If we talk about dementia, the most common problem really is mild cognitive impairment.
This isn't dementia, it's the goofiness you get after being on bypass. You know, all the patients after they've been on cardiac bypass are just not the same, and they're a little kind of bewildered. It takes about 18 months for them to get better.
But many people do actually develop forms of dementing disease. And the younger you are, the more likely it is that you actually have an underlying pathologic process with a name added to it, like Alzheimer's or frontotemporal dementia or Lewy Body Disease.
And the older you are, the less likely it is to be a specific disease and more likely just to be little strokes from vascular disease. Just as you get in your legs from peripheral vascular disease, you get it in your brain.
The most common thing that people fear is called Alzheimer's disease. And it really is caused by a deposition of amyloid protein around your neurons, which causes the brain to atrophy. And if this is the normal side of the brain,
the abnormal would be on this side. You get these plaques and tangles. So instead of having a nice healthy brain like this, you wind up with a shrunken atrophic brain like that. The key structure in your brain for integrating memories is your hippocampus.
And if you divide your brain into kind of like RAM and your hard drive, the thing that links your RAM and your active memory and integrates it into permanent memory would be your hippocampus. And it's a beautiful structure,
it's got a lovely shape. It's got this little kind of curved shape. And often when I'm driving along, I'll see something that looks like that shape. Like, look at the rear lights on a Honda Civic. It looks exactly like a hippocampus.
Or at my daughter's birthday, the cake looked exactly like hippocampus. And often you'll be doing something and you're walking along and you see a tree that looks like the Carotid bifurcation. Or a tree in bloom, and it'll look like the lungs.
So there many shapes you see in nature, which are normal healthy things, and they have shapes that are analogous to anatomic structures. And it's a beautiful thing. Maybe I'm just abnormal, but I can't help but...
I'll be walking down the street and there'll be a branch in the tree. And I see these branches coming off it perpendicularly, and they look like the lenticulostriate arteries coming off the middle cerebral artery. So you might find things like this later as you walk around.
So there are things you can do about Alzheimer's disease. There are drugs, and then there's this whole exciting field of placing depth electrodes in people's brains and stimulating specific parts of the brain electrically, with essentially a pacemaker to overcome the dementing process, which is fabulous.
Imagine if you could be brighter, more alert, if you could reverse that process by putting depth electrodes under stereotactic guidance into the brain and stimulating it. And different parts of the brain have different results.
Potentially you could make somebody miserable if you put one of these electrodes in the nucleus ambiguous. You could make them miserable permanently. It could be a punishment. Or you could make them brighter by putting it at a different area
and amping up their intellectual activity.
So that'll wake you up. In terms of imaging assessment, imaging is critical, both MR and CT. And imaging over time, so sequential studies. Baseline six months, 18 months, two years, three years.
And you see brain volume loss over time in specific areas. And those areas that atrophy are specific to certain types of dementia. Certain diseases pick out different areas of the brain and cause them to waste. And this results
in certain specific kinds of cognitive deficits, and these can be tested for. And you can have specific neuropsychological testing that will detect errors of essentially function in patients with wasting of brain in specific territories. So I'm gonna show you some of these.
So this is a scoring system to look at the hippocampus. And you can see normal happy hippocampus here, and then you can see well, there's a little more space around it. And then over here, well, there's quite a bit of space around it now.
And then there's a lot of CSF in that lateral ventricle now. And then it gets worse and it gets worse. And that might take about three years to occur, and that would give you the inability to integrate your RAM, your active constant current memory, into your permanent hard drive.
And it may also make you forget things. We all forget things as we age. There's a normal forgetting process that increases with time. It's bothersome, it happens to me. It happened to me last night, very bothersome,
but it isn't abnormal. But in these people, they've got it to a stage where it is abnormal. So again here, you see pictures of the hippocampus, and they decrease in size over about 36 months. When I was a fellow, I spent thousands of hours
measuring hippocampal volumes, and trying to assign to those volumes certain degrees of dementia in patients and in epileptics. It's interesting. People with epilepsy also get hippocampal volume loss, and they wind up getting debilitated over time functionally.
It's a terrible disease. But this is a process which results in dementia. Here in the axial plane on MRI, on FLARE imaging, look at the Sylvian fissure here. And then about six months later, look at it here. So the brain is shrinking.
And this person has an increasing problem in integration of new knowledge and remembrance of old things. Here again, look at the CSF space around the hippocampus. And then here, and the overall brain volume is reduced. And then as you look further back,
in the coronal plane going back towards the occiput you see more volume loss.
Now, there are other types of things that can cause you to get demented. What I showed you first was Alzheimer's. This is just multi-infarct dementia.
So say you've smoked all your life. Maybe you have afib. Maybe you've got a dodgy left ventricle, and your aorta's full of plaque from too many bear claws at Tim Hortons or whatever. Or you're a diabetic
or you're a chronic hypertensive that's poorly controlled. Over time, you'll have insults to your brain and you will have small strokes. Not big enough to make you have a difficulty with your leg or arm or speech, but enough to hurt white matter.
And here you can see that these are three different people, and this is a grade one, grade two, grade three white matter disease. This is also associated with dementia. Okay, I'm gonna skip these. If you do a PET scan on these people,
you inject FDG or some other agent, you'll find that their brains are less active in some areas than others. On the left side, this would be a normal brain. The cortex is uniformly active. In the middle we see Alzheimer's disease,
where the parietal lobes are not metabolizing as much glucose as the frontal lobes. And that's a characteristic pattern of Alzheimer's disease. And you can see that the gyrite on that image are more prominent than on this image. So the volume is down.
On the far right one, that's something called frontotemporal dementia, or Pick's disease because it picks out the frontal lobes. And there you can see that the frontal lobes are less metabolically active. There's less red up there.
And again, you see a decrease in volume in that region. So these scoring systems exist, and they can be used to assess the degree of white matter disease. When you give a score to something, you can then communicate what you see.
That's the beauty of scoring things. It's a grade one, it's a grade two, and then you can have a probability of a certain kind of outcome based on that.
We always think of stroke as ischemic disease that results in a brain insult,
that has a specific physical manifestation of a hemiparesis or a drooping corner of the mouth or slurred speech or aphasia. Or the inability speak properly, dysphasia, or absence of speech, aphasia. And what we forget is that stroke itself
can have dementia associated with it. If you take out specific territories, like a laser-guided bomb you can absolutely make people demented overnight, because they just can't compute. Here we see somebody with bilateral medial-thalamic,
the yellow arrows, medial-anterior-thalamic infarcts. Really bad place to have a stroke.
This is a person who had a stroke in the area of the right hippocampus. So we've shown that hippocampal volume loss is a bad thing. With a stroke in that territory, it's clearly a bad thing.
So you can have strategic strokes and specific distributions that result in specific cognitive defects. So not only does this person have to overcome the left-sided physical weakness, the visual changes that occur
because of the ischemia down in the occipital pole, but now they've got cognitive interpretive problems that disable them from remembering what they're learning. So specific vessels, particularly the posterior cerebral arteries, supply specific territories that affect the hippocampus.
So there, you see the yellow arrows pointing to where the posterior cerebral arteries should be. It's absent. And on the right, you see the ischemia on diffusion-weighted imaging, which detects ischemia very beautifully,
in the thalamus and in the hippocampus.
The blood supply of the hippocampus is well understood. It's the posterior cerebral artery, which I tend to imitate vessels. It's not a good thing. But basically if that's the basilar tip
and I'm an aneurysm, right? So the PCA's go back like that. But before they do, they swing forward and they come back. And as they go forward, they supply the hippocampus. So taking out the PCA's really, really bad for brain cognitive function.
There is a little hippocampal infarct. Okay, and there we see it on the coronal T2 image in the hippocampus. A normal hippocampus, edematous ischemic hippocampus. Okay. Now, another wonderful little blood vessel in the brain
is called the anterior choroidal artery. It's this tiny one, whoops, up here. And it's really, really small, and it kind of looks like the Nike swoosh. It comes off the posterior wall of the internal carotid, and it goes like that.
And it supplies the internal capsule of the brain. And if your nobble that, it doesn't matter how good your brain is, none of the signals can get out of the brain in that side. And it's a devastating stroke. So this is a very important territory,
because you get ischemia in these kind of central wiring areas, the wiring harness of the brain, and people are significantly disabled as a result of it.
Okay, I'm gonna skip through all of this. I talked about amyloid being deposited in Alzheimer's.
There's another kind of amyloid that isn't deposited in nerves, but is deposited in vessels. And here you see these little black dots, and these are gradient echo images, SWI or mag-transfer images, which are oriented towards the visualization
of hemosiderin and calcium. And so these little black dots are little hemorrhages. And these occur in people with amyloid angiopathy. Amyloid now deposited in vessels, making them friable, which results in hemorrhage. So these people have a characteristic MRI,
it's a mini kind of thing. You look at that, as I would or you would or a computer would, and you say this is amyloid angiopathy. I know what this is, just like you look at your Aunt Norah
and you know it's your Aunt Norah because that's what she looks like. And these cause multiple small hemorrhage infarcts and you get demented from that, too. Sometimes they bleed and you get Loeber hemorrhages. Now I mentioned something earlier
that picked out the frontal lobes, Pick's disease. So here you see the frontal lobes are atrophic and the ventricles are huge. So frontal lobe is essential for artistic endeavor, complex thought, integration of complex things, memory, personality.
I used to jokingly say that you just needed one lobe to be continent, one frontal lobe to be continent and socially acceptable. But if you lose two, you are neither of those things. And it's a devastating type of... And that sounds awfully insensitive, doesn't it?
But I don't mean it to be, really. But when your brain is like this, you're pretty much in terrible trouble cognitively. But that's the disease. Frontotemporal dementia picks out the frontal lobes. Just remember that, picking out the frontal lobes.
Now, this is what Robin Williams had. Poor guy. He was such a gifted comedian. You can imagine him as an inventor. The rate of association of thought which gave him that gifted, unexpected humor
is actually very similar in many ways, I think, to the synapses which occur in the event of mind that creates devices. But he would've realized that his speed of association was slowing down, that he was impaired in thought
and that he was facing a significant problem. He learned that he had Lewy body dementia and he decided to end his life, which is a terrible thing. There is no specific appearance of this disease. It may appear clinically like Parkinson's disease, but that's what he had.
So you get a little volume loss, the space around the hippocampus gets a bit bigger. The hippocampi themselves are smaller. And it's a non-specific appearance.
progressive supranuclear palsy.
And it has a classic appearance. On the sagittal images, it looks like a hummingbird. So you see the hummingbird on the left. You see the chubby tummy and the breast, and you see the beak. And this is what they look like in real life.
So progressive supranuclear palsy, it used to have a different name. It's one of these atypical Parkinsonian syndromes. So there you go, that's the progressive dementia. And gait problems occur from this disease, characteristically causing this kind of wasting
of the brain stem. See it? Once you see it, it's hard not to see it.
Okay, multisystem atrophy. It used to be called Shy-Drager syndrome,
so we all learned that in med school. But this has a characteristic appearance, too. It's a Parkinsonian-like disease, and it looks like a hot cross bun. So in the brain stem, in the pons... I find it best to create these analogies
so I can remember them, but it kind of puts you off hot cross buns, which I really like. Hot cross buns with salty butter, brilliant. So there's the pons, and you see that appearance. And then on the right, you see the hot cross buns.
So that's what multisystem atrophy does, and it's a really bad, bad disease. It's a miserable dementing process. It's a terrible disease. There's another appearance of it. Looks like a hot cross bun.
If you were English, you might say it looked like a St. George's cross
Okay, mad cow disease. Rare, fortunately, and has a characteristic appearance. The cortex is bright on diffusion and on FLARE.
And you get this cortical, kind of inflammatory, ischemic type process. And in the pons, sorry, in the thalamus, in a posterior aspect of the thalamus, you get what's called the hockey stick sign, which would be easy for you guys to remember.
And it sort of looks like a musical note or a hockey stick, because it is this area of high signal that occurs in the thalamus. So that's mad cow disease.
Okay, Huntington's disease.
Here, your brain loses the caudate nucleus, so these guys. These guys are really critical to cognitive reasoning. And over time, they shrink. So here you see a patient with caudate, caudate, and here they're gone. And there are famous examples of Huntington's disease.
Arlo Guthrie, you're probably too young to know him. He was a musician. And his son, both of them, both of them had this. No, Arlo was the son. I forgot the father's name.
But Arlo knew he was getting it and still wrote music. And he was like, a Jack Kerouac type figure. If you go up to that great bookstore up there, you'll find things on him. So caudate wasting is classic for Huntington's disease.
Now, the most common thing we see in Toronto, actually,
probably on-call at nighttime, are the traumatized brains of the alcoholic and schizophrenic population who live on University Avenue. And they all go to Mount Sinai and they get their head CTs, and they've had some unfortunate event.
Over time, they have repetitive trauma. And the brain shears against the inferior aspect of the frontal lobes, shear against the inner table of the frontal bone. Or the temporal lobes bang into the interior aspects of the middle cranial fossa
and hit the greater wing of sphenoid. And and because the brain goes forward, it comes back, and then they get a contrecoup injury in the region of the occipital poles. So they lose the temporal lobes, they lose their hippocampus,
and they lose their frontal lobes. And they get a traumatic brain injury. Now, our hockey players get this too. And you know, you've gotta wonder. Poor Sidney Crosby. What's gonna happen to him as he ages?
So I'm part of our concussion group. I race cars as a hobby, and I'm very aware that you have rules around concussion and hockey and horse riding and sailing. We have no rules around it in motor racing. Kids can go-kart
and they can do 90 miles an hour in a go-kart. And they have the little skinny necks, the big heavy helmet. And there are no rules to talk about when they can go back to racing after a concussion. So normally, you see nothing. But if you do see something,
you might just see these little black dots. And they look like the little black dots you get in amyloid angiopathy. It's hemociderin. A shearing injury, as the cortex and the gray matter moves separate from the white matter
at different speeds. And they get little hemorrhages in their brain. And this is associated with cognitive impairment.
Okay, this is one of my favorite characters in... Ever, like ever. So he invented the cyclotron.
And from that we have molecular imaging, and from that we have PET. And how he invented the cyclotron was in 1914, he asked his boss Rutherford if he should go on vacation. And he said, "Oh yeah, off you go." So he went to Germany and he got arrested.
And he spent four years in a horse box, and he was a physicist, we thought, for four years in isolation in this horse box. While he was there, he came up with the concept of the neutron, and he invented a way of identifying it using a cyclotron.
So in 1919, he built this and he eventually got a Nobel Prize. And then he started the British atomic bomb program. A gifted, gifted man. So he built this huge cyclotron, and he produced positrons from it.
And today we have these cyclotrons because of him and the horse box, which is a phenomenal indication of the need for isolation if you want to invent or think deeply. (audience chuckling)
The opposite of how much of us live. And so from this, we have PET CT and PET MR, from him in 1914, like 100 years ago. Now this is a really cool interaction when we do we PET. And we forget that what we're actually looking at is the positron is antimatter.
And when it hits an electron, it's an annihilation reaction and energy is released as a waveform. And that's detected by the PET CT detector, which doesn't spin unlike other CT scanners, the PET detector.
So this is really pure quantum physics, created in the mind of a man as a prisoner of war. It's quite an incredible story.
But this allows us to image dementia and traumatic brain injury. When a tracer has been developed,
initially people bind it with carbon, because you can bind anything to carbon. But that has a very short half life. And for it to become commercially available and used by many, many centers, you have to attach it to an isotope with a longer half life,
which is fluorine. That's why you use FDG, because it lasts for ages whereas carbon lasts for less than an hour. So in the early research stages, you always have carbon-11 and then things attached to it. And Pittsburgh came up with one agent
which helps identify amyloid, and somebody else came up with somebody, with another agent that allows you to develop tau, which is the thing that is found in concussions from trauma. Okay, so you can image the brain of people with these different diseases.
And on the right, you see imaging of a person's brain who has amyloid deposition from Alzheimer's dementia. And it's imaging of the amyloid plaques. These are images of football players with concussions and dementia. This is normal, healthy distribution.
And this person who is mildly demented in the middle, you can see there's some deposition in the territories where you get traumatic injury to your brain. And on the far right, this guy is clearly very demented and he has distribution everywhere. - [Man] Trump?
(audience chuckling) - Sadly, no. So this is tau protein occurring in traumatic brain injury, with increasing distribution on the far right in somebody with tremendous dementia.
Now there are things you can do about this, as I mentioned.
You can put stimulators into peoples' brains, and you can amplify that which is still there by putting these depth electrodes there. And here's a person who's got volume loss there in a stereotactic frame. And these are depth electrodes going down into their brain,
in this case for Parkinson's disease in the sub-thalamic nuclei. These are made of platinum and iridium. And basically, you increase the energy going through them until you get the response you want. And they have a pacemaker-type unit,
which is placed under the clavicle. There are different territories you can stimulate. One of my med students drew this. And basically, you can stimulate the hippocampus and the fornix. And this person has atrophy.
You see all the space around the hippocampi and the brain volume loss. And then you put in depth electrodes down into the fornix, and you can halt or slightly improve the progression of their disease, and use electrical stimulation
to reverse the process somewhat. It's imperfect, but it's very, very interesting.
Okay, there's one reversible form of dementia, and that's called normal pressure hydrocephalus. And basically, this is like hydrocephalus that you see in children,
except it's not a high pressure in the brain. People, the three Ws. These people are wet, wobbly, and wacky. They pee in their pants, they are falling over all the time, and they're demented.
And this is reversible. So you put in shunt catheters. Now, I think this is one of the worst-managed diseases ever. And I have some patents in this area. I wanted to do something about this because my cousin Oliver had untreated hydrocephalus
when I was a kid, and I probably was, I stayed away from him. Intellectually he was fine, but he had the head the size of a basketball. And you know, these catheters are thick-walled, narrow lumen, and they're not coated with anything.
It's archaic, and we could do such a better job by... If you can do radial access, we can do that better. So on the left side, you see a patient with enlarged ventricles. The brain is pushed to the side, and on the right side you see the brain
of the same person after shunting. So brain has plasticity and can respond to these things. And it is one of the few reversible forms of dementia. It's about 15% of demented people. And it requires careful identification of these people.
Now, currently shunts are misplaced,
and you'll see shunts in all sorts of places. They're placed by the least-trained neurosurgeon, often at the bedside, blindly. It is medieval. And you'll see them causing strokes, you'll see them in the wrong place,
you'll see hemorrhage along their tract about 15% of the time. So I was bothered by this, so I got a box of heads. It's not often people say that. And so I practiced for several nights in a row, different boxes, right?
And then I used a burr hole, which is just like opening a bottle of wine, and a micropuncture kit. And I passed a wire into the ventricles, and I found I could do it with CT fluoro reliably. And then you can move around in the ventricles.
So then I used a little microcatheter, and I was able to navigate. And I was able to stent the aqueduct to Sylvius. So this is really simple. But people in different silos don't think like us, and we don't cross-pollinate enough.
So there's lots of things we could do that are fun. This is a live patient, and she had slit ventricles. And this is just a Toshiba, you know, fourth slice CT with CT fluoro. And that's a micropuncture,
a needle going into her ventricle, hitting it the first time. And then exchanged over a wire and placed a shunt. And you know, normally there's all this kind of back and forth. And over time, people lose brain.
So this is the way, I think, we should do it. I did that nine years ago. And you know, it was very elegant.
Okay, let's talk about back pain in the elderly. Every Friday and Thursday, I treat two people and I see about five other patients.
And I love treating elderly people. I have sort of two parts of my practice in terms of spine intervention. One is women who can't sit. There's a whole population of women who can't sit. Women get back pain for different reasons than men,
and yet we read their MRIs just the same and it's wrong. Because women have all this stuff in their pelvis that can compress the sciatic nerves, and endometriosis can go anywhere, and implant and lumbar sacral nerves can cause pain. So I have all these women who come into my office
and they stand. And often they turn out to have Tarlov cysts in the sacrum. And I've treated about 213 of them, published a paper in AJR and that. Then there's the other population, the elderly patients. And these folks, they have backs like this.
And they've had multiple compression fractions treated by vertebroplasty. They have spinal stenosis. There's nothing wrong with their brains, and yet because they can't walk they wind up in a nursing home
because they can no longer live independently. So I'm fortunate to work in a Portuguese neighborhood. I see a ton of little old ladies right before Easter and right before Christmas, Little Nonas. And I sort of do little nerve blocks,
and then they go home for Easter and for Christmas, and they can bake and they're all happy. And they come back next year. It's great, it's lovely. And it's very low stress and it has a big impact on social networks.
And it's terrific. Now, the conventional surgical alternative of this will be this. So Peter and I and others have developed methods of treating compression fractures. And I had the pleasure working with Cook
for many, many, many years on this, and I've accomplishments I didn't disclose because all the Cook vertebroplasty stuff is mine. But you know, if you have one fracture the risk of another one goes way up. If you have two fractures, the risk increase 12 times.
If you three fractures, the risk goes up 75 times, which is pretty bad. The cement we inject, it comes from the per specs in the cockpit of this airplane, the Spitfire. It's polymethylmethacrylate.
And so you know, it's an embolization of a vertebral body under X-ray guidance. That's how I see it. Here you see the injection of cement. You see the little particles, the little fishies going in. And then we watch it carefully
to make sure you don't fill the epidural space or it goes to the lungs or anything like that. It's one of the simplest things I do, but it brings great pleasure because people get pain relief. It's a very simple reason that I like being a doctor. I'm not sure I can express it any more complex.
So there you go, anyway. So the cements, I worked very hard to make them dense enough. I now have four different cements. One is really dense for L45. One is really hot.
Oh, and you can navigate vertebral bodies by using curved needles and things.
This is one of my new cements called Exofix. It's for tumor. It polymerizes to 88 degrees Centigrade, so it can cause an RF type energy deposition
in the vertebral body. There's another one that's really cold for osteoporosis, because you don't wanna kill the residual viable bone. There's one that's really dense, and there's one that responds to parathyroidoma. PTH.
You should learn about FORTEO, it's fantastic. It's the only anabolic bone agent. All these etidronate things, they actually stop bone turnover and impair bone growth. So I'm running out of time. Oh, I made a device that vibrates,
that allows you to deliver cement at ultra-low pressure. It's a little ball bearing in a raceway. You attach compressed air, you put the needle through the middle, and you get lovely bone cement distribution.
They call it benign, but it actually has a malignant outcome because people die.
Or by plating. And so I've been working on using ultrasound-guided nerve blocks, and then the injection of cement into the region of the rib fracture. So we can have an active program to treat rib fractures.
Elderly women or men with osteoporosis who fall and break ribs, if they have more than four rib fractures they have a 40% mortality. This is the kind of stupid benign disease that people shouldn't die of.
Peter and I worked very hard on the use of my ozone device to treat herniated discs. O3 shrinks discs. This is... Go on, play. Darn, okay.
So O3 is very astringent, and it...
I thought it was gonna play, darn. Okay. It basically would've dissolved that glove. That's what you would've seen. So this young lady had an L5 S1 disc herniation.
That's my needle going into L5 S1 under X-ray guidance using an extended Scottie dog approach. There's the gas in the nucleus pulposus. This is her disc initially, and that's the disc at six weeks. So it shrinks discs.
And in our trial, we have 68% at one-year success rate. This is an outpatient procedure. It takes about 30 minutes to do it, and it's same-day procedure. And there she is again on the left side, pre, and on the right, post.
You see the decreased mass effect on the exiting nerve root.
The last thing I wanna talk to you about. You're at tremendous risk of DNA damage from your occupation, from X-ray exposure. And it's a serious problem. In fact, there's a paper last year
that US X-ray techs have like, a three or fourfold increase of brain tumors. And so when you look at medical imaging volumes, they continue to go up 80 million CTs a year. Most of them elective, but 30% of them emergent. The younger you are when you're exposed to radiation,
the greater the risks you have, because your life expectancy is longer. So X-rays impinge on water molecules, and then they split them and they create free radicals, which attack your DNA. And then your DNA responds to this
by putting oxygen molecules on those free radicals. So it's an oxidated injury. And that oxidated injury can be countered by antioxidants, okay? So there are methods in our bodies for repaiting this DNA damage.
There are two in particular, H2 Alpha and P53. You've heard of BRCA one and two, breast cancer-related genes. Well, the defect in BRCA one and two is actually a P53 repair mechanism. So these are essential to maintaining the integrity
and competence of our DNA. Bottom line is, factors that increase your risks of DNA damage from radiological studies. X-ray or CT or Nuc Med, or MRI. MRI causes DNA damage, as Peter Canaday published recently.
CT with contrast while on chemotherapy. Each thing... CT with contrast causes more DNA damage than CT alone. CT with contrast in a patient on chemo causes more damage than CT with contrast. Genetic inability to repair your DNA
is something that we should look for in ourselves before we pick our professions. The cancer risks have been identified and published in the Canadian Medical Association Journal. Every 10 millisieverts of low-dose ionizing radiation is associated with a 3% increased risk of developing...
A malignancy. So we published this paper in the Canadian Association Radiologist Journal. Flight crews are considered radiation workers, by the way. So if you work for Air Canada or any airline, whether you're a pilot or a stewardess,
you're considered a radiation worker because there's solar radiation you get. It's related to altitude. So we stand in X-ray beams all the time doing procedures. We know that when we did this in the 1900s, it worked out badly, yet we still do it.
Initially these are radiologists sitting in front of their patients in the beam. And this is Conrad Rontgen's wife's hand, as you know. But ultimately radiologists, and this is an image of a radiologist's hand. They lost fingers and they lost noses,
and they died of oncologic problems. This is the left leg of a bunch of us standing here. You can see we have no hair on our left leg. That's because it's beside the X-ray tube. And so we're in the beam during these procedures. So I just published in JVIR a very...
It was a hard paper to write on cataractogenesis and our understanding of that. And basically, the cataracts you get from X-ray exposure in the angio suite is different from the cataracts you get from aging. It's in the posterior chamber of the cataract.
It's a specific thing. This is another paper that I've been involved in. The dose to the left side of her head is six times higher than the dose to the right. And this correlates to the paper from Japan discussing 31 left-sided brain tumors
in Japanese interventional cardiologists. So should we be screened for mutations that impair our ability to repair DNA damage from X-ray exposure? It's worthwhile considering. Because if you have a BRCA one and two mutation,
if you are Ashkenazi Jewish, male or female, you've got a 2% chance of having this. Now if you'd have a mammogram, they would say you should have an MRI instead. But would you choose interventional radiology as your field rather than ultrasound?
So it's something to think about. So what happened was, this is my son with our dog. And we went for a walk. We bumped into a guy, and it turns out the two dogs played together. And he told me that, we talked about what we worked on.
And he asked me what I was thinking about or working on, and I told him about the antioxidant project. And unbelievably he said, "Oh, I make antioxidants." I met this person because of the dog. So we did a trial using his antioxidant. And then I was out in Dalhousie,
and I found they have a lot of apples out in Nova Scotia. And they try to do different things with the apples, and they extract from the skin of the apple something called quercetin, which is what stops apples going brown. And you bite into them when you break the skin.
So we added quercetin to our formulation. I'm not sure if you can read this, but basically beta-Carotene, vitamin C, quercetin, alpha lipoic acid is a formulation we came up with. I've just published this in March,
giving that formulation to patients who are having bone scans. On the left in blue is the pre-bone scan level of DNA breaks. On the right in red is the number of breaks these five patients had after injection of technetium MDP.
Okay, now the next group got pre-medicated with our formulation, and this is what happened. So on the left is their baseline, and on the right in red is the number of breaks they had after.
So we can pre-medicate people against DNA breaks. That's pretty darn cool. So I think we should probably take something like this on a daily basis, and probably all our patients should receive similar pre-medication
prior to procedures or dental X-rays. And maybe we should do it prior to airline flights, too. Now, weirdest thing. So the company who I hope are gonna make this for me, in terms of coincidences, are in Quebec near the airport on Kieran Street.
(audience chuckling) I apologize for going over. I tried to fit too much as usual. - [Man] You've still got time. - Do I? Well.
(audience laughing) No, I think I have quite enough. Thank you very much. (audience applauding) Oh, one last thing. My research, I should mention this.
This is Ron Joyce, the founder of Tim Hortons. And that was his spine I showed you, with the multiple fractures. He's been a wonderful supporter of my research. He donated to the research program, and that's how I have the time to do all these crazy things.
He's a terrific person. So he and Tim Horton funded Tim Hortons. And he's the guy who opened their first shop in Hamilton. - Okay, as usual I feel completely inadequate after listening to all that. At any rate.
So if that didn't give you guys something to think about, then there's no hope for you. So do you have any questions for Dr. Murphy? (incoherent chattering) - There are different kinds of tremor, and there are things that can be done about that.
There are certain strategies, cognitive therapies, behavioral therapies. But if it's severe, if it's affecting your life, there are procedures you can have. But there are also cool technologies to reduce the impact. There's a wonderful fork,
and it has in the handle a tool which assesses the frequency of your tremor. And it neutralizes the movement of the spoon or the fork. So only the handle is moving, but this portion isn't oscillating. So you can eat.
It's a really cool, I love that kind of inventiveness. They have things you can do. You can have MR-focused ultrasound ablation of the portion of the thalamus which would cause the tremor. Or you can have depth electrode placement and ablation of that focal area,
whether it's unilateral or bilateral. Or you can have radiation therapy. And you can burn a two or three millimeter hole in the thalamus and affect that center that would be causing that tremor. So there are many things that can be done for that.
Okay, any other questions? Okay, thank you very much. (audience applauding)
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