Dyskinesia
 

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!

This is me too
 

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.

dyskinesias
 

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.....:)

(sigh)
 

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

another example
 

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.

Lindy
 

In the white rat thread you had some questions concerning dyskinesia and dystonia: Lindy's question; So my question is to all of you who are experiencing dyskinesias, is where from the patient perspective is a way of knowing? At the moment I am veering towards dystonia as an end of dose thing, and dyskinesia as a peak dose thing, rather than looking at the actual quality of the movement and discomfort. And I know I may be very very wrong in my thinking. But I WOULD like to understand this thing. And why some of us get such dramatic and negative results from l-dopa and some of us go a long way on a little.....


For me dyskinesia is more of a problem when I am on good, and there us any excitability. I sort of flail back and forth even when sitting and resting. the only time I am not doing so is when I sleep - no extra movements at all.

Dystonia, on the otherhand, is painful writhing and twisting of muscles throughout my body. These seem to exacerbate during peak dose. And just recently, my dyskinesia comes at end of dose as well at peak dose. Go figure! But this is why I am speculating that advancement of the disease is causing my "off" dyskinesias.

Peg

Lindy
 

I found another perspective of dyskinesia, which blames it all on long-term drug use.

Tardive Dyskinesia (from Wemove.org)
In general, tardive dyskinesia (TD) refers to a wide variety of involuntary, repetitive, persistent, stereotypic movements caused by the use of drugs that block dopamine receptors. These drugs that block dopamine receptors are known as dopamine-receptor antagonists or DRAs. Involuntary movements such as those associated with dystonia, myoclonus, tics, and tremor, and restlessness with muscle quivering and the urge to move (akathisia) may be manifestations of TD. When used in the classic sense, TD refers to an iatrogenic disorder produced by the long-term use of drugs to treat schizophrenia that act by blocking dopamine receptors.

Dyskinesia is from the Greek words, dys and kinEsis, meaning difficulty of movement. Tardive comes from the French word (tardif) for tardy or late, meaning that the dyskinesias appear late in the course of therapy with a drug that blocks dopamine receptors (DRAs). These movements do not occur as an immediate response to the use of the drug.

i think there is more of that than we think
 

once again we are discussing something with each other that the experts don't know the answers to. The Bachmann Strauss Foundation was nice enough to invite us but I don't think it ever occurred to them to pay our way as an expert.

My neuro defines dystonia as when there is twisting of muscles. dykinesia is when you have involuntary movement.

That definition works for me up to a point. I'm off in the a.m. and my shoulders head and neck are actually twisting. In fact my entire right side is turning inward. Could this be from all the pushing and pulling of muscles from dystonia? Dystonia means no dopamine for me and only dopamine will relieve it.

But my face, throat, voice are all caving in like a much older person with no teeth and that happens increasingly through out the day Ranting is a possibility at any time....i just can talk away for hours ....problem is nobody can hear me or understand me.

My neuro will give me botox around the face and neck if my family physician writes the prescription. He's been ripped off by promises to pay that don't come thru. HOW DARE THEY MAKE IT SO HARD FOR US! The things we need - like a voice and a mouth and teeth are for the rich.
This is becoming quite difficult. i'm sitting here with a jaw that is turning black from the difficult removal of my teeth. I've had to add a painkiller that makes me feel like I've taken LSD. i'm on an antibiotic that interferes with my meds.

i have aquatics in less than an hour, i have to drive myself because my faithful friend had to have foot surgery, the instructor is the :killer - we all love her she makes us work. And i made her a tape of all fast dance songs that she might use today. all pain tonite is my own doing.

Anyway tardive dyskinesia is often located around the lower face and neck so a good database would solve some of this. it concerns me that the bachmann strauss foundation after nine yrs and olanow and ted dawson involved still doesn't know what dystonia is??????

so a prestigious group of NEW YORK city's finest are going to "interact" with patients.

Does this mean we get to touch them?

Catch up people - someone should fund a patient group, we should be making our own "observations".

p\od at all of this...u don't learn about the engine if you don't have a car!! They should be flying us up for extensive observations all the time. It's not like we are getting a free trip to nyc as so many of them do. We're there for very serious reasons and too tired for anything else. How would they know who to pick?Apparently people are rated and handpicked. How should they choose who goes?

By their qualifications. You can find people online who are knowledgeable and physically fit the bill in days. you must go to them, the grassroots are getting angry. it's not just the well known pwp - we were a community long before 23andme came on the scene and it is about to get much bigger. almost round the clock you can communicate online. iF you are going to live in an ivory tower we will find another way. So if you aren't going to communicate with the commoners, we have other choices. I'm talking to anyone who feels the sting of this, not particular person , but many at one time. just call them and ask them you have hundreds of thousands around the world but they are suppposed to come to you?/

THEY CAN"T AFFORD IT.

Revolution anyone?
Ii warned about my behavior in advance ....i'm in pain and i am going to go kick about and probably feel great. here'sthe video of one song that i put on the cd - it's for listening fun...remember that? it doesn't mean i am a nasty girl or that i want to be a nasty girl. it is a great aquatic execise

http://www.youtube.com/watch?v=6R4hsN6snFc

glub glub i feel better just listening to this. remember, there won't be a video at class- it's about the beat. i'm getting on now. Tardive dyskinesia needs to be throughly researched now. if you read the description i 'd say it's one part of my multi -faceted kinetic nightmare.

i'm off to the NIH on Monday for their screening required for certain clinical trials. What do I have to do to make the Clinical trial honor roll?, hee hee

have a sense of humor will you? we are all dying here.

Dr. Lieberman, now of the Ali center,used to have a website with a wealth of info drawn from his many years of experience with thousands of patients. When he announced the impending closure of the site, I archived a bunch of it and had not looked at it since. Dusted it off today-


"dyskinesia , a rapid, jerk-like movement of brief duration is more LIKELY to be regulated by the AMPA receptors: receptors that generate brief currents. Whereas a dystonia , a prolonged twisting movement is more LIKELY to be regulated by the NMDA receptors: receptors that generate prolonged currents. It's unknown, at this time, whether AMPA receptors actually incite dyskinesia or whether NMDA receptors actually incite dystonia. It's thought, however, that, given the types of current the receptors generate it's more likely AMPA receptors regulate dyskinesias while NMDA receptors regulate dystonias.

Current is carried through AMPA receptors mainly by the movement of sodium ions from outside the cell into the cell. Some AMPA receptors in regions of the brain such as the striatum, the hippocampus (where memory is stored), and the cerebellum (which coordinates movement) are also affected by the movement of the calcium ion. This movement plays a key role in the regulation of several second messenger systems (chemicals inside the cell that carry messages from one part of the cell to another)."

Rick & Ron
 

Ron & Rick
I'm sure glad we have you two to keep us straight in thiis confusing episode called "Life with PD!"
Peg

Dyskenisia
 

I always thought dystonia is a spasm or a cramp of both voluntary and involuntary muscles, like I experience in my feet and calf muscles and facial cramps similar to Bell’s Palsy. Dyskinesia on the other hand is what I have seen in the public face of Michael J Fox. My cramps are relieved by Sinemet.

I used to like Dr Liebermans open honest answers on his Ask the Doctor site, full of information, and wish it was still up. There are others, but he was the original! And missed.....

Lindy

Thanks Rick for something that looks a little less based on guesswork than the others.....