Talk:Tardive dyskinesia
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[edit] president bush
does president bush suffer from tardive dyskinesia?
Kingturtle 02:57, 12 October 2005 (UTC)
- Was this intended as a joke or a serious comment? The link is broken. JMPZ 05:36, 6 April 2007 (UTC)
[edit] Thanks for the heads up.
I suffered three severe bouts which nearly killed me when my tongue swelled, and my neck and throat muscles went into a tonic spasm.
I apparently suffer massive twitching bouts in my sleep, three years on. Thanks for the info.--218.215.195.80 06:22, 30 August 2006 (UTC)
[edit] MUST ??
"The devastating impact of tardive dyskinesia illustrates why patients and/or their families (guardians and/or caregivers/nurses) must receive full information about the neuroleptic before starting treatment (informed consent)."
I rewrote to " Some believe the devastating impact of tardive dyskinesia illustrates why patients and/or their families (guardians and/or caregivers/nurses) should receive full information about the neuroleptic before starting treatment (informed consent)."
Feel free to revert, it just struck me as an opinion, even if it is one I agree with! DisneyFreak96 20:18, 26 October 2006 (UTC)
[edit] Pharmacogenetics of Tardive Dyskinesia
I've just read a Medscape article "Pharmacogenetics and Psychotropic Drugs" (2000) by Takuya Saito. It has an interesting subsection on the frequency of TD in patients with different alleles in two genes: for the D3 receptor and for CYP1A2.
Medscape demands a free registration to read its articles, so I quote:
"Gene Polymorphisms and Tardive Dyskinesia (TD) A recent study published in Molecular Psychiatry [2] points out that genetic make-up in individuals may contribute to predisposition to side effects. Pharmacodynamics (ie, how a medication affects the body) and pharmacokinetics (ie, how the body metabolizes a medication) are influenced by genes. Kennedy and others[3] studied 2 genes and their association with TD. One gene is dopamine D3 receptor, which involves pharmacodynamics of antipsychotics. The other is CYP1A2, which involves pharmacokinetics of antipsychotics. Kennedy studied 248 schizophrenia patients diagnosed by the Diagnostic and Statistical Manual of Mental Disorders, third edition, revised (DSM-III-R), and he and his associates evaluated the severity of TD using the abnormal involuntary movement scale (AIMS) 2 weeks after typical antipsychotics were discontinued. An association study was conducted using an SNP, which changes an amino acid from ser to gly. In Ser/ser genotype, AIMS was 3.47. In ser/gly, AIMS was 3.92. In gly/gly, AIMS was 14.20. There was a statistical significance between the D3 receptor polymorphism and AIMS (F[2,95]=8.25, P < .0005), and gly/gly genotype was associated with high AIMS score. The study group also investigated an association between CYP1A2 and TD. There is an SNP (C->A change) in first intron of CYP1A2 gene, which affects the gene expression of CYP1A2. In the same sample, in A/A genotype, AIMS was 5.2. In A/C genotype, AIMS was 6.6. In C/C genotype, AIMS was 17.8. There was statistical significance between the CYP1A2 polymorphism and AIMS (F[2,82] = 7.41, P < .0007), and C/C genotype was associated with high AIMS score. Kennedy and colleagues also conducted association studies using dopamine D2, D4 polymorphisms, and CYP2D6 polymorphisms, but they did not find any association. They also tested interaction between the dopamine D3 polymorphism and the CYP2D6 polymorphism toward TD. They found that these 2 polymorphisms had an additive effect for TD. These findings have been replicated, and SNPs may have benefit to predict potential side effects from medications."
Maybe we should include the "pharmacogenetics" section in the article and fill it with appropriate information? --CopperKettle 14:23, 27 November 2006 (UTC)
[edit] Long-term condition
i disagree Tardive Dyskinesia is a long term condition
i was in a mental hospital for a few days
shortly after release the cogentin was no longer working but the thorazine was
i developed tardive dyskinesia for a few days
my tongue was stuck out
and it was difficult to talk
Festus Christopher King (fcking2000@yahoo.com)
- That would be an extra-pyramidal effect, not tardive. Midgley 23:33, 23 March 2006 (UTC)
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- I'm taking a Psych Nursing class at the moment. Based on that and what Wiki has to say about Extrapyramidal Symptoms (EPS), Tardive Dyskinesia IS an EPS. -- Nick
I have moved this comment thread into a topic. It was located at the top of the page. JMPZ 01:37, 5 April 2007 (UTC)
Sorry, you are incorrect. The person above was referring to a dystonic reaction, which is a short-term (meaning it appears within hours/days) side effect of many serotonin and dopamine agonist drugs (aka "antipsychotics"). Tardive dyskinesia is a delayed response which has a different (though related) pathophysiology. —Preceding unsigned comment added by 68.149.145.163 (talk) 09:33, 23 April 2008 (UTC)
[edit] Introduction could be more concise, on-topic
The introduction provides plenty of information about what drugs cause tardive dyskinesia, as well as which types of drugs are better or worse than others.
This information should probably be moved below the contents links. After reading the introduction, I knew what caused the symptoms, but not what the symptoms were. The introduction should contain a summary / overview of the symptoms and what causes them (but not a discussion of which neuroleptics cause it to what degree). JMPZ 01:37, 5 April 2007 (UTC)
For example, what on earth is this statement doing in the introduction? "The use of MDMA (ecstasy) has been shown to enhance the effects of L-Dopa while reducing the associated dyskinesia in primates with simulated Parkinson's disease." JMPZ 02:16, 5 April 2007 (UTC)
[edit] About 5% year-by-year increase in TD
I've added a ref (PMID 8100643) supporting that statement. Just was reading a case story in JAMA and stumbled upon a similar statement with citations:
Tardive dyskinesia occurs with a frequency of approximately 5% per year of exposure to conventional neuroleptics and is not dose-related.(62) Elderly individuals have much higher rates of adverse neurological effects, including a 30% incidence of tardive dyskinesia during the first year of exposure.(63)
Still not sure about the "no upper limits" though. Best regards, CopperKettle 05:59, 8 April 2007 (UTC)
[edit] Increasing dose
I've read that increasing the dose of the neuroleptic actually reduces tardive dyskinesia. I guess this is because the syndrome is caused by a sensitization of dopamine receptors? Maybe increasing the dose overcomes the sensitization, reducing symptoms? Anyone else heard about this?
- I haven't heard about that. However, I would be interested in reading a source about it. Neitherday 23:18, 12 April 2007 (UTC)
[edit] introduction
I removed this: "Year-long implants that are being developed using the older typicals[citation needed], e.g., haloperidol, one of the worst offenders when it comes to tardive dyskinesia[citation needed]. " because it's ungrammatical and hence meaningless. I can think of at least three very different things it might be trying to express, depending on how you fix the grammar. Anyone who likes this bit should turn it into an ACTUAL SENTENCE and have a think about whether it means what they want it to mean. --snaxalotl 20 july 2007
"only clozapine has been shown to have a lower risk of tardive dyskinesia than older antipsychotics" this seems to be unnecessarily absolute for a statement sourced from a textbook. I think there might be a couple of papers suggesting otherwise for Quetiapine, for example
