We all have a personal bubble, an invisible zone of privacy around our bodies. When strangers cross this boundary, it makes us feel uncomfortable. But not all of us – Daniel Kennedy from the California Institute of Technology has been studying a woman known only as SM, who lacks any sense of personal space.
SM suffers from a rare genetic disorder called Urbach-Wiethe disease, that causes parts of the brain’s temporal lobes to harden and waste away. This brain damage has completely destroyed SM’s amygdalae, a pair of small, almond-shaped structures that help us to process emotions.
Kennedy asked her to say when she felt most comfortable as a female experimenter walked towards her. On average, she preferred a distance of around a foot, about half the usual two-foot gap that 20 other normal people demanded. SM’s lack of boundaries remained whether she walked towards her partner or vice versa, whether they were looking away or at each other, and whether they started close by or far apart.
The fact that SM had a boundary at all was probably because at close distances, it’s hard to see people. She said time and time again that she was actually comfortable at any distance, and during one trial, she actually walked all the way to her partner until they were actually touching. Even when they were making direct eye contact and touching nose-to-nose, she only rated the experience as 1 on a comfort scale of 1 to 10, where 1 is perfectly comfortable and 10 is a level of discomfort that only the British can survive. When a male stranger talked to her up close, she again rated the chat as a 1 (even though he gave it a 7).
SM has been working with this group of researchers, led by Ralph Adolphs, for over a decade but her comfort didn’t stem from simply knowing her partner well. When Kennedy tested two other people who also knew the scientists equally well, but didn’t have damaged amygdalae, they were much less accommodating with their personal space than SM was. Nor did SM simply put her discomfort to heel – she knew that Kennedy was “up to something”, but so did the male stranger and that did nothing to allay his discomfort.
In fact, it was clear that SM understood the concept of personal space. She thought it was smaller than most people’s, and she said that she didn’t want to make other people too uncomfortable by standing too close to them. She estimated that people feel most comfortable about 1.5 feet apart – that’s an underestimate but it’s still larger than her own preference.
Kennedy’s experiments suggest that our sense of personal space comes from the amydgala. Indeed, when he scanned the brains of a small group of volunteers, their amygdalae were more active when someone was standing close to the scanner than when they were keeping their distance.
Kennedy thinks that the amygdala, with its pivotal role in emotional processing, governs the emotional kick we feel when people enter our personal zone. Without it, we remain unfazed by close proximity. What’s less clear is how this affect changes as we get to know people better. Why is it that friends and loved ones are allowed (or positively encouraged) to stay nearer than strangers are?
Other aspects of SM’s ability to deal with emotions are off-kilter too. For a start, she knows no fear – not in a Batman way, but in the sense that she can’t recognise the emotion in the eyes of others Way back in 1994, Adolphs’ group showed that SM can reasonably recognise the emotions in most facial expressions, but she falters when the face in question is afraid. And even though she’s a talented artist, she can’t draw a scared face, once claiming that she didn’t know what such a face would look like.
Now, Naotsugu Tsuchiya, working in Adolphs’ team, has found that SM’s knowledge of fear is a little more complicated. When asked to classify angry and fearful faces, or threatening and harmless scenes, SM did so completely normally when she had to do it quickly. Even though she felt that the scared faces were less intense than volunteers with intact amygdalae, she classified them correctly, with similar reaction times.
In a similar experiment, Tsuchiya showed SM faces that had been gradually morphed from fearful to neutral expressions. When she had unlimited time, it took much more severe expressions for her to recognise a face as fearful. But when she had to quickly pick scared faces from a set, her performances were indistinguishable from other people.
This means that the amygdala isn’t always necessary to know fear. It’s not needed for the earliest stages where our brain starts to process fearful images below the level of our consciousness. Instead, Tsuchiya suggests that after this first level of analysis is over, the amygdala helps us to use the results to make social judgments – to explicitly recognise fear for what it is and to assess the relevance of those first subconscious twinges.
Reference: Nature Neuroscience doi:10.1038/nn.2381 and 10.1038/nn.2380
More on the amygdala:
This is a repost from the old WordPress incarnation of Not Exactly Rocket Science
You are being hunted, chased through a labyrinth by a relentless predator. Do you consider your options and plan the best possible escape, or do you switch off and rely solely on instinct? A new study provides the answer – you do both, flicking from one to the other depending on how far away the threat is.
Earlier studies have found that different parts of a rodent’s brain are activated in the face of danger, depending on how imminent that danger is. Now, scientists at University College London has found the same thing in human brains.
It would be a poor strategy to stick to the same defensive behaviours in all situations. Simply put, there are threats and there are threats, and we need different kinds of behaviour to cope with different scales of danger. When a predator is fifty feet away, we have the time and space to consider our options and plan an escape. But when it’s five feet away, such luxuries are ill-afforded and behaviour needs to be fast and reflexive. In the millisecond between life and death, the best laid plans of mice and men take a back seat in the light of three simple options – fight, flight or freeze.
This sounds fairly obvious, but Dean Mobbs and colleagues actually watched the switch taking place by scanning the brains of several volunteers as they were being chased by a predator. Of course, ethics committees would frown on letting a bear loose on some volunteers, so the experiment was done in a virtual Pacman-like game, where people had to flee a virtual predator through a maze. But they weren’t completely let off the hook; if they were caught, they received an electric shock.
A couple of weeks ago, I wrote about propranolol, a drug that can erase the emotion of fearful memories. When volunteers take the drug before recalling a scary memory about a spider, it dulled the emotional sting of future recollections. It’s not, however, a mind-wiping pill in the traditional science-fiction sense, and it can’t erase memories as was so widely reported by the hysterical mainstream media.
The research that’s published today is a different story. Jin-Hee Han from the University of Toronto has indeed found a way to erase a specific fearful memory, but despite the superficial similarities, this is a very different story to the propranolol saga. For a start, Han worked in mice not humans. And unlike the propranolol researchers, who were interested in developing ways of treating people with post-traumatic stress disorder, Han’s goal was to understand how memories are stored in the brain. Erasing them was just a step towards doing that.
Han’s found that a protein called CREB is a molecular beacon that singles out neurons involved in remembering fearful experiences. When a rat experiences something scary, the CREB-neurons in a part of its brain called the amygdala are responsible for storing that memory – for producing what neuroscientists call its “trace”. When Han killed the amygdala’s CREB-neurons, he triggered selective amnesia in the rats, abolishing the specific fears they had been trained to feel. The memory loss was permanent.
This is a major piece of work. Scientists have long believed that memories are represented by specific collections of neurons. But these neurons don’t occur in a neat, tidy clump; they’re often widely spread out, which makes finding the cells that make up any particular memory incredibly challenging. Han has done this by using the CREB protein as a marker. And in doing so, he had highlighted the vital role of this protein in our memories.
I stress again that this isn’t about erasing memories in and of itself. Doing so is just a means to an end – identifying a group of neurons involved in storing a specific memory. For reasons that should become clear in this article, Han’s technique isn’t exactly feasible in humans! Whether this will stop the inevitable run-for-the-hills editorials is perhaps unlikely, but enough speculation: on with the details.
The wiping of unwanted memories is a common staple of science-fiction and if you believe this weekend’s headlines, you might think that the prospect has just become a reality. The Press Association said that a “drug helps erase fearful memories“, while the ever-hyperbolic Daily Mail talked about a “pill to erase bad memories“. The comparisons to The Eternal Sunshine of the Spotless Mind were inevitable, but the actual study, while fascinating and important, isn’t quite the mind-wiper these headlines might have you believe.
The drug in question is propranolol, commonly used to treat high blood pressure and prevent migraines in children. But Merel Kindt and colleagues from the University of Amsterdam have found that it can do much more. By giving it to people before they recalled a scary memory about a spider, they could erase the fearful response it triggered.
The critical thing about the study is that the entire memory hadn’t been erased in a typical sci-fi way. Kindt had trained the volunteers to be fearful of spidery images by pairing them with electric shocks. Even after they’d been given propranolol, they still expected to receive a shock when they saw a picture of a spider – they just weren’t afraid of the prospect. The drug hadn’t so much erased their memories, as dulled their emotional sting. It’s more like removing all the formatting from a Word document than deleting the entire file. Congatulations to Forbes and Science News who actually got it right.
Kindt’s work hinges on the fact that memories of past fears aren’t as fixed as previously thought. When they are brought back to mind, proteins at the synapses – the junctions between two nerve cells – are broken down and have to be created from scratch. This process is called “reconsolidation” and scientists believe that it helps to incorporate new information into existing memories. The upshot is that when we recall old memories, they have to be rebuilt on some level, which creates an opportunity for changing them.
A few years ago, two American scientists managed to use propranolol to banish fearful responses in rats. They injected the animals in their amygdalae, a part of their brains involved in processing emotional memories. The drug didn’t stop a fearful memory from forming in the first place, but it did impair the memory when the rats tried to retrieve it. Now, Kindt has shown that the chemical has the same effect in humans.