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New Treatments for Neurovascular Disorders

Posterior circulation. Gait and limited ataxia and dysarthria may be prominent. Vertigo and headache, perhaps less common. PCA is a beautiful vessel of course, at the very top of the basilar system. How it wraps around the ambient cistern, how it hugs the peduncles as it is heading back, how it supplies that whole portion of the thalamus back there and then heads right towards calcarine cortex. The beautiful syndromes of PCA all the way back. I tried to summarize them for you there. The thalamic and subthalamic supply arises from the proximal PCA, but there is this one variant that I’m interested in. I didn’t put it in because I found it in the exams I reviewed, but it’s just a nice variant.

Weber’s, very simply: W. Unilateral III with corticospinal tract involvement. Three as it’s coming out so a fascicular III. Benedikt’s: III plus corticospinal tract in the peduncle, plus red nucleus, plus brachium conjunctivum. So in all fairness, actually B is a little more proximal than C, but you know, B and C are in the middle. In other words, you are clipping III, fascicular III, corticospinal tract in the peduncle, red nucleus on that side and a brachium conjunctivum or superior cerebellar peduncle right at the crossing point.

Hemorrhage. Now this discussion takes two parts. The first is, there is the whole discussion about the typical hypertensive hemorrhage. Typical hypertensive hemorrhage, classical localizations. I list them for you there; putamen, lobes, then thalamus. I didn’t think the lobes were up there. I thought it was putamen, thalamus, cerebellum, pons. That’s what I always learned. But according to Case from 1982 - I provide the reference - they put the lobes up there. The bottom line is knowing that the putamen is number one. That’s where the hypertensive hemorrhages happen. But increasingly as people have been treating blood pressure so well over so long, we have seen the development of the non-hypertensive hemorrhages, which has been the subject of review articles by Carlos Case for at least the past five or seven years. So I’ve tried to take a few of those and summarize them for you. These are the things - not hypertensive - associated with intraparenchymal hemorrhage. Notice that I’ve moved completely from hemorrhages as a result of an ischemic lesion and like re-perfusion hemorrhage in a stroke. These are the primary parenchymal hemorrhages.

Oral anticoagulants. I can’t tell you the number of times I’ve ordered a CT scan in somebody on Coumadin - just because I’m worried about that - but the story is different typically in people who have anticoagulation-related disturbances. It’s the story of a more insidious thing like a subdural over time. It’s more insidious. Bleeding, kind of a leaching out of blood. The worst cases of hemorrhages that I’ve seen that weren’t hypertensive in nature.

Now a little more about amyloid angiopathy. A steadily increasing frequency with age. About 10% in patients in the sixth decade to as high as 60% in those greater than 90 of age. The deposition of amyloid is in the media and adventitia. I did see one case in which they presented a green filter picture of it and it really showed rather nicely the media and adventitia involved by this.

I sort of went over this whole issue of the different kinds of angiomas. Did I make that reasonably clear? Let’s just review that. There’s a difference, at least in terms of the pathology of these things. There is no intervening normal brain tissue in the cavernous type. There is intervening brain tissue in the venous type.

Hemorrhage in the posterior fossa. I haven’t seen a lot of cases like that. I guess they just get referred on to neurosurgery. But the teaching is that if the hemorrhage is larger than 3 cm you are thinking about ventriculostomy, decompression and very possibly evacuation of the hemorrhage in the posterior fossa.

A little bit about subarachnoid hemorrhage. For whatever reason, they love to talk about subarachnoid hemorrhage particularly in the orals, but there are a modicum of questions in the written portion of the exam as well.

Now we will launch into our discussion of saccular aneurysms. The prevalence of unruptured aneurysms in the general population is on the low side. Annual risk in un-ruptured aneurysms appears to be a function of size. Now greater than 1 cm associated with high risk. But the figure that I’ve seen more recently is 7 mm. I hope that they don’t try to give you grief on that.

The medical management of the complications: the major complications of subarachnoid hemorrhage - I take this from a large series on the subject - here are the major problems. Vasospasm of course, hydrocephalus a little bit later on, typically a week or more out. Edema often associated with vasospasm and associated infarct.

Treatment, medical treatment I think should be apparent to all of you. It has to do with intensive management and control of excessive blood pressure fluctuations really, because you want neither low blood pressure, which increases the likelihood of vasospasm, or high blood pressure which increases the likelihood of re-bleeding, highest in the first 48 hours after presentation. Hydrocephalus is a later manifestation.

The last page has to do simply with the so-called International Cooperative Study on the timing of aneurysm surgery to make this point. If the Hunt and Hess presentation is early, I or II, not III or IV, if mental status is preserved with no focal deficit, you tend to be more aggressive.