Re: Jane Questions...

[Guest guest]

Hi Jane, good luck with your book.

My Warren first showed problems with dizziness, lack of balance and fear of

driving,slowness in walking (he shuffled along like Charlie Chaplin) these

were things we noticed about 3-4 years ago but he wasn't dx'd until Dec

1999. Also his short term memory was starting to go, he had had angina a

couple years before and the Dr's told him that this happens sometimes and it

would return, it didn't!

After he retired and we settled down after 4 months of travelling he started

have dreams and talking in his sleep, which he never had done before, and we

laughed about what he said in his dreams. He really tried to act out a lot

of things but nothing that would harm me. Until now we didn't think much

about it but realize it was probably the start of this. This was 12 years

ago. Now he moves a lot and legs run and talks in a jumble that is not

understandable.

Hope this helps

Jane Questions...

Greeting all,

Thank you so much for the input I have gotten on these scientific questions.

You have helped a lot. Also, yesterday I went to Borders and learned quite

a bit. Better than a library!

I am not planning on writing about glial cells (I understand better what

they are now) or synuclien or any other mumbo-jumbo, because readers don't

really care (except a few specific cases I can think of...!) But you gotta

know what the heck you are writing about.

I will be reading every day (one has to...catching up after two weeks

off-line was a chore. Phew!)

My next question is: what were the first symptoms you noticed? It sounds

like violent dreaming is a big one. What about balance, dropping things,

forgetfulness, or....?

Please chime in with ANY information you think might be interesting or

helpful. Thanks again, and here's to insight, acceptance, and enlightenment

in the new year!

Jane

12/31/00 11:08 AM, woodford at haq@... wrote:

> hello Jane,

>

> It sounds like a wonderful idea to write a book. If you are going to

include

> some science along with all these wonderful anecdotes from the MSA

patients,

> though, you need to get some basic understanding of the Nervous System.

>

> A simple book, such as a nurse's Neurology book would help you.

>

> Firstly, the glial cells are not stimulating neurons, i.e. they do not

> directly send impulses to other neurons or to muscles. Glial cells are

> supporting cells of the nervous system, and there are several types.

>

> Neurons that send impulses do so by way, mostly, of

> neurotransmitters---chemicals that cross the space to other neurons or to

> muscles. There are many types of neurotransmitters, from the first and

well

> known, acetylcholine, to norepinephrine to dopamine and to less known

smaller

> molecules called neuropeptides. Acetylcholine and norepinephrine are the

main

> neurotransmitters that supply the peripheral striated muscles and smooth

> muscles. Dopamine is a neurotransmitter in the brain, among many other

> neurotransmitters. It is especially present in the basal ganglia, a part

of

> the brain that deals with motor function, and dopamine there is what is

> missing in Parkinson's Disease.

>

> Messages from the brain get sent through many relay sites to the final

> peripheral nerve that stimulates muscle. So malfunction can occur in the

> brain, at the relay sites, or at the final neuromuscular junction. This

can be

> caused by a lack of neurotransmitter, or by a deficit of neuronal

capacity.

>

> I'm sure others can answer you specific questions more completely, but I

can

> address part of them. Some can't be answered at all.

>

> 1) There are researchers who are really hot about inclusions and about

ASN.

> Read their papers, but don't believe everything you read. This may just be

a

> coincidental finding, as aluminum was in Alzheimer's brains.

>

> 2) Cytoplasmic inclusions can not be thought of as tumors because they are

in

> individual cells and don't make up a mass of cells.

>

> 3)I don't think that anyone knows this.

>

> 4) Right now there is what I consider an artificial division in types of

MSA

> based on regions of the brain affected. Since there have been few

autopsies to

> show that diagnoses based on functional deficits are correct, I believe

this

> to be yet shown to be a viable division. The MSA web site has information

on

> these purported types.

>

> 5) I don't know.

>

> 6) Orthostatic hypotension is caused, as I understand it, because the

neurons

> to the smooth muscle of the blood vessels do not produce enough

norepinephrine

> to automatically constrict the vessels, thus not raising the blood

pressure to

> compensate for standing, as it normally would. In Pure Autonomic Failure

it

> was thought that the deficit was in the peripheral nerves, yet I have read

> that in MSA, the deficit of orthostatic hypotension is in brain control of

the

> autonomic system (not the same location as the basal ganglia or the

> cerebellum). Conflicting ideas.

>

> 7.) Ask the experts.

>

> 8.) Ibid.

>

> 9) The first quote means that synucleins, in very similar forms, are found

> throughout the vertebrate kingdom. Their DNA patterns are very similar.

> The second quote means they are RELATIVELY abundant in neurons, as opposed

to

> other cells, like, say, liver cells. And, back to anatomy---the end of a

> neuron has special sturctures called presynpatic terminals. Terminals,

meaning

> the ends of the neurons, and presynaptic, meaning that portion which comes

> before the space between the neuron and the next neuron or the muscle. The

> space is called the synapse, across which the neurotransmitter chemicals

pass.

>

> I hope this has helped some.

>

> Don't be dismayed at the wealth of information that is contradictory, or

> doesn't make sense. In research, that is the period in which the most

> discoveries are made because there is a big dialogue among researchers,

and a

> sound explanation comes out eventually.

>

> Barbara J. Woodford, Ph.D., retired neuroanatomist and neuroscientist.

>

> [Jane wrote]

>

> My name is Jane. I wrote to the group already once or twice, a few weeks

> ago. I was hired as a caregiver for a man with SDS, three years ago. The

> experience had a profound effect on me, and I want to write a book about

the

> experience, about him, and SDS. I have set aside the next two months to

> write, and will see how it goes.

>

> I have been listening to you all for about 6 weeks now, and feel I almost

> know some of you. It is a privilege. I have some questions, and surely

> more will follow. I hope you won¹t mind my asking. Ask me anything you

like

> about my background, the tone of the intended book, etcSanything. I have

> several goals for this book, but one huge one is to bring attention to

MSA,

> specifically SDS. I figure attention can¹t help but bring money to

> research.

>

> Anyway, right now, I¹m wrestling with exactly what MSA is, how it is

caused,

> etc. Following, I will write how it all works as I understand it. I¹m

> hoping you all can set me straight on the errant parts. Also, I have

about

> 10 questions, and I hope someone (like Bill & Charlotte, the treasure

trove

> of valuable information!) can help me out.

>

> Thanks a million in advance for any help you can give me. If you feel I

am

> being intrusive, please tell me, and I¹ll buzz off. I just want to

> understand as much as I possibly can about this awful disease, and see

what

> I can create.

>

>

> MSA AS I understand it:

>

> In normal brain cell function, the neurons (the glial cells?) creat the

> messages for autonomic nerve function. Their messages are sent to the

> muscles through nurotransmitters. Dopamine aids in transferring

information

> by keeping the (neurons? nurotransmitters?) sensitive.

>

> Alpha-synuclein is a protein, (ASN) that normally occurs in our brains.

In

> MSA, ASN is hyperproduced and forms aggregates that attach themselves to

> the neurons (glial cells). Now the message cannot be sent because the

glial

> cells (GC) lose sensitivity, and the GCs cannot " speak to " the NTs. Or

are

> they just " speech impaired, " and the message dies on the vine, or are the

> messages intermittently sent?

>

> The GCs eventually die.

>

> Sinemet is levodopa plus a catalyst. Levodopa becomes Dopamine in the

> brain. It has the ability to go through the blood stream to the brain,

> whereas Dopamine cannot.

>

> Dopamine goes to the nurotransmitters to help bring the message across to

> the muscles. The less dopamine, the less efficiency.

>

>

> Whew! Okay, now for the questionsS.

>

> 1.) How are the Alpha-synuclein (ASN) inclusions different from Lewy

> Bodies?

> 2.) Could the Glial Cytoplasmic Inclusions be thought of as clumps, or

> tumors?

> 3.) What malfunctions first: the neurons, or the nurotransmitters?

> 4.) Specifically, what regions of the brain are attacked in SDS? Are they

> always the exact same regions or can there be variation?

> 5.) What symptoms indicate an Autoimmune Dysfunction?

> 6.) What exactly causes low BP upon rising? (cellular level)

> 7.) Where should ASN be in the first place?

> 8.) Is the intended function of ASN known?

> 9.) What does this mean? " Synucleins are highly conserved proteins in

> vertebratesS " ? And this S " especially abundant in neurons and typically

> enriched at presynaptic terminals. " ?

>

>

>

>

>

>

>