Tuesday, May 24, 2011

Tardive Dyskinesia, It's 'Mentally Healthy' For You

Back to Psychiatry 101.

1: No Cures
2: No Science
3: No Side Effects, because there is no such Thing as a "Side Effect".

There are only Direct Effects, and Tardive Dyskinesia is a Direct Effect of being Poisoned by Any of 22 of the 23 Psychiatric Drugs in our FDA Reported Adverse Reaction pages.

Abilify: Tardive Dyskinesia
Adderall: Tardive Dyskinesia
Celexa: Tardive Dyskinesia
Clozapine: Tardive Dyskinesia
Cymbalta: Tardive Dyskinesia
Depakote: Tardive Dyskinesia
Effexor: Tardive Dyskinesia
Geodon: Tardive Dyskinesia
Klonopin: Tardive Dyskinesia
Lamactil: Tardive Dyskinesia
Lexapro: Tardive Dyskinesia
Neurontin: Tardive Dyskinesia
Paxil: Tardive Dyskinesia
Prozac: Tardive Dyskinesia
Risperdal: Tardive Dyskinesia
Ritalin/Concerta: Tardive Dyskinesia
Seroquel: Tardive Dyskinesia
Strattera: Tardive Dyskinesia
Tegretol: Chorea
Wellbutrin: Tardive Dyskinesia
Xanax: Tardive Dyskinesia
Zoloft: Tardive Dyskinesia
Zyprexa: Tardive Dyskinesia

So Remember, Class, when You Buy 'Mental Health' that Psychiatry Has NO actual 'Mental Health' to Sell. What it Does have to Sell is Paperwork (to cover its Own Butt) justifying all the money it's sucking up while what it's actually selling You IS:

Tardive dyskinesia
From Wikipedia, the free encyclopedia
Not to be confused with dyskinetic cerebral palsy..

Based upon the Crackpot Theories of:




DopamineICD-10G24.0ICD-9333.85OMIM272620

DiseasesDB12909eMedicineneuro/362

Tardive dyskinesia (English pronunciation: /ˈtɑrdɨv ˌdɪskɨˈniːʒə/) is a difficult-to-treat form of dyskinesia (disorder resulting in involuntary, repetitive body movements) that can be tardive (having a slow or belated onset).[1] It frequently appears after long-term or high-dose use of antipsychotic drugs,[N 1] or in children and infants as a side effect from usage of drugs for gastrointestinal disorders prevention.[N 2][2]

Tardive dyskinesia is characterized by repetitive, involuntary, purposeless movements, such as grimacing, tongue protrusion, lip smacking, puckering and pursing of the lips, and rapid eye blinking. Rapid movements of the extremities may also occur. Impaired movements of the fingers may also appear. For comparison, patients with Parkinson's disease have difficulty moving, while patients with tardive dyskinesia have difficulty not moving.

Other closely related neurological disorders have been recognized as variants of tardive dyskinesia. Tardive dystonia is similar to standard dystonia but permanent. Tardive akathisia involves painful feelings of inner tension and anxiety and a compulsive drive to move the body.[citation needed] In the extreme, the individual undergoes internal torture and can no longer sit still. Tardive tourettism is a tic disorder that can closely mimic Tourette Syndrome, sometimes to the point where the two can only be distinguished by the details of their onsets. Tardive myoclonus, a rare disorder, presents as brief jerks of muscles in the face, neck, trunk, and extremities.

Tardive dyskensia is often misdiagnosed as a mental illness rather than a neurological disorder, and as a result patients are prescribed neuroleptic drugs which enhance the probability that the patient will develop a severe and disabling case. In such cases, it is critical to properly identify the signs of the disorder and stop neuroleptic treatment as early as possible. The neuroleptic drugs have a tendency to suppress or mask the very symptoms they are causing, thus making disorder identification more difficult. The symptoms may then abruptly break out after drug usage is reduced or stopped. Doctors must be very careful to limit the use of neuroleptics, and thoroughly examine patients periodically for signs of abnormal movements. Physicians should educate patients and families about the dangers of tardive dyskinesia.[2]

Cause

Despite the fact that tardive dyskinesia was described 50 years ago, its mechanism is poorly understood. The most compelling line of evidence suggests that tardive dyskinesia may result primarily from neuroleptic-induced dopamine supersensitivity in the nigrostriatal pathway, with the D2 dopamine receptor being most affected. Neuroleptics act primarily on this dopamine system, and older neuroleptics, which have greater affinity for the D2 binding site, are associated with high risk for tardive dyskinesia.[3] The D2 hypersensitivity hypothesis is also supported by evidence of a dose-response relationship, withdrawal effects, studies on D2 agonists and antagonists, animal studies, and genetic polymorphism research.[3]

Given similar doses of the same neuroleptic, differences among individuals still exist in the likelihood of developing tardive dyskinesia. Such individual differences may be due to genetic polymorphisms, which code for D2 receptor binding site affinity, or prior exposure to environmental toxins. Decreased functional reserve or cognitive dysfunction, associated with aging, mental retardation, alcohol and drug abuse, or traumatic head injuries, has also been shown to increase risk of developing the disorder among those treated with neuroleptics.[3] Antipsychotic drugs can sometimes camouflage the signs of tardive dyskinesia from occurring in the early stages; this can be from the individual having an increased dose of an antipsychotic drug, although when tardive dyskinesia worsens the signs become visible (Videbeck 2006).[citation needed]

Other dopamine antagonists and antiemetics can cause tardive dyskinesia, such as metoclopramide and promethazine, used to treat gastrointestinal disorders. While newer atypical antipsychotics such as olanzapine and risperidone appear to have fewer dystonic effects, only clozapine has been shown to have a lower risk of tardive dyskinesia than older antipsychotics.[4] There has been a reported case of the anti-psychotic medication Aripiprazole, a partial agonist at D2 receptors, leading to tardive dyskinesia.[5]

The available research seems to suggest that the concurrent prophylactic use of a neuroleptic and an antiparkinsonian drug is useless to avoid earlyextrapyramidal side-effects and may render the patient more sensitive to tardive dyskinesia. Since 1973 the use of these drugs has been found to be associated with the development of tardive dyskinesia.[6][7] Since some of the symptoms of tardive dyskinesia can be interpreted as schizophrenia by doctors, they may prescribe additional neuroleptic drugs to treat it, leading to increased risk of more prevalent tardive dyskinesia. Several studies have indicated that long-term neuroleptic use is associated with both cognitive deterioration and atrophy of the brain.[8][9]


Treatment

Primary prevention of tardive dyskinesia is achieved by using the lowest effective dose of a neuroleptic for the shortest time (Although, with diseases of chronic psychosis such as schizophrenia, this strategy must be balanced with the fact that increased dosages of neuroleptics are more beneficial in preventing recurrence of psychosis). If tardive dyskinesia is diagnosed, the causative drug should be discontinued. Tardive dyskinesia may persist after withdrawal of the drug for months, years or even permanently.

The dopamine-depleting drug tetrabenazine has been used to treat tardive dyskinesia[10][11] and other movement disorders.

Zofran has shown some benefit in experimental studies on tardive dyskinesia and a variety of anti-Parkinsonian medications are used such as Aricept, Baclofen,Requip and Mirapex. Clonidine is used for dystonic spasms and can be of help. Botox injections are used for minor focal dystonia, but not in more advanced tardive dyskinesia.[12] A review paper found Benzodiazepines[N 3] to be effective in alleviating the symptoms of tardive dyskinesia.[13] However, like mostanticonvulsants, benzodiazepines may cause tremors as well as benzodiazepine withdrawal syndrome upon rapid discontinuation.

Natural remedies, such as vitamin E (Alpha-Tocopherol), rhodiola, omega 3 fatty acids or melatonin can be used, although they have not proven efficacy in controlled studies.

In males, the branched-chain amino acid formula Tarvil, containing the amino acids valine, isoleucine, and leucine in a 3:3:4 ratio has been reported as beneficial for motor symptoms. [14]

Epidemiology

Tardive dyskinesia most commonly occurs in patients with psychiatric conditions who are treated with antipsychotic medications for many years. One study reported that within the first four years of using antipsychotic medications, 18.5 percent of young adults develop symptoms. Furthermore, 31 percent of those over 55 years of age develop tardive dyskinesia symptoms in the same time frame.[15] Other estimates suggest that it occurs in 15-30% of patients receiving treatment with antipsychotic neuroleptic medications for 3 months or longer.[citation needed] “A study being conducted at the Yale University School of Medicine has estimated that 32% of patients develop persistent tics after 5 years on major tranquilizers, 57% by 15 years, and 68% by 25 years.”[16] Other estimates suggest that with each year of neuroleptic use, 5% of the patients will show signs of tardive dyskinesia, i.e., 5% after one year, 10% after two years, 15% after three years with no clear upper limit.[17] Eventually, according to these estimates, if on the drugs long enough, the majority of patients will develop the disorder.[18] The incidence of tardive dyskinesia varies with the type of neuroleptic (e.g., haloperidol (Haldol) more often than perphenazine (Trilafon)), daily dose and duration of treatment (the higher the daily dose and the longer the duration of treatment, the higher the risk).

The elderly and female patients are more prone to develop tardive dyskinesia.[citation needed] Cigarette smokers also have a higher prevalence of tardive dyskinesia.[citation needed] Children and adolescents are much more sensitive to the early and late extrapyramidal side-effects of neuroleptics than adults.[citation needed] Because of this, treatment of youngsters with neuroleptics may be contraindicated, and many authorities believe that they should be initiated only as a last resort, using the lowest dose regime possible and the shortest duration of treatment in accordance with good patient management.[citation needed]

Tardive dyskinesia can become disabling socially and cause people to self isolate, due to the societal stigma as well. Patients and/or their families (guardians and/or caregivers/nurses) should receive full information about the neuroleptic before starting treatment (informed consent).[citation needed] The benefits need to be weighed by the individual patient/guardian and their physician. However, the antipsychotic clozapine is not known to cause tardive dyskinesia and can be an option and is not used on a more widespread basis because of blood dyscrasias as well as other side effects of concern.[citation needed].

The still hypothetical conditions tardive psychosis, tardive dysphrenia and tardive dysmentia remain little understood and as yet unconfirmed.[citation needed] New classes of antipsychotics in study such as glycine and other NMDA receptor modulators in not affecting the dopaminergic system in Phase II FDA studies have been shown not to cause tardive dyskinesia and may, once realized as FDA approved antipsychotics, be a new treatment modality that will not create this condition.[citation needed]

See also

Notes

  1. ^ Compazine, Risperdal
  2. ^ Propulsid, Reglan
  3. ^ Benzodiazepine drugs e.g. Ativan, Valium, or Klonopin

References

  1. ^ tardive dyskinesia at Dorland's Medical Dictionary
  2. ^ a b Breggin 2001
  3. ^ a b c Hoerger 2007
  4. ^ Craig & Stitzel; Modern Pharmacology (6th ed) pp. 401.
  5. ^ Abbasian, C. (2009) A case of aripiprazole and tardive dyskinesia, J Psychopharmacol, vol.23, no.2:214-215
  6. ^ Crane 1973a
  7. ^ Crane 1973b
  8. ^ Breggin 1990
  9. ^ Gualtieri & Barnhill 1988
  10. ^ Rauchverger, Isakov & Jabarin 2007
  11. ^ Fernandez & Friedman 2003
  12. ^ Brašić & Bronson 2010
  13. ^ Soares-Weiser & Bhoopathi 2006
  14. ^http://www.ncbi.nlm.nih.gov/pubmed/12777270
  15. ^ Saltz, Woerner & Kane 1991
  16. ^ Glenmullen 2000 ::referring to Glazer, Morgenstern & Doucette 1993
  17. ^ Jeste & Caligiuri 1993
  18. ^ Whitaker , Robert - Mad in America: Bad Science, Bad Medicine, and the Enduring Mistreatment of the Mentally Ill, Perseus Pub., c2002

Bibliography

External links

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2 comments:

Kris said...

I agree with your post about anti-psychotic drugs, but you seem to list drugs that don't have that side effect or in fact correct that side effect.

The trouble is that some psychiatrists used those drugs to partially correct the symptom but not the cure. Nevertheless including drugs that improve or correct the problem and listing them as causing the problem needs to be revised.

Gabapentin for instance is used for RLS, which is usually treated with dopamine agonist, since anti-psychotics are dopamine antagonist, your post needs revision.

Similarly, wellbutrin is unlikely to cause TD, because it isn't antagonizing dopamine, SSRIS usually don't either although they have other serious side effects,



June 8, 2015 at 11:39 AM
D Bunker said...

Hi Kris;
Thanks for your interest and your comment.

However, reports received by FDA differ with your conclusions RE: causation.

Neurontin/Gabapentin:

"Between 2004 and 2006 the FDA MedWatch program received 5,418 Individual Safety Reports naming Neurontin (gabapentin) the Primary Suspect Drug for 2,672 distinct adverse reactions"

http://psychroachesadverseevent.blogspot.com/2009/03/neurontin-adverse-reactions.html

Welbutrin:

"Between 2004 and 2006 the FDA MedWatch program received 10,728 Individual Safety Reports naming Wellbutrin (bupropion) the Primary Suspect Drug for 1,773 distinct adverse reactions"

http://psychroachesadverseevent.blogspot.com/2009/03/wellbutrin-adverse-reactions.html

If the drug specific links don't read properly in the comment box, you can go to the main URL below and access them alphabetically.

http://psychroachesadverseevent.blogspot.com

June 9, 2015 at 4:21 PM

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