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Old 08-10-2013, 08:26 PM
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reverett123 reverett123 is offline
In Remembrance
 
Join Date: Aug 2006
Posts: 3,772
15 yr Member
reverett123 reverett123 is offline
In Remembrance
reverett123's Avatar
 
Join Date: Aug 2006
Posts: 3,772
15 yr Member
Default "Nip it in the bud!

....as Barney Fife would say. Once established it can be a *****. From Wikipedia-
"dyskinesia (DD), which occur when the drug concentration rises or falls. If dyskinesia becomes too severe or impairs the patient's quality of life, a reduction in L-Dopa might be necessary, however this may be accompanied by a worsening of motor performance. Therefore, once established, LID is difficult to treat.[5] Amongst pharmacological treatment, N-methyl-D-aspartate (NMDA) antagonist, (a glutamate receptor), amantadine, has been proven to be clinically effective in a small number of placebo controlled randomized controlled trials, while many others have only shown promise in animal models,.[4][7] Attempts to moderate dyskinesia by the use of other treatments such as bromocriptine (Parlodel), a dopamine agonist, appears to be ineffective.[8] In order to avoid dyskinesia, patients with the young-onset form of the disease or young-onset Parkinson's disease (YOPD) are often hesitant to commence L-DOPA therapy until absolutely necessary for fear of suffering severe dyskinesia later on. Alternatives include the use of DA agonists (i.e. ropinirole or pramipexole) in lieu of early L-DOPA use which delays the use of L-DOPA. Additionally, a review (Stocchi, F., Clin Neuropharmacol, 2010, 33, 198) shows that highly soluble L-DOPA prodrugs may be effective in avoiding the in vivo blood concentration swings that potentially lead to motor fluctuations and dyskinesia.

Patients with prominent dyskinesia resulting from high doses of antiparkinsonian medications may benefit from deep brain stimulation (DBS), which benefits the patient in two ways: 1) DBS allows a reduction in L-DOPA dosage of 50-60% (thus tackling the underlying cause); 2) DBS treatment itself (in the subthalamic nucleus or globus pallidus) can reduce dyskinesia.[9]

The use of MDMA ("Ecstasy") has been shown to enhance the effects of L-DOPA while reducing the associated dyskinesia in primates with advanced PD.[10] Its serotonergic actions may be responsible for this effect."


I thnk that dextrometorphan is an NDMA antagonist. It might be worth tryind a low dose there.

-Rick

Quote:
Originally Posted by Jim091866 View Post
I ssem to be having lots of end of dose dyskinesia. My carbidopa doseage has been reasonably stable. Anyone found anything that works for this problem. I seem to recall amantadine? Thanks.
__________________
Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000.
Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well.
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