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Does Keppra Cause OCD Like Symptoms?
Question: Dear Dr. Solanki,
During 2009 i was taking Lamictal 100mg, Solian 100 mg, Klonopin 3 mg and Lexapro 10 mg. I had then some "ocd/phobia like" troubles probably linked to dopaminergic activity of Solian at low dose (it's even worse when i take Solian 200 mg), but it happened that these symptoms -and it's not exactly OC because there are no rituals or compulsive attitude and so on- disappeared changing Lamictal for Keppra. As far as i know, Keppra is linked to calcium channels and these channels can act on dopamine (to release it or stop it). ¿Some kind of relation is possible? Because if not, there will be no explanation of an "OC/phobia like" symptom disappearing from Lamictal to Keppra. The symptom was gone during 4 years and it appeared again changing from Keppra to Neurontin.
I want so insist that i don't have OC, is just "like OC" but a problem with images without any rituals, compulsive attitudes and so on.
I would like to have your opinion, thanks XXXXXXX
During 2009 i was taking Lamictal 100mg, Solian 100 mg, Klonopin 3 mg and Lexapro 10 mg. I had then some "ocd/phobia like" troubles probably linked to dopaminergic activity of Solian at low dose (it's even worse when i take Solian 200 mg), but it happened that these symptoms -and it's not exactly OC because there are no rituals or compulsive attitude and so on- disappeared changing Lamictal for Keppra. As far as i know, Keppra is linked to calcium channels and these channels can act on dopamine (to release it or stop it). ¿Some kind of relation is possible? Because if not, there will be no explanation of an "OC/phobia like" symptom disappearing from Lamictal to Keppra. The symptom was gone during 4 years and it appeared again changing from Keppra to Neurontin.
I want so insist that i don't have OC, is just "like OC" but a problem with images without any rituals, compulsive attitudes and so on.
I would like to have your opinion, thanks XXXXXXX
Brief Answer:
yes keppra has role
Detailed Answer:
Hello XXXXXXX
Thanks for contacting me directly.
First of all some neurobilogy of OC:
The many clinical drug trials that have been conducted support the hypothesis that dysregulation of serotonin is involved in the symptom formation of obsessions and compulsions in the disorder. Data show that serotonergic drugs are more effective in treating OCD than drugs that affect other neurotransmitter systems.
Role of epinephrine is also inconclusive.
There is debate over role of dopamine. But yes some studies are there suggesting role of dopamine in OCD.
http://www.yyyyyyyyyyyyyyyyyy/pubmed/0000
http://www.yyyyyyyyyyyyyyyyyyyy/pubmed/0000
We have seen both OC symptoms after use of anti psychotic in patients and improvement of OC symptoms after adding anti psychotic medicine to SSRI.
This means some role of dopamine is there but how it works and what role is still a research topic.
A higher than usual incidence of nonspecific EEG abnormalities occurs in patients with OCD. Sleep EEG studies have found abnormalities also.
Considering above pathology in OCD keppra may be working in OC as follows.
It binds to synaptic vesicle protein SV2A, which is involved in synaptic vesicle
exocytosis. It opposes the activity of negative modulators of GABA- and glycine-gated currents and partially inhibits N-type calcium currents in neuronal cells. With these mechanisms it exerts its antiepileptic effects. As i mentioned some abnormalities in EEG in OCD so keppra is likely working through this anti-epileptic mechanism (in epilepsy EEG abnormalities are evident).
Now role of keppra in doapmine regulation:
http://www.yyyyyyyyyyyyyyyyyy/0000
It increases dopamine level in general but with genetic variation it decreases the dopamine level. So yes keppra was working in OC symptoms through dopamine also likely.
However it is not established drug for OCD. I found one proposed trial but it was closed due to some unknown reason.
https://www.yyyyyyyyyyyyyyyyy.gov/yy/show/yyyyy/NCT0000
Hope this answer will help to clarify your doubts.
Regards,
Dr.Chintan Solanki.
yes keppra has role
Detailed Answer:
Hello XXXXXXX
Thanks for contacting me directly.
First of all some neurobilogy of OC:
The many clinical drug trials that have been conducted support the hypothesis that dysregulation of serotonin is involved in the symptom formation of obsessions and compulsions in the disorder. Data show that serotonergic drugs are more effective in treating OCD than drugs that affect other neurotransmitter systems.
Role of epinephrine is also inconclusive.
There is debate over role of dopamine. But yes some studies are there suggesting role of dopamine in OCD.
http://www.yyyyyyyyyyyyyyyyyy/pubmed/0000
http://www.yyyyyyyyyyyyyyyyyyyy/pubmed/0000
We have seen both OC symptoms after use of anti psychotic in patients and improvement of OC symptoms after adding anti psychotic medicine to SSRI.
This means some role of dopamine is there but how it works and what role is still a research topic.
A higher than usual incidence of nonspecific EEG abnormalities occurs in patients with OCD. Sleep EEG studies have found abnormalities also.
Considering above pathology in OCD keppra may be working in OC as follows.
It binds to synaptic vesicle protein SV2A, which is involved in synaptic vesicle
exocytosis. It opposes the activity of negative modulators of GABA- and glycine-gated currents and partially inhibits N-type calcium currents in neuronal cells. With these mechanisms it exerts its antiepileptic effects. As i mentioned some abnormalities in EEG in OCD so keppra is likely working through this anti-epileptic mechanism (in epilepsy EEG abnormalities are evident).
Now role of keppra in doapmine regulation:
http://www.yyyyyyyyyyyyyyyyyy/0000
It increases dopamine level in general but with genetic variation it decreases the dopamine level. So yes keppra was working in OC symptoms through dopamine also likely.
However it is not established drug for OCD. I found one proposed trial but it was closed due to some unknown reason.
https://www.yyyyyyyyyyyyyyyyy.gov/yy/show/yyyyy/NCT0000
Hope this answer will help to clarify your doubts.
Regards,
Dr.Chintan Solanki.
Above answer was peer-reviewed by :
Dr. Chakravarthy Mazumdar
Dear Dr. Solanki,
Thank you for your explanation. As i said, at the end of 2009 with change from Lamictal to Keppra the symptoms were gone. Now, they are still there, but not so strong since two weeks, in a similar dose to the one of the end of 2009, i mean Klonopin 3mg (the same), Lexapro 15 mg (5 mg more), Keppra 1000mg (the same) and Solian 100 mg (the same). But during the last two years before the accident with Neurontin(may 2014) i was on Lexapro 0.75 mg and Klonopin 1 mg. Maybe these drugs lost their cumulative effect? maybe i have to wait for this effect again, say for example more or least 6 weeks for the full effect of Lexapro, since it worked before during some years at 10 mg?
Thanks beforehand, XXXXXXX
Thank you for your explanation. As i said, at the end of 2009 with change from Lamictal to Keppra the symptoms were gone. Now, they are still there, but not so strong since two weeks, in a similar dose to the one of the end of 2009, i mean Klonopin 3mg (the same), Lexapro 15 mg (5 mg more), Keppra 1000mg (the same) and Solian 100 mg (the same). But during the last two years before the accident with Neurontin(may 2014) i was on Lexapro 0.75 mg and Klonopin 1 mg. Maybe these drugs lost their cumulative effect? maybe i have to wait for this effect again, say for example more or least 6 weeks for the full effect of Lexapro, since it worked before during some years at 10 mg?
Thanks beforehand, XXXXXXX
Brief Answer:
yes wait it will work likely
Detailed Answer:
Dear XXXXXXX
According to guidelines in any psychiatric problem in past if any drug was effective the same drug should be used as first choice when similar episodes/symptoms come again.
Yes you thought right.Lexapro (SSRI) works gradually. Specifically in OC symptoms it takes more time than that in depression. You are already on 5 mg dose higher dose than previous. At 4 weeks noticeable improvement should be there, if not dose should be increased. At 4 weeks if improvement is there better to wait for more 4 weeks to see full effect.
Feel free to discuss further.
Take care.
yes wait it will work likely
Detailed Answer:
Dear XXXXXXX
According to guidelines in any psychiatric problem in past if any drug was effective the same drug should be used as first choice when similar episodes/symptoms come again.
Yes you thought right.Lexapro (SSRI) works gradually. Specifically in OC symptoms it takes more time than that in depression. You are already on 5 mg dose higher dose than previous. At 4 weeks noticeable improvement should be there, if not dose should be increased. At 4 weeks if improvement is there better to wait for more 4 weeks to see full effect.
Feel free to discuss further.
Take care.
Above answer was peer-reviewed by :
Dr. Raju A.T
Dear Dr. Solanki,
Thanks for your clear answer.
I have a last doubt.
There is release of dopamine with Solian at low dose, but according to you there is no clear relation established between this and Keppra. But according to books on cellular physiology, dopamine release depends on levels of cytosolic calcium (higher cytosolic calcium, higher dopamine release). You wrote that Keppra inhibits N-type calcium currents in neuronal cells. As far as i understand, calcium is then lower in those cells: if the relation "higher cytosolic means higher dopamine release" is right according to books, the opposite can be true? I hardly see how an antiepileptic could increase dopamine levels, including an antiepileptic (Keppra, in this case) which stops Levodopa induced effects. ¿Why what works with Keppra doesn't works with Lamictal or Neurontin? I know that in psychiatry there are a lot of things not investigated, but i guess some relations between meds are possible to establish.
Thanks beforehand, XXXXXXX
Thanks for your clear answer.
I have a last doubt.
There is release of dopamine with Solian at low dose, but according to you there is no clear relation established between this and Keppra. But according to books on cellular physiology, dopamine release depends on levels of cytosolic calcium (higher cytosolic calcium, higher dopamine release). You wrote that Keppra inhibits N-type calcium currents in neuronal cells. As far as i understand, calcium is then lower in those cells: if the relation "higher cytosolic means higher dopamine release" is right according to books, the opposite can be true? I hardly see how an antiepileptic could increase dopamine levels, including an antiepileptic (Keppra, in this case) which stops Levodopa induced effects. ¿Why what works with Keppra doesn't works with Lamictal or Neurontin? I know that in psychiatry there are a lot of things not investigated, but i guess some relations between meds are possible to establish.
Thanks beforehand, XXXXXXX
Brief Answer:
dopaminergic system is very complicated
Detailed Answer:
Hello XXXXXXX
I appreciate your interest for details. However to clear you about dopaminergic system I need to write lots of pages.
In neuronal cells there 5 types of Doapmine receptors D1,D2,D3,D4,D5 and they distributed differently in different parts of brain. And different drugs also act differently on this receptors.
The dopamine D2 receptor was initially distinguished from the D1 receptor on the basis of its high affinity for butyrophenones. Moreover D2 receptor stimulation was observed to inhibit rather than stimulate adenylate cyclase activity. Subsequently, the D2 receptor subtype was found to display interactions with a variety of G-proteins, leading to diverse second messenger effects such as the modulation of Ca2+ and K+ channel function and the alteration of phosphoinositide production. The intracellular consequences of D2 receptor activation appear to depend upon the cell type in which the receptor is expressed.
D1 is related to parkinsonism and D2 is related to psychosis/OCD.
Role of calcium in neurons is for feedback. Dopamine release does not depend solely on calcim cytosolic calcium. It is rather more complicated.
In your case role of keppra for OC symptoms is a research topic I guess. At present hope for improvement. I will search more on this topic and will make a note when get time. In our next communication I hope I can give more clear idea if I find.
Sorry for limitation from my side.
All the best.
dopaminergic system is very complicated
Detailed Answer:
Hello XXXXXXX
I appreciate your interest for details. However to clear you about dopaminergic system I need to write lots of pages.
In neuronal cells there 5 types of Doapmine receptors D1,D2,D3,D4,D5 and they distributed differently in different parts of brain. And different drugs also act differently on this receptors.
The dopamine D2 receptor was initially distinguished from the D1 receptor on the basis of its high affinity for butyrophenones. Moreover D2 receptor stimulation was observed to inhibit rather than stimulate adenylate cyclase activity. Subsequently, the D2 receptor subtype was found to display interactions with a variety of G-proteins, leading to diverse second messenger effects such as the modulation of Ca2+ and K+ channel function and the alteration of phosphoinositide production. The intracellular consequences of D2 receptor activation appear to depend upon the cell type in which the receptor is expressed.
D1 is related to parkinsonism and D2 is related to psychosis/OCD.
Role of calcium in neurons is for feedback. Dopamine release does not depend solely on calcim cytosolic calcium. It is rather more complicated.
In your case role of keppra for OC symptoms is a research topic I guess. At present hope for improvement. I will search more on this topic and will make a note when get time. In our next communication I hope I can give more clear idea if I find.
Sorry for limitation from my side.
All the best.
Above answer was peer-reviewed by :
Dr. Raju A.T
Dear Dr. Solanki,
Thanks a lot for your answer, i was just trying to know if there are any relations between Keppra and Solian. My EEG was normal in 2009 and i wrote that i don't have OC problems because there are no rituals nor compulsive actions and my problem appeared as an accident when my psychiatrist decided to give me a lower dose of Solian (from 400 mg to 200 mg and then to 100 mg). I have "OC/phobia like" but i don't have OC disorder symptoms and i react at the second week to higher dose of Lexapro, I guess that i have something between "psychosis" and "OCD" (or "anxiety" with some images)but it's just a problem of a troubling image. If i react strongly at the second week to higher dosage of Lexapro, so it is not the reaction of the week four to an OC disorder. I was just trying to understand relations between meds since my psychiatrist don't understand very well and there is an empirical experience (with changes between doses in Solian, with changes between antiepileptic meds, and so on) which can suggest some probable inferences even if, of course, nobody is going to find my case in a book. Thank you for your help. I will try after some time other questions, since i was also asking if Lexapro has cumulative effects, not asking how many weeks it takes to Lexapro to fight and OCD i don't have (i always write "OCD/phobia LIKE"). I have a chemical imbalance.
Best regards, XXXXXXX
Hi,
In summary, every time i ask, with some exceptions, side effects or maybe some intolerances (each person is unique and it can happen) to certain kind of meds are taken for a disease (for example, dopaminergic effect D2 with Solian at low dosage is taken for an OCD i don't have because i don't have rituals nor compulsive attitudes nor abnormalities in EEG nor this problem before 2009), so i receive good information (thanks!), but also all the time a diagnosis of things i don't have instead of the possibility of reasoning close to my experience. Instead of having a particular experience, i have always a diagnosis of a disease even if i say that i don't have the disease (for example, "role of Keppra in OC" when i never said that i have a true OC, but a dopaminerghic symptom and OCD/phobia LIKE). I think this is a limitation: i don't need a name on a disease (it's worse if i don't have it), but an approach to a personal experience (difficult to hear CLEARLY, as far as i can see, since the SENSE of my questions are not appearing in the answers). But thanksanyway!
All the best, XXXXXXX
Thanks a lot for your answer, i was just trying to know if there are any relations between Keppra and Solian. My EEG was normal in 2009 and i wrote that i don't have OC problems because there are no rituals nor compulsive actions and my problem appeared as an accident when my psychiatrist decided to give me a lower dose of Solian (from 400 mg to 200 mg and then to 100 mg). I have "OC/phobia like" but i don't have OC disorder symptoms and i react at the second week to higher dose of Lexapro, I guess that i have something between "psychosis" and "OCD" (or "anxiety" with some images)but it's just a problem of a troubling image. If i react strongly at the second week to higher dosage of Lexapro, so it is not the reaction of the week four to an OC disorder. I was just trying to understand relations between meds since my psychiatrist don't understand very well and there is an empirical experience (with changes between doses in Solian, with changes between antiepileptic meds, and so on) which can suggest some probable inferences even if, of course, nobody is going to find my case in a book. Thank you for your help. I will try after some time other questions, since i was also asking if Lexapro has cumulative effects, not asking how many weeks it takes to Lexapro to fight and OCD i don't have (i always write "OCD/phobia LIKE"). I have a chemical imbalance.
Best regards, XXXXXXX
Hi,
In summary, every time i ask, with some exceptions, side effects or maybe some intolerances (each person is unique and it can happen) to certain kind of meds are taken for a disease (for example, dopaminergic effect D2 with Solian at low dosage is taken for an OCD i don't have because i don't have rituals nor compulsive attitudes nor abnormalities in EEG nor this problem before 2009), so i receive good information (thanks!), but also all the time a diagnosis of things i don't have instead of the possibility of reasoning close to my experience. Instead of having a particular experience, i have always a diagnosis of a disease even if i say that i don't have the disease (for example, "role of Keppra in OC" when i never said that i have a true OC, but a dopaminerghic symptom and OCD/phobia LIKE). I think this is a limitation: i don't need a name on a disease (it's worse if i don't have it), but an approach to a personal experience (difficult to hear CLEARLY, as far as i can see, since the SENSE of my questions are not appearing in the answers). But thanksanyway!
All the best, XXXXXXX
Brief Answer:
yes it is not OC, they are more psychotic symptoms
Detailed Answer:
Hi XXXXXXX
Sorry for late reply due to busy Sunday!
Thanks for clarification about OC symptoms. Even I was thinking that these are not OC symptoms but you were mentioning every time 'OC'. However it was my mistake that I never question you for the same though I doubted. Now I can say they are not at all OC symptoms. They are psychotic symptoms due to solian likely.
How does solian work?
In low doses, this drug binds far more to the high affinity DA presynaptic autoreceptors (increasing the release of dopamine) than to the low affinity DA postsynaptic receptors (blockade of which results in antipsychotic activity). Thus, in low doses, these drugs INCREASE the DA tone, potentially worsening psychosis.
In high doses, there is still binding to the DA autoreceptors, resulting in increased DA release. However, the DA postsynaptic receptors are effectively blocked, and DA tone is DECREASED.
When it was started at 400 mg and reduced to 100 mg possibility of psychotic symptoms are there. So your symptoms are more towards psychotic category not even OC like.
To revert back these symptoms something which can reduce dopamine tone is needed.
As I mentioned before keppra is likely opposing action of solian by reducing dopamine tone through some unknown mechanism in your case.
Role of NMDA is a research hot topic in psychiatry. You can find some mechanism of keppra in reducing side effects of levodopa through below article.
http://jpet.aspetjournals.org/content/310/1/386.full
It is possible that keprra is working through NMDA receptor and decreasing DA tone.
Hope you will feel some sense in answer now.
Thanks for questioning as with your unique case I do lot of search and learn before giving you answer.
Wish you good health.
If still any query there, I will be happy to answer. If not, you can close the discussion and if feasible give your feedback and rating so I can improve my service. In future you can contact me directly on this site if you wish with this link:
http://bit.ly/yyyyyyyyyyy
by clicking on 'Ask me a question' on same page.
Take care.
yes it is not OC, they are more psychotic symptoms
Detailed Answer:
Hi XXXXXXX
Sorry for late reply due to busy Sunday!
Thanks for clarification about OC symptoms. Even I was thinking that these are not OC symptoms but you were mentioning every time 'OC'. However it was my mistake that I never question you for the same though I doubted. Now I can say they are not at all OC symptoms. They are psychotic symptoms due to solian likely.
How does solian work?
In low doses, this drug binds far more to the high affinity DA presynaptic autoreceptors (increasing the release of dopamine) than to the low affinity DA postsynaptic receptors (blockade of which results in antipsychotic activity). Thus, in low doses, these drugs INCREASE the DA tone, potentially worsening psychosis.
In high doses, there is still binding to the DA autoreceptors, resulting in increased DA release. However, the DA postsynaptic receptors are effectively blocked, and DA tone is DECREASED.
When it was started at 400 mg and reduced to 100 mg possibility of psychotic symptoms are there. So your symptoms are more towards psychotic category not even OC like.
To revert back these symptoms something which can reduce dopamine tone is needed.
As I mentioned before keppra is likely opposing action of solian by reducing dopamine tone through some unknown mechanism in your case.
Role of NMDA is a research hot topic in psychiatry. You can find some mechanism of keppra in reducing side effects of levodopa through below article.
http://jpet.aspetjournals.org/content/310/1/386.full
It is possible that keprra is working through NMDA receptor and decreasing DA tone.
Hope you will feel some sense in answer now.
Thanks for questioning as with your unique case I do lot of search and learn before giving you answer.
Wish you good health.
If still any query there, I will be happy to answer. If not, you can close the discussion and if feasible give your feedback and rating so I can improve my service. In future you can contact me directly on this site if you wish with this link:
http://bit.ly/yyyyyyyyyyy
by clicking on 'Ask me a question' on same page.
Take care.
Note: For further follow up on related General & Family Physician Click here.
Above answer was peer-reviewed by :
Dr. Chakravarthy Mazumdar
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