PSP

PSP, the major features of that disorder there. To organize your trivia, I just gave you that little vignette a little while ago. You know what I mean by supranuclear gaze palsy, you know that there is a difference in the disease processes at different ages; Niemann-Pick in youth, Whipple’s in middle age and PSP in older ages. Men tend to be involved, and there is a picture associated with progressive supranuclear palsy. It has been termed, rather maliciously it seems to me, as the “stupid gaze” of PSP. They don’t like PSP. They also talk about the idiot pleasure of multiple sclerosis, and all that. They are brutal in these descriptions. But in PSP, I hate to tell you, it is rather accurate. So it’s the kind of thing where you walk into your clinic in the morning, you’ve had a cup of coffee at Starbuck’s – this is the life of a movement disorders person – you walk in, you pass by the usual hyperkinetics and then you come to one guy who is sitting there going… then you ask him to generate a saccade because you’re a very good neurologist, I’m a very good neurologist and so that’s why I shall test saccade. “Look here, now quickly look here.” Right? Now what do they have to do? They have to go through some lurching and entire movement of the head. “You don’t have to move the body, I’m just asking you to move your eyes.” And the reason why is because early in this disease they lose that saccade. But that happens in a lot of extrapyramidal diseases. You watch the saccade in the parkinsonian, its sort of slow and viscous and sort of saccadic inclusions in smooth pursuit. That’s an early finding. It’s seen in Huntington’s disease too. Then as time goes on they lose their capacity to generate saccade entirely, as they lose down-gaze first, up-gaze later. Giving rise eventually to virtual ophthalmo-paresis. But it’s supranuclear because you can overcome it with head movement in the oculo-cephalic maneuver.
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Okay, so here’s a story. This guy I trained with – and this guy was smart – I went to a very competitive program and this guy was smart. And he was like a M.D., Ph.D., he had published in Embo Journal. I didn’t even know what Embo Journal was. This guy is getting into all these journals. I’ve been giving these talks for a lot of years and about three years ago I see him in the audience, and I figure he’s going to give talk or something. He comes up to me and says, “I missed the Board by one.” He missed the Board by one? This is a guy who on his NCAT’s scored, like they had to rearrange the scoring system for this guy. He scored on his SAT’s … that’s why I hate the Boards. That’s why I like to give these talks because it’s different. It’s a different approach to how to deal with this. It’s a different way of organizing your data, if you know what I mean. It doesn’t reflect on your capacity as a clinician, to be perfectly honest.
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Machado-Joseph’s disease. I mention it because there is a lot of interest in the spinal cerebral ataxia’s. Seven types have been identified. I’ve seen seven and they are all CAG, Triplet repeat diseases. Basically there are now chromosomal associations for at least five of the seven types. But the concept here is that all these ataxias, they think, are associated with Triplet repeat disease. You’ve got to know a little bit about the Triplet repeat diseases. The paradigmatic Triplet diseases: Huntington’s disease. Autosomal dominant, one of the few associated with chromosome 4. The characteristic presentations of Huntington’s disease – I’m speaking to a sophisticated audience, I will not dwell on the obvious – but Huntington’s disease can present with the early behavioral disturbances without a movement disorder at all. It can present in its rigid form early on, it can present in its hyperkinetic form early on. Many different forms of the disease. There are a few things that we know; the length of the triplet repeat seems to predict the earlier presentation of the disorder but beyond that, we don’t know. The protein product from that gene abnormality in chromosome 4, the significance of that protein product is not clear. Huntington is the name of the protein product and we don’t know the significance of why that particular protein product is involved in the pathogenesis of that disorder. There is the phenomenon of anticipation, that is to say, earlier onset with length of triplet repeats.

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