Deutetrabenazine in Post-Thalamic Infarction Hemichorea: A Case Report and Literature Review

Deutetrabenazine in Post-Thalamic Infarction Hemichorea: A Case Report and Literature Review | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Deutetrabenazine in Post-Thalamic Infarction Hemichorea: A Case Report and Literature Review Xiaoxuan Wu, Yanfei Sun, Sixuan Li, Baiyu Wang, Ying Xing, Chunpeng Xu This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-6905162/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 11 You are reading this latest preprint version Abstract Background Chorea, a hyperkinetic movement disorder, manifests as involuntary, irregular, rapid, and large-amplitude dance-like movements, such as limb flailing, twisting, and facial grimacing. It can be a primary symptom of neurological disorders directly affecting the basal ganglia, such as Huntington's disease, or a secondary manifestation of various systemic diseases, including infections, autoimmune diseases, drug-induced disorders, metabolic diseases, neurodegenerative diseases, and stroke. Among these, acute cerebrovascular disease is a common cause of chorea. While some patients experience rapid relief of choreiform movements with appropriate symptomatic treatment, others may suffer from refractory chorea that remains difficult to cure despite prolonged pharmacological intervention. Case presentation We present a rare case of refractory post-thalamic infarction hemichorea. After the failure of conventional anti-dopaminergic therapy during the acute phase of cerebral infarction, the patient's symptoms were rapidly controlled with deutetrabenazine without significant adverse effects. Conclusions This report aims to enhance the understanding of treatment strategies for refractory post-stroke chorea and emphasize the potential efficacy of deutetrabenazine in such cases, providing an alternative therapeutic approach for refractory post-stroke hemichorea. Hemichorea Thalamic infarction Deutetrabenazine Movement disorders Stroke Treatment Chorea Figures Figure 1 Figure 2 Figure 3 Background Hemichorea is a common hyperkinetic movement disorder resulting from extrapyramidal system damage, characterized with involuntary, irregular dance-like movements on one side of the body or face. The extrapyramidal system primarily coordinates motor functions, with various motor and non-motor cortical regions projecting to striatal medium spiny neurons and the subthalamic nucleus. The internal segment of the globus pallidus serves as the main output nucleus, connecting back to the cortex via the thalamus. The striatum has two main projections: a direct pathway to the internal segment of the globus pallidus and an indirect pathway through the external segment of the globus pallidus and subthalamic nucleus to the internal segment. The indirect pathway is modulated by the substantia nigra pars compacta, exerting an inhibitory effect. Movement disorders associated with cerebrovascular disease often involve lesions in the basal ganglia region. In addition to the basal ganglia, the damage of the neostriatum and subthalamic nucleus can also lead to hemichoreiform movements[ 1 ]. Among the secondary causes of chorea, cerebrovascular disorders—particularly ischemic strokes—are the most common, represent the leading etiology[ 2 ]. Hemichorea acts as the most frequent involuntary movement disorder after stroke. Some post-stroke hemichorea cases that are secondary to cerebral infarction have shown refractory characteristics[ 3 ]. However, current treatment for hemichorea focuses primarily on suppressing dopaminergic function in the extrapyramidal circuit. For post-stroke hemichorea, treatment typically involves controlling cerebrovascular risk factors, addressing the issue of potential diseases, and adjunctive therapy with haloperidol for dopamine blockade[ 4 , 5 ]. Here, we present a case of refractory post-thalamic infarction hemichore that showed significant improvement with the assistance of Deutetrabenazine after prolonged unsuccessful conventional treatments. Case presentation A 53-year-old hypertensive woman was referred to our neurology department after 21 days of persistent right-sided hemiparesis. Previous treatment at the other hospital included antiplatelet aggregation and circulation-improving medications, which failed to alleviate the limb weakness. 7 days after the onset of right-sided limb weakness, the patient developed involuntary movements in the right limb. The involuntary movements, initially characterized by uncontrollable twisting of the right limbs, got worse with both voluntary movement and emotional excitement. Prior to admission, an acute left thalamic infarction has been confirmed. In consideration of the patient's behavior of hemi-choreiform movements, the therapeutic regimen was expanded haloperidol in addition to antiplatelet and circulation-improving medications. So the pre-admission treatment included intravenous injection of Urinary Kallidinogenase (0.15 PNA unit once a day) for cerebral microcirculation improvement, oral administration of clopidogrel (75 mg per day) for antiplatelet therapy, rosuvastatin (10 mg per day) for lipid control, amlodipine besylate (5 mg per day) for blood pressure management, metformin hydrochloride (0.5 g, three times per day) and dapagliflozin (10 mg per day) for glycemic regulation, bicyclol (50 mg, three times per day) for hepatoprotection, haloperidol (2 mg, three times per day for chorea control. However, after these treatment, the patient's limb weakness showed no improvement, and the right-sided involuntary movements worsened, which made her unable to care for herself. The symptom progression and medication regimen during the first 21 days are summarized as follows (Fig. 1 ). The complexity and refractory characteristic of this case have been evidenced by the lack of response to conventional therapy, and the subsequent worsening of her involuntary movement. These findings suggest the patient need for alternative strategies targeting distinct pathophysiological pathways. During hospitalization, the patient underwent comprehensive diagnostic evaluations including physical examination, laboratory tests (complete blood count, metabolic panel), and neuroimaging, along with electroencephalography (EEG) to establish the diagnosis and rule out differentials. The muscle tension on the right side was decreased, while left-sided muscle tension was normal. Similarly, the muscle strength was grade III on the right but grade V on the left, indicating right limb motor impairment. Sensory examination was unremarkable. The National Institutes of Health Stroke Scale (NIHSS) score was 4 (2 points for right upper limb, 2 points for right lower limb). The Abnormal Involuntary Movement Scale (AIMS) score was 20 (4 points each for right upper limb, right lower limb, severity of abnormal movements, impact on daily life, and patient’s awareness of movements). The Activity of Daily Living Scale (ADL) score was 39. In summary, the patient presents with mild right-sided hemiparesis (NIHSS 4), severe choreiform movements (AIMS 20), and complete dependence in activities of daily living (ADL 39), reflecting significant neurological disability requiring comprehensive care. The laboratory tests including complete blood count, lipid profile, renal function, electrolytes, thyroid function, and tumor markers were normal. The Aspartate Aminotransferase (AST) was 82.35 U/L, with random blood glucose at 6.99 mmol/L and fasting blood glucose at 5.96 mmol/L. Normal video-EEG monitoring findings excluded epileptic origin of the involuntary movements. The Diffusion-weighted imaging (DWI, Fig. 2 A) showed restricted diffusion in the left thalamus, with corresponding findings on the ADC and FLAIR sequences (Figs. 2 B and 2 C). Transcranial Doppler ultrasound revealed left vertebral artery occlusion. Neuroimaging confirmed an acute left thalamic infarction, which correlated well with the patient's clinical presentation. During hospitalization, the treatment regimen has been modified by gradually reduced the dosage of haloperidol by 2 mg per day over three consecutive days while introducing deutetrabenazine (6 mg daily) on the third day. The cardiac rhythm and emotional state of the patient were closely monitored, with no significant abnormalities detected. On the second day with the treatment of deutetrabenazine, the frequency of limb twisting decreased, by the seventh day of hospitalization, involuntary movements of the patient had significantly reduced, The significant clinical improvement following deutetrabenazine therapy confirms its therapeutic value for this patient's movement disorder. Table 1 Longitudinal clinical outcomes after the treatment of deutetrabenazine. Parameter Admission the seventh day of hospitalization 28-Day Follow-Up 3-Month Follow-Up NIHSS Score 4 2 0 0 AIMS Score 20 15 10 4 ADL Score 39 23 18 17 PHQ-9 Score \ 3 2 2 ECG Findings Normal Normal Normal Normal (PHQ-9: Patient Health Questionnaire-9) Discussion and Conclusions To systematically evaluate both therapeutic effects and potential adverse reactions of the novel therapy, we conducted the following comprehensive assessments. When compared with previous symptoms, the muscle tension and strength has been improved, with right-sided strength increasing to grade IV. As for the assessment using standardized rating scales, the NIHSS score has been improved to 2 (1 point each for right upper and lower limbs), AIMS score decreased to 15 (3 points each for right upper limb, right lower limb, severity of abnormal movements, impact on daily life, and patient awareness), and ADL score has also been improved to 23, suggesting that deutetrabenazine demonstrated rapid efficacy with no observed adverse effects. After discharge, the patient underwent rehabilitation for 28 days, showing only minimal residual uncontrollable movements, and the patient regained independent ambulation and self-care ability Table 1 ). During a three-month follow-up, the patient experienced mild lower limb twisting twice after the discontinuation of deutetrabenazine. However, the above undesirable symptom has been resolved by resuming the medication of deutetrabenazine. Currently, the patient maintains good symptom control with a low dosage of 6 mg deutetrabenazine daily without significant side effects. Hemichorea is a hyperkinetic movement disorder that may be induced by various etiologies. Treatment outcomes are influenced by multifactorial determinants. Of these, Choreiform movements caused by autosomal dominant mutations are designated as Huntington's disease, is primarily treated with tetrabenazine[ 7 ] and deutetrabenazine[ 8 ] to deal with undesired symptoms and improve the quality of the life. NKH is characterized by choreiform movements due to impaired glucose metabolism [ 9 ], with most of the NKH cases can be resolved efficiently after glucose correction[ 10 ]. However, the patients who suffer from stroke-induced hemichorea continued to exhibit significant and persistent limb movement impairmen after treatment, which severely hinders them to perform daily activities and thus causes considerable distress. The most common diseased regions that result in post-stroke hemichorea are basal ganglia (caudate nucleus, putamen, and globus pallidus) and subthalamic nucleus[ 11 , 12 ]. Clinical studies suggest that the recovery degree of post-stroke hemichorea may be related to the location of the lesion. Except from the lesion locations, different treatment approach significantly impacts prognosis. The control of the underlying cerebral infarction and pharmacological intervention for hyperkinetic movements are both required for acute post-stroke hemichorea. For refractory cases, surgical options such as pallidotomy, thalamotomy, and deep brain stimulation [15] may be conducive to reducing choreiform movements. However, due to the risks associated with invasive surgeries, these interventions are typically considered only for patients without cognitive impairment[ 10 , 13 ].Therefore, there is an urgent need for targeted, non-invasive conservative therapies to manage refractory post-stroke hemichorea. Recently, anti-dopaminergic medications are the mainstay of chorea treatment. Antipsychotics, with their potent dopamine-blocking effects, are commonly used as first-line agents. Conventional therapeutics often relies on dopamine receptor antagonists such as haloperidol, which exert rapid anti-dopaminergic effects. However, their application is limited by adverse effects including tardive dyskinesia and neuroleptic malignant syndrome[ 14 ], and its efficacy in treating hemichorea remains uncertain [ 15 ]. Dopamine-depleting agents have offered another important treatment option. Deutetrabenazine, a dopamine-consuming agent, inhibits vesicular monoamine transporter 2 to prevent monoamine release. It has been used for decades to treat various hyperkinetic movement disorders [ 16 – 19 ]. Compared to dopamine receptor blockers, such as antipsychotics, deutetrabenazine shows significant advantage in avoiding tardive dyskinesia risks [ 20 ]. Therefore, deutetrabenazine is currently recommended as a first-line treatment for Huntington's chorea (Level A evidence) [ 21 ] and has been reported effective in treating chorea associated with non-ketotic hyperglycemia [ 10 ]. However, its use in post-stroke hemichorea must not be neglected. In this report, deutetrabenazine achieved rapid improvement of symptoms resist to conventional haloperidol treatment, suggesting a potential new therapeutic approach for post-stroke hemichorea. When using deutetrabenazine, several issues are needed to be considered. First of all, we should pay attention to common adverse effects including sedation, depression, anxiety, akathisia, agitation, dysphagia, parkinsonism, and dystonia, some of which seem to relate to the peak concentrations of active circulating metabolites. To minimize dopaminergic fluctuations and associated psychomotor abnormalities, we employed a cross-tapering strategy, gradually replacing haloperidol with deutetrabenazine. Secondly, deutetrabenazine may exacerbate depression and suicidal behavior, particularly in predisposed patients. Therefore, it is contraindicated in predisposed patients with no pharmacological intervention or inadequately treatment due to the high suicide risks [ 22 ]. As for our patient, we carefully screened for the depressive history and used the PHQ-9 scale for rapid assessment, then closely monitored her emotional changes during treatment to minimize adverse events. Thirdly, while deutetrabenazine has proved its ability to revolutionize Huntington's chorea treatment, its potential in refractory post-stroke hemichorea remains underrecognized. Fourthly, high drug costs also limit access for many potentially benefiting patients. Notwithstanding these limitations, the deutetrabenazine has shown impressive efficacy and significant safety in dealing with Huntington's disease, which will definitely expanding the usage of it. If deutetrabenazine can be approved for secondary hyperkinetic movement disorders like post-stroke chorea in the future, increased availability and reduced costs could benefit more patients.it could benefit more patients. This report highlights the efficacy of deutetrabenazine in managing refractory post-stroke hemichorea, particularly in patients unresponsive to conventional dopamine-blocking agents like haloperidol. This report aims to enhance understanding of treatment strategies for refractory post-stroke chorea and highlight the potential utility of deutetrabenazine in such cases, offering an alternative therapeutic approach for refractory post-stroke hemichorea. Our findings advocate for expanded clinical trials to validate its efficacy and safety in cerebrovascular chorea. Abbreviations MRI: Magnetic resonance imaging EEG：electroencephalography NIHSS：National Institutes of Health Stroke Scale AIMS：Abnormal Involuntary Movement Scale ADL：Activity of Daily Living Scale AST ：Aspartate Aminotransferase DWI：Diffusion-weighted imaging NKH：non-ketotic hyperglycemia PHQ-9: Patient Health Questionnaire-9 Declarations Acknowledgements We thank the patient for providing consent to publish this case. Author Contributions XW wrote the manuscript. YS collected the data. SL and BW prepared figures. YX and CX revised the manuscript. All authors read and approved the final manuscript. Funding This study did not receive any funding or grants from the institution. Data availability The data underlying this article were provided by the China-Japan Union Hospital of Jilin University.Data will be shared on request to the corresponding author with permission. Ethics declarations Ethics approval and consent to participate The patient has provided consent for the publication of this case report. Consent for publication Written informed consent was obtained from the patient for the publication of this case report and accompanying images. Competing interests The authors declare no competing interests. References Mehanna R, Jankovic J. Movement disorders in cerebrovascular disease. The Lancet Neurology. 2013;12:597–608. Piccolo I, Defanti CA, Soliveri P, Volontè MA, Cislaghi G, Girotti F. Cause and course in a series of patients with sporadic chorea. J Neurol. 2003;250:429–35. Ghika-Schmid F, Ghika J, Regli F, Bogousslavsky J. Hyperkinetic movement disorders during and after acute stroke: The lausanne stroke registry. J Neurol Sci. 1997;146:109–16. Yi J, Zhang L, Zhang T, Li J, Zhang Y, Zhou M. Cerebral infarction in centrum semiovale presenting with hemichorea: A case report and literature review. Front Neurol. 2023;14:1249464. Lopes J, Antunes E, Oliveira B, Gomes V, Caridade S. Hyperglycemic hemichorea: A case report. Cureus. 2023. https://doi.org/10.7759/cureus.39240. Takamatsu K. [diabetic chorea]. Brain Nerve. 2014;66:121–8. Suchowersky O. Evidence-based guideline: Pharmacologic treatment of chorea in huntington disease: report of the guideline development subcommittee of the American academy of neurology. Neurology. 2013;80:970–970. Huntington Study Group, Frank S, Testa CM, Stamler D, Kayson E, Davis C, et al. Effect of deutetrabenazine on chorea among patients with huntington disease: A randomized clinical trial. JAMA. 2016;316:40–50. Nath J, Jambhekar K, Rao C, Armitano E. Radiological and pathological changes in hemiballism‐hemichorea with striatal hyperintensity. Magnetic Resonance Imaging. 2006;23:564–8. Bendi VS, Matta A, Torres-Russotto D, Shou J. Case report: Bilateral chorea/ballismus: detection and management of a rare complication of non-ketotic hyperglycaemia. BMJ Case Reports. 2018;2018. Li Z-S, Fang J-J, Xiang X-H, Zhao G-H. Hemichorea due to ipsilateral thalamic infarction: A case report. WJCC. 2021;9:5287–93. Hernandez Fustes OJ, Puppi Munhoz R, Arteaga Rodriguez C, Hernandez Fustes OJ. Chorea as the first manifestation of cerebral infarction. Cureus. 2020. https://doi.org/10.7759/cureus.7384. Edwards TC, Zrinzo L, Limousin P, Foltynie T. Deep brain stimulation in the treatment of chorea. Movement Disorders. 2012;27:357–63. Rahman S, Marwaha R. Haloperidol. In: StatPearls [Internet]. StatPearls Publishing; 2023. Nakano N, Uchiyama T, Okuda T, Kitano M, Taneda M. Successful long-term deep brain stimulation for hemichorea—hemiballism in a patient with diabetes: Case report. Journal of Neurosurgery. 2005;102:1137–41. Dalby MA. Effect of Tetrabenazine on Extrapyramidal Movement Disorders. BMJ. 1969;2:422–3. Kingston D. TETRABENAZINE FOR INVOLUNTARY MOVEMENT DISORDERS. Medical Journal of Australia. 1979;1:628–30. Huang CY, McLEOD JG, Holland RT, Elliot C. Tetrabenazine in the treatment of huntington’s chorea. Medical Journal of Australia. 1976;1:583–4. Jankovic J, Orman J. Tetrabenazine therapy of dystonia, chorea, tics, and other dyskinesias. Neurology. 1988;38:391–391. Bashir H, Jankovic J. Deutetrabenazine for the treatment of Huntington’s chorea. Expert Rev Neurother. 2018;18:625–31. Huntington Study Group, Frank S, Testa CM, Stamler D, Kayson E, Davis C, et al. Effect of deutetrabenazine on chorea among patients with huntington disease: A randomized clinical trial. JAMA. 2016;316:40. Coppen EM, Roos RAC. Current pharmacological approaches to reduce chorea in huntington’s disease. Drugs. 2017;77:29–46. Additional Declarations No competing interests reported. Cite Share Download PDF Status: Under Review Version 1 posted Reviews received at journal 30 Jul, 2025 Reviewers agreed at journal 24 Jul, 2025 Reviews received at journal 22 Jul, 2025 Reviewers agreed at journal 22 Jul, 2025 Reviews received at journal 20 Jul, 2025 Reviewers agreed at journal 16 Jul, 2025 Reviewers invited by journal 15 Jul, 2025 Editor invited by journal 17 Jun, 2025 Editor assigned by journal 17 Jun, 2025 Submission checks completed at journal 17 Jun, 2025 First submitted to journal 16 Jun, 2025 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-6905162","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":486524413,"identity":"e55fdce0-8c37-45a8-acfa-1544f4a0f137","order_by":0,"name":"Xiaoxuan Wu","email":"","orcid":"","institution":"China-Japan Union Hospital of Jilin University","correspondingAuthor":false,"prefix":"","firstName":"Xiaoxuan","middleName":"","lastName":"Wu","suffix":""},{"id":486524414,"identity":"069b072a-c95c-4dd3-b411-5a13627a8c2c","order_by":1,"name":"Yanfei Sun","email":"","orcid":"","institution":"Changchun Normal 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11:38:22","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-6905162/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-6905162/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":87050713,"identity":"2061466d-573f-4389-86f9-c10270a54a79","added_by":"auto","created_at":"2025-07-18 14:59:03","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":29521,"visible":true,"origin":"","legend":"\u003cp\u003eSymptom progression and medication regimen before admission\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-6905162/v1/d8fae7119685dc24496ea57d.png"},{"id":87050714,"identity":"ae7555bb-c9f9-452c-8b42-e8944a0d3e3d","added_by":"auto","created_at":"2025-07-18 14:59:03","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":161787,"visible":true,"origin":"","legend":"\u003cp\u003eDWI (b=1000) revealed restricted diffusion in the left thalamus (Figure 2A), with corresponding findings on the ADC and FLAIR sequences (Figures 2B and 2C\u003cem\u003e).\u003c/em\u003e\u003c/p\u003e","description":"","filename":"2.png","url":"https://assets-eu.researchsquare.com/files/rs-6905162/v1/08c8177c1e9446da4ee7a850.png"},{"id":87053643,"identity":"2bab27a5-cc72-46ce-a0cb-295c8b04ffb1","added_by":"auto","created_at":"2025-07-18 15:15:03","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":158634,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003e(A–G) \u003c/strong\u003eSagittal T1-weighted MRI images excluding striatal hyperintensity.\u003c/p\u003e","description":"","filename":"3.png","url":"https://assets-eu.researchsquare.com/files/rs-6905162/v1/a411cc1c8054174667ab1fe1.png"},{"id":87053646,"identity":"30dfe672-18d3-4e1b-94d1-0861ee245d76","added_by":"auto","created_at":"2025-07-18 15:15:07","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":800968,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-6905162/v1/a8d33d8a-6aa5-4edd-b4b3-29d40336c2a3.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Deutetrabenazine in Post-Thalamic Infarction Hemichorea: A Case Report and Literature Review","fulltext":[{"header":"Background","content":"\u003cp\u003eHemichorea is a common hyperkinetic movement disorder resulting from extrapyramidal system damage, characterized with involuntary, irregular dance-like movements on one side of the body or face. The extrapyramidal system primarily coordinates motor functions, with various motor and non-motor cortical regions projecting to striatal medium spiny neurons and the subthalamic nucleus. The internal segment of the globus pallidus serves as the main output nucleus, connecting back to the cortex via the thalamus. The striatum has two main projections: a direct pathway to the internal segment of the globus pallidus and an indirect pathway through the external segment of the globus pallidus and subthalamic nucleus to the internal segment. The indirect pathway is modulated by the substantia nigra pars compacta, exerting an inhibitory effect. Movement disorders associated with cerebrovascular disease often involve lesions in the basal ganglia region. In addition to the basal ganglia, the damage of the neostriatum and subthalamic nucleus can also lead to hemichoreiform movements[\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. Among the secondary causes of chorea, cerebrovascular disorders\u0026mdash;particularly ischemic strokes\u0026mdash;are the most common, represent the leading etiology[\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. Hemichorea acts as the most frequent involuntary movement disorder after stroke. Some post-stroke hemichorea cases that are secondary to cerebral infarction have shown refractory characteristics[\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. However, current treatment for hemichorea focuses primarily on suppressing dopaminergic function in the extrapyramidal circuit. For post-stroke hemichorea, treatment typically involves controlling cerebrovascular risk factors, addressing the issue of potential diseases, and adjunctive therapy with haloperidol for dopamine blockade[\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]. Here, we present a case of refractory post-thalamic infarction hemichore that showed significant improvement with the assistance of Deutetrabenazine after prolonged unsuccessful conventional treatments.\u003c/p\u003e"},{"header":"Case presentation","content":"\u003cp\u003eA 53-year-old hypertensive woman was referred to our neurology department after 21 days of persistent right-sided hemiparesis. Previous treatment at the other hospital included antiplatelet aggregation and circulation-improving medications, which failed to alleviate the limb weakness. 7 days after the onset of right-sided limb weakness, the patient developed involuntary movements in the right limb. The involuntary movements, initially characterized by uncontrollable twisting of the right limbs, got worse with both voluntary movement and emotional excitement.\u003c/p\u003e\u003cp\u003ePrior to admission, an acute left thalamic infarction has been confirmed. In consideration of the patient's behavior of hemi-choreiform movements, the therapeutic regimen was expanded haloperidol in addition to antiplatelet and circulation-improving medications. So the pre-admission treatment included intravenous injection of Urinary Kallidinogenase (0.15 PNA unit once a day) for cerebral microcirculation improvement, oral administration of clopidogrel (75 mg per day) for antiplatelet therapy, rosuvastatin (10 mg per day) for lipid control, amlodipine besylate (5 mg per day) for blood pressure management, metformin hydrochloride (0.5 g, three times per day) and dapagliflozin (10 mg per day) for glycemic regulation, bicyclol (50 mg, three times per day) for hepatoprotection, haloperidol (2 mg, three times per day for chorea control. However, after these treatment, the patient's limb weakness showed no improvement, and the right-sided involuntary movements worsened, which made her unable to care for herself. The symptom progression and medication regimen during the first 21 days are summarized as follows (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). The complexity and refractory characteristic of this case have been evidenced by the lack of response to conventional therapy, and the subsequent worsening of her involuntary movement. These findings suggest the patient need for alternative strategies targeting distinct pathophysiological pathways.\u003c/p\u003e\u003cp\u003e\u003c/p\u003e\u003cp\u003eDuring hospitalization, the patient underwent comprehensive diagnostic evaluations including physical examination, laboratory tests (complete blood count, metabolic panel), and neuroimaging, along with electroencephalography (EEG) to establish the diagnosis and rule out differentials. The muscle tension on the right side was decreased, while left-sided muscle tension was normal. Similarly, the muscle strength was grade III on the right but grade V on the left, indicating right limb motor impairment. Sensory examination was unremarkable. The National Institutes of Health Stroke Scale (NIHSS) score was 4 (2 points for right upper limb, 2 points for right lower limb). The Abnormal Involuntary Movement Scale (AIMS) score was 20 (4 points each for right upper limb, right lower limb, severity of abnormal movements, impact on daily life, and patient’s awareness of movements). The Activity of Daily Living Scale (ADL) score was 39. In summary, the patient presents with mild right-sided hemiparesis (NIHSS 4), severe choreiform movements (AIMS 20), and complete dependence in activities of daily living (ADL 39), reflecting significant neurological disability requiring comprehensive care. The laboratory tests including complete blood count, lipid profile, renal function, electrolytes, thyroid function, and tumor markers were normal. The Aspartate Aminotransferase (AST) was 82.35 U/L, with random blood glucose at 6.99 mmol/L and fasting blood glucose at 5.96 mmol/L. Normal video-EEG monitoring findings excluded epileptic origin of the involuntary movements. The Diffusion-weighted imaging (DWI, Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003eA) showed restricted diffusion in the left thalamus, with corresponding findings on the ADC and FLAIR sequences (Figs.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003eB and \u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003eC). Transcranial Doppler ultrasound revealed left vertebral artery occlusion. Neuroimaging confirmed an acute left thalamic infarction, which correlated well with the patient's clinical presentation.\u003c/p\u003e\u003cp\u003e\u003c/p\u003e\u003cp\u003e\u003c/p\u003e\u003cp\u003eDuring hospitalization, the treatment regimen has been modified by gradually reduced the dosage of haloperidol by 2 mg per day over three consecutive days while introducing deutetrabenazine (6 mg daily) on the third day. The cardiac rhythm and emotional state of the patient were closely monitored, with no significant abnormalities detected. On the second day with the treatment of deutetrabenazine, the frequency of limb twisting decreased, by the seventh day of hospitalization, involuntary movements of the patient had significantly reduced, The significant clinical improvement following deutetrabenazine therapy confirms its therapeutic value for this patient's movement disorder.\u003c/p\u003e\u003cp\u003e\u003c/p\u003e\u003cdiv class=\"gridtable\"\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e\u003ctable float=\"Yes\" id=\"Tab1\" border=\"1\"\u003e\u003ccaption language=\"En\"\u003e\u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e\u003cdiv class=\"CaptionContent\"\u003e\u003cp\u003eLongitudinal clinical outcomes after the treatment of deutetrabenazine.\u003c/p\u003e\u003c/div\u003e\u003c/caption\u003e\u003ccolgroup cols=\"5\"\u003e\u003c/colgroup\u003e\u003cthead\u003e\u003ctr\u003e\u003cth align=\"left\" colname=\"c1\"\u003e\u003cp\u003eParameter\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c2\"\u003e\u003cp\u003eAdmission\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c3\"\u003e\u003cp\u003ethe seventh day\u003c/p\u003e\u003cp\u003eof hospitalization\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c4\"\u003e\u003cp\u003e28-Day Follow-Up\u003c/p\u003e\u003c/th\u003e\u003cth align=\"left\" colname=\"c5\"\u003e\u003cp\u003e3-Month Follow-Up\u003c/p\u003e\u003c/th\u003e\u003c/tr\u003e\u003c/thead\u003e\u003ctbody\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003eNIHSS Score\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e4\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e2\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e0\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e0\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003eAIMS Score\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e20\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e15\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e10\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e4\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003eADL Score\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e39\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e23\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e18\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e17\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003ePHQ-9 Score\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003e\\\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003e3\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003e2\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003e2\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003ctr\u003e\u003ctd align=\"left\" colname=\"c1\"\u003e\u003cp\u003e\u003cb\u003eECG Findings\u003c/b\u003e\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c2\"\u003e\u003cp\u003eNormal\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c3\"\u003e\u003cp\u003eNormal\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c4\"\u003e\u003cp\u003eNormal\u003c/p\u003e\u003c/td\u003e\u003ctd align=\"left\" colname=\"c5\"\u003e\u003cp\u003eNormal\u003c/p\u003e\u003c/td\u003e\u003c/tr\u003e\u003c/tbody\u003e\u003ctfoot\u003e\u003ctr\u003e\u003ctd colspan=\"5\"\u003e(PHQ-9: Patient Health Questionnaire-9)\u003c/td\u003e\u003c/tr\u003e\u003c/tfoot\u003e\u003c/table\u003e\u003c/div\u003e\u003cp\u003e\u003c/p\u003e"},{"header":"Discussion and Conclusions","content":"\u003cp\u003eTo systematically evaluate both therapeutic effects and potential adverse reactions of the novel therapy, we conducted the following comprehensive assessments. When compared with previous symptoms, the muscle tension and strength has been improved, with right-sided strength increasing to grade IV. As for the assessment using standardized rating scales, the NIHSS score has been improved to 2 (1 point each for right upper and lower limbs), AIMS score decreased to 15 (3 points each for right upper limb, right lower limb, severity of abnormal movements, impact on daily life, and patient awareness), and ADL score has also been improved to 23, suggesting that deutetrabenazine demonstrated rapid efficacy with no observed adverse effects. After discharge, the patient underwent rehabilitation for 28 days, showing only minimal residual uncontrollable movements, and the patient regained independent ambulation and self-care ability Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). During a three-month follow-up, the patient experienced mild lower limb twisting twice after the discontinuation of deutetrabenazine. However, the above undesirable symptom has been resolved by resuming the medication of deutetrabenazine. Currently, the patient maintains good symptom control with a low dosage of 6 mg deutetrabenazine daily without significant side effects.\u003c/p\u003e\u003cp\u003eHemichorea is a hyperkinetic movement disorder that may be induced by various etiologies. Treatment outcomes are influenced by multifactorial determinants. Of these, Choreiform movements caused by autosomal dominant mutations are designated as Huntington's disease, is primarily treated with tetrabenazine[\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e] and deutetrabenazine[\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e] to deal with undesired symptoms and improve the quality of the life. NKH is characterized by choreiform movements due to impaired glucose metabolism [\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e], with most of the NKH cases can be resolved efficiently after glucose correction[\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]. However, the patients who suffer from stroke-induced hemichorea continued to exhibit significant and persistent limb movement impairmen after treatment, which severely hinders them to perform daily activities and thus causes considerable distress. The most common diseased regions that result in post-stroke hemichorea are basal ganglia (caudate nucleus, putamen, and globus pallidus) and subthalamic nucleus[\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e, \u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e]. Clinical studies suggest that the recovery degree of post-stroke hemichorea may be related to the location of the lesion. Except from the lesion locations, different treatment approach significantly impacts prognosis. The control of the underlying cerebral infarction and pharmacological intervention for hyperkinetic movements are both required for acute post-stroke hemichorea. For refractory cases, surgical options such as pallidotomy, thalamotomy, and deep brain stimulation\u003csup\u003e[15]\u003c/sup\u003e may be conducive to reducing choreiform movements. However, due to the risks associated with invasive surgeries, these interventions are typically considered only for patients without cognitive impairment[\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e, \u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e].Therefore, there is an urgent need for targeted, non-invasive conservative therapies to manage refractory post-stroke hemichorea. Recently, anti-dopaminergic medications are the mainstay of chorea treatment. Antipsychotics, with their potent dopamine-blocking effects, are commonly used as first-line agents. Conventional therapeutics often relies on dopamine receptor antagonists such as haloperidol, which exert rapid anti-dopaminergic effects. However, their application is limited by adverse effects including tardive dyskinesia and neuroleptic malignant syndrome[\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e], and its efficacy in treating hemichorea remains uncertain [\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e].\u003c/p\u003e\u003cp\u003eDopamine-depleting agents have offered another important treatment option. Deutetrabenazine, a dopamine-consuming agent, inhibits vesicular monoamine transporter 2 to prevent monoamine release. It has been used for decades to treat various hyperkinetic movement disorders [\u003cspan additionalcitationids=\"CR17 CR18\" citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e–\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e]. Compared to dopamine receptor blockers, such as antipsychotics, deutetrabenazine shows significant advantage in avoiding tardive dyskinesia risks [\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e]. Therefore, deutetrabenazine is currently recommended as a first-line treatment for Huntington's chorea (Level A evidence) [\u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e] and has been reported effective in treating chorea associated with non-ketotic hyperglycemia [\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]. However, its use in post-stroke hemichorea must not be neglected. In this report, deutetrabenazine achieved rapid improvement of symptoms resist to conventional haloperidol treatment, suggesting a potential new therapeutic approach for post-stroke hemichorea.\u003c/p\u003e\u003cp\u003eWhen using deutetrabenazine, several issues are needed to be considered. First of all, we should pay attention to common adverse effects including sedation, depression, anxiety, akathisia, agitation, dysphagia, parkinsonism, and dystonia, some of which seem to relate to the peak concentrations of active circulating metabolites. To minimize dopaminergic fluctuations and associated psychomotor abnormalities, we employed a cross-tapering strategy, gradually replacing haloperidol with deutetrabenazine. Secondly, deutetrabenazine may exacerbate depression and suicidal behavior, particularly in predisposed patients. Therefore, it is contraindicated in predisposed patients with no pharmacological intervention or inadequately treatment due to the high suicide risks [\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e]. As for our patient, we carefully screened for the depressive history and used the PHQ-9 scale for rapid assessment, then closely monitored her emotional changes during treatment to minimize adverse events. Thirdly, while deutetrabenazine has proved its ability to revolutionize Huntington's chorea treatment, its potential in refractory post-stroke hemichorea remains underrecognized. Fourthly, high drug costs also limit access for many potentially benefiting patients.\u003c/p\u003e\u003cp\u003eNotwithstanding these limitations, the deutetrabenazine has shown impressive efficacy and significant safety in dealing with Huntington's disease, which will definitely expanding the usage of it. If deutetrabenazine can be approved for secondary hyperkinetic movement disorders like post-stroke chorea in the future, increased availability and reduced costs could benefit more patients.it could benefit more patients.\u003c/p\u003e\u003cp\u003eThis report highlights the efficacy of deutetrabenazine in managing refractory post-stroke hemichorea, particularly in patients unresponsive to conventional dopamine-blocking agents like haloperidol. This report aims to enhance understanding of treatment strategies for refractory post-stroke chorea and highlight the potential utility of deutetrabenazine in such cases, offering an alternative therapeutic approach for refractory post-stroke hemichorea. Our findings advocate for expanded clinical trials to validate its efficacy and safety in cerebrovascular chorea.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003eMRI: Magnetic resonance imaging\u003c/p\u003e\n\u003cp\u003eEEG：electroencephalography\u003c/p\u003e\n\u003cp\u003eNIHSS：National Institutes of Health Stroke Scale\u003c/p\u003e\n\u003cp\u003eAIMS：Abnormal Involuntary Movement Scale\u003c/p\u003e\n\u003cp\u003eADL：Activity of Daily Living Scale\u003c/p\u003e\n\u003cp\u003eAST\u0026nbsp;：Aspartate Aminotransferase\u003c/p\u003e\n\u003cp\u003eDWI：Diffusion-weighted imaging\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eNKH：non-ketotic hyperglycemia\u003c/p\u003e\n\u003cp\u003ePHQ-9: Patient Health Questionnaire-9\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eAcknowledgements\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWe thank the patient for providing consent to publish this case.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthor Contributions \u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eXW wrote the manuscript. YS collected the data. SL and BW prepared figures. YX and CX revised the manuscript. All authors read and approved the final manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis study did not receive any funding or grants from the institution.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eData availability\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe data underlying this article were provided by the China-Japan Union Hospital of Jilin University.Data will be shared on request to the corresponding author with permission.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eEthics declarations\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eEthics approval and consent to participate\u003c/p\u003e\n\u003cp\u003eThe patient has provided consent for the publication of this case report.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication \u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWritten informed consent was obtained from the patient for the publication of this case report and accompanying images.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests \u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare no competing interests.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eMehanna R, Jankovic J. Movement disorders in cerebrovascular disease. The Lancet Neurology. 2013;12:597\u0026ndash;608.\u003c/li\u003e\n\u003cli\u003ePiccolo I, Defanti CA, Soliveri P, Volont\u0026egrave; MA, Cislaghi G, Girotti F. Cause and course in a series of patients with sporadic chorea. J Neurol. 2003;250:429\u0026ndash;35.\u003c/li\u003e\n\u003cli\u003eGhika-Schmid F, Ghika J, Regli F, Bogousslavsky J. Hyperkinetic movement disorders during and after acute stroke: The lausanne stroke registry. J Neurol Sci. 1997;146:109\u0026ndash;16.\u003c/li\u003e\n\u003cli\u003eYi J, Zhang L, Zhang T, Li J, Zhang Y, Zhou M. Cerebral infarction in centrum semiovale presenting with hemichorea: A case report and literature review. Front Neurol. 2023;14:1249464.\u003c/li\u003e\n\u003cli\u003eLopes J, Antunes E, Oliveira B, Gomes V, Caridade S. Hyperglycemic hemichorea: A case report. Cureus. 2023. https://doi.org/10.7759/cureus.39240.\u003c/li\u003e\n\u003cli\u003eTakamatsu K. [diabetic chorea]. Brain Nerve. 2014;66:121\u0026ndash;8.\u003c/li\u003e\n\u003cli\u003eSuchowersky O. Evidence-based guideline: Pharmacologic treatment of chorea in huntington disease: report of the guideline development subcommittee of the American academy of neurology. Neurology. 2013;80:970\u0026ndash;970.\u003c/li\u003e\n\u003cli\u003eHuntington Study Group, Frank S, Testa CM, Stamler D, Kayson E, Davis C, et al. Effect of deutetrabenazine on chorea among patients with huntington disease: A randomized clinical trial. JAMA. 2016;316:40\u0026ndash;50.\u003c/li\u003e\n\u003cli\u003eNath J, Jambhekar K, Rao C, Armitano E. Radiological and pathological changes in hemiballism‐hemichorea with striatal hyperintensity. Magnetic Resonance Imaging. 2006;23:564\u0026ndash;8.\u003c/li\u003e\n\u003cli\u003eBendi VS, Matta A, Torres-Russotto D, Shou J. Case report: Bilateral chorea/ballismus: detection and management of a rare complication of non-ketotic hyperglycaemia. BMJ Case Reports. 2018;2018.\u003c/li\u003e\n\u003cli\u003eLi Z-S, Fang J-J, Xiang X-H, Zhao G-H. Hemichorea due to ipsilateral thalamic infarction: A case report. WJCC. 2021;9:5287\u0026ndash;93.\u003c/li\u003e\n\u003cli\u003eHernandez Fustes OJ, Puppi Munhoz R, Arteaga Rodriguez C, Hernandez Fustes OJ. Chorea as the first manifestation of cerebral infarction. Cureus. 2020. https://doi.org/10.7759/cureus.7384.\u003c/li\u003e\n\u003cli\u003eEdwards TC, Zrinzo L, Limousin P, Foltynie T. Deep brain stimulation in the treatment of chorea. Movement Disorders. 2012;27:357\u0026ndash;63.\u003c/li\u003e\n\u003cli\u003eRahman S, Marwaha R. Haloperidol. In: StatPearls [Internet]. StatPearls Publishing; 2023.\u003c/li\u003e\n\u003cli\u003eNakano N, Uchiyama T, Okuda T, Kitano M, Taneda M. Successful long-term deep brain stimulation for hemichorea\u0026mdash;hemiballism in a patient with diabetes: Case report. Journal of Neurosurgery. 2005;102:1137\u0026ndash;41.\u003c/li\u003e\n\u003cli\u003eDalby MA. Effect of Tetrabenazine on Extrapyramidal Movement Disorders. BMJ. 1969;2:422\u0026ndash;3.\u003c/li\u003e\n\u003cli\u003eKingston D. TETRABENAZINE FOR INVOLUNTARY MOVEMENT DISORDERS. Medical Journal of Australia. 1979;1:628\u0026ndash;30.\u003c/li\u003e\n\u003cli\u003eHuang CY, McLEOD JG, Holland RT, Elliot C. Tetrabenazine in the treatment of huntington\u0026rsquo;s chorea. Medical Journal of Australia. 1976;1:583\u0026ndash;4.\u003c/li\u003e\n\u003cli\u003eJankovic J, Orman J. Tetrabenazine therapy of dystonia, chorea, tics, and other dyskinesias. Neurology. 1988;38:391\u0026ndash;391.\u003c/li\u003e\n\u003cli\u003eBashir H, Jankovic J. Deutetrabenazine for the treatment of Huntington\u0026rsquo;s chorea. Expert Rev Neurother. 2018;18:625\u0026ndash;31.\u003c/li\u003e\n\u003cli\u003eHuntington Study Group, Frank S, Testa CM, Stamler D, Kayson E, Davis C, et al. Effect of deutetrabenazine on chorea among patients with huntington disease: A randomized clinical trial. JAMA. 2016;316:40.\u003c/li\u003e\n\u003cli\u003eCoppen EM, Roos RAC. Current pharmacological approaches to reduce chorea in huntington\u0026rsquo;s disease. Drugs. 2017;77:29\u0026ndash;46.\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-neurology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"nurl","sideBox":"Learn more about [BMC Neurology](http://bmcneurol.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/nurl","title":"BMC Neurology","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Hemichorea, Thalamic infarction, Deutetrabenazine, Movement disorders, Stroke, Treatment, Chorea","lastPublishedDoi":"10.21203/rs.3.rs-6905162/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-6905162/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e\u003cp\u003eChorea, a hyperkinetic movement disorder, manifests as involuntary, irregular, rapid, and large-amplitude dance-like movements, such as limb flailing, twisting, and facial grimacing. It can be a primary symptom of neurological disorders directly affecting the basal ganglia, such as Huntington's disease, or a secondary manifestation of various systemic diseases, including infections, autoimmune diseases, drug-induced disorders, metabolic diseases, neurodegenerative diseases, and stroke. Among these, acute cerebrovascular disease is a common cause of chorea. While some patients experience rapid relief of choreiform movements with appropriate symptomatic treatment, others may suffer from refractory chorea that remains difficult to cure despite prolonged pharmacological intervention.\u003c/p\u003e\u003ch2\u003eCase presentation\u003c/h2\u003e\u003cp\u003eWe present a rare case of refractory post-thalamic infarction hemichorea. After the failure of conventional anti-dopaminergic therapy during the acute phase of cerebral infarction, the patient's symptoms were rapidly controlled with deutetrabenazine without significant adverse effects.\u003c/p\u003e\u003ch2\u003eConclusions\u003c/h2\u003e\u003cp\u003eThis report aims to enhance the understanding of treatment strategies for refractory post-stroke chorea and emphasize the potential efficacy of deutetrabenazine in such cases, providing an alternative therapeutic approach for refractory post-stroke hemichorea.\u003c/p\u003e","manuscriptTitle":"Deutetrabenazine in Post-Thalamic Infarction Hemichorea: A Case Report and Literature Review","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-07-18 14:58:58","doi":"10.21203/rs.3.rs-6905162/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"editorInvitedReview","content":"","date":"2025-07-30T13:50:28+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"223853369492916921183291426649980275581","date":"2025-07-24T13:09:11+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-07-22T12:32:17+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"210003306848178311056379250517648669058","date":"2025-07-22T12:12:25+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-07-20T10:59:55+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"130655430995028349804282516280978297983","date":"2025-07-16T13:57:56+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2025-07-15T15:40:00+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2025-06-17T13:27:20+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2025-06-17T05:47:24+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2025-06-17T05:45:07+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Neurology","date":"2025-06-16T11:31:36+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-neurology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"nurl","sideBox":"Learn more about [BMC Neurology](http://bmcneurol.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/nurl","title":"BMC Neurology","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"4e4d113f-e2ba-4153-b881-71f857b0102d","owner":[],"postedDate":"July 18th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2025-07-18T14:58:58+00:00","versionOfRecord":[],"versionCreatedAt":"2025-07-18 14:58:58","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-6905162","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-6905162","identity":"rs-6905162","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}