The Problem with Empathy: Bridging the Gap

The Problem of Empathy: Bridging the Gap between Neuroscience and Psychoanalysis toward understanding Autism.

Initial Submission 11/11/07

The Problem of Empathy: Bridging the Gap Between Neuroscience and Psychoanalysis Toward Understanding Autism Perhaps, one day in the future, a bridge between clinical psychoanalytic observations and neuro-scientific findings regarding autistic states will be discovered. I would like to believe that I might contribute to building that bridge in some small way. Frances Tustin, 1994a

Introduction By the end of her life in 1994, Frances Tustin had made a vital contribution to the psychoanalytic understanding of the development of autistic states in children and adults, and she had formulated guidelines for psychoanalytic treatment based upon that understanding. A tireless advocate for these children and their parents, her thoughts expressly reached into a future toward a time when discoveries in neuro-science might cross paths with her own, leading to more effective handling of this tragic disorder, one that reportedly affects 1 out of 150 children and their families. Inspired by Tustin’s dedication and indebted to her ideas, I find that over the year’s I’ve been collecting up the pieces to a kind of jigsaw puzzle related to the problem of autism. This has been something of a personal journey for me, passing by experimental psychology, through psychoanalysis, with a recent detour into the world of neuroscience. It is my hope that this paper may serve to take the reader along on this journey with me, as I endeavor to put together this puzzle, concluding with a multi-dimensional sketch of autism, pointing the way toward some areas for further discussion and for future study. The Journey Begins in Berkeley in the 1960’s While majoring in psychobiology at UCLA, I was introduced to experiments conducted at UC Berkeley’s biology laboratories (Bennett, Diamond, Krech & Rosenzweig, 1964), which were perhaps impelled by a socio-political climate in which animal rights activists were lobbying for a more humane treatment of lab animals. These researchers used rats selected for genetic uniformity, to ensure that the results of their experiments were not due to genetic differences. Once weaned from their mothers, they were raised in one of three environmental conditions. One set of rats was raised in a deprived environment, isolated in a dark and quiet room, but with as much access to food and water as the other rats. A second set of rats was raised in a minimal social condition, housed three to a cage within the bustling environment of the lab. The third group lived in the rat equivalent of a summer camp: 12 to a cage, in an enriched environment where they played with toys and mazes daily and were frequently handled by the scientists. The Berkeley team discovered that rats raised in the "enriched" environment, with toys and social interaction, were not only smarter than rats raised in impoverished conditions of social isolation and sensory deprivation, but the improvement in performance also correlated with a significantly larger cerebral cortex: the area of the brain that determines intelligence, personality and motor function, and is involved in the interpretation of sensory impulses, and therefore the capacity to plan and to organize. So the researchers concluded, after ruling out competing theories, that a combination of intellectual and social stimulation was necessary for the cortical gains observed in their rats. What’s more, further research showed that such cortical growth also occurs in adult rats placed in an enriched environment. Additional studies at the University of Illinois by Volkmar and Greenough (1972) suggested that enriched environments also enhance the brain's ability to process information. They found that the increase in cortical weight is accompanied by an increase in the number of dendritic branches -- or the tendrils that receive communications from other neurons -- in layer IV of the cortex the, which is an area important to communication between the brain’s relay station, the thalamus, and the cortex. Greenough (1988) also found that rats originally raised in a deprived environment, if placed in an enriched environment, also develop larger brains with more neural connections and their performance improves on subsequent tests. These findings suggest that previously stultified brain development can be set back on track through environmental improvements. Furthermore, Greenough, Black and Wallace (1987) demonstrated that in humans, a critical component of an enriched environment is that it must induce learning. In other words, they found that real learning from experience, not just rote exercise, has a dramatic influence on the physical structure of the brain. And although the exact relationship between these changes in physical structure and intellect remained unclear to them, their experiments provide evidence of actual links between the physical stuff we’re made of and our abstract qualities of intelligence and creativity. They also suggest and reinforce the sense that all aspects of the mind - from memory, to dreams, to emotions - have physical correlates, and that sensory deprivation and constricted “experience” may result in atrophy of the physical structure as well as the function of the brain. I remember wondering, when I first read these studies, if they also have implications for the ways in which certain kinds of psychotherapies work, perhaps setting physiological as well as psychic and emotional development back on track in humans. But what sort of psychotherapy and what varieties of constricted development might this model apply to? It was only in my first year of graduate school that I came across this next piece of my puzzle on the way toward addressing this question. The Work of Frances Tustin It was in the early 1980’s that I was initially introduced to the work of Frances Tustin, who had been trained at the famed Tavistock Center and at Great Ormond Street Hospital in London where she treated autistic and psychotic children in analysis. Tustin’s keen capacity for observation, her third ear for listening to a child’s unconscious process, and her finely honed insight as well as eye-sight, enabled her to identify what forces moved these children to do the things they did and would not do. Tustin (1981) came to understand that the ‘impressive caesura of birth,’ originally referred to by Freud, might include the shock of the premature awareness of bodily separateness experienced by the infant: ‘premature’ in the sense that it has occurred before the infant has developed the capacity to sufficiently sort out his feelings, emotions and anxieties from his bodily sensations, while, at the same time, he has yet to sort himself out fully from his mother. This shock appears to give rise to certain existential dreads of being ‘gone’ or of having lost an essential bodily bit, for example the nipple on the breast, initially experienced as part of the baby’s mouth; or the joints that connect his body parts, originally experienced as the mother’s arms; or, in some cases, an entire half of the baby’s body, originally experienced as the mother. Tustin (1981) explained that, in health, in spite of the caesura of birth, there is a gradual transition from the sensations associated with being inside the womb to being outside of it in that tactile sensations of being in a 'watery medium’ are carried over into the child's earliest experience of the post-natal environment. She observed that under good-enough circumstances, if the awareness of separateness threatens to overwhelm the infant, he may communicate his primal terrors to a normally attentive mother, and perhaps, because of the mother’s ability to empathize with the plight of her baby and to modify his ordeal by filtering it through her own previously digested experience of the ups and downs of being and living, she attenuates her baby’s fears by communicating with and lending her confidence to him through the many ways in which she attends to him. Tustin thought that, when these events go well-enough, the commonsensical, empathic yet individual qualities of the post-natal womb of the mother’s mind foster psychological integrations in the neonate, just as the hail and hearty physical womb of the mother’s body promoted bodily integrations in the fetus. However, some mothers have been unable to negotiate their own feelings of separateness in infancy, such that when these feelings are re-kindled in the peri-natal period of motherhood, they constitute a source of stress and strain -- a pre-occupation, if you will. And when a mother is pre-occupied, either by circumstance or character, or when feelings of inadequacy, loneliness, and depression prevail, she may lack the necessary peace of mind essential for mental and emotional sensitivity to her own infantile experience, let alone those similar-if-different experiences arising in her baby. Unfortunely, if Mother is unable to feel, to think about and to sort our these feelings for herself, she may not have nor be able to convey a sense of being able to hold, to catch, to sooth, to bond with, to separate from and to preserve her infant’s entirety. So what’s a mother to do? Tustin (1994b) observed that such well-meaning mothers often instinctively compensate for this deficit by becoming physically over-protective. However, such an undue focus on the physical may create a state of what Tustin called “dual unity” or “adhesive unity,” wherein the emphasis is on a sensation of being, rather than the sense of well-being. This overemphasis upon tactile contact leaves the baby extremely vulnerable in times of Mother’s physical absence. Thus, in her last paper, Tustin clarified that, in her view, psychogenic autism is A protective reaction that develops to deal with the stress associated with a traumatic disruption of an abnormal. perpetuated state of adhesive unity with the mother - autism being a reaction that is specific to trauma. It is a two-stage illness. First, there is a perpetuation of dual unity, and then the traumatic disruption of this and the stress that it arouses (1994b, p. 14). I wish here to underscore that Tustin (1972) fully acknowledged the innate disposition and sensitivities of each baby alongside the impact of the environment. Instead of ‘refrigerator mothers’ (Kanner 1943), she observed that these mothers are, generally speaking, loving mothers who seem to be preoccupied with their own struggles to survive while feeling unsupported, unsure of themselves, or depressed and helpless before and/or after the birth of their babies. She suggested that this pre-occupation interferes with the establishment of what Winnicott called ‘normal primary maternal pre-occupation’ (Winnicott 1962/1965) with what the baby is going through and his needs and desires, as separate and distinct from Mother’s. Regrettably, such feelings of insecurity are more common in new mothers than we like to think, as many are increasingly geographically or emotionally cut-off from the close and affectionate support of their families. Additionally, sometimes their husbands are themselves preoccupied, for example with the pressures of providing for an expanding family or their own insecurity about the prospect of becoming a father, and are therefore unavailable to lend emotional support to the neonatal couple: support that is both necessary for healthy bonding and for timely separation. Perhaps these environmental conditions, increasingly prevalent in our culture, may be at least one factor contributing to the frightening increase in the incidence of autism in the past three decades. Tustin (1990) suggested that, under optimal conditions, mother and baby match each other’s rhythms, gestures, vocalizations or actions. They are both complete and similar-if-separate from birth. And under these conditions, normal developmental imitation gradually evolves into a process of introjective identification. This means that there exists a relationship that is complementary and reciprocal, rather than competitive or parasitic. However, when the inadequately prepared infant experiences too great a gap between himself and a now suddenly separate Mother, he may protectively and perhaps reflexively withdraw into his own disconnected sensual experiences. In this instance, imitation is of a fusional nature, and adhesive rather than introjective identification prevails, as the sensual experiences that had once linked mother and infant become autosensual and therefore increasingly cut-off from the experience of human contact and from relationship. In reporting the experience of her patient John, Tustin (1972) wrote that, when he emerged from his autistic shell, he was able to tell her of the sudden wrenching away of the nipple from the mouth it was originally felt to be a part of. This event had been perceived by John as a sensation of the "black hole with the nasty prick" (1990, p.78). Tustin noted that this sort of ‘happening’ is one version of the ‘nameless dread’ (Bion 1962) of pre-mature twoness: premature in that the infant has yet to be adequately helped to tolerate such situations. Jean, another of Tustin’s (1986) patients, emerged from her shell after much therapy and described the nature of the terror she endured during the breaks in analysis. Jean felt that she and her analyst were “two jugs pouring water into each other, only Jean’s jug had a hole in it and the water spilled out of her” (p. 198). She also said that she felt, “deep down, as if she were a waterfall, falling forever out of control into a bottomless abyss, into nothingness” (p. 198). Jean emphasized that it was the “feeling of being out of control, as much as the falling, that was unbearable” (p.198) as she felt that she was losing herself. Tustin was able to speak to Jean about her waterfall feelings being ‘deep down,’ in that they came from the very beginnings of life, when her body was felt, not just as fluid, but as composed of fluids that could be spilled out and lost. Thus, the baby-Jean was in danger of losing all sense of having a body, of existing. Worse than the fear of dying, where at least her body would be left behind, Jean’s fear was one of complete annihilation: “She would be a no-body, a non-entity” (p. 198). Such fears of being gone were heard repeatedly in the communications of Tustin’s patients, as well as in those child cases for which she was consulted. All in all, the sense of catastrophe surely seems to be at the heart of the matter when instead of normally timed differentiation and integration, explosive disintegration or paralyzed unintegration is the order of the day. It is important to note that it is the awareness of this state that has to be avoided by the child, in the interest of psychic survival. And Tustin discovered that infant’s like John and Jean rally extra-ordinary, auto-generated protections in an effort to block out the awareness of the gap between self and other. Her theory of autistic objects (1980) and autistic shapes (1984) addresses these autosensual tactics and makes more comprehensible the myriad idiosyncratic and often covert activities engaged in by the autistic child: activities that function to enclose them in an impenetrable world apart from our own. Tustin (1990) noticed how autosensual maneuvers -- for example repetitive movements, echolalia, and retention of feces or urine -- serve to create a protective exoskeleton made up of sensation-dominated delusions that block out both the insufferable awareness of two-ness and the overwhelming ecstasy of at-one-ment, when such awareness threatens the baby’s developing sense of personal continuity and integrity. Here, Tustin observed that these delusions are the ‘thing-in-itself,’ not to be confused with more sophisticated mental representations like metaphors. With the elaboration of her models of autistic objects and autistic shapes, Tustin developed a coherent picture of autism that complements current observations from both behavioral and neurobiological disciplines. She distinguished autistic objects from ordinary inanimate or animate objects, in that autistic objects are not related to as objects in the ordinary sense, but instead are used for the tactile sensations that they engender upon the surface of the skin. Tustin observed that autistic children use toys, not in the course of child’s-play as a mode of expression, or in therapy for communicating their experience, but for the sensations that these objects engender upon the surface of the skin. For example, a toy car might be turned upsidedown and the wheels spun for hours, creating a sensation for the child of being fused with the wheels going round and round. Thus, he is able to gain a sensation of going ‘round forever without beginnings or endings: a sensation of timelessness and immortality. Or when held tightly in the palm of the hand, the car becomes a source of comfort, as the child can feel himself to actually be that hard durable ‘thing.’ Additionally, the idiosyncratic shape produced in the palm of the child’s hand by the object can afford him an additional soothing sensation, since, as this shape is idiosyncratic, it belongs to him and him alone and thus cannot be taken away. To be clear, Tustin differentiated autistic shapes from objective shapes -- such as a square or a circle -- in that these are eccentric, endogenous impressions or swirls of sensation -- produced upon the surface of the skin or upon the internal surfaces of the body -- with the aid of bodily substances like pee and poo, or malleable materials like clay, or impressable objects like the toy car. Of course, one difficulty with this survival strategy is that, although the child may tentatively gain a sensation of invulnerability or safety by fusing with these inanimate objects and often use people in this way as well, they cease to develop their own sense of growing or a growing sense of being truly lively, animate, flesh-and-blood creatures. Instead they come to feel, as one patient of mine put it in retrospect, “Like an inanimate thing in a world of the dead.” It is important to notice that the key word in Tustin’s psychology is 'sensation.' Such sensations, as are provided by the autistic use of objects and the creation of autistic shapes, may not only be tactile, but may be visual, auditory, olfactory or gustatory sensations as well, all felt as tactile in nature, perhaps through an abnormally sustained capacity for what Stern (1985) called amodal perception1. We only need to recall expressions such as, “His eyes were glued onto me” or “he was lost in the music” or “the smell of perfume captivated him” to get the gist of the allenveloping tactile sensations derived from various perceptual modalities. These sensations, by rights of their denial of physical distance, either function to distract attention away from feelings of indefensible anxiety -– by providing an illusion of safety, strength and impermeability -- or they may have a numbing or tranquilizing effect on the individual, which serves to protect him from such feared sensations of bodily catastrophe as falling forever, liquefying, spilling, evaporating, burning or freezing. Unfortunately, in their extreme form, and when used to excess, the child becomes addicted to this mode of bodily and psychic survival. Tustin (1990) underscored the fact that the protective shell of autism constitutes a barrier to the potentially healing effects of human relationships and what Bion (1962) called ‘learning from experience.’ But fortunately, this self-protective encapsulation gradually becomes less necessary as the child, in the course of intensive analytic psychotherapy, begins to develop what another of Tustin’s patients called the ‘rhythm of safety’ (1986, p.268). This is a mind-body state in which sensory experiences and individual bodily-rhythms become re-associated with a relational, cooperatively founded tempo involving self and other. In this kind of treatment, the consistency of time and place, along with the firm and benign attitude and empathically founded understanding of the therapist, can provide a mental and emotional as well as physical ambient cadence that enfolds the child securely in relationship, gradually replacing the reliance on autogenerated sensations that had previously helped the child to ‘get a grip on himself.’ I wondered if, on a neuro-physiological level, the autistic child’s auto-sensuous manoeuvres might function by inhibiting the workings of various areas of the brain, creating a vicious cycle where learning from experience, most especially the experience of and with others, becomes increasingly truncated, resulting in the stultification of neural as well as emotional and mental development. And is it possible that this stultification may, in turn, 1 The innate general capacity of the infant to take information received in one sensory modality and somehow translate it into another sensory modality. further interfere with learning, leading to the eventual atrophy of various regions of the brain? In other words, if what the infant perceives is too much to bear, might it be that what Meltzer (1973) referred to as a “dismantling of the apparatus of perception”(p. 108)2 not only occurs in phantasy by actually occurs in reality? And can we think of this situation as the connected with what neurologists call brain damage or even retardation in autistic children? Certainly we know that autistic infants are often mistakenly thought to be deaf. So, if autosensual manoeuvres are effective in blocking out some unbearable awareness, might it be said that the infant creates and lives within a deprived environment that functions in much the same way as the dark, isolated cage in the Berkeley experiments, where physical provisions are adequate for survival, while mental and emotional supplies are deficient for growth of the mind? I’m reminded here of Melanie Klein’s (1930) observation of her autistic patient Dick who retreated into what she called ‘the dark, empty, mummy’s body,’ when he could not bear the feelings engendered by his premature empathy for and identification with the mother. Perhaps some light might be shed upon these questions as we consider the next piece of my puzzle. The Rome Studies Through my personal association with Tustin, I became aware of the work of Gianotti & de Astis (1978, 1989), two psychoanalytic psychiatrists treating autistic children and conducting research at the Pediatric NPI of the University of Rome. Their studies involved the intensive, psychoanalytically informed psychotherapy with 39 psychotic and autistic children, additionally diagnosed as having significant neuropathy, a factor frequently thought to be causal in autism. As is still often the case, the consequences of such a diagnosis by medical experts would rule out any possibility of normal psychic or intellectual development in these children, and consequently psychoanalysis would be contraindicated. However, DeAstis and Gianotti had followed Tustin’s work, and that of Donald Meltzer and his group, who were all treating autism psychotherapeutically with remarkable success. So they resolved to proceed with an analytic protocol. 2 Meltzer (1973) defined dismantling as the most primitive working of obsessional mechanisms that, unlike the splitting processes described by Melanie Klein, which make use of the sadistic drives, dismantling, which is reversible at any time, instead relies on a relaxation of the attention function. Much to the surprise of the organicists at the University, after these children had been engaged in an intensive psychoanalytic process for up to five years, neuropathy was absent in follow-up brain studies. These findings in the test children corresponded to a marked improvement in their cognitive and emotional functioning. Tustin, who consulted on each one of the cases seen in the Rome study and who conducted seminars in Rome for the therapists, suggested, “To the superficial observer, the type of autism that mainly originates from psychological disturbances can look virtually the same as that which originates from gross organic [brain] damage” (Tustin 1990, p. 10). In light of the Rome results, I became convinced that psychoanalysis was the kind of therapy that might set physiological as well as psychic development back on track in humans afflicted with pervasively constricting developmental disorders. So it was that, with these studies in the back of my mind, I was intrigued to read about the work being done by researchers in another part of Italy on ‘mirror neurons.’ The Discovery of Mirror Neurons As the story goes, a group of neuroscientists at The University of Parma (Rizzolatti et al 1996) fell into this line of research strictly by chance. They were working with monkeys, testing neurons that fired whenever the monkey would grab for a peanut and assumed that these were motor neurons. However, one day a scientist came into the lab and when he grabbed a peanut, the monkey's cells fired too. The monkey hadn't moved, only the human had moved, suggesting that these neurons equate seeing something with doing something. The head of the lab, Dr. Rizzolatti, thought it was surprising that these cells, which are involved with motor planning for the monkey, turn out to be interested in the movements of others as well –- even the movements of a member of another species! These neurons eventually came to be called ‘mirror neurons,’ because it appears that the brain mirrors the movements it sees. This serendipitous discovery got these and other scientists thinking and conducting more experiments, and soon it became clear that mirror neurons are a people thing as well (Iacoboni et al. 1999), with the data suggesting that mirror neuron systems are fully developed in human infants (Falck-Ytter, Gredebäck & von Hofsten 2006), and that these systems help them to make sense of other peoples' actions. These findings are consistent with those from psychoanalytic prenatal and infant observation that demonstrate a baby’s capacity to make rudimentary meaning out of his perceptions right from the moment of birth and even before that in utero (Piontelli 1992, Mancia 1981, Levin & Trevarthen 2000, Cramer and Brazelton 1990.) Presently, we know that humans learn by looking and imitating, and that once we've watched, copied and learned a series of movements, we not only have these in our minds, but if we see somebody else making these movements, we can share the experience, moving with others in our imagination, so to speak. What’s more, it appears that the incredibly rich body of knowledge we’ve acquired in this way can be applied to the problem of comprehending the world. The Parma group posited that these mirror neurons might be the brain's method of translating what we see so that we can relate to the world. Many different functions for mirror neuron systems have since been suggested. Some studies link mirror neurons to understanding goals and intentions. For example, since mirror neurons are found in the inferior parietal lobe -- the region of the brain recognized as an association cortex which integrates sensory information and codes the same act in a different way according to the final goal or context of the action -- they are thought to be the neural basis for predicting another individual’s subsequent actions and inferring intentionality. Mirror neurons have also been linked to empathy, because certain brain regions (in particular the anterior insula and inferior frontal cortex) are active when a person experiences an emotion and also when they see another person demonstrate an emotion. Most recently, Keysers & Gazzola at the University of Parma demonstrated that people who are more empathic have stronger activations both in the mirror system for action and the mirror system for emotion, providing direct support for the idea that mirror systems are linked to empathy. Mirror neurons have also been found in the inferior frontal cortex, close to Broca's area, the language center of the brain. This has lead to suggestions that human language evolves from a system where gesture is linked to performance and to understanding implemented by mirror neurons. Mirror neurons are also thought to have the potential to provide a mechanism for action-understanding, imitation-learning, and the simulation of other people's behaviors. And as we know, babies understand language long before they can speak. The mirror system seems also to be involved in the way that we tap into and harness our own abilities and project them out into the world. And people are ordinarily good at watching and translating what they see. Perhaps that's why sports fans tense with the action, and wince, and leap. Because if you know the game, then your neurons are firing as if you’re playing. Professor Marco Iacoboni and his team at U.C.L.A. (1999) suggest that mirror neurons tie us not just to other people's actions, but also to other people's feelings. He found that the part of the brain that's working when you make a face is the same part that’s activated when you see a face. Normally, when we imitate faces there’s an even bigger neural response. Thus it appears that by sending messages to the limbic or emotional system in our brains, mirror neurons help us tune into each other’s feelings, and Iacoboni suggests that that's empathy. Iacoboni strongly believes that there’s a unifying mechanism that allows people to actually connect at a very basic level. In a way, he’s saying that there are neurons in our brains whose job it is to enable us to experientially live in other people's minds, and even to live in other people's bodies. In other words, we have the capacity to identify with others. As psychoanalysts, this comes as no surprise since identification is at the heart of what we call countertransference, a useful thing to pay attention to if you wish to understand the subtle, nonverbal or infra-verbal communications coming from a patient. As analysts, it’s our business to read other people's minds. Here, I am not suggesting that we use telepathy, but we can unconsciously adopt another person's point of view. We analysts call this introjective identification. And it appears that, in health, all human beings do this. So the question arises, if mirror neurons help us to connect emotionally, then what about people who have trouble connecting? For example, autistic children who have trouble with normal developmental imitation, with empathy, with communicative language and with using and comprehending metaphors. This question brings me to the fifth piece of my puzzle, discovered at UCSD around the turn of the century. Broken Mirrors and Autism It's been known for some time that children with autism can be quite intelligent, although they have profound deficits in social interaction. Tustin (personal communication 1985) used to say that “when autistic children come out of their shell, they are really quite artistic as well.” We know that through behavior therapy, sensory integration and the like, autistic children can be taught to speak, read and write. But they still avoid eye contact, often misunderstand questions and they cannot comprehend metaphor. In short, they can’t truly relate to others. These days, when so many children are diagnosed somewhere along the autistic spectrum, everyone wants to know exactly what causes this. So Ramachandran and Oberman (2006) at UCSD designed an experiment. They recorded the mu waves in the brains of test children using an EEG while they opened and closed their hands, and while they looked at a movie of somebody else opening and closing their hands. They state that for most children, the brainwaves are suppressed whether they're doing or seeing this action. But for children with autism, the mu wave suppression that takes place when they’re ‘doing,’ does not occur when they’re watching someone else’s action or even when they’re imitating another’s action. This finding suggests that autism might have something to do with what Ramashandran calls “broken mirror” neurons. This finding is also in harmony with Tustin’s (1972, 1981) observation that what appears on the surface to be normal developmental imitation of another in the autistic child, is really a state of imitative fusion that actually serves to block out the awareness of otherness. According to Ramachandran what we do know is that healthy human beings are intensely social creatures, inventing shared ways to connect, like games, handshakes, dances, language and storytelling. So, he concludes that deep down in our cells, we are normally built to be together. However (and this is key), unlike any other system in our bodies -- for example the digestive system, motoric system, and visual system -- there would be very little point in having a mirror system if you lived in isolation, no point in having a mirror system if you don't want or can’t bear to interact or relate to other people. So, if Tustin is right -- that children at risk for autism cannot bear to be aware of otherness and therefore cannot tolerate true interaction with others, and if their idiosyncratic, auto-sensuous behaviors function to block out any awareness of otherness -- could the broken, deficient or dysfunctional mirror systems occur as a result of these addictive behaviors that distract attention away from the perception of otherness? And could it also be that these behaviors, and the subsequent shutting down of mirror systems, enclose the autistic child in an isolated and insulated state, akin to the deprived environment described in the Berkeley rat studies? Might it be conceivable that these mirror systems were at one time turned on, and that relating to a depressed or pre-occupied mother was too much to bear for some children? Could it be that their subsequent prolonged engagement in auto-sensuousness actually functions to shut down the mirror systems? In health, human beings are able to effortlessly understand each other’s actions and intensions, because an action performed by one person activates the neural pathways responsible for performing the same action in another person’s brain. The observer seems to ‘understand,’ on a visceral level, what the actor is doing because a mirror mechanism affords him an experience in his mind that approximates the experience of the actor. Although scientists say that they don’t know which genetic and environmental risk factors can prevent the development of mirror neurons or alter their function, many research groups are now actively pursuing this hypothesis because it predicts symptoms that are unique to autistic spectrum disorders. For example, mirror neurons have been embraced by simulation theorists who talk about 'theory of mind' (Baron-Cohen, Leslie & Frith 1985), which refers to our ability to infer another person's mental state and their beliefs and desires from their experiences or behavior. According to simulation theory, a theory of mind is available to us when we subconsciously put ourselves in the shoes of the person we're observing and, accounting for relevant differences, imagine what we would desire and believe in the same scenario. In short, we identify! Today mirror neurons are thought to be the mechanism by which we ‘simulate’ others in order to better understand them. Therefore, the discovery of mirror neurons has been taken by some as a validation of simulation theory. Another finding from this research, connected to the phenomenon of empathy, is that stronger EEG responses related to mirror neuron systems have been recorded in women as compared to men. This is consistent with the idea that women tend to be more empathic, that the mirror neuron system is related to empathy, and that weak responses in the mirror neuron system could be linked to a so-called masculine mind and to autism, which is diagnosed to a far greater extent in males than in females (Baron-Cohen 2003). These results make me wonder if, as mothers, might women be naturally endowed with a greater capacity for empathy? This would surely be adaptive, as we know that empathy is the basic communicative link between mothers and infants (Bion 1962). Perhaps we might wonder what impact the use of labor inducing and anesthetic drugs have upon what Winnicott (1961) called ‘primary maternal preoccupation’, an empathic state of heightened and exclusive sensitivity in the mother towards her infant upon which his existence may depend? Additionally, might a deficiency in a mother’s capacity for empathy leave her baby both under-stimulated and frustrated in his attempts to engage with Mother? Could it be that some infants, while initially lacking an active response from the mother, reflexively shut-down their mirror systems, since the operation of such systems would be experienced as painfully unnecessary when social connection is felt to be thwarted, unsatisfying and even traumatic? This state of affairs might be analogous to findings in the field of linguistics (Fauconnier 1985) that demonstrate that, up until 6 months of age, all babies are able to perceive all allophonic contrasts of the world's languages, no matter where they’re born. However, we know that the requisite phonemes for most languages ‘drop out’ of the baby’s babbling repertoire if he doesn’t hear such sounds in his environment during a certain critical period. Perhaps these two situations are examples of a ‘use it or lose it’ tendency in the human organism. Furthermore, speaking of empathy and language, the UCSD Group discovered that people with autism show reduced mirror neuron activity in a part of the brain’s pre-motor cortex, perhaps explaining their inability to assess the intentions of others. They’ve also found evidence that the dysfunction of mirror neurons in the insula and anterior cingulate cortex is linked to related symptoms such as the absence of empathy, and deficits in the angular gyrus may result in language deficits, all known to be connected with autism. So it follows that, if the mirror systems are shut off or broken and the neural activity that would ordinarily allow a child to understand intentionality is absent, one might wonder if, when the autistic child’s auto-sensuous behaviors are interrupted, could it be that he suddenly finds himself in an incomprehensible and therefore frightening world where seemingly ordinary events are experienced as extraordinary? Could it be that the tantrums we see in the autistic child are signs that this interruption has occurred? Is it possible that new or extraordinary happenings are instinctively anticipated as so very threatening to the survival of the relatively inexperienced child, that these are massively blocked out of awareness and thus they might appear (to the observer) to go unnoticed by the autistic child? In addition to explaining the primary signs of autism, Ramashandran (2006) and his colleagues believe that mirror neuron theory can also account for some of the less well-known symptoms. For instance, they know that children with autism have problems interpreting proverbs and metaphors. For example, when they told one of their subjects to ‘get a grip on himself,’ the child took the message concretely and started grabbing his own body. Now, we know that understanding metaphor requires the ability to extract a common denominator from superficially dissimilar entities. For example, take the bouba/kiki effect, discovered by German-American psychologist Wolfgang Köhler (1929). In a replication of his study, Ramachandran & Hubbard (2001) two crudely drawn shapes (one jagged and one curvy) were shown to an audience. They were asked, “Which of these shapes is bouba and which is kiki?” No matter what language the subjects spoke, 98 percent designated the curvy shape as ‘bouba’ and identified the jagged one as ‘kiki,’ suggesting that the human brain is somehow able to tease out abstract properties from shapes and sounds that are shared, not idiosyncratic. These researchers believe that this type of “cross-domain mapping” is analogous to metaphor, and must involve neural circuits similar to those in the mirror neuron system. Consistent with this hypothesis, autistic children perform poorly on the bouba/kiki test, as do non-autistic subjects with damage to the angular gyrus, which is at the crux of the visual, auditory and tactile centers of the brain, another site where mirror neurons have been detected. I wonder if one way of understanding this phenomenon may be derived from Tustin’s (1984) observation that, for the autistic child, words are not ordinarily used for communication, but rather they are idiosyncratically used as a shape producing object or as a hard autistic object. Tustin found that the tactile sensations of tongue in mouth, made by the utterance of certain words, provide a calming or soothing sensation for the child, while other words produce sensations of filling the mouth, perceived as a black hole, thus blocking out the insufferable awareness of otherness and loss, felt as a ‘nasty prick’. Additionally, Tustin observed that jagged edges are often a relieving sight to the autistic child, who can feel himself to actually be the hard edges that he sees and therefore is reassured of his “thereness” and durability, while rounded shapes can be felt to provide a tactile sensation of soothing softness, of timelessness and continuity. Tustin highlights the need to take into consideration the idiosyncratic and concrete nature of the autistic child’s world. For example, when her patient David (1972) had emerged from his shell, he was able to tell her that he had felt that the words ‘Tustin’ and ‘Austin’ were the same (the latter referring to a little toy Austin Martin car that he gripped in his hand as a hard autistic object). These words felt the same on his tongue and lips, and the sensation was the same when the sight of them met his eyes or the sound of them filled his ears. This use of words does not allow for shared meaning, nor does it allow for meaningful discrimination. For the autistic child, words are frequently an agglomeration and agglutination of tactile shapes and objects that function to block out the awareness of difference and similarity between two lively entities, rather than an acknowledgement of and an attempt to communicate with other human beings, since in order for connections to be made, separateness must be tolerated. Now, here’s the crucial question: if autistic children suffer from ‘broken mirrors,’ can they be repaired? Researchers believe that the discovery of mirror neuron deficiencies in autism may open up new approaches to diagnosing and treating the disorder. Ramachandran & Oberman (2006) propose that pediatricians might use the lack of mu-wave suppression (or perhaps the failure to mimic a mother sticking out her tongue) as a tool to diagnose children with autism in early infancy so that therapy can begin as quickly as possible. I would also suggest that a similar test of the post-partum mothers might identify those who, while preoccupied and taken-up with their own predicament, may unwittingly employ concrete obsessional activities that result in a shut-down of their own mirror systems, and thus they may be temporarily lacking in empathy and further tuned-out to the emotional experience of their infants. In such cases, perhaps infant observers (and other engaged in identifying and intervening with mothers and infants at risk for difficulties in bonding and attachment) might be able to assist in supporting these developmental achievements by lending their own empathic understanding to the nursing couple, as is being done in parts of Australia (Salo

  1. and Europe (e.g. the work of Haag, Houzel, Lechevalier in France, Maiello in Italy & Tavistock Centre workers in England). Ramachandran & Oberman (2006) suggest that “salience landscape theory” can explain other symptoms of autism, for example repetitive motions such as rocking to and fro, avoidance of eye contact, hypersensitivity, and aversion to certain sounds, all symptoms that cannot be explained by the mirror neuron hypothesis. They point out that when perceptions – for example, sights, sounds and smells – are processed by sensory areas in the brain, information is relayed to the amygdala, which acts as a portal to the emotion-regulating limbic system. Using input from an individual’s stored knowledge, the amygdala determines how the person should respond emotionally—for example, with fear at the sight of a mad dog or indifference when confronted with trivia. Messages then cascade from the amygdala to the rest of the limbic system and eventually reach the autonomic nervous system, which prepares the body for action. So if a person is faced with a mad dog, his heart rate will rise and his body will sweat to dissipate the heat from muscular exertion. Autonomic arousal, in turn, will feed back into the brain, amplifying the emotional response. Over time, the amygdala creates what they call a ‘salience landscape.’ Autistic children are thought to have a distorted salience landscape, perhaps because of altered connections between the cortical areas that process sensory input and the amygdala, or between the limbic structures and the frontal lobes that regulate subsequent behavior. As a consequence of these abnormal connections, any trivial event or object might set off an extreme emotional storm in the child. This hypothesis is thought to offer an explanation as towhy autistic children avoid eye contact and other novel sensations that might trigger an insufferable upheaval of emotions. According to Ramachandran & Oberman (2006), salience landscape theorists believe that such distorted perceptions of emotional significance might explain why many autistic children become preoccupied with trifles such as train schedules, while expressing no interest at all in things that most children find salient. The UCSD Group found support for this hypothesis when they monitored autonomic responses in autistic children, by measuring the increase in skin conductance related to perspiration. In contrast with control subjects, they found that children with autism have a higher level of autonomic arousal. And although they become agitated, when exposed to trivial objects and events, they often ignore stimuli that trigger expected responses in the control group (Ramachandran & Oberman 2006). However, the question remains, how could a child’s salience landscape become so distorted? The UCSD people found that nearly one third of autistic children have had temporal lobe epilepsy in infancy, related to repeated random volleys of nerve impulses traversing the limbic system. They conjecture, that these seizures eventually scramble the connections between the visual cortex and the amygdala, indiscriminately enhancing some links while diminishing others. They also recognize that both environmental and genetic causes could apply here as well. Such findings on autonomic responses are thought to provide an explanation for the clinical observation that high fever sometimes temporarily alleviates the symptoms of autism (Ramachandran & Oberman 2006). Accordingly, since they know that the autonomic nervous system is involved in controlling body temperature, and because fever and the emotional upheavals of autism appear to be regulated by the same neural pathways, these researchers suspect that fever can mitigate emotion. Initially, upon reading their hypothesis, I was reminded of Tustin’s (1990, p.140) observation that autistic children seem to have an immunity to common childhood illnesses, and that when they begin to emerge from the autistic shell, they not only suffer from emotional meltdowns, but also loosen their immunity to the ordinary fevers, colds, influenza, mumps, measles and chicken pox of childhood. Thus, she found that psychosomatic disturbances appear when the protective shell of the autism is lifted. So, might this be another way to find meaning in the UCSD data? ‘Salience landscape theory’ appears also to provide an explanation for the repetitive motions and head banging seen in children with autism. Researchers seem to be onto the idea that self-stimulation somehow dampens the child’s autonomic storms. And since studies found that self-stimulation not only has a calming effect, but also leads to a measurable reduction in skin conductance in autistic children, these researchers are working on a possible symptomatic therapy for autism: a portable device that could monitor an autistic child’s skin conductance, detect autonomic arousal, and turn on another device-- called a squeeze vest -- that provides comforting pressure by gently tightening around the child’s body (Ramachandran & Oberman 2006). Now, if we take into consideration Tustin’s theory of autism, might we understand that the proposed squeeze-vest would function as a ‘second skin’ (Bick 1968, 1986), to supplement the failing auto-sensual maneuvers that the autistic child employs to do this, thus reinstating the sensation of being held together when the sense of being held together in the empathic understanding of another is insufficient? Although not as simple or as cost efficient as a squeeze-vest, could it be that empathic human understanding might offer both a symptomatic relief and, gradually over time, an internalized mental structure that hold’s both body and mind together in times of stress? UCSD’s two-theory explanation for the symptoms of autism—mirror neuron dysfunction and distorted salience landscape—are seen as complimentary and these researchers believe that it’s possible that the same event that distorts a child’s salience landscape also shuts down the mirror neuron systems. Alternatively, the altered limbic connections are thought to be a side effect of the same “event” -– whether genetic or environmental -- that triggers dysfunctions in the mirror neuron system. But all agree that “the ultimate cause of autism remains to be discovered.” Putting it All Together: Discussion and Tentative Conclusions In concluding, I will summarize by pulling together my puzzle and will leave off with some further questions for study and research. Arguably, the Parma group sheds a ray of light on the neurological areas involved in autism and specifically the problem of empathy, with their discovery of mirror neuron systems. Through continuing research based on their findings, the UCSD group and others have been able to identify a possible connection between the dysfunction of these systems and the problematics observed in autism. However, I’d like to underscore that it’s explicitly stated in all these studies that scientists have yet to identify which genetic and/or environmental factors actually lead to the development and functioning of mirror neuron systems and which of these factors may prevent their development or impede their functioning. The same goes for factors that can lead to a distorted salience landscape or those that aid in the development of one that is relevant and true. Now, since the possibility that an individual’s mirror neurons may be dormant or suppressed (rather than altogether lost or irreparably broken) is clearly considered by all, the question remains as to what if any therapeutic process might possibly revive or restore this neural capacity and it’s related mental and emotional functioning? What therapeutic process might mitigate the distortions in the experiences of the child to create a more helpful and accurate salience landscape? Perhaps psychoanalytic understanding, with its penchant for the discovery of the meaning of things, can offer a new and salient landscape map of the territory other disciplines have been exploring. Take Tustin’s observations, that the autistic child is intrinsically bright and sensitive, let’s say too smart for his own good. And what if he comes into the world genetically endowed with all mirror systems going full bore within the first year of life and thus is exquisitely tuned into his environment? Now, let’s say that the infant -- by rights of his capacity to perceive his mother’s insecurities, to empathize with her, and to feel her pain -- becomes flooded with her (as well as his own) infantile terrors of separateness? So, what’s a baby to do? In such cases, Tustin suggests that that the baby may take over the mother’s function of holding and containing his bodily essences, as-yet-undifferentiated from their mental and emotional counterparts, through autochthonous activities that afford him a sensation of being held together, safe within a second skin. But when auto-sensuousness replaces mental and emotional activity, keeping out unwanted or insufferable stimulation and happenings, the baby may become enclosed in an impoverished environment. Could this result in stultification of cortical development and truncation of neural connections, furthering isolation, and so forth? We might think of this situation as a virtual Möbius strip, where neural systems needed for interaction with the environment are disabled, and the interaction with the environment necessary for further neural development becomes increasingly deficient. Curiously, a Möbius strip is an excellent model for the world that the autistic child attempts to maintain, as described in the popular limerick, often associated with this design, which reads, A mathematician confided That a Möbius strip is one-sided, And you'll get quite a laugh, If you cut one in half, For it stays in one piece when divided. Indeed, Tustin underscores the autistic child’s aversion to the state of two-ness and the effect he can have upon his environment while avoiding this reality. For example, echolalia is often reinforced by the parents and caretakers, who feel compelled to repeat what they say to the child many times, just in order to get his attention. Thus, they are forced to go the child’s autistic way. So Tustin warns, “If as therapists, we unduly collude with the child’s use of words as objects, we risk leaving him in the grip of his pathology, with no possibility for developing genuine relationships characterized by effort and co-operation.” She also described how, “Mother and child become autistic objects for each other; [living] in a sensation-dominated cocoon in which they fit each other predictably and perfectly. They become each other’s ecstasy. Some autistic children come into therapy with a history of such an idyllic infancy. But the benefits from such an infancy are spurious”(Tustin 1981, p. 119.) Often children seem to be developing normally until such time as an event, such as the birth of a sibling, abruptly interrupts this blissful state of affairs. She points out that, “A beneficial feature of the bearable lack of fit of the ‘good-enough mother’ is that it provides a space in which chance happenings can occur. Such chance happenings are agents for transformation and change” (Tustin 1981, p119.) I would add that these are opportunities for learning from experience in contrast with rote memorization and repetition. You will recall that the Berkeley scientists found that opportunities for learning from experiences were a necessary component of an enriched environment essential for cortical development, especially neural connectivity. Tustin cautioned that, “The mother and baby who become entrancing autistic objects for each other and fit each other perfectly, prevent the possibility of such a space. This means that the child’s mental development is massively stunted and goes awry, because agents of change are shut out” (1981, p119). Tustin thought that the father could be one such agent, playing an important role in supporting the nursing couple through the trials and tribulations aroused by the lack of a perfect fit, and the realization that they cannot absolutely control one another. An absent, passive or too malleable father is easily used as yet another autistic object. However, father’s interested and firmly supportive presence can serve as a bounding third party that holds mother and infant together in ever growing and changing experiences, and can facilitate a safe and sound separateness that may be able to be tolerated. The therapist may be able to function in this way as well, to help the child to sort himself out safely from his objects and to mitigate, through empathic understanding, the ‘black hole experience’ that has necessitated the rigid defensive structures that have isolated him from life. Surely the Rome study attests to the possibility that neural as well as emotional and mental development that has been thwarted, stultified and perverted on all scales and measures, can be set back on track through analytic therapy, which provides a firm, empathic (yet not entangling or collusive) experience that serves to open the child’s mind to the riches available in his environment, freeing him from his caged isolation.

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