New Treatments for Movement Disorders

I am going to be spending more time talking about differential diagnosis in a little bit, but there have been a number of articles in our literature, in the movement disorders literature, in recent years talking about the thing we tend to confuse most readily with idiopathic disease, and that’s multiple system atrophy. Now multiple system atrophy comprises three different entities. The three different entities are OPCA, Shy-Drager, striatonigral degeneration. So the three are olivopontocerebellar atrophy, striatonigral degeneration and Shy-Drager. Now why are these three together? Well, because they have been identifying some highly clinically heterogeneous but what seems to draw them together is the presence of these argyrophilic cytoplasmic inclusion bodies, typically in oligodendrocytes. This list from Quinn is really to point out to you some of those things that are heralds of multiple system atrophy in the same way that we can think of the kinds of heralds for idiopathic disease. So, say for example, if I see somebody with disproportionate antecholis. Not just the sort of flexed posture, but actually that neck tucked down forward, I’m beginning to think of something else. If I’m hearing the story of wife complaining violently because husband with this disproportionate antecholis spends the entire night keeping her up with outrageous stridorous snoring, suggesting abductor vocal paresis – another characteristic feature of multiple system atrophy – in association with sleep apnea. I love this one. The involuntary sign, which actually to be perfectly honest is entirely non-specific in my clinic. Other things, other kinds of autonomic features, Raynaud’s phenomenon and of course the story of early urinary or bowel difficulties that you certainly would not expect in idiopathic disease in its early course, say within its first 5-7 years. I also find in this population that they are exquisitely sensitive – for whatever reason – to levodopa. These are the people who get very nauseous on it, or very orthostatic on it and at very low doses.
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So now some comments from Quinn’s list about some characteristic clinical features of this entity, multiple system atrophy, and three diagnostic entities that he thinks are most commonly confused with idiopathic disease. Ole Hornikowitz who was responsible for really describing in the greatest detail, in the late 50’s and early 60’s, the specific apparently specific cell loss to the pars compacta of the nigra, has made some arguments recently that it is striking to him how much – if you take a look at quantitative dopamine in the brain of parkinsonian’s – that the area that seems to be hardest hit is the putamen. Now a little bit later we are going to go through that horrendous wiring diagram that for some reason is so … everybody talks about it. For those people who go to the movement disorder section, I don’t know of any talk that doesn’t go over that ridiculous wiring diagram. So just in case they hit you with it – you know, movement disorders is not all of clinical neurology – but just in case I’m going to walk you through that diagram a little bit later on and why, in that diagram, the putamen might be of significance. But the point here is that the putamen seems to be hit relatively hard. This is a graph showing the relative dopamine ratio from caudate to putamen in, for example, three different related parkinsonian disorders. Or differential diagnosis of parkinsonism. He goes on to say that if you start talking about comparing dopamine in putamen versus the place where we think the lesion is in Parkinson’s disease, we find surprisingly that the putamen seems more hit than the nigra. Which seems strange. Except to say that that’s the projection pathway, so maybe that’s the reason why. But Hornikowitz is making the point that just when you think that you know what’s going on in Parkinson’s disease, the pathology is restricted to the nigra – well, of course it’s not. Extra-nigral involvement is one of the key features of this disease and that the extent of that extra-nigral involvement is going to play an important part in levodopa response, for example. And that’s basically the argument that Hernikowitz is making.

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