No need to apologize. I was just happening to read between the lines wondering why the Stalevo was prescribed too. I just figured that someone new to the wacky world of PD diagnosis would be confused by these seemingly contradictory results.

Nicole, if you haven't given up on us entirely...there is no one definitive biochemical test for PD- no blood work, no spit test, no really 100 % accurate brain scan even. More thorough neurologists make the diagnosis after excluding any other possible look-a-like disorders or abnormalities via MRI; then add in clinical observation and patient histories/symptoms. Sometimes, doctors will prescribe a "dopamine challenge" to see if the patient responds positively to levodopa- this will be another indicator to the doctor that it's PD. From my readings, the only way to date that confirms a 100% accurate diagnosis of idiopathic PD is to check the brain for Lewey bodies upon autopsy- sorry to be so grim. I'm not sure if this Lewey bodies presence is still the defining test- if I'm wrong, please correct!

Hope that helps,

Laura

is this weird
and requip makes me confused anxious andworry let alone tremors turn into convulsions and I mean convulsions

Hi,

Not weird. PD is considered these days more a spectrum disorder; we all experience it differently. There have been at least two identified clinical sub-types of PD: 1) Tremor Dominant 2) Postural-Instability-Gait-Rigidity. According to studies, consider yourself lucky if you are tremor predominant, the course of disease progression is slower; my neuro, even said it's a "milder" PD. (Jankovic, McDermott, et al. Neurology. 1990. 40(10).

You are fortunate if you only have tremor after 8 years. I was misdiagnosed for 8 years with Essential Tremor. Upgraded to PD last year, I now have some slowness and rigidity, still tremor only on one side, but it now amps up.

I too have noticed that an agonist can seem to super charge my tremor. After a while, one begins to wonder where the PD symptoms begin and the drug side effects end. Sadly, we have no other choice.

I am very interested in the article you quoted re. clinical sub types of PD.

Unfortunately I cannot access the article unless I join various sites which I am not qualified to do.

Can you tell me anymore of the findings of this study ?

Thank you,
Neil.

Neil,

Unfortunately, Neurology is a subscription only journal; I do not have free access. You might want to inquire at your library to see if they can get a copy of the article for you.

I can't tell you much else other than Jankovic's observations on subtype were conducted in 1985 and it has since become recognized by neurologists as such; many of us here on the forum, and researchers, believe that PD is a spectrum disorder- not a catch all disease.

PDOnline Research has an interesting thread based on Jankovic's observation of subtypes...mainly, shouldn't we apply knowledge of subtypes within clinical trials? Could this be an explanation as to why meds are so variable in efficacy for us?

Also, see this article by Weiner "There is No Parkinson Disease" - this is a full text link.

Hope this helps,

Laura

MJFF is very interested in seeing if we can "validate" subtypes...such information would certainly be useful in the clinic (better inform families about expected course of disease, provide treatment guidance to physicians) but could also prove to be extremely informative for clinic trials (design and recruitment exclusion/inclusion criteria)...you can look at the projects we funded last summer via the press release below and/or our searchable grants database at michaeljox.org.

http://www.michaeljfox.org/newsEvent...cle.cfm?ID=197

Debi

Robert -

I've never been on Stalevo, but I did not respond at all to generic sinemet, got really sick on requip and then discovered Mirapex. Great help. Later, I tried Sinemet again, but used the name brand type, and it worked. Tried the generic since, and no response. We are highly individualized, in other words. You may well not have Parkinson's, or you may not have found the right mediation.

Hang in there - it seems we all have to become our own advocates...

Neil and all other interested folks,

I was curious as to the outcome of the MJFF initiative which dates from 2007. Here's a summary of outcomes at PDOnline Research

Mainly, research seemed to confirm existence of subtypes. While other could not corraborate. Some even suggested there are no subtypes but just a representation of the various stages of disease progression and response to meds. This may be a viable explanation for some PWP, but I think that anyone who knows a few PWP would beg to differ on this.

Laura

Mainly, research seemed to confirm existence of subtypes. While other could not corraborate. Some even suggested there are no subtypes but just a representation of the various stages of disease progression and response to meds. This may be a viable explanation for some PWP, but I think that anyone who knows a few PWP would beg to differ on this.

Laura[/QUOTE]

Laura,
Good point. To me, the basic classification of subtypes based on physical features of PD are tremor-dominant and rigidity dominant types. That is the first thing I noticed about PD (tremor vs rigidity) and is not a response to meds atleast during the early stages of PD. I just started reading about PD sub-types a few days ago and like you surprised by what I found out there.

Have you seen any studies that classify Tremor vs rigidity as the first order of classification??

Some time ago, there was a poll going on this subject, does anyone remember what the conclusions were?

Thanks
girija

girija and others-

The little noticed study from St. Judes a month ago provides a partial explanation for at leas two and possibly three subtypes based on age at onset and the role of environment. Bear with me while I explain my reasoning.

The St. Jude team Found that spraying influenza H5N1 into a mouse's nose led to a ten-day progression along the route's described by Braak- nose to olfactory bulb and gastric wall to vagal nerve to brainstem to SN. This resulted in the activation of microglia and neuronal damage plus alpha-synuclein clumping, all leading to PD.

In short they showed that viral (and probably bacterial) impacts can trigger the immune system cascade that leads to PD. This cascade, once begun, requires, we are told, at least 20 years to prodce symptoms. If that 20 years was a firm figure, which it is not, then it would be possible to trace a 70 years old man's tremor back to a long-forgotten cold at the age of 50. This viral induction could explain the standard senior onset subtype of PD, the closest thing there is to "normal" PD.

However, there is another and far more elaborate cascade that would account for young onset. P.M. Carvey at Rush and J.S. Hong and Bin Liu have shown that there is another path leading to the same cascade described by the St. Jude team. Pre-natal exposure to bacterial endotoxins triggers the same cascade once puberty is passed. This would indicate first symptoms at about the age of 35 to 40 - young onset. The endotoxin also shows synergetic actions with various toxins, metals, etc. The fetal exposure also affects the endocrine stress response in a manner that might explain our unique relationship to same.

Finally, the third variety could result from a viral exposure at any age with a "plain vanilla" course of progression.

Note that this also accounts for the complexity of PD.


Laura,
Good point. To me, the basic classification of subtypes based on physical features of PD are tremor-dominant and rigidity dominant types. That is the first thing I noticed about PD (tremor vs rigidity) and is not a response to meds atleast during the early stages of PD. I just started reading about PD sub-types a few days ago and like you surprised by what I found out there.

Have you seen any studies that classify Tremor vs rigidity as the first order of classification??

Some time ago, there was a poll going on this subject, does anyone remember what the conclusions were?

Thanks
girija[/QUOTE]