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First, the term EPS, which stands for “extrapyramidal symptoms,” is outdated and should be discontinued in practice.¹ This is because it lacks specificity and can potentially refer to symptoms of tardive dyskinesia (TD), drug-induced parkinsonism, or acute medication-induced movement disorders, conditions that differ in pathophysiology, presentation, and treatment strategy.² 

Several important differences exist between the characteristic movements associated with TD and those associated with drug-induced parkinsonism. TD movements are most often described as choreic (irregular, dance-like), athetotic (slow, writhing), and/or stereotypic (repetitive, purposeless).³ These are all hyperkinetic, involuntary movements.³ Patients with TD may demonstrate movements in the orofacial region, including movements of the tongue, lower face, and jaw.⁴ You might notice chewing movement in the jaw; protrusion, curling, or twisting of the tongue; lip smacking, puckering, or grimacing; and increased eye blinking.^1,3,5 Beyond orofacial movements, you may also notice purposeless or repeated movements in the arms or legs, tapping, or dancing movements in the fingers and toes. Finally, rocking, jerking, or flexing movements may be observed in the trunk or hips.⁶ Movements of the limbs and extremities do not necessarily present on both sides of the body in patients with TD.⁵

Drug-induced parkinsonism, on the other hand, is generally characterized by bradykinesia, rigidity, and tremor.^7,8 Bradykinesia, or reduced or slowed movement, is one hallmark feature of parkinsonism and is distinct from what is seen in patients with TD.^3,5 There may be decreased blink rate and decreased facial expression. Gait may consist of shortened strides with reduced arm swing.³ Voluntary finger-tapping movements may be slow and small.³ In addition, the only hyperkinetic (extra, involuntary) movement that is seen in drug-induced parkinsonism is tremor. A distinguishing feature of tremor is that it is a rhythmic (generally 3-6 Hz) back-and-forth movement, and is commonly (but not always) symmetric.^8,9 This is in contrast to the hyperkinetic stereotypic movements often seen in TD, which can be repetitive, but are not rhythmic. Additionally, patients with drug-induced parkinsonism may have rigidity (increased resistance on passive movement) in the neck and extremities.⁵ Note that a patient may have a parkinsonian tremor without much bradykinesia or prominent bradykinesia without any tremor.³ Similarly, the presence/extent of rigidity is highly variable.¹⁰ Nonetheless, clues to drug-induced parkinsonism include the presence of bradykinesia or tremor.

Another key difference between drug-induced parkinsonism and TD is the time of onset and effect of dosage changes. Drug-induced parkinsonism typically begins days, weeks, or sometimes months after antipsychotic initiation. It generally improves after antipsychotic discontinuation and worsens with increased dosage.^7,9,11,12 On the other hand, TD typically develops over months to years of antipsychotic use,¹³ and is often irreversible.^9,14 With TD, an increased dosage may temporarily improve or mask symptoms, whereas a decreased dosage could temporarily worsen or reveal TD symptoms.⁹

For more information on differentiating between these 2 drug-induced movement disorders, check out the differential diagnosis slide library and listen to experts discuss their approaches to recognizing tardive dyskinesia.​

1. Savitt D, Jankovic J. Tardive syndromes. J Neurol Sci. 2018;389:35-42. 
2. D’Souza RS, Hooten WM. Extrapyramidal symptoms. In: StatPearls. Treasure Island (FL): StatPearls Publishing; August 3, 2021.
3. Hauser RA, Meyer JM, Factor SA, et al. Differentiating tardive dyskinesia: a video-based review of antipsychotic-induced movement disorders in clinical practice. CNS Spectr. 2022;27(2):208-217.
4. Factor SA, Burkhard PR, Caroff S, et al. Recent developments in drug-induced movement disorders: a mixed picture. Lancet Neurol. 2019;18(9):880-890.
5. Caroff SN, Campbell EC. Drug-induced extrapyramidal syndromes: implications for contemporary practice. Psychiatr Clin North Am. 2016;39(3):391-411.
6. Data on file. Neurocrine Biosciences, Inc.
7. Caroff SN. Overcoming barriers to effective management of tardive dyskinesia. Neuropsychiatr Dis Treat. 2019;15:785-794.
8. Susatia F, Fernandez HH. Drug-induced parkinsonism. Curr Treat Options Neurol. 2009;11(3):162-169.
9. Ward KM, Citrome L. Antipsychotic-related movement disorders: drug-induced parkinsonism vs. tardive dyskinesia-key differences in pathophysiology and clinical management. Neurol Ther. 2018;7(2):233-248.
10. Hardie RJ, Lees AJ. Neuroleptic-induced Parkinson’s syndrome: clinical features and results of treatment with levodopa. J Neurol Neurosurg Psychiatry. 1988;51(6):850-854.
11. Tarsy D. Neuroleptic-induced extrapyramidal reactions: classification, description, and diagnosis. Clin Neuropharmacol. 1983;6 Suppl 1:S9-S26.
12. Shin HW, Chung SJ. Drug-induced parkinsonism. J Clin Neurol. 2012;8(1):15-21.
13. Fahn S, Jankovic J, Hallet M. The tardive syndromes: phenomenology, concepts on pathophysiology and treatment, and other neuroleptic-induced syndromes. In: Fahn S, Jankovic J, Hallet M, eds. Principles and Practice of Movement Disorders. 2nd ed. Saunders; 2011:415-446.
14. Caroff SN, Hurford I, Lybrand J, Campbell EC. Movement disorders induced by antipsychotic drugs: implications of the CATIE schizophrenia trial. Neurol Clin. 2011;29(1):127-148, viii.

According to a modified Delphi consensus study of best practices in screening, diagnosis, and treatment of tardive dyskinesia (TD), a clinical assessment for TD should be performed at every clinical visit in patients taking antipsychotics, regardless of the patient’s risk for TD.¹ This includes both semi-structured and less frequent structured assessments. Per panel recommendations, a semi-structured assessment should include the following: asking the patient whether they have noticed any abnormal movements, visual observation by the assessor of psychomotor abnormalities; a caregiver report of recent abnormal movements; a patient report of a history of movement of psychomotor changes; and patient complaints about changes in movements being distressing or interfering with everyday functioning and quality of life.¹ 

The MIND-TD Questionnaire can help facilitate a dialogue about abnormal movements with patients at risk for TD and may be a helpful tool for these brief TD assessments—whether they take place in person or via telehealth. Please note that the MIND-TD questionnaire is not a validated diagnostic instrument. The MIND-TD Questionnaire consists of 2 parts. Part 1, the MIND questions, includes 4 questions that ask about unwanted movements, the impact of these movements, whether they have been noticed by others, and how they might affect daily function. These questions can be administered through video or audio-only telehealth, when necessary, by either a clinician or medical staff member.² If you suspect abnormal movements, part 2 of the questionnaire consists of a thorough interview administered by the treating clinician. This part can also be conducted by video or audio-only telehealth.^2,3 If there is any suspicion about movement abnormalities that may be present, an in-person followup is critical.⁴ Part 2 of the MIND-TD Questionnaire can be used when visual observation of the patient is possible, and can help differentiate movements associated with TD from those associated with other drug-induced movement disorders. 

1. Caroff SN, Citrome L, Meyer J, et al. A modified Delphi consensus study of the screening, diagnosis, and treatment of tardive dyskinesia. J Clin Psychiatry. 2020;81(2):19cs12983.
2. Lundt L, Jain R, Matthews D, et al. Development of a MIND-TD questionnaire as a screening tool for tardive dyskinesia. Poster presented at: Neuroscience Education Institute Congress; November 4-7, 2021; Colorado Springs, CO.

3. Data on file. Neurocrine Biosciences, Inc.
4. Psychiatry & Behavioral Health Learning Network. Can the AIMS exam be conducted via telepsychiatry? December 9, 2019. Accessed October 19, 2021. https://www.psychcongress.com/article/can-aims-exam-be-conducted-telepsychiatry ​

Tardive dyskinesia (TD) is characterized by persistent, hyperkinetic, and involuntary movements of the mouth, jaw, tongue, face, trunk, or extremities. Most often, these movements are described as choreic (irregular and dance-like), athetotic (slow and writhing), and/or stereotypic (repetitive, purposeless).¹ Although oro-buccal-lingual and limb movements tend to be most common, truncal movements are still observed in a significant proportion of patients. Common truncal movements include swaying, twisting, backwards arching, rocking, thrusting of the hips and pelvis, and jerking motions,² as well as irregular respirations.^2,3 According to a 2019 survey of 101 patients diagnosed with TD, 13% of patients experienced rocking, jerking, flexing, or thrusting movements of the trunk or hips compared with 51% of patients who experienced repetitive movements of the tongue, jaw, or lips; and 57% of patients who experienced repetitive movements of the arms or legs.² 

1. Hauser RA, Meyer JM, Factor SA, et al. Differentiating tardive dyskinesia: a video-based review of antipsychotic-induced movement disorders in clinical practice. CNS Spectr. 2022;27(2):208-217.

2. Data on file. Neurocrine Biosciences, Inc.

3. Lundt L, Jain R, Matthews D, et al. Development of a MIND-TD questionnaire as a screening tool for tardive dyskinesia. Poster presented at: Neurocrine Institute Congress; November 4-7, 2021; Colorado Springs, CO.