Artery of Percheron Infarction: A Rare Cause of Coma with Favorable Recovery Following Early MRI Diagnosis and Multidisciplinary Management

Artery of Percheron Infarction: A Rare Cause of Coma with Favorable Recovery Following Early MRI Diagnosis and Multidisciplinary Management | 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 Artery of Percheron Infarction: A Rare Cause of Coma with Favorable Recovery Following Early MRI Diagnosis and Multidisciplinary Management Sakshi Puri, Dr Insha Aleena, Dr Manoj Kumar Mahata This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-6985292/v1 This work is licensed under a CC BY 4.0 License Status: Published Journal Publication published 30 Jan, 2026 Read the published version in Discover Neuroscience → Version 1 posted 11 You are reading this latest preprint version Abstract Background: The artery of Percheron (AOP) is a rare anatomical variant in which a solitary arterial trunk arises from one posterior cerebral artery to supply the bilateral paramedian thalami and rostral midbrain. Infarction in this territory is an uncommon cause of ischemic stroke and frequently presents with non-localizing features such as altered sensorium, vertical gaze palsy, memory impairment, or coma. Diagnosis is often delayed due to nonspecific clinical signs and limitations of early neuroimaging. Case Presentation: We present a case of a 62-year-old male who arrived with sudden-onset coma (Glasgow Coma Scale score of 7). Initial non-contrast CT and CT angiography were unremarkable. However, persistent altered consciousness and signs of third cranial nerve involvement prompted an MRI brain, which demonstrated bilateral paramedian thalamic and rostral midbrain infarctions, consistent with AOP occlusion. The patient was outside the thrombolysis window. He was managed with dual antiplatelet therapy, anticoagulation for newly diagnosed atrial fibrillation, and supportive neurocritical care. Two weeks later, he experienced transient deterioration due to post-stroke seizures, confirmed by EEG and effectively managed with antiepileptic therapy. At 6 weeks post-event, he had achieved functional independence with minimal residual deficits, including mild dysphagia and ptosis. Conclusion: AOP infarction should be suspected in patients presenting with acute unexplained coma or bilateral thalamic involvement. MRI is the diagnostic modality of choice. Early recognition facilitates appropriate medical and rehabilitative strategies. Despite the initial severity, favorable outcomes are achievable with timely diagnosis and multidisciplinary care. Artery of Percheron bilateral thalamic infarction ischemic stroke coma vertical gaze palsy MRI brain posterior circulation stroke midbrain infarction post-stroke seizures neurorehabilitation Figures Figure 1 Figure 2 Figure 3 MANUSCRIPT INTRODUCTION The artery of Percheron (AOP) is a rare anatomical variant in which a single perforating artery from the P1 segment of one posterior cerebral artery supplies the bilateral paramedian thalami and rostral midbrain. AOP infarction accounts for a small subset of ischemic strokes and often presents with non-localizing symptoms such as coma, vertical gaze palsy, and memory impairment. Diagnosis is frequently delayed, as early CT imaging is often unremarkable and the vessel itself is rarely visualized. MRI remains the gold standard for detection. We report a case highlighting diagnostic challenges and favorable recovery following multidisciplinary management. KEY HIGHLIGHTS Artery of Percheron (AOP) infarction is a rare stroke subtype caused by occlusion of a solitary thalamic perforating artery. It typically presents with non-localizing symptoms such as coma, vertical gaze palsy, or memory impairment. Early diagnosis is often missed on initial CT; MRI with DWI/FLAIR sequences is critical for detection and thus our case highlights favorable functional recovery despite delayed presentation, with management guided by early MRI and a multidisciplinary approach. Prompt supportive care, seizure control, and rehabilitation are vital for improved outcomes in AOP infarction. INTRODUCTION The artery of Percheron (AOP) is a rare anatomical variant of the posterior cerebral circulation, first described by French neurologist Gérard Percheron in 1973. This variant is characterized by a solitary perforating arterial trunk arising from one posterior cerebral artery (PCA) that supplies the bilateral paramedian thalami and rostral midbrain. It is estimated to occur in approximately 4–12% of the population [1] . The vascular supply to the thalami is complex and is classified into four major configurations. In the Type 2b pattern—commonly referred to as the AOP variant—a single perforating artery from either the left or right PCA supplies both paramedian thalami. Given the thalamus’s role as a critical relay center for sensory and motor pathways and its involvement in consciousness, alertness, and sleep-wake regulation, infarcts in this region may present with a broad and often non-specific spectrum of clinical manifestations [2] . AOP infarction is a rare cause of ischemic stroke, accounting for approximately 0.1–2% of all cases. Pure thalamic infarcts constitute around 3–4% of ischemic strokes, and among these, AOP occlusion is implicated in approximately 4–35% of cases [3] . The variability in reported incidence reflects both the rarity of this vascular configuration and the diagnostic challenges it presents. Imaging findings may be subtle in the acute phase, and clinical presentations—including altered mental status, vertical gaze palsy, memory disturbances, and coma—often mimic other central nervous system pathologies. Due to its rarity and heterogeneous presentation, AOP infarction is frequently underdiagnosed or misdiagnosed. Management remains largely supportive, as many patients present beyond the window for thrombolytic therapy, and there is limited consensus regarding long-term rehabilitation and prognosis. Here, we report the case of a 62-year-old male who presented with a Glasgow Coma Scale (GCS) score of 7 and was subsequently diagnosed with bilateral thalamic infarction due to AOP occlusion. The patient was managed conservatively and demonstrated substantial functional recovery, ultimately achieving independence in daily activities, albeit with mild residual deficits and ongoing enteral feeding via a Ryle’s tube. This case highlights the diagnostic and therapeutic challenges of AOP infarction and emphasizes the potential for meaningful recovery with timely recognition and comprehensive supportive care. CASE DESCRIPTION A 62-year-old male presented to the emergency department in an acutely drowsy state. He was last seen well the previous night, but was found unarousable the next morning. On arrival, his Glasgow Coma Scale (GCS) score was E1V1M5, totaling 7. The patient had no known comorbidities apart from hyperuricemia, which was under medical management. Due to the severely altered level of consciousness, calculation of the National Institutes of Health Stroke Scale (NIHSS) was not feasible. On examination, the patient was noted to have right-sided pupil dilation and gaze deviation to the right. Muscle tone was normal in all four limbs, and bilateral plantar responses were equivocal. Other systemic examinations were unremarkable. His vital parameters were stable: pulse rate 66/min, blood pressure 150/80 mmHg, and oxygen saturation of 96% on 2L/min supplemental oxygen. Initial laboratory investigations including arterial blood gas (ABG) analysis were within normal limits. A non-contrast computed tomography (CT) of the brain did not reveal any acute intracranial bleed or evident lesion. CT angiography was subsequently performed to evaluate for a posterior circulation stroke; however, no large vessel occlusion was identified. Given the unclear etiology of the altered mental status, further evaluations were performed including toxicological screening and urine drug testing, all of which were negative. Magnetic resonance imaging (MRI) of the brain was then conducted, which demonstrated bilateral infarcts in the ventromedial thalami and rostral midbrain, consistent with an artery of Percheron (AOP) infarction [Figure 1 ]. MR Angiography was not evident of any Large vessel occlusion. [Figure 2 ] Routine blood investigations, including complete blood count, liver and renal function tests, electrolytes, and thyroid function, were within normal limits. Stroke workup revealed the following: HbA1c 5.7%, homocysteine 10.3 µmol/L, vitamin B12 277 pg/mL, and LDL cholesterol 151 mg/dL. Transthoracic echocardiography showed preserved left ventricular function (EF 60%). A 24-hour Holter monitor revealed episodes of atrial fibrillation. As the patient presented outside the thrombolysis window, intravenous thrombolytic therapy was not administered. He was initiated on dual antiplatelet therapy (aspirin and clopidogrel, 150 mg each), low molecular weight heparin, and statin therapy. Following detection of atrial fibrillation, anticoagulation was transitioned from heparin to apixaban (5 mg twice daily). The patient showed gradual clinical improvement but had persistent right third nerve palsy resulting in ptosis. He began mobilizing independently and, at discharge, was neurologically improved though he required nasogastric feeding due to dysphagia. Two weeks later, he re-presented in a drowsy state. Laboratory investigations remained within normal limits. Repeat CT brain showed established infarcts in the bilateral thalami and midbrain without evidence of infarct progression [Figure 3 ]. Electroencephalography (EEG) revealed encephalopathic changes consistent with seizure activity. Antiepileptic therapy was adjusted accordingly. The patient was managed conservatively with antiepileptics, apixaban, a single antiplatelet agent, statins, beta blockers (including amiodarone), and physiotherapy. At 1.5 months post-stroke, the patient demonstrated significant recovery. He remained mildly dysphagic and had persistent right eye ptosis but was functionally independent in most daily activities with minimal assistance. This case highlights the diagnostic and therapeutic complexities of AOP infarction and underscores the value of a multidisciplinary approach for favorable long-term outcomes. DISCUSSION Artery of Percheron (AOP) infarction is a rare variant of posterior circulation stroke resulting from occlusion of a solitary arterial trunk originating from the P1 segment of one posterior cerebral artery (PCA). This single perforating vessel supplies the bilateral paramedian thalami and, variably, the rostral midbrain. The clinical presentation is highly heterogeneous and depends on the extent of ischemia and the structures involved. Three primary patterns of infarction associated with AOP occlusion have been described: bilateral paramedian thalamic with midbrain infarction (43%), bilateral paramedian thalamic infarction without midbrain involvement (38%), and bilateral paramedian thalamic with anterior thalamic and midbrain infarction (19%) [4] . The classic clinical triad—altered mental status or coma, vertical gaze palsy, and memory impairment—is characteristic but inconsistently observed in clinical settings. Other presenting features may include hypersomnolence due to involvement of the ascending reticular activating system, dysarthria or aphasia if the dominant thalamus is affected, and neuropsychiatric symptoms such as apathy, disinhibition, or agitation that may mimic primary psychiatric disorders. Hemiparesis or ataxia can result from midbrain involvement, particularly of the corticospinal tracts or cerebellothalamic pathways. In our patient, key findings included altered sensorium, vertical gaze palsy, and right third cranial nerve involvement, consistent with midbrain extension of the infarct [5] . The diagnostic challenge of AOP infarction stems from its non-localizing symptomatology and broad differential diagnosis. Conditions to be considered include deep cerebral venous thrombosis, top-of-the-basilar syndrome, Wernicke’s encephalopathy, bilateral thalamic glioma or lymphoma, metabolic or toxic encephalopathies, viral encephalitis (e.g., West Nile virus, Japanese encephalitis), basilar artery thrombosis, and autoimmune or inflammatory encephalopathies. Initial imaging, particularly non-contrast CT, is frequently unremarkable in the early stages of AOP infarction. CT or MR angiography often fails to visualize the AOP due to its diminutive caliber. However, associated findings such as P1 segment occlusion or other PCA abnormalities may serve as indirect indicators. A 2021 case report documented delayed diagnosis in a patient presenting within the thrombolysis window, whose initial CT and CTA were unremarkable despite fluctuating consciousness [6 ] . MRI with diffusion-weighted imaging (DWI), apparent diffusion coefficient (ADC) mapping, and FLAIR sequences remains the gold standard for diagnosis. The “midbrain V-sign”—a V-shaped hyperintensity in the midbrain on axial DWI or FLAIR—has been reported in AOP infarcts with a sensitivity of 67% [7] . In our case, prompt MRI confirmed the diagnosis, although the patient had presented outside the thrombolytic window. When diagnosed early, intravenous thrombolysis may improve outcomes and remains the treatment of choice in eligible patients [8] . Management of AOP infarction is largely supportive and aligned with standard ischemic stroke protocols. These include initiation of antiplatelet or anticoagulation therapy based on underlying etiology, statins for secondary prevention, and supportive care tailored to neurological deficits. In our patient, anticoagulation was initiated for new-onset atrial fibrillation. Seizure management is another critical aspect; our patient developed post-stroke seizures during the subacute phase, which were successfully treated with antiepileptics. A retrospective series of 18 patients with bilateral paramedian thalamic infarction reported that 61% regained the ability to perform activities of daily living independently [9] . Persistent deficits may include vertical gaze palsy, cognitive dysfunction, third nerve palsy with ptosis, and dysphagia. Disruption of the ascending dopaminergic and noradrenergic pathways from the reticular activating system is believed to underlie hypersomnolence and arousal deficits [10] . Recovery is typically slow and may necessitate prolonged neurorehabilitation involving multidisciplinary care. Mechanical thrombectomy is not feasible in AOP infarction due to the small vessel caliber. Therefore, a high index of suspicion, early MRI evaluation, and a coordinated therapeutic strategy are vital for optimizing outcomes in affected individuals. CONCLUSION Artery of Percheron infarction should be considered in patients presenting with unexplained altered consciousness, memory disturbances, or signs suggestive of bilateral thalamic involvement. Early MRI is essential for diagnosis, as conventional CT and angiographic modalities often fail to visualize the lesion. While direct identification of the AOP is rarely possible, the characteristic imaging pattern of bilateral paramedian thalamic infarction—when interpreted in the context of compatible clinical features—is highly suggestive. Prompt recognition, individualized medical management, seizure control, and structured rehabilitation are key to achieving favorable long-term outcomes in this rare but potentially reversible condition. Declarations FINANCIAL DISCLOSURE OR FUNDING – Nil CONFLICT OF INTEREST – There are no conflicts of interest CONSENT TO PUBLISH DECLERATION AND INFORMED CONSENT - We certify that we have obtained all appropriate patient consent forms. In the form , the patient has given consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published , and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. REGISTRATION DETAILS FOR CLINICAL TRIAL – NOT APPLICABLE Ethics Approval and Consent to Participate - Ethical approval was not required for this single-patient case report, in accordance with institutional guidelines. Written informed consent was obtained from the patient for participation and publication. Data Availability Statement – The data supporting the findings of this case report are not publicly available due to patient privacy and confidentiality concerns but are available from the corresponding author upon reasonable request and with appropriate ethical approvals. All data generated or analysed during the case reporting are included in this published article . AUTHOR CONTRIBUTIONS – Dr Sakshi Puri – Concept , design , definition if intellectual content , manuscript preparation and editing Dr Insha Aleena –Design , Data acquisition , manuscript preparation and editing , literature search Dr Manoj Kumar Mahata – Concept , Manuscript editing , Literature review , Data acquisition References Jones J, Tao W, Sharma R, et al. Artery of Percheron. Reference article, Radiopaedia.org. https://doi.org/10.53347/rID-5936. Accessed May 30, 2025. Ratanpara L, Xalxo N, Chauhan PR, Mehra S. Artery of Percheron, an uncommon variant of posterior cerebral circulation: a case report. Cureus. 2024;16(3):e57266. Doi:10.7759/cureus.57266. Kumral E, Evyapan D, Kutluhan S. Pure thalamic infarctions: clinical findings. J Stroke Cerebrovasc Dis. 2000;9(6):287–97. Doi:10.1053/jscd.2000.18741. Kichloo A, Jamal SM, Zain EA, Wani F, Vipparala N. Artery of Percheron infarction: a short review. J Investig Med High Impact Case Rep. 2019;7:2324709619867355. Doi:10.1177/2324709619867355. Phate N, Pawar T, Andhale A, Singh RK, Talwar D, Acharya S, et al. Artery of Percheron stroke: a case report with a diagnostic challenge. Cureus. 2022;14(2):e21939. Doi:10.7759/cu2324709619867355. Badu-Boateng C, Jeyanesan D, Easaw J, Lloyd M. Artery of Percheron infarct: hiding in plain sight. Clin Med (Lond). 2021;21:e405–7. Doi:10.7861/clinmed.2021-0383Zai Lazzaro NA, Wright B, Castillo M, Fischbein NJ, Glastonbury CM, Hildenbrand PG, et al. Artery of Percheron infarction: imaging patterns and clinical spectrum. AJNR Am J Neuroradiol. 2010;31(7):1283–9. Doi:10.3174/ajnr.A2044. Cassourret G, Prunet B, Sbardella F, Bordes J, Maurin O, Boret H. Ischemic stroke of the artery of Percheron with normal initial MRI: a case report. Case Rep Med. 2010;2010:425734. Doi:10.1155/20Neuroradiol. D Xu Z, Sun L, Duan Y, Zhang J, Zhang M, Cai X. Assessment of Percheron infarction in images and clinical findings. J Neurol Sci. 2017;383:87–92. Saida IB, Saad HB, Zghidi M, Ennouri E, Ettoumi R, Boussarsar M. Artery of Percheron stroke as an unusual cause of hypersomnia: a case series and a short literature review. Am J Mens Health. 2020;14(4):155798832093894. Additional Declarations No competing interests reported. Cite Share Download PDF Status: Published Journal Publication published 30 Jan, 2026 Read the published version in Discover Neuroscience → Version 1 posted Editorial decision: Revision requested 26 Aug, 2025 Reviews received at journal 13 Aug, 2025 Reviews received at journal 11 Aug, 2025 Reviewers agreed at journal 06 Aug, 2025 Reviews received at journal 05 Aug, 2025 Reviewers agreed at journal 05 Aug, 2025 Reviewers agreed at journal 04 Aug, 2025 Reviewers invited by journal 22 Jul, 2025 Editor assigned by journal 15 Jul, 2025 Submission checks completed at journal 10 Jul, 2025 First submitted to journal 10 Jul, 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. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. 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-6985292","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":489255737,"identity":"9ae5471d-c000-41bd-bff5-133850e3cb65","order_by":0,"name":"Sakshi Puri","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAABC0lEQVRIie3PMUvDQBTA8RcC53J0TgmYr/CgcCAc6QdxSTi4ToWMDgVPhHYRujrZT+DqHDnIFJo14mIXnQQhawdfsnRKmlHw/sPBhffjXQBcrj8ZAx8wuGQXhi4o6fDu8hFEzia8nUPdEjOCgE6fgqS92e7bIIk2hWqyzHprWBbhTVbFzxtLW1byuo9gqYvwEa3PYK+nJb6rlzIlUuil6SOwWPscLWPeg5gaIiIn4hnbS6Lt131DhDOft2SvRHUYJlDrPOSoA8Y6kseiPrMF609NRCLjE3VlUCWipi3JwL9EWz1r+DG43e2+X9/MMZ6LanH4+FnJ/oed4t2ZdpPJ+fETmY8bdrlcrv/UL+ePXZYZKVpmAAAAAElFTkSuQmCC","orcid":"","institution":"Apollo Gleneagles Hospitals","correspondingAuthor":true,"prefix":"","firstName":"Sakshi","middleName":"","lastName":"Puri","suffix":""},{"id":489255738,"identity":"7128f20d-5be4-424d-a5ad-c5e2c6f6e2ba","order_by":1,"name":"Dr Insha Aleena","email":"","orcid":"","institution":"Apollo Gleneagles Hospitals","correspondingAuthor":false,"prefix":"Dr","firstName":"Insha","middleName":"","lastName":"Aleena","suffix":""},{"id":489255739,"identity":"827bc6f1-5714-452a-8a71-b463df5b0e48","order_by":2,"name":"Dr Manoj Kumar Mahata","email":"","orcid":"","institution":"Apollo Gleneagles Hospitals","correspondingAuthor":false,"prefix":"Dr","firstName":"Manoj","middleName":"Kumar","lastName":"Mahata","suffix":""}],"badges":[],"createdAt":"2025-06-26 16:23:12","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-6985292/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-6985292/v1","draftVersion":[],"editorialEvents":[{"content":"https://doi.org/10.1186/s13064-026-00233-0","type":"published","date":"2026-01-30T15:59:02+00:00"}],"editorialNote":"","failedWorkflow":false,"files":[{"id":87720780,"identity":"1c81e168-0e43-401c-9c61-f8e2dffc3f02","added_by":"auto","created_at":"2025-07-28 09:49:30","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":245260,"visible":true,"origin":"","legend":"\u003cp\u003eDWI , ADC AXIAL AND CORONAL \u0026nbsp;SEQUENCES OF MRI BRAIN SHOWING BILATERAL THALAMI INFARCTS\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-6985292/v1/4c3f2b227901155cf5c684cb.png"},{"id":87721983,"identity":"3c6087fd-022a-4dd6-8949-2bcc02d3ee90","added_by":"auto","created_at":"2025-07-28 09:57:30","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":211710,"visible":true,"origin":"","legend":"\u003cp\u003eMRI ANGIOGRAPHY AXIAL VIEW IMAGE SHOWING NO LARGE VESSEL OCCLUSION\u003c/p\u003e","description":"","filename":"2.png","url":"https://assets-eu.researchsquare.com/files/rs-6985292/v1/c478d211865b9d5126b40cf0.png"},{"id":87720776,"identity":"806a99e3-2e63-4356-b343-165bc8503883","added_by":"auto","created_at":"2025-07-28 09:49:30","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":160303,"visible":true,"origin":"","legend":"\u003cp\u003eFOLLOW UP REPEAT CT SCAN SHOWING BILATERAL THALAMI INFARCT WITH NO INCREASE IN SIZE\u003c/p\u003e","description":"","filename":"3.png","url":"https://assets-eu.researchsquare.com/files/rs-6985292/v1/87b6c035d4fc646d59d4db21.png"},{"id":101690826,"identity":"83b54d6f-2a8d-4df3-8ffd-75a127e13b4d","added_by":"auto","created_at":"2026-02-02 16:09:31","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1170209,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-6985292/v1/52f5c7cf-2eac-4f39-a3a1-76174d7c7885.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Artery of Percheron Infarction: A Rare Cause of Coma with Favorable Recovery Following Early MRI Diagnosis and Multidisciplinary Management","fulltext":[{"header":"MANUSCRIPT INTRODUCTION ","content":"\u003cp\u003eThe artery of Percheron (AOP) is a rare anatomical variant in which a single perforating artery from the P1 segment of one posterior cerebral artery supplies the bilateral paramedian thalami and rostral midbrain. AOP infarction accounts for a small subset of ischemic strokes and often presents with non-localizing symptoms such as coma, vertical gaze palsy, and memory impairment. Diagnosis is frequently delayed, as early CT imaging is often unremarkable and the vessel itself is rarely visualized. MRI remains the gold standard for detection. We report a case highlighting diagnostic challenges and favorable recovery following multidisciplinary management.\u003c/p\u003e"},{"header":"KEY HIGHLIGHTS ","content":"\u003col\u003e\n \u003cli\u003eArtery of Percheron (AOP) infarction is a rare stroke subtype caused by occlusion of a solitary thalamic perforating artery.\u003c/li\u003e\n \u003cli\u003eIt typically presents with non-localizing symptoms such as coma, vertical gaze palsy, or memory impairment.\u003c/li\u003e\n \u003cli\u003eEarly diagnosis is often missed on initial CT; MRI with DWI/FLAIR sequences is critical for detection and thus our case highlights favorable functional recovery despite delayed presentation, with management guided by early MRI and a multidisciplinary approach.\n \u003c/li\u003e\n\u003c/ol\u003e\u003cp\u003ePrompt supportive care, seizure control, and rehabilitation are vital for improved outcomes in AOP infarction.\u003c/p\u003e"},{"header":"INTRODUCTION","content":"\u003cp\u003eThe artery of Percheron (AOP) is a rare anatomical variant of the posterior cerebral circulation, first described by French neurologist Gérard Percheron in 1973. This variant is characterized by a solitary perforating arterial trunk arising from one posterior cerebral artery (PCA) that supplies the bilateral paramedian thalami and rostral midbrain. It is estimated to occur in approximately 4–12% of the population \u003csup\u003e[1]\u003c/sup\u003e.\u003c/p\u003e\u003cp\u003eThe vascular supply to the thalami is complex and is classified into four major configurations. In the Type 2b pattern—commonly referred to as the AOP variant—a single perforating artery from either the left or right PCA supplies both paramedian thalami. Given the thalamus’s role as a critical relay center for sensory and motor pathways and its involvement in consciousness, alertness, and sleep-wake regulation, infarcts in this region may present with a broad and often non-specific spectrum of clinical manifestations \u003csup\u003e[2]\u003c/sup\u003e.\u003c/p\u003e\u003cp\u003eAOP infarction is a rare cause of ischemic stroke, accounting for approximately 0.1–2% of all cases. Pure thalamic infarcts constitute around 3–4% of ischemic strokes, and among these, AOP occlusion is implicated in approximately 4–35% of cases \u003csup\u003e[3]\u003c/sup\u003e. The variability in reported incidence reflects both the rarity of this vascular configuration and the diagnostic challenges it presents. Imaging findings may be subtle in the acute phase, and clinical presentations—including altered mental status, vertical gaze palsy, memory disturbances, and coma—often mimic other central nervous system pathologies.\u003c/p\u003e\u003cp\u003eDue to its rarity and heterogeneous presentation, AOP infarction is frequently underdiagnosed or misdiagnosed. Management remains largely supportive, as many patients present beyond the window for thrombolytic therapy, and there is limited consensus regarding long-term rehabilitation and prognosis.\u003c/p\u003e\u003cp\u003eHere, we report the case of a 62-year-old male who presented with a Glasgow Coma Scale (GCS) score of 7 and was subsequently diagnosed with bilateral thalamic infarction due to AOP occlusion. The patient was managed conservatively and demonstrated substantial functional recovery, ultimately achieving independence in daily activities, albeit with mild residual deficits and ongoing enteral feeding via a Ryle’s tube. This case highlights the diagnostic and therapeutic challenges of AOP infarction and emphasizes the potential for meaningful recovery with timely recognition and comprehensive supportive care.\u003c/p\u003e"},{"header":"CASE DESCRIPTION","content":"\u003cp\u003eA 62-year-old male presented to the emergency department in an acutely drowsy state. He was last seen well the previous night, but was found unarousable the next morning. On arrival, his Glasgow Coma Scale (GCS) score was E1V1M5, totaling 7. The patient had no known comorbidities apart from hyperuricemia, which was under medical management. Due to the severely altered level of consciousness, calculation of the National Institutes of Health Stroke Scale (NIHSS) was not feasible. On examination, the patient was noted to have right-sided pupil dilation and gaze deviation to the right. Muscle tone was normal in all four limbs, and bilateral plantar responses were equivocal. Other systemic examinations were unremarkable. His vital parameters were stable: pulse rate 66/min, blood pressure 150/80 mmHg, and oxygen saturation of 96% on 2L/min supplemental oxygen.\u003c/p\u003e\u003cp\u003eInitial laboratory investigations including arterial blood gas (ABG) analysis were within normal limits. A non-contrast computed tomography (CT) of the brain did not reveal any acute intracranial bleed or evident lesion. CT angiography was subsequently performed to evaluate for a posterior circulation stroke; however, no large vessel occlusion was identified. Given the unclear etiology of the altered mental status, further evaluations were performed including toxicological screening and urine drug testing, all of which were negative.\u003c/p\u003e\u003cp\u003eMagnetic resonance imaging (MRI) of the brain was then conducted, which demonstrated bilateral infarcts in the ventromedial thalami and rostral midbrain, consistent with an artery of Percheron (AOP) infarction [Figure \u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e]. MR Angiography was not evident of any Large vessel occlusion. [Figure \u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e] Routine blood investigations, including complete blood count, liver and renal function tests, electrolytes, and thyroid function, were within normal limits. Stroke workup revealed the following: HbA1c 5.7%, homocysteine 10.3 µmol/L, vitamin B12 277 pg/mL, and LDL cholesterol 151 mg/dL. Transthoracic echocardiography showed preserved left ventricular function (EF 60%). A 24-hour Holter monitor revealed episodes of atrial fibrillation. As the patient presented outside the thrombolysis window, intravenous thrombolytic therapy was not administered. He was initiated on dual antiplatelet therapy (aspirin and clopidogrel, 150 mg each), low molecular weight heparin, and statin therapy. Following detection of atrial fibrillation, anticoagulation was transitioned from heparin to apixaban (5 mg twice daily). The patient showed gradual clinical improvement but had persistent right third nerve palsy resulting in ptosis. He began mobilizing independently and, at discharge, was neurologically improved though he required nasogastric feeding due to dysphagia.\u003c/p\u003e\u003cp\u003eTwo weeks later, he re-presented in a drowsy state. Laboratory investigations remained within normal limits. Repeat CT brain showed established infarcts in the bilateral thalami and midbrain without evidence of infarct progression [Figure \u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003e]. Electroencephalography (EEG) revealed encephalopathic changes consistent with seizure activity. Antiepileptic therapy was adjusted accordingly. The patient was managed conservatively with antiepileptics, apixaban, a single antiplatelet agent, statins, beta blockers (including amiodarone), and physiotherapy. At 1.5 months post-stroke, the patient demonstrated significant recovery. He remained mildly dysphagic and had persistent right eye ptosis but was functionally independent in most daily activities with minimal assistance. This case highlights the diagnostic and therapeutic complexities of AOP infarction and underscores the value of a multidisciplinary approach for favorable long-term outcomes.\u003c/p\u003e"},{"header":"DISCUSSION","content":"\u003cp\u003eArtery of Percheron (AOP) infarction is a rare variant of posterior circulation stroke resulting from occlusion of a solitary arterial trunk originating from the P1 segment of one posterior cerebral artery (PCA). This single perforating vessel supplies the bilateral paramedian thalami and, variably, the rostral midbrain. The clinical presentation is highly heterogeneous and depends on the extent of ischemia and the structures involved.\u003c/p\u003e\u003cp\u003eThree primary patterns of infarction associated with AOP occlusion have been described: bilateral paramedian thalamic with midbrain infarction (43%), bilateral paramedian thalamic infarction without midbrain involvement (38%), and bilateral paramedian thalamic with anterior thalamic and midbrain infarction (19%) \u003csup\u003e[4]\u003c/sup\u003e. The classic clinical triad\u0026mdash;altered mental status or coma, vertical gaze palsy, and memory impairment\u0026mdash;is characteristic but inconsistently observed in clinical settings.\u003c/p\u003e\u003cp\u003eOther presenting features may include hypersomnolence due to involvement of the ascending reticular activating system, dysarthria or aphasia if the dominant thalamus is affected, and neuropsychiatric symptoms such as apathy, disinhibition, or agitation that may mimic primary psychiatric disorders. Hemiparesis or ataxia can result from midbrain involvement, particularly of the corticospinal tracts or cerebellothalamic pathways. In our patient, key findings included altered sensorium, vertical gaze palsy, and right third cranial nerve involvement, consistent with midbrain extension of the infarct \u003csup\u003e[5]\u003c/sup\u003e.\u003c/p\u003e\u003cp\u003eThe diagnostic challenge of AOP infarction stems from its non-localizing symptomatology and broad differential diagnosis. Conditions to be considered include deep cerebral venous thrombosis, top-of-the-basilar syndrome, Wernicke\u0026rsquo;s encephalopathy, bilateral thalamic glioma or lymphoma, metabolic or toxic encephalopathies, viral encephalitis (e.g., West Nile virus, Japanese encephalitis), basilar artery thrombosis, and autoimmune or inflammatory encephalopathies.\u003c/p\u003e\u003cp\u003eInitial imaging, particularly non-contrast CT, is frequently unremarkable in the early stages of AOP infarction. CT or MR angiography often fails to visualize the AOP due to its diminutive caliber. However, associated findings such as P1 segment occlusion or other PCA abnormalities may serve as indirect indicators. A 2021 case report documented delayed diagnosis in a patient presenting within the thrombolysis window, whose initial CT and CTA were unremarkable despite fluctuating consciousness \u003csup\u003e[6 ]\u003c/sup\u003e.\u003c/p\u003e\u003cp\u003eMRI with diffusion-weighted imaging (DWI), apparent diffusion coefficient (ADC) mapping, and FLAIR sequences remains the gold standard for diagnosis. The \u0026ldquo;midbrain V-sign\u0026rdquo;\u0026mdash;a V-shaped hyperintensity in the midbrain on axial DWI or FLAIR\u0026mdash;has been reported in AOP infarcts with a sensitivity of 67% \u003csup\u003e[7]\u003c/sup\u003e. In our case, prompt MRI confirmed the diagnosis, although the patient had presented outside the thrombolytic window. When diagnosed early, intravenous thrombolysis may improve outcomes and remains the treatment of choice in eligible patients\u003csup\u003e[8]\u003c/sup\u003e.\u003c/p\u003e\u003cp\u003eManagement of AOP infarction is largely supportive and aligned with standard ischemic stroke protocols. These include initiation of antiplatelet or anticoagulation therapy based on underlying etiology, statins for secondary prevention, and supportive care tailored to neurological deficits. In our patient, anticoagulation was initiated for new-onset atrial fibrillation. Seizure management is another critical aspect; our patient developed post-stroke seizures during the subacute phase, which were successfully treated with antiepileptics. A retrospective series of 18 patients with bilateral paramedian thalamic infarction reported that 61% regained the ability to perform activities of daily living independently \u003csup\u003e[9]\u003c/sup\u003e.\u003c/p\u003e\u003cp\u003ePersistent deficits may include vertical gaze palsy, cognitive dysfunction, third nerve palsy with ptosis, and dysphagia. Disruption of the ascending dopaminergic and noradrenergic pathways from the reticular activating system is believed to underlie hypersomnolence and arousal deficits \u003csup\u003e[10]\u003c/sup\u003e. Recovery is typically slow and may necessitate prolonged neurorehabilitation involving multidisciplinary care.\u003c/p\u003e\u003cp\u003eMechanical thrombectomy is not feasible in AOP infarction due to the small vessel caliber. Therefore, a high index of suspicion, early MRI evaluation, and a coordinated therapeutic strategy are vital for optimizing outcomes in affected individuals.\u003c/p\u003e"},{"header":"CONCLUSION","content":"\u003cp\u003eArtery of Percheron infarction should be considered in patients presenting with unexplained altered consciousness, memory disturbances, or signs suggestive of bilateral thalamic involvement. Early MRI is essential for diagnosis, as conventional CT and angiographic modalities often fail to visualize the lesion. While direct identification of the AOP is rarely possible, the characteristic imaging pattern of bilateral paramedian thalamic infarction\u0026mdash;when interpreted in the context of compatible clinical features\u0026mdash;is highly suggestive. Prompt recognition, individualized medical management, seizure control, and structured rehabilitation are key to achieving favorable long-term outcomes in this rare but potentially reversible condition.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eFINANCIAL DISCLOSURE OR FUNDING\u003c/strong\u003e – Nil\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCONFLICT OF INTEREST\u003c/strong\u003e – There are no conflicts of interest\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCONSENT TO PUBLISH DECLERATION AND INFORMED CONSENT\u003c/strong\u003e- \u0026nbsp;We certify that we have obtained all appropriate patient consent forms. In the form , the patient has given consent for his images and other clinical information to be reported in the journal. \u0026nbsp;The patient understands that his name and initials will not be published , and due efforts will be made to conceal their identity, \u0026nbsp;but anonymity cannot be guaranteed.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eREGISTRATION DETAILS FOR CLINICAL TRIAL\u003c/strong\u003e – NOT APPLICABLE\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eEthics Approval and Consent to Participate\u003c/strong\u003e - Ethical approval was not required for this single-patient case report, in accordance with institutional guidelines. Written informed consent was obtained from the patient for participation and publication.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eData Availability Statement\u0026nbsp;\u003c/strong\u003e– The data supporting the findings of this case report are not publicly available due to patient privacy and confidentiality concerns but are available from the corresponding author upon reasonable request and with appropriate ethical approvals. All data generated \u0026nbsp;or analysed during the case reporting are included in this published article .\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAUTHOR CONTRIBUTIONS\u003c/strong\u003e –\u003c/p\u003e\n\u003cp\u003eDr Sakshi Puri – Concept , design , definition if intellectual content , manuscript preparation and editing\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eDr Insha Aleena –Design , Data acquisition , manuscript preparation and editing , literature search\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eDr Manoj Kumar Mahata – Concept , Manuscript editing , Literature review , Data acquisition\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eJones J, Tao W, Sharma R, et al. Artery of Percheron. Reference article, Radiopaedia.org. https://doi.org/10.53347/rID-5936. Accessed May 30, 2025.\u003c/li\u003e\n\u003cli\u003eRatanpara L, Xalxo N, Chauhan PR, Mehra S. Artery of Percheron, an uncommon variant of posterior cerebral circulation: a case report. Cureus. 2024;16(3):e57266. Doi:10.7759/cureus.57266.\u003c/li\u003e\n\u003cli\u003eKumral E, Evyapan D, Kutluhan S. Pure thalamic infarctions: clinical findings. J Stroke Cerebrovasc Dis. 2000;9(6):287\u0026ndash;97. Doi:10.1053/jscd.2000.18741.\u003c/li\u003e\n\u003cli\u003eKichloo A, Jamal SM, Zain EA, Wani F, Vipparala N. Artery of Percheron infarction: a short review. J Investig Med High Impact Case Rep. 2019;7:2324709619867355. Doi:10.1177/2324709619867355.\u003c/li\u003e\n\u003cli\u003ePhate N, Pawar T, Andhale A, Singh RK, Talwar D, Acharya S, et al. Artery of Percheron stroke: a case report with a diagnostic challenge. Cureus. 2022;14(2):e21939. Doi:10.7759/cu2324709619867355.\u003c/li\u003e\n\u003cli\u003eBadu-Boateng C, Jeyanesan D, Easaw J, Lloyd M. Artery of Percheron infarct: hiding in plain sight. Clin Med (Lond). 2021;21:e405\u0026ndash;7. Doi:10.7861/clinmed.2021-0383Zai\u003c/li\u003e\n\u003cli\u003eLazzaro NA, Wright B, Castillo M, Fischbein NJ, Glastonbury CM, Hildenbrand PG, et al. Artery of Percheron infarction: imaging patterns and clinical spectrum. AJNR Am J Neuroradiol. 2010;31(7):1283\u0026ndash;9. Doi:10.3174/ajnr.A2044.\u003c/li\u003e\n\u003cli\u003eCassourret G, Prunet B, Sbardella F, Bordes J, Maurin O, Boret H. Ischemic stroke of the artery of Percheron with normal initial MRI: a case report. Case Rep Med. 2010;2010:425734. Doi:10.1155/20Neuroradiol. D\u003c/li\u003e\n\u003cli\u003eXu Z, Sun L, Duan Y, Zhang J, Zhang M, Cai X. Assessment of Percheron infarction in images and clinical findings. J Neurol Sci. 2017;383:87\u0026ndash;92.\u003c/li\u003e\n\u003cli\u003eSaida IB, Saad HB, Zghidi M, Ennouri E, Ettoumi R, Boussarsar M. Artery of Percheron stroke as an unusual cause of hypersomnia: a case series and a short literature review. Am J Mens Health. 2020;14(4):155798832093894.\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"discover-neuroscience","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"ndev","sideBox":"Learn more about [Neural Development](http://neuraldevelopment.biomedcentral.com/)","snPcode":"13064","submissionUrl":"https://submission.nature.com/new-submission/13064/3","title":"Discover Neuroscience","twitterHandle":"@BioMedCentral","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"em","reportingPortfolio":"BMC/SO AJ","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Artery of Percheron, bilateral thalamic infarction, ischemic stroke, coma, vertical gaze palsy, MRI brain, posterior circulation stroke, midbrain infarction, post-stroke seizures, neurorehabilitation","lastPublishedDoi":"10.21203/rs.3.rs-6985292/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-6985292/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground:\u003c/h2\u003e\u003cp\u003eThe artery of Percheron (AOP) is a rare anatomical variant in which a solitary arterial trunk arises from one posterior cerebral artery to supply the bilateral paramedian thalami and rostral midbrain. Infarction in this territory is an uncommon cause of ischemic stroke and frequently presents with non-localizing features such as altered sensorium, vertical gaze palsy, memory impairment, or coma. Diagnosis is often delayed due to nonspecific clinical signs and limitations of early neuroimaging.\u003c/p\u003e\u003ch2\u003eCase Presentation:\u003c/h2\u003e\u003cp\u003eWe present a case of a 62-year-old male who arrived with sudden-onset coma (Glasgow Coma Scale score of 7). Initial non-contrast CT and CT angiography were unremarkable. However, persistent altered consciousness and signs of third cranial nerve involvement prompted an MRI brain, which demonstrated bilateral paramedian thalamic and rostral midbrain infarctions, consistent with AOP occlusion. The patient was outside the thrombolysis window. He was managed with dual antiplatelet therapy, anticoagulation for newly diagnosed atrial fibrillation, and supportive neurocritical care. Two weeks later, he experienced transient deterioration due to post-stroke seizures, confirmed by EEG and effectively managed with antiepileptic therapy. At 6 weeks post-event, he had achieved functional independence with minimal residual deficits, including mild dysphagia and ptosis.\u003c/p\u003e\u003ch2\u003eConclusion:\u003c/h2\u003e\u003cp\u003eAOP infarction should be suspected in patients presenting with acute unexplained coma or bilateral thalamic involvement. MRI is the diagnostic modality of choice. Early recognition facilitates appropriate medical and rehabilitative strategies. Despite the initial severity, favorable outcomes are achievable with timely diagnosis and multidisciplinary care.\u003c/p\u003e","manuscriptTitle":"Artery of Percheron Infarction: A Rare Cause of Coma with Favorable Recovery Following Early MRI Diagnosis and Multidisciplinary Management","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-07-28 09:49:25","doi":"10.21203/rs.3.rs-6985292/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2025-08-26T09:40:38+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-08-13T20:47:54+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-08-11T21:48:36+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"75010064595499421345092582737343839226","date":"2025-08-06T13:22:16+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-08-05T18:44:29+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"216031155806305923598277755698585922315","date":"2025-08-05T18:34:30+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"227727822544257352026398997703982723993","date":"2025-08-04T23:56:46+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2025-07-22T14:37:54+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2025-07-15T13:41:58+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2025-07-10T13:16:13+00:00","index":"","fulltext":""},{"type":"submitted","content":"Discover Neuroscience","date":"2025-07-10T11:31:44+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"discover-neuroscience","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"ndev","sideBox":"Learn more about [Neural Development](http://neuraldevelopment.biomedcentral.com/)","snPcode":"13064","submissionUrl":"https://submission.nature.com/new-submission/13064/3","title":"Discover Neuroscience","twitterHandle":"@BioMedCentral","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"em","reportingPortfolio":"BMC/SO AJ","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"723d9b4d-ff23-4769-b1e2-28ef4ee2f1cc","owner":[],"postedDate":"July 28th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"published-in-journal","subjectAreas":[],"tags":[],"updatedAt":"2026-02-02T16:06:41+00:00","versionOfRecord":{"articleIdentity":"rs-6985292","link":"https://doi.org/10.1186/s13064-026-00233-0","journal":{"identity":"discover-neuroscience","isVorOnly":false,"title":"Discover Neuroscience"},"publishedOn":"2026-01-30 15:59:02","publishedOnDateReadable":"January 30th, 2026"},"versionCreatedAt":"2025-07-28 09:49:25","video":"","vorDoi":"10.1186/s13064-026-00233-0","vorDoiUrl":"https://doi.org/10.1186/s13064-026-00233-0","workflowStages":[]},"version":"v1","identity":"rs-6985292","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-6985292","identity":"rs-6985292","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}