A case report of posterior circulation stroke in a young patient caused by Bow Hunter Syndrome

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Abstract Background : Bow Hunter’s syndrome is an uncommon cause of transient vertebrobasilar insufficiency and posterior circulation stroke, resulting from dynamic mechanical compression of the vertebral artery during head rotation. Due to its low prevalence and variable clinical presentation, it may go unrecognized in young patients presenting with posterior circulation ischemic stroke. Case presentation : We report the case of a young male patient who presented with vertigo, vomiting, and occipital headache exacerbated by head rotation. Brain computed tomography (CT) revealed hypodense areas involving the cerebellar hemispheres and brainstem, with cerebellar infarctions confirmed on MRI. Computed tomography angiography (CTA) demonstrated asymmetric left vertebral artery course at V1 segment, hypoplasia of the V2 segment, as well as an anatomical variant of the left posterior inferior cerebellar artery (PICA). Dynamic digital subtraction angiography (DSA) showed cessation of flow during leftward head rotation at the left V1 level. Endovascular treatment with stent placement across the V1–V2 left segments was performed, achieving flow restoration and complete clinical recovery. Conclusion : Bow Hunter’s syndrome should be considered in patients with posterior circulation ischemic events and symptoms triggered by head movement. Dynamic angiographic studies remain essential for diagnosis, and endovascular treatment represents a safe and effective therapeutic option.
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A case report of posterior circulation stroke in a young patient caused by Bow Hunter Syndrome | 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 A case report of posterior circulation stroke in a young patient caused by Bow Hunter Syndrome Alvaro Santiago Quimbaya-Rodriguez, Juan Camilo Rubiano-Castaño, and 3 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-9024842/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Background : Bow Hunter’s syndrome is an uncommon cause of transient vertebrobasilar insufficiency and posterior circulation stroke, resulting from dynamic mechanical compression of the vertebral artery during head rotation. Due to its low prevalence and variable clinical presentation, it may go unrecognized in young patients presenting with posterior circulation ischemic stroke. Case presentation : We report the case of a young male patient who presented with vertigo, vomiting, and occipital headache exacerbated by head rotation. Brain computed tomography (CT) revealed hypodense areas involving the cerebellar hemispheres and brainstem, with cerebellar infarctions confirmed on MRI. Computed tomography angiography (CTA) demonstrated asymmetric left vertebral artery course at V1 segment, hypoplasia of the V2 segment, as well as an anatomical variant of the left posterior inferior cerebellar artery (PICA). Dynamic digital subtraction angiography (DSA) showed cessation of flow during leftward head rotation at the left V1 level. Endovascular treatment with stent placement across the V1–V2 left segments was performed, achieving flow restoration and complete clinical recovery. Conclusion : Bow Hunter’s syndrome should be considered in patients with posterior circulation ischemic events and symptoms triggered by head movement. Dynamic angiographic studies remain essential for diagnosis, and endovascular treatment represents a safe and effective therapeutic option. Bow Hunter’s Syndrome Vertebral Artery Posterior Circulation Stroke Young Stroke Case Report Figures Figure 1 Figure 2 Figure 3 Figure 4 Introduction Transient vertebrobasilar insufficiency is an uncommon cause of posterior circulation infarction, resulting from stenosis or occlusion of the vertebral artery (VA) during head rotation, which leads to vertebrobasilar ischemia. Since its first description in 1978 by Sorensen [ 1 ] in a young patient (39 years old) who, during archery practice, developed Wallenberg’s syndrome and pyramidal tract involvement due to unidirectional hyperrotation of the head to stabilize the arrow while aiming, the term Bow Hunter’s Syndrome (BHS) was coined. Common presenting symptoms include visual disturbances, vertigo, syncope, nausea, and headache [ 2 ]. Given the limited number of reported cases, the exact incidence of this syndrome remains unknown; however, it has been described predominantly in males aged 50–70 years with chronic comorbidities such as hypertension, hyperlipidemia, osteoarthritis, diabetes, tobacco use, and coronary artery disease [ 2 – 3 ]. Management of BHS usually involves conservative neck immobilization, anticoagulant therapy, and, in some cases, surgical intervention for bony decompression or vertebral artery stenting [ 3 ]. We report the case of a previously healthy young male patient presenting with an ischemic posterior circulation stroke. Case Presentation A 44-year-old Latin male, former professional soldier, presented to the emergency department referred from a primary care facility due to a chief complaint of “dizziness.” He reported a two-day history of vertiginous sensation characterized by a sudden-onset illusion of environmental rotation, accompanied by vomiting and oppressive frontal headache, with exacerbation of symptoms upon head movements. He had no relevant comorbidities. He was an ex-smoker, having quit 15 years earlier, and reported no family medical history. On physical examination, the patient was alert and oriented. Muscle strength, tone, and reflexes were normal in all four limbs. Neurological examination revealed non-fatigable horizontal nystagmus with a fast phase to the right, left truncal and appendicular ataxia, and left pyramidal tract signs. A 24-hour Holter monitor was within normal limits. Transthoracic echocardiography demonstrated concentric left ventricular remodeling. Autoimmune screening (ANA, ENA, lupus anticoagulant, anti-DNA) and HIV tests were negative. Functional antithrombin, coagulation factor V, and complement components C3 and C4 were within normal ranges. Non-contrast head CT on admission showed hypodense areas along the cefebellum, vermis, pons and midbrain (Fig. 1 , a and b). No hemorrhages were depicted. Non-contrast brain MRI (Fig. 1 , c and d) demonstrated acute cerebellar infarctions, predominantly involving the left hemisphere. CT head and neck angiography (Fig. 2 ) revealed that the left vertebral artery originated from the aortic arch, entered the foraminal canal at the C5 level and exhibited a reduction in caliber along its V2 segment. Additionally, a common origin of the posterior inferior cerebellar artery (PICA) from the left vertebral arteries was identified as an anatomical variant. Digital Subtraction Angiography (DSA) (Fig. 3 ) demonstrated a normal right vertebral artery (a) and (b and c) focal narrowing of the proximal V2 segment of the left vertebral artery. (d) During left cervical rotation, absence of flow was observed from the V1 left segment, caused by external muscular compression. Additionally, (e) a common trunk of the posterior inferior cerebellar arteries (PICA) arising from the left vertebral artery and supplying both cerebellar hemispheres was identified. In a second procedure, a stent was deployed across the V1–V2 segments of the left vertebral artery, achieving adequate contrast medium flow on dynamic imaging (Fig. 4 ). The patient was discharged 72 hours after the procedure, without new neurological focalization signs and with secondary prevention using statins and antiplatelet agents. Discussion Posterior circulation stroke (PCS) refers to a neurological deficit secondary to hypoperfusion of the brainstem, cerebellum, thalamus, and/or occipitoparietal lobes [ 4 ], which are territories primarily supplied by the vertebrobasilar system. The vertebral arteries usually originate from the subclavian arteries, traverse the six transverse foramina of the cervical vertebrae, pass through the superior vertebral notch located on the arch of the atlas, and turn medially and laterally toward the dura mater, where they give rise to the posterior inferior cerebellar artery (PICA) and the anterior spinal artery (ASA). They then converge to form the basilar artery at the pontomedullary junction, which gives off branches including the anterior inferior cerebellar arteries (AICA), pontine perforating arteries, and superior cerebellar arteries, finally terminating as the posterior cerebral arteries (PCA) [ 5 ]. PCS accounts for approximately 20% of all cerebrovascular events annually in the United States [ 6 ]. Among young patients, the main causes of PCS include cardioembolic disease, arterial dissection, and vasculopathies. Bow Hunter’s Syndrome (BHS), also known as rotational vertebral artery occlusion, is a rare cause of transient vertebrobasilar insufficiency induced by dynamic neck motion. Compression of the vertebral artery by surrounding soft tissue or posterior cervical bony abnormalities leads to recurrent symptoms and/or ischemic stroke [ 2 – 3 ]. The pathophysiology of BHS has been explained by the “two-hit theory.” First, one vertebral artery may be hypoplastic or stenotic due to congenital or acquired causes, or show anatomic variants in PICA origin; subsequently, the dominant vertebral artery becomes compromised by extrinsic factors [ 7 ]. These may include muscular or tendinous insertions, osteophytes, degenerative cervical disease—particularly at the atlantoaxial level (C1–C2)—fibromuscular membranes, hypertrophy of the atlanto-occipital membrane, or other craniovertebral junction abnormalities. At the subaxial level, compression may occur due to the anterior scalene or longus colli muscles, deep cervical fascia, cervical sympathetic chain, or cervical spondylosis [ 8 ]. To date, no incidence data for BHS are available. Reported cases include all age groups, including pediatric and adolescent populations [ 3 ]. The most frequently affected age range is between the fifth and seventh decades of life, with a male-to-female ratio of 2:1. The vertebral artery segments most commonly involved are V1 (80%), V2 (74%), and V3–V4 (61%). Regarding laterality, the syndrome occurs on the left side in 49.5% of cases, on the right in 36.7%, and bilaterally in 13.7% [ 3 ]. The most frequent symptoms include syncope (69%), vertigo (49%), dizziness (45%), visual disturbances (43%), paresthesias (21%), nausea or vomiting (19%), headache (9%), and nystagmus (7%) [ 3 , 9 – 10 ]. CT angiography may demonstrate a reduction in the caliber of the affected vertebral artery. Furthermore, evaluation in bone window settings can help identify degenerative or congenital bony abnormalities. Dynamic digital subtraction angiography (DSA) confirms the diagnosis of BHS [ 9 ]. Regarding management, there are currently no standardized treatment guidelines. Reported therapeutic options include conservative approaches (such as cervical collar use) with secondary prevention, and surgical techniques including decompression, spinal fusion, combined decompression and fusion, vertebral artery stenting, and PICA–PICA bypass [ 3 ]. In some case series, decompression and fusion have been associated with recurrence and persistent symptoms in 5–8% of patients, respectively. Endovascular management has also been reported in isolated cases, with satisfactory outcomes to date. Conclusion This case illustrates an uncommon cause of vertebrobasilar insufficiency with posterior fossa ischemic stroke, secondary to muscular compression of the V1 segment of the left vertebral artery at its entry into the foraminal canal at C5, along with focal narrowing of the proximal V2 segment and the presence of a common trunk giving rise to the posterior inferior cerebellar arteries. The condition was successfully treated by endovascular intervention. The use of multiple diagnostic modalities—particularly dynamic Digital Subtraction Angiography (DSA)—enabled definitive confirmation of Bow Hunter’s syndrome, while CT and MRI were essential in excluding other abnormalities that could modify the management of this entity. Declarations Funding No funding was necessary and none was received for this case. Author contributions A.D, P.R.and M.C were actively involved in the critical review of the intellectual content of the manuscript, the selection and analysis of the images included, and the final approval of the version submitted for publication. A.Q. and J.C.R contributed to the drafting and preparation of the manuscript, performed a critical review of its academic and methodological content, and approved the final version for submission. All authors reviewed and approved the final manuscript and agree to be accountable for all aspects of the work. Competing interest The authors declare no competing interests. Clinical trial number: Not aplicable. Ethics approval This case report was approved by the Institutional Ethics Committee of the Hospital Militar Central in Bogotá DC. The study was conducted in accordance with the ethical principles of the Declaration of Helsinki. Consent to participate and publication Informed consent was obtained from all the individual participants for participation in this study. The consent form has been signed and is in possession of the authors. Data availability The datasets generated during and/or analysed during the current study are available from the corresponding author on reasonable request. References Sorensen B. Bow Hunter’s Stroke. Neurosurgery. 1978; 2 (3): 259 – 61. https://doi.org/10.1227/00006123-197805000-00013 Duan G, Xu J, Shi Jm Cao Y. Advances in the pathogenesis, diagnosis and treatment of Bow Hunter’s Syndrome: A comprehensive review of the literature. Intervent Neurol. 2016;5(1–2):29–38. 10.1159/00044430 . Jost GF, Dailey AT. Bow hunter’s syndrome revisited: 2 new cases and literature review of 124 cases. Neurosurg Focus. 2015;38(4):E7. doi.org/10.3171/2015.1.FOCUS14791 . Schneider AM, Neuhaus AA, Hadley G, Balami JS, Harston GW, De Luca GC, Buchan AM. Posterior circulation ischaemic stroke diagnosis and management. Clin Med. 2023;23(3):219–27. https://doi.org/10.7861/clinmed.2022-0499 . Salerno A, Strambo D, Nannoni S, Duner V, Michel P. Patterns of ischemic posterior circulation strokes: A clinical, anatomical, and radiological review. Int J Stroke. 2022;17(7):714–22. 10.1177/17474930211046758 . Mozaffarian D, Benjamin E, Go A, Arnett D, Blaha M, Cushman M, et al. Heart Disease and Stroke Statistics – 2016 Update: A Report From the American Heart Association. Circulation. 2016;133(4):e38–360. https://doi.org/10.1161/CIR.0000000000000350 . Choi KD, Choi JH, Kim JS, Kim HJ, Kim MJ, Lee TH et al. Rotational Vertebral Artery Occlusion: Mechanism and Long-term outcome. 2013; 44 (7); 1817–24. https://doi.org/10.1161/STROKEAHA.113.001219 Fujimoto S, Terai Y, Itoh T. Rotational stenosis of the first segmento f the vertebral artery through compression by the cervical sympathethic chain – case report. Neurol Med Chir. 1988;28(10):1020–23. https://doi.org/10.2176/nmc.28.1020 . Rastogi V, Rawis A, Moore O, Victorica B, Khan S, Saravanapavan P, et al. Rare etiolology of Bow Hunter’s Syndrome and Systemic Reviw of Literature. J Vasc Interv Neurol. 2015;8(3):7–16. PMCID: PMC4535600. Go G, Hwang SH, Park IS, Park H. Rotational Vertebral Artery Compression: Bow Hunter’s Syndrome. J Korean Neurosurg Soc. 2013;54(3):243–45. https://doi.org/10.3340/jkns.2013.54.3.243 . Additional Declarations No competing interests reported. Cite Share Download PDF Status: Posted Version 1 posted 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. 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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-9024842","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":613594729,"identity":"7fdb69e9-71b3-49a6-9e83-e58b2b61d441","order_by":0,"name":"Alvaro Santiago Quimbaya-Rodriguez","email":"data:image/png;base64,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","orcid":"","institution":"Universidad Militar Nueva Granada","correspondingAuthor":true,"prefix":"","firstName":"Alvaro","middleName":"Santiago","lastName":"Quimbaya-Rodriguez","suffix":""},{"id":613594730,"identity":"3de9e0e6-1f56-42fb-9925-a7b6bc07676f","order_by":1,"name":"Juan Camilo Rubiano-Castaño","email":"","orcid":"","institution":"Universidad Militar Nueva Granada","correspondingAuthor":false,"prefix":"","firstName":"Juan","middleName":"Camilo","lastName":"Rubiano-Castaño","suffix":""},{"id":613594731,"identity":"8becb9de-e32a-446b-b7c3-8dcffcb6d6d5","order_by":2,"name":"Marco Charry","email":"","orcid":"","institution":"Hospital Militar Central, Bogotá D.C","correspondingAuthor":false,"prefix":"","firstName":"Marco","middleName":"","lastName":"Charry","suffix":""},{"id":613594732,"identity":"3546fbba-9177-46e5-8b16-ac2f182b8cc2","order_by":3,"name":"Pilar Rodriguez","email":"","orcid":"","institution":"Hospital Militar Central, Bogotá D.C","correspondingAuthor":false,"prefix":"","firstName":"Pilar","middleName":"","lastName":"Rodriguez","suffix":""},{"id":613594733,"identity":"bfa1e91f-f077-4243-a2fe-2c5cffee776b","order_by":4,"name":"Angel Donato","email":"","orcid":"","institution":"Hospital Militar Central, Bogotá D.C","correspondingAuthor":false,"prefix":"","firstName":"Angel","middleName":"","lastName":"Donato","suffix":""}],"badges":[],"createdAt":"2026-03-04 02:23:38","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-9024842/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-9024842/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":105905336,"identity":"91811554-9123-478b-964e-71fe94fc1327","added_by":"auto","created_at":"2026-04-01 10:11:51","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":358947,"visible":true,"origin":"","legend":"\u003cp\u003eNon-contrast head CT, axial (a) and sagittal (b) planes, shows hypodense confluent areas involving cerebellum and vermis (white arrow), pons and midbrain (dotted white arrow). Non-contrast brain MRI: Axial DWI b-1000 (c) and ADC (d) reveals a restricted diffusion area consistent with cerebellar infarction (white arrow). No diffusion-weighted abnormalities are identified in the brainstem (not shown).\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-9024842/v1/8fa2b15313aa56e5f45edc7e.png"},{"id":105906756,"identity":"c991f6c1-0b3e-4388-9e1e-23a2e0068450","added_by":"auto","created_at":"2026-04-01 10:24:16","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":304252,"visible":true,"origin":"","legend":"\u003cp\u003eHead and neck CT angiography. Axial image (a) shows the origin of the left vertebral artery from the aortic arch (white arrow). Sagittal reconstruction (b) demonstrates its entry into the foraminal canal at the C5 level (white dotted arrow). Coronal multiplanar reconstruction (c) reveals narrowing and wall irregularity of the V2 segment of the left vertebral artery (black arrow).\u003c/p\u003e","description":"","filename":"2.png","url":"https://assets-eu.researchsquare.com/files/rs-9024842/v1/41c0a5ca89e429b8a49d038c.png"},{"id":105874923,"identity":"293fa1ef-680b-440f-9934-55b22e7534cf","added_by":"auto","created_at":"2026-04-01 05:32:34","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":428375,"visible":true,"origin":"","legend":"\u003cp\u003eDigital Subtraction Angiography (DSA). (a) Right vertebral artery angiography and (b) left vertebral artery angiography in neutral position, demonstrating segmental narrowing of the left vertebral artery at the \u0026nbsp;proximal V2 segment (white arrow). With right cervical rotation (c) no changes were observed. With left cervical rotation (d), absence of contrast flow is depicted (black arrow). The yellow arrow indicates the trachea as a laterality marker. Image (e) shows the common origin of the posterior inferior cerebellar arteries (PICA) (dotted arrow) arising from the left vertebral artery.\u003c/p\u003e","description":"","filename":"3.png","url":"https://assets-eu.researchsquare.com/files/rs-9024842/v1/899a184a5d95cab14c085759.png"},{"id":105874926,"identity":"d42a0f34-a340-4ce9-935a-65b747c00d09","added_by":"auto","created_at":"2026-04-01 05:32:34","extension":"png","order_by":4,"title":"Figure 4","display":"","copyAsset":false,"role":"figure","size":277700,"visible":true,"origin":"","legend":"\u003cp\u003eDigital Subtraction Angiography (DSA) of the left vertebral artery. Image (a) shows a segmental narrowing of the V2 segment (white arrow). Image (b) obtained after stent deployment, demonstrates adequate contrast flow in the neutral position. Image (c) shows preserved contrast flow during left cervical rotation. The yellow arrow indicates the trachea as a laterality marker.\u003c/p\u003e","description":"","filename":"4.png","url":"https://assets-eu.researchsquare.com/files/rs-9024842/v1/1bcbb722439788787a6df65d.png"},{"id":109172168,"identity":"226dc4d8-d6f4-4080-a3f8-59beb37fe892","added_by":"auto","created_at":"2026-05-13 09:03:18","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1734815,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-9024842/v1/b697b756-68fd-4214-a57e-4e9985433620.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"A case report of posterior circulation stroke in a young patient caused by Bow Hunter Syndrome","fulltext":[{"header":"Introduction","content":"\u003cp\u003eTransient vertebrobasilar insufficiency is an uncommon cause of posterior circulation infarction, resulting from stenosis or occlusion of the vertebral artery (VA) during head rotation, which leads to vertebrobasilar ischemia. Since its first description in 1978 by Sorensen [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e] in a young patient (39 years old) who, during archery practice, developed Wallenberg\u0026rsquo;s syndrome and pyramidal tract involvement due to unidirectional hyperrotation of the head to stabilize the arrow while aiming, the term \u003cem\u003eBow Hunter\u0026rsquo;s Syndrome (BHS)\u003c/em\u003e was coined.\u003c/p\u003e \u003cp\u003eCommon presenting symptoms include visual disturbances, vertigo, syncope, nausea, and headache [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. Given the limited number of reported cases, the exact incidence of this syndrome remains unknown; however, it has been described predominantly in males aged 50\u0026ndash;70 years with chronic comorbidities such as hypertension, hyperlipidemia, osteoarthritis, diabetes, tobacco use, and coronary artery disease [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eManagement of BHS usually involves conservative neck immobilization, anticoagulant therapy, and, in some cases, surgical intervention for bony decompression or vertebral artery stenting [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eWe report the case of a previously healthy young male patient presenting with an ischemic posterior circulation stroke.\u003c/p\u003e"},{"header":"Case Presentation","content":"\u003cp\u003eA 44-year-old Latin male, former professional soldier, presented to the emergency department referred from a primary care facility due to a chief complaint of \u0026ldquo;dizziness.\u0026rdquo; He reported a two-day history of vertiginous sensation characterized by a sudden-onset illusion of environmental rotation, accompanied by vomiting and oppressive frontal headache, with exacerbation of symptoms upon head movements.\u003c/p\u003e \u003cp\u003eHe had no relevant comorbidities. He was an ex-smoker, having quit 15 years earlier, and reported no family medical history. On physical examination, the patient was alert and oriented. Muscle strength, tone, and reflexes were normal in all four limbs. Neurological examination revealed non-fatigable horizontal nystagmus with a fast phase to the right, left truncal and appendicular ataxia, and left pyramidal tract signs.\u003c/p\u003e \u003cp\u003eA 24-hour Holter monitor was within normal limits. Transthoracic echocardiography demonstrated concentric left ventricular remodeling. Autoimmune screening (ANA, ENA, lupus anticoagulant, anti-DNA) and HIV tests were negative. Functional antithrombin, coagulation factor V, and complement components C3 and C4 were within normal ranges.\u003c/p\u003e \u003cp\u003eNon-contrast head CT on admission showed hypodense areas along the cefebellum, vermis, pons and midbrain (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e, a and b). No hemorrhages were depicted. Non-contrast brain MRI (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e, c and d) demonstrated acute cerebellar infarctions, predominantly involving the left hemisphere. CT head and neck angiography (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e) revealed that the left vertebral artery originated from the aortic arch, entered the foraminal canal at the C5 level and exhibited a reduction in caliber along its V2 segment. Additionally, a common origin of the posterior inferior cerebellar artery (PICA) from the left vertebral arteries was identified as an anatomical variant.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eDigital Subtraction Angiography (DSA) (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003e) demonstrated a normal right vertebral artery (a) and (b and c) focal narrowing of the proximal V2 segment of the left vertebral artery. (d) During left cervical rotation, absence of flow was observed from the V1 left segment, caused by external muscular compression. Additionally, (e) a common trunk of the posterior inferior cerebellar arteries (PICA) arising from the left vertebral artery and supplying both cerebellar hemispheres was identified.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eIn a second procedure, a stent was deployed across the V1\u0026ndash;V2 segments of the left vertebral artery, achieving adequate contrast medium flow on dynamic imaging (Fig.\u0026nbsp;\u003cspan refid=\"Fig4\" class=\"InternalRef\"\u003e4\u003c/span\u003e). The patient was discharged 72 hours after the procedure, without new neurological focalization signs and with secondary prevention using statins and antiplatelet agents.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003ePosterior circulation stroke (PCS) refers to a neurological deficit secondary to hypoperfusion of the brainstem, cerebellum, thalamus, and/or occipitoparietal lobes [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e], which are territories primarily supplied by the vertebrobasilar system.\u003c/p\u003e \u003cp\u003eThe vertebral arteries usually originate from the subclavian arteries, traverse the six transverse foramina of the cervical vertebrae, pass through the superior vertebral notch located on the arch of the atlas, and turn medially and laterally toward the dura mater, where they give rise to the posterior inferior cerebellar artery (PICA) and the anterior spinal artery (ASA). They then converge to form the basilar artery at the pontomedullary junction, which gives off branches including the anterior inferior cerebellar arteries (AICA), pontine perforating arteries, and superior cerebellar arteries, finally terminating as the posterior cerebral arteries (PCA) [\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e].\u003c/p\u003e \u003cp\u003ePCS accounts for approximately 20% of all cerebrovascular events annually in the United States [\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]. Among young patients, the main causes of PCS include cardioembolic disease, arterial dissection, and vasculopathies. Bow Hunter\u0026rsquo;s Syndrome (BHS), also known as rotational vertebral artery occlusion, is a rare cause of transient vertebrobasilar insufficiency induced by dynamic neck motion. Compression of the vertebral artery by surrounding soft tissue or posterior cervical bony abnormalities leads to recurrent symptoms and/or ischemic stroke [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eThe pathophysiology of BHS has been explained by the \u0026ldquo;two-hit theory.\u0026rdquo; First, one vertebral artery may be hypoplastic or stenotic due to congenital or acquired causes, or show anatomic variants in PICA origin; subsequently, the dominant vertebral artery becomes compromised by extrinsic factors [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e]. These may include muscular or tendinous insertions, osteophytes, degenerative cervical disease\u0026mdash;particularly at the atlantoaxial level (C1\u0026ndash;C2)\u0026mdash;fibromuscular membranes, hypertrophy of the atlanto-occipital membrane, or other craniovertebral junction abnormalities. At the subaxial level, compression may occur due to the anterior scalene or longus colli muscles, deep cervical fascia, cervical sympathetic chain, or cervical spondylosis [\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eTo date, no incidence data for BHS are available. Reported cases include all age groups, including pediatric and adolescent populations [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. The most frequently affected age range is between the fifth and seventh decades of life, with a male-to-female ratio of 2:1. The vertebral artery segments most commonly involved are V1 (80%), V2 (74%), and V3\u0026ndash;V4 (61%). Regarding laterality, the syndrome occurs on the left side in 49.5% of cases, on the right in 36.7%, and bilaterally in 13.7% [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. The most frequent symptoms include syncope (69%), vertigo (49%), dizziness (45%), visual disturbances (43%), paresthesias (21%), nausea or vomiting (19%), headache (9%), and nystagmus (7%) [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eCT angiography may demonstrate a reduction in the caliber of the affected vertebral artery. Furthermore, evaluation in bone window settings can help identify degenerative or congenital bony abnormalities. Dynamic digital subtraction angiography (DSA) confirms the diagnosis of BHS [\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eRegarding management, there are currently no standardized treatment guidelines. Reported therapeutic options include conservative approaches (such as cervical collar use) with secondary prevention, and surgical techniques including decompression, spinal fusion, combined decompression and fusion, vertebral artery stenting, and PICA\u0026ndash;PICA bypass [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. In some case series, decompression and fusion have been associated with recurrence and persistent symptoms in 5\u0026ndash;8% of patients, respectively. Endovascular management has also been reported in isolated cases, with satisfactory outcomes to date.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eThis case illustrates an uncommon cause of vertebrobasilar insufficiency with posterior fossa ischemic stroke, secondary to muscular compression of the V1 segment of the left vertebral artery at its entry into the foraminal canal at C5, along with focal narrowing of the proximal V2 segment and the presence of a common trunk giving rise to the posterior inferior cerebellar arteries. The condition was successfully treated by endovascular intervention. The use of multiple diagnostic modalities\u0026mdash;particularly dynamic Digital Subtraction Angiography (DSA)\u0026mdash;enabled definitive confirmation of Bow Hunter\u0026rsquo;s syndrome, while CT and MRI were essential in excluding other abnormalities that could modify the management of this entity.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNo funding was necessary and none was received for this case.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthor contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eA.D, P.R.and M.C were actively involved in the critical review of the intellectual content of the manuscript, the selection and analysis of the images included, and the final approval of the version submitted for publication.\u003c/p\u003e\n\u003cp\u003eA.Q. and J.C.R contributed to the drafting and preparation of the manuscript, performed a critical review of its academic and methodological content, and approved the final version for submission.\u003c/p\u003e\n\u003cp\u003eAll authors reviewed and approved the final manuscript and agree to be accountable for all aspects of the work.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interest\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare no competing interests.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eClinical trial number:\u0026nbsp;\u003c/strong\u003eNot aplicable.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eEthics approval\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis case report was approved by the Institutional Ethics Committee of the Hospital Militar Central in Bogot\u0026aacute; DC. The study was conducted in accordance with the ethical principles of the Declaration of Helsinki.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent to participate and publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eInformed consent was obtained from all the individual participants for participation in this study. The consent form has been signed and is in possession of the authors.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eData availability\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe datasets generated during and/or analysed during the current study are available from the corresponding author on reasonable request.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eSorensen B. Bow Hunter\u0026rsquo;s Stroke. Neurosurgery. 1978; 2 (3): 259\u0026thinsp;\u0026ndash;\u0026thinsp;61. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1227/00006123-197805000-00013\u003c/span\u003e\u003cspan address=\"10.1227/00006123-197805000-00013\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDuan G, Xu J, Shi Jm Cao Y. Advances in the pathogenesis, diagnosis and treatment of Bow Hunter\u0026rsquo;s Syndrome: A comprehensive review of the literature. Intervent Neurol. 2016;5(1\u0026ndash;2):29\u0026ndash;38. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.1159/00044430\u003c/span\u003e\u003cspan address=\"10.1159/00044430\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eJost GF, Dailey AT. Bow hunter\u0026rsquo;s syndrome revisited: 2 new cases and literature review of 124 cases. Neurosurg Focus. 2015;38(4):E7. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003edoi.org/10.3171/2015.1.FOCUS14791\u003c/span\u003e\u003cspan address=\"10.3171/2015.1.FOCUS14791\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSchneider AM, Neuhaus AA, Hadley G, Balami JS, Harston GW, De Luca GC, Buchan AM. Posterior circulation ischaemic stroke diagnosis and management. Clin Med. 2023;23(3):219\u0026ndash;27. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.7861/clinmed.2022-0499\u003c/span\u003e\u003cspan address=\"10.7861/clinmed.2022-0499\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSalerno A, Strambo D, Nannoni S, Duner V, Michel P. Patterns of ischemic posterior circulation strokes: A clinical, anatomical, and radiological review. Int J Stroke. 2022;17(7):714\u0026ndash;22. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.1177/17474930211046758\u003c/span\u003e\u003cspan address=\"10.1177/17474930211046758\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMozaffarian D, Benjamin E, Go A, Arnett D, Blaha M, Cushman M, et al. 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Rotational Vertebral Artery Occlusion: Mechanism and Long-term outcome. 2013; 44 (7); 1817\u0026ndash;24. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1161/STROKEAHA.113.001219\u003c/span\u003e\u003cspan address=\"10.1161/STROKEAHA.113.001219\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eFujimoto S, Terai Y, Itoh T. Rotational stenosis of the first segmento f the vertebral artery through compression by the cervical sympathethic chain \u0026ndash; case report. Neurol Med Chir. 1988;28(10):1020\u0026ndash;23. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.2176/nmc.28.1020\u003c/span\u003e\u003cspan address=\"10.2176/nmc.28.1020\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eRastogi V, Rawis A, Moore O, Victorica B, Khan S, Saravanapavan P, et al. Rare etiolology of Bow Hunter\u0026rsquo;s Syndrome and Systemic Reviw of Literature. J Vasc Interv Neurol. 2015;8(3):7\u0026ndash;16. PMCID: PMC4535600.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGo G, Hwang SH, Park IS, Park H. Rotational Vertebral Artery Compression: Bow Hunter\u0026rsquo;s Syndrome. J Korean Neurosurg Soc. 2013;54(3):243\u0026ndash;45. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.3340/jkns.2013.54.3.243\u003c/span\u003e\u003cspan address=\"10.3340/jkns.2013.54.3.243\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"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":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Bow Hunter’s Syndrome, Vertebral Artery, Posterior Circulation Stroke, Young Stroke, Case Report","lastPublishedDoi":"10.21203/rs.3.rs-9024842/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-9024842/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eBackground\u003c/strong\u003e: Bow Hunter’s syndrome is an uncommon cause of transient vertebrobasilar insufficiency and posterior circulation stroke, resulting from dynamic mechanical compression of the vertebral artery during head rotation. Due to its low prevalence and variable clinical presentation, it may go unrecognized in young patients presenting with posterior circulation ischemic stroke.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCase presentation\u003c/strong\u003e: We report the case of a young male patient who presented with vertigo, vomiting, and occipital headache exacerbated by head rotation. Brain computed tomography (CT) revealed hypodense areas involving the cerebellar hemispheres and brainstem, with cerebellar infarctions confirmed on MRI. Computed tomography angiography (CTA) demonstrated asymmetric left vertebral artery course at V1 segment, hypoplasia of the V2 segment, as well as an anatomical variant of the left posterior inferior cerebellar artery (PICA). Dynamic digital subtraction angiography (DSA) showed cessation of flow during leftward head rotation at the left V1 level. Endovascular treatment with stent placement across the V1–V2 left segments was performed, achieving flow restoration and complete clinical recovery.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConclusion\u003c/strong\u003e: Bow Hunter’s syndrome should be considered in patients with posterior circulation ischemic events and symptoms triggered by head movement. Dynamic angiographic studies remain essential for diagnosis, and endovascular treatment represents a safe and effective therapeutic option.\u003c/p\u003e","manuscriptTitle":"A case report of posterior circulation stroke in a young patient caused by Bow Hunter Syndrome","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-04-01 05:32:26","doi":"10.21203/rs.3.rs-9024842/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"b7d31f24-98b2-4b00-945b-57ba33d8c661","owner":[],"postedDate":"April 1st, 2026","published":true,"recentEditorialEvents":[{"type":"decision","content":"Withdrawn","date":"2026-05-13T08:48:23+00:00","index":"","fulltext":""}],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2026-05-13T09:02:16+00:00","versionOfRecord":[],"versionCreatedAt":"2026-04-01 05:32:26","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-9024842","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-9024842","identity":"rs-9024842","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}

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