Hi Lindy,
Started a new thread as you suggested, so as not to hijack Rick's thread. The Dystonia Society defines dystonia as:
"Dystonia is a common neurological movement disorder characterised by sustained and involuntary muscle contractions or muscle spasms. These spasms can cause twisting, repetitive movements or abnormal postures and are sometimes accompanied by tremor."
The more questions you ask, the more others raise their heads. The Medical Dictionary has a series of dyskinesias:
"dyskinesia /dys·ki·ne·sia/ (-kĭ-ne´zhah) distortion or impairment of voluntary movement, as in tic or spasm.dyskinet´ie.

biliary dyskinesia derangement of the filling and emptying mechanism of the gallbladder.
dyskinesia intermit´tens intermittent disability of the limbs due to impaired circulation.
orofacial dyskinesia facial movements resembling those of tardive dyskinesia, seen in elderly, edentulous, demented patients.
primary ciliary dyskinesia any of a group of hereditary syndromes characterized by delayed or absent mucociliary clearance from the airways, often accompanied by lack of motion of sperm.
tardive dyskinesia an iatrogenic disorder of involuntary repetitive movements of facial, buccal, oral, and cervical muscles, induced by long-term use of antipsychotic agents, sometimes persisting after withdrawal of the agent"

I suffer from what I have always called dyskinesia. This is writhing around, unable to keep still, impossible to write, or do anything intricate. The constant movement wears me out, and I get very hot and perspire. It is difficult to have a meal with raging DK, and the people sitting next to me are advised to wear their raincoats!!! The drug amantadine is prescribed to calm it down, and it works reasonably well for about 6 months and then loses its effectiveness.

Blue Dalia,
Interesting your DK starts when you increase your dose of comptan/levodopa, which is more support for the theory that DK is cauised by levodopa, not agonist or others. You don't take an agonist ?
Ron

Ron, I don't take an agonist. If there's a side effect, I get it. LOL. I was on mirapex years ago and had to stop because of compulsive behaviours.

Right now I'm taking 1/2 tablet of levodopa/carbidopa 25/100, every 3 or 4 hrs, and 200 mg of amantadine a day.

The goal is to get me totally off all PD drugs as I am very sensitive to them.

Ron-
My statement about agonists being causal in my case is based entirely on my experience with requip - stop it and dk goes down, start it back up and dk follows.

Here's another for you that I haven't seen elsewhere. Sunlight triggers mine but what is unusual is that sunlight in my peripheral vision is far worse than straight ahead, especially if just on one side as in driving an automobile. Cup a hand to shield the side toward the window and it decreases markedly.

I'll add one thing - the greatest single trigger for me is talking on the phone!

Well, not the sunlight part. I know for sure that agonist + levodopa cause dyskinesia for me. Two simple reasons: 1) I can isolate as Rick has done

and 2) I feel "toxic" as in too much levodopa in my system.

Hi All,
I just saw this paper, looks interesting (based on the abstract). I have not read it yet to summarize or comment on it.

Glutamate NMDA Receptor Dysregulation in Parkinson's Disease with Dyskinesias

Imtiaz Ahmed; Subrata K. Bose; Nicola Pavese; Anil Ramlackhansingh; Federico Turkheimer; Gary Hotton; Alexander Hammers; David J. Brooks

Authors and Disclosures

Posted: 04/18/2011; Brain. 2011;134(4):979-986. © 2011 Oxford University Press

*


processing....



* Abstract and Introduction
* Materials and Methods
* Results
* Discussion

* References

Abstract and Introduction
Abstract

Levodopa-induced dyskinesias are a common complication of long-term therapy in Parkinson's disease. Although both pre- and post-synaptic mechanisms seem to be implicated in their development, the precise physiopathology of these disabling involuntary movements remains to be fully elucidated. Abnormalities in glutamate transmission (over expression and phosphorylation of N-methyl-D-aspartate receptors) have been associated with the development of levodopa-induced dyskinesias in animal models of Parkinsonism. The role of glutamate function in dyskinetic patients with Parkinson's disease, however, is unclear. We used 11C-CNS 5161 [N-methyl-3(thyomethylphenyl)cyanamide] positron emission tomography, a marker of activated N-methyl-D-aspartate receptor ion channels, to compare in vivo glutamate function in parkinsonian patients with and without levodopa-induced dyskinesias. Each patient was assessed with positron emission tomography twice, after taking and withdrawal from levodopa. Striatal and cortical tracer uptake was calculated using a region of interest approach. In the 'OFF' state withdrawn from levodopa, dyskinetic and non-dyskinetic patients had similar levels of tracer uptake in basal ganglia and motor cortex. However, when positron emission tomography was performed in the 'ON' condition, dyskinetic patients had higher 11C-CNS 5161 uptake in caudate, putamen and precentral gyrus compared to the patients without dyskinesias, suggesting that dyskinetic patients may have abnormal glutamatergic transmission in motor areas following levodopa administration. These findings are consistent with the results of animal model studies indicating that increased glutamatergic activity is implicated in the development and maintenance of levodopa-induced dyskinesias. They support the hypothesis that blockade of glutamate transmission may have a place in the management of disabling dyskinesias in Parkinson's disease.
Introduction

Dopamine replacement with oral levodopa remains the most effective treatment available for reversing the motor symptoms of Parkinson's disease. However, long-term use of levodopa in patients with Parkinson's disease is invariably associated with the development of abnormal involuntary movements known as dyskinesias, which may become as disabling as the parkinsonian symptoms themselves. A review of the cumulative literature suggests that levodopa-induced dyskinesias (LID) are experienced by 40% of patients with Parkinson's disease 4–6 years after starting levodopa, and up to 90% of patients by 9–15 years of treatment (Ahlskog and Muenter, 2001).

The pathogenic mechanisms underlying LID in Parkinson's disease are still being elucidated. The progressive loss of dopaminergic.................................

Ron, your descriptions clarify things for me, what I am getting are dystonias, Your description of your personal experience of dyskinesia is exactly what I have seen with real PwP, but descriptions of dyskinesia often sound closer like this:

"twisting, repetitive movements or abnormal postures"

This is exactly what I get when I am walking, not at peak dose at all, but when wearing off.

Thanks, and for the thread, there do seem to be questions.

I thought the main reason for people delaying l-dopa was to avoid the likelihood of dyskinesia. Are there are people on agonists only who get dyskinesia?

I would like to know more about this.....

Laura and Rick you always make me want to know more.....

I believe girija has pegged my source of dyskinesia and dystonia:
Levodopa-induced dyskinesias are a common complication of long-term therapy in Parkinson's disease. Although both pre- and post-synaptic mechanisms seem to be implicated in their development, the precise physiopathology of these disabling involuntary movements remains to be fully elucidated (posted by girija)

Sound like everyone is different..I only get dyskinetic when there isn't enough levodopa in my system, especially when Stalevo is wearing off for the day..If I take a teaspoon of Zandopa in the middle of the day, I am almost symptomless for hours

I dont take agonists anymore..Too expensive, and Mirapex is about as effective as an asprin for me

I take approximately 1400 mg of sinemet a day - 2 25/100s every 2 hours; 200 mg of amantadine, and nortyriptyline, which i have been given permission to play around with as I'm on a low dose. i am not dyskinetic except around the mouth i'm not sure what's going on there.

i asked my neuro just yesterday about the sinemet dosage and he suggested that it's because i take smaller dosages frequently and my system uses it up before it gets overload. if I were to take 4 every 4 hours i would have dyskinesia. CR is too uneven. Agonists add to the sinemet dose. I don't want that at this point.

I was also relieved to learn that I am at the high end of the recommended range of sinemet dosage.

My neuro quipped, "You certainly are not a moneymaker." All of my medicines are old and they work.