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New Treatments for Neurovascular Disorders

Point number one. There are these percentages for overall stroke types. So embolic, the most common at about 34% arterial disease, large vessel disease, accounting for 34%, 31% to embolism. Basically a rule of thirds. Then about one-fifth to lacunas and 10% to hypertensive hemorrhage and that is what they quote you.

Point number three relates to a very simple issue and that is that our job at the bedside - and this was raised in an article that has been quoted just far too often.

Okay, point number four: afro and Asian Americans may be particularly prone to the involvement of intracranial vessels. A couple of questions that I saw on that. As all of you know, diabetes and hypertension associated with lipohyalinotic change in end arteries, particularly as I mentioned, ventricular striates coming off the MCA system and thalamo-perforates coming off the PCA system. Atrial fibrillation, obviously a risk factor in cardiogenic embolization.

Okay, point 5A then just talks a little bit about how transient ischemic events precede the stroke that happens. We know of course about large vessel thrombotic disease and transient monocular blindness as a classical syndrome. I say transient monocular blindness rather than amaurosis fugax because people are using TMB much more than amaurosis fugax as a term these days.

Now we need to talk a little bit about these big therapeutic trials, and again I hesitate a bit because Iím entering into the world of controversy. What does not seem controversial, however, is the report about symptomatic high grade carotid disease. The answer is, surgery. Above what percentage of stenosis? About 75% symptomatic, hemispheric involvement, on the appropriate side, obviously. Yes, the indication for surgery.

I list in point six, six major AF studies that argue almost to a man, to a person, that low dose - Coumadin light, as we say - is good treatment for long term atrial fibrillation to mitigate or to decrease the likelihood of stroke in the longer term in known embolic disease.

Then with great fear and trembling I enter the discussion of the lytic therapies in stroke. Now Iím basing this discussion mainly on two major studies in lytic therapies and specifically Iím talking about tissue plasminogen activator here. Iím talking about the ECAS and the NINDS study. As you see in my notes there, the bottom line is that these were different studies. The ECAS study looks at the use of TPA within the first six hours, and NINDS in three. The issue here is that window of time from onset of symptoms to presentation and the earlier intervention and the use of TPR. Assuming that you donít have hemorrhage. Thatís the big one.

Transient ischemia. Now if I hear another medical student say, "Well, the definition of a transient ischemic attack is a clinical deficit that lasts for less than 24 hours and then gets betterÖ" I will puke and die. In that order, with a little seizure along the way. Because, to be perfectly honest with you, I think that definition clinically is perfectly useless to me because a transient ischemic attack, to me, lasts a really short time. Less than 20 minutes. If itís over an hour, Iím thinking stroke. Iím thinking stroke that maybe I can see clinically if I spend enough time there, or something. But Iím in stroke territory if itís over an hour. Because most transient ischemic attacks, and certainly transient monocular blindness, are brief. Really brief.

Now I want to talk about - hereís the fact attack now - specific weird things in stroke that you either should see pictures of or know a little bit about clinically. Letís begin with giant cell arteritis. Giant cell arteritis, thereís a weird thing about giant cell arteritis and that is, letís say for example that you are a giant cell arteritis. You are a disease process and you eat away at large extracranial vessels and the moment that you walk into the foramen magnum you say, "Whoa, I stop here." If you are giant cell arteritis it looks strange and it probably has to do with the difference in the media layer, the internal media layer, between the intracranial vasculature.

So you have the intensive care people all over you because this guy is clipping off cerebral cortex like it is going out of style, and you donít have the faintest clue whatís going on. So youíve gotten a leptomeningeal biopsy and the neurosurgeon says Ö he doesnít want to do it. Youíve got the angiographers, he doesnít want to do it.

Of these different entities, the one I want to spend a little bit of time talking about is the antiphospholipid antibody syndrome. Because I think it has a little bit more substance as a clinical entity. Antiphospholipid antibody syndrome has a kind of story to it. Let me try to give you a case of this story. Relatively young woman comes in with this history of family who had a lot of blood clots in the legs, for reasons that are entirely unclear to her. And unfortunately, very sad to say, in her early married life had a number of spontaneous abortions.

Fibromuscular dysplasia: itís a non-inflammatory process, medium and small vessels. Of course in the differential diagnosis for hypertension in the young person, since the renals are involved.

Migraine. Now there is this whole big literature that grows every day about the relationship between migraine and stroke. Perhaps you should be familiar with those studies, looking at the incidence of stroke risk factors in migraine populations, and they find that there are more risk factors in migraineurs when compared to age-matched populations.

Lou Kaplan, previously at Tufts and now at Harvard, makes the argument that one of the most undersold stroke diagnoses is vertebral dissection. Let me tell you about a case. A true case. A 38-year-old woman admitted to the far side of the hospital, where I have to go a long way to see her - this is entirely germane because I was being called there every hour when I was a first year resident - tells me this story because she comes in with fibromyalgia and a variety of other problems. She was in a car accident - but of course she was in a car accident - developed intractable neck pain and was describing for her nurse visual hallucinations.

I always found that discussing particular stroke syndromes was like a Ö people say, "Just read it." Well, youíve got to get a lecture on it. Youíve got to hear some of this. So letís talk about individual vessels and their associated stroke syndromes, sort of one by one. MCA we should all be familiar with. No? I mean seriously, we are pretty familiar with it. Those strokes in the MCA distribution more toward the back, more toward the front, certainly in the left hemisphere we should feel comfortable with that.

What about some of the other vessels? Letís review them. ACA, the one to know about is the recurrent artery or arteries of Heubner. It is recurrent because it takes off from the A1 division of ACA - what is the A1 division of ACA? Well, letís take MCA as an example. So your ICA, you are coming up and you become MCA the moment you give off ACA, now you are MCA. MCA dives parallel to the floor now in the sylvian fissure and then will become the candelabra at the end, in the superior and inferior divisions.

Another arterial syndrome that I think needs to be known about Ö everybody talks about the anterior choroidal, just like I was talking about with the Irving Cooper story. But hereís the anterior choroidal syndrome. So it originates from the ICA, the internal choroidal artery. A few millimeters distal to the PCOM and it supplies the optic tract and a little bit of medial temporal lobe, thalamus, posterior limb of the internal capsule.

In the posterior circulation. My chief of service was telling me, as I was priding myself on being able to tell him about Wallenbergís syndrome, he stopped me in mid-track. He said, "Youíre a neurologist now. Weíd be very proud of you if you knew the Wallenbergís syndrome as a medical resident, but now you are a neurologist. We assume that you know the Wallenbergís syndrome. Now letís talk about some other stuff." The problem was, all I knew about was the Wallenbergís syndrome. I didnít know there was anything else.

Of all these things to keep in mind, I like the one about the medial PICA. I also want to emphasize for you those things that predict for bad course in PICA in Wallenbergís syndrome. And they areÖ hereís the story. A guy comes in, a known hypertensive. Nauseous as hell, feels funny on his right face, ipsilateral hemiataxia, Hornerís on this side, decreased pain.

ICA, very similar to PICA as the name suggests. I had one guy, really weird, a colleague who said if he has two daughters heís going to name them Ica and Pica, and I said, you know what? You need a life. Whatís the difference between ICA and PICA, at least characteristically? The difference is deafness. ICA is the only stroke syndrome that I know of associated with unilateral deafness.