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Buddy
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11 Jan 2007, 4:00 pm

:D
Did you know that parkinson's and asperger's are nurobological disorders that means that the symptoms are similar I have a friend who has parkinson's and we compare notes both disorders affect balance and walking and doing simple tasks.



SteveK
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11 Jan 2007, 4:20 pm

Buddy wrote:
:D
Did you know that parkinson's and asperger's are nurobological disorders that means that the symptoms are similar I have a friend who has parkinson's and we compare notes both disorders affect balance and walking and doing simple tasks.


DIFFERENT CAUSE!
DIFFERENT SYMPTOMS for the most part! I don't have any parkinsons symptoms!
DIFFERENT TREATMENTS, etc....
PARKINSONS is progressive, AS isn't

So they're both neurological and can affect nerves. BIG DEAL!

Steve



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11 Jan 2007, 8:18 pm

They're completely different, even though they both affect the brain - kind of like a burn on your arm and a broken arm are completely different - and I've never really noticed anything affected with me about balance / walking / simple tasks. It seems I can balance better than most people :P



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11 Jan 2007, 9:26 pm

My mom has Parkinson's and I may have AS, they are leagues apart. Parkinson's involves involuntary muscle movement while AS seems to impact portions of the brain responsible for interpersonal communication and trickles into other aspects of that person's life.



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11 Jan 2007, 9:51 pm

I took the anti-parkinson's drug Selegiline for many years at the typical anti-parkinson's dose of 10 mg daily (about 100% inhibition of MAO-B). As an experimental
treatment of social phobia. http://en.wikipedia.org/wiki/Deprenyl


Studies have showed that phenelzine was superior to moclobemide in treating social phobia (its now called social anxiety disorder). Phenelzine inhibits both MAO-B and
MAO-A , but moclobemide only inhibits MAO-A. So a leading resercher in the field of
social phobia speculated that MAO-B inhibition may be a factor in the therapeutic effects of phenelzine. Before he even ran his study I did my on anecdotal research
and proved that the MAO-B inhibitor selegiline did not have a strong therapetic effect
for social phobia. Oh the increase potency of phenelzine maybe due to its effects on
GABA. http://en.wikipedia.org/wiki/Phenelzine Phenelzine is the most potent anti-depressant if it fails one likely is a good canidate for ECT.

I did have a since of well being and wanted to keep taking the selegiline. I took it for many more years at lowwer doses. One thing I noted is I shaked my legs less when
taking it. Which got me speculating that many of the stims from ASD may infact be
dopamine related.



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11 Jan 2007, 10:25 pm

Parky's is also fatal.


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11 Jan 2007, 11:13 pm

Sophist wrote:
Parky's is also fatal.


WHO even CARES! As I said, it is progressive. If you have it sooner or later you will WELCOME death!

Steve



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11 Jan 2007, 11:22 pm

TheMachine1 wrote:
I did have a since of well being and wanted to keep taking the selegiline. I took it for many more years at lowwer doses. One thing I noted is I shaked my legs less when
taking it. Which got me speculating that many of the stims from ASD may infact be
dopamine related.


Are you sure it wasn't because of the sense of well being?

HECK, I did that kind of rocking today when I was browsing in some stores. It was kind of nice. I can't explain it, but I guess you guys know what I am talking about. I felt fine BEFORE it. I could have stopped, and STILL felt fine. STILL, I started doing it, and didn't WANT to stop. I used to think it was just a funny habit, or whatever, even though it has no set pattern on when it starts. It was kind of nostalgic as I did it as a child. Still, it is a characteristic stim, unusual, controllable, and starts by itself, so I guess it is a stim.

Steve



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11 Jan 2007, 11:32 pm

SteveK wrote:
TheMachine1 wrote:
I did have a since of well being and wanted to keep taking the selegiline. I took it for many more years at lowwer doses. One thing I noted is I shaked my legs less when
taking it. Which got me speculating that many of the stims from ASD may infact be
dopamine related.


Are you sure it wasn't because of the sense of well being?

HECK, I did that kind of rocking today when I was browsing in some stores. It was kind of nice. I can't explain it, but I guess you guys know what I am talking about. I felt fine BEFORE it. I could have stopped, and STILL felt fine. STILL, I started doing it, and didn't WANT to stop. I used to think it was just a funny habit, or whatever, even though it has no set pattern on when it starts. It was kind of nostalgic as I did it as a child. Still, it is a characteristic stim, unusual, controllable, and starts by itself, so I guess it is a stim.

Steve


Maybe but other self-testing I find SSRI's tend to make my leg shaking worst. I think
there is a mechanism in which SSRI's (Paxil, Zoloft,Prozac)can interfere with dopamine levels. So that is part of my logic in my theory. Its been about year since
I ran out of selegiline. Since I quite my job about two years ago my research budget has been reduce to the point that restocking selegiline is not going to happen.



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12 Jan 2007, 12:24 am

SteveK wrote:
Sophist wrote:
Parky's is also fatal.


WHO even CARES! As I said, it is progressive. If you have it sooner or later you will WELCOME death!


Not everyone with a progressive disease particularly welcomes death because of the disease. (Look at Stephen Hawking.)

There is some sort of thing that can happen to some autistic people that looks a lot like Parkinson's in a few respects (I know several people who have it, I might have a variant of it) but it's unknown whether it just spontaneously happens or if it's an aftereffect of neuroleptics or something else like that (or of course a combination). It's written about in Tony Attwood's book and a couple other places.


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12 Jan 2007, 12:47 am

anbuend wrote:
SteveK wrote:
Sophist wrote:
Parky's is also fatal.


WHO even CARES! As I said, it is progressive. If you have it sooner or later you will WELCOME death!


Not everyone with a progressive disease particularly welcomes death because of the disease. (Look at Stephen Hawking.)

There is some sort of thing that can happen to some autistic people that looks a lot like Parkinson's in a few respects (I know several people who have it, I might have a variant of it) but it's unknown whether it just spontaneously happens or if it's an aftereffect of neuroleptics or something else like that (or of course a combination). It's written about in Tony Attwood's book and a couple other places.


I said sooner or later. ALSO, stephen hawkings, as bad as he is, is FAR better off than most in his place. He has a chair, keyboard, job, reputation, etc....

Steve



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12 Jan 2007, 1:19 am

Its been said by some "experts" all people will infact develop parkinson if they live long enough. Thats one of the few know health benfits of smoking. Smokers seem to develop parkinson less often than other groups. Though they also tend to die younger to so I'm not sure if that was factored in the data. African Americans are less likley to develop parkinson compared to whites. Oh back to smoking nicotine has an effect on dopamine plus tobacco also has a MAO-B inhibitor. Smokers typically have 40% inhibition of MAO-B which means they are on a anti-parkinson drug. Selegiline is known to be neuroprotective. It prevents/reduces that unavoidable parkinson that we
will all theoretically develop if we live long enough. So its possible tobacco has the same mechanism of action.

I would not be so quick to discount the realtionship between earily onset parkinson and autism the OP is suggesting. If a person had less dopamine neuron density from the beginning of their life in a number of areas of their brains such as one that control motor functions and other location related to social cogntion . Then one could theorise
a single genetic factor could put a person at risk of both autism and earily onset parkinson. I remember one study in with dopamine activity was less in social phobics.
As Rdos would suggest there is some strong overlap between social phobia and aspergers.


Quote:
Striatal Function in Generalized Social Phobia: A Functional Magnetic Resonance Imaging Study.
Sareen J, Campbell DW, Leslie WD, Malisza KL, Stein MB, Paulus MP, Kravetsky LB, Kjernisted KD, Walker JR, Reiss JP.

Department of Psychiatry.

BACKGROUND: Although evidence suggests the involvement of the amygdala in generalized social phobia (GSP), few studies have examined other neural regions. Clinical, preclinical, and dopamine receptor imaging studies demonstrating altered dopaminergic functioning in GSP suggest an association with striatal dysfunction. This is the first functional magnetic resonance imaging (fMRI) study to use a cognitive task known to involve the striatum to examine the neural correlates of GSP. We examined whether subjects with GSP had differential activation in striatal regions compared with healthy control subjects while engaged in a cognitive task that has been shown to activate striatal regions reliably. METHODS: Ten adult, unmedicated subjects with a primary DSM-IV diagnosis of GSP and 10 age-, gender-, and education-matched healthy comparison subjects underwent fMRI while performing the implicit sequence learning task. RESULTS: The GSP and healthy comparison subjects did not differ significantly on the behavioral performance of the task. Subjects with GSP, however, had significantly reduced neural activation related to implicit learning compared with healthy comparison subjects in the left caudate head, left inferior parietal lobe, and bilateral insula. CONCLUSIONS: These findings support the hypothesis that GSP is associated with striatal dysfunction and further the neurobiological understanding of this complex anxiety disorder.

PMID: 17097072 [PubMed - as supplied by publisher]

Quote:
Am J Psychiatry. 1997 Feb;154(2):239-42.
Links
Comment in:
Am J Psychiatry. 2001 Feb;158(2):327-8.
Dopamine reuptake site densities in patients with social phobia.
Tiihonen J, Kuikka J, Bergstrom K, Lepola U, Koponen H, Leinonen E.

Department of Forensic Psychiatry, University of Kuopio, Finland.

OBJECTIVE: It has been suggested that social phobia is associated with dysfunction of the noradrenergic and dopaminergic systems, but there are no published anatomic data on the monoaminergic abnormalities found in the brains of phobic patients. The authors studied the density of dopamine reuptake sites in patients with social phobia. METHOD: The study included 11 patients with social phobia and 28 healthy comparison subjects, 11 of whom were age- and gender-matched to the patients for the analyses. Measurement of the density of dopamine reuptake sites was performed by using a 123I-labeled cocaine analogue, [123I]beta-CIT, with single photon emission computed tomography (SPECT). RESULTS: Blind quantitative analysis revealed that striatal dopamine reuptake site densities were markedly lower in the patients with social phobia than in the age- and gender-matched comparison subjects. CONCLUSIONS: The results indicate that social phobia may be associated with a dysfunction of the striatal dopaminergic system.

PMID: 9016274 [PubMed - indexed for MEDLINE]



renaeden
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12 Jan 2007, 9:00 am

SteveK wrote:
WHO even CARES! As I said, it is progressive. If you have it sooner or later you will WELCOME death!
Steve

Some people may care. It is still an interesting subject.



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12 Jan 2007, 2:42 pm

SteveK wrote:
Sophist wrote:
Parky's is also fatal.


WHO even CARES! As I said, it is progressive. If you have it sooner or later you will WELCOME death!

Steve


Just definition-wise, there's a difference between "progressive" and "fatal". I was just clarifying further.


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normal2357
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21 Sep 2018, 8:59 pm

I have just been dx with Parkinson I am also an aspie
The early symptoms of PD closely mimic Aspergers. Beware of this. It is affecting every bit of my life
i am 62 years old.