Merkan

The thread about dopamine agonists and supportive agents (e.g levodopa and reuptake inhibitors)

69 posts in this topic

Just wondering, what's the recommended dosage of Sinemet and do you guys take the regular or extended release tablets?

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Im wondering whether you have experienced any side effects/ withdrawal symptoms. I do not want to get addicted to anything so am refusing to take benzo's but really hating this hppd hell and really need something for those bad days. Also does it help with your visuals? My visuals have ramped up as of late and making it hard to see.

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Just wondering, what's the recommended dosage of Sinemet and do you guys take the regular or extended release tablets?

[Disclaimer] Ok, none of us are doctors [End Disclaimer]

As for dose, Sinemet 25/100 (most common preparation): ½ pill 2 or 3 times per day should do. If it is going to help you, you will notice the effect in as little 30 minutes or as long as a few days. You probably do not want to go higher than a full pill 3 times a day. Always start low and be patient.

So far, regular works better for me and another member.

I’m wondering whether you have experienced any side effects/ withdrawal symptoms. I do not want to get addicted to anything so am refusing to take benzo's but really hating this hppd hell and really need something for those bad days.

Note in Jay’s thread: http://hppdonline.co...-sinemet-trail/

"My neuro said I could stay on this low dose for life, if needed. No addiction, no tolerance, very little side effects."

[This info is nice since it comes from an actual doctor – Note: low dose]

When you discontinue using it, then things gradually return as they were in the course of 1-4 weeks. However, in my case, some symptoms seem to be permanently resolved. Hopefully others will experience this as well.

Also does it help with your visuals? My visuals have ramped up as of late and making it hard to see.

It depends on your visuals. Contrast, night vision, visual acuity (sharpness vs cloudy), depth perception, halos, glare, motional latency & frames, and negative afterimages are the most likely to respond.

Non-visual symptoms that it may help are: anhedonia (motivation, enthusiasm, labido), depression, anxiety, insomnia, and (for some) DR.

Visuals unlikely to respond are: visual snow, color confusion, CEVs, OEVs, pariedolias.

There is quite a variance with individuals. Combination with other meds such as Keppra may be important – just work with one at a time to gain a feel/understanding of how you respond.

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Awesome thanks so much! I am going to ask my psychiatrist for this. I took dexedrine today (2.5 mg) to study for a test and almost all my symptoms except visual snow and and a bit of afterimages are gone! Feels good! Dexedrine or dextroamphetamine works mostly on dopamine I think so dopamine does play a big role in our disorder. Sinemet which increases dopamine hopefully will have a similar effect but without the speedy feeling these adhd medicines have.

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yea i got an appointment with a neuro Nov. 1st. really looking forward to trying this but also dont wanna get to optimistic for fear of failure. ive been on klonopin .5mg/ twice a day for like 3 years and idk if im getting used to it or what. i just had sinus surgery on Thursday so that could be affecting things.

does sinemet interact well with klono? and does it improve memory? ot fogginess? i think i might try and cut my dosage a bit but my anxiety is awful. maybe Sinemet will help that and the DP/DR.

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I took dexedrine today ... almost all my symptoms except visual snow and and a bit of afterimages are gone

If you had success with Dexedrine, then it is likely you will improve with Sinemet. Dexedrine increases DA and NE about the same (NE is more stimulating than DA). Sinemet mostly increases DA and doesn't make one feel speedy.

does sinemet interact well with klono

Yes, no problem. It is compatible with most meds. Anti-psychotics however do the opposite as Sinemet (anti-psychotics = anti-dopamine)

does it improve memory? or fogginess?

It usually helps thinking but it may not be the complete answer. In general, if you have any dopamine weakness, Sinemet will help things work better - and 'things' are a broad list.

Sinemet often helps anxiety. Some get help with DR but it may also require Keppra.

Do you feel that Klonopin is making you feel foggy or other negative effects?

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I took dexedrine today ... almost all my symptoms except visual snow and and a bit of afterimages are gone

If you had success with Dexedrine, then it is likely you will improve with Sinemet. Dexedrine increases DA and NE about the same (NE is more stimulating than DA). Sinemet mostly increases DA and doesn't make one feel speedy.

does sinemet interact well with klono

Yes, no problem. It is compatible with most meds. Anti-psychotics however do the opposite as Sinemet (anti-psychotics = anti-dopamine)

does it improve memory? or fogginess?

It usually helps thinking but it may not be the complete answer. In general, if you have any dopamine weakness, Sinemet will help things work better - and 'things' are a broad list.

Sinemet often helps anxiety. Some get help with DR but it may also require Keppra.

Do you feel that Klonopin is making you feel foggy or other negative effects?

see im at a point where idk if its the klonopin causing the fogginess or its the attempted withdrawal from it but that was like 4-5 months ago.

i was looking at keppra but then sinemet came about and i dont want sinemet, keppra, and klonopin you know? also i dont wanna wait the 2 years that it would take to get completely off klono to get on sinemet. so any suggestions or ideas would help.

thanks

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Just wondering, if adderall increases dopamine and nonrepinephrine, then why does it affect our symptoms so negatively?

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Just wondering, if adderall increases dopamine and nonrepinephrine, then why does it affect our symptoms so negatively?

Sinemet is pre-cursor to dopamine I think whereas amphetamines are going to deplete the dopamine and make other problems.

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Just wondering, if adderall increases dopamine and nonrepinephrine, then why does it affect our symptoms so negatively?

Plus amphetamines cause pupil dilation which will severely increase visual symptoms.

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what im confused about is if Klonopin decreases dopamine and helps people, how can Sinemet increase dopamine and help as well? i seem really stupid bu jw lol.

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what im confused about is if Klonopin decreases dopamine and helps people, how can Sinemet increase dopamine and help as well? i seem really stupid bu jw lol.

I don't think Clonazepam (Klonopin) to my knowledge effects the dopamine systems in the brain, I could be wrong though.

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Different types of drugs may increase dopamine/serotonin/norepinephrine in the brain but most drugs have a selective affinity for a certain area in the brain or a certain type of dopaminergic/serotonergic receptor, and there are many different types of receptors. Two drugs that work by "increasing serotonin" can thus have vastly different and even opposite affects as most neurotransmitters are used for countless functions in different parts of the brain. Klonopin indirectly works on dopamine as it works on GABA receptors which mostly inhibit dopamine release.

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i was looking at keppra but then sinemet came about and i dont want sinemet, keppra, and klonopin you know? also i dont wanna wait the 2 years that it would take to get completely off klono to get on sinemet. so any suggestions or ideas would help.

If you wish to try Sinemet, there is no need to change anything else that you are taking – keep the Klonopin the same.

what im confused about is if Klonopin decreases dopamine and helps people, how can Sinemet increase dopamine and help as well?

"Clonazepam exerts its action by binding to the benzodiazepine site of the GABA receptors, which causes an enhancement of the electric effect of GABA binding on neurons, resulting in an increased influx of chloride ions into the neurons. This results in an inhibition of synaptic transmission across the central nervous system. Benzodiazepines, however, do not have any effect on the levels of GABA in the brain ... decreases the utilization of 5-HT (serotonin) by neuronsClonazepam decreases release of acetylcholine in cat brain and decreases prolactin release in rats" http://en.wikipedia....wiki/Clonazepam

Klonopin isn’t known for reducing dopamine (though the effect on prolactin in rats indicate the opposite effect - increase). By reducing both acetylcholine and serotonin, it will help ‘balance’ the ratio if you have low dopamine (another important topic). However, in the end, Klonopin acts like it increases GABA (through benzo receptors), which reduces brain activity. GABA does the opposite of Glutamate. These two neurotransmitters account for about 80% of all the body’s neurotransmitters. There are many complex feedback loops between all the brains systems but, again, Klonopin isn’t known for reducing dopamine.

Klonopin, by design, is an antiseizure drug. These drugs reduce brain activity. Thus also calm anxiety (an overactivity) and make a person drowsy. If it doesn’t make you drowsy, then you may have an overactive brain.

Just wondering, if adderall increases dopamine and norepinephrine, then why does it affect our symptoms so negatively?

Good question and leads to a distinction between meds. There are many drugs that increase dopamine or its effect: Requip, Wellbutrin, Selegiline, Adderall, Dexedrine, COMT inhibitors, amphetamines, methamphetamine, cocaine, LSD, etc… Each of these drugs work in different ways. [ And a few report positive results from Adderall. ]

Point 1 -- Sinemet (carbidopa/levodopa) is unique in that because levodopa as a precursor, it is not as forceful as many drugs. It will cause increase throughout the brain but it doesn’t cause huge changes unless there is a shortage in an area – then it is largely supplying a need.

Point 2 -- Most drugs affect several areas and are complex. Take Wellbutrin as an example. It is a weak DA reuptake inhibitor [makes it stay in the synapses longer so is more effective] yet at the same time tends to reduce the production of DA, it is a weak NE reuptake inhibitor, it reduces acetylcholine (nicotinic), and weakly inhibits the H1 histamine receptor.

Point 3 – Chain reaction. Norepinephrine is closely related to dopamine (one peroxide molecule different). Norepinephrine is made from dopamine (just as dopamine is made from levodopa). Epinephrine is made from Norepinephrine. Epinephrine IS adrenaline.

Both epinephrine and norepinephrine are stimulating by nature. Whereas dopamine is more ‘enabling’. All drugs that increase DA will exert some increase in NE. Some drugs increase NE a lot – and this often makes HPPD symptoms worse. Furthermore, if a drug forces dopamine too high, then this will likely have negative effects as well. (see next post for some more details)

So by increasing levodopa, you increase dopamine, norepinephrine, and epinephrine. Ultimately in the end, how much of any drug you take will determine its effects and side-effects.

500px-Catecholamines_biosynthesis.svg.png

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Sinemet and PFC (prefrontal cortex).

The PFC is where executive functions are performed – something that many of us complain about. "Executive function is an umbrella term for cognitive processes such as planning, working memory, attention, problem solving, verbal reasoning, inhibition, mental flexibility, multi-tasking, initiation and --monitoring of actions" -- http://en.wikipedia....xecutive_system

There is a close relationship between dopamine and norepinephrine (see post above). Again using PD (the ‘gold standard’ disease of low dopamine): "Parkinson’s patients have marked PFC cognitive deficits, … show a progressive profile of deficits resembling frontal lobe lesions. These include working memory deficits, impaired recency judgement, decreased planning, and impaired set-shifting. Depletion of NE in the PFC may contribute to the array of PFC cognitive deficits … Ironically, the medications given to Parkinson’s patients often worsen their cognitive impairment. High doses of [sinemet] (which increases both dopaminergic and NE transmission) … are often required to restore movement … However, these doses are often too high for the caudate and PFC. These sites have a more modest depletion, and in the case of the PFC, requires more delicate catecholaminergic manipulations. Thus, patients are often left with substantial cognitive impairment." – Brain Norepinephrine, Norepinephrine and cognitive disorders, p417

To better understand what is happening here, small increases of NE in the PFC improve the ability to focus and remain undistracted. Larger increases of NE do the opposite and stimulate the amygdala (fight/flight) and ‘alertness’.

Point 1 -- Some are wondering if Sinemet will improve fogginess and thinking ability. Low doses of Sinemet may help because of small increases of DA and NE in the PFC. Large doses may make thinking worse.

Point 2 – This is another reason for low doses. PD patients who are advanced must take a high doses in order to walk, thus part of the problem reported in the above quote.

Again, the chart above shows the trickledown effect of levodopa -> dopamine -> norepinephrine -> epinephrine.

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Someone's said (i think was you Visual) something about Sinemet and interaction with SSRI. I take 20mg of paroxetine everyday and i dont really know if it will cause some trouble with sinemet, i think you or other member said a paroxetine dose will low the effect of sinemet.

Maybe im wrong.

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Someone's said (i think was you Visual) something about Sinemet and interaction with SSRI. I take 20mg of paroxetine everyday and i dont really know if it will cause some trouble with sinemet, i think you or other member said a paroxetine dose will low the effect of sinemet.

Maybe im wrong.

Strictly speaking, they are not opposites. And some people with Parkinson’s disease do take SSRIs. They are on opposite ends of the circadian rhythm – dopamine is highest in AM and lowest in PM while serotonin is lowest in AM and highest in PM.

I am one of those who feels worse with increasing serotonin (something some HPPD sufferers report) but since you are taking one, it apparently doesn’t bother you. My experience with Lexapro (a SSRI) was I needed to take more Sinemet. And all meds tried that increase serotonin increase anxiety (a lot) and make vision worse (a little).

Here is a New York Times article http://health.nytime.../treatment.html "Although depression is very common in PD, there have been surprisingly few controlled studies. Antidepressants used for PD include tricyclics, particularly amitriptyline (Elavil). Some studies have found that selective serotonin-reuptake inhibitors (SSRIs) -- which include fluoxetine (Prozac), sertraline (Zoloft), and paroxetine (Paxil) -- may worsen symptoms of Parkinson's. Doctors should monitor patients taking SSRIs."

Obviously if Paxil is making you feel better, then you may wish to keep using it. And while you don’t have PD, the above quote indicates some problems with the two – it isn’t interaction but rather the underlying need these people have.

Hope this helps…

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Didnt know where to post, figured this would be the best spot...went to the neurologist, was hesitant to give me sinemet, instead sent me to get a neuropsychiatric exam so he could pinpoint what areas of my cognition were affected and thus close in on the brain areas that need help...fucking sucks...gotta wait 3 weeks til the exam when my insurance goes through and then who knows...back to being perma bummed

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just keep scheduling app w/ different nuero's, that's what i'm going to do. If they want to do testing I'll tell them to fuck off and go to the next. I always schedule my doc app. in bunches, so when one goes wrong I don't have to wait long. When you find one you like just cancel the other appointments so you don't get charged. Look up your insurance online, you'll find every type of doc in all your surrounding cities.

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Thanks a lot for the info Visual. My Dr. told me that i have to take the 20mg of paroxetine for at least a year (to March-April 2012) but i think i cant wait that time.

I will show your post from The New York Times to my Dr.

PD: I completely sure the ssri med are f'ck my vision.

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Didnt know where to post, figured this would be the best spot...went to the neurologist, was hesitant to give me sinemet, instead sent me to get a neuropsychiatric exam so he could pinpoint what areas of my cognition were affected and thus close in on the brain areas that need help...fucking sucks...gotta wait 3 weeks til the exam when my insurance goes through and then who knows...back to being perma bummed

That's foolish. Taking an exam is going to allow him to exactly pinpoint what the problem is? He must be the smartest man on earth who is able to cure anything then with his fool-proof testing.

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i guess it just shows which areas of my cognition are most affected, and then he can hone in on an area of my brain, depending on their corresponding functions...yea it's dumb, but i just figure if it gets me through his door again talking about meds i might be able to get a script in the future

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went to the neurologist, was hesitant to give me sinemet, instead sent me to get a neuropsychiatric exam so he could pinpoint what areas of my cognition were affected and thus close in on the brain areas that need help

It isn’t so easy to get a doctor to prescribe stuff for you. Doubly frustrating is not even knowing if a specific med, such as Sinemet, will work for you. There are a lot of docs willing to try meds, but it is often limited to ones they have experience with.

In general it takes developing a working relationship with a doctor over time. And a lot of these guys are a pain in the rear end. I’ve heard doctors say blatantly incorrect things. Part of the problem is the lack of number of cases. Most docs deal with the same old issues day in and day out. Take diabetes, it must be very boring to be an endocrinologist – the same answer: ‘lose weight, eat less, exercise, take insulin’ … then much of the time patients don’t really comply. (given that 95%+ of all diabetes is the result of lifestyle)

As far as Neurocognitive testing goes, this is a very good idea if you can get it paid for. These tests are often about 8 hours and ‘exercise’ different parts of the brain to identify strong and weak areas. The quote in post #17 about cognitive problems with PD was, in the end, established by these tests. These tests will show LOTS of things that will NOT show on a MRI.

1998 has good advice about scheduling several doctors. At the same time, go ahead and see if you can get the testing done – the doctor is actually doing you a good service on this point.

Summery – Try to work with your general doctor. If he won’t help, then seek a doctor familiar with treating brain injuries. Also, if someone is involved in research as well, then they may be more alert to try things (not just the same old boring things). If one doc won’t help, then shop around – you are buying a service, so require that they perform it.

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