I don't really know much about the neurotoxicity of neuroleptics. I just know that factors like reduced blood flow or down regulation ( even though some evidence points out, that the body increases dopamin receptors ) can contribute to neurotoxicity. Why I want to know it? I took Risperidon 1mg for around 10 days and Aripiprazol 10 mg for 4 weeks. After that I reduced it to zero over 20 days, because my psychatric ward didn't want to advice me and I couldn't get any appointment by any neurologist. I am still hampered in life with cognitive deficiencies and parathesias. I am hoping to recover through neuroplasticy. I am around 22 so my brain still grows, even though I am not sure if it can grow right now, since I have not been able to find out how long these drugs bind to the receptors. Is a recovery possible?
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N&PD Moderators: Skorpio | thegreenhand
Neuroleptic neurotoxicity
- Thread starter mb-909
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dopamimetic
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I think it greatly varies between individuals. While some have no problems with prolonged neuroleptic intake or even positive reaction on them, for me they are among the worst drugs ever, getting worse with potency increasing.
^i definitely agree. the only favorable risk-benefit ratio i see with using neuroleptics is to control psychosis.
op, the drugs binding remains as far as their activity. those who witness cognitive impairment far beyond that are usually psychiatrically ill.
op, the drugs binding remains as far as their activity. those who witness cognitive impairment far beyond that are usually psychiatrically ill.
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Anti-psychotics are serious drugs. They should only be used when indicated. But, for instance, seroquel is one that has low D2 binding affinity and is used to good results in bi-polar disorder. The same goes for abilify. For some reason everyone I've met who's been prescribed geodon is female. Weird. Werd.
I would think that you're not experiencing their lingering effects on your brain. Why did you get off it in the first place?
I would think that you're not experiencing their lingering effects on your brain. Why did you get off it in the first place?
Trying2Iso
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I take abilify, i have not noticed any changes, and i'm actually getting better marks in college than i was before the medication. i feel smarter tbh...
entirely probable as seen in schizophrenic patients.
wezface
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I hadn't attributed it to that but since starting Abilify (I have treatment resistant depression and am on Lexapro and Abilify as well as gabapentin, milnacipran (Savella), ropinirole and tizanidine for chronic pain/spasms) I can think more clearly as well, though the akasthisia/involuntary movements are incredibly uncomfortable and annoying.
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Abilify is the best for schoolwork imo.
I personally couldn't focus without a typical anti-psychotic, but to each their own.
The akathesia (as you describe it) is probably just restlessness. I had that. It actually went away. That was the major factor in me going off my medication in the past. Please give it a couple months. And perhaps ask about cogentin, though it will make you less cognitively adept. Right now, your health should come before anything else.
I personally couldn't focus without a typical anti-psychotic, but to each their own.
The akathesia (as you describe it) is probably just restlessness. I had that. It actually went away. That was the major factor in me going off my medication in the past. Please give it a couple months. And perhaps ask about cogentin, though it will make you less cognitively adept. Right now, your health should come before anything else.
First of all, I was diagnosed with F21 or severe Depression, depending on the doctor you ask. I stopped using it, because I don't want to suffer brain shrinkage anymore. I can not think of anything positive, besides a little better concentration. Right now, I would guess that I am around 80-90 % of my oldself. The tremors are nearly away, but my creativity is gone and I still have brain zaps. Some people rellay depend on these drugs, but most of them just need a good psychotherapy. These drugs are way worse than you think. I might post a way bigger post of the trouble I have, later on, I need to eat something first ^^.
wezface
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I have actually had akasthisia/tremors/jerks for quite some time, before starting the abilify. I have fibromyalgia (or something, still being tested for MS) and the Abilify has only made these things worse. I do get them regularly, though.
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^Oh okay.
The literature doesn't support your claim, mb. .2% more shrinkage per year isn't significant. And your claim about psychotherapy is just banal.
The literature doesn't support your claim, mb. .2% more shrinkage per year isn't significant. And your claim about psychotherapy is just banal.
I am still suffering from neuroleptics. Therefor I am a little bit biased, so take the following post with a grain of salt.
Neuroleptics, also called antipsychotics, are medications used against all kind of mental illnesses. Once these illnesses were thought to be neurotransmitter imbalances. As of today we know that this is not the case. People with psychosis, who are not treated by neuroleptics, don't differ much from healthy people in terms of brain shrinkage. The thougt of bigger brain shrinkage induced by shizophrenia was directly linked to the dose and culmutive length of treatment with psychotics. Atypical and the old antipsychotics don't differ much from the negative side effects. In case of brain atrophy the biggest change happens within the first few months and slows down over time for first time treaties. These big changes do not happen for long term treaties by changing medications. The brain shrinkage is not that big, but it is still worrying that it happenes.
These medications are perscribed, because they are lessening the negative symptoms associated with psychotics and are told to not cause dependency. But in my case and several others experiencing withdrawal symptoms by reducing or quiting neuroleptics it speaks for dependency. The side effects include diziness, loss of sight, tremors and so on. They make you numb. You are turned into a zombie. It not only causes damage to the brain, but to all other organs as well.
Abilify (aripiprazol) is perscribed even for teenagers, which are still developping. By blocking the receptors in the brain, brain growth can be stopped and might lead to problems later on. If these changes are reversible is not known.
So why are these strong medications available for nearly everybody? Most of the studies on these subjects are sponsored directly by big pharma industries paying scientists extra bucks for a positive result. Sometimes these studies are not carried out by these scientists just signatured by them. Big pharma industries not only give free book samples to universities but also sponsor them for pharma developing. The biggest problem is hereby that the principles of medications for psychotics is written by the big pharma industries and the new doctors and psychologists believe them blindly. Negative studies are often published too late. The worst part of all, is that the psychologists, scientists and the industry as well can't be belonged for their actions. And so the long term project with antipsychotics goes on. By the way: antidepressants are not much better.
In some cases a treatment is necessary and therefor the lowest possible dose should be find to reduce the long term side effects. But for a good treatment you need a good psychotherapy, too, because the drug only lessens the symptoms, but not the cause.
But who tells us what it means to be mentally ill? Why do the doctors differ with their prognosis and their diagnosis? Is it not normal to be sick or better called different?
Neuroleptics, also called antipsychotics, are medications used against all kind of mental illnesses. Once these illnesses were thought to be neurotransmitter imbalances. As of today we know that this is not the case. People with psychosis, who are not treated by neuroleptics, don't differ much from healthy people in terms of brain shrinkage. The thougt of bigger brain shrinkage induced by shizophrenia was directly linked to the dose and culmutive length of treatment with psychotics. Atypical and the old antipsychotics don't differ much from the negative side effects. In case of brain atrophy the biggest change happens within the first few months and slows down over time for first time treaties. These big changes do not happen for long term treaties by changing medications. The brain shrinkage is not that big, but it is still worrying that it happenes.
These medications are perscribed, because they are lessening the negative symptoms associated with psychotics and are told to not cause dependency. But in my case and several others experiencing withdrawal symptoms by reducing or quiting neuroleptics it speaks for dependency. The side effects include diziness, loss of sight, tremors and so on. They make you numb. You are turned into a zombie. It not only causes damage to the brain, but to all other organs as well.
Abilify (aripiprazol) is perscribed even for teenagers, which are still developping. By blocking the receptors in the brain, brain growth can be stopped and might lead to problems later on. If these changes are reversible is not known.
So why are these strong medications available for nearly everybody? Most of the studies on these subjects are sponsored directly by big pharma industries paying scientists extra bucks for a positive result. Sometimes these studies are not carried out by these scientists just signatured by them. Big pharma industries not only give free book samples to universities but also sponsor them for pharma developing. The biggest problem is hereby that the principles of medications for psychotics is written by the big pharma industries and the new doctors and psychologists believe them blindly. Negative studies are often published too late. The worst part of all, is that the psychologists, scientists and the industry as well can't be belonged for their actions. And so the long term project with antipsychotics goes on. By the way: antidepressants are not much better.
In some cases a treatment is necessary and therefor the lowest possible dose should be find to reduce the long term side effects. But for a good treatment you need a good psychotherapy, too, because the drug only lessens the symptoms, but not the cause.
But who tells us what it means to be mentally ill? Why do the doctors differ with their prognosis and their diagnosis? Is it not normal to be sick or better called different?
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i think you're right in that they're medications handed out lightly by physicians for indications which pharmaceutical companies have lobbied for. they have a dangerous adverse effect profile aside from being neurotoxic, they can increase the risk of cardiovascular disease, diabetes, and obesity.
instances of psychosis and paranoid delusions however do at times, require the use of anti-psychotics.
instances of psychosis and paranoid delusions however do at times, require the use of anti-psychotics.
r. Nancy C. Andreasen concentrates on the big questions. A neuroscientist and psychiatrist at the University of Iowa, she uses M.R.I. to ask questions like: How do the nervous systems of extremely creative people differ from those of the rest of us? How is the brain physiology of the mentally ill different from that of normal people? For nearly two decades, she has been conducting a study that tracks long-term changes in the brain. We spoke this summer when she visited New York City. An edited version of a three-hour conversation follows:
Q. HOW DID YOU BECOME A PSYCHIATRIST?
A. I was an English professor in the early 1960s. I’d done a book on John Donne. Then, in 1964, I gave birth to my first child and nearly died from a postpartum infection — the very thing that had killed millions of birthing women in the centuries before antibiotics. As I recovered, I realized I had been given back my life, and that caused me to rethink everything in it. I decided to quit literature studies and go back to school to become a doctor.
From the outset, I knew I wanted to do research and patient care. Because I relish complexity, I chose psychiatry — it’s more complicated than neurology. And I chose brain research because the brain is the most complicated organ in the body. I wanted to do something as important as the discovery of penicillin, the thing that had saved me.
Q. YOU PIONEERED THE USE OF IMAGING TECHNOLOGY FOR LEARNING ABOUT THE PHYSIOLOGY OF THE BRAIN. HOW DID THE IDEA OF USING CAT SCANS AND M.R.I.’S AS A RESEARCH TOOL COME TO YOU?
A. My first patient was a schizophrenic. After working with him, I wanted to understand how this terrible disease developed, how to stop it and to find better treatments. Right away, I began searching for new tests to assay brain activities. With the technology we had at that time, you couldn’t see brain differences easily. A lot of our information came from autopsies done on patients, but that was of limited use because you had nothing to compare it to.
But then, in the early 1970s, CT scans came along. They got pictures of the inside of a living patient’s brain. I recognized the potential immediately. The problem was convincing my colleagues. CT scans involved exposing patients to radiation. When I went to the human experimentation committee at my medical school, they went, “We don’t want you subjecting patients to radiation. Besides, you’re not going to find anything that way, anyway.” It took a long time to convince them.
Q. TODAY, IMAGING STUDIES ARE ONE OF THE MAINSTAYS OF NEUROSCIENCE. WHEN DID ATTITUDES CHANGE?
A. In the early 1980s, when magnetic resonance imaging came on line. M.R.I.’s did not expose patients to radiation, and you could see brain structures in exquisite detail. I decided to use it for a longitudinal study of brain changes over a long period of time. We’re asking: Is schizophrenia a neurodegenerative disease like Alzheimer’s?
In 1989, I began to collect subjects — some with schizophrenia and some not — and began taking pictures of their brains. With the schizophrenics, we began seeing them at the first onset of their disease, which is usually at around age 24. We recruited about 538 people with schizophrenia. Eighteen years later, we’re still following 305.
Q. AND WHAT HAVE YOU FOUND?
A. I haven’t published this yet. But I have spoken about it in public lectures. The big finding is that people with schizophrenia are losing brain tissue at a more rapid rate than healthy people of comparable age. Some are losing as much as 1 percent per year. That’s an awful lot over an 18-year period. And then we’re trying to figure out why. Another thing we’ve discovered is that the more drugs you’ve been given, the more brain tissue you lose.
Q. WHY DO YOU THINK THIS IS HAPPENING?
A. Well, what exactly do these drugs do? They block basal ganglia activity. The prefrontal cortex doesn’t get the input it needs and is being shut down by drugs. That reduces the psychotic symptoms. It also causes the prefrontal cortex to slowly atrophy.
If I were developing new drugs, I’d switch targets. Till now it’s been chemically formulated targets. I believe we should be thinking more anatomically and asking, “With schizophrenics, which brain regions are functioning abnormally?”
Q. ARE YOU WORRIED YOUR FINDINGS MIGHT BE MISUSED?
A. The reason I sat on these findings for a couple of years was that I just wanted to be absolutely sure it was true. My biggest fear is that people who need the drugs will stop taking them.
Q. WHAT ARE THE POLICY IMPLICATIONS OF THIS FINDING?
A. Implication 1: that these drugs have to be used at the lowest possible dose, which often doesn’t happen now. There’s huge economic pressure to medicate patients very rapidly and to get them out of the hospital right away. Implication 2: we need to find other drugs that work on other systems and parts of the brain. Implication 3: whatever medications we use need to be combined with more nonmedication-oriented treatments, like cognitive or social therapies.
Q. IN YOUR LONGITUDINAL STUDY, ARE YOU ALSO LOOKING AT HOW THE NORMAL BRAIN AGES?
A. Yes. I’ve been asking, “At what point is human brain maturation complete and at what point do our brains naturally decline and lose tissue?” The answer is: the human brain continues to mature till about 25. At about 25, it plateaus for about 20 years, and at about 45, we start to lose brain tissue.
But it’s interesting: we lose brain tissue, but we don’t necessarily lose cognitive capacities. A lot of people at 50, 60, 70 or 80 are quite sharp. I can quantify their brain tissue and see they’ve lost quite a bit from what would be normal for a 45-year-old, but their cognitive abilities are not at all impaired.
- New York Times
Q. HOW DID YOU BECOME A PSYCHIATRIST?
A. I was an English professor in the early 1960s. I’d done a book on John Donne. Then, in 1964, I gave birth to my first child and nearly died from a postpartum infection — the very thing that had killed millions of birthing women in the centuries before antibiotics. As I recovered, I realized I had been given back my life, and that caused me to rethink everything in it. I decided to quit literature studies and go back to school to become a doctor.
From the outset, I knew I wanted to do research and patient care. Because I relish complexity, I chose psychiatry — it’s more complicated than neurology. And I chose brain research because the brain is the most complicated organ in the body. I wanted to do something as important as the discovery of penicillin, the thing that had saved me.
Q. YOU PIONEERED THE USE OF IMAGING TECHNOLOGY FOR LEARNING ABOUT THE PHYSIOLOGY OF THE BRAIN. HOW DID THE IDEA OF USING CAT SCANS AND M.R.I.’S AS A RESEARCH TOOL COME TO YOU?
A. My first patient was a schizophrenic. After working with him, I wanted to understand how this terrible disease developed, how to stop it and to find better treatments. Right away, I began searching for new tests to assay brain activities. With the technology we had at that time, you couldn’t see brain differences easily. A lot of our information came from autopsies done on patients, but that was of limited use because you had nothing to compare it to.
But then, in the early 1970s, CT scans came along. They got pictures of the inside of a living patient’s brain. I recognized the potential immediately. The problem was convincing my colleagues. CT scans involved exposing patients to radiation. When I went to the human experimentation committee at my medical school, they went, “We don’t want you subjecting patients to radiation. Besides, you’re not going to find anything that way, anyway.” It took a long time to convince them.
Q. TODAY, IMAGING STUDIES ARE ONE OF THE MAINSTAYS OF NEUROSCIENCE. WHEN DID ATTITUDES CHANGE?
A. In the early 1980s, when magnetic resonance imaging came on line. M.R.I.’s did not expose patients to radiation, and you could see brain structures in exquisite detail. I decided to use it for a longitudinal study of brain changes over a long period of time. We’re asking: Is schizophrenia a neurodegenerative disease like Alzheimer’s?
In 1989, I began to collect subjects — some with schizophrenia and some not — and began taking pictures of their brains. With the schizophrenics, we began seeing them at the first onset of their disease, which is usually at around age 24. We recruited about 538 people with schizophrenia. Eighteen years later, we’re still following 305.
Q. AND WHAT HAVE YOU FOUND?
A. I haven’t published this yet. But I have spoken about it in public lectures. The big finding is that people with schizophrenia are losing brain tissue at a more rapid rate than healthy people of comparable age. Some are losing as much as 1 percent per year. That’s an awful lot over an 18-year period. And then we’re trying to figure out why. Another thing we’ve discovered is that the more drugs you’ve been given, the more brain tissue you lose.
Q. WHY DO YOU THINK THIS IS HAPPENING?
A. Well, what exactly do these drugs do? They block basal ganglia activity. The prefrontal cortex doesn’t get the input it needs and is being shut down by drugs. That reduces the psychotic symptoms. It also causes the prefrontal cortex to slowly atrophy.
If I were developing new drugs, I’d switch targets. Till now it’s been chemically formulated targets. I believe we should be thinking more anatomically and asking, “With schizophrenics, which brain regions are functioning abnormally?”
Q. ARE YOU WORRIED YOUR FINDINGS MIGHT BE MISUSED?
A. The reason I sat on these findings for a couple of years was that I just wanted to be absolutely sure it was true. My biggest fear is that people who need the drugs will stop taking them.
Q. WHAT ARE THE POLICY IMPLICATIONS OF THIS FINDING?
A. Implication 1: that these drugs have to be used at the lowest possible dose, which often doesn’t happen now. There’s huge economic pressure to medicate patients very rapidly and to get them out of the hospital right away. Implication 2: we need to find other drugs that work on other systems and parts of the brain. Implication 3: whatever medications we use need to be combined with more nonmedication-oriented treatments, like cognitive or social therapies.
Q. IN YOUR LONGITUDINAL STUDY, ARE YOU ALSO LOOKING AT HOW THE NORMAL BRAIN AGES?
A. Yes. I’ve been asking, “At what point is human brain maturation complete and at what point do our brains naturally decline and lose tissue?” The answer is: the human brain continues to mature till about 25. At about 25, it plateaus for about 20 years, and at about 45, we start to lose brain tissue.
But it’s interesting: we lose brain tissue, but we don’t necessarily lose cognitive capacities. A lot of people at 50, 60, 70 or 80 are quite sharp. I can quantify their brain tissue and see they’ve lost quite a bit from what would be normal for a 45-year-old, but their cognitive abilities are not at all impaired.
- New York Times
what does that say that we don't already know? nowhere does it say that the schizophrenic brain does not lose brain tissue without the use of anti-psychotics. it only states that brain tissue is lost more rapidly with the use of anti-psychotics which can be deduced using logic. if anti-psychotics are neurotoxic and schizophrenics are proven to suffer cognitive decline then the combination of both would probably amplify this symptom or set of symptoms.
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Not significant at all, depending on dosage and individual metabolism, etc.
I should have stated that "neurotoxic" is a very subjective and loaded word.
There's a lot I want to respond to but I'll keep it short:
1: the loss isn't significant
2: schizophrenics are notorious for smoking and being overweight, the latter of which probably contributes more to cognitive decline than anti-psychotics
3: lots of schziophrenics are very smart
4: if untreated, though in the beginning they may appear very smart, their cognition will probably decline drastically
paranoid android
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I have never been on Abilify but i have been on Quetiapine, Risperidone and Olanzapine long term. I was on Quetiapine for a few years at doses of 300-400mg's a day and i still take it now if i am starting to get manic. I was on Olanzapine only for a short time as i used to get the sample packs of Zyprexa Zydis but they stopped handing them out and even the generic Olanzapine tablets cost a fortune. I was on Risperidone for maybe a year or more at doses of up to 4mg's depending on how Manic i was.
I have not noticed any negative effects on my cognitive abilities at all and if anything it they sort of help me in that regard as they slow my brain down to normal speed instead of having those godforsaken racing thoughts. Risperidone does sometimes have a blunting effect on me at doses of over 2mg's a day if i am not manic. I find Risperidone to be the worst for causing that zombie effect by far and i have taken old typical anti-psychotics such as Largactil/Thorazine, Stemetil/Compazine and Methotrimeprazine aka Levomepromazine (trade name Nozinan). The Nozinan is a low potency anti-psychotic but due to it's really strong anti-cholinergic and anti-histaminic effects it's so sedating it makes Quetiapine look like Dextroamphetamine.
I personally wouldn't worry about it unless your taking really potent and nasty D2 antagonists like Haldol. Clopixol, Pimozide aka Orap or any of the other really potent typical anti-psychotics. Granted Risperidone is also a really potent D2 antagonist and like Haldol causes very little sedation but causes that shitty zombie effect. Generally it's the really potent D2 antagonists without much in the way of anti-cholinergic or H1 antagonism that are the worst for causing movement disorders associated with anti-psychotics.
I would be really interested in trying Clozapine as it's a D3 antagonist as well as being a 5-HT1a receptor antagonist as well as having some effect on the Gaba-B receptor. It is not known for causing movement disorders at all and get's the best rep out of all of them for treating Schizophrenia, Bipolar disorder as well as Major depression. Of course the nasty side effects like agranulocytosis as well as the cardiac problems makes it a drug of last resort really. I really wish they would get around to marketing DHA-Clozapine which apparently bypasses these side effects.
I have not noticed any negative effects on my cognitive abilities at all and if anything it they sort of help me in that regard as they slow my brain down to normal speed instead of having those godforsaken racing thoughts. Risperidone does sometimes have a blunting effect on me at doses of over 2mg's a day if i am not manic. I find Risperidone to be the worst for causing that zombie effect by far and i have taken old typical anti-psychotics such as Largactil/Thorazine, Stemetil/Compazine and Methotrimeprazine aka Levomepromazine (trade name Nozinan). The Nozinan is a low potency anti-psychotic but due to it's really strong anti-cholinergic and anti-histaminic effects it's so sedating it makes Quetiapine look like Dextroamphetamine.
I personally wouldn't worry about it unless your taking really potent and nasty D2 antagonists like Haldol. Clopixol, Pimozide aka Orap or any of the other really potent typical anti-psychotics. Granted Risperidone is also a really potent D2 antagonist and like Haldol causes very little sedation but causes that shitty zombie effect. Generally it's the really potent D2 antagonists without much in the way of anti-cholinergic or H1 antagonism that are the worst for causing movement disorders associated with anti-psychotics.
I would be really interested in trying Clozapine as it's a D3 antagonist as well as being a 5-HT1a receptor antagonist as well as having some effect on the Gaba-B receptor. It is not known for causing movement disorders at all and get's the best rep out of all of them for treating Schizophrenia, Bipolar disorder as well as Major depression. Of course the nasty side effects like agranulocytosis as well as the cardiac problems makes it a drug of last resort really. I really wish they would get around to marketing DHA-Clozapine which apparently bypasses these side effects.
I just know that Haldol is one of the most neurotoxic drugs out there and it can lead to brain shrinkage in some brain areas of up to 4,7 % in the first year. What does it matter, if your total brain shrinkage is around 0.2-0.6 % if you have these big changes in some areas? That is my biggest concern. Some say that Abilify is as efficient as Haldol after only 3 days of use and it has a T1/2 of 75 hours compared to Haldol's 6-32 hours. I found out that Abilify leads to changes lasting up to 12 weeks after quitting... I am in week 7 and I am feeling smarter overall, even though my thoughts are racing again one day, I am going to learn to adapt to it, because it can be a big advantage if used correctly. It is not a bad thing, because it shows that your brain works great! Risperidon is pretty much like Haldol and shows big changes as well. Does anybody have some studies on Abilify since the producer has said that they won't start other studies in the future, which is a crime if you ask me.
Dresden
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They're all neurotoxic. I've been taking one or another typical or atypical antipsychotic for 19 years, and I can't stop. I've tried more than once. It's terrible. But at least I'm not in a psychiatric hospital. Plus, neuroleptics are great for toning down an amphetamine binge or aborting a psychedelic trip turned bad. I've been taking Haldol for 4 years. Just this past year, I successfully reduced my dosage from 20mg/night to 10mg/night, but it didn't help any with my 50 lb. weight gain. If 10mg of Haldol at night gave me akathisia on a regular basis, then I would force myself to go off it. I hate akathisia! Worst feeling ever. And I feel so sorry for those usually middle age men or women on the bus with obvious, uncontrolled, and socially debilitating involuntary muscle movements. I know it's tardive dyskinesia, which is one thing I've been lucky not to get so far. Knocks on wood.