Like the Bloodhound Gang song ‘The Bad Touch’ states, we are indeed mammals.
In his book Why is Sex Fun? Jared Diamond calls his opening chapter ‘The animal with the weirdest sex life’. That animal is the human. We are mammals, and a lot of what we have learned about how our brain controls our sex lives comes from research done on animals, typically rodents and small mammals. But there are significant differences between animal and human sexuality, so extrapolating from the sex life of animals and applying the findings to humans is problematic.
In regard to our sex lives, says Diamond, ‘we are the ones who are bizarre’ when compared to the thousands of other mammalian species on the planet. He provides many examples of our peculiarity. Humans, for example, do not just have sex to reproduce but have sex for fun, at any time, typically in private and often with the same partner over a long period of time. In contrast, other mammals have sex for the sole purpose of reproduction, at specific times only, typically in public and with many partners. Animal sexuality is largely dependent on hormonal mechanisms, while human sexuality involves a myriad factors in addition to hormones, including mood and personality.
Yet even though the use of animal models is obviously limited, there is a relationship between particular brain regions implicated in animal research and observations in humans. One brain region that will feature throughout this book is the temporal lobe; you have two of them, one on each side or hemisphere of your brain, behind your ears. Within the temporal lobe is a structure called the amygdala (pronounced ahMIGdala; plural amygdalae), which could arguably be referred to as your sexiest brain bit. By ‘sexiest’, I mean the part of the brain that has most commonly been associated with changes in sex drive and behaviour.
Over 130 years ago, in 1888, scientists Sanger Brown and Edward Schäfer were conducting experiments on rhesus monkeys. They removed both temporal lobes of these monkeys in an operation called a ‘bilateral temporal lobectomy’. In their reports about how the monkeys behaved after surgery, they made a brief reference to one female monkey who showed ‘uncontrollable passion on the approach of other monkeys, so that it is now necessary to shut her up in a cage by herself ‘. Fifty years later, German psychologist Heinrich Klüver was performing behavioural experiments on monkeys, and noted that when they were given the psychoactive compound mescal they made chewing and licking movements and had convulsions; similar symptoms had been described in humans who had epilepsy, specifically temporal lobe seizures – or seizures that arise from atypical activity of the nerve cells in the temporal lobe. Klüver then teamed up with American neurosurgeon Paul Bucy to perform temporal lobe resections (that is, removal of parts of the temporal lobe) of rhesus monkeys, and they unexpectedly discovered an intriguing syndrome that now bears their names: Klüver-Bucy syndrome. The symptoms of the syndrome are visual agnosia (an inability to recognise objects by sight), hyperorality (a tendency to examine all objects by mouth), hypermetamorphosis (an irresistible impulse to react and attend to visual stimuli), emotional changes (an absence of fear and anger, often referred to as the ‘taming effect’), changes in dietary habits and – you guessed it – hypersexuality (a dramatic increase in sex drive).
This research was the first to demonstrate that the temporal lobes are involved in controlling sexual behaviour. The monkeys manifested hypersexuality about three to six weeks after they had undergone bilateral temporal lobectomy, and it involved both a quantitative increase and qualitative change in sexual behaviour. They engaged in indiscriminate mounting of animals of the same and the opposite sex, and of inanimate objects. They had sexual intercourse for up to half an hour, only to mount again immediately after dismounting, as though they had overdosed on Viagra. Males lifted up other males by their erect penises. They orally and manually explored their genitals while in all kinds of positions, for example biting their own penises while suspending themselves upside down from the top of their cage and swinging back and forth. In other words, they wanted sex all the time, and in any way they could get it. These behaviours were not seen in monkeys that had undergone unilateral (one-sided) temporal lobectomy, or in monkeys that had not been operated on at all.
Subsequent reports of partial or complete Klüver-Bucy syndrome in humans then confirmed the temporal lobe’s role as one of our brain’s most important regions for sexual behaviour. The first published case of the syndrome in humans appeared in 1955. A 19-year-old man had undergone a bilateral temporal lobectomy to treat his temporal lobe epilepsy. After the surgery he showed all the symptoms of Klüver-Bucy syndrome except hyperorality. His hypersexuality was expressed through sexual disinhibition, increased masturbation and out-of-character homosexual tendencies. He also had a dense amnesia (memory loss). It’s surprising that he underwent this surgery in the first place; perhaps his surgeon had not yet heard of the devastating case of Henry Molaison, better known as ‘HM’. HM had undergone the same operation two years earlier to treat his severe epilepsy and had been left with a global amnesia. He could not learn new things and also could not recall the 11 years before his surgery; if you talked to him, he would forget you and the conversation as soon as you left the room. HM is undoubtedly the most famous neuropsychological case study of all time, and he taught us a lot about memory, in particular how the hippocampi (singular: hippocampus) – two seahorse-shaped structures, one within each temporal lobe – are crucial for making memories. There are no reports that HM had Klüver-Bucy syndrome, despite his surgery including resection of his amygdalae.
Twenty years later, the first report of full-blown human Klüver-Bucy syndrome was published. A 20-year-old man who had damage to both his temporal lobes due to herpes encephalitis, a rare type of brain inflammation, showed visual agnosia and prosopagnosia (inability to recognise faces) instead of the ‘psychic blindness’ observed in Klüver’s monkeys, and placidity and flattened affect – that is, a general lack of emotional expression – as opposed to the monkeys’ loss of fear and anger. In this case, the subject’s sexual orientation changed from a heterosexual to a homosexual preference. This is one common feature of the hypersexuality described in human Klüver-Bucy syndrome; the other typical feature is sexual disinhibition. For example, in addition to all the other symptoms of the syndrome, a 32-year-old woman with herpes encephalitis had no interest in having sex with her husband but made sexual advances, both ‘manually and orally’, towards female hospital staff. A 57-year-old man who had a severe traumatic brain injury in a car accident made indiscriminate sexual advances towards male and female staff in hospital, and a 52-year-old lawyer who developed seizures showed no overt hypersexuality but rubbed his genitals so frequently that he developed an abrasion on the shaft of his penis.
Human Klüver-Bucy syndrome has been reported in people with a range of neurological conditions, including herpes encephalitis, temporal lobe epilepsy, stroke affecting bilateral temporal lobes, and Alzheimer’s dementia. What all of these conditions have in common is that they involve the temporal lobes. Every human diagnosed with the syndrome has bilateral temporal damage, and in most cases the damage includes the amygdala. This is certainly the case if hypersexuality is a feature, and echoes what has been found in animal research. Following on from Klüver and Bucy’s research, further studies of primates, cats and rodents focused on the amygdala; destruction of both amygdalae in these animals revealed the same sexual changes that had been observed in rhesus monkeys who had been given bilateral temporal lobectomies. Although the temporal lobe is widely considered to be a critical part of the brain in controlling our sex drives and behaviours, it is the amygdala that takes the award for the structure within the temporal lobe that is most commonly implicated in cases of altered sexual behaviour via brain injury or disease.
In neuroanatomy textbooks, the amygdala is always referred to as an ‘almond-shaped’ structure. This analogy reminds me of my neuroanatomy class which was scheduled just before lunch. I always felt hungry while dissecting my assigned human brain, and although I was in awe of this firm jelly thing that was responsible for everything the person had ever felt, remembered or dreamed of, I couldn’t shake the thought that it looked like something you could throw into a stir-fry. The amygdala is found in the middle of each temporal lobe, so we have two amygdalae – one in our right temporal lobe and one in our left. It’s about the size of a five-cent piece. It plays a crucial role in processing our emotions, and abuts the hippocampus, which is critical for memory. We know that memories and emotions are closely intertwined, so it makes sense that these two structures are neighbours.
Thirteen different nuclei make up the amygdala, and each nucleus interconnects with different brain regions, including the olfactory bulbs (involved in processing smells) and the hypothalamus. The hypothalamus, in turn, regulates our endocrine system (hormones) and our autonomic nervous system (bodily functions such as heart rate and breathing). Each amygdala is also connected to other brain regions, such as the frontal lobes, including the medial, orbital and prefrontal regions. These rich interconnections are important to bear in mind when we consider the amygdala’s role in sexual behaviour. It does not act alone; rather, it is part of a wider ‘sexual neural network’. Other brain structures and regions that are part of this network will feature throughout this book.
FOR MY PHD RESEARCH, I SPENT FOUR YEARS INVESTIgating changes in sex drive and behaviour after epilepsy surgery. My supervisor was in charge of a service that offered pre- and post-operative counselling to patients who were undergoing neurosurgery for epilepsy, and she had found that some had reported hypersexuality after their operations. These patients told her their sex drives had increased dramatically, and some had even confided that they had experienced a change in sexual orientation. In some cases, the partners of patients had confirmed this surprising surgical outcome (see Chapter 3). The purpose of my PhD was to explore why this was happening. Was it because they were having fewer seizures, so they were more confident, more ‘in the mood’ for sex? Or was it to do with the part of the brain that had been removed? Was it perhaps a combination of both these reasons?
We already knew about cases of hypersexuality as part of human Klüver-Bucy syndrome, so there was no doubt about the potential role of the temporal lobe. I interviewed over 70 people who had undergone neurosurgery for epilepsy to find out about their sex lives. I also looked at their brain scans before they had surgery. I was particularly focused on their amygdalae. I wanted to know if the size of their amygdalae had any impact on what happened to their sex lives after surgery. I spent months of my life staring at the brain scans of these patients, locating their amygdalae and literally colouring them in (with numerous clicks of the computer mouse) to then determine their size. This can now be done in a more automatic way, but back in the early 2000s when I was doing this work, it was laborious. There were no automatic computer algorithms for determining the volume of various brain structures. I had to carefully identify the structure on each image on which it appeared, then painstakingly colour it in until there was no sign of it. Then I could tap in the code to add up those coloured pixels and the computer would spit out a number that represented the calculated volume.
My supervisor for the neuroimaging part of my thesis had a team of ‘neuro nerds’ (neurologists, neuropsychologists, neuroscientists) in his lab, all doing different research projects for various degrees. The lab was in the basement of the hospital; my supervisor jokingly referred to it as the laboratoire, but it was far from the luxurious abode that this pronunciation suggests. I referred to it as ‘the dungeon’, which I think was a more accurate description. It was windowless, cold and bare – just desks and computers, and people staring at screens covered in images of brains. My supervisor had a favourite saying – ‘Life is short’ – which only exacerbated my desperation to escape the dungeon and get on with what I felt was ‘real’ work: seeing patients. Spending hours staring at brain scans in the dungeon turned me off ever wanting to do neuroimaging research again.
Nevertheless, I found the idea that there could be a link between a patient’s amygdala size and sexual outcome after surgery fascinating, so I persisted with my amygdala painting for many months. In addition to all the patients’ brain scans, I also had to measure the amygdalae of healthy people as a comparison ‘control’ group. I had 45 patients and 46 healthy people, so 91 brain scans to review, with two amygdalae to measure on each, making a grand total of 182 amygdalae. Initially, each one took hours, but I got quicker at it over time. In the end, all that amygdalae painting paid off. When I did my statistical analyses, I was surprised to find that I had actually found something. There was a significant relationship between the size of the amygdala in the healthy temporal lobe of patients – that is, the opposite or ‘contralateral’ lobe to the one where the seizures were coming from – and the person’s sex drive after they had a unilateral temporal lobectomy. The bigger the amygdala in the healthy temporal lobe, the better the person’s sexual outcome. There was also a significant positive relationship between the volume of the contralateral amygdala and the maximum degree of sexual change. Patients who reported a post-operative increase in sex drive had a significantly larger amygdala in their healthy temporal lobe when compared to patients who reported a sexual decrease or no change, and when compared with the control group of healthy people. These findings provided the first evidence ever recorded for an association between amygdala size and human sexual behaviour. When it comes to amygdala size and sexual outcome after temporal lobectomy, bigger is better.
So why would a bigger amygdala be better? One possibility is that the amygdala, through its extensive connections with the hypothalamus, plays an inhibitory role – in other words, it puts the brakes on – in the regulation of the endocrine or hormonal mechanisms of sexual behaviour. Removing the temporal lobe, including the amygdala, on the side where the seizures come from gets rid of this inhibition (brakes off) on the hypothalamus, which leads to a post-operative increase in sexual behaviour. The connections between the remaining amygdala and hypothalamus could also account for variations in sexual outcome.
An alternative explanation is based on the amygdala’s role in emotional processing. It is thought the amygdala regulates the attachment of emotional significance to things and applies reinforcing or discriminative properties to sensory stimuli. In other words, it helps us decide what or who we should or shouldn’t approach, feel attracted to or run away from, love or hate. For example, if you were walking home in the dark and were approached by a tall, aggressive-looking person asking for money, your amygdala would be responsible for alerting you to the potential dangers of this situation, and kickstart your emotional (fear) and behavioural (fight-or-flight) responses. So, according to this proposal, amygdala damage does not disrupt a specific sexual/endocrinological mechanism. Rather, it disturbs the emotional processing of stimuli, which then causes inappropriate and indiscriminate responses. This theory suggests that rather than playing an inhibitory role, the amygdala has a positive effect on sexual behaviour by allowing the appropriate attachment of emotional significance to sexual cues. A larger amygdala may function better in its role in processing emotional and specifically sexual information and the attachment of significance to it, which would increase the likelihood of a sexual response, resulting in an increased sex drive. A bigger amygdala would help you to notice and feel aroused by a sexual cue and make you more likely to accept that cue and go for it.
What about the cases of hypersexuality after temporal lobe surgery, when some patients’ partners complained that they couldn’t keep up with their loved one’s newfound post-surgical sexual desires? Could that be human Klüver-Bucy syndrome? I don’t think so. The sexual increase described by the patients I interviewed was qualitatively different from the reports of hypersexuality in Klüver-Bucy syndrome in both animals and humans. Hypersexual animals who have bilateral amygdala damage show indiscriminate sexual behaviour towards inappropriate objects; for example, they will attempt to mount inanimate objects. Similarly, hypersexual changes in human Klüver-Bucy syndrome involve indiscriminate sexual behaviours, ranging from sexual advances (verbal or physical) towards strangers to homosexual advances that were previously uncharacteristic in the patient. Sexual movements such as hip thrusting, and exhibitionistic behaviours such as disrobing and public masturbation have also been described. These behaviours represent a decrease in selectivity of the target of sexual advances, and of the time and place of sexual expression.
In contrast, the post-operative sexual increase described by the patients who had undergone temporal lobectomy mostly involved an increase in sex drive without indiscriminate sexual behaviour. Using the term ‘hypersexuality’ in relation to Klüver-Bucy syndrome confuses these two kinds of sexual behaviour – increased sex drive and indiscriminate sexual behaviour – and my research suggests that these are two distinct outcomes that may be caused by distinct neurological mechanisms. The fact that I found a positive relationship between amygdala size and sexual outcome also supports the notion that the patients I studied did not have Klüver-Bucy syndrome; if they did, I would have found a smaller dysfunctional amygdala associated with increased sexual behaviour.
‘Bigger is better’ was the title of one of the talks I gave about my PhD research. It was fun thinking of titles. It was around the time that Sex and the City was a huge hit, so ‘Sex and the single amygdala’ was another one I used. ‘The amygdala and sexual outcome after epilepsy surgery: Does size matter?’ was the title of the research study I presented at my first overseas conference in the United States. It certainly caught people’s attention (see Chapter 3). But after four years of thinking and writing about a single topic, and many months in ‘the dungeon’, as soon as the PhD was done I yearned to run away to a new life – and that’s exactly what I did. I wanted to work as a clinician and explore the world, so I moved to London. I was lucky to get a job at the National Hospital for Neurology and Neurosurgery, a world-renowned specialist hospital; I was thrilled to find out that many famous neurologists had worked there. My ‘sexy’ PhD faded into the background as I was trained in the busy life of a clinical neuropsychologist. Until I met a patient who brought it all back…