Psycho-Babble Medication Thread 1029742

Shown: posts 1 to 20 of 20. This is the beginning of the thread.

 

question about tardive dyskinesia pathophysiology

Posted by neuroscience on October 25, 2012, at 13:35:55

I'm reading a book called Neurology for the Non-Neurologist (6th Edition), and on page 281 it talks about TD pathophysiology and says:

"Although choreiform movements may begin when the neuroleptic is chronically administered without a change in dose, the most common clinical setting in which the movement disorder emerges is after the dose is lowered or discontinued. This latter setting is in keeping with the postulate of lowering the pharmacologic blockade of the dopamine receptor and allowing normal dopaminergic mechanisms to resume their interaction with the already hypersensitized receptor. Although there is much evidence in animal models to support this notion, there have been inconsistencies."

My question is: what inconsistencies?

 

Re: question about tardive dyskinesia pathophysiology » neuroscience

Posted by Phillipa on October 25, 2012, at 14:44:50

In reply to question about tardive dyskinesia pathophysiology, posted by neuroscience on October 25, 2012, at 13:35:55

No idea hoping someone can answer this for you. Phillipa

 

Lou's response-psad » neuroscience

Posted by Lou Pilder on October 25, 2012, at 15:38:25

In reply to question about tardive dyskinesia pathophysiology, posted by neuroscience on October 25, 2012, at 13:35:55

> I'm reading a book called Neurology for the Non-Neurologist (6th Edition), and on page 281 it talks about TD pathophysiology and says:
>
> "Although choreiform movements may begin when the neuroleptic is chronically administered without a change in dose, the most common clinical setting in which the movement disorder emerges is after the dose is lowered or discontinued. This latter setting is in keeping with the postulate of lowering the pharmacologic blockade of the dopamine receptor and allowing normal dopaminergic mechanisms to resume their interaction with the already hypersensitized receptor. Although there is much evidence in animal models to support this notion, there have been inconsistencies."
>
> My question is: what inconsistencies?

neuro,
The reason fo the inconsistancies is that the cause of TD is much more than what they think.
Let us go to tobacco smoking. Not all smokers get lung cancer, and some non-smokers get lung cancer. Causality is a long involved process to determine sometimes in relation to this. Some people get TD in the first week as akethisia. Some years later or not at all. But there is a causality relationship with the drug and TD. But corrolation does not prove causality.
It has been reveald to me what causes these movement conditions as a result of taking mind-altering drugs. And it has been revealed to me healing. This healing I am not permitted to post here due to prohibitons to me by Mr Hsiung. It involves the foundation of Judaism as revealed to me. There could be people here to tell you to use human acheivement in relation to taking more drugs and they are permitted to do so even though the condition is induced by a drug. I know of cases healed by divine accomplishment. Look at the admin board here and a member calls this B*llsh*t and says that I believe it. Sadly. Mr Hsiung to this day alllows defamation to be posted to me including insulting Judaism and Islam and other faiths. This could keep you from having dialog with me, yet it is allowed here.
Lou

 

Re: Lou's response-psad » Lou Pilder

Posted by schleprock on October 25, 2012, at 18:21:20

In reply to Lou's response-psad » neuroscience, posted by Lou Pilder on October 25, 2012, at 15:38:25

Lou, what are you going to be for Halloween.

 

Re: question about tardive dyskinesia pathophysiology » neuroscience

Posted by phidippus on October 25, 2012, at 21:36:56

In reply to question about tardive dyskinesia pathophysiology, posted by neuroscience on October 25, 2012, at 13:35:55

If they did not elaborate on the inconsistencies, it would be hard to postulate exactly what they were.

What did you think about my idea of treating with Keppra?

Eric

 

Re: Lou's response-psad

Posted by jono_in_adelaide on October 25, 2012, at 22:39:59

In reply to Re: Lou's response-psad » Lou Pilder, posted by schleprock on October 25, 2012, at 18:21:20

Tetrabenzine is effective in treating TD, but it can cause depression

 

Re: question about tardive dyskinesia pathophysiology

Posted by neuroscience on October 26, 2012, at 8:05:46

In reply to Re: question about tardive dyskinesia pathophysiology » neuroscience, posted by phidippus on October 25, 2012, at 21:36:56

> If they did not elaborate on the inconsistencies, it would be hard to postulate exactly what they were.
>
> What did you think about my idea of treating with Keppra?
>
> Eric

Keppra seems promising like Nootropyl is. I believe its use was based on the neurotoxic hypothesis. Dopamine receptor blockade leads to an increase of dopamine turnover thus producing excessive free oxyradicals that damage striatal neurons.

My original question has to do with the hypothesis that TD is caused by an alteration of sensitivity and number of dopamine receptors.

 

Re: Lou's response-psad

Posted by neuroscience on October 26, 2012, at 8:16:58

In reply to Re: Lou's response-psad, posted by jono_in_adelaide on October 25, 2012, at 22:39:59

> Tetrabenzine is effective in treating TD, but it can cause depression

ANd (i'd say worse still), akathisia

This reminds me of something I read recently of a woman who developed TD after 8 years of risperidone. She was given several things (including keppra actually), that didn't work or produced side-effects too nasty. So she was given Tetrabenzine, at a dose of 125/mg day, finally suppressing the TD but unfortunately causing severe akathisia (subjective and objective).

The akathisia went away when the TBZ was stopped but TD reemerged.

They ultimately performed bilateral globus pallidus deep brain stimulation on her which resulted in the nearly complete relief of the TD.

 

Re: Lou's response-psad

Posted by neuroscience on October 26, 2012, at 8:42:28

In reply to Lou's response-psad » neuroscience, posted by Lou Pilder on October 25, 2012, at 15:38:25

I already figured that the reason for inconsistencies is that the dopamine receptor sensitivity hypothesis is wrong or incomplete. But I didn't ask for the reason of the inconsistencies, but for the inconsistencies themselves. If anyone knows them.

It's a complicated subject that I may research myself anyway.

>
> neuro,
> The reason fo the inconsistancies is that the cause of TD is much more than what they think.

 

Re: question about tardive dyskinesia pathophysiology » neuroscience

Posted by phidippus on October 26, 2012, at 17:09:53

In reply to Re: question about tardive dyskinesia pathophysiology, posted by neuroscience on October 26, 2012, at 8:05:46

>TD is caused by an alteration of sensitivity and number of dopamine receptors.

This sounds logical. Sounds like Parkonsonism.

Eric

 

Re: question about tardive dyskinesia pathophysiology

Posted by neuroscience on October 27, 2012, at 1:59:55

In reply to Re: question about tardive dyskinesia pathophysiology » neuroscience, posted by phidippus on October 26, 2012, at 17:09:53

> >TD is caused by an alteration of sensitivity and number of dopamine receptors.
>
> This sounds logical. Sounds like Parkonsonism.
>
> Eric

I'm hoping it's wrong. I'm taking B-6 300mg at the moment because I'm thinking the neurotoxicity hypothesis is correct.

 

Re: question about tardive dyskinesia pathophysiology

Posted by phidippus on October 27, 2012, at 18:22:13

In reply to Re: question about tardive dyskinesia pathophysiology, posted by neuroscience on October 27, 2012, at 1:59:55

what does the neurotoxicity hypothesis state?


Eric

 

Re: question about tardive dyskinesia pathophysiology

Posted by neuroscience on October 28, 2012, at 2:06:16

In reply to Re: question about tardive dyskinesia pathophysiology, posted by phidippus on October 27, 2012, at 18:22:13

> what does the neurotoxicity hypothesis state?
>
>
> Eric
Dopamine receptor blockade leads to an increase of dopamine turnover thus producing excessive free oxyradicals that damage striatal neurons.

Also, there is this from Lerner, V. and C. Miodownik (2011). "Motor symptoms of schizophrenia: is tardive dyskinesia a symptom or side effect? A modern treatment." Curr Psychiatry Rep 13(4): 295-304.:

"To date, several neurochemical hypotheses have been proposed for the development of TD, including a disturbed balance between dopamine and cholinergic systems; dysfunctions of striatonigral, γ-aminobutric acid (GABA)ergic neurons; and excitotoxicity [38, 39]. Recently, the role of oxidative stress and structural abnormality in the pathophysiology of TD has gained impetus. Induction of free radicals by neuroleptic drugs leading to oxidative stress and resultant structural abnormality could be the key factor in the pathogenesis of TD. The studies by Lerner et al. [40] and Libov et al. [41] support the neurotoxicity hypothesis. It also has been supported by reports that chronic neuroleptic treatment increases free radical production and causes structural damage [37]. In 2005, Tan and colleagues [42] reported that brain-derived neurotrophic factor appears to exert a protective effect in the nervous system against TD in patients with schizophrenia.
Previously, it was suggested that only antipsychotic agents could cause TD. However, in recent years, many reports have suggested that various psychotropic medications, such as antihistamines, antidepressants, anticholinergics and other agents, can cause TD (Table 1)."

you can read the whole thing here:
http://rd.springer.com/article/10.1007/s11920-011-0202-6/fulltext.html

 

Re: question about tardive dyskinesia pathophysiology

Posted by neuroscience on October 28, 2012, at 7:17:54

In reply to question about tardive dyskinesia pathophysiology, posted by neuroscience on October 25, 2012, at 13:35:55

I believe the basic answer to my question is this: the theory of hypersensitivity doesn't explain all the clinical findings of tardive dyskinesia because there are people who are exposed to dopamine receptor-blocking drugs who don't develop TD.

 

Re: question about tardive dyskinesia pathophysiology » neuroscience

Posted by phidippus on October 28, 2012, at 15:41:13

In reply to Re: question about tardive dyskinesia pathophysiology, posted by neuroscience on October 28, 2012, at 2:06:16

>Induction of free radicals by neuroleptic drugs leading to oxidative stress and resultant structural abnormality could be the key factor in the pathogenesis of TD.

This could very well be right.

So what are you trying to do medicinally?

Eric

 

Re: question about tardive dyskinesia pathophysiology » neuroscience

Posted by phidippus on October 28, 2012, at 15:45:29

In reply to Re: question about tardive dyskinesia pathophysiology, posted by neuroscience on October 28, 2012, at 7:17:54

>hypersensitivity doesn't explain all the clinical findings of tardive dyskinesia because there are people who are exposed to dopamine receptor-blocking drugs who don't develop TD.

Maybe those who don't get TD don't suffer from hypersensitivity.

Eric

 

Re: question about tardive dyskinesia pathophysiology » neuroscience

Posted by phidippus on October 28, 2012, at 15:48:04

In reply to Re: question about tardive dyskinesia pathophysiology, posted by neuroscience on October 28, 2012, at 2:06:16

Thanks, looks like a good read.

Eric

 

Re: question about tardive dyskinesia pathophysiology

Posted by neuroscience on October 28, 2012, at 16:14:49

In reply to Re: question about tardive dyskinesia pathophysiology » neuroscience, posted by phidippus on October 28, 2012, at 15:41:13

> >Induction of free radicals by neuroleptic drugs leading to oxidative stress and resultant structural abnormality could be the key factor in the pathogenesis of TD.
>
> This could very well be right.
>
> So what are you trying to do medicinally?
>
> Eric

Vitamin B-6, I'm at 300mg a day right now, I'm not sure I'd go higher than 400mg.

 

Re: question about tardive dyskinesia pathophysiology

Posted by neuroscience on November 1, 2012, at 7:28:30

In reply to Re: question about tardive dyskinesia pathophysiology » neuroscience, posted by phidippus on October 28, 2012, at 15:45:29

> >hypersensitivity doesn't explain all the clinical findings of tardive dyskinesia because there are people who are exposed to dopamine receptor-blocking drugs who don't develop TD.
>
> Maybe those who don't get TD don't suffer from hypersensitivity.
>
> Eric

One of the hypotheses is that TD _causes_ hypersensitivity.

 

Re: question about tardive dyskinesia pathophysiology

Posted by neuroscience on November 1, 2012, at 7:30:26

In reply to Re: question about tardive dyskinesia pathophysiology, posted by neuroscience on November 1, 2012, at 7:28:30

> > >hypersensitivity doesn't explain all the clinical findings of tardive dyskinesia because there are people who are exposed to dopamine receptor-blocking drugs who don't develop TD.
> >
> > Maybe those who don't get TD don't suffer from hypersensitivity.
> >
> > Eric
>
> One of the hypotheses is that TD _causes_ hypersensitivity.
>
>

OOps :O

I meant to say that the hypothesis is that the neuroleptic causes hypersentivity, which then leads to TD.


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