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
Wellbutrin: Tardive Dyskinesia
Xanax: Tardive Dyskinesia
Zoloft: Tardive Dyskinesia
Zyprexa: Tardive Dyskinesia
From Wikipedia, the free encyclopedia
Not to be confused with dyskinetic cerebral palsy..
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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). 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]
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. 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.
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. 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.
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. 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).
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. There has been a reported case of the anti-psychotic medication Aripiprazole, a partial agonist at D2 receptors, leading to tardive dyskinesia.
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. 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.
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.
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. A review paper found Benzodiazepines[N 3] to be effective in alleviating the symptoms of tardive dyskinesia. However, like mostanticonvulsants, benzodiazepines may cause tremors as well as benzodiazepine withdrawal syndrome upon rapid discontinuation.
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. Other estimates suggest that it occurs in 15-30% of patients receiving treatment with antipsychotic neuroleptic medications for 3 months or longer. “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.” 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. Eventually, according to these estimates, if on the drugs long enough, the majority of patients will develop the disorder. 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. Cigarette smokers also have a higher prevalence of tardive dyskinesia. Children and adolescents are much more sensitive to the early and late extrapyramidal side-effects of neuroleptics than adults. 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.
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). 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..
The still hypothetical conditions tardive psychosis, tardive dysphrenia and tardive dysmentia remain little understood and as yet unconfirmed. 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.
- ^ tardive dyskinesia at Dorland's Medical Dictionary
- ^ a b Breggin 2001
- ^ a b c Hoerger 2007
- ^ Craig & Stitzel; Modern Pharmacology (6th ed) pp. 401.
- ^ Abbasian, C. (2009) A case of aripiprazole and tardive dyskinesia, J Psychopharmacol, vol.23, no.2:214-215
- ^ Crane 1973a
- ^ Crane 1973b
- ^ Breggin 1990
- ^ Gualtieri & Barnhill 1988
- ^ Rauchverger, Isakov & Jabarin 2007
- ^ Fernandez & Friedman 2003
- ^ Brašić & Bronson 2010
- ^ Soares-Weiser & Bhoopathi 2006
- ^ Saltz, Woerner & Kane 1991
- ^ Glenmullen 2000 ::referring to Glazer, Morgenstern & Doucette 1993
- ^ Jeste & Caligiuri 1993
- ^ Whitaker , Robert - Mad in America: Bad Science, Bad Medicine, and the Enduring Mistreatment of the Mentally Ill, Perseus Pub., c2002
- Breggin, Peter R., M.D. (2001), Tardive Dyskinesia Legal Settlement, Breggin.com
- Breggin, Peter R., M.D. (Summer/Autumn 1990), "Brain damage, dementia and persistent cognitive dysfunction associated with neuroleptic drugs. Evidence, etiology, implications.", JMB (New York: Institute of Mind and Behavior: Journal of Mind and Behavior) vol.11 (no.3-4): 425–464, ISBN 0-93019-505-1, ISSN 0271-0137 .pdf (scan) (11.3MB)
- Brašić, James Robert, MD; Bronson, Brian, MD (21 January 2010), Tardive Dyskinesia: Treatment & Medication
- Crane, George E. (Sep 1973a), "Is tardive dyskinesia a drug effect?", AJP (American Psychiatric Association: American Journal of Psychiatry) vol.130 (no.9): 1043–4,ISSN 0002-953X, OCLC 104768868, PMID 4727768
- Crane, George E. (Oct 1973b), "Rapid reversal of tardive dyskinesia", AJP (American Psychiatric Association: American Journal of Psychiatry) vol.130 (no.10): 1159,ISSN 0002-953X, OCLC 104790755, PMID 4728916
- Fernandez, Hubert H., MD; Friedman, Joseph H., MD (Jan 2003), "Classification and Treatment of Tardive Syndromes", Neurologist (Baltimore US-MD: Williams & Wilkins: The Neurologist) vol.9 (no.1): 16–27, doi:10.1097/01.nrl.0000038585.58012.97, ISSN 1074-7931, OCLC 111183504, PMID 12801428
- Hoerger, Michael (2007), "The primacy of neuroleptic-induced D2 receptor hypersensitivity in tardive dyskinesia", Psychiatry Online (Psychiatry Online) vol.13 (no.12): 18–26
- Glazer, William M.; Morgenstern, Hal; Doucette, John T. (Apr 1993), "Predicting the Long-Term Risk of Tardive Dyskinesia in Outpatients Maintained on Neuroleptic Medications", JCP (Memphis US-TN: Physicians Postgraduate Press: Journal of Clinical Psychiatry) vol.54 (no.4): 133–9, ISSN 0160-6689, OCLC 119262955,PMID 8098030
- Glenmullen, Joseph (2000), "Ch.1.", Prozac Backlash, New York: Joseph Glenmullen. Simon & Schuster, p. 38 .pdf
- Gualtieri, C. Thomas; Barnhill, L.J. (1988), Wolf, Marion E.; Mosnaim, A.D., eds., "Tardive Dyskinesia, Biological Mechanisms & Clinical Aspects", Tardive Dyskinesia in Special Populations (Washington, D.C.: American Psychiatric Press): pp. 137–154, ISBN 0-88048-176-5
- Jeste, Dilip V.; Caligiuri, Michael P. (Feb 1993), "Tardive Dyskinesia", Schizophr Bull (Schizophrenia Bulletin) vol.19 (no.2): 303–315, doi:10.1093/schbul/19.2.303,PMID 8100643
- Rauchverger, Boris, MD; Isakov, Victoria, MD; Jabarin, Mahmoud, MD (Fall 2007), "Olanzapine-Induced Tardive Dystonia Successfully Treated by Tetrabenazine", JNCN(American Neuropsychiatric Association: The Journal of Neuropsychiatry and Clinical Neurosciences) vol.19 (no.4): 484–5, doi:10.1176/appi.neuropsych.19.4.484-a,ISSN 0895-0172, OCLC 264210333, PMID 18070868
- Soares-Weiser, Karla; Bhoopathi, Paranthaman Sethupathi; Bhoopathi, Paranthaman Sethupathi (19 July 2006), "Benzodiazepines for Neuroleptic-Induced Tardive Dyskinesia", Cochrane Library (The Cochrane Database of Systematic Reviews) 3 (rev.3): CD000205, doi:10.1002/14651858.CD000205.pub2, OCLC 109974960,PMID 16855954 Umbrich, P; Soares, KV; Walker, Paul (2003), "-", Cochrane database of systematic reviews (Online) (rev.2): CD000205,doi:10.1002/14651858.CD000205, OCLC 111195192, PMID 12804389
- Saltz, Bruce L., MD; Woerner, Margaret G., PhD; Kane, John M., MD; Lieberman, JA; Alvir, JM; Bergmann, KJ; Blank, K; Koblenzer, J et al. (6 November 1991), "Prospective Study of Tardive Dyskinesia Incidence in the Elderly", JAMA (Chicago US-IL: American Medical Association: Journal of the American Medical Association) vol.266(no.17): 2402–6, doi:10.1001/jama.266.17.2402, ISSN 0098-7484, OCLC 116673469, PMID 1681122
- tardive at NINDS
- Jenelle's story report on a patient at antipsychiatry.org.
- Tardive Dyskinesia at Psyweb.com at psyweb.com
- Photographs and Video of TD (biased view of psychiatry) at yoism.org
- Practical Gastroenterology article with Plain English description of all symptoms of EPS-TD and links to testing guidelines. at reflux.org