AT FIRST the unhappy 33-year-old-let’s call her Marnie-didn’t stand out from the hundreds of patients that psychiatrist Don Condie saw every month at the Massachusetts General Hospital in Boston. Indeed, he treated Marnie for depression for two-and-a-half years without ever suspecting her secret. Then her mother died and Marnie began to reveal her true selves.
After her mother’s death, Marnie became withdrawn and felt hopeless. She hoarded her medicines, hinted at suicide and needed a spell in hospital. While she was there Condie saw her, but instead of the depressed patient he expected to see, he found himself talking to a bright, energetic and optimistic woman-nothing like the usual Marnie. She even introduced herself to him as if they hadn’t met before, not as Marnie, but as Mimi. Mimi told him that she could fool everyone by imitating Marnie so well that they wouldn’t notice the switch-even Marnie didn’t know she existed.
Mimi gradually began to unveil Marnie’s horrifying past, including years of beatings, sexual abuse and psychological torment at the hands of her alcoholic, criminally violent mother. Mimi explained that her job was to deal with problems that were just too painful for Marnie, such as the explosion of feelings unleashed by her mother’s death. As he listened, Condie realised that Marnie was suffering from something far more mysterious and difficult to treat than depression-multiple personality disorder or MPD.
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After years of therapy with Marnie, Mimi, and the several other personalities that subsequently emerged, Condie teamed up with Guochuan Tsai, a neurobiologist and brain imaging expert at the McLean Hospital in Belmont, Massachusetts. They realised that, with Marnie’s help, they could do something nobody had done before-peer inside a human brain as it shrugs off one identity and slips into another. Their findings are helping to piece together a brain-based understanding of this mysterious, personality-splintering disease.
A physical basis for MPD, and even the reality of the condition, is by no means a given. Many psychiatrists, especially in Britain, think the disorder is nonsense (91av, 17 June 1995, p 14). They’ve seen it mutate over the past decade from a condition so rare that most therapists never saw a single case into a near epidemic, especially in North America. They scoff at reports of patients who spin off hundreds or even thousands of personalities.
Tom Fahy, a psychiatrist at the Maudsley Hospital, London, is one of the critics who believe most MPD cases are the creation of misguided therapists. Through the use of hypnosis, drugs and group pressure, he suspects, aggressive therapists persuade vulnerable patients into believing and acting as multiples. Other critics say MPD is trumped up by attention-seeking patients, or by criminals trying to dodge responsibility for their crimes.
But after years of debate, Fahy wants to move on. “It’s silly to argue whether it exists or not,” he says. “You can’t deny that MPD patients exist. The question is, how has this patient got into such a bizarre mental state?” While Fahy is looking primarily to cultural causes, Condie and Tsai chose to address the question by studying Marnie’s brain in action.
Therapists who believe in MPD have developed a more or less consistent psychological explanation, that it is the mind’s escape from unendurable childhood abuse, usually before the age of five-an explanation popularised by the film Sybil. “It’s chronic trauma,” says Condie, “where you know you’re going to be abused over and over again, by the same person, and there’s no escape. The only escape is inside your own mind.”
But if it is a form of escape, then surely it is like escaping into a nightmare. Imagine competing for control of mind and body, not to mention your home and bank balance with a terrified child, strangers with different sexual proclivities, and a collection of hostile or suicidal toughs. You never meet them and don’t know what they’re up to, although some of them know all about you. But you find their clothes in your closet, you’re blamed for their bad behaviour and you have to clean up the messes they make. And even when you manage to stay in charge, you’re plagued by them arguing, shouting or crying inside your head. No wonder Marnie, like most people with MPD, hid this terrifying reality for years.
But how in escaping does one personality fragment into many others? Some theorists suggest that the overwhelming stress of living such a chaotically divided life tears at the fragile web of a child’s developing memory, so the child cannot weave experiences together into a coherent whole. Instead, islands of memory and behavioural traits develop independently. Eventually they emerge as autonomous personalities competing for control of mind and body.
For example, as a child, Marnie learned to trick her mother into thinking she’d already punished her by pounding on her own thighs until they were covered in bruises. Eventually, a separate male personality developed to inflict the beatings. The outcome is too close to Invasion of the Body Snatchers to be believed without a fight. Perhaps that’s one reason MPD is such a contentious diagnosis. That and a reluctance to admit that anyone could so grossly mistreat a child.
Traumatic shrinkage
The continuing battle over the diagnosis makes it all the more exciting that Condie and Tsai have finally been able to peer into the brain of a patient with MPD. Their preliminary studies showed what’s now been found in many people who’ve lived through protracted trauma: a dramatically shrunken hippocampus. All the other areas of Marnie’s brain were well within the average volumes, while her hippocampus was less than half the normal size-as shrunken as if she suffered from Alzheimer’s disease.
Brain researchers have known for years that the hippocampus, a pair of finger-sized curls of tissue cradled between the temples, plays a key role in memory. It is most active when a person consciously recalls information they have learned-lists of words for example, but more importantly, personal experiences-what you have heard, seen and felt. In addition, patients with severe hippocampal damage can neither build nor recall new memories. “If it’s damaged bilaterally,” says John Aggleton, a neuroscientist at the University of Wales, in Cardiff, “then you get a profound loss of new learning. You can’t remember conversations you’ve had, places you’ve been, or what you’ve done. Yet your other cognitive abilities remain intact.”
To some, her shrivelled hippocampus did not come as a complete surprise. In 1995, researchers at Yale University and at the University of California, San Diego, reported that patients with combat-related post-traumatic stress disorder (PTSD), and adults with PTSD following childhood abuse, also have smaller hippocampuses, along with memory and thinking deficits. Stress and depression are closely linked; indeed one study of women with a history of depression also uncovered a degree of hippocampal damage and memory problems.
After surveying human and animal studies linking stress and hippocampal decline, Robert Sapolsky from Stanford University suggests that extreme levels of glucocorticoids, steroid hormones released by the body under stress, are toxic to the hippocampus. They can disrupt cell function, cause structural changes and eventually cell death. Conversely, Barry Jacobs and Casimir Fornal at Princeton University showed that Prozac, used for treating depression, stimulates the birth of new neurons in the hippocampus (91av, 6 November, p 6). “We know that stress hormones can be neurotoxic,” says Condie. “But we don’t know if it’s neurotoxicity or a combination of things causing the volume change.”
A large number of studies have shown that the memory formation controlled by the hippocampus is also intimately linked to emotion, probably modulated by its next-door neighbour, the amygdala. The hippocampus reacts strongly to stress hormones and also to drugs like Valium and the body’s own anti-anxiety agents. Recent research in rats shows that emotional arousal, for example from a mild electric shock, switches a protein called CREB from an inactive to an active form in the hippocampus. High levels of activated CREB help lay down long-lasting memories, while low levels cause amnesia (91av, 27 March, p 16).
Joseph LeDoux, a neuroscientist at New York University, adds that someone with an intact amygdala but a damaged hippocampus may form emotional memories, for example, fear of a certain place or person, without conscious memory of what caused the fear. “You get a powerful emotional memory, but a weaker memory for the experience,” he says.
Putting all this together-a shrunken, damaged hippocampus and wildly fluctuating levels of stress hormones and neurotransmitters-makes memory distortions seem inevitable. And, as Vilayanur Ramachandran, director of the Center for Brain and Cognition at the University of California, San Diego, pinpoints in his idea of the mnemonic self, memory underlies who we are. Store memories abnormally and you may never be able to find them again. Land on a different island of memories and you’re a different person.
Stanford University’s John Gabrieli, who studies the neuroscience of human memory, also links it to personality formation. “The hippocampus binds together information from many different parts of the brain into a memory of an experience,” he says. “Without access to these memories, your identity can’t grow or develop.” And the absence of coherent memory for personal experiences, the kind of amnesia caused by hippocampal damage, is MPD’s calling card.
What Condie and Tsai really wanted to know was what lies beneath the memory separation and the switch from one dissociated personality to another. They used functional magnetic resonance imaging, fMRI, to address this question. By the time they did their study, a dozen years had passed since Marnie’s mother’s death. Marnie was working steadily in a professional role and seemed to be coping better with her personal life too. Intriguingly, through years of therapy, she had also developed an unusual ability to shift personalities at her therapist’s request, allowing the researchers a unique opportunity to watch the change happening.
The fMRI scanner records hundreds of images per second, revealing in exquisite detail where brain activity is drawing oxygen from the blood. Condie and Tsai monitored Marnie’s brain for a total of 90 minutes, in two sessions separated by several weeks. Using taped directions, Condie directed Marnie to switch to a personality named Guardian, an 8-year-old girl who appeared frequently during therapy. Guardian’s role since childhood had been to watch over Marnie, for example, while her mother tormented her. In the experiment, Guardian would press a button to signal to the experimenters that she had taken control, a process that took about 30 seconds. Marnie would signal her return the same way.
To see whether real personality switches were different from the effects of imagination or effort, Marnie was also asked to imagine being an 8-year-old girl named Player, who was not a real alter ego. Although she found it exhausting, Marnie made the transitions dozens of times while the researchers measured how the activity in the different regions of Marnie’s brain changed as each personality or the imagined character emerged.
As suspected from the preliminary studies, the hippocampus emerged as the star of the identity-shifting drama. But just what its activity means is not easy to interpret. As Marnie’s awareness faded and Guardian took centre stage, activity throughout the hippocampus and in the surrounding temporal cortex ebbed. And as Guardian stepped aside and Marnie re-emerged, the right side of the hippocampus lit up with renewed activity (see Diagram). When Marnie pictured herself as Player, rather than a real alter ego, her brain activity didn’t change.
These findings, coupled with the known links between stress, hippocampal damage and memory abnormalities, have led Tsai towards a brain-based theory of MPD. “The label is misleading,” he says. “It’s not multiple personalities in the same body, but the brain’s reaction to damage. I think it’s a form of brain damage from repetitive and overwhelming stress in early childhood or from overwhelming trauma in life.”
Flashback
The American Psychiatric Association has already acknowledged the problem with the name of the condition, and since 1993 has labelled it Dissociative Identity Disorder, or DID. Dissociation is a disruption in normally integrated consciousness. It ranges from the everyday, such as momentarily forgetting a familiar name or realising you’ve driven miles while thinking of something else, to the pathological-episodes of amnesia, flashbacks or periods of highly abnormal behaviour. At dissociation’s extreme, say believers, lurks multiplicity-coexisting selves with distinct life experiences, memories and personalities.
Tsai speculates that Marnie’s abnormally small hippocampus, almost certainly the result of the abuse she suffered early in life, may misfire in a way that makes possible the extreme dissociation required to switch personalities. He points out that everyone can dissociate, when they daydream, for example. “But some people’s brains get changed early in life, become more vulnerable to trauma, so the switch can go back and forth more easily,” he says. “We really don’t know, but if the wiring is not as sound as it should be, it might easily get inhibited or over-excited, and that might tip the balance between the two personalities.”
David Healy, who heads the department of psychological medicine at the University of Wales College of Medicine in Bangor, finds the brain imaging results intriguing. “There would have to be some physiological underpinnings to the phenomenon of MPD,” he says. “You could describe this as a very graphic illustration of the idea that when a particular personality comes into play, it doesn’t have access to the full range of brain resources.”
He thinks differences between children’s brains might determine who would react to extreme stress by developing dissociative symptoms and eventually MPD. And he’s not surprised to find the hippocampus lurking at the heart of MPD. “It’s no surprise that it’s the structure that might be involved when people are asked to remember what they did, or who they are.”
It is tempting to suggest that decreased hippocampal activity as Guardian emerges is suppressing and preventing access to memories that are Marnie, while the upsurge of activity as Marnie returns is the vital trigger to bring her memories back online. But the researchers and other experts are quick to point out that their findings are too preliminary to support such detailed conclusions.
Daniel Schacter, a brain researcher at Harvard University, warns about pushing the findings too far. “It’s certainly very suggestive,” he says, “but it’s one finding, one patient, one study. Imaging studies are very easy to over-interpret, especially in an exotic subject like this.”
While agreeing with Condie and Tsai’s interpretation of what the hippocampus does, Fahy, the Maudsley psychiatrist, echoes Schacter’s cautionary note. “The important thing with these kinds of studies is not to take them literally, to think that a light flashing in one part of the brain represents a different personality,” he says. “That would be absurd.”
Although Tsai very much wants to repeat their findings with other MPD patients, getting to watch Marnie’s injured brain perform its remarkable sleight of hand has strengthened his belief that neuroscience’s high-powered new tools can illuminate the damage or dysfunction in more detail, and eventually lead to better treatments for MPD and many other mental disorders. But for now, it’s no small feat that they have spotlighted the hippocampus as the battleground where traumatic stress, memory and our sense of who we are collide.