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Old 12-23-2011
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Default EPS and antipsychotics

Guys, correct me if what i've got in my head is wrong.

There are 2 pathways in basal ganglia- 1. direct, helps in movement. 2. indirect- movement decreased. Dopamine plays a role in the first one.

In a patient with parkinsonism, since Dopamine is decreased and ACh is increased, indirect pathway predominates that explains why the patient has bradykinesia, rigidity n stuff.

Now, a patient taking anti-psychotics, will have again depressed dopamine level, so shouldnt the EPS that occurs in this patient have all the symptoms of parkinsonism? Why does a Patient with EPS have dystonia, akethesia which you'd rather expect in someone with depressed indirect pathway??


Someone pls clear this for me...
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Its due to the fact that prolonged inhibition of dopamine leads to Over expression of dopamine receptors,due to which even low quantities of dopamine cause symptoms of dopamine excess
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Does that mean, the direct pathway predominates and the indirect becomes dummy?
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Quote:
Originally Posted by callmerocky2 View Post
Does that mean, the direct pathway predominates and the indirect becomes dummy?
okay there are two pathways in basal ganglia

1)dopamine binds to D1 in exciatatory pathway and stimulate the excitatory pathway(increased motion)

2)dopamine binds to D2 in inhibitory pathway and inhibit the inhibitory pathway(increased motion)

so dopamine loss in parkinson results in decreased motion(bradykinesia and etc)

its straight from FA pg 400
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Originally Posted by indigo View Post
Its due to the fact that prolonged inhibition of dopamine leads to Over expression of dopamine receptors,due to which even low quantities of dopamine cause symptoms of dopamine excess

ok, if that is the case then how does anti-muscarinic work in EPS, cuz according to what you are saying the DA activity is exaggerated and hence Ach activity should be low.
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Originally Posted by step_enhancer View Post
okay there are two pathways in basal ganglia

1)dopamine binds to D1 in exciatatory pathway and stimulate the excitatory pathway(increased motion)

2)dopamine binds to D2 in inhibitory pathway and inhibit the inhibitory pathway(increased motion)

so dopamine loss in parkinson results in decreased motion(bradykinesia and etc)

its straight from FA pg 400
That doesnt expalin why there's dystonia and akathesia in EPS
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That doesnt expalin why there's dystonia and akathesia in EPS
okay for that i checked up kaplan -i took notes from dr raymond lecture (long time ago)

EPS side effects of tardive dyskinesia etc r due to DA production increase + receptor upregulation (km increases) i.e in response to dopamine blockade by the antipsychotics .

this is what he told.
hope it helps
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Originally Posted by step_enhancer View Post
okay for that i checked up kaplan -i took notes from dr raymond lecture (long time ago)

EPS side effects of tardive dyskinesia etc r due to DA production increase + receptor upregulation (km increases)

this is what he told.
hope it helps

I'm trying to put this together. If EPS is due to increased Dopamine activity then Ach activity should be decreased, then why is Anti-muscarinic given for EPS when the Ach activity is already low.. can you figure that out?? I'm going nuts..haha
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Also if anti-psychotics upregulate DA receptors and if there's exaggerated DA response then shouldnt that patient become psychotic again?
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Originally Posted by callmerocky2 View Post
Also if anti-psychotics upregulate DA receptors and if there's exaggerated DA response then shouldnt that patient become psychotic again?
dopamine is present is different regions of brain causing diff functions

remember super high yield dopamine in 3 pathways

1) tuberoinfundibular pathway

Responsible for dopamine dependent prolactin tonic inhibiton
That leads to antipsychotics causing galactorhea and amenorhea

2)mesolimbic mesocortical pathway

dopamine resposible for regulating behavior.hyperactive in schizophreania

3)nigrostriatal pathway

dopamine neurons project from substatia nigra to caudate nucleus and putamen.coordination of movement.

so may be -due to anipsychotics dopamine blockade in mesolimbic pathway production increase in nigrostiatal pathway causing EPS symptoms.

just get a broad idea.....i think it shld be clear now.

and whenever dop inc acetylcholine dec i dont think its that simple corelation .its neurology things dont happen acc to simple logic
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Old 12-23-2011
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nice topic by the way it made me hooked on

EPS symptoms-
4hr acute dystonia
4d akinesia(parkinsonion sympotoms)
4wk akathesia(restlessness)
4mo tardive dykinesia

dopamine dynamics in nigrostriatal pathway

dopamine totally blocked - no motion acute dystonia

dopamine now increasing (reflex) recetor upregulation- so dopamine blocked (but less than previously) -akinesia (parkinsonion)

dopmaine increasing plus blockade by drug-akethesia-compelling desire to move but cannot move.

4 months -dopamine production increases alot alot receptor upregulated so now drug cannot block rather motion increased- so tardive dyskinesia steriotyped oral facial movemnets

now it makes sense. nice topic btw

Last edited by step_enhancer; 12-23-2011 at 10:48 AM.
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hmm.. Everything's falling in place except ACh, right?
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Quote:
Originally Posted by callmerocky2 View Post
hmm.. Everything's falling in place except ACh, right?
EPS Side effect like acute dystonia ,parkinsoninism Rx is antimuscarninc

coz it decreases acetylcholine and helps to decrease rigidity and tremor.

its kind of you are managing the patient not curing him .

one more reason why we give them antimuscarininc coz we cannot give them dopamine agonist to manage these symoitoms coz it will worsen psychosis so we r left no choice than to give antimuscarininc.
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Old 12-24-2011
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@Step_enhancer.. based on what you said and after referring a couple of books i've come to this conclusion.

In parkinson's there is no DA, so even if there is upregulation of receptors, you'll only find symptoms of increased Ach like resting tremors, rigidity and bradykinesia.

Where as in pt taking antipsychotics, only the DA receptors are blocked but DA by itself is present. And since DA is not acting cuz of its receptor blockage, Ach increases giving rise to parkinson's like symptoms initially. As upregulation of DA recpetor occurs, we get signs of EPS like dystonia, akathesia etc.

So the idea to give Anti-muscarinic is to make sure the DA that is present does not have to work too hard to act on the receptors that are not blocked, thereby preventing upregulation.

But if upregulation does occur and if the person develops tardive dyskinesia, we have to switch to atypical anti-psychotics..

This also explains why a person on typical psychotics like thioridazine or cholropropamzine does nt have EPS as S/E cuz those drugs have Anti-Muscarinic property but on the other hand a person on haloperidol has EPS cuz it has low Anti-M property..

CORRECT ME IF I'M WRONG..

ANYWAY, THANKS A LOT STEP_ENHANCER.. IT WAS GREAT FUN TRYING TO FIGURE THAT OUT..
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Old 12-24-2011
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yes i think its fair enough.

but my friend do not spend more time on this. i have done many qs but did not come across these concepts you will not be tested on such deep mechanisms .

but reason its good to go deep in concepts sometimes coz it will make us remember the main points (atleast)

Gluck
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  #16  
Old 12-24-2011
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haha.. no, i wasnt devoting all my time towards this, just that it kept bothering me so during my breaks i looked up for it
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