Sidelined: Sports Concussions Educator Guide

Dr. Pratik Mukherjee, a radiologist specializing in brain imaging, sits in front of an MRI scanner at the UCSF China Basin campus in San Francisco.

Studying the damage caused by a concussion at its source, inside the brain, is no easy feat. As Dr. Geoffrey Manley, Chief of Neurosurgery at San Francisco General Hospital told me, "What we’re dealing with is one of the most complicated injuries in the most complicated organ in the body. The brain has millions of cells that use many, many neurotransmitters to be able to talk to different regions of the brain, so it’s very complicated."

It's also an injury that afflicts two million people in the U.S. each year, according to the Centers for Disease Control.

Today, new brain imaging tools are revealing how concussions, which result from a blow to the head that causes the brain to move inside the skull cavity, are more serious than previously thought, producing actual damage to the brain's intricate network of wires that connect key regions of mental activity.

"The white matter of the brain is essentially the wiring of the brain," said Dr. Pratik Mukherjee, a professor of radiology at the U.C. San Francisco Medical Center. "Brain cells have a transmission unit called the axon, which is a long cable, essentially, that runs for a long distance throughout the brain. And bundles of these axons are called white matter fibers. And they are by analogy the fiber optic cables that produce long-range connection in the brain," he added.

Diffusion Tensor Imaging, a new, advanced form of Magnetic Resonance Imaging, measures the rate of water movement along the brain's bundle of white matter fibers. Additionally, scientists can also measure changes in the rate of water flow, which would occur in the event of damage to the white matter following, for example, a moderate to severe brain concussion. (Degenerative brain diseases like Alzheimer's Disease can also change the movement of water along white matter fibers). Even more impressively, the direction of this water movement can be tracked, thereby allowing scientists to create 3-D maps which show the connections the fibers make between key brain regions. The different colors in these brain visualizations refer to the different directions the white mater fibers are oriented in the brain, such as up-down and left-right.

A slide taken from a D.T.I.-rendered visualization of the brain. The arrow points to a region in the frontal lobe that is vulnerable to damage from concussions. Image courtesy Dr. Alexander Leemans.

Although D.T.I. is not currently in widespread clinical use, it is nonetheless proving to be a promising research tool to better understand the structural damage that concussions can cause.

"The evidence is that the concussions, especially the ones causing rotational injury to the head, cause microscopic damage to these white matter fibers. And that causes a disconnection of brain regions that should be in communication. And that we believe is the cause of the altered thinking, the altered memory, the altered attention that many concussion patients suffer from," said Dr. Mukherjee.

This damage is not even visible with Computed Tomography, an x-ray scanning procedure, which has been routinely administered for decades to brain injured patients.

"A C.T. scan is actually very good for the early phases of trauma," said Dr. Manley. "It tells us whether or not there’s a skull fracture, it tells us whether or not there’s bleeding in the brain. However, we’ve learned over the years that an M.R.I. scan is far more sensitive for looking at abnormalities of soft tissue, and the soft tissue that we’re talking about is the brain. So in fact, an M.R.I. scan gives you a much better picture of the brain than a C.T. scan does," he added.

Dr. Geoffrey Manley looks at M.R.I brain scans with his colleague, Dr. Alisa Gean, at San Francisco General Hospital.

Advanced MRI machines that are powered with magnets twice as strong as those employed in conventional MRI machines can now reveal small areas of bleeding, or "micro-bleeds", in the brain after concussions.

During our filming for this story, Dr. Mukherjee shared with me two sets of scans, one of which was generated with a conventional C.T. scanner, while the other was generated with advanced M.R.I. technology. Both sets of scans were performed on the same concussion-injured patient. Dr. Mukherjee pointed out a black dot on the M.R.I. scans in the left frontal lobe of the patient's brain.

"This black dot is a micro-bleed, which indicates that there has been damage to the white matter in this location," he said. "This indicates tearing at the level of the brain cells, as well as bleeding in the adjacent blood vessels," he added.

Damage to the frontal lobe can cause impairments in attention and focus, which Dr. Mukherjee said can be confirmed with timed tests of mental activity given to patients who have suffered concussions.

Joe Redmond, center, suffered a concussion from a helmet-to-helmet hit while playing on Marin Catholic High School's football team. He lost consciousness after the hit and experienced headaches, confusion and a loss of memory afterwards.

The new imaging tools are highlighting other regions of the brain that are also vulnerable to damage with concussions. For example, patients who have suffered moderate to severe concussions often complain of memory impairments. Dr. Mukherjee's research is showing that the hippocampus – a structure long known to play a critical role in memory formation and learning – can actually shrink following concussions.

"It can help explain why some concussion patients have long-term problems with memory, with attention and with other problems with mood and thought," said Dr. Mukherjee.

But most concussion patients don't suffer any perceptible long-term damage from concussions. In fact, about half the people who suffer concussions recover from their injury in seven to ten days. Nonetheless, they may experience the sluggishness, headaches and mental 'fogginess' that often result from concussions.

In this group of individuals, the neurological effects of the concussion injury may be due more to neurochemical changes than actual structural damage to the brain's white matter.

Eric Freitag, a neuropscyhologist based in Walnut Creek, helps roughly 60 to 70 mostly adolescent athletes each year get back on track following their concussion injuries. I asked him to explain to me how a concussion can disrupt the neurochemical activity of brain cells.

"At the moment of impact of a concussion, all cells in the brain fire. And the brain is asking for more energy, but also in that moment of impact, you have a dramatic decrease in brain blood flow," Freitag said. The energy the brain uses is in the form of glucose which is carried in the blood flowing into the brain.

"So when the brain is asking for more energy, your body can’t provide it. And it’s this metabolic mismatch that causes the symptoms of a concussion. It causes the confusion, it can cause the loss of consciousness, and also other neurological symptoms that can occur for minutes, hours, days, weeks and sometimes months," he added.

Both Dr. Mukherjee and Dr. Manley stress that additional work must be done before the widespread adoption of advanced M.R.I imaging techniques in clinical settings like an emergency room. Nonetheless, they hope that the technological advances in brain imaging will help clinicians more nimbly diagnose and more effectively treat this complex and all-too common injury.

"In the future, a patient will come in, we will have an M.R.I, we will have a blood test where we can go back and we can say, ‘this is the diagnosis that you carry, this is my specific treatment for you.’ But the only way that we’re going to get there is with the same kind of focus, comprehensive and well-funded effort that’s been applied to cancer and heart disease," he said.

A special thanks to Dr. Alexander Leemans for the kind use of his 3D tractography brain imagery and animations.

Meditation is associated with stronger connections between brain regions. Photo courtesy of R_x - renee barron.

Meditation is the practice of focusing your mind on a single thought or idea for an extended period of time in order to achieve some benefit. The goals of meditation can vary and include increased focus, increased awareness or “presence,” better memory, decreased stress and achieving a state of enlightenment. Physiological advantages have also been reported, such as decreased blood pressure and pain reduction.

Though meditation has been practiced all over the world for thousands of years, the mechanism by which it works is still largely unknown. A recent study published in the journal NeuroImage suggests that mediation may work by strengthening the connections between brain regions, thereby building more robust neural networks.

The study compared age and gender matched meditators with non-meditators. Researchers used a method called diffusion tensor imaging (DTI) that detects the size and direction of white matter tracts in the brain. White matter is made up of long neuronal processes called axons that transmit information from one area of the brain to another. DTI is used to measure the integrity of white matter tracts and is thought to indicate the strength of neural connections.

Meditators had stronger DTI measures than non-meditators, particularly in the corticospinal tract (axons from the brain to the rest of the body), the superior longitudinal fasciculus (connections between executive brain areas and sensory regions) and the uncinate fasciculus (connects executive brain areas to emotion and memory regions). Meditators also seemed to have less age-related degeneration.

Though this was not a randomized controlled trial and cannot determine if mediation was the cause of the structural changes, this study opens a new area of research for exploring the role of meditation and brain training in strengthening and preserving the neural connections necessary for memory and other important cognitive tasks.

I might be better off NOT knowing some things about my genes.

Last blog I talked about how I was able to wrest information about my APOE gene from my 23andMe data. I wanted to know because of this gene’s link to late onset Alzheimer’s disease.

APOE comes in three versions: e2, e3, and e4. People with two e4 versions are around 15 times more likely to end up with Alzheimer’s than are people with two e3 versions. And if these e4 folks do get the disease, it tends to come at an earlier age.

I found out that I actually have two e2 versions which protects me somewhat from getting late onset Alzheimer’s. Good news? I guess…

In all of this, I didn’t ask whether this information is worth knowing. Being e2/e2 doesn’t mean I won’t get Alzheimer’s…it just means I am at a lower risk. But at least I didn’t find out I was e4/e4. Then I’d know I was more likely to get Alzheimer’s but not be able to do anything medically useful with that information.

Being e4/e4 would not have meant that I would for sure end up with Alzheimer’s. So it wouldn’t be like having two copies of the delta-508 marker of the CFTR gene. In that case, I would almost certainly have developed cystic fibrosis. No, two copies of e4 would just mean that I was at a higher risk.

And knowing this wouldn’t be able to help me medically at all. There aren’t any good preventative measures I could take to stave off Alzheimer’s.

Now this isn’t always true with these kinds of increased risk genetic markers—some are definitely worth knowing. Women who have certain BRCA1/BRCA2 markers are at an increased risk for getting breast or ovarian cancer. They can choose to screen early (and often) in the hope of catching the cancer early when it is more treatable. Or, more drastically, they can choose to have their breasts and/or ovaries removed. Neither is really an option for Alzheimer’s.

So knowing my APOE status isn’t really that useful medically (at least not yet). I can’t do anything useful with the information other than wait and see if I end up with Alzheimer’s. Which is pretty much what I would have done without the test.

I’m bringing all of this up because 23andMe is now offering people their APOE information (with an upgrade to their new chip, of course). People can now find out their particular combination of e2, e3, and e4 markers*.

In the past, the question was whether or not direct to consumer (DTC) genetic testing companies should offer such a test. That ship has either sailed or is getting ready to leave the harbor. The test will be made available to people who really want the information.

So now the key question is whether knowing your APOE status is worth it. The answer to this question will be different for different people. Given this, the most important thing is for people to have the information they need to make the right choice about whether they want to know their APOE status or not.

One way to figure this out is with a genetic counselor but most DTC tests don’t mandate that you need to talk to one before you are tested. This means it is absolutely critical that the online information provided by DTC companies are presented in an easy to understand way that does not oversell the genetic test. The DTC companies need to be upfront in the fact that this test is not predictive and that there are no proven preventative measures that can keep Alzheimer’s at bay.

I’ll let you all judge how well 23andMe has done at letting people know about what you can learn from the APOE test and what you can do with that knowledge. Click here to read what they have to say.

* You have always been able to get your APOE status with a more expensive genetic test from deCODEme.

Learn more about how genes and the environment work together to cause Alzheimer's.

I put this video in the last blog but it probably should have gone in this one. It shows the unintended consequences of finding out you are e4/e4.

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I was having lunch with a colleague the other day and we got to talking about genetic testing (yes, we are that geeky). I told him about how my 23andMe test had missed my being prediabetic. This says a lot about what 23andMe’s test can tell me about my risk for diabetes. Not much.

Now as I have said before, the fact that 23andMe can’t tell me that I’m likely to become diabetic from their DNA test isn’t their fault (other than, perhaps, some overselling on their part). Diabetes research just isn’t far enough along to be able to accurately predict whether someone will get diabetes or not. Or to make any really meaningful prediction about diabetes at all.

We then got to talking about Alzheimer’s. Turns out his family tree is littered with Alzheimer’s on both his mother’s and father’s side. He ran into a similar problem–23andMe doesn’t report anything for Alzheimer’s.

But here the situation is a bit different than for diabetes. There are a couple of DNA markers that can tell us a lot about our future risk for late onset Alzheimer’s. It just so happens that 23andMe doesn’t report on them.

These markers deal with the APOE gene. This gene comes in three common versions: e2, e3, and e4. People with two copies of the e4 version are 15 times more likely to develop Alzheimer’s and if they do end up with the disease, it tends to come earlier. (One copy of e4 increases your risk about 3 times.)

With a little help from my colleague, I decided to dig a bit deeper into Alzheimer’s and see what I could figure out from what 23andMe did provide. Turns out I can figure out a whole lot about my APOE status. And that I can help other people figure out more from their results too.

The two markers (also called SNPs) that deal with APOE and Alzheimer's are rs429358 and rs7412. Here, according to SNPedia, are the combinations of these markers that tell you your APOE status:

To my surprise, 23andMe gives information on one of them, rs7412. Even though this isn’t usually enough to tell whether you have the dreaded e4 version or not, in my case it was. I almost certainly do not have any versions of e4 (yay!).

See, my results at rs7412 are TT*. If I am interpreting these results correctly, this means I almost certainly have two copies of the e2 version of the APOE gene. In terms of my Alzheimer's risk this is great news as being e2/e2 actually lowers your risk for getting the disease. (There is a chance I could be e1 but this doesn’t seem to be a very common version at all.)

Of course this doesn’t mean I won’t get Alzheimer’s…I still might. After all, the risk for someone over 85 getting Alzheimer’s is almost 50%. Even though this number lumps e4 and e2 folks together, e2 people do not have a 0% risk for Alzheimer's nor do e4 people have a 100% chance. People with e4 are just more likely to have Alzheimer's than e2 people.

It might help to think about getting Alzheimer's like drawing an inside straight in poker. Everyone might do it but people who are playing with wildcards are more likely to get it. These are the e4 folks. But it isn’t a for sure thing…you still may not draw the straight even with deuces wild.

Same thing with not having e4. Now I am less likely to draw that inside straight because there are no wild cards but it can still happen.

Because I was TT at rs7412, my case was pretty easy to figure out. Next blog I’ll try to help people out who are TC or CC at rs7412.

*Remember, we have two copies of each of our genes. So I have a T at rs7412 in one copy and a T at rs7412 in my other copy.

A video showing why knowing your APOE status isn't necessarily a good thing.

Learn more about current Bay Area genetic research from KQED's Forum.

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As I have blogged about before, a big part of sexual preference is biological. Research shows that some people are hardwired to prefer the same sex. This is true in animals as well.

What scientists haven’t had much luck at yet is finding out why this is. There have been studies that have implicated the X chromosome (although not convincingly). And others that have pointed to brain structure. But none of these studies really gets at what is going on in these folks’ brains that makes them prefer relationships with the same sex.

A new study out suggests that, at least in mice, the neurotransmitter serotonin may play a big role. Scientists created a strain of mice that lacked most of a certain kind of serotonin receptors in the brain (central serotonin receptors). These mice were healthy and happy. And the males were not at all fussy about whom they hooked up with.

When scientists put wild type* male mice in a cage with other males, they mostly ignored the other mice. The male mice lacking their central serotonin receptors reacted differently. They got busy with the male mice almost every time.

These mice aren’t homosexual though. Given a choice of a male or female, they didn’t really care; they went after both at about the same rate. The genetically altered mice were more bisexual than homosexual.

The researchers did lots of other experiments as well that showed that these mice were not oversexed or lacking anything in particular. They just liked the boys as much as the girls.

What this study tells us is that in mice, serotonin plays a big role in sexual preference through these particular brain neurons. What it doesn’t tell us is if the same thing is true in people. After all, picking a mate is very different in mice as compared to people.

But there are hints that serotonin works differently in the brains of bisexual and homosexual men. For example, certain selective serotonin reuptake inhibitors (or SSRIs) have different effects in bisexual and homosexual men compared to heterosexual men. Still, this isn’t yet enough to finger serotonin use as the main driver of sexual preference in people.

What it does do though is provide scientists some direction for their research. Instead of wading through all 20,000+ genes, they can start out focusing on those that deal with serotonin. This will greatly simplify the research and if serotonin does play a role, then scientists will find the genetic variations involved sooner rather than later.

And frankly, given the slow progress thus far, focusing on serotonin genes won’t set the field back too far. It is probably worth taking the research in this direction.

* Wild type just means a mouse (or any living thing) that hasn’t been tampered with. In this case, it is a run of the mill lab mouse.

A more in depth look at the story from blogger Ed Yong at Not Exactly Rocket Science.

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Stanford University.

On Wednesday, scientists at Stanford Medical School released new images they’ve produced showing a slice of a mouse’s cerebral cortex. The images, captured using a technology called array tomography, show individual neurons and synapses. Synapses – which are less than a thousandth of a millimeter in diameter – allow brain cells to communicate with each other.

The idea, said Stephen Smith, a professor of molecular and cellular physiology at Stanford Medical School, is that one day scientists might be able to map the changes in individual synapses that occur when people, say, learn a new skill, or experience pain or disease.

That’s a tall order, considering the number of synapses there are in a human brain. Smith says in the human cerebral cortex alone, there are 125 trillion synapses – as many stars as you’d find in 1,500 Milky Ways.

These images – set, in this video, to music composed by Smith’s daughter – are a step in that direction. Smith said the images “have revealed to me, in a way I wasn’t entirely prepared for, how incredibly beautiful the insides of the brain are.”

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Zoloft is a popular drug used for the treatment of depression symptoms.

Depression is hardly new. The Roman physician Galen, in the second century A.D., expounded on the prevailing medical view that four bodily fluids, or humors, existed within all people but that the unique variation of these humors within people resulted in individual differences among people in their behavior and temperament. An excess of black bile, for example, indicated a melancholic personality.

Fortunately, a lot of scientific progress has been made since then in understanding depression to be an organic, brain-based medical condition that afflicts millions. In fact, an individual has a ten to fifteen percent lifetime risk of developing a major depressive episode. But as Dr. Karl Deisseroth, a Stanford neuroscientist and psychiatrist, told me during our interview for “Illuminating Depression”, “Diagnosis is a big challenge because in psychiatry, we don’t have a lab test. There’s not a blood draw that you can do as you might to check how your liver is doing or how your thyroid function is doing.” So given that the diagnosis of depression is based on clinical observation (most often done by a primary care physician), one can’t help feel that hard, empirical understanding of depression is somewhat lacking, especially when compared to diseases of other organs like the heart and lungs where tests do exist to gauge the presence of pulmonary and cardiovascular diseases.

This was the most interesting observation for me when working on this story. Imagine a medical disease that afflicts eighteen million people in the U.S. (26 million if you include Bipolar Disorder), for which more than 160 million prescriptions were filled in 2008, that is one of the leading causes of disability in the U.S., but a disease for which no definitive medical model of pathology exists. Increasingly, doctors are prescribing antidepressants to treat not just depression but a host of other medical conditions, including chronic pain and insomnia, some of which can co-occur with depression. Sure, we’ve made strides since the time of Galen’s bodily humors and the Freudian view of misplaced hostility and mourning to explain depression, but in some respects, we’re still in the dark about why some people get depression while others don’t, why some people respond to one treatment and not another, or why one person will suffer from a form of depression that is less or more severe than another person. This lack of clear, empirical understanding comes at an awful price to victims of depression, as they encounter remarks from people that tell them to “snap out of it”, implying that they somehow can control the emotional crumbling and dark ideations that accompany the disease.

The consequence of all this is that it’s incredibly tough to create effective, lasting treatments for the disease if we can’t exactly track how the disease affects not only specific regions of the brain but the activity among individual brain cells in regions that may not have even been known to play an integral role in the disease. My layperson’s view is that treating depression currently is a bit like bringing in a car to the mechanic and telling him to fix it but there’s a catch – the mechanic can’t get under the hood to observe directly what’s wrong with the car. We suspect that the problem is with the engine but good luck with opening it up and peering into its pistons. So the mechanic attempts to work on the engine but indirectly, and whatever repairs are attempted may affect the engine but they may also have unwanted effects on the car’s transmission, muffler, timing belt, etc.

Fortunately, advances in imaging techniques like two-photon microscopy and fMRI are elucidating the activity of the depressed brain, allowing the previously impenetrable forest of billions of neurons to be explored, to see their pathways altered, their branches pruned by the disease. And scientists like Philippe Goldin and Kelly Werner are compiling biomarkers like DNA and brain blood flow activity to see if those biomarkers can help predict if people suffering from anxiety and/or depression will respond more favorably to cognitive behavioral therapy than to mindfulness meditation, for example. Dr. Deisseroth is using genetically engineered, photosensitive proteins implanted into rodents’ brains to control brain activity at the level of individual neurons.

Dr. M. Bret Schneider told me during our interview, “A real cure for depression is gonna involve being able to selectively affect those portions of the brain which don’t function properly in depression… But fathoming the huge number of possibilities in each brain with every brain being a little bit different than every other one, is gonna require individualized solutions and will be a scientific feat.” I suppose that with a disease as complex as depression, where one’s individual genetic makeup can influence the kinds of side effects one may experience with an antidepressant, it’s apropos that the future of treating and eventually curing it will entail personalized medicine. Until then, let’s hope that more people bring psychiatry into the research lab to study illnesses like depression, for it’s only through the methodical rigor of science that we have the best hope for curing depression.

Watch the Illuminating Depression television story online.

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This radio story tries to cram a lot into five minutes, so if you don't find what you need here, put a comment on the blog, below and I'll see if I can't provide a lead to more information.

Transcranial magnetic stimulation interested me, in part, because of how non-invasive it is. Dr. Bret Schneider, who offers TMS from his private practice in Portola Valley, was one of several experts to suggest that TMS machines might one day be available for home use. Of course, that's a long way off. TMS is expensive: about $5,000 for an initial round of treatment. It's still much easier and cheaper to simply pop a pill each morning. And researchers are still working out how effective it can be.

Studies show that TMS brings a remission in depression to about a third of patients to try it. Another third experience some improvement, and a final third are unaffected. Dr. Schneider says he sees much better success rates on patients who combine TMS with antidepressant drugs (TMS without drugs, he says, is like "trying to drive a car with no gas.") Finally, the FDA approval covers only one TMS machine on the market, Neurostar, although some physicians use other techniques, off-label.

You can find links to the abstracts of clinical studies performed on TMS and depression through a search at pubmed.com. This meta-analysis compares 30 double-blind studies, covering a total of 1164 patients (606 received TMS, 558 received sham treatments).

But TMS is just one in a class of "brain stimulation" depression treatments — an important fact that didn't make it into the story. Others include vagus nerve stimulation, deep brain stimulation and, of course, electroshock convulsive therapy — which is offered here in the Bay Area at the UCSF Langley Porter Psychiatric Institute to severely depressed patients (as well as, less commonly, people suffering from manic depression and schizophrenia).

Quest TV will cover TMS and other depression treatments in greater depth later this season, so stay tuned. For a sneak peak at some of what you'll find on the show, check out Stanford scientist Karl Deisseroth's groundbreaking work using light-sensitive proteins to stimulate neural circuits — work that could someday help treat not just depression, but other brain diseases as well.

Listen to the Depression Advancements radio report online or check out the slideshow below of Dr. Bret Schneider, a consulting assistant professor at Stanford University and a practicing psychiatrist in Portola Valley, discussing depression and the brain.

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Now I'm just about the most rational, science-y person you'll ever meet. But the conversation with my wife had me thinking, what "weird" things do I believe in?

Even I have beliefs I can't explain. I have innumerable superstitions. For example, I always put on my right shoe first so it will bring me good luck for the day. I've had a tarot reading done and yes, I read the daily horoscope from time to time. I find my mind's contradictions amazing. My rational brain doesn't believe that these will bring me more happiness or wealth… no chance. But deep down, I want to believe in the power of a horoscope.

On Friday, March 6th, explore why people believe weird things with a talk by renowned skeptic, Michael Shermer. In Scientific American, he's written about the science behind our need to find patterns and the biological reasons why the brain might cause "paranormal experiences." He'll discuss superstitions, pseudoscience, and paranormal claims . For a preview, check out Michael's video Out of Body Experiences.

Michael Shermer presents "Why People Believe Weird Things", Friday 3/6 7 PM at Ohlone College. Tickets are $10 and can be purchased online. For more info, visit Ohlone College's website.

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Though it was McCarthy who persuaded his nine other colleagues at the conference to adopt the term "artificial intelligence" to describe the nascent field, the seeds of artificial intelligence were planted earlier. Alan Turing, who was instrumental in breaking the German's Enigma code during WWII, published a paper in 1950 that laid out what came to be known as the "Turing Test:" if a machine could carry out a conversation with a human in such a sophisticated manner as to trick the human into thinking that he or she was conversing with another human, then the machine would have displayed true "intelligence."

But nearly 60 years later, the world still awaits a machine capable of exhibiting "general A.I.", instead of the "narrow A.I." demonstrated by IBM's chess-playing Deep Blue or Stanford University's Stanley, an autonomous robotic vehicle, or other impressive albeit limited applications of A.I. For example, Deep Blue may be able to beat Gary Kasparov at chess but can it beat a 10 year-old at a game of checkers? The lack of a general A.I. is made even more stark when juxtaposed with Moore's Law, a maxim that goes back to 1965 when Intel founder Gordon Moore postulated that the number of transistors on a computer chip would double roughly every 18 months.

There's even a term – "Singularity" – that is being used to describe the moment when technological progress will leapfrog and herald the creation of computers that not only achieve human-like intelligence, but also give rise to a progeny of computers who will be smarter then their digital forbears. Though he didn't coin the term (sci-fi writer Vernor Vinge did), the most famous exponent of this belief is inventor Ray Kurzweil. He places the Singularity as occurring sometime before 2050 and believes that with the advent of this unheralded technological progress, mankind may solve some of our society's most pressing ills, such as global warming, and even conquer death, by uploading one's consciousness into a virtual medium.

Though this seems a far stretch from engineering a domestic robot like Stanford's Artificial Intelligence Robot, top A.I. researchers like Stanford's Andrew Ng and Daphne Koller do believe that computing systems will some day be as smart or smarter than humans. When I spoke with Dharmendra Modha about his work into cognitive computing at IBM, he talked effusively about creating an "i-Brain," a digital accessory that people could carry around, making decisions and processing information like its human cousin. But if you're like me, and lament those moments when you've misplaced your keys or other instances of poor neural performance, you can't help but think that such a device can't arrive soon enough. On second thought, I'll wait until v2.0 hits the shelves.

Watch the Artificial Intelligence: Thinking Big television story report online.

And don't miss our Web Extra: A Dose of A.I. In this QUEST web exclusive, Stanford University computer science professor and artificial intelligence (A.I.) researcher Daphne Koller provides an elegant explanation of how A.I. can be employed in the examining room to diagnose a patient's illness more accurately than a human clinician. Find out more and learn how medical diagnosis is just the tip of the iceberg when it comes to tasks that rely on making sense of a sea of data to arrive at an informed conclusion.