Tardive dyskinesia

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Tardive dyskinesia
ICD-10 G24.0
ICD-9 333.85
OMIM 272620
DiseasesDB 12909

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List of terms related to Tardive dyskinesia

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [3]

Overview

Tardive dyskinesia is a neurological disorder caused by the long-term or high-dose use of dopamine antagonists, usually antipsychotics. These neuroleptic drugs are generally prescribed for psychiatric disorders. Other dopamine antagonists that can cause tardive dyskinesia are drugs for gastrointestinal disorders (for example metoclopramide) and neurological disorders. Some drugs that are not intended to affect dopamine, such as SSRI antidepressants, may also cause tardive dyskinesia. While newer atypical antipsychotics such as olanzapine and risperidone appear to have less dystonic effects, only clozapine has been shown to have a lower risk of tardive dyskinesia than older antipsychotics.[1]

The term tardive dyskinesia was introduced in 1964. Dyskinesia refers to an impairment of voluntary movement. The resultant tics and other movements are often referred to as dyskinesias. Dyskinesia is sometimes caused by long-term use of anti-psychotic drugs or other dopamine antagonists like the antiemetic metoclopramide. The effect of these drugs can be tardive, meaning the dyskinesia continues or appears even after the drugs are no longer taken. As far as treatment of iatrogenic tardive dyskinesia is concerned, neuroleptic drugs should be withdrawn for a period of 3-6 months to see if this resolves the issue, but the problem may fail to improve or may even exacerbate. In this situation, it would be sensible to trial the patient on tetrabenazine 25-50 mg/8h PO.(Oxford Handbook of Clinical Medicine).

In context of Parkinson's disease, dyskinesias are often the result of chronic levodopa (L-dopa) therapy. These motor fluctuations occur in more than half of PD patients after 5 to 10 years of levodopa therapy, with the percentage of affected patients increasing over time.[2]

Dyskinesias most commonly occur at the time of peak L-dopa plasma concentrations and are thus referred to as peak-dose dyskinesias. As patients advance, they may evidence diphasic dyskinesias, which occur when the drug concentration rises or falls.

The use of MDMA has been shown to enhance the effects of L-Dopa while reducing the associated dyskinesia in primates with simulated Parkinson's disease.[3]

Features

Tardive dyskinesia is characterized by repetitive, involuntary, purposeless movements. Features of the disorder may include grimacing, tongue protrusion, lip smacking, puckering and pursing of the lips, and rapid eye blinking. Rapid movements of the arms, legs, and trunk may also occur. Impaired movements of the fingers may appear as though the patient is playing an invisible guitar or piano. 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 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.

Cause

The cause of tardive dyskinesia appears to be related to damage to the system that uses and processes the neurotransmitter dopamine. It is thought that postsynaptic dopaminergic receptors become supersensitive to stimulation as a result of the use of neuroleptic drugs and that this supersensitivity causes the symptoms of tardive dyskinesia. 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 have been found to be associated with the development of tardive dyskinesia (Crane, 1973). 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.[4][5]

Differential Diagnosis of Tardive dyskinesia

One the basis of stiffness and fever it can be differentiated from:


Differential Diagnosis of Fever and Stiffness
Disease Diagnosis Treatment
Symptoms Signs Laboratory Findings
Tetanus[6][7]
  • Not significant
Neuroleptic Malignant Syndrome [8][9]
Viral Meningitis[10][11][12]
Stiff man syndrome
  • Marked rigidity
  • Spasms
    • Intermittent
    • Painful
    • Absent during sleep
Drug induced (Tardive dyskinesia)[13][14][15]
  • History of intake of the offending drug for at least one month
  • Eye deviation
  • Head and neck jerky movements
  • No tonic contraction of the muscles between the spasms
Strychnine poisoning[16][17][18][19]
  • Hx of up to date tetanus immunizations
  • History of intentional or accidental intake
    • Strychnos nux vomica seeds
    • Rodenticide
  • Hypervigilance
  • Anxiety
  • Mydriasis
  • Hypereflexia
  • Clonus
  • Facial and neck stiffness
  • Blood assay
  • Tissue assay
  • Urine assay
  • Initial stabilization
  • High dose Benzodiazepines
  • Intubation and airway securing
Hypocalcaemia[20][21]
Parkinson's disease[22][23]
  • Clinical diagnosis
  • Improvement with dopaminergic therapy confirms diagnosis

Causes

Cardiovascular No underlying causes
Chemical / poisoning No underlying causes
Dermatologic No underlying causes
Drug Side Effect Asenapine maleate, Chlorpromazine, Clozapine, Fluphenazine, Iloperidone, Loxapine, Metoclopramide, Olanzapine, Perphenazine, Prochlorperazine, Thioridazine hydrochloride, Thiothixene, Trifluoperazine
Ear Nose Throat No underlying causes
Endocrine No underlying causes
Environmental No underlying causes
Gastroenterologic No underlying causes
Genetic No underlying causes
Hematologic No underlying causes
Iatrogenic No underlying causes
Infectious Disease No underlying causes
Musculoskeletal / Ortho No underlying causes
Neurologic No underlying causes
Nutritional / Metabolic No underlying causes
Oncologic No underlying causes
Opthalmologic No underlying causes
Overdose / Toxicity No underlying causes
Psychiatric No underlying causes
Pulmonary No underlying causes
Renal / Electrolyte No underlying causes
Rheum / Immune / Allergy No underlying causes
Trauma No underlying causes
Miscellaneous No underlying causes

Treatment

Primary prevention of tardive dyskinesia is achieved by using the lowest effective dose of a neuroleptic for the shortest time. If tardive dyskinesia is diagnosed, the causative drug should be reduced or discontinued if possible. Tardive dyskinesia may persist after withdrawal of the drug for months, years, or even permanently. There is no known cure for tardive dyskinesia, but preliminary research suggests that the atypical neuroleptic clozapine (Clozaril®) may improve the state of the patient. Improvements are also seen in some cases, if the high potency benzodiazepines - lorazepam (Ativan®), diazepam (Valium®), or clonazepam (Klonopin®)--are used. The findings about the effects of natural substances, such as vitamin E (Alpha-Tocopherol) or melatonin, are inconclusive.

Natural remedies are unproven, since they are seldom tested in a controlled setting such as a drug trial. Preliminary research indicates that alternating rest, and regular exercise also negate the symptoms of tardive dyskinesia, necessary for all mental health outpatients who maintain anti-psychotic neuroleptic drug regimes, for on-going 'wellness'. Switching to a newer drug with fewer side effects might be an option for a patient in a controlled or monitored environment.

Epidemiology

Tardive dyskinesia most commonly occurs in patients with psychiatric conditions who are treated with antipsychotic medications for many years. Some 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.”[24] 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.[25] Eventually, according to these estimates, if on the drugs long enough, the majority of patients will develop the disorder.[26] 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 a social handicap. 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.

Controversy

Peter Breggin has discussed tardive dyskinesia in the context of his criticism of biological psychiatry. However, his hypotheses are not widely accepted by mainstream psychiatric professionals. [27][28][29][30]

See also

References

  1. Craig & Stitzel; Modern Pharmacology (6th ed) pp. 401.
  2. Obeso JA, et al. The evolution and origin of motor complications in Parkinson's disease. Neurology. 2000;55 (suppl 4):S13-S20.
  3. Iravani, M., Jackson, M., Kuoppamäki, M., Smith, L. & Jenner, P. (2003). 3,4-Methylenedioxymethamphetamine (Ecstasy) Inhibits Dyskinesia Expression and Normalizes Motor Activity in 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine-Treated Primates, Journal of Neuroscience, 23, 9107–9115
  4. Breggin, P. R. (1990) Brain damage, dementia and persistent cognitive dysfunction associated with neuroleptic drugs. Evidence, etiology, implications. Journal of Mind and Behavior, 11, 425 64
  5. Gualtieri, C. T. and Barnhill, L. J. (1988) Tardive dyskinesia in special populations. In M. E. Wolf and A. D. Mosnaim (eds) Tardive dyskinesia. Washington DC: American Psychiatric Press.
  6. Woldeamanuel YW, Andemeskel AT, Kyei K, Woldeamanuel MW, Woldeamanuel W (2016). "Case fatality of adult tetanus in Africa: Systematic review and meta-analysis". J Neurol Sci. 368: 292–9. doi:10.1016/j.jns.2016.07.025. PMID 27538652.
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  8. Hosseini S, Elyasi F (2017). "Olanzapine-Induced Neuroleptic Malignant Syndrome". Iran J Med Sci. 42 (3): 306–309. PMC 5429500. PMID 28533580.
  9. Leenhardt F, Perier D, Pinzani V, Giraud I, Villiet M, Castet-Nicolas A; et al. (2017). "Pharmacist intervention to detect drug adverse events on admission to the emergency department: Two case reports of neuroleptic malignant syndrome". J Clin Pharm Ther. doi:10.1111/jcpt.12531. PMID 28488314.
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  11. Leen WG, Willemsen MA, Wevers RA, Verbeek MM (2012). "Cerebrospinal fluid glucose and lactate: age-specific reference values and implications for clinical practice". PLoS One. 7 (8): e42745. doi:10.1371/journal.pone.0042745. PMC 3412827. PMID 22880096.
  12. Tyler KL (2004). "Herpes simplex virus infections of the central nervous system: encephalitis and meningitis, including Mollaret's". Herpes. 11 Suppl 2: 57A–64A. PMID 15319091.
  13. Deng ZD, Li DY, Zhang CC, Pan YX, Zhang J, Jin H; et al. (2017). "Long-term follow-up of bilateral subthalamic deep brain stimulation for refractory tardive dystonia". Parkinsonism Relat Disord. doi:10.1016/j.parkreldis.2017.05.010. PMID 28552340.
  14. "Valbenazine (Ingrezza) for tardive dyskinesia". Med Lett Drugs Ther. 59 (1521): 83–84. 2017. PMID 28520698.
  15. Voelker R (2017). "Tardive Dyskinesia Drug Approved". JAMA. 317 (19): 1942. doi:10.1001/jama.2017.5537. PMID 28510661.
  16. Charlotte Duverneuil, Geoffroy Lorin de la Grandmaison, Philippe de Mazancourt & Jean-Claude Alvarez (2004). "Liquid chromatography/photodiode array detection for determination of strychnine in blood: a fatal case report". Forensic science international. 141 (1): 17–21. doi:10.1016/j.forsciint.2003.12.010. PMID 15066709. Unknown parameter |month= ignored (help)
  17. B. A. Smith (1990). "Strychnine poisoning". The Journal of emergency medicine. 8 (3): 321–325. PMID 2197324. Unknown parameter |month= ignored (help)
  18. B. J. Maron, J. R. Krupp & B. Tune (1971). "Strychnine poisoning successfully treated with diazepam". The Journal of pediatrics. 78 (4): 697–699. PMID 5547830. Unknown parameter |month= ignored (help)
  19. B. Oberpaur, A. Donoso, C. Claveria, C. Valverde & M. Azocar (1999). "Strychnine poisoning: an uncommon intoxication in children". Pediatric emergency care. 15 (4): 264–265. PMID 10460082. Unknown parameter |month= ignored (help)
  20. Chhabra P, Rana SS, Sharma V, Sharma R, Bhasin DK (2016). "Hypocalcemic tetany: a simple bedside marker of poor outcome in acute pancreatitis". Ann Gastroenterol. 29 (2): 214–20. doi:10.20524/aog.2016.0015. PMC 4805743. PMID 27065735.
  21. Desai M, Kolla PK, Reddy PL (2013). "Calcium unresponsive hypocalcemic tetany: gitelman syndrome with hypocalcemia". Case Rep Med. 2013: 197374. doi:10.1155/2013/197374. PMC 3792521. PMID 24171002.
  22. Olanow CW, Watts RL, Koller WC (2001). "An algorithm (decision tree) for the management of Parkinson's disease (2001): treatment guidelines". Neurology. 56 (11 Suppl 5): S1–S88. PMID 11402154.
  23. Connolly BS, Lang AE (2014). "Pharmacological treatment of Parkinson disease: a review". JAMA. 311 (16): 1670–83. doi:10.1001/jama.2014.3654. PMID 24756517.
  24. Glenmullen, Joseph. Prozac Backlash. ©2000 by Joseph Glenmullen. Simon & Schuster, Inc. New York. page 38. [1]
    Referring to W. M. Glazer, H. Morgenstern, and J. T. Doucette, "Predicting the Long-Term Risk of Tardive Dykinesia [tics] in Outpatients Maintained on Neuroleptic [major tranquilizer] Medications," Journal of Clinical Psychiatry 54 (1993): 133-139. [2]
  25. Jeste D, Caligiuri M. (1993) Tardive dyskinesia. Schizophr Bull. 1993;19:303-316. PMID 8100643
  26. Whitaker , Robert - Mad in America: Bad Science, Bad Medicine, and the Enduring Mistreatment of the Mentally Ill, Perseus Pub., c2002
  27. Breggin, P. R. (1983) Psychiatric drugs. New York: Springer
  28. Breggin, P. R. (1991) Toxic psychiatry. New York: St. Martin's Press
  29. Psychiatrist and Psychiatry Critic, Peter Breggin, On Tardive Dyskinesia
  30. Psychiatrist and Psychiatry Critic, Peter Breggin, On Neuroleptics



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