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What Causes Rapid Movement Of Eyes And No Control Of Nerves And Muscles In Eyes?
Question: Hi,
I take Lexapro 5 mg, Klonopin 4 mg, Solian 100 mg aand Keppra 1000mg for anxiety. In low dose, from 100 mg to 200 mg (it's worse for me with 200 mg), Solian has a well known dopaminergic effect and i had had serious troubles with this. I had had an "ocd like symptom" but is just "like", not exactly ocd: my eyes move quickly, i feel i don't have control of nerves and muscles of the eyes, i have troubles with their movement and eyes focuses on open windows of cars (something strange): when my eyes see those windows, my eyes cannot recognize the dephtness of the image, the foreground and the rest, and my mind cannot do any right association neither look normally to this image.
The problem is being corrected with Keppra and Klonopin (so, antiepileptics) until now with good results and i have nothing abnormal in electroencephalogram, but i would like to know if a dopaminergic effect of a med can create this strange sensation of "flat image", problems to understand the relief of the image, all this corrected strangely by antiepileptics.
I've been told by a neurologist here that it can be a problem with dopaminergic brain pathways (if there is not a seizure in temporal lobe), including the mesolimbic system. As far as i understand, dopa comes to action with Solian (amisulpride) in prefrontal cortex. I would like to know if this brain pathway can create some kind of NEUROPHYSIOLOGICAL compulsive behavior (in this case, looking at open windows of cars without ANY reason), including the movement of the eyes, and what kind of relation there is between mesolimbic system and temporal lobe, because of course i am not neurologist.
Thanks beforehand,
XXXXX
I take Lexapro 5 mg, Klonopin 4 mg, Solian 100 mg aand Keppra 1000mg for anxiety. In low dose, from 100 mg to 200 mg (it's worse for me with 200 mg), Solian has a well known dopaminergic effect and i had had serious troubles with this. I had had an "ocd like symptom" but is just "like", not exactly ocd: my eyes move quickly, i feel i don't have control of nerves and muscles of the eyes, i have troubles with their movement and eyes focuses on open windows of cars (something strange): when my eyes see those windows, my eyes cannot recognize the dephtness of the image, the foreground and the rest, and my mind cannot do any right association neither look normally to this image.
The problem is being corrected with Keppra and Klonopin (so, antiepileptics) until now with good results and i have nothing abnormal in electroencephalogram, but i would like to know if a dopaminergic effect of a med can create this strange sensation of "flat image", problems to understand the relief of the image, all this corrected strangely by antiepileptics.
I've been told by a neurologist here that it can be a problem with dopaminergic brain pathways (if there is not a seizure in temporal lobe), including the mesolimbic system. As far as i understand, dopa comes to action with Solian (amisulpride) in prefrontal cortex. I would like to know if this brain pathway can create some kind of NEUROPHYSIOLOGICAL compulsive behavior (in this case, looking at open windows of cars without ANY reason), including the movement of the eyes, and what kind of relation there is between mesolimbic system and temporal lobe, because of course i am not neurologist.
Thanks beforehand,
XXXXX
Brief Answer:
Dopamine involved in vision processes too.
Detailed Answer:
Hello and thanks for using HCM.
I have read your query and understand your concerns.
Amisulpride is an antipsychotic atypical drug that blocks the dopamine receptors whenever they are found.
Dopamine is a neurotransmitter involved in regulating mood, behavior, but also retinal dopamine and associated receptors are involved in vision processes related to resolution, light adaption, contrast sensitivity.
Briefly, Amisulpride doesn't affect, or block only dopamine receptors in the prefrontal cortex, dopaminergic pathway includes dopamine neurons in the ventral tegmental area that project to prefrontal cortex, amygdala, hippocampus ( temporal lobe ), nucleus acumbens, substantia nigra and striatum. (motivation, reward, pleasure, fine motor function, compulsion).
So, if you experienced OCD-like symptoms related to Amisulpride effects, there are two components to consider:
1. Neuropsychological symptoms related to Dopaminergic pathways function affected by Amisulpride.
2. Vision distortion related to retinal dopamine and receptors affected too by Amisulpride.
Vision distortion could be explained also by disfunction of fine motor function of the eyes muscles affected by antidopaminergic effects of Amisulpride.
Hope you found the answer helpful.
Take care.
Dopamine involved in vision processes too.
Detailed Answer:
Hello and thanks for using HCM.
I have read your query and understand your concerns.
Amisulpride is an antipsychotic atypical drug that blocks the dopamine receptors whenever they are found.
Dopamine is a neurotransmitter involved in regulating mood, behavior, but also retinal dopamine and associated receptors are involved in vision processes related to resolution, light adaption, contrast sensitivity.
Briefly, Amisulpride doesn't affect, or block only dopamine receptors in the prefrontal cortex, dopaminergic pathway includes dopamine neurons in the ventral tegmental area that project to prefrontal cortex, amygdala, hippocampus ( temporal lobe ), nucleus acumbens, substantia nigra and striatum. (motivation, reward, pleasure, fine motor function, compulsion).
So, if you experienced OCD-like symptoms related to Amisulpride effects, there are two components to consider:
1. Neuropsychological symptoms related to Dopaminergic pathways function affected by Amisulpride.
2. Vision distortion related to retinal dopamine and receptors affected too by Amisulpride.
Vision distortion could be explained also by disfunction of fine motor function of the eyes muscles affected by antidopaminergic effects of Amisulpride.
Hope you found the answer helpful.
Take care.
Above answer was peer-reviewed by :
Dr. Raju A.T
Dear Dr. Erion,
Thank you very much for your clear answer, it's helpful, especially about dopaminergic brain pathways, thanks.
As far as i know and as i was told here in HCM by psychiatrists, Solian in low dose (100mg-300mg) has at the same time antidopaminergic effects (it blocks D2D3) and dopaminergic ones, it enhances dopamine release according to psychiatrists here in HCM and in a lot of scientific articles (that's why Amisulpride 100-300 mg helps in patients with negative symptoms of schizophrenia). I understand what you say about ANTIdopaminergic effect of Solian and maybe they act in my problems of vision, but these problems are essentially with dimension, relief and depthness looking at windows of cars (some kind of problem to RECOGNIZE the dimension) -i have no problems with light, contrast and so on. My other question is: if Solian has a dopaminergic action (and according to pschiatrists of HCM it has at low dose under 400 mg), it can create some kind of compulsion or a compulsion? (it seems to me that it can, according to one of the paragraphs of your answer and to your point number 1, but i would like to be sure, since you talk about symptoms but in the other sense -antidopaminergic). I also ask this because antiepileptics like Klonopin and Keppra (as far as i know Keppra fights Levodopa in some cases) are helpful to revert my symptom and maybe they are controlling this strange compulsion which has a neurophysiological origin and not an emotional one.
Thank you for your patience, i'll be waiting for your answer
Best regards,
XXXXX
Thank you very much for your clear answer, it's helpful, especially about dopaminergic brain pathways, thanks.
As far as i know and as i was told here in HCM by psychiatrists, Solian in low dose (100mg-300mg) has at the same time antidopaminergic effects (it blocks D2D3) and dopaminergic ones, it enhances dopamine release according to psychiatrists here in HCM and in a lot of scientific articles (that's why Amisulpride 100-300 mg helps in patients with negative symptoms of schizophrenia). I understand what you say about ANTIdopaminergic effect of Solian and maybe they act in my problems of vision, but these problems are essentially with dimension, relief and depthness looking at windows of cars (some kind of problem to RECOGNIZE the dimension) -i have no problems with light, contrast and so on. My other question is: if Solian has a dopaminergic action (and according to pschiatrists of HCM it has at low dose under 400 mg), it can create some kind of compulsion or a compulsion? (it seems to me that it can, according to one of the paragraphs of your answer and to your point number 1, but i would like to be sure, since you talk about symptoms but in the other sense -antidopaminergic). I also ask this because antiepileptics like Klonopin and Keppra (as far as i know Keppra fights Levodopa in some cases) are helpful to revert my symptom and maybe they are controlling this strange compulsion which has a neurophysiological origin and not an emotional one.
Thank you for your patience, i'll be waiting for your answer
Best regards,
XXXXX
Brief Answer:
Different mechanisms involved.
Detailed Answer:
Welcome back XXXXXXX
Solian blocks D2,D3 receptors, blocking this way dopamine to bind with these receptors, and this is believed to be one of the mechanisms of action that improves positive symptoms in schizophrenia.
Negative symptoms of schizophrenia are thought to be related to a hypoactive pathway from ventral tegmental area to prefrontal cortex where is found a D1 receptor predominantly.
I think blocking of dopamine from binding with D2 receptors "leaves" more dopamine in disposition of mesocortical pathway ( to prefrontal cortex), improving thus negative symptoms.
One of mechanisms thought to cause OCD is the hyperactive mesocortical pathway (prefrontal cortex), but low basal ganglia serotonin activity is needed as well.
It is said also that low doses of Solian (about 50 mg) result in an increase of dopamine.
It is important to distinguish the start of the OCD symptoms, if they started AFTER Solian use, or if there were minor OCD symptoms before Solian use.
Keppra has shown some effects in improving symptoms related to Levodopa long use in Parkinson's.
Klonopin and Keppra revert OCD symptoms most probably by stabilizing hyperactive neuronal pathways.
Hope I've been of help.
Best regards.
Different mechanisms involved.
Detailed Answer:
Welcome back XXXXXXX
Solian blocks D2,D3 receptors, blocking this way dopamine to bind with these receptors, and this is believed to be one of the mechanisms of action that improves positive symptoms in schizophrenia.
Negative symptoms of schizophrenia are thought to be related to a hypoactive pathway from ventral tegmental area to prefrontal cortex where is found a D1 receptor predominantly.
I think blocking of dopamine from binding with D2 receptors "leaves" more dopamine in disposition of mesocortical pathway ( to prefrontal cortex), improving thus negative symptoms.
One of mechanisms thought to cause OCD is the hyperactive mesocortical pathway (prefrontal cortex), but low basal ganglia serotonin activity is needed as well.
It is said also that low doses of Solian (about 50 mg) result in an increase of dopamine.
It is important to distinguish the start of the OCD symptoms, if they started AFTER Solian use, or if there were minor OCD symptoms before Solian use.
Keppra has shown some effects in improving symptoms related to Levodopa long use in Parkinson's.
Klonopin and Keppra revert OCD symptoms most probably by stabilizing hyperactive neuronal pathways.
Hope I've been of help.
Best regards.
Above answer was peer-reviewed by :
Dr. Chakravarthy Mazumdar
Dear Dr. Erion
Thank you very much for your clear answer.
The "ocd like" symptoms -they are not exactly OCD, because there are no rituals, for example, and it's just the compulsion looking at the windows of cars- started after lowering Solian from 400 mg (positive symptoms) to 200 mg first and then 100 mg. So i guess it can be dopamine in the prefrontal cortex. This is my last question: please confirm me that this possibility exists (a compulsion from neurophysiological origin then due to dopamine in prefrontal cortex), even if of course not all patients have this problem. This hypothesis is possible, right?
High doses of serotonin are not eliminating my problem, so thanks a lot for your clear information about effects of Klonopin and Keppra.
Regards,
XXXXX
Thank you very much for your clear answer.
The "ocd like" symptoms -they are not exactly OCD, because there are no rituals, for example, and it's just the compulsion looking at the windows of cars- started after lowering Solian from 400 mg (positive symptoms) to 200 mg first and then 100 mg. So i guess it can be dopamine in the prefrontal cortex. This is my last question: please confirm me that this possibility exists (a compulsion from neurophysiological origin then due to dopamine in prefrontal cortex), even if of course not all patients have this problem. This hypothesis is possible, right?
High doses of serotonin are not eliminating my problem, so thanks a lot for your clear information about effects of Klonopin and Keppra.
Regards,
XXXXX
Brief Answer:
In my opinion the hypothesis is possible.
Detailed Answer:
Hello again XXXXXXX
Since OCD-like symptoms started after lowering of Solian, the possibility to be dopamine related could be true.
OCD is known to be related to inheritance too, and symptoms become visible when neurotransmitters disbalance take place.
Hope I helped you.
Wishing you good health.
In my opinion the hypothesis is possible.
Detailed Answer:
Hello again XXXXXXX
Since OCD-like symptoms started after lowering of Solian, the possibility to be dopamine related could be true.
OCD is known to be related to inheritance too, and symptoms become visible when neurotransmitters disbalance take place.
Hope I helped you.
Wishing you good health.
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Above answer was peer-reviewed by :
Dr. Neel Kudchadkar
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