I've just been reading the PD UK forum and noticed that, on some threads, people are beginning to talk about 'coming off all meds'. I must stress you shouldn't do this by yourself. Get advice from the powers that be.
I'm OK today. I am taking absolutely NO PD drugs and feel OK. I had a crappy nights sleep again and feel stiff and sore. The word OK is the right word. I couldn't run an Olympic race but can so the housework. This is no better or worse than when I was on Sinemet and Mirapexin. My shakes aren't too bad.
I have become truly concerned about the longevity of PD drugs. I have heard they only last 2/5/10 years and then stop helping. IF this is the case I think that's another reason to not start (or stop taking) PD drugs until you really have to. Is there any real evidence of this? Comments please!
I wish all you PWP a great day!
Chris
The question really is whether the neurones switch off dopamine production/control at the same rate or faster when on meds.
ReplyDeleteThe whole system is geared to pushing a swathe of drugs onto the PDer, each with its own side effects. In the end everyone forgets which side is up.
from the Viartis website ( see line 8) there are numerous references elsewhere if you google it.
L-DOPA
The most widely used form of treatment is L-dopa in various forms. L-dopa is transfomed into dopamine in the dopaminergic neurons by L-aromatic amino acid decarboxylase (often known by its former name dopa-decarboxylase). However, only 1-5% of L-DOPA enters the dopaminergic neurons. The remaining L-DOPA is often metabolised to dopamine elsewhere, causing a wide variety of side effects. Due to feedback inhibition, L-dopa results in a reduction in the endogenous formation of L-dopa, and so L-dopa eventually becomes counterproductive. Mucuna pruriens is a natural source of therapeutic quantities of L-dopa.
Sinemet consists of L-dopa and Carbidopa (a dopa decarboxylase inhibitor that helps to prevent the metabolism of L-dopa before it reaches the dopaminergic neurons). There is also a controlled release version, Sinemet CR, that spreads out the effect of the L-dopa.
Madopar consists of L-dopa and Benserazide (a dopa decarboxylase inhibitor that helps to prevent the metabolism of L-dopa before it reaches the dopaminergic neurons). There is also a controlled release version called Madopar CR that spreads out the effect of L-dopa.
Parcopa consists of L-dopa and Carbidopa, the same as Sinemet, but is in orally disintegrating tablets.
Duodopa is a combination of L-dopa and Carbidopa, dispersed as a viscous gel. Using a patient-operated portable pump, the drug is continuously delivered via a tube directly into the upper small intestine, where it is rapidly absorbed.
Stalevo consists of L-dopa, Carbidopa and Entacopone (Comtan). Entacapone (Comtan) inhibits the COMT enzyme, thereby prolonging the effects of L-dopa, and so has been used to complement L-dopa. Tolcapone does the same, but can have serious side effects.
DOPAMINE AGONISTS
Dopamine agonists are drugs that mimic dopamine by stimulating the dopamine receptors. The dopamine agonists include Bromocriptine (Parlodel), Pramipexole (Mirapex), Ropinirole (Requip), Cabergoline (Dostinex, Cabaser), Lisuride (Revanil), Rotigotine (Neupro) which is applied using a transdermal patch, and Apomorphine hydrochloride (Apokyn) which is administered via injection or infusion. Pergolide (Permax) has been widely withdrawn from use. Besides the side effects they cause, dopamine agonists cause the dopamine receptors to become progressively less sensitive, thereby eventually increasing the symptoms.
MAO-B INHIBITORS
MAO-B inhibitors do not directly increase the formation of dopamine or its activity. MAO-B inhibitors instead reduce the symptoms by inhibiting monoamine oxidase-B (MAO-B), which inhibits the breakdown of dopamine secreted by the dopaminergic neurons. The most common MAO-B inhibitors are Selegiline (Eldepryl) and Rasagiline (Azilect). MAO-B inhibitors cause widespread side effects.