All I know is, it made me feel really awful even on a minimal dose, and when I quit it after a few days, I was speeding for five days. Couldn’t sleep from beginning to end. The idiot doctor didn’t believe me and thought I was experiencing nocebo. Clearly a complicated medication as it agonises both serotonin and dopamine. I’m over sensitive to both, also why Ropinirole didn’t work for me. Might work for someone else, of course.
That makes sense to me. It's clearly a powerful drug, best left as a 'last resort' option if someone finds themselves unable to get through the withdrawal.
Yes, exactly, I was offered it in lieu of low dose quetiapine which I have had to use for insomnia over the years, but sadly it had the opposite effect (and it’s a completely different medication so I don’t understand the rationale, I thought the doctor was an impostor!). It would be very hard to get hold of also as I think only a psychiatrist would prescribe it and they are not typically reliable and don’t understand about restless legs one bit!
They suggest it may just be for Augmentation with sensitised D2 receptors, not augment free RLS. They reference a number of articles where it did not work or variable responses in RLS. The dose used was about 10% used in schizophrenia. The biggest thing was that they had to stop the DA before starting Aripiprazole where having a medication to take while tapering is really what is needed.
It's a tiny 'experiment' rather than a controlled trial under strict conditions.My view is that, once augmentation hits, it's always best to get off ALL dopamine agonists completely. However, I know that some people cannot manage this, and they are probably the ones who might want to try it for a short 'trial basis'.
Interesting, and scary stuff! But then again RLS is scary stuff! I would use a lot of caution as most antidepressants are fraught with discontinuation syndrome - trading one evil for another.
Agreed. It's definitely a 'last resort' option in my opinion, after everything else has failed.
“Abilify is a “dopamine stabilizer,” meaning it can act as a dopamine receptor antagonist when the dopamine system is overactive, and a partial agonist when dopamine levels are low. It is able to do this because it has a very high affinity for dopamine receptors, so it binds to the receptor in place of dopamine. Abilify still activates the receptor but does so at a much weaker level than dopamine itself would. Ultimately, this should reduce the overactivation of the dopamine system and reduce chorea.”
What? Does the drug have a mind of its own? I’m beginning to think that magnesium (and we probably have to try to figure out which form) is our best bet for giving our receptors a leg up. No pun intended. One too many people swear by it, and everything I read indicates that like Abilify, it acts on dopamine receptors. It seems to increase the dopamine pool (per some articles) yet mainly it blocks its release??? Whenever I read “block dopamine release” I immediately think to myself “eureka, that’s what we need… in the long run.” This is the most informative paragraph I have ever read with regards to magnesium’s mode of action:
“Magnesium also potentiates the function of GABAA receptors suggesting a putative Mg2+ binding site on the GABAA receptor protein (Möykkynen et al., 2001).
Dopamine is considered the most important molecule in development of pharmacodependence. Indeed, substances that result in pharmaco- dependence strongly increase the level of dopamine in the midbrain. As an example, morphine produces a dose-dependent increase in dopamine-containing neurons in the substantia nigra and ventral tegmentum in rat brain (Trulson and Arasteh, 1985). Magnesium can reduce dopamine release in some brain structures through direct presynaptic action at the level of some dopaminergic synapses, by inhibiting calcium induced brain dopamine release, and by decreasing the stimulatory action of glutamate upon dopamine release. Brain dopamine level in mice is significantly increased following icv administration of CaCl2. Magnesium, an antagonist to calcium, inhibits the dopamine release (Sutoo and Akiyama, 2000).
There are NMDA receptors at the level of some dopaminergic nerve endings whose stimulation also increases dopamine release. The reduction in NMDA receptor stimulation by magnesium can reduce dopamine release induced by the addictive substance (Chéramy et al., 1994). Extracellular Mg2+ blocks NMDA ion channels in a voltage dependent manner and increases the receptor affinity for glycine (Paoletti et al., 1995). Glycine inhibits the glutamate-evoked release of noradrenaline, and possibly other catecholamines (Johnson et al., 1994). In this way, the facilitating effect of magnesium on glycine linkage at its binding sites could reduce the glutamate stimulating effect of presynaptic catecholamine release (dopamine release being an essential step of addiction development). A selective inhibitor of the glycine transporter (Gly T1) significantly increased dopamine release (Bennett and Gronier, 2005). This fact indicates that glycine reduces dopamine release, in this way decreasing the intensity of addictive processes. Notably, magnesium increases both glycine synthesis and release.”
Bottom line, a little afternoon magnesium can’t hurt, whereas the antipsychotics can.
Seems like you really covered all the bases on behalf of your wife. Not eating after an earlyish dinner is helpful for many. I’m not big on iron infusions and in my case it would make matters worse because of the hepcidin increase it causes. I believe RLS is worse in the evenings because of a drop in serum iron (not ferritin). I believe that ferritin has very little to do with RLS. I take 50mg of ferrous bisglycinate on an empty stomach one hour before bed. My RLS is gone in one hour for one night. Iron taken this way is to RLS what aspirin is to a headache. I’ve attached a post with what I believe is a more potent way to up-regulate receptors. It’s a long post. Pay attention to RKM7’s story.
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Augmentation?
Can augmentation be avoided on DA's?
Augmentation
