One of the most distinctive signs of autism is a lack of direct eye contact.  Undeniably involved in social interaction, eye contact is, well, easy to see, especially when abnormal.  Surprisingly, however, there are no interventions specifically designed to improve or facilitate eye contact in autism.  Granted, some behavioral therapies involve training individuals with autism to look at others’ eyes. But, this type of behavioral training doesn’t seem to elicit natural eye contact.

Think back two posts ago.  I mentioned how some everyday experiences can cause stress reactions in people with autism.  Add eye contact to that list.  Several studies have shown that direct eye gaze from others can bring on physiological signs of stress in those with autism.  Again, here’s where our lab’s research comes to bat.  In a recently completed study, we hypothesized that by blocking the stress response system in people with autism, eye contact may be become more easy.  Just as in the other study, we used propranolol, a drug designed to block receptors in the brain that are a part of the stress response system.

In this study, we examined eye contact via a machine that tracks the location of eye gaze.  This machine, called an eye tracker, can tell us where a participant is looking and how long they look there.  To mimic the direct gaze of another person, we used video clips of people looking directly at the video camera.  We had research participants with autism view 32 of these clips on two different study days.  Just as before, we compared the effects of propranolol, given on one study day, versus placebo (a sugar pill), given on the other.  Overall, we hoped to see a benefit of propranolol in improving eye contact, or increasing the time the participants spent looking at the eyes of the people in the video clips.

Here’s the interesting part about science. 99.999% of the time, you don’t find exactly what you expect.  We did not see differences between propranolol and placebo in eye contact.  However, we did find that propranolol significantly decreased the amount of time our participants spent looking at the people’s mouths in the video clips.  What does this mean?  We are not entirely sure.
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Is looking someone in the mouth an impairment linked to reduced eye contact or is it an adaptive strategy used to cope with the stress of eye contact?  And how does the effect of propranolol on mouth gaze fit into the picture?  As is common in the field of autism research, our findings produced more questions than answers.  All the more reason to keep asking.

​[This post was originally published at my previous blog, Neurolore.]

It’s awkward. We do it because we have to, not because we like it. And did I mention, it’s awkward?

We’re talking networking.

Yes, we normally cringe at the thought of another schmooze fest at the office, but when it comes to the brain, networking is not only important, but crucial.  For any behavior or any cognitive process to occur, multiple areas of our brain must work in concert.  These areas may be distant from each other in the brain, but become active at the same time or deactivate together.  This pairing of activity may imply that the areas involved are necessary for whatever behavior is taking place.  This is called functional connectivity.  The areas are connected, not physically, but in terms of what they are used for.

Within the brain, there are countless functionally connected networks designed to carry out the processes of everyday life.  What’s surprising though is how we have networks that are active even when we are doing nothing at all, like when we sleep.  These networks, called resting state networks, are the least understood.  It’s not quite clear what these networks are for.  Furthermore, in the case of a mental disorder, such as schizophrenia, these resting state networks seem to be disrupted.  They are less connected, or have weaker connections. Clearly, there some importance to these networks.

Here’s where my project comes in.  It has been shown that individuals with autism have less functional connectivity at resting state than those without autism.  There might be disruptions in the resting state networks.  But which networks and which areas are involved in this disruption?  In my project, I am analyzing data from fMRI scans of individuals with autism and control participants without autism.  During the scans, the participants were instructed to lie still in the scanner, thinking about nothing in particular for 5 minutes.  With the data analysis technique I’m using, I’ll be able to determine which of 90 areas in the brain are functionally connected when a participant is at rest.  I’ll also be able to visualize the resting state networks of the participants by constructing graphs of the functionally connected areas.  With this, I hope to find differences between the autism group and the control group in the graphed networks.  The differences may include changes in the strength of certain connections or even discrepancies in which areas are connected.
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What’s to be gained here?  We already know that functional connectivity is decreased in autism. However,  studies like this one will allow us to gain knowledge of the overall properties of the resting state networks of people with autism.  Are their networks under-connected, over-connected, or completely different?  To know these things will bring us closer to understanding the nature of this disorder, and more importantly, how we can better help.
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[This post was originally published at my previous blog, Neurolore.]

The almost cliché concept, “fight-or-flight,” is well-ingrained in our minds. Walking down a path, you suddenly realize that the stick you were headed toward is actually a snake.  You are on Facebook at work and your boss appears out of thin air.  Or, as a professor recently described, you are hiking in the woods and you come across a bear with a gun. Not just a bear. One with opposable thumbs and a firearm. Regardless of the event (no matter how implausible) the reaction is the same: your heart races, your palms sweat, and your breathing becomes rapid.  Your body is preparing you either to roundhouse kick the gun from the bear’s mutant-hand or to run away faster than Michael Johnson.

What would it be like if this same reaction occurred when you tried to remember the list of grocery items you wanted to pick up? Or when an acquaintance starts a conversation with you?

According to several studies, these seemingly commonplace events are often quite stressful for people with autism, even stressful enough to bring on fight-or-flight symptoms. Behind these symptoms is a brain chemical called norepinephrine that runs the stress response system.  Here’s where our lab comes into the picture.  We are hypothesizing that blocking the function of norepinephrine in the brain will reduce stress in people with autism, thus improving their cognitive and social abilities.  To block norepinephrine, we are using a drug called propranolol, which is typically prescribed for hypertension or test anxiety. Propranolol works by blocking receptors in the brain that normally respond to norepinephrine.

In a current study, we are comparing the effect of propranolol to that of placebo (or a sugar-pill) on a range of cognitive and social tasks completed by participants who have autism. These tasks involve things like remembering and repeating back lists of words or choosing between two topics and participating in a short conversation (sound familiar?). Our hypothesis is that propranolol, by blocking the stress response, will improve performance on these tasks. If this turns out to be true, we will have identified a drug (that is already on the market and is relatively cheap) as a potential treatment for some core features of autism.

Let’s be clear: propranolol is not and never will be a cure for autism.  In fact it’s quite likely that there never will be a cure, or even just one drug that solves everything.  What we are trying to do is to improve the daily life of someone with autism. To allow him to handle the stressors of the everyday things a little more easily. To help her engage the world a little bit more. For me, that’s an important enough goal as any.

[This post was originally published at my previous blog, Neurolore.]

Don’t you just love how during finals your world becomes a little microcosm of nothing but studying and coffee? That would be what happened to me last week, when Tuesday Thoughts weren’t, well, thought of until Thursday afternoon.
What reminded me of my endeavor to blog regularly was something one of my lab mates shared with me.  Last week, Autism Speaks posted a link to a blog post on it’s Facebook page.  In the post, an MD/PhD student at Albert Einstein College of Medicine discussed the potential links between autism incidence and increased parental age.

The striking thing is nature of the 110 Facebook comments that followed the link.  Parents, caregivers, and even people without children with autism lashed out against the study, the student, and science as a whole.  Talk about public communication backfiring. These individuals seemed to interpret the post as an expression of blame against parents who had their children at older ages.  Interestingly, their responses didn’t admonish this supposed blaming.  They simply repositioned it the FDA, pharmaceutical companies, and researchers.

My question is: Should we be playing this blame game?

In the post against which so many argued, the grad student humbly admits what all autism researchers know to be true:  We know X,Y, & Z about autism, which begs A to Z more questions. The clash between scientists and the community regarding autism stems out of this predicament.  There is still a lot we don’t know.

Understandably so, parents of children with autism are desperate for answers. And researchers are desperately trying to provide them. What’s for certain is that no one should be blamed when so many questions remain unanswered. The blame game is only throwing a road block in the long path ahead.

[This post was originally published at my previous blog, Neurolore.]