Scientific Cafe 2012: Brain Myths

Last night was BAW's first Scientific Café of 2012, with the topic being "Brain Myths," a topic that I've written about before, and the discussion of which I feel is crucial in dispelling popular misconceptions regarding the brain and its functions as well as being particularly suited to the Café’s general audience.

The guest speakers were Dr. Ed Ruthazer (McGill; Montreal Neurological Institute), Dr. Natasha Rajah (McGill; Douglas Institute), Dr. Michael Fehlings (University of Toronto), and Dr. David Ragsdale (McGill; MNI). I'll provide a quick recap of the topics covered by each of the guests along with some of my own comments.

Dr. Ruthazer focused primarily on experience and perception, and how these originate within the brain. Recent advances in technology have allowed us to make incredible leaps in our understanding of perception; in particular, it's possible to reconstruct one's visual experience using imaging techniques, albeit with (currently) limited accuracy and resolution. As technology advances, it will increasingly become possible to reconstruct one's experiences through analysis of brain activity. Future technology may also lead to a complicated (but fascinating) ethical and philosophical issue: if consciousness is an epiphenomenon of brain activity, and we eventually become capable of producing sophisticated artificial 'brains', what are the consequences of producing artificial intelligence and sentience that mimics or rivals our own?

Dr. Rajah focused on myths related to memory. One common misconception is that our brains act as 'recorders' that faithfully encode events for subsequent accurate retrieval. However, work from Dr. Elizabeth Loftus and others has shown that our own memories are in fact rather fallible, in that memories can be modulated or even (in some cases) inserted, with the manipulated individual confident that their adulterated memories are both accurate and their own. In fact, stating that we believe something reinforces that belief, leading to false confidence in a fallible memory if it is declared often enough. Similarly, repressed memories are controversial in this field, with the general consensus being that traumatic events would normally be remembered to some extent, and that repressed memories are likely to be false memories. Finally, myths regarding memory loss in popular media can be misleading, as common misconceptions regarding amnesia are produced from inaccurate fiction.

Dr. Fehlings lamented the fact that there are very few examples of clinical neuroscientists or neurosurgeons in popular fiction (with Dr. Frankenstein, or his younger Mel Brooks equivalent, as rare examples). In the scientific world, however, we are rapidly gaining an understanding of brain regeneration and repair following injury. One example he mentioned is adult neurogenesis, which I've previously written about here, as well as the therapeutic potential of implanted neural stem cells. In closing, he stressed the importance of translational research, in which new insight into brain repair and regeneration gleaned from basic science is applied at a clinical level to patients of neurotrauma.

Finally, Dr. Ragsdale focused on more philosophical concerns related to neuroscience. In particular, if the mind is an epiphenomenon of brain activity, what is the mechanism by which this occurs? If our consciousness is a product of deterministic forces (i.e. underlying neurobiology and its features), do we actually have free will? One experiment exploring the latter described how the neural activity underlying a voluntary action actually precedes the conscious decision to perform the action by roughly a half-second. So if our brains are making our decisions for us, is free will an illusion? He concluded with the importance of creative thinking in neuroscience research, in that our understanding of our brain is still very incomplete, and so there is still lots of room for wild new ideas about the brain to lead to insight about ourselves.

If you couldn't make it to the event, I hope this provided a rough explanation of the type of topics covered. I would definitely recommend checking out any future Science Cafés, as they're stimulating and worthwhile events that make complicated topics accessible to a general audience.

The origins of empathy?

Neuroscience is uniquely suited to investigate the biological underpinnings of the features and traits that make us human, including morality, complex emotions and higher-order cognition. However, as we continually learn more about our behaviour and its origins, one unavoidable and startling possibility is frequently made clear; many quintessentially 'human' characteristics may not be unique to ourselves. One recent example is empathy, the experience of feeling and understanding the state of another agent. Empathy may cause one to respond altruistically; for example, to relieve the suffering or discomfort of another in unfortunate circumstances. Biologists have found evidence of altruistic behaviour across the animal kingdom, presumably due to evolutionary pressures favouring those behaviours that promote species survival and not due to active cognition. However, recent studies have raised the startling possibility that the experience of empathy may be older (evolutionarily) than we think, that we may not be alone in our understanding of the states of others, and that our own understanding of the mental states of animals may be even more primitive than we hold them to be.

Some of the recent evidence suggesting that rodents may have the capacity for empathy comes from pain research here at McGill. Mice in the presence of another mouse in pain are more sensitive to pain themselves, but only if the mouse is familiar (a 'roommate', essentially), and not if the alternate mouse is unfamiliar. To put it another way, if a mouse sees a 'friend' in pain, their understanding (such as it is) of the familiar mouse's experience can affect their own perception of pain, as part of a phenomenon termed “emotional contagion” that is believed to be a precursor to empathic behaviour.

A brand-new study has potentially added some exciting insight to the issue of empathy precursors in animals. A team from the University of Chicago developed a novel method of examining empathy-related behaviour, in which one rat is held in a restraining device that can be released by another rat. After learning how to open the restraining cage, the freely-moving rat chose to free its restrained companion, but not empty restrainers or those containing a toy rat. Notably, female rats seemed to show more altruistic behaviour than males. In a subsequent experiment, this team showed that if a second restrainer containing chocolate was placed alongside a trapped rat, the free rat was equally likely to initially open the chocolate restrainer (and enjoy the chocolate alone) or to open the rat restrainer and share the chocolate, suggesting that freeing the trapped companion is as motivating to the rat as a tasty treat. The authors of this study suggest that these results indicate empathy on the part of the freely-moving rat, in that it is highly motivated to rescue a companion animal that it perceives as distressed, even when doing so costs the rat resources (in terms of sharing the chocolate).

However, is this really the case? In the scant time since this article was published, alternative explanations for the rats' behaviour have arisen. One possibility is that the freely-moving rat becomes distressed by the trapped rat (either by their vocal cries, a released scent, or another signal), and the free rat is opening the restrainer to extinguish these cues and reduce its own distress, as opposed to 'helping' the other rat. Supporting this hypothesis, the animals emitted more frequent 'alarm calls' when an animal was trapped, explaining why the free animals were more motivated to open only those cages containing a trapped companion. This would not be empathic behaviour, as the freely-moving rat is merely acting to reduce its own distress, rather than altruistically 'rescuing' the trapped rat. In addition, the evolutionary advantages of empathic experiences in rodents are unclear.

So the animal empathy issue, new as it is, remains somewhat murky. It seems that rodents possess the capacity for emotional contagion, a primitive precursor for actual empathy. The more recent research raises the possibility for empathy underlying altruistic behaviour in rats, although the evidence so far is insufficient to conclude that this is the case. However, these studies provide clear research directions for future studies investigating the origins of our own uniquely human condition. We already know that human infants display empathy- and morality-related behaviour, as well as a basic understanding of the mental experiences of others (“theory of mind”), as early as one to two years of age. Taken together, these avenues of research bring us closer to understanding the evolutionary and developmental origins of those traits that make us human, to whatever extent we can say they remain uniquely ours.

[Adapted from a post originally posted here.]

Brains need love too

I recently saw the new ad campaign from the institute where I work (the Douglas Institute), ‘Brains need love too’. Seeing as the campaign touches on brain awareness-related topics (including the brain's involvement in psychiatric illness), as well as today being Valentine’s Day, I thought it deserved sharing. The video is extremely open-ended, with the actual message of the campaign open to the interpretation of the viewer, at least until they visit the campaign’s web site. Here are the initial interpretations I took away from it:

- Psychiatric conditions are neurobiologically based, as implied with the opening shots of brains labelled by psychiatric diagnosis. I’m assuming the reasoning behind this is that it has traditionally been believed that stigma against mental illness could be ameliorated in the general public if it was more widely known that mental illness is fundamentally due to the structure and function of the brain itself, as opposed to any personal weakness of afflicted persons themselves. Although it’s noble to attempt to combat stigma by replacing popular misconceptions with fact, however, recent studies showing that stigma against mental illness persists even in the face of improvement of the public’s understanding of the origins of mental illness sadly cast doubt on the effectiveness of this particular strategy.

- People are more than their labels, another anti-stigma message. Outside of its labelled container, the brain reveals it’s capable of experiencing life just like anyone else.

- Take care of your brain, not meant as an anti-stigma message but more of a suggestion that all of our brains, well, ‘need love too’. Speaking of which, Brain Awareness Week is coming up in the near future, so get involved if you need some spring brain-awareness-lovin’. I’m assuming the figurative message here is to be aware that your brain needs care, if not by skateboarding and psychedelic brain-tossing, then by nutrition, exercise, mental stimulation, paying attention to your mental and emotional functioning, and not-sniffing-glue-or-opening-doors-with-your-head-or-something. They’re pretty vague on this one.

Overall, it’s charming and cute, and I like the bold approach of using real (albeit calf) brains up-close and bloody to show that something that may seem disquieting to us (in this case, a bloody brain) is capable of experiencing cognition, emotions and the world around us. Similarly, although mental illness can be disquieting to those with a stigma against it, psychiatric patients are fully capable of these same experiences. Also, regarding the brain images, I feel obligated to point out that we’re talking about something we’ve all got, which is processing this sentence right now within your own head, and while you don’t necessarily have to realize how cool that is, you should at least try to get over your squeamishness over the look of your own brain. It is, after all, what ‘you’ really look like.

It’s a bit difficult to determine the overarching message of the campaign from the 62-second ad alone; it does seem to be necessary to go to the campaign website for clarification, where there’s a slightly vague description urging people to take care of their brains and, more usefully, a list of diverse resources for information on the brain as well as psychiatric disorders and treatment. However, despite this it’s a well-produced and genuinely endearing ad. So go love your brain.

-Ian Mahar

(Adapted from a post previously appearing here)

New neurons and a new therapeutic target

The recent discovery that the human brain produces new neurons throughout life has led us to re-evaluate how we think about our brains and their plasticity, as well as examine potential new targets for psychiatric treatment.

In the narrow space between your ears, a roughly three-pound lump of tissue (composed mostly of water) contains everything that makes you who you are. Your brain is responsible for all of your memories, emotions, actions and aspirations. The human brain is also the source of all of our joy and misery, and understanding its workings offers hope for the amelioration of psychiatric suffering and, possibly, greater potential for happiness and enjoyment of life. However, one difficulty in dealing with the complexity of psychiatric disorders is that frequently multiple theories arise to help explain the origin or cause of any particular condition. 

Depression is one example of this; there are many hypotheses attempting to explain this debilitating condition that affects more than 120 million people worldwide. One of the most widely-known theories is the 'monoaminergic theory' of depression, which focuses on neurotransmitters (chemicals used by neurons for communication) like serotonin. However, in this article I will try to give a brief review of a more recent theory, the 'neurogenic theory' of depression.

Up until relatively recently, it was believed that the brain stopped producing new neurons after development; as the famous neuroscientist Santiago Ramon y Cajal said around a century ago, "In the adult centers, the nerve paths are something fixed, and immutable: everything may die, nothing may be regenerated". However, the creation of new neurons in the mature brain, a process known as 'adult neurogenesis', was confirmed relatively recently in humans.

But there are some mysterious aspects to this phenomenon. For one thing, there initially seems to be only two clearly neurogenic areas in the brain; the olfactory bulb, and the dentate gyrus of the hippocampus. There's some early evidence to suggest other parts of the brain may be neurogenic as well, but even in these areas, the number of new cells produced seems to be limited at best. So this raises some questions; why just these few areas in particular, and not others? And what is the function of these new cells?

Although adult neurogenesis is still a relatively new discovery, it's become something of a hot topic in neuroscience, so we have some preliminary answers to the questions I just posed. For one thing, these new neurons seem to have special properties, in that immature neurons seem more 'plastic' or flexible in their firing responses than other cells. We also have some hints at their function, particularly with hippocampal neurogenesis; it's been shown to be involved in learning and memory and, most importantly for this entry, has been associated with emotional functioning.

This brings us back to the neurogenic theory of depression, an idea that essentially states that if the rate of production of these new 'special' neurons decreases, depressive symptoms may appear or be increased in severity, whereas increases in the rate of adult hippocampal neurogenesis can reduce the severity or appearance of depressive symptoms. Although this idea is only a few years old, there's some evidence supporting it. For one thing, factors that seem to make depression worse, such as stress, also decrease hippocampal neurogenesis, and factors that have been shown to improve depressive symptoms, such as antidepressant drugs and electroconvulsive treatment, also increase hippocampal neurogenesis. Human depressed patients also show decreased volume of the hippocampus. In addition, the delay between starting antidepressant medication and the amelioration of depressive symptoms, roughly four to six weeks, closely mirrors the time necessary for newly-proliferated cells spurred by this medicine to develop into functional neurons. And finally, experiments using animal models have shown that factors that increase neurogenesis also induce antidepressant behaviour.

So the neurogenic theory of depression, although it's still a relatively new idea, has the potential to offer exciting insight into depression and other psychiatric conditions, including treatment applications; if increasing the rate of neurogenesis can improve depression and depressive symptoms, then we can potentially develop new medications and treatments aimed specifically at increasing adult neurogenesis.

It's important to keep in mind that a lot of the theories scientists have developed concerning psychiatric illness are still preliminary, and a lot of important research is still needed before we can provide the definitive answers patients and their families are desperate to hear. However, the silver lining is that we're constantly getting closer to finding those answers, and offering hope to those searching for it.

- Ian Mahar

[Adapted from an article initially published here]