Identifying Tardive Dyskinesia: Risk Factors, Functional Impact, and Diagnostic Tools

Abstract

Tardive dyskinesia (TD) is an involuntary movement disorder induced by dopamine-receptor blocking agents (DRBAs), including antipsychotics. Because the introduction of second-generation antipsychotics has reduced but not eliminated the risk for TD as had been hoped, recognizing and treating TD are important skills for clinicians. Many patients rely on DRBAs for chronic conditions. To minimize the risk of patients’ involuntary movements becoming permanent, they must be detected early and treated. To improve the early recognition and diagnosis of TD, clinicians must know the risk factors, understand the functional impairment, regularly and systematically assess their patients, and appropriately apply diagnostic criteria.

J Clin Psychiatry 2020;81(1):TV18059BR1C

From the Pharmacotherapy Division, The University of Texas at Austin College of Pharmacy, and Pharmacotherapy Education and Research Center, School of Medicine, UT Health San Antonio.
From the Series: Revisiting Tardive Dyskinesia: Focusing on the Basics of Identification and Treatment
To cite: Saklad SR. Identifying tardive dyskinesia: risk factors, functional impact, and diagnostic tools. J Clin Psychiatry. 2020;81(1):TV18059BR1C.
To share: https://doi.org/10.4088/JCP.TV18059BRIC
© Copyright 2019 Physicians Postgraduate Press, Inc.

Support Statement

Supported by an educational grant from Teva Pharmaceuticals.

Learning Objectives

After completing this educational activity, you should be able to:

• Recognize risk factors for TD in patients being treated with antipsychotics
• Evaluate patients for TD at recommended intervals with standardized tools and criteria

Release, Review, and Expiration Dates

This brief report activity was published in December 2019 and is eligible for AMA PRA Category 1 Credit™ through December 31, 2021. The latest review of this material was October 2019.

Statement of Need and Purpose

Many clinicians are unable to identify risk factors for TD, are unfamiliar with diagnostic criteria, and do not regularly assess patients for TD. New medications for TD are available, evidence-based treatment recommendations have been published, and research has explored longer-term safety and efficacy with new medications. But clinicians may be slow to implement treatment strategies due to underestimation of the social and occupational impact that TD has on patients’ lives and uncertainty about what to do due to lack of training. Education is therefore needed on the risk factors that should alert clinicians to monitor certain patients especially closely for TD and strategies to assess all patients being treated with dopamine-blocking agents and provide an accurate diagnosis. Clinicians also need awareness of the burden of TD and need up-to-date, evidence-based, expert guidance on using new medications in the treatment of TD, including longer-term use. This activity was designed to meet the needs of participants in CME activities provided by the CME Institute of Physicians Postgraduate Press, Inc., who have requested information on TD.

Disclosure of Off-Label Usage

Dr Saklad has determined that, to the best of his knowledge, no investigational information about pharmaceutical agents or device therapies that is outside US Food and Drug Administration–approved labeling has been presented in this activity.

Review Process

The faculty member(s) agreed to provide a balanced and evidence-based presentation and discussed the topic(s) and CME objective(s) during the planning sessions. The faculty’s submitted content was validated by CME Institute staff, and the activity was evaluated for accuracy, use of evidence, and fair balance by the Chair and a peer reviewer who is without conflict of interest.

Acknowledgment

This activity is derived from the teleconference series “Revisiting Tardive Dyskinesia: Focusing on the Basics of Identification and Treatment,” which was held in July and August 2019 and supported by an educational grant from Teva Pharmaceuticals. The opinions expressed herein are those of the faculty and do not necessarily reflect the opinions of the CME provider and publisher or the commercial supporter.

Faculty Affiliation

Stephen R. Saklad, PharmD, BCPP
Pharmacotherapy Division, The University of Texas at Austin College of Pharmacy, and Pharmacotherapy Education and Research Center, School of Medicine, UT Health San Antonio

Financial Disclosure

The faculty for this CME activity and the CME Institute staff were asked to complete a statement regarding all relevant personal and financial relationships between themselves or their spouse/partner and any commercial interest. The Accreditation Council for Continuing Medical Education (ACCME) defines a commercial interest as any entity producing, marketing, re-selling, or distributing health care goods or services consumed by, or used on, patients. The ACCME defines relevant financial relationships as financial relationships in any amount occurring within the past 12 months that create a conflict of interest. The CME Institute has resolved any conflicts of interest that were identified. No member of the CME Institute staff reported any relevant personal financial relationships. Faculty financial disclosures are as follows:

Dr Saklad is a consultant for Texas Health and Human Services, San Antonio State Hospital, Alkermes, Intra-Cellular Therapeutics, and Otsuka; has received grant/research support from Alkermes; and is a member of the speakers/advisory boards for Alkermes and Neurocrine. The Chair for this activity, Leslie L. Citrome, MD, MPH, is a consultant for Acadia, Alkermes, Allergan, Eisai, Impel, Indivior, Intra-Cellular Therapeutics, Janssen, Lundbeck, Merck, Neurocrine, Noven, Osmotica, Otsuka, Pfizer, Shire, Sunovion, Takeda, Teva, and Vanda; is a member of the speakers/advisory boards for Acadia, Alkermes, Allergan, Janssen, Lundbeck, Merck, Neurocrine, Otsuka, Pfizer, Shire, Sunovion, Takeda, and Teva; and is a stock shareholder of Bristol-Myers Squibb, Eli Lilly, Johnson & Johnson, Merck, and Pfizer

Accreditation Statement

The CME Institute of Physicians Postgraduate Press, Inc., is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

Credit Designation

The CME Institute of Physicians Postgraduate Press, Inc., designates this enduring material for a maximum of 0.50 AMA PRA Category 1 Credit™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Note: The American Nurses Credentialing Center (ANCC) and the American Academy of Physician Assistants (AAPA) accept certificates of participation for educational activities certified for AMA PRA Category 1 Credit™ from organizations accredited by the ACCME.

To obtain credit for this activity, study the material and complete the CME Posttest and Evaluation.

MOC Approval Statement

Through the American Board of Medical Specialties (“ABMS”) ongoing commitment to increase access to practice relevant Continuing Certification Activities through the ABMS Continuing Certification Directory, Identifying Tardive Dyskinesia: Risk Factors, Functional Impact, and Diagnostic Tools has met the requirements as a MOC Part II CME Activity (apply toward general CME requirement) for the following ABMS Member Boards:

MOC Part II CME Activity

Psychiatry and Neurology

Available Credit

• 0.50 AMA PRA Category 1 Credit™
• 0.50 Participation

This CME activity is expired. For more CME activities, visit cme.psychiatrist.com.
Find more articles on this and other psychiatry and CNS topics:
The Journal of Clinical Psychiatry
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Introduction

Tardive dyskinesia (TD) is a potentially permanent, hyperkinetic movement disorder associated with the use of dopamine-receptor blocking agents (DRBAs).¹ It is commonly believed that TD is associated only with antipsychotics, but other DRBAs are associated with this neurologic disorder, such as the pro-motility agent metoclopramide. It is important to realize that this disabling movement disorder may occur not only in patients taking antipsychotics but also in patients taking other DRBAs.

The prevalence of TD is higher than commonly realized. A meta-analysis² of 41 studies included over 11,000 patients with an average age of 43 years. Two-thirds of these patients were male, and more than three-quarters had a schizophrenia spectrum disorder. The overall prevalence of TD in this sample was 25%. The TD rate for those with current SGA use was lower than in those with current FGA use (21% vs 30%, respectively), and the small number of patients with current SGA use without any prior FGA exposure had a prevalence rate of only 7.2%.²

The management of this abnormal and involuntary motor disturbance remains a significant challenge for clinicians whose patients rely on DRBAs for chronic conditions. Also, TD must be detected early to minimize the risk of the patient’s iatrogenic movement disorder becoming permanent. To improve the early recognition and diagnosis of TD, clinicians must know the risk factors, understand the functional impairment, regularly and systematically assess their patients, and appropriately apply diagnostic criteria.

Functional Impact of TD

Patient Perspectives
Despite its prevalence, many people with TD are unaware of their movements until a family member, friend, or clinician notices them, as was the case for this patient:

A study⁴ of patients with schizophrenia (N = 607) at a state mental hospital in Singapore reported that 40% met criteria for TD, yet 67% were unaware of their abnormal movements. The finding that two-thirds of patients with schizophrenia lacked awareness of their TD suggests that many patients are not likely to voluntarily mention this side effect at clinical visits and clinicians must be proactive in screening.

The abnormal involuntary movements of TD contribute to functional impairment, negatively affecting patients’ quality of life. To investigate the burden of TD in a real-world population of patients taking antipsychotics, a study⁵ evaluated health-related quality of life using the EQ-5D-5L questionnaire in participants without visible signs of involuntary movements (Cohort 1) and participants with visible signs and clinical assessment of possible TD (Cohort 2). In all but 1 domain, a higher percentage in Cohort 2 reported having moderate to extreme problems  (AV 1).⁵ Those with probable TD also had greater impairment across all three domains of the Sheehan Disability Scale, including work/school, social life, and family life/home responsibilities compared to those without TD.

AV 1. Self-Reported Quality of Life in Patients With and Without TD

Data from Caroff et al.⁵

An observational study⁶ of patients with schizophrenia, bipolar disorder, and major depressive disorder compared self-report questionnaires of participants with TD (N = 79) and without TD (N = 90). TD patients had significantly worse scores on the physical component summary of the SF‑12v2 Health Survey (P = .003), the Q-LES-Q-SF (P < .001), and the SW-ISMI (P < .001) than non-TD patients. Greater TD severity was associated with lower overall quality of life, greater social withdrawal, and decreased physical and mental health.

Patient Perspectives
The embarrassment and stigma associated with obvious involuntary movements often lead patients with TD to avoid social contact, as the following patient comment describes:

Risk Factors for TD

The risk-benefit ratio of DRBAs must be evaluated and individualized for each patient, meaning that clinicians must consider the type and dose of antipsychotic, as well as other interventions (eg, psychosocial) that could be used instead as a preventive measure against TD.⁷ Communicating clearly and documenting their discussions with patients about treatment options for their situation are essential tasks for clinicians. All patients taking DRBAs should be educated on the risk and symptoms of TD.

The pathophysiology of TD is unknown but is believed to involve postsynaptic dopamine receptor hypersensitivity.⁸ Other prominent explanatory models for TD include GABA depletion, cholinergic deficiency, neurotoxicity and oxidative stress, changes in synaptic plasticity, and defective neuroadaptive signaling.⁹

Factors increasing the risk of TD may involve the patient directly or maybe non-patient (eg, treatment, illness) factors. Both patient and non-patient factors can be non-modifiable or modifiable.¹⁰

Non-modifiable factors. Non-modifiable factors for TD include the following¹⁰:

Modifiable factors. Modifiable risk factors include comorbid diabetes, smoking, and alcohol and substance abuse.¹⁰ Although these factors are common in patients with mental illness, they are areas that clinicians can work with patients to try to improve.

Modifiable treatment factors that are associated with increased risk of TD include the development of acute EPS and the use of FGA (over SGA) medications.¹⁰ Higher antipsychotic doses are also associated with increased risk. People who metabolize medications less effectively have a higher risk. To reduce TD risk, clinicians should only use DRBAs when indicated and minimize the dose and duration of exposure to DRBA medications as clinically appropriate.

A possible risk factor for TD is intermittent antipsychotic treatment.^11–13 Patients often stop taking medication for a weekend or other period of time, called a “drug holiday.”

Finally, patients exposed to concomitant anticholinergic medications have increased risk of TD.¹⁰ Anticholinergic medications that cross the blood-brain barrier can include agents used to treat acute EPS, Parkinson’s disease, gastrointestinal problems, and enuresis. Clinicians should avoid these medications, if possible, because they can worsen symptoms of TD and cause cognitive impairment and many other problems.¹⁴

Diagnostic Tools for TD

Early recognition of abnormal movements is essential to the prevention and management of TD. To diagnose TD, clinicians must be familiar with diagnostic criteria, differential diagnosis, and use of an assessment tool for abnormal movements, such as the AIMS.

Criteria. The Schooler-Kane criteria¹⁵ for TD were developed to aid research but are now widely used in clinical practice to determine probable TD. Schooler–Kane criteria require: 1) at least 3 months of cumulative exposure to a DRBA; 2) at least moderate dyskinetic movements in 1 body area (≥ 3 score on AIMS) or mild dyskinetic movements in 2 body areas (≥ 2 score on AIMS); and 3) absence of other conditions that might cause involuntary movements.

The DSM-5 criteria¹⁶ for TD are not as specific as Schooler-Kane criteria in the time requirement for DRBA exposure, stating that involuntary movements develop with the use of neuroleptic medication for “at least a few months” and that the time may be shorter for older adults.¹⁷ The involuntary movements are frequently observed in the tongue, jaw, the perioral area, and also in the trunk and the extremities. Common orofacial movements include chewing; lip smacking, puckering, or pursing; tongue protrusion; grimacing; or cheek bulging.¹⁸ TD can also appear as contracting, twisting, or writhing movements of the fingers, hands, arms, or legs. These involuntary movements are present for at least 4 weeks and fit any 1 of several patterns: choreiform, athetoid, or rhythmic.¹⁶ Choreiform movements are rapid, jerky, and non-repetitive, while athetoid movements are slow, sinuous, and widely continual. Frequently, these 2 types of movement occur in combination and are called choreoathetoid movements.

TD is diagnosed if involuntary movements develop during exposure to a DRBA, within 4 weeks of withdrawal from an oral DRBA, or within 8 weeks of withdrawal from a long-acting injectable DRBA.¹⁶ Generally, the more severe forms of TD would appear during the constant dosing of a DRBA.

Differential diagnosis. TD is a diagnosis of exclusion because many other conditions and syndromes can cause abnormal movements that resemble TD and must be ruled out, such as the following¹⁷:

• Spontaneous dyskinesias occurring in the elderly and patients with schizophrenia
• Oral movements from ill-fitting dentures and other dental problems
• Drug-induced dyskinesias from antiparkinsonian drugs or stimulants
• Autism
• Chronic motor tic disorder
• Huntington’s disease
• Meige’s syndrome
• Restless legs syndrome
• Rett’s syndrome
• Senile chorea
• Sydenham’s chorea
• Tourette syndrome
• Wilson’s disease

Spontaneous dyskinesias are fairly common in elderly patients and patients with schizophrenia who have never been exposed to DRBAs. For example, a study¹⁹ reported that dyskinetic movements were more common among patients with schizophrenia who were never exposed to DRBAs (N = 94) than among patients with other psychiatric diagnoses (N = 179). The dyskinetic movements were most often noted in the same body areas typically associated with TD. Spontaneous dyskinesias are some of the most difficult to differentiate because they look the same as TD.

While TD is the most common abnormal movement syndrome,²⁰ clinicians should be familiar with the other tardive syndromes (AV 2).^21,22

AV 2. The Tardive Syndromes

Based on Truong and Frei²¹ and AAN.²²

Drug-induced dyskinesias from antiparkinsonian drugs or stimulants can present a diagnostic challenge because amphetamines and methamphetamines interact with some of the same neurotransmitter transporter systems that are involved in the treatment of TD.²³

Distinguishing characteristics can help clinicians determine if patients have TD versus drug-induced parkinsonism (previously called pseudoparkinsonism). The first characteristic to consider is that the onset of TD occurs months to years after DRBA initiation, and drug-induced parkinsonism occurs hours to weeks after starting an antipsychotic or after increasing the dose.²⁴ Second, increasing the antipsychotic dose will improve TD but worsen drug-induced parkinsonism within hours or weeks, while decreasing the dose worsens TD but improves drug-induced parkinsonism within days to weeks. Third, the addition of an anticholinergic medication can worsen TD but improve drug-induced parkinsonism. Finally, clinicians may be able to differentiate the motor symptoms between these conditions because individuals with TD tend to have arrhythmic movements (generally choreoathetoid) of the face, trunk, and extremities, and individuals with drug-induced parkinsonism have rhythmic tremor, rigidity, shuffling gait, or restlessness.

Abnormal Involuntary Movement Scale. A rating scale cannot be used to diagnose TD, but it can establish the presence of abnormal movements, which is a criterion of TD. A rating scale, such as the AIMS, can lead to timely identification and improved outcomes.^17,25 The AIMS is recommended for clinical screening for TD and follow-up of patients diagnosed with the disorder. Other rating scales may also be used as long as training is provided. Whatever scale is used, a baseline exam is essential to document the status of patients’ movements before treatment begins.

In addition to conducting an initial assessment before treatment, the APA guideline²⁶ recommends that patients be evaluated for TD every 6 months while receiving an FGA and every 12 months while receiving an SGA. Patients with risk factors for TD, such as those who are older, female, and/or smoke or use recreational drugs, should be examined every 3 months while receiving an FGA and every 6 months while taking an SGA. Clinicians may assess more frequently as indicated or if other guidelines or laws apply.

The AIMS exam was published in 1976²⁷ and is accessible to the public at no cost. The AIMS exam has 14 items²⁸ and takes about 10 minutes to administer. Clinicians should observe patients unobtrusively at rest either before or after administering the exam, such as while they are sitting in the waiting room. For the assessment, patients should be seated in a firm chair or stool without arms and remove their shoes and socks. Clinicians should ask patients if they have experiences of involuntary movements and, if so, whether they are bothered by them. So that abnormal movements are not confused with actions such as chewing gum, the examiner should ask patients about any problems with their teeth or gums, if they have dentures, and if they are chewing anything. Because the abnormal movements are increased when the patient is distracted by performing other movements, the examiner looks for evidence of involuntary movements in the patient’s entire body while asking them to perform tasks that include sticking out their tongues, tapping their thumbs to each finger, and extending their limbs.^27,29 These tasks occupy the patient’s attention and decrease their ability to suppress the abnormal movements.

In my experience, it is best to wait to fill out the AIMS form until after the assessment is completed, as it may be disconcerting to patients. Patients always watch what their health care provider is writing down. Unless I am taking a history (in which case the patient expects note-taking behavior), I always write notes after the interview with the patient is completed, and usually out of sight of the patient.

For scoring movements on the AIMS 5-point scale (from 0 = none, normal to 4 = severe), clinicians should keep in mind that minimal is the extreme edge of normal. So, a questionable movement would be rated as 1 = minimal, and 2 = mild is the first point where movements are definitively abnormal. For the global judgments section, the overall severity is the highest rating assigned to any of the specific body areas, and the incapacitation score is the functional impairment due to the patient’s abnormal movements. Finally, the patient’s awareness of their abnormal movements and level of distress due to their abnormal movements are rated on an adjusted scale of 0 = no awareness to 4 = awareness with severe distress. Training (such as videos provided by the College of Psychiatric and Neurologic Pharmacists) and experience using the scale will improve the clinician’s accuracy and reliability of their ratings.

Conclusion

The involuntary movements of TD can decrease patients’ quality of life, cause embarrassment, and lead to social withdrawal. Clinicians must evaluate patients taking DRBAs for TD risk factors and regularly assess them for TD using a rating scale such as the AIMS. Familiarity with tools and diagnostic criteria will enable clinicians to conduct a differential diagnosis.

 Clinical Points

• Consider all patients taking DRBAs to be at risk for symptoms of TD.
• Along with regular assessments for TD using tools, be sure to discreetly observe the patient at rest before and/or after the clinical assessment.

© Copyright 2019 Physicians Postgraduate Press, Inc.

References

1. Lerner PP, Miodownik C, Lerner V. Tardive dyskinesia (syndrome): current concept and modern approaches to its management. Psychiatry Clin Neurosci. 2015;69(6):321–334. Pubmed CrossRef
2. Carbon M, Hsieh C-H, Kane JM, et al. Tardive dyskinesia prevalence in the period of second-generation antipsychotic use: a meta-analysis. J Clin Psychiatry. 2017;78(3):e264–e278. Pubmed CrossRef
3. McEvoy JP. Living with tardive dyskinesia. The CME Institute: Patients. https://www.cmeinstitute.com/patients/Pages/home.aspx. Published 2018. Accessed October 18, 2019.
4. Chong SA, Remington G, Mahendran R, et al. Awareness of tardive dyskinesia in Asian patients with schizophrenia. J Clin Psychopharmacol. 2001;21(2):235–237. Pubmed CrossRef
5. Caroff SM, Cutler A, Lenderking WR, et al. Quality of life and functional impairment results: a prospective real-world dyskinesia screening study and registry in patients taking antipsychotic agents. Value Health. 2018;21(suppl 1):S188. CrossRef
6. McEvoy J, Carroll B, Gandhi S, et al. Effect of tardive dyskinesia on quality of life: patient-reported symptom severity is associated with deficits in physical, mental, and social functioning (P4.077). Neurology. 2018;90(15 suppl):P4.077.
7. Correll CU, Rubio JM, Kane JM. What is the risk-benefit ratio of long-term antipsychotic treatment in people with schizophrenia? World Psychiatry. 2018;17(2):149–160. Pubmed CrossRef
8. Margolese HC, Chouinard G, Kolivakis TT, et al. Tardive dyskinesia in the era of typical and atypical antipsychotics, part 1: pathophysiology and mechanisms of induction. Can J Psychiatry. 2005;50(9):541–547. Pubmed CrossRef
9. Rana AQ, Chaudry ZM, Blanchet PJ. New and emerging treatments for symptomatic tardive dyskinesia. Drug Des Devel Ther. 2013;7:1329–1340. Pubmed CrossRef
10. Solmi M, Pigato G, Kane JM, et al. Clinical risk factors for the development of tardive dyskinesia. J Neurol Sci. 2018;389:21–27. Pubmed CrossRef
11. Branchey M, Branchey L. Patterns of psychotropic drug use and tardive dyskinesia. J Clin Psychopharmacol. 1984;4(1):41–45. Pubmed CrossRef
12. Shenoy RS, Sadler AG, Goldberg SC, et al. Effects of a six-week drug holiday on symptom status, relapse, and tardive dyskinesia in chronic schizophrenics. J Clin Psychopharmacol. 1981;1(3):141–145. Pubmed CrossRef
13. Sampson S, Mansour M, Maayan N, et al. Intermittent drug techniques for schizophrenia. Cochrane Database Syst Rev. 2013;(7):CD006196. Pubmed CrossRef
14. Cornett EM, Novitch M, Kaye AD, et al. Medication-induced tardive dyskinesia: a review and update. Ochsner J. 2017;17(2):162–174. Pubmed
15. Schooler NR, Kane JM. Research diagnoses for tardive dyskinesia. Arch Gen Psychiatry. 1982;39(4):486–487. Pubmed CrossRef
16. American Psychiatric Association. Diagnostic and Statistical Manual for Mental Disorders. Fifth Edition. Washington, DC: American Psychiatric Association; 2013.
17. Citrome L, Dufresne R, Dyrud JM. Tardive dyskinesia: minimizing risk and improving outcomes in schizophrenia and other disorders. Am J Manag Care. 2007;12(suppl). http://www.ajmc.com/journals/supplement/2007/2007-12-vol12-n1-decisionmakernews/dec07-2760p1-12. Accessed October 21, 2019.
18. Kane JM. Assessing patients for tardive dyskinesia. J Clin Psychiatry. 2017;78(9):e1428. Pubmed CrossRef
19. Fenton WS, Blyler CR, Wyatt RJ, et al. Prevalence of spontaneous dyskinesia in schizophrenic and non-schizophrenic psychiatric patients. Br J Psychiatry. 1997;171(3):265–268. Pubmed CrossRef
20. Waln O, Jankovic J. An update on tardive dyskinesia: from phenomenology to treatment. Tremor Other Hyperkinet Mov (N Y). 2013;3:tre-03-161-4138-1. Pubmed
21. Truong DD, Frei K. Setting the record straight: the nosology of tardive syndromes. Parkinsonism Relat Disord. 2019;59:146–150. Pubmed CrossRef
22. American Academy of Neurology. Treating and managing tardive syndromes. 2013. https://www.aan.com/Guidelines/Home/GetGuidelineContent/613. Accessed October 21, 2019.
23. Müller T. Valbenazine granted breakthrough drug status for treating tardive dyskinesia. Expert Opin Investig Drugs. 2015;24(6):737–742. Pubmed CrossRef
24. Ward KM, Citrome L; Tardive Dyskinesia-Key Differences in Pathophysiology and Clinical Management. Antipsychotic-related movement disorders: drug-induced parkinsonism vs tardive dyskinesia-key differences in pathophysiology and clinical management. Neurol Ther. 2018;7(2):233–248. Pubmed CrossRef
25. Palmer M, Campbell AR, Finegan A, et al. Identification, assessment, and clinical management of tardive dyskinesia: an update. Psychiatr Times. 2019;36(7). https://www.psychiatrictimes.com/cme/identification-assessment-and-clinical-management-tardive-dyskinesia-update. Accessed September 26, 2019.
26. Lehman AF, Lieberman JA, Dixon LB, et al; American Psychiatric Association; Steering Committee on Practice Guidelines. Practice guideline for the treatment of patients with schizophrenia, second edition. Am J Psychiatry. 2004;161(suppl):1–56. Pubmed
27. Guy W. ECDEU Assessment Manual for Psychopharmacology. Revised Edition. Washington, DC: US Department of Health, Education, and Welfare; 1976.
28. Kane JM, Correll CU, Nierenberg AA, et al; Tardive Dyskinesia Assessment Working Group. Revisiting the Abnormal Involuntary Movement Scale: proceedings from the Tardive Dyskinesia Assessment Workshop. J Clin Psychiatry. 2018;79(3):17cs11959. Pubmed CrossRef
29. Menzies V, Farrell SP. Schizophrenia, tardive dyskinesia, and the Abnormal Involuntary Movement Scale (AIMS). J Am Psychiatr Nurses Assoc. 2002;8(2):51–56. CrossRef