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late-occurring (especially with reference to symptoms of a disease); "tardive dyskinesia"
abnormality in performing voluntary muscle movements

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2017/11/26 23:35:52」(JST)

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Tardive dyskinesia (TD) is a disorder that results in involuntary, repetitive body movements.^[1] This may include grimacing, sticking out the tongue or smacking of the lips.^[1] Additionally there may be rapid jerking movements or slow writhing movements.^[1] In about 20% of people, decreased functioning results.^[3]

Tardive dyskinesia occurs in some people as a result of long-term use of neuroleptic medications (antipsychotics, metoclopramide).^[1]^[2] These medications are usually used for mental illness, but may also be given for gastrointestinal or neurological problems.^[1] The condition typically only develops after months to years of use.^[1]^[3] The diagnosis is based on the symptoms after ruling out other potential causes.^[1]

Efforts to prevent the condition include not using or using the lowest possible dose of neuroleptics.^[3] Treatment include stopping the neuroleptic medication if possible or switching to clozapine.^[1] Other medications such as valbenazine, tetrabenazine, or botulinum toxin may be used to lessen the symptoms.^[1]^[4] With treatment some see a resolution of symptoms while others do not.^[1]

Rates in those on atypical antipsychotics are about 20% while those on typical antipsychotics have rates of about 30%.^[5] Risk is greater in older people.^[3] The term "tardive dyskinesia" first came into use in 1964.^[3]

Signs and symptoms

Tardive dyskinesia is characterized by repetitive, involuntary movements. Some examples of these types of involuntary movements include:^[6]

Grimacing
Tongue movements
Lip smacking
Lip puckering
Pursing of the lips
Excessive eye blinking

Rapid, involuntary movements of the limbs, torso, and fingers may also occur.^[7] In some cases, an individual's legs can be so affected that walking becomes difficult or impossible.^[8] These symptoms are the opposite of patients who are diagnosed with Parkinson's disease. Parkinson's patients have difficulty moving, whereas tardive dyskinesia patients have difficulty not moving.^[9]

Respiratory irregularity, such as grunting and difficulty breathing, is another symptom associated with tardive dyskinesia, although studies have shown that the prevalence rate is relatively low.^[10]

Tardive dyskinesia is often misdiagnosed as a mental illness rather than a neurological disorder,^[11] and as a result patients are prescribed neuroleptic drugs, which increase the probability that the patient will develop a severe and disabling case, and shortening the typical survival period.^[12]

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 some extreme cases, afflicted individuals experience so much internal torture that they lose their ability to sit still. Tardive tourettism is a tic disorder featuring the same symptoms as Tourette syndrome. The two disorders are extremely close in nature and often can only be differentiated by the details of their respective onsets. Tardive myoclonus, a rare disorder, presents as brief jerks of muscles in the face, neck, trunk, and extremities.^[9]

"AIMS Examination": This test is used when psychotropic medications have been prescribed because patients sometimes develop tardive dyskinesia due to prolonged use of antipsychotic medications. The Abnormal Involuntary Movement Scale (AIMS) examination is a test used to identify the symptoms of tardive dyskinesia (TD). The test is not meant to tell whether there is an absence or presence of tardive dyskinesia. It just scales to level of symptoms indicated by the actions observed. The levels range from none to severe. The AIMS examination was constructed in the 1970s to measure involuntary facial, trunk, and limb movements. It is best to do this test before and after the administration of the psychotropic drugs. Taking the AIMS consistently can help to track severity of TD over time.^[13]^[14]

Cause

Tardive dyskinesia was first described in the 1950s shortly after the introduction of chlorpromazine and other antipsychotic drugs.^[15] However, the exact mechanism of the disorder remains largely uncertain. 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.^[16] 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.^[16]

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.^[16] Antipsychotic drugs can sometimes camouflage the signs of tardive dyskinesia from occurring in the early stages; this can happen from the individual having an increased dose of an antipsychotic drug. Often the symptoms of tardive dyskinesia are not apparent until the individual comes off of the antipsychotic drugs; however, when tardive dyskinesia worsens, the signs become visible.^[17]

Other dopamine antagonists and antiemetics can cause tardive dyskinesia, such as metoclopramide and promethazine, used to treat gastrointestinal disorders. Atypical antipsychotics are considered lower-risk for causing TD than their typical counterparts with their relative rates of TD of 13.1% and 32.4% respectively in short-term trials with haloperidol being the main typical antipsychotic utilised in said trials.^[18] Quetiapine and clozapine are considered the lowest risk agents for precipitating TD.^[18] From 2008, there have been reported cases of the anti-psychotic medication aripiprazole, a partial agonist at D2 receptors, leading to tardive dyskinesia.^[19] As of 2013, reports of tardive dyskinesia in aripiprazole have grown in number.^[20] The available research seems to suggest that the concurrent prophylactic use of a neuroleptic and an antiparkinsonian drug is useless to avoid early extrapyramidal 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.^[21]^[22]

Risk factors

An increased risk of tardive dyskinesia has been associated with smoking in some studies,^[23]^[24] although a negative study does exist.^[25] There seems to be a cigarette smoke-exposure-dependent risk for TD in antipsychotic-treated patients.^[26] Elderly patients are also at a heightened risk for developing TD,^[6] as are females and those with organic brain injuries or diabetes mellitus and those with the negative symptoms of schizophrenia.^[18] TD is also more common in those that experience acute neurological side effects from antipsychotic drug treatment.^[18] Racial discrepancies in TD rate also exist, with Africans and African Americans having higher rates of TD after exposure to antipsychotics.^[6] Certain genetic risk factors for TD have been identified including polymorphisms in the genes encoding the D₃, 5-HT_2A and 5-HT_2C receptors.^[27]

Prevention

Prevention of tardive dyskinesia is achieved by using the lowest effective dose of a neuroleptic for the shortest time. However, 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.^[28]^[29] Some studies suggest that physicians should consider using atypical antipsychotics as a substitute to typical antipsychotics for patients requiring medication. These agents are associated with fewer neuromotor side effects and a lower risk of developing tardive dyskinesia.^[30]

Recent studies have tested the use of melatonin, high dosage vitamins, and different antioxidants in concurrence with antipsychotic drugs (often used to treat schizophrenia) as a way of preventing and treating tardive dyskinesia. Although further research is needed, studies reported a much lower percentage of individuals developing tardive dyskinesia than the current prevalence rate for those taking antipsychotic drugs.^[31]

Treatment

Valbenazine has been approved by the FDA for tardive dyskinesia.^[32] Tetrabenazine, which is a dopamine depleting drug, is sometimes used to treat tardive dyskinesia and other movement disorders.^[7] However, it is only approved to treat chorea associated with Huntington's disease. The related VMAT2 inhibitor, reserpine, has also been tried in one small randomised double-blind placebo-controlled trial as a treatment for TD with success,^[33] as has α-methyldopa.^[33] Ondansetron has shown some benefit in experimental studies on tardive dyskinesia and a variety of anti-Parkinsonian medications are used such as donepezil,^[34]^[35] baclofen,^[36]^[37]^[38] and pramipexole.^[39] Clonidine may also be useful in the treatment of TD, although dose-limiting hypotension and sedation may hinder its usage.^[40] Botox injections are used for minor focal dystonia, but not in more advanced tardive dyskinesia.^[41] Benzodiazepines are an effective treatment for TD, however their use is limited by the development of tolerance which requires ever increasing doses of the benzodiazepines to be used to attenuate TD symptoms. The most popular benzodiazepine for the treatment of TD is clonazepam.^[42] Vitamin B6 has been reported to be an effective treatment for TD in two randomised double-blind placebo-controlled trials.^[43]^[44] In males, the branched-chain amino acid formula Tarvil, containing the amino acids valine, isoleucine, and leucine in a 3:3:4 ratio was reported as beneficial for motor symptoms in a small, non-blinded study.^[45]

Epidemiology

Tardive dyskinesia most commonly occurs in patients with psychiatric conditions who are treated with antipsychotic medications for many years. The average prevalence rate has been estimated to be around 30% for individuals taking antipsychotic medication, such as that used to treat schizophrenia.^[46] 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."^[47] More drastic data was found during a longitudinal study conducted on individuals 45 years of age and older who were taking antipsychotic drugs. According to this research study, 26% of patients developed tardive dyskinesia after just one year on the medication. Another 60% of this at-risk group developed the disorder after 3 years, and 23% developed severe cases of tardive dyskinesia within 3 years.^[48] According to these estimates, the majority of patients will eventually develop the disorder if they remain on the drugs long enough.^[49]

Elderly patients are more prone to develop tardive dyskinesia, and elderly women are more at-risk than elderly men. The risk is much lower for younger men and women, and also more equal across the sexes.^[50] Patients who have undergone electro-convulsive therapy or have a history of diabetes or alcohol abuse also have a higher risk of developing tardive dyskinesia.^[30]

Several studies have recently been conducted comparing the prevalence rate of tardive dyskinesia with second generation, or more modern, antipsychotic drugs to that of first generation drugs. The newer antipsychotics appear to have a substantially reduced potential for causing tardive dyskinesia. However, some studies express concern that the prevalence rate has decreased far less than expected, cautioning against the overestimation of the safety of modern antipsychotics.^[31]^[51]

A physician can evaluate and diagnose a patient with tardive dyskinesia by conducting a systematic examination. The physician should ask the patient to relax, and look for symptoms like facial grimacing, eye or lip movements, tics, respiratory irregularities, and tongue movements. In some cases, patients experience nutritional problems, so a physician can also look for a gain or loss in weight.^[30]

Apart from the underlying psychiatric disorder, tardive dyskinesia may cause afflicted people to become socially isolated. It also increases the risk of dysmorphophobia and can even lead to suicide. Emotional or physical stress can increase the severity of dyskinetic movements, whereas relaxation and sedation have the opposite effect.^[52]

References

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^ ^a ^b ^c "Tardive Dyskinesia". NORD (National Organization for Rare Disorders). 2015. Archived from the original on 28 August 2017. Retrieved 11 June 2017.
^ ^a ^b ^c ^d ^e ^f Vijayakumar, D; Jankovic, J (May 2016). "Drug-Induced Dyskinesia, Part 2: Treatment of Tardive Dyskinesia". Drugs. 76 (7): 779–87. PMID 27091214.
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^ ^a ^b ^c "Tardive Dyskinesia". Medscape Reference. WebMD. 9 February 2012. Archived from the original on 3 December 2013. Retrieved 25 November 2013.
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1. 遅発性ジスキネジア：臨床的特徴および診断 tardive dyskinesia clinical features and diagnosis
2. 遅発性ジスキネジア：予防および治療 tardive dyskinesia prevention and treatment
3. 遅発性ジスキネジア：病因および疫学 tardive dyskinesia etiology and epidemiology
4. 統合失調症に対する薬物療法：副作用マネージメント pharmacotherapy for schizophrenia side effect management
5. 第1世代抗精神病剤：薬理学、投与、および副作用の比較 first generation antipsychotic medications pharmacology administration and comparative side effects

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NAID 40019989729

抑肝散の臨床応用 : 統合失調症, パーソナリティ障害, ジスキネジアなど

精神神經學雜誌 = Psychiatria et neurologia Japonica 114(6), 708-718, 2012-06-25
NAID 10030970681

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リンク元	「遅発性ジスキネジア」「TD」
関連記事	「tardive」

「遅発性ジスキネジア」

Classification	V · T · D ICD-10: G24.0; ICD-9-CM: 333.85; OMIM: 272620; DiseasesDB: 12909;
External resources	MedlinePlus: 000685; eMedicine: neuro/362;

Tardive dyskinesia
Synonyms	Linguofacial dyskinesia, tardive dystonia, tardive oral dyskinesia
	Tardive dyskinesia is believed to involve the neurotransmitter dopamine.
Pronunciation	/ˈtɑːrdɪv ˌdɪskɪˈniːʒə/;
Specialty	Psychiatry
Symptoms	Involuntary, repetitive body movements
Causes	Neuroleptic medications (antipsychotics, metoclopramide)
Diagnostic method	Based on symptoms after ruling out other potential causes
Similar conditions	Huntington's disease, cerebral palsy, Tourette syndrome, dystonia
Prevention	Using lowest possible dose of neuroleptic medication
Treatment	Stopping neuroleptic medication if possible, switching to clozapine
Medication	Valbenazine, tetrabenazine, botulinum toxin
Prognosis	Variable
Frequency	20% (atypical antipsychotics) 30% (typical antipsychotics)
	[edit on Wikidata]

　　[★]

英: tardive dyskinesia
同: 遅発性ジスキネジー
関: ジスキネジア dyskinesia

[show details]

遅発性ジスキネジア : 約 11,000 件
晩発性ジスキネジア : 10 件
遅発性ジスキネジー : 約 17,500 件

「TD」

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「tardive」

　　[★]

adj.

晩期の、晩発の/晩発性の、遅発性の

関: delayed, late-onset, tardy, tardiness 緩慢

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[NORD2015-2] "Tardive Dyskinesia". NORD (National Organization for Rare Disorders). 2015. Archived from the original on 28 August 2017. Retrieved 11 June 2017.

[Vi2016-3] ^ ^a ^b ^c ^d ^e ^f Vijayakumar, D; Jankovic, J (May 2016). "Drug-Induced Dyskinesia, Part 2: Treatment of Tardive Dyskinesia". Drugs. 76 (7): 779–87. PMID 27091214.

[NIH2017-4] "Tardive Dyskinesia Information Page". National Institute of Neurological Disorders and Stroke. Archived from the original on 2017-07-04.

[Car2017-5] Carbon, M; Hsieh, CH; Kane, JM; Correll, CU (March 2017). "Tardive Dyskinesia Prevalence in the Period of Second-Generation Antipsychotic Use: A Meta-Analysis". The Journal of Clinical Psychiatry. 78 (3): e264–e278. PMID 28146614.

[MSR-6] "Tardive Dyskinesia". Medscape Reference. WebMD. 9 February 2012. Archived from the original on 3 December 2013. Retrieved 25 November 2013.

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[13] Encyclopedia of Mental Disorders

[14] Montana State Hospital

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[crane_1973A-21] Crane, GE (1973). "Is tardive dyskinesia a drug effect?". The American Journal of Psychiatry. 130 (9): 1043–44. PMID 4727768.

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[26] Diehl, A; Reinhard, I; Schmitt, A; Mann, K; Gattaz, WF (January 2009). "Does the degree of smoking effect the severity of tardive dyskinesia? A longitudinal clinical trial". European Psychiatry. 24 (1): 33–40. doi:10.1016/j.eurpsy.2008.07.007. PMID 18774276.

[27] Segman, RH; Heresco-Levy, U; Finkel, B; Inbar, R; Neeman, T; Schlafman, M; Dorevitch, A; Yakir, A; Lerner, A; Goltser, T; Shelevoy, A; Lerer, B (November 2000). "Association between the serotonin 2C receptor gene and tardive dyskinesia in chronic schizophrenia: additive contribution of 5-HT2Cser and DRD3gly alleles to susceptibility" (PDF). Psychopharmacology. 152 (4): 408–13. doi:10.1007/s002130000521.

[28] Rauchverger, B; Isakov, V; Jabarin, M (2007). "Olanzapine-induced tardive dystonia successfully treated by tetrabenazine". The Journal of neuropsychiatry and clinical neurosciences. 19 (4): 484–5. doi:10.1176/appi.neuropsych.19.4.484-a. PMID 18070868.

[29] Fernandez, Hubert H.; Friedman, Joseph H. (2003). "Classification and Treatment of Tardive Syndromes". The Neurologist. 9 (1): 16–27. doi:10.1097/01.nrl.0000038585.58012.97. PMID 12801428.

[pmid16001096-30] Saltz, Bruce L.; Robinson, Delbert G.; Woerner, Margaret G. (2004). "Recognizing and Managing Antipsychotic Drug Treatment Side Effects in the Elderly". Primary Care Companion to the Journal of Clinical Psychiatry. 6 (Suppl 2): 14–9. PMC 487007 . PMID 16001096.

[Lerner.2C_V._2011_pp._109.E2.80.9334-31] Lerner, Vladimir (2011). "Handbook of Schizophrenia Spectrum Disorders, Volume III": 109–34. doi:10.1007/978-94-007-0834-1_6. ISBN 978-94-007-0833-4. |chapter= ignored (help)

[FDAApprove-32] Commissioner, Office of the. "Press Announcements - FDA approves first drug to treat tardive dyskinesia". www.fda.gov. Archived from the original on 12 April 2017. Retrieved 12 April 2017.

[TD1981-33] Huang, CC; Wang, RI; Hasegawa, A; Alverno, L (1981). "Reserpine and alpha-methyldopa in the treatment of tardive dyskinesia" (PDF). Psychopharmacology. 73 (4): 359–62. doi:10.1007/BF00426466. PMID 6789358.

[34] Caroff, SN; Campbell, EC; Havey, J; Sullivan, KA; Mann, SC; Gallop, R (October 2001). "Treatment of tardive dyskinesia with donepezil: a pilot study". Journal of Clinical Psychiatry. 62 (10): 772–775. doi:10.4088/JCP.v62n1004. PMID 11816865.

[35] Ogunmefun, A; Hasnain, M; Alam, A; Osuala, T; Regenold, WT (February 2009). "Effect of donepezil on tardive dyskinesia". Journal of Clinical Psychopharmacology. 29 (1): 102–04. doi:10.1097/JCP.0b013e3181934475. PMID 19142126.

[36] Korsgaard, S (July 1986). "Baclofen (Lioresal) in the treatment of neuroleptic-induced tardive dyskinesia". Acta Psychiatrica Scandinavica. 54 (1): 17–24. doi:10.1111/j.1600-0447.1976.tb00090.x. PMID 782159.

[37] Gerlach, J; Rye, T; Kristjansen, P (March 1978). "Effect of baclofen on tardive dyskinesia" (PDF). Psychopharmacology. 56 (2): 145–51. doi:10.1007/BF00431840. PMID 417365.

[38] Stewart, RM; Rollins, J; Beckham, B; Roffman, M (December 1982). "Baclofen in tardive dyskinesia patients maintained on neuroleptics". Clinical Neuropharmacology. 5 (4): 365–73. doi:10.1097/00002826-198212000-00004. PMID 6130838.

[39] Erkan, A; Pirildar, S; Acarer, A; Akdeniz, F (2011). "Efficacy of Low-dose Pramipexole Augmentation in the Treatment of Refractory Psychotic Depression Complicated with Tardive Dyskinesia A Case Report" (PDF). Bulletin of Clinical Psychopharmacology (in Turkish). 21 (4): 353–55. doi:10.5455/bcp.20111029071711. Archived (PDF) from the original on 2012-01-13.

[TD2011-40] Aia, PG; Revuelta, GJ; Cloud, LJ; Factor, SA (2011). "Tardive Dyskinesia" (PDF). Current Treatment Options in Neurology. 13 (3): 231–41. doi:10.1007/s11940-011-0117-x. PMID 21365202.

[41] Brasic, James Robert (February 9, 2012). Benbadis, Selim, R, ed. "Tardive Dyskinesia". eMedicine. Archived from the original on August 27, 2009.

[42] Bhoopathi, Paranthaman Sethupathi; Soares-Weiser, Karla (2006). Bhoopathi, Paranthaman Sethupathi, ed. "Benzodiazepines for neuroleptic-induced tardive dyskinesia". Cochrane Database of Systematic Reviews (3): CD000205. doi:10.1002/14651858.CD000205.PUB2. PMID 16855954.

[43] Lerner, V; Miodownik, C; Kaptsan, A; Cohen, H; Matar, M; Loewenthal, U; Kotler, M (September 2001). "Vitamin B6 in the Treatment of Tardive Dyskinesia: A Double-Blind, Placebo-Controlled, Crossover Study" (PDF). The American Journal of Psychiatry. 158 (9): 1511–14. doi:10.1176/appi.ajp.158.9.1511. PMID 11532741.

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[45] Richardson, Mary Ann; Bevans, Margaret L.; Read, Laura L.; et al. (2003). "Efficacy of the Branched-Chain Amino Acids in the Treatment of Tardive Dyskinesia in Men". American Journal of Psychiatry. 160 (6): 1117–24. doi:10.1176/appi.ajp.160.6.1117. PMID 12777270.

[46] Llorca, Pierre-Michel; Chereau, Isabelle; Bayle, Frank-Jean; et al. (2002). "Tardive dyskinesias and antipsychotics: A review". European Psychiatry. 17 (3): 129–38. doi:10.1016/S0924-9338(02)00647-8. PMID 12052573.

[47] Glenmullen, Joseph (2001). Prozac Backlash: Overcoming the Dangers of Prozac, Zoloft, Paxil, and Other Antidepressants With Safe, Effective Alternatives. New York: Simon & Schuster. p. 38. ISBN 978-0-7432-0062-2. ^{[unreliable medical source?]} ::referring to Glazer, William M.; Morgenstern, Hal; Doucette, John T. (1993). "Predicting the long-term risk of tardive dyskinesia in outpatients maintained on neuroleptic medications". Journal of Clinical Psychiatry. 54 (4): 133–9. PMID 8098030.

[48] Jeste, Dilip V.; Caligiuri, Michael P.; Paulsen, Jane S.; et al. (1995). "Risk of Tardive Dyskinesia in Older Patients: A Prospective Longitudinal Study of 266 Outpatients". Archives of General Psychiatry. 52 (9): 756–65. doi:10.1001/archpsyc.1995.03950210050010. PMID 7654127.

[49] Whitaker, Robert (2002). Mad in America: Bad Science, Bad Medicine, and the Enduring Mistreatment of the Mentally Ill. Perseus. ^{[page needed]}

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tardive dyskinesia