Browse

Journals By Subject

Life Sciences, Agriculture & Food
Chemistry
Medicine & Health
Materials Science
Mathematics & Physics
Electrical & Computer Science
Earth, Energy & Environment
Architecture & Civil Engineering
Education
Economics & Management
Humanities & Social Sciences
Multidisciplinary

Books

Publish Conference Abstract Books
Upcoming Conference Abstract Books
Published Conference Abstract Books
Publish Your Books
Upcoming Books
Published Books

Proceedings

Events

Events
Five Types of Conference Publications

Join

Join as Editorial Board Member
Become a Reviewer

Information

For Authors
For Reviewers
For Editors
For Conference Organizers
For Librarians
Article Processing Charges
Special Issue Guidelines
Editorial Process
Manuscript Transfers
Peer Review at SciencePG
Open Access
Copyright and License
Ethical Guidelines
Submit an Article
Case Report | | Peer-Reviewed

Remission of Aripiprazole-induced Tardive Dyskinesia with Valbenazine and Vitamin E Combination Therapy: A Case Report

Nicholas Coyne*,  Emma Coyne,  Michael Watcher,  Ankit Chalia,  Michael Ang-Rabanes,  Raja Mogallapu
Published in American Journal of Psychiatry and Neuroscience (Volume 13, Issue 3)
Received: 12 July 2025     Accepted: 28 July 2025     Published: 12 August 2025
Views:       Downloads:
Download PDF
Abstract

Antipsychotic medications comprise a cornerstone for the management of multiple psychopathologies, but their use is associated with significant side effects. Tardive dyskinesia (TD) is one such effect that is particularly troublesome. TD is clinically distressing, hard to treat, and poorly understood by the medical community. Due to these challenges, second-generation antipsychotics, such as aripiprazole, tend to be favored for their reduced risk of TD; however, rare cases of aripiprazole-induced TD have been documented. This report presents a novel case of TD secondary to aripiprazole monotherapy, managed successfully with Valbenazine and Vitamin E. A 39-year-old woman with schizophrenia was treated with aripiprazole, titrated to 30 mg daily. Though her psychotic symptoms improved significantly, she developed clinically distressing moderate-severe TD symptoms after one year of treatment. Her dose of aripiprazole dose was reduced, and a combination of Valbenazine 40 mg and Vitamin E 400 mg daily was initiated. This intervention led to substantial improvement, allowing the patient to achieve remission of TD symptoms and improvement in her psychiatric symptoms. This improvement persisted for over a year, even after the patient independently elected to discontinue Valbenazine therapy. Although recent case reports display clozapine as therapeutic for Aripiprazole-induced TD, the risks associated with clozapine necessitate alternative strategies for management of TD symptoms. The successful use of Valbenazine and Vitamin E in this case suggests a potentially safer and more accessible treatment option. This case study also supports the oxidative stress hypothesis of TD pathogenesis, and highlights the need for early screening, recognition, and intervention in TD to improve patient outcomes.

Published in American Journal of Psychiatry and Neuroscience (Volume 13, Issue 3)
DOI 10.11648/j.ajpn.20251303.11
Page(s) 77-84
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2025. Published by Science Publishing Group
Previous article
Keywords

Aripiprazole, Tardive Dyskinesia, Valbenazine, Vitamin E, Antipsychotics, Extrapyramidal Symptoms

1. Introduction
Antipsychotic medications are fundamental for the management of many pathologies. Although most commonly used for schizophrenia, these agents are frequently used on and off-label for conditions including bipolar disorder, autism spectrum disorder, treatment-resistant major depressive disorder, and more
[1-3]
. While robust literature supports that these medications are highly effective, their efficacy must be carefully balanced with their extensive side effect profile
[4]
. Such effects include, anticholinergic/antihistaminergic effects, sedation, epileptogenic effects, QTc prolongation, and increased risk of mortality
[1]
. A unique set of adverse reactions associated with this class of medications are the extra-pyramidal symptoms (EPS): a group of motor disorders caused by Dopamine 2 (D2) dopamine receptor antagonism classified as akathisia, dystonia, parkinsonism, and tardive dyskinesia (TD)
[1]
. TD is a particularly challenging side effect for clinicians and patients alike. This side effect is clinically distressing for patients, often persists despite cessation of the causative drug, and remains to be poorly understood by the medical community
[5, 6]
. In light of these challenges, many clinicians prefer second generation antipsychotics (SGA’s), particularly aripiprazole, over first generation antipsychotics (FGA’s) due to the decreased risk for patients to develop TD
[7]
.
The comparative reduction in TD risk of SGA’s vs FGA’s is due to differences in each class’s pharmacologic mechanism of action. Positive symptoms of schizophrenia (i.e., delusions, hallucinations) are suspected to be caused by excess dopaminergic signaling throughout the mesolimbic pathway
[8]
. FGA’s show robust reduction in positive symptoms by antagonizing D2 receptors. However, this receptor antagonism occurs diffusely throughout the brain. It is theorized that D2 blockage in the nigrostriatal pathway can lead to the development of EPS, such as TD
[9]
. Rather than receptor antagonism, SGA’s employ various mechanisms to decrease dopamine signal transduction. Aripiprazole is one such SGA with a particularly interesting mechanism; the drug displays partial 5-HT1A agonism, 5-HT2A antagonism, and dynamic D2 receptor modulation
[10]
. The effects on these receptors allow for functional antagonistic effects in signaling pathways with excess dopamine, and agonistic effects in pathways with deficient dopamine, yielding a stabilization of dopaminergic activity
[10]
. Aripiprazole’s mechanism allows for a reduction in schizophrenia symptomatology with less of a detrimental effect on homeostatic dopamine signaling
[10]
.
The impetus for the use of aripiprazole can be partially explained by the relative risk-reduction of EPS, particularly TD, compared to other antipsychotic medications
[11]
. In addition to selecting this drug with the goal of preventing TD, research shows that patients who develop TD can achieve reduction or remission of symptoms by switching to aripiprazole
[12-14]
. However, despite its more favorable profile, aripiprazole itself has been shown to cause TD
[15]
. Literature regarding the treatment of TD that develops in patients taking aripiprazole is limited, with most cases necessitating clozapine to induce remission of symptoms
[16, 17]
. These limitations underscore the need for alternative therapeutic strategies. This report details a novel case of TD secondary to aripiprazole therapy, where remission was achieved using a combination of Valbenazine and Vitamin E. The findings add to the growing body of evidence surrounding the management of TD, particularly in cases where aripiprazole is implicated as the causative agent.
The Abnormal Involuntary Movement Scale (AIMS) is a rating scale used to assess TD in patients taking psychiatric medications
[18]
. It is one of the most widely used tools for the objective clinical evaluation of TD
[18, 19]
, and is available in the public domain, allowing for unrestricted use and reproduction. The scale has demonstrated validity and high inter-rater reliability, particularly among experienced raters
[20, 21]
. Clinical trials suggest that a decrease in AIMS score of 2 or more points on the AIMS indicates a clinically significant improvement in symptoms
[22]
.
The AIMS assessment consists of two phases: (1) an examination phase, where patient is instructed to follow several simple commands, followed by (2) a scoring phase, where the clinician evaluates the presence of involuntary movements throughout the preceding maneuvers
[18]
. The scale consists of 12 total items - the first seven assessing dyskinesias in the patient’s face, jaw, tongue, extremities, and trunk, while the remaining five items holistically evaluate the significance of these dyskinesias
[18]
. Each item is scored on a scale of 0-4 (0 = no abnormal movements, 4 = severe dyskinesia)
[18]
.
In this case report, the authors used the sum of the first 7 items, generating a total severity score ranging from 0 to 28. This sum total was used to monitor for changes in the patient’s dyskinesias over time. In this case report, the authors used the sum of the first 7 items, generating a total severity score ranging from 0 to 28. This sum total was used to monitor for changes in the patient’s dyskinesias over time.
2. Case Presentation
A 39-year-old woman with a medical history of hypertension and obesity, but no prior psychiatric diagnoses, presented to an outpatient psychiatry clinic due to a three-year history of auditory hallucinations and paranoid delusions without significant mood disturbances. The patient was provisionally diagnosed with schizophrenia, and Aripiprazole 10 mg daily was initiated to mitigate her symptoms of psychosis while minimizing the risk of extrapyramidal side effects.
Over the next several months, the patient’s Aripiprazole was gradually increased to 30 mg daily, which correlated with a marked reduction in her psychotic symptoms and improved sociability. To establish a baseline for potential extrapyramidal symptoms, an Abnormal Involuntary Movement Scale (AIMS) assessment was conducted; the assessment yielded a score of 0, indicating no observable TD at that time.
Shortly thereafter, the patient reported a possible manifestation of early TD in the form of new- intermittent episodes of shakiness. At the next appointment, although her psychotic symptoms were well-controlled, the patient expressed growing concern about newly observed involuntary lip, tongue, and jaw movements. An AIMS evaluation resulted in a score of 10, indicating the presence of moderate TD. This finding prompted immediate intervention - the patient’s Aripiprazole dosage was reduced to 25 mg, and she was initiated on Valbenazine 40 mg and Vitamin E 400 mg daily to address her new motor symptoms. These adjustments to the medication regimen allowed her to maintain control of her hallucinations and delusions, while experiencing increased comfort and functionality in daily activities secondary to a reduction in TD symptoms, as evidenced by a gradual reduction in AIMS scores back to 0.
With her psychotic symptoms remaining well-controlled for months and no signs of TD present, the patient’s Aripiprazole dosage was reduced from 25 mg to 10 mg in an effort to limit the patient’s total exposure to the medication. Unfortunately, the dose reduction coincided with an exacerbation of psychotic symptoms. After a thorough discussion of potential therapeutic options, and a failed attempt at alternative pharmacotherapy due to denial by the patient’s insurance, the clinician and the patient engaged in shared decision-making, and the patient elected to gradually increase her dose of Aripiprazole once more.
At the clinicians next follow up visit with the patient, she disclosed that she had independently discontinued Valbenazine therapy, citing personal preference. However, she reported satisfactory control of her psychotic symptoms without experiencing any re-emergence of TD on a regimen of only Aripiprazole 20 mg and Vitamin E 400 mg daily. Both the patient and clinician agreed on periodic follow-ups to monitor for any emerging motor symptoms and ensure sustained efficacy of her treatment plan. As of her most recent visit nearly one year after discontinuing Valbenazine, the patient maintains adequate control of psychiatric symptoms while maintaining consistent AIMS scores of 0.
Table 1. Significant Developments in the Presented Case. When administered, Items 1-7 of AIMS were summed to generate a single value representative of the patient’s TD symptoms. (ARIP = Aripiprazole; VBZ = Valbenazine; Vit. E = Vitamin E).

Date

Clinical Summary

AIMS Score

Pharmacologic Management

01/2021

Marked psychotic symptoms, excess sleep, social isolation

N/A

Start ARIP 10 mg, gradually increase dose over subsequent visits

03/2022

Clinical improvement achieved (Reduced psychotic symptoms, improved sociability and participation in household activities)

0

Continue ARIP 30 mg

06/2022

New onset involuntary lip, tongue, jaw movements

10

Decrease ARIP to 25 mg Start VBZ 40 mg Start Vit. E 400 mg

03/2023

TD symptoms resolve, continued control of psychiatric symptoms

0

-

03/2024

Clinically well-appearing, clinician desires to mitigate total exposure to antipsychotic medication

N/A

Decrease ARIP to 10 mg

04/2024

Recurrence of psychotic symptoms occurs

0

Increase ARIP to 15 mg

06/2024

Decrease in psychotic symptoms, patient desires dose increase

2

Increase ARIP to 20 mg

08/2024

Patient independently discontinues VBZ, psychotic symptoms well controlled

1

Discontinue VBZ per patient request Continue ARIP 20 mg and Vit. E 400 mg

10/2024

Clinically stable, no significant changes

0

-

01/2025

As above

0

-

04/2025

Most recent appointment, patient maintains adequate control of psychiatric symptoms without reemergence of TD

0

Continue ARIP 20 mg and Vit. E 400 mg
3. Discussion
Tardive dyskinesia (TD) is a multifaceted and poorly understood disorder, most commonly associated with the prolonged use of antipsychotic medications
[23]
. Its clinical relevance lies in its potential to significantly impair quality of life and complicate the long-term management of psychiatric disorders. When antipsychotic therapy is indicated, aripiprazole is often chosen by clinicians due to its relatively decreased incidence of TD
[24, 25]
. However, it is vital to consider that all antipsychotic medications, including aripiprazole, can lead to the development of TD
[7]
. As such, the regular screening of patients on antipsychotic medications for TD symptoms is warranted.
When considering the management of the patient who develops TD, in moderate to severe cases, the standard of care typically includes vesicular monoamine transporter 2 (VMAT2) inhibitors, such as Valbenazine, which reduce dopaminergic signaling by inhibiting dopamine transport into presynaptic vesicles
[26]
. Additionally, de-escalating or discontinuing the offending antipsychotic medication may be considered, though this approach risks exacerbating the underlying psychiatric condition
[26, 27]
. While these treatments address the symptoms of TD, they do not target its underlying pathophysiology. Furthermore, the use of VMAT2 inhibitors may cause additive side effects such as somnolence, nausea, and parkinsonism
[15, 28, 29]
. Emerging evidence suggests that transitioning to Aripiprazole may reduce or even remit TD symptoms induced by other antipsychotics
[11, 30-33]
. However, data remains limited, particularly regarding the medication’s efficacy across diverse patient populations and in cases where Aripiprazole itself is the causative agent.
Recent case reports have highlighted clozapine as a potential therapeutic option for Aripiprazole-induced TD
[16, 17, 34]
. However, clozapine use is associated with significant drawbacks, including the risk of agranulocytosis and the need for intensive hematologic monitoring, which may limit its feasibility in certain patient populations
[35-37]
. This case report introduces an alternative approach using a combination of Valbenazine and Vitamin E, offering a potentially safer and more accessible treatment option for Aripiprazole-induced TD.
Valbenazine, a VMAT2 inhibitor, is well-established as a standard treatment for TD of varying etiologies
[34, 38-42]
. This case adds to the existing evidence by demonstrating its efficacy in addressing TD symptoms specifically associated with Aripiprazole therapy. The justification for VMAT2 inhibitor therapy lies in one of the theorized mechanisms for TD pathogenesis - chronic blockade of dopamine receptors by antipsychotic agents promotes “super-sensitivity” of the receptors, causing a net increase in dopamine signaling in particular neurologic regions (i.e., the basal ganglia), evoking movement symptoms
[43-47]
. By decreasing the transport of monoamines (such as dopamine) into presynaptic vesicles, less dopamine is released by presynaptic neurons, causing a decrease in the total dopaminergic signaling and reducing the movement symptoms of TD
[43-47]
. In this case, we expand upon this literature to show that VMAT2 inhibitors are effective when TD occurs due to aripiprazole therapy. The use of Valbenazine rather than clozapine avoids the need for frequent laboratory testing and avoids the risk of agranulocytosis, myocarditis, and cardiomyopathy, and decreases the risk of seizure
[23]
. In contrast to Clozapine, Valbenazine can also be used in patients with comorbidities or a history of cardiac pathologies, epilepsy, and myelosuppression
[23, 37]
. By allowing for a safer, less cumbersome course of therapy for the patient, Valbenazine is an attractive choice for the treatment of TD secondary to Aripiprazole therapy.
The efficacy of VMAT2 inhibitors in TD management is supported by the dopamine receptor super-sensitivity hypothesis
[45]
. In contrast, Vitamin E targets a different proposed mechanism of TD pathogenesis: oxidative stress-induced neurodegeneration
[48-53]
. A well-known antioxidant, Vitamin E has demonstrated cytoprotective effects against oxidative damage
[49-60]
and may help mitigate neurodegeneration associated with chronic antipsychotic use, potentially conferring a neuroprotective effect in TD
[49]
. Presently, there is no existing research assessing the efficacy of Vitamin E in conjunction with other TD treatments, such as VMAT2 inhibitors. However, the authors believe that given the safety of Vitamin E at appropriate doses, the low cost of the compound, and the tendency for patients to view natural substances such as vitamins in a positive light, Vitamin E may represent a viable adjunctive therapy for TD
[59, 61-68]
. Vitamin E may be especially beneficial early in TD pathogenesis, potentially delaying or reducing the need for VMAT 2 therapy.
This case underscores the importance of maintaining a high index of suspicion for TD in patients taking antipsychotic medications. The recent expansion of indications for antipsychotics have increased the number of patients at risk of developing TD
[2, 69]
. Evidence suggests that early detection and prompt intervention can significantly enhance the reversibility of TD symptoms and prevent symptom progression
[31, 70]
. In the subject of this report, the timely initiation of Valbenazine and Vitamin E therapy contributed to the successful remission of her symptoms. Therefore, the authors suggest that regularly screening this patient population for TD with a tool such as the AIMS may facilitate earlier diagnosis and improve clinical outcomes.
This report highlights the potential of combining Valbenazine and Vitamin E as a treatment for Aripiprazole-induced TD. However, further research, including randomized controlled trials, is needed to validate this approach and establish its generalizability across diverse patient populations. Additionally, the timing of the intervention coincided with a small reduction in the dosage of Aripiprazole, further limiting the ability to attribute remission of symptoms to the intervention.
The findings from this case study add to the growing base of literature to help better understand the phenomenon of TD. The case bolsters the notion that VMAT2 inhibitors are effective for TD and posits that augmenting with Vitamin E may further improve patient outcomes. The pharmacologic intervention employed in this report poses an alternative to clozapine therapy for patients who develop TD secondary to Aripiprazole therapy. The case also emphasizes the importance of early detection and intervention for TD symptoms, suggesting that routine screening can improve patient outcomes. If a patient experiences TD, in particular if symptoms occur secondar to Aripiprazole therapy, clinicians may consider the use of Vitamin E and Valbenazine as a means to alleviate motor symptoms without necessarily discontinuing Aripiprazole.
4. Conclusions
This case highlights the critical need for early recognition and intervention in TD to improve patient outcomes. The AIMS scale, which can be quickly and easily administered by clinicians, may serve as a practical means to detect early manifestations of TD. The observed remission of aripiprazole-induced TD with valbenazine and vitamin E suggests a more easily accessible therapeutic approach for this population than prior literature has reported. Furthermore, the sustained remission of TD symptoms with vitamin E monotherapy supports the hypothesis that oxidative stress contributes to TD pathogenesis. Given vitamin E’s safety and accessibility, clinicians may consider its use early in the course of TD. Further research is required to validate these findings and explore their applicability to broader patient populations.
Abbreviations

TD

Tardive Dyskinesia

EPS

Extra-pyramidal Symptoms

SGA’s

Second Generation Antipsychotics

FGA’s

First Generation Antipsychotics

D2

Dopamine 2 (as in, Dopamine 2 Receptor)

AIMS

Abnormal Involuntary Movement Scale

ARIP

Aripiprazole

VBZ

Valbenazine

Vit. E

Vitamin E

VMAT2

Vesicular Monoamine Transporter 2
Author Contributions
Nicholas Coyne: Conceptualization, Supervision, Visualization, Writing - original draft, Writing-Review & Editing
Emma Coyne: Conceptualization, Visualization, Writing - original draft, Writing-Review & Editing
Michael Watcher: Writing- Review & Editing
Ankit Chalia: Visualization, Writing-Review & Editing
Michael Ang-Rabanes: Writing-Review & Editing
Raja Mogallapu: Conceptualization, Supervision, Visualization, Writing-Review & Editing
Funding
This work is not supported by any external funding.
Conflicts of Interest
The authors declare no conflicts of interest.
References
[1] Chokhawala K, Stevens L. Antipsychotic Medications. StatPearls [Internet] Treasure Island (FL): StatPearls Publishing; 2024 [cited 2024 Jun 23]. Available from:

http://www.ncbi.nlm.nih.gov/books/NBK519503/f

[2] Carton L, Cottencin O, Lapeyre-Mestre M, et al. Off-Label Prescribing of Antipsychotics in Adults, Children and Elderly Individuals: A Systematic Review of Recent Prescription Trends. CPD 2015; 21: 3280-97.

https://doi.org/10.2174/1381612821666150619092903

[3] O’Brien PL, Cummings N, Mark TL. Off-Label Prescribing of Psychotropic Medication, 2005-2013: An Examination of Potential Influences. PS 2017; 68: 549-58.

https://doi.org/10.1176/appi.ps.201500482

[4] Huhn, Maximilian, Adriani Nikolakopoulou, Johannes Schneider-Thoma, et al. Comparative efficacy and tolerability of 32 oral antipsychotics for the acute treatment of adults with multi-episode schizophrenia: a systematic review and network meta-analysis. The Lancet 2019; 394: 939-51.

https://doi.org/10.1016/s0140-6736(19)31135-3

[5] Cornett EM, Novitch M, Kaye AD, et al. Medication-Induced Tardive Dyskinesia: A Review and Update. Ochsner J 2017; 17: 162-74.
[6] Jackson R, Brams MN, Carlozzi NE, et al. Impact-Tardive Dyskinesia (Impact-TD) Scale: A Clinical Tool to Assess the Impact of Tardive Dyskinesia. J Clin Psychiatry [Internet] 2022 [cited 2024 Nov 10]; 84. Available from:

https://doi.org/10.4088/jcp.22cs14563

[7] Ostuzzi G, Mazzi MA, Terlizzi S, et al. Factors associated with first- versus secondgeneration long-acting antipsychotics prescribed under ordinary clinical practice in Italy. Mazza M, editor. PLoS ONE 2018; 13: e0201371.

https://doi.org/10.1371/journal.pone.0201371

[8] Brisch R, Saniotis A, Wolf R, et al. The role of dopamine in schizophrenia from a neurobiological and evolutionary perspective: old fashioned, but still in vogue. Front Psychiatry 2014; 5: 47.

https://doi.org/10.3389/fpsyt.2014.00047

[9] Debrey SM, Goldsmith DR. Tardive Dyskinesia: Spotlight on Current Approaches to Treatment. Focus (Am Psychiatr Publ) 2021; 19: 14-23.

https://doi.org/10.1176/appi.focus.20200038

[10] Tuplin EW, Holahan MR. Aripiprazole, A Drug that Displays Partial Agonism and Functional Selectivity. Curr Neuropharmacol 2017; 15: 1192-207.

https://doi.org/10.2174/1570159X15666170413115754

[11] Schwartz T, Raza S. Aripiprazole (abilify) and tardive dyskinesia. P T 2008; 33: 32-4.
[12] Chan C-H, Chan H-Y, Chen Y-C. Switching antipsychotic treatment to aripiprazole in psychotic patients with neuroleptic-induced tardive dyskinesia: a 24-week follow-up study. International Clinical Psychopharmacology 2018; 33: 155-62.

https://doi.org/10.1097/YIC.0000000000000208

[13] Osorio RS, Agüera-Ortiz L, Hurtado De Mendoza A, et al. Treatment of Tardive Dyskinesia with Aripiprazole. Neurotox Res 2010; 17: 432-4.

https://doi.org/10.1007/s12640-009-9123-0

[14] Rajarethinam R, Dziuba J, Manji S, et al. Use of aripiprazole in tardive dyskinesia: An open label study of six cases. The World Journal of Biological Psychiatry 2009; 10: 416-9.

https://doi.org/10.1080/15622970902995612

[15] Gettu N, Saadabadi A. Aripiprazole. StatPearls [Internet] Treasure Island (FL): StatPearls Publishing; 2024 [cited 2024 Oct 17]. Available from:

http://www.ncbi.nlm.nih.gov/books/NBK547739/

[16] Joe S, Park J, Lim J, et al. Remission of irreversible aripiprazole-induced tardive dystonia with clozapine: a case report. BMC Psychiatry 2015; 15: 253.

https://doi.org/10.1186/s12888-015-0644-1

[17] Aguilar L, Lorenzo C, Fernández-Ovejero R, et al. Tardive Dyskinesia After Aripiprazole Treatment That Improved With Tetrabenazine, Clozapine, and Botulinum Toxin. Front Pharmacol 2019; 10: 281.

https://doi.org/10.3389/fphar.2019.00281

[18] Rush AJ, First MB, Blacker D, et al., editors. Handbook of psychiatric measures. 2nd ed. Washington, DC: American Psychiatric Pub; 2008.
[19] Kane JM, Correll CU, Nierenberg AA, et al. Revisiting the Abnormal Involuntary Movement Scale: Proceedings From the Tardive Dyskinesia Assessment Workshop. J Clin Psychiatry [Internet] 2018 [cited 2025 Feb 7]; 79. Available from:

https://doi.org/10.4088/jcp.17cs11959

[20] Lane RD, Glazer WM, Hansen TE, et al. Assessment of Tardive Dyskinesia Using the Abnormal Involuntary Movement Scale: The Journal of Nervous and Mental Disease 1985; 173: 353-7.

https://doi.org/10.1097/00005053-198506000-00005

[21] Gerlach J, Korsgaard S, Clemmesen P, et al. The St. Hans Rating Scale for extrapyramidal syndromes: reliability and validity. Acta Psychiatr Scand 1993; 87: 244-52.

https://doi.org/10.1111/j.1600-0447.1993.tb03366.x

[22] Stacy M, Sajatovic M, Kane JM, et al. Abnormal involuntary movement scale in tardive dyskinesia: Minimal clinically important difference. Movement Disorders 2019; 34: 1203-9.

https://doi.org/10.1002/mds.27769

[23] Vasan S, Padhy RK. Tardive Dyskinesia. StatPearls [Internet] Treasure Island (FL): StatPearls Publishing; 2024 [cited 2024 Oct 17]. Available from:

http://www.ncbi.nlm.nih.gov/books/NBK448207/

[24] Miller DD, Eudicone JM. Comparative Assessment of the Incidence and Severity of Tardive Dyskinesia in Patients Receiving Aripiprazole or Haloperidol for the Treatment of Schizophrenia: A Post Hoc Analysis. J Clin Psychiatry 2007; 68: 1901-6.

https://doi.org/10.4088/jcp.v68n1210

[25] Crystal S, Olfson M, Huang C, et al. Broadened Use Of Atypical Antipsychotics: Safety, Effectiveness, And Policy Challenges: Expanded use of these medications, frequently offlabel, has often outstripped the evidence base for the diverse range of patients who are treated with them. Health Affairs 2009; 28: w770-81.

https://doi.org/10.1377/hlthaff.28.5.w770

[26] Keepers GA, Fochtmann LJ, Anzia JM, et al. The American Psychiatric Association Practice Guideline for the Treatment of Patients With Schizophrenia. AJP 2020; 177: 868.

https://doi.org/10.1176/appi.focus.18402

[27] Goldberg JF. Tardive Dyskinesia: Assessing and Treating a Debilitating Side Effect of Prolonged Antipsychotic Exposure. PN 2021; 56: appi. pn.2021.3.10.

https://doi.org/10.1176/appi.pn.2021.3.10

[28] Vesicular Monoamine Transporter 2 (VMAT2) Inhibitors. LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet] Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases; 2012 [cited 2024 Oct 17]. Available from:

http://www.ncbi.nlm.nih.gov/books/NBK548187/

[29] Vasireddy RP, Sokola B, Guduru Z. New generation VMAT2 inhibitors induced parkinsonism. Clinical Parkinsonism & Related Disorders 2020; 3: 100078.

https://doi.org/10.1016/j.prdoa.2020.100078

[30] Brown HE, Flaherty AW, Goff DC, et al. A Case of Dramatic Improvement of Severe Tardive Dyskinesia After Switch to Aripiprazole. Prim Care Companion CNS Disord [Internet] 2011 [cited 2024 Oct 17]; Available from:

https://doi.org/10.4088/pcc.11l01188

[31] Wu W-Y, Chan H-Y, Tan HK-L. Suppression of antipsychotic-induced tardive dyskinesia with aripiprazole in an elderly patient with bipolar I disorder. Acta Neuropsychiatr 2014; 26: 61-4.

https://doi.org/10.1017/neu.2013.50

[32] Mangalwedhe S, Mahadevaiah M, Pandurangi A, et al. Aripiprazole in the treatment of paliperidone-induced tardive dyskinesia. J Sci Soc 2015; 42: 204.

https://doi.org/10.4103/0974-5009.165582

[33] Kang N-R, Kim M-D. Tardive dyskinesia: treatment with aripiprazole. Clin Psychopharmacol Neurosci 2011; 9: 1-8.

https://doi.org/10.9758/cpn.2011.9.1.1

[34] Zutshi D, Cloud LJ, Factor SA. Tardive Syndromes are Rarely Reversible after Discontinuing Dopamine Receptor Blocking Agents: Experience from a University-based Movement Disorder Clinic. Tremor Other Hyperkinet Mov (N Y) 2014; 4: 266.

https://doi.org/10.7916/D8MS3R8C

[35] Correll CU, Agid O, Crespo-Facorro B, et al. A Guideline and Checklist for Initiating and Managing Clozapine Treatment in Patients with Treatment-Resistant Schizophrenia. CNS Drugs 2022; 36: 659-79.

https://doi.org/10.1007/s40263-022-00932-2

[36] Kar N, Barreto S, Chandavarkar R. Clozapine Monitoring in Clinical Practice: Beyond the Mandatory Requirement. Clin Psychopharmacol Neurosci 2016; 14: 323-9.

https://doi.org/10.9758/cpn.2016.14.4.323

[37] Haidary HA, Padhy RK. Clozapine. StatPearls [Internet] Treasure Island (FL): StatPearls Publishing; 2024 [cited 2024 Oct 17]. Available from:

http://www.ncbi.nlm.nih.gov/books/NBK535399/

[38] Witek N, Comella C. Valbenazine in the Treatment of Tardive Dyskinesia. Neurodegener Dis Manag 2019; 9: 73-81.

https://doi.org/10.2217/nmt-2019-0001

[39] Gupta H, Moity AR, Jumonville A, et al. Valbenazine for the Treatment of Adults with Tardive Dyskinesia. Health Psychol Res 2021; 9: 24929.

https://doi.org/10.52965/001c.24929

[40] Touma KTB, Scarff JR. Valbenazine and Deutetrabenazine for Tardive Dyskinesia. Innov Clin Neurosci 2018; 15: 13-6.
[41] Citrome L. Valbenazine for tardive dyskinesia: A systematic review of the efficacy and safety profile for this newly approved novel medication-What is the number needed to treat, number needed to harm and likelihood to be helped or harmed? Int J Clin Pract 2017; 71: e12964.

https://doi.org/10.1111/ijcp.12964

[42] Caroff SN, Aggarwal S, Yonan C. Treatment of tardive dyskinesia with tetrabenazine or valbenazine: a systematic review. J Comp Eff Res 2018; 7: 135-48.

https://doi.org/10.2217/cer-2017-0065

[43] Sreeram V, Shagufta S, Kagadkar F. Role of Vesicular Monoamine Transporter 2 Inhibitors in Tardive Dyskinesia Management. Cureus 2019; 11: e5471.

https://doi.org/10.7759/cureus.5471

[44] 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: 1-6.

https://doi.org/10.1017/S1092852917000621

[45] Golsorkhi M, Koch J, Pedouim F, et al. Comparative Analysis of Deutetrabenazine and Valbenazine as VMAT2 Inhibitors for Tardive Dyskinesia: A Systematic Review. Tremor and Other Hyperkinetic Movements 2024; 14: 13.

https://doi.org/10.5334/tohm.842

[46] Frei K. Tardive dyskinesia: Who gets it and why. Parkinsonism & Related Disorders 2019; 59: 151-4.

https://doi.org/10.1016/j.parkreldis.2018.11.017

[47] Ali Z, Roque A, El-Mallakh RS. A unifying theory for the pathoetiologic mechanism of tardive dyskinesia. Medical Hypotheses 2020; 140: 109682.

https://doi.org/10.1016/j.mehy.2020.109682

[48] Cho C-H, Lee H-J. Oxidative stress and tardive dyskinesia: Pharmacogenetic evidence. Progress in Neuro-Psychopharmacology and Biological Psychiatry 2013; 46: 207-13.

https://doi.org/10.1016/j.pnpbp.2012.10.018

[49] Takeuchi H, Mori Y, Tsutsumi Y. Pathophysiology, prognosis and treatment of tardive dyskinesia. Ther Adv Psychopharmacol 2022; 12: 20451253221117313.

https://doi.org/10.1177/20451253221117313

[50] Cadet JL, Perumal AS. Chronic treatment with prolixin causes oxidative stress in rat brain. Biological Psychiatry 1990; 28: 738-40.

https://doi.org/10.1016/0006-3223(90)90461-a

[51] Jeste DV, Lohr JB, Manley M. Study of neuropathologic changes in the striatum following 4, 8 and 12 months of treatment with fluphenazine in rats. Psychopharmacology 1992; 106: 154-60.

https://doi.org/10.1007/BF02801966

[52] Kropp S, Kern V, Lange K, et al. Oxidative Stress During Treatment With First- and Second-Generation Antipsychotics. JNP 2005; 17: 227-31.

https://doi.org/10.1176/jnp.17.2.227

[53] Goh XX, Tang PY, Tee SF. Blood-based oxidation markers in medicated and unmedicated schizophrenia patients: A meta-analysis. Asian Journal of Psychiatry 2022; 67: 102932.

https://doi.org/10.1016/j.ajp.2021.102932

[54] Soares-Weiser K, Maayan N, Bergman H. Vitamin E for antipsychotic-induced tardive dyskinesia. Cochrane Database Syst Rev 2018; 1: CD000209.

https://doi.org/10.1002/14651858.CD000209.pub3

[55] Edwards G, Olson CG, Euritt CP, et al. Molecular Mechanisms Underlying the Therapeutic Role of Vitamin E in Age-Related Macular Degeneration. Front Neurosci 2022; 16: 890021.

https://doi.org/10.3389/fnins.2022.890021

[56] Ungurianu A, Zanfirescu A, Nițulescu G, et al. Vitamin E beyond Its Antioxidant Label. Antioxidants 2021; 10: 634.

https://doi.org/10.3390/antiox10050634te

[57] Duncan RS, Hurtado DT, Hall CW, et al. Differential Mechanisms of Action and Efficacy of Vitamin E Components in Antioxidant Cytoprotection of Human Retinal Pigment Epithelium. Front Pharmacol 2022; 12: 798938.

https://doi.org/10.3389/fphar.2021.798938

[58] Yamauchi R. Vitamin E: Mechanism of Its Antioxidant Activity. FSTI 1997; 3: 301-9.

https://doi.org/10.3136/fsti9596t9798.3.301

[59] Rizvi S, Raza ST, Ahmed F, et al. The role of vitamin e in human health and some diseases. Sultan Qaboos Univ Med J 2014; 14: e157-165.
[60] Burton GW, Joyce A, Ingold KU. Is vitamin E the only lipid-soluble, chain-breaking antioxidant in human blood plasma and erythrocyte membranes? Archives of Biochemistry and Biophysics 1983; 221: 281-90.

https://doi.org/10.1016/0003-9861(83)90145-5

[61] Lappas CM, Coyne N, Dillard AJ, et al. Do Physicians Prefer Natural Drugs? The Natural Versus Synthetic Drug Bias in Physicians. European Journal of Health Psychology 2023; 30: 40-7.

https://doi.org/10.1027/2512-8442/a000116

[62] Meier BP, Dillard AJ, Osorio E, et al. A Behavioral Confirmation and Reduction of the Natural versus Synthetic Drug Bias. Med Decis Making 2019; 39: 360-70.

https://doi.org/10.1177/0272989X19838527

[63] Meier BP, Dillard AJ, Lappas CM. Naturally better? A review of the natural-is-better bias. Social & Personality Psych 2019; 13: e12494.

https://doi.org/10.1111/spc3.12494

[64] Meier BP, Lappas CM. The Influence of Safety, Efficacy, and Medical Condition Severity on Natural versus Synthetic Drug Preference. Med Decis Making 2016; 36: 1011-9.

https://doi.org/10.1177/0272989X15621877

[65] Scott SE, Rozin P. Actually, natural is neutral. Nat Hum Behav 2020; 4: 989-90.

https://doi.org/10.1038/s41562-020-0891-0

[66] Roberts LJ, Oates JA, Linton MF, et al. The relationship between dose of vitamin E and suppression of oxidative stress in humans. Free Radic Biol Med 2007; 43: 1388-93.

https://doi.org/10.1016/j.freeradbiomed.2007.06.019

[67] Davey PJ, Schulz M, Gliksman M, et al. Cost-effectiveness of vitamin E therapy in the treatment of patients with angiographically proven coronary narrowing (CHAOS trial). The American Journal of Cardiology 1998; 82: 414-7.

https://doi.org/10.1016/s0002-9149(98)00354-3

[68] Kappus H. Tolerance and safety of vitamin E: A toxicological position report. Free Radical Biology and Medicine 1992; 13: 55-74.

https://doi.org/10.1016/0891-5849(92)90166-e

[69] Browne S, Roe M, Lane A, et al. Quality of life in schizophrenia: relationship to sociodemographic factors, symptomatology and tardive dyskinesia. Acta Psychiatr Scand 1996; 94: 118-24.

https://doi.org/10.1111/j.1600-0447.1996.tb09835.x

[70] Mehta SH, Morgan JC, Sethi KD. Drug-induced Movement Disorders. Neurologic Clinics 2015; 33: 153-74.

https://doi.org/10.1016/j.ncl.2014.09.011

Cite This Article
Plain Text BibTeX RIS

  • APA Style

    Coyne, N., Coyne, E., Watcher, M., Chalia, A., Ang-Rabanes, M., et al. (2025). Remission of Aripiprazole-induced Tardive Dyskinesia with Valbenazine and Vitamin E Combination Therapy: A Case Report. American Journal of Psychiatry and Neuroscience, 13(3), 77-84. https://doi.org/10.11648/j.ajpn.20251303.11

    Copy | Download

    ACS Style

    Coyne, N.; Coyne, E.; Watcher, M.; Chalia, A.; Ang-Rabanes, M., et al. Remission of Aripiprazole-induced Tardive Dyskinesia with Valbenazine and Vitamin E Combination Therapy: A Case Report. Am. J. Psychiatry Neurosci. 2025, 13(3), 77-84. doi: 10.11648/j.ajpn.20251303.11

    Copy | Download

    AMA Style

    Coyne N, Coyne E, Watcher M, Chalia A, Ang-Rabanes M, et al. Remission of Aripiprazole-induced Tardive Dyskinesia with Valbenazine and Vitamin E Combination Therapy: A Case Report. Am J Psychiatry Neurosci. 2025;13(3):77-84. doi: 10.11648/j.ajpn.20251303.11

    Copy | Download 

  • @article{10.11648/j.ajpn.20251303.11,
  author = {Nicholas Coyne and Emma Coyne and Michael Watcher and Ankit Chalia and Michael Ang-Rabanes and Raja Mogallapu},
  title = {Remission of Aripiprazole-induced Tardive Dyskinesia with Valbenazine and Vitamin E Combination Therapy: A Case Report
},
  journal = {American Journal of Psychiatry and Neuroscience},
  volume = {13},
  number = {3},
  pages = {77-84},
  doi = {10.11648/j.ajpn.20251303.11},
  url = {https://doi.org/10.11648/j.ajpn.20251303.11},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajpn.20251303.11},
  abstract = {Antipsychotic medications comprise a cornerstone for the management of multiple psychopathologies, but their use is associated with significant side effects. Tardive dyskinesia (TD) is one such effect that is particularly troublesome. TD is clinically distressing, hard to treat, and poorly understood by the medical community. Due to these challenges, second-generation antipsychotics, such as aripiprazole, tend to be favored for their reduced risk of TD; however, rare cases of aripiprazole-induced TD have been documented. This report presents a novel case of TD secondary to aripiprazole monotherapy, managed successfully with Valbenazine and Vitamin E. A 39-year-old woman with schizophrenia was treated with aripiprazole, titrated to 30 mg daily. Though her psychotic symptoms improved significantly, she developed clinically distressing moderate-severe TD symptoms after one year of treatment. Her dose of aripiprazole dose was reduced, and a combination of Valbenazine 40 mg and Vitamin E 400 mg daily was initiated. This intervention led to substantial improvement, allowing the patient to achieve remission of TD symptoms and improvement in her psychiatric symptoms. This improvement persisted for over a year, even after the patient independently elected to discontinue Valbenazine therapy. Although recent case reports display clozapine as therapeutic for Aripiprazole-induced TD, the risks associated with clozapine necessitate alternative strategies for management of TD symptoms. The successful use of Valbenazine and Vitamin E in this case suggests a potentially safer and more accessible treatment option. This case study also supports the oxidative stress hypothesis of TD pathogenesis, and highlights the need for early screening, recognition, and intervention in TD to improve patient outcomes.},
 year = {2025}
}

    Copy | Download 

  • TY  - JOUR
T1  - Remission of Aripiprazole-induced Tardive Dyskinesia with Valbenazine and Vitamin E Combination Therapy: A Case Report

AU  - Nicholas Coyne
AU  - Emma Coyne
AU  - Michael Watcher
AU  - Ankit Chalia
AU  - Michael Ang-Rabanes
AU  - Raja Mogallapu
Y1  - 2025/08/12
PY  - 2025
N1  - https://doi.org/10.11648/j.ajpn.20251303.11
DO  - 10.11648/j.ajpn.20251303.11
T2  - American Journal of Psychiatry and Neuroscience
JF  - American Journal of Psychiatry and Neuroscience
JO  - American Journal of Psychiatry and Neuroscience
SP  - 77
EP  - 84
PB  - Science Publishing Group
SN  - 2330-426X
UR  - https://doi.org/10.11648/j.ajpn.20251303.11
AB  - Antipsychotic medications comprise a cornerstone for the management of multiple psychopathologies, but their use is associated with significant side effects. Tardive dyskinesia (TD) is one such effect that is particularly troublesome. TD is clinically distressing, hard to treat, and poorly understood by the medical community. Due to these challenges, second-generation antipsychotics, such as aripiprazole, tend to be favored for their reduced risk of TD; however, rare cases of aripiprazole-induced TD have been documented. This report presents a novel case of TD secondary to aripiprazole monotherapy, managed successfully with Valbenazine and Vitamin E. A 39-year-old woman with schizophrenia was treated with aripiprazole, titrated to 30 mg daily. Though her psychotic symptoms improved significantly, she developed clinically distressing moderate-severe TD symptoms after one year of treatment. Her dose of aripiprazole dose was reduced, and a combination of Valbenazine 40 mg and Vitamin E 400 mg daily was initiated. This intervention led to substantial improvement, allowing the patient to achieve remission of TD symptoms and improvement in her psychiatric symptoms. This improvement persisted for over a year, even after the patient independently elected to discontinue Valbenazine therapy. Although recent case reports display clozapine as therapeutic for Aripiprazole-induced TD, the risks associated with clozapine necessitate alternative strategies for management of TD symptoms. The successful use of Valbenazine and Vitamin E in this case suggests a potentially safer and more accessible treatment option. This case study also supports the oxidative stress hypothesis of TD pathogenesis, and highlights the need for early screening, recognition, and intervention in TD to improve patient outcomes.
VL  - 13
IS  - 3
ER  -

    Copy | Download

Author Information
Download PDF
Submit an Article

About Us

Science Publishing Group (SciencePG) is an Open Access publisher, with more than 300 online, peer-reviewed journals covering a wide range of academic disciplines.

Learn More About SciencePG

Products

Information

Important Link

Copyright © 2012 -- 2025 Science Publishing Group – All rights reserved.