DSM-5 Diagnostic Criteria for Tardive Dyskinesia
- Involuntary athetoid or choreiform movements (lasting at least a few weeks) generally of the tongue, lower face and jaw, and extremities (but sometimes involving the pharyngeal, diaphragmatic, or trunk muscles) developing in association with the use of a neuroleptic medication for at least a few months.
- Symptoms may develop after a shorter period of medication in older persons.
- In some patients, movements of this type may appear after discontinuation, or after change or reduction in dosage, of neuroleptic medications (in which case the condition is called neuroleptic withdrawal-emergent dyskinesia). Withdrawal-emergent dyskinesia is usually time-limited, so dyskinesia persisting more than 4 to 8 weeks is considered tardive dyskinesia.8
The Schooler-Kane Diagnostic Criteria for Tardive Dyskinesia
- At least 3 months of cumulative antipsychotic exposure
- Abnormal Involuntary Movement Scale: at least moderate in ≥1 area, or at least mild in ≥2 areas
- Absence of other causal conditions
- Meets criteria 1-3: Probably tardive dyskinesia
- Meets criteria 1-3 but movements suppressed within 2 weeks by antipsychotic drugs: Masked tardive dyskinesia
- Movements not observed on subsequent examination within 3 months: Transient tardive dyskinesia
- Movements observed within 2 weeks of antipsychotic drug discontinuation: Withdrawal tardive dyskinesia
- Movements persist for 3 months: Persistent tardive dyskinesia9
Dr Correll stresses the importance of using a standardized rating scale, notably the Abnormal Involuntary Movement Scale.10 Additional scales are the Simpson Dyskinesia Scale11 and the Extrapyramidal Symptom Rating Scale.12 It is important to note that these are screening and not diagnostic tools, and should be used in conjunction with diagnostic criteria.1
Assessment tools can be used to facilitate communication, as some patients are reluctant or unable to describe these effects. The scales create a structure and framework for discussion, giving clinicians “information regarding the severity, frequency, and impact of involuntary movement symptoms” and enabling patients to ‘recognize and describe their symptoms.’ “1
The American Psychiatric Association recommends that all patients taking an antipsychotic medication be monitored for movement disorders; those taking FGAs should be assessed every 6 months, whereas patients taking SGAs should be assessed every 12 months.13 Patients with additional risk factors and patients who recently initiated antipsychotic treatment and are showing signs of early involuntary movement should also be monitored more frequently.13
Pharmacotherapies for Treating Tardive Dyskinesia
Until recently, there were few treatment options available for tardive dyskinesia. An older strategy was for patients to switch from an FGA to an SGA. Other suggested treatments included branched-chain amino acids, which, although no longer available as a brand, can still be obtained in compounding pharmacies.1 Additional proposed treatments included donepezil, melatonin, vitamin B6, and vitamin E, but they had “mixed results” in clinical trials.
In 2013, the American Academy of Neurology released evidence-based guidelines for the treatment of tardive dyskinesia.14,15 These were updated in 2018 and are summarized below.
American Academy of Neurology Recommended and Nonrecommended Agents for Treating Tardive Dyskinesia
Insufficient Evidence/Not Recommended
- Discontinuing medication associated with tardive dyskinesia
- Switching from FGA to SGA
- Raising antipsychotic dose
- Vitamin E
- Vitamin B6
- Yi-gan san
- Biperidin discontinuation
- Botulinum toxin type A
- Electroconvulsive treatment (ECT)
- Eicosapentaenoic acid
- Clonazepam (Level B)
- Ginkgo biloba (Level B)
- Amantadine (Level C)
- Tetrabenazine (Level C)
- Deutetrabenazine (Level A)
- Valbenazine (Level A)
- Pallidal deep brain stimulation for intractable tardive dyskinesia (Level C)
The guideline update reflects the 2017 US Food and Drug Administration’s approval of 2 novel agents, valbenazine and deutetrabenazine, which are reversible vesicular monoamine transporter-2 inhibitors.16,17
By inhibiting the vesicular monoamine transporter type 2, these agents reduce dopamine storage and release. Reduction in dopamine in turn curtails the overstimulation of supersensitive D2 dopamine receptors in the motor striatum, which causes tardive dyskinesia, leading to “less ‘go’ and more ‘stop’ ” signals.18
Nonpharmacologic Interventions for Tardive Dyskinesia
Amid the focus on pharmacotherapies, it is sometimes easy to lose sight of the importance of nonpharmacologic interventions.
“We know that abnormal involuntary movements get worse when people are stressed, and abate during sleep,” Dr Correll stated.
Interventions to increase relaxation show some promise.19,20 However, “the data are not strong,” Dr Correll noted.
Nevertheless, “this is just conjecture, but it may be that mindfulness or yoga can assist with relaxation,” Dr Correll said.
He cautioned that these approaches will likely bring only in bringing temporary relief, rather than having a long-term effect, as they do not remove the basic pathophysiological issue that underlies the tardive dyskinesia.
Because tardive dyskinesia “can affect functioning and be embarrassing” and can also cause anxiety,21 providing education and support to patients and families is very important. Resources for patients can be found below.
Resources for Patients with Tardive Dyskinesia
Phone: (703) 524-7600
TTY: (703) 516-7227
NAMI HelpLine: (800) 950-NAMI (6264)
E-mail: [email protected]
Phone: (203) 744-0100
Voice mail: (800) 999-NORD (6673)
TTY: (203) 797-9590
E-mail: [email protected]
Tardive Dyskinesia/Tardive Dystonia National Association
Phone: (206) 522-3166
E-mail: [email protected]
- Correll CU, Kane JM, Citrome LL. Epidemiology, prevention, and assessment of tardive dyskinesia and advances in treatment. J Clin Psychiatry. 2017;78(8):1136-1147.
- Schonecker M. [Paroxysmal dyskinesia as the effect of megaphen]. Nervenarzt. 1957;28(12):550-553 [Article in German]
- Tarsy D, Lungu C, Baldessarini RJ. Epidemiology of tardive dyskinesia before and during the era of modern antipsychotic drugs. Handb Clin Neurol. 2011;100:601-616.
- Dhir A, Schilling T, Abler V, Potluri R, B Carroll B. Estimation of epidemiology of tardive dyskinesia in the United States. Neurology. 2017;88(16 Supplement):P2.018.
- Carbon M, Hsieh CH, Kane JM, Correll CU. Tardive dyskinesia prevalence in the period of second-generation antipsychotic use: a meta-analysis. J Clin Psychiatry. 2017;78(3):e264-e278.
- Cornett EM, Novitch M, Kaye AD, Kata V, Kaye AM. Medication-induced tardive dyskinesia: a review and update. Ochsner J. 2017;17(2):162-174.
- Correll CU, Leucht S, Kane JM. Lower risk for tardive dyskinesia associated with second-generation antipsychotics: a systematic review of 1-year studies. Am J Psychiatry. 2004;161(3):414-425.
- American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 5th ed. Washington, DC: American Psychiatric Association; 2013.
- Schooler NR, Kane JM. Research diagnoses for tardive dyskinesia. Arch Gen Psychiatry. 1982;39(4):486-487.
- National Institute for Mental Health. Abnormal Involuntary Movement Scale. https://www.aacap.org/App_Themes/AACAP/docs/member_resources/toolbox_for_clinical_practice_and_outcomes/monitoring/AIMS.pdf. Accessed March 9, 2018.
- Simpson GM, Lee JH, Zoubok B, Gardos G. A rating scale for tardive dyskinesia. Psychopharmacology (Berl). 1979;64(2):171-179.
- Chouinard G, Margolese HC. Manual for the Extrapyramidal Symptom Rating Scale (ESRS). Schizophr Res. 2005;76(2-3):247-265.
- Lehman AF, Lieberman JA, Dixon LB, et al. Practice guideline for the treatment of patients with schizophrenia, second edition. Am J Psychiatry. 2004;161(2 Suppl):1-56.
- Bhidayasiri R, Fahn S, Weiner WJ, et al. Evidence-based guideline: treatment of tardive syndromes: report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology. 2013;81(5):463-469.
- Bhidayasiri R, Jitkritsadakul O, Friedman JH, Fahn S. Updating the recommendations for treatment of tardive syndromes: A systematic review of new evidence and practical treatment algorithm [published online February 5, 2018]. J Neurol Sci. doi: 10.1016/j.jns.2018.02.010
- Ingrezza (valbenazine): highlights of prescribing information. April 2017. https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/208772lbl.pdf. Accessed March 9, 2018.
- Austedo (deutetrabenazine): highlights of prescribing information. August 2017. Available at: https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/208082s000lbl.pdf. Accessed March 9, 2018.
- Stahl SM. Mechanism of action of vesicular monoamine transporter 2 (VMAT2) inhibitors in tardive dyskinesia: reducing dopamine leads to less “go” and more “stop” from the motor striatum for robust therapeutic effects. CNS Spectr. 2018;23(1):1-6.
- Cotton DH. The effects of progressive relaxation training and EMG biofeedback on tardive dyskinesia: A single case design study. Clin Biofeedback Health. 1986;9(1):3-8.
- Johnson PR. A behavioral approach to management of neuroleptic-induced tardive dyskinesia: progressive relaxation training. http://arizona.openrepository.com/arizona/handle/10150/193579. Accessed March 9, 2018.
- American Academy of Neurology. Treating and managing tardive syndromes. https://www.aan.com/Guidelines/Home/GetGuidelineContent/614. March 9, 2018.
This article originally appeared on Psychiatry Advisor