![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 9 of 9. This is the beginning of the thread.
Posted by neuroscience on October 15, 2012, at 4:38:58
Hello, my first post. How is everyone?
My information on the pathogenesis of dyskinesias is maybe out of date. I was wondering if there was any knew discoveries on this. Particularly on TA.
"The pathogenesis of the tardive dyskinesia syndromes is unknown. No one hypothesis is able to explain the disorder, and more than one factor may be necessary.
These factors include the development of dopamine-receptor supersensitivity, activation of dopamine D1 receptors, and loss of G-aminobutyric acid activity in the
subthalamic nucleus." --Merritt Neurology 10th edition
Posted by Lou Pilder on October 15, 2012, at 6:27:27
In reply to Tardive Akathisia Pathogenesis, posted by neuroscience on October 15, 2012, at 4:38:58
> Hello, my first post. How is everyone?
>
> My information on the pathogenesis of dyskinesias is maybe out of date. I was wondering if there was any knew discoveries on this. Particularly on TA.
>
> "The pathogenesis of the tardive dyskinesia syndromes is unknown. No one hypothesis is able to explain the disorder, and more than one factor may be necessary.
> These factors include the development of dopamine-receptor supersensitivity, activation of dopamine D1 receptors, and loss of G-aminobutyric acid activity in the
> subthalamic nucleus." --Merritt Neurology 10th editionneuroscience,
The condition of tardive dyskinesia/dystonia/other appears in a percentage of people that take psychotropic drugs. The condition can be irreverible and life-ruining.
Yet today, millions of people take psychotropic drugs. Maybe they don't know what these drugs are and where they were developed and for what reason. They may also not know the chemical composition of the drugs and their history.
Many of the chemical constituants of some of the psychotropic drugs are the same as used in {nerve agents} used in mass-murder. And in agents used in riot control. And in inecticides, rat poison and chemical dyes. The chemicals way to kill is well-known as to how the nerves are shut down to cause death. This method of death is well-documented but I am prohibited from posting here this educational material by the nature of prohibitions made to me here by Mr Hsiung. I did start to develop this educational material here but was stopped by Mr Hsiung. You could do a search such as ,[Lou, Effexor] or ,[Lou, thlaidomide], or[Lou, phenol] and that might direct you to a thread here where I was stopped from continuing.
Now understand that when knowledge is prohibited from being told, an indoctrination could be fostered by the one prohibiting the knowledge from being told. An indoctrination that could lead to the deaths of pople that are prohibited from knowing what can not be told to them that could save their lives.
So let it be with those that want to still my voice in any way, be it the prohibition of posting of facts, facts that I think cold mark the difference between life and death, or the prohibiting me from posting the foundation of Judaism as revealed to me that IMHHHO could lead people out of the darkness of depression and addiction, save them from the horrors of tardive dyskinesia, and give them their lives back.
I would like to tell you the answer to your question for I know it, but I am prohibited from posting it here by the nature of the prohibitions posted to me here by Mr Hsiung.
I ask you, what benefit could outweigh the risk of one from taking psychotropic drugs that could cause tardive dyskinesia and such? And it is generally accepted that 42,000 people died just last year from psychotropic drugs and my math shows that with the marketing continuing on television that million of people could die from these drugs going forward and summing all the people that have died in the last 50 years from these drugs. Yet today, people in this community post to others to take chemicals that could rob them of their lives or leave them in a condition of disfigurement for the rest of their lives or give them diabetes that could lead to their blindness or amputation of their limbs and other life-ruining conditions.
Lou
Posted by neuroscience on October 15, 2012, at 6:55:24
In reply to Lou's response-knrvehyjentz, posted by Lou Pilder on October 15, 2012, at 6:27:27
I can understand your desire to warn people about TD Lou.
On the topic of pathophysiology, there is something I just read from Motor Symptoms of Schizophrenia: Is Tardive Dyskinesia a Symptom or Side Effect? A Modern Treatment:
"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."
The neurotoxicity hypothesis seems promising.
Posted by Lou Pilder on October 15, 2012, at 7:27:34
In reply to Re: Lou's response-knrvehyjentz, posted by neuroscience on October 15, 2012, at 6:55:24
> I can understand your desire to warn people about TD Lou.
>
> On the topic of pathophysiology, there is something I just read from Motor Symptoms of Schizophrenia: Is Tardive Dyskinesia a Symptom or Side Effect? A Modern Treatment:
>
> "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."
>
> The neurotoxicity hypothesis seems promising.neuroscience,
You wrote,[...the neurotoxicity hypothosis seems promising...]
In my study of {nerve agents}, I have found that the chemicals in psychotropic drugs that cause TD and such have a way to migrate to {brain componants} and chemically alter the brain componant to produce brain damage. The chemicals could lodge in the part of he brain that controls, let's say,sleep, or any other function.
I do have an undergraduate background in cell physiology. I have found that the chemicals can alter the mitichondria in a manner that could induce cell-death. A lot of this I am prohibited from posting here. And by the nature of the prohibitions to me here, I think that people here could be cheated out of knowing what IHHHHO could save their lives. You could go to the administraive board here and see years of outstanding requests from me to Mr Hsiung. Outstanding requests that I think if were responded to, could mark the difference between life and death to some here and prevent Jews and Islamic people and others from being victims of violence. And since the forum is for support and education, the statements there that could arouse antisemitic feelings, or be an insult to Islam, that are left to stand, could lead some to consider them to be supportive. And what do they support?
Lou
Posted by phillipa on October 15, 2012, at 9:40:52
In reply to Tardive Akathisia Pathogenesis, posted by neuroscience on October 15, 2012, at 4:38:58
Wecome to babble. Do you currently have TD? Hopefully soon someone from the boards will offer some advise to you. Phillipa
Posted by neuroscience on October 15, 2012, at 10:15:20
In reply to Re: Tardive Akathisia Pathogenesis » neuroscience, posted by phillipa on October 15, 2012, at 9:40:52
> Wecome to babble. Do you currently have TD? Hopefully soon someone from the boards will offer some advise to you. Phillipa
I have tardive akathisia a subtype of td
Posted by neuroscience on October 15, 2012, at 10:38:53
In reply to Re: Lou's response-knrvehyjentz, posted by neuroscience on October 15, 2012, at 6:55:24
> I can understand your desire to warn people about TD Lou.
>
> On the topic of pathophysiology, there is something I just read from Motor Symptoms of Schizophrenia: Is Tardive Dyskinesia a Symptom or Side Effect? A Modern Treatment:
>
> "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."
>
> The neurotoxicity hypothesis seems promising.Libov, I., et al. (2007). "Efficacy of piracetam in the treatment of tardive dyskinesia in schizophrenic patients: a randomized, double-blind, placebo-controlled crossover study." J Clin Psychiatry 68(7): 1031-1037.
The above article I cited is extremely interesting to me. It supports the neurotoxicity hypothesis.
Piracetam is a potent antioxidant and a cerebral neuroprotector.
Posted by phidippus on October 15, 2012, at 19:35:23
In reply to Re: Tardive Akathisia Pathogenesis, posted by neuroscience on October 15, 2012, at 10:15:20
How long have you had TD and what medications caused it?
Eric
Posted by neuroscience on October 16, 2012, at 2:51:20
In reply to Re: Tardive Akathisia Pathogenesis » neuroscience, posted by phidippus on October 15, 2012, at 19:35:23
> How long have you had TD and what medications caused it?
>
> EricI think it's difficult to know what medications caused it exactly as some of them mask the symptoms but I was on Geodon when this happened. I've had this akathitic dyskinesia for about 8 1/2 years. In my case when it didn't take many years to develop it. Maybe like a couple years at most.
And the kicker: I had bad anxiety. No psychosis or schizophrenia or mania. But was still given Geodon, Seroquel, Abilify and some I probably forget.
I'm doing research on piracetam because there is good evidence that the dyskinesias is caused by neurotoxic pathogenesis.
This is the end of the thread.
Psycho-Babble Medication | Extras | FAQ
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.org
Script revised: February 4, 2008
URL: http://www.dr-bob.org/cgi-bin/pb/mget.pl
Copyright 2006-17 Robert Hsiung.
Owned and operated by Dr. Bob LLC and not the University of Chicago.