Quote:
Originally Posted by lindylanka
The other is increase in joint pain, something that I was prepared to live with if it improved OAB. From the outset my urologist has discussed with me that this class of drugs bring some improvement as a side-benefit for PD, and I would agree with this. These side-benefits are with mobility, smoother faster movement, and less wearing off in terms of mobility, though other wearing off signs are more sudden and acute. With all there was this trade off in terms of pain when sinemet wore off, to a degree that does not happen when I am on just the sinemet/entacapone PD regime I use. Taking the anti-ch pills in the night gave me dystonia so I took them in the morning instead, and it resolved. The difference between them and the patch is that it is active over a much longer period. I am now experiencing acute wearing off dystonia, expecially if I leave it too long between sinemet doses, as TMJ type pain, and nocturnal foot dystonias, and I would also correlate early morning lower back dystonia and internal dystonias with this. All resolve when sinemet kicks in. All I had to a degree BEFORE going on sinemet, i.e. when untreated. None were a problem last year when I spent nearly 4 months off anti-ch meds and only on sinemet. I went onto Kentera because the OAB became unbearable. So my conclusion from this was the same as yours Paula, that when sinemet is at it's lowest there is a corresponding increase in acetycholine DESPITE being on the patch. In other words an imbalance. And perhaps taking this medication means my body is no longer regulating acetycholine naturally??
Lindy
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Lindy,
Blech, sorry you have to go through this. It seems with every drug it's one step forward, two steps back.
I found this at at the Net Doctor UK site where it explains how Kentera works:
Kentera patches contain the active ingredient oxybutynin hydrochloride, which is a type of medicine called an anticholinergic (or antimuscarinic) muscle relaxant. It works by relaxing the involuntary muscle that is found in the wall of the bladder.
The muscle in the wall of the bladder is called the detrusor muscle. It can sometimes contract in uncontrollable spasms, and this is often referred to as having an overactive or unstable bladder.
Oxybutynin works by relaxing the detrusor muscle in the wall of the bladder. It does this by blocking receptors called cholinergic (or muscarinic) receptors that are found on the surface of the muscle cells. This prevents a natural body chemical called acetylcholine from acting on these receptors.
Normally when acetylcholine acts on these receptors, it causes the detrusor muscle to contract and the bladder to empty. By blocking acetylcholine, oxybutynin helps the muscle in the bladder wall to relax. This reduces unstable, involuntary contractions of the bladder,
I am confused; however, as to why it would cause "more" dystonia or muscular problems. As an anticholinergic it is in the same league as Amantadine which helps
lower our acetylcholine levels. This is why it is prescribed because it helps prevent the bladder from spasms which result in overactive bladder issues.
On the other hand, if your doctor also gave you Aricept for some reason, that is an cholinesterase inhibitor and this
increases acetyl choline; thus, in essence canceling out effects of the patch.
So I guess I am in the dark as to how this would make your dystonia worse from a neurotransmitter perspective unless it somehow makes things more off balance. If anything, as you experience more mobility with Kentera, I would think that the anti-cholinergic aspect would play in your wearing off too, that you would have less acetyl choline, unless there is some sort of weird symptom rebound going on? I also don't see much out there on side effects...some do report muscle pain. I wonder if because it is fairly new how there may be some negatives that are relatively unknown. Have you asked your neurologist for feedback?
I'm stumped.
Laura