration of amphetamine on days 1 and 3 (triangle) and phenoxybenzamine on days 6 through 10 (arrows). Note that hypersexuality (star) occurred on day 10 following prolonged hippocampal and amygdala seizures.

abolishing the postictal hypersexuality. In addition, spontaneous seizures occurred between the periods of the electrically induced seizures. The subject was then given a 3-day rest period and the spontaneous seizures ceased. During the next period of 6 days, the animal continued on amphe tamine (1 mg/kg) and hypersexual manifestations returned to 3 + and the average seizure duration became longer, 194 sec. The postictal hypersex ual drive was so strong that the animal also attempted to copulate with the coat sleeve of the experimenter’s arm. Amphetamine [0.33 mg/kg in S4 and S5 (fig. 3, 4) and 1.0 mg/kg in S14] did not appear to greatly influence the onset of postictal hypersex uality. In S14 the amphetamine was given daily and the onset day of post ictal hypersexuality was on the 15th day. A pomorphine Depressing Effects on Postictal Hypersexuality In subject S9, during an 8-day sequence of repeatedly induced daily seizures, apomorphine (0.5 mg/kg) was administered during the first 4 days and was increased to 1.0 mg/kg during the second 4 days. Postictal Downloaded by: Univ. of California Santa Barbara 128.111.121.42 - 6/18/2018 10:21:13 AM

Seizure duration, sec

200

Amphetamine


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Fig. 5. Limbic seizure durations related to postictal hypersexuality and adminis tration of apomorphine. Note the selective prolongation of the amygdala and hippo campal discharges during apomorphine injection and the associated development of the hypersexuality (subject 9).

hypersexuality ranged from 3 + to 4 + during the first 4 days of stimula tion and it decreased to 2 + during the second 4 days of stimulation. The seizure durations simultaneously were decreased from an average of 124 to 114 sec between the first and second periods of stimulation. Seizure Accumulation Effects on Hypersexuality In S9 during a 17-day stimulation period, there were 5 days of single stimulation sessions randomly combined with 12 days of double stimula tion sessions, during which time apomorphine (1.0 mg/kg) was given on each of those days. Postictal hypersexuality occurred in 11 of the 12 dou ble stimulation session days, in contrast to only 2 of the 5 single stimula tion days. The average seizure duration for the former was 150 sec and the latter 130 sec. In the same subject, however, the onset day of hyper sexuality was not shortened by the double stimulation sessions when com pared to the single stimulation sessions in other subjects.


Apomorphine Differential Effects on Limbic and Basal Ganglia Discharges Apomorphine appears to facilitate the prolongation of electrically in duced seizures in certain limbic structures. In S9 (fig. 5), the discharges

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Fig. 6. Limbic and basal ganglia discharge durations correlated with the adminis tration of apomorphone and development of postictal hypersexuality. Note the selective prolongation of the amygdala and hippocampal discharges during the ad ministration of apomorphine and the occurrence of hypersexuality (subject 10).

from the amygdala and hippocampus following the administration of apo morphine (1.0mg/kg) were doubled in duration with no significant change in those of the gyrus proreus. Hypersexuality also developed postictally. In S10 (fig. 6), the administration of apomorphine and the repeated electrical induction of seizures selectively prolonged the amygdala and hippocampal discharges, in contrast to discharges elicited from the cau date nucleus, putamen and septal structures. Associated with the prolong ation of the discharges and the administration of apomorphine, postictal hypersexuality had developed.


Apomorphine Facilitated Hypersexuality In S12, administration of apomorphine (1 mg/kg) on each of 3 conse cutive days resulted in a 4 + postictal hypersexual behavior associated

Feline Limbic Seizures and Hypersexuality Hypersexuality related to amydala-globus pallidus seizure durations and apomorphine 100 - A - 12

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Hypersexual Stim. 66 Seiz. 28 Apomorphine 1.0 m g / k g

Not hypersexual Stim. 55 Seiz. 19

75 -

50 -

25

R S -F

LGO LGP-IC No drug

RA-GP

LGP-IC RA-GP Apomorphine x 6

Fig. 7. Limbic and basal ganglia discharge durations related to administration of apomorphine and postictal hypersexuality. Note that hypersexuality occurred with the prolonged seizure duration and with the apomorphine (subject 12).


with an average seizure duration of 235 sec. The postictal hypersexuality was very markedly attenuated during the 3 subsequent days during which time the apomorphine was only given on 1 of those 3 days and the aver age seizure duration for each of those days was 390 sec. In the same sub ject, hypersexuality occurred during the application of apomorphine and prolongation of seizures (fig. 7). In S10, the postictal hypersexuality drive was increased by increasing the dose of apomorphine from 0.5 to 1.0 mg/kg. The animal copulated with the coat sleeve of the experimenter’s forearm with the elevated dose and had no significant change in seizure duration. In S5, apomorphine (1.0 mg/kg) may have contributed to the in creased level of postictal hypersexuality, while the seizure duration was shorter than on the previous day when no apomorphine was administered (fig. 8). In the same subject, discharges from the hippocampus alone did not elicit any postictal hypersexuality, whereas discharges elicited from combined stimulations of the hippocampus and amygdala did elicit the postictal hypersexual change (fig. 8).

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r

Apomorphine 0.1 mg/kg

No LH

Stimulation, mA

Fig. 8. Hippocampal seizures alone and combined hippocampal-amygdala sei zures elicited without apomophine on day 1 and following apomorphine on day 2. Postictal hypersexuality only occurred following combined amygdala-hippocampal seizures and not following hippocampal seizures alone. Note that apomorphine po tentiated the level of sexual drive which was associated with a relatively shorter sei zure (subject 5).

Phenoxybenzamine Effect on Postictal Hypersexuality In S5, administration of phenoxybenzamine 1.0mg/kg during the last 5 days of a 10 day sequence of stimulations was accompanied by postictal hypersexuality on the 10th day following the induction of a prolonged hippocampal and amygdaloid discharge. It should be noted that the cin gulate discharges elicited in the presence of amphetamine during the first 6 days of the period were no longer present after the 2nd day of phenoxy benzamine administration (fig. 4).


Haloperidol Effects on Postical Hypersexuality In S5, administration of 0.5 mg/kg of haloperidol on 2 successive days did not produce hypersexuality following amygdala and hippocampus stimulations. The subject then had 4 days rest, following which the amyg dala and hippocampus were stimulated again on two successive days. The longest seizures were 95 and 268 sec on the first and second days, re spectively, and hypersexuality reached a 3 + level following the second day of stimulation. In SI 4, both pre- and postictal hypersexuality occurred during the dai ly administration of amphetamine. Haloperidol combined with the am-

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I

I

I

I

i

.

I

I

I

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Sexual drive Seizure, sec

Sexual drive

Seizure, sec


Daily stim ulation sessions

Fig. 9. Hypersexuality and the daily longest seizure duration correlated with si multaneous administration of amphetamine and phenoxybenzamine. Haloperidol was substituted on each fifth stimulation day from day 7 through day 27 and phenoxybenzaminc alone was given on days 37 through 41. Note that a 2+ postictal hy persexuality still was present after the castration which had abolished the sponta neously preexisting hypersexuality. Values for day 40 not available (subject 20).

phetamine resulted in abolishing the preictal 3 + to 4 + hypersexual drive after the second day. The postictal hypersexual drive remained at a level of 2 + and was not abolished until haloperidol alone was given. After ha loperidol was discontinued, the postictal hypersexuality returned to 3 + in 2 days and preictal hypersexuality returned in 3 days.


Phenoxybenzamine, Amphetamine and Haloperidol Effects on Hypersexuality (S20, fig. 9) Daily administration of amphetamine and phenoxybenzamine com bined with haloperidol (on each sequential fifth day of stimulation) result ed in a progressive prolongation of seizure duration with an associated progressively increased postictal sexual drive. Haloperidol alone appeared to facilitate the sexual drive, especially in the early period of injection, followed by a delayed tendency to depress the sexuality. Note the phenoxy benzamine alone, after having been given in conjunction with amphet-

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Fig. 10. Pre- and postictal hypersexuality is related to daily longest limbic sei zure durations. Note that during trials 56 through 64 when seizure durations be came longer than in the preceding 6 days, there occurred postictal attentuation of the hypersexual drive in 5 of 9 sessions, whereas there was postictal facilitation rather than depression during the previous period of shorter discharge durations (subject 14).

amine, resulted in an abrupt depression of sexuality with a gradual return over the 5-day period of administration. During this 5-day period of de pressed sexuality, the postictal sexuality was at a higher level than the spontaneous sexuality. The abolished spontaneous hypersexuality result ing from castration became 2 + postictally.


Discharge Duration and Hypersexuality With the progressively increasing seizure durations there was a pro gressively increasing state of hypersexuality, reaching a maximum at a particular seizure duration, which, if exceeded, would depress and even abolish the previoulsy acquired sexual drive. The following examples con sider details of the seizure durations under two separate headings, as if the drug effects were only expressed through altering seizure durations. (1) Increased seizure duration with decreased sexuality. In S14 during the course of a 15-day stimulation period without drugs, the seizures were relatively short, averaging 99.8 sec in the first 6 days. At that time, there was a postictal potentiation of the. sexual drive in 50% of the stimulation


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Subject 19

Phenoxybenzamine

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52 53 54

55

Haldol -

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60 61

62

63

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64 65

66

Testosterone

Daily stim ulation sessions

Fig. 11. Hypersexuality correlated with daily seizure durations and the adminis tration of haloperidol, phenoxbenzamlne, amphetamine, and testosterone. This sub ject was spontaneously hypersexual before implantation of the electrodes. After electrode implantation no spontaneous hypersexuality existed during the first 4 days of stimulation, at which time a 4 + postictal hypersexual drive occurred. Sponta neous hypersexuality returned on the fourth day. The discharges tended to decrease or abolish the spontaneous sexual drive through the fourth and fifth days. Pro longed administration of haloperidol and phenoxybenzamine depressed the hyper sexual system to the point of not responding even to testosterone (subject 19).


sessions and no change in the other 50%. In the subsequent 9 days, the seizures became abruptly prolonged, averaging 188.2 sec, and postictal hypersexuality was depressed in 55% of the stimulations and unchanged in the others (fig. 10). In S20 (fig. 9), the daily sequence of longest seizure durations could be separated into four periods related to the pre- and postictal sexual drive. The average seizure durations in each of the four periods were (1) nonhypersexual period, 17.5 sec (days 1 through 6); (2) postictal hypersexual period, 52.1 sec (days 7 through 12); (3) pre- and postictal period of in creasing hypersexuality, 75.6 sec (days 13 through 24), and (4) pre- and

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postictal period of decreasing sexuality, 79.0 sec (days 25 through 30), and 92.0 sec (days 37 through 41). In SI 9 (fig. 11), the changes in seizures durations could be separated into four periods according to the pre- and poststimulation sexual drive patterns. The average seizure durations were (1) for the dissimilar preand poststimulation hypersexuality, 43.8 sec (days 1 through 9); (2) for the similar pre- and poststimulation sustained hypersexuality, 80.4 sec (days 10 through 14); (3) for the depressed pre- and poststimulation hy persexuality, 103.8 sec (days 15 through 19), 101.2 sec (days 21 through 25), and 119.1 sec (days 27 through 45), and (4) for the abolished hypersexual state, 127.9 sec (days 46 through 66). (2) Increased seizure duration with increased sexuality. Although am phetamine was given daily in subject S14, postictal hypersexuality first developed on the 15th stimulation day following a 144 sec seizure. The longest seizure during the previous 15 stimulation days was 107 sec. The average seizure duration for the 4 days immediately preceding the onset day of hypersexuality was 56 sec, in contrast to 136 sec for the subsequent 4 days of hypersexuality. In S4 an exceptionally long discharge on the eighth stimulation day was followed by postical hypersexuality (fig. 5). Limbic-Basal Ganglia Structures and Hypersexuality The structures from which postictal hypersexuality were most easily elicited were from varying combinations of the hippocampus, amygdala, septum (bed nucleus of stria terminalis), ventromedial hypothalamic area, the ventromedial supraoptic area, globus pallidus, putamen and caudate-accumbens nucleus. Stimulations of the following structures individual ly did not induce postictal hypersexuality: hippocampus, cingulate gyrus, putamen, caudate nucleus, internal capsule and thalamus.

Discussion


These studies suggest that increased dopaminergic activity facilitates the development of hypersexuality associated with limbic seizures. It should be noted that the 7 subjects receiving amphetamine, phenoxybenzamine and apomorphine, individually or in combination, developed hy persexuality on the seventh through 15th stimulation day, whereas the 1 subject (S17) receiving haloperidol during the first 20 stimulation days developed hypersexuality on the 46th day. Although the onset day of hy


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persexuality may be advanced by increased dopaminergic activity, the ac tual day of onset appears to be more directly related to the change in sei zure duration, from short to long. At first the hypersexuality appears only as a postictal event. With a subsequently greater increase in seizure dura tion, interictal or spontaneous hypersexuality also appears. Further pro longation of the seizures is accompanied by a decreased hypersexuality, as shown in figure 10. With continued seizure prolongation, the sexual drive may even be abolished (fig. 11). This change from no hypersexual drive to progressively increasing hypersexuality to eventual abolishment of sex uality in relation to the evolution of seizures, from short durations to pro gressively longer durations, has been designated the ‘hypersexual growth and decay curve’ associated with limbic or temporal lobe seizures [1], Accentuating the dopaminergic activity appears to stimulate, sustain or enhance hypersexuality once it is established. In support of this state ment, it is pertinent to note that combined administration of amphetamine and phenoxybenzamine, which tends to accentuate the dopaminergic component of the catecholamine activity, was effective in sustaining the seizure induced hypersexuality despite periodic administration of haloperidol, a blocker of dopamine transmission (fig. 9). Haloperidol appears to have an early potentiating effect on the hypersexuality followed by a sub sequent attenuation which is overcome by the combined amphetamine and phenoxybenzamine. Note that with phenoxybenzamine alone, without the amphetamine, there is a marked reduction in the hypersexuality on day 37 (fig. 9). It is further significant that haloperidol (0.5 mg/kg) tem porarily abolished a 4 + hypersexuality in S19 (fig. 11). The hypersexual ity was partially restored to between zero and 2 + by phenoxybenzamine (1 mg/kg) and subsequently completely abolished by haloperidol (1 mg/kg). Both amphetamine and testosterone did not restore the seizureinduced hypersexuality following the last administration of haloperidol (fig. 11). These observations suggest that dopamine, which was found to stimulate copulatory behavior in rats [20], also facilitates the develop ment of hypersexuality associated with limbic or temporal lobe seizures in the cat. References


1 Andy, O.: Hypersexuality and limbic system seizures. Pavlov. J. biol. Sci. 12 (4): 187-228 (1977). 2 Blumer, D.: Changes of sexual behavior related to temporal lobe disorders in man. J. Sex Res. 6: 173-180 (1970).

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3 Blumer, D. and W alker, A.: Sexual behavior in temporal lobe epilepsy. Archs Neurol. 16: 37-43 (1967). 4 C lemente , C.: Emotional changes and lesions of ‘temporal lobe’ structures. Clin. Res. 7: 1-3 (1959). 5 F alconer, M.; H ill, D.; M eyer, A. ; M itchell , W., and P ond , D.: Treatment of temporal-lobe epilepsy by temporal lobectomy. Lancet i: 827-835 (1955). 6 G astaut, H. ci C ollomb, H.: Etude du comportement sexuel chez les épilep tiques psychomoteurs. Annls méd. phys. 112: 657-696 (1954). 7 G essa, G. and T agliamonte, A.: Role of brain monoamines in male sexual be havior. Life Sci. 14: 425-426 (1974). 8 G reen , L ; C lemente , C., and G root , J. d e : Rhinencephalic lesions and behav ior in cats. J. comp. Neurol. 108: 505-545 (1957). 9 G ullotta, F.; F e e n e y , D., and G ilmore , W.: Effects of experimental epilepsy on the sexual behavior of cats. Neurosci. Abstr. 2: 261 (1976). 10 H ill , D.; P ond , D.; M itchell , W., and F alconer, M.: Personality changes fol lowing temporal lobectomy for epilepsy. J. ment. Sci. 103: 18-27 (1957). 11 Katahira, K. and T sukahara, S.: Hypersexuality following unilateral amygdalectomy in the cat. Fukushima J. med. Sci. 20: 67-69 (1974). 12 K l i n g , A. and H u i t , P. J.: Effect of hypothalamic lesions on the amygdala syn drome in the cat. Am. med. Ass. Archs Neurol. Psychiat. 79: 511-517 (1958). 13 K luver, H. and Bucy, P.: Preliminary analysis of functions of the temporal lobes in monkeys. Archs Neurol. Psychiat. 42: 979-1000 (1939). 14 M eyers, R.: Evidence of a locus of the neural mechanisms for libido and penile potency in the septo-fornico-hypothalamic region of the human brain. Trans. Am. neurol. Ass. 86: 81-85 (1961). 15 M ichael, R.: ‘Hypersexuality’ in male cats without brain damage. Science 134: 553 (1961). 16 P e t e r s , U.: Sexualstôrungen bei psychomotorischer Epilepsie. J. Neuro-Visceral Rel., suppl. 19, pp. 491-497 (1971). 17 S avard, R. and W alker, E.: Changes in social functioning after surgical treat ment for temporal lobe epilepsy. Social Work 10: 87-95 (1965). 18 Schreiner , L. and K ling , A.: Behavioral changes following rhinencephalic inju ry in cats. J. Neurophysiol. 16: 643-659 (1953). 19 Schreiner , L. and K ling , A.: Effects of castration on hypersexual behavior in duced by rhinencephalic injury in cats. Am. med. Ass. Archs Neurol. Psychiat. 72: 180-186 (1954). 20 T agliamonte, A.; F ratta, W.; D el F iacco, M., and G essa, G.: Evidence that brain dopamine stimulates copulatory behaviour in male rats. Riv. Farm. Terap. iv: 177-181 (1973). 21 T a y l o r , D.: Appetitive inadequacy in the sex behavior of temporal lobe epilep tics. J. Neuro-Visceral Rel., suppl. 10, pp. 486-490 (1971). J. A n d y , Neurosurgery Center for Seizure and Behavioral Disorders, De partment of Neurosurgery, University of Mississippi Medical Center, Jackson, MS 39216 (USA) Downloaded by: Univ. of California Santa Barbara 128.111.121.42 - 6/18/2018 10:21:13 AM

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