A rare clinical presentation of acute ischaemic myelopathy of the conus medullaris: a case report | 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 rare clinical presentation of acute ischaemic myelopathy of the conus medullaris: a case report Fernando Martins Braga, Javier Pizarro, Hatice Kumru This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-7398122/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: Conus medullaris infarction is a rare cause of acute spinal cord injury that can mimic Guillain-Barré syndrome (GBS) or cauda equina syndrome. Early diagnosis is important for management and prognosis. We report a case in a patient without major vascular risk factors. Case presentation: A 68-year-old man with a history of Pott's disease and smoking presented with sudden left foot numbness that progressed within hours to bilateral leg weakness, back pain, urinary retention, and a T10 sensory level. Examination showed complete flaccid paraplegia (American Spinal Injury Association Impairment Scale, AIS, Grade A) with normal upper limb function. MRI revealed T12–L1 conus medullaris oedema without evidence of compression. Cerebrospinal fluid analysis and autoimmune/infectious workup were unremarkable. High-dose methylprednisolone was administered for suspected Guillain–Barré syndrome, with minimal clinical improvement. CT angiography showed only mild aortoiliac atherosclerosis. Acute ischaemic myelopathy of the conus medullaris was diagnosed. Rehabilitation started at 7 weeks led to partial recovery of strength in the hip flexors and quadriceps, as well as independent wheelchair mobility at 12 weeks. Conclusions: This case demonstrates the diagnostic challenges of conus medullaris infarction. Clinicians should consider spinal cord ischaemia in acute paraplegia with early urinary retention and normal CSF, even in individuals without significant vascular risk factors. Rehabilitation can produce significant recovery despite poor initial presentation. spinal cord injury ischaemic SCI conus medullaris differential diagnoses acute myelopathy Figures Figure 1 Background Spinal cord infarction is an uncommon neurological emergency, representing a small fraction of all strokes and acute myelopathies. Infarction of the conus medullaris is particularly rare and often under-recognised in clinical practice [ 1 , 2 ]. The conus, located at the T12–L1 vertebral levels, contains both upper and lower motor neuron structures and is supplied by a terminal vascular network, making it susceptible to ischaemic injury when perfusion is impaired [ 3 ]. Clinical presentation can be abrupt, with motor, sensory, and sphincter deficits that may mimic peripheral nervous system disorders. Such overlap often leads to diagnostic delay, especially in the absence of significant vascular risk factors. Magnetic resonance imaging (MRI) plays a key role in excluding compressive or inflammatory causes, though early ischaemic changes in the spinal cord may be subtle or absent [ 2 ]. We present a case of acute ischaemic myelopathy involving the conus medullaris in an older adult lacking major cardiovascular risk factors such as hypertension, dyslipidaemia, obesity, or a current smoking habit. This report illustrates the unusual clinical presentation, details the diagnostic reasoning, and describes functional outcomes following neurorehabilitation, adding to the sparse literature on this rare condition. Case Description and Findings A 68-year-old man with a history of smoking and resolved Pott's disease developed acute-onset paraesthesia in his left foot after waking up asymptomatic. Four hours after onset, lower limb ischaemia was ruled out in the emergency department. Over the subsequent hours, sensory and then motor symptoms progressed bilaterally, ascending to T10, with severe lumbar pain and urinary retention. Neurological examination revealed flaccid paraplegia. The Lower Extremity Motor Score (LEMS) for the right/left sides was as follows: L3: 4/3, L4: 4/3, L5 and S1: 0/0. He demonstrated hypoesthesia and areflexia in the lower limbs, with preserved upper limb function. Guillain-Barré Syndrome (GBS) was initially suspected, and cerebrospinal fluid (CSF) analysis was performed, which was unremarkable—showing no pleocytosis or albuminocytological dissociation. Empirical treatment with high-dose methylprednisolone (1 g/day for 5 days), however, yielded no improvement. MRI showed oedema at T12–L1 without compression. Serological tests were negative for autoimmune markers (anti-MOG, anti-NMO) and infectious panels. Within 24 hours, the condition progressed to complete paraplegia (LEMS: L3 0/0, L4 0/1, L5-S1 0/0), anaesthesia and analgesia with a neurological level at T10 and classified as American Spinal Injury Association Impairment Scale (AIS) A. Thoracoabdominal CT and cardiac evaluation showed only mild aortoiliac atheromatosis, with no embolic source identified. Under suspicion of ischaemia of the conus medullaris, prophylaxis with acetylsalicylic acid and statin therapy was initiated. Follow-up MRI at two weeks showed involution of the conus and decreased signal abnormality, consistent with evolving ischaemia (Fig. 1 ). (Placeholder for Fig. 1 ) Seven weeks post-onset, the individual was admitted to rehabilitation with paraplegia at the L1 level (AIS A). Initial rehabilitation assessment revealed mild motor strength at the L2–L3 myotomes (psoas and quadriceps strength: 1 on the right, 2 on the left) and absent sphincter control. Sensation was preserved up to L1. A 10-week MRI demonstrated resolution of the swelling and new atrophy of the T11–L1 segment, with necrotic-malacic changes. At 12 weeks, motor strength improved to grade 2 (right) and grade 3 (left) in the psoas and quadriceps (L2–L3), with no improvement at L4–S1 bilaterally. Intermittent catheterisation was required due to persistent urinary incontinence. He experienced neuropathic pain below the knees, which was controlled with gabapentin. Although non-ambulatory, he achieved independence in basic activities of daily living using a self-propelled wheelchair and was able to take a few steps with an orthosis and a walker. Discussion Our case, characterised by abrupt unilateral sensory onset that rapidly progressed to bilateral deficits with early urinary incontinence, a normal CSF analysis that excluded inflammatory or infectious aetiologies, and compatible sequential MRI changes, is most consistent with ischaemic injury of the conus medullaris. Epidemiological, Clinical and Diagnostic Features Ischaemic myelopathy represents 6–8% of acute myelopathies and 0.3-1% of strokes. Conus medullaris infarctions (T12-L1) are exceptionally rare [ 1 , 2 ], and their clinical presentation can mimic Guillain-Barré syndrome [ 4 ], delaying diagnosis. However, acute urinary retention, T10 sensory level, and normal cerebrospinal fluid distinguished this central process from peripheral mimics, supporting spinal ischaemia. Spinal cord infarction typically affects younger individuals and women more than cerebral stroke. Lower thoracic segments are most often involved [ 5 ]. Classic features include abrupt-onset pain in 60–70% of cases, localised on the affected dermatomal level [ 6 ], followed by weakness, sensory loss, and sphincter dysfunction, peaking within 12–24 hours. Novy et al. report 59% of segmental back pain and over 80% of radicular radiation [ 7 ]. Our patient’s evolution—from unilateral paraesthesia to bilateral symptoms with lumbar pain and peaking within 12–24 hours—fits this pattern. Additionally, the absence of inflammatory markers (normal CSF, negative serologies), combined with MRI showing evolving oedema without compression, helped exclude other aetiologies such as compressive myelopathies, tumours/metastases, vascular malformations, demyelinating disorders [ 8 ], or mimics like GBS. Aetiological Insights and Diagnostic Pitfalls Spinal cord infarctions can result from various conditions, such as aortic disease, embolism, vertebral dissection, disc-induced radicular artery compression, or hypercoagulable states, including antiphospholipid syndrome and malignancy. Up to 30% remain cryptogenic [ 3 , 5 ]; our individual had only mild atheromatosis, which suggests this category. Involvement of the conus medullaris may reflect vulnerability of the terminal supply zone of the artery of Adamkiewicz, which typically arises between T8–L1 [ 3 ]. MRI is not very sensitive in detecting acute spinal cord ischaemia but remains essential to rule out other causes. Conus infarctions lack specific MRI markers, often delaying diagnosis. The "snake-eyes sign"—bilateral symmetric T2 hyperintensities on axial sequences—may suggest poor prognosis when present [ 9 ]. In atypical presentations, integrating clinical features with imaging evolution, including diffusion-weighted sequences–which may support the diagnosis despite common susceptibility artifacts–, and CSF analysis remains essential, particularly when no clear aetiology is found. Prognostic Implications and Rehabilitation Predicting outcomes in spinal cord infarction is challenging. Poor prognostic indicators include AIS classification, bladder dysfunction, proprioceptive loss, older age, female sex, and lack of improvement within the first 24 hours [ 5 , 10 ]. Additionally, delayed admission to rehabilitation has been associated with increased complication risk [ 10 ]. Functional recovery tends to favour motor over sensory or sphincter domains, with 70% showing some improvement but persistent gait impairment or bladder dysfunction remaining common [ 7 ]. Our individual's presentation with complete paraplegia (AIS A), concomitant urinary and faecal incontinence, and minimal early recovery would, therefore, typically indicate a poor functional outcome based on these established parameters. However, longitudinal studies have demonstrated that meaningful late recovery can occur even in severe cases, with 41% of initially wheelchair-dependent patients eventually regaining ambulatory capacity [ 11 , 12 ], and 33% recovering bladder function [ 12 ]. Our patient's partial motor recovery at the L2-L3 myotomes after 12 weeks, though modest, aligns with these observations and supports the need for sustained rehabilitation effort. Conclusions Acute ischaemic myelopathy of the conus medullaris represents a rare neurological emergency requiring prompt recognition. The rarity of this condition should not rule out its consideration in the differential diagnosis of acute paraplegia. It is important to maintain suspicion for spinal cord infarction when patients present with sudden-onset paraesthesia rapidly progressing to bilateral deficits, particularly with early sphincter dysfunction and severe segmental pain. The clinical presentation can closely mimic conditions such as GBS or other conus medullaris affectation aetiologies, making careful neurological examination and appropriate imaging essential for accurate diagnosis. While prognosis remains reserved in cases with complete paraplegia and sphincter involvement, the potential for significant functional improvement should not be underestimated. Early rehabilitation and continuous therapeutic efforts may lead to significant benefits, as demonstrated by the partial motor recovery observed in this patient. Clinicians should maintain awareness of conus medullaris ischaemic myelopathy as a potential cause of acute spinal cord dysfunction, even without major vascular risk factors. Declarations Ethics approval and consent to participate Not applicable. Consent for publication Written informed consent was obtained from the patient for publication of this case report and accompanying images. Availability of data and materials No datasets were generated or analysed during the current study. Competing interests The authors declare that they have no competing interests. Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors. Authors’ contributions FMB extracted the clinical data and drafted the manuscript. JP contributed to the development of the discussion section. HK reviewed and critically revised the manuscript. All authors read and approved the final manuscript. Acknowledgements Work performed at XXXX. References Weng YC, Chin SC, Wu YY, Kuo HC. Clinical, neuroimaging, and nerve conduction characteristics of spontaneous Conus Medullaris infarction. BMC Neurol. 2019 Dec;19(1):328. Tan YJ, Manohararaj N. Isolated Infarctions of the Conus Medullaris: Clinical Features and Outcomes. Journal of Stroke and Cerebrovascular Diseases. 2021 Oct;30(10):106055. Alektoroff K, Kettner M, Papanagiotou P. Spinale Ischämie. Radiologe. 2021 Mar;61(3):263–6. Tham SL, Prasad K, Umapathi T. Guillain–Barré syndrome mimics. Brain and Behavior. 2018 May;8(5):e00960. Nasr DM, Rabinstein A. Spinal Cord Infarcts: Risk Factors, Management, and Prognosis. Curr Treat Options Neurol. 2017 Aug;19(8):28. Vargas MI, Gariani J, Sztajzel R, Barnaure-Nachbar I, Delattre BM, Lovblad KO, et al. Spinal Cord Ischemia: Practical Imaging Tips, Pearls, and Pitfalls. AJNR Am J Neuroradiol. 2015 May;36(5):825–30. Novy J, Carruzzo A, Maeder P, Bogousslavsky J. Spinal Cord Ischemia: Clinical and Imaging Patterns, Pathogenesis, and Outcomes in 27 Patients. Arch Neurol. 2006 Aug 1;63(8):1113. Yadav N, Pendharkar H, Kulkarni GB. Spinal Cord Infarction: Clinical and Radiological Features. Journal of Stroke and Cerebrovascular Diseases. 2018 Oct;27(10):2810–21. Zhang QY, Xu LY, Wang ML, Cao H, Ji XF. Spontaneous conus infarction with ‘snake-eye appearance’ on magnetic resonance imaging: A case report and literature review. World J Clin Cases. 2023 Mar 26;11(9):2074–83. Bonavita J, Torre M, Capirossi R, Baroncini I, Brunelli E, Chiarottini G, et al. Outcomes Following Ischemic Myelopathies and Traumatic Spinal Injury. Topics in Spinal Cord Injury Rehabilitation. 2017 Oct;23(4):368–76. Nedeltchev K, Loher TJ, Stepper F, Arnold M, Schroth G, Mattle HP, et al. Long-Term Outcome of Acute Spinal Cord Ischemia Syndrome. Stroke. 2004 Feb;35(2):560–5. Robertson CE, Brown RD, Wijdicks EFM, Rabinstein AA. Recovery after spinal cord infarcts: Long-term outcome in 115 patients. Neurology. 2012 Jan 10;78(2):114–21. 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. 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-7398122","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":520408505,"identity":"1137e0e6-1037-49be-bf88-8d364bcbfbb6","order_by":0,"name":"Fernando Martins Braga","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA3ElEQVRIiWNgGAWjYBAC9gYQacDAwE+0Fp4DQOIAUItkAwNjwwHitYAsOkC0FrHDzz5/KLhjb3x+jfnjjzl2eeYMzA8f3cCnRTrNeMYBg2eJ2268MWw4uC252LKBzdg4B48We+kEY6BfDieY3TgD0sKcuOEAD5s0Pi080umfQVrsjWeAtdQToyUHbAvjBv4ekJbDRGkpZjhjcDhxxg22whlntx1P3HCYgF+ADtvMUPHnsD1//+ENHyq3VSduON788DE+LQggkQBlMBOlHAT4DxCtdBSMglEwCkYYAAAQYFUHEYSIhQAAAABJRU5ErkJggg==","orcid":"","institution":"Fundació Institut Guttmann Hospital de Neurorehabilitació","correspondingAuthor":true,"prefix":"","firstName":"Fernando","middleName":"Martins","lastName":"Braga","suffix":""},{"id":520408506,"identity":"83fcb92d-f6b4-494d-9631-d3eae80fa192","order_by":1,"name":"Javier Pizarro","email":"","orcid":"","institution":"Hospital Clínico Universidad de Chile","correspondingAuthor":false,"prefix":"","firstName":"Javier","middleName":"","lastName":"Pizarro","suffix":""},{"id":520408507,"identity":"e81c33ef-7fb7-47a5-b6d7-ef0e36b4b8b0","order_by":2,"name":"Hatice Kumru","email":"","orcid":"","institution":"Fundació Institut Guttmann Hospital de Neurorehabilitació","correspondingAuthor":false,"prefix":"","firstName":"Hatice","middleName":"","lastName":"Kumru","suffix":""}],"badges":[],"createdAt":"2025-08-18 09:38:18","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-7398122/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-7398122/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":92252059,"identity":"fd775592-00b5-4848-9a4b-88ab5e2e8b48","added_by":"auto","created_at":"2025-09-26 10:48:54","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":615712,"visible":true,"origin":"","legend":"\u003cp\u003eSerial sagittal T2-weighted MRI findings in evolving conus medullaris ischaemia. (A) Day 1: Subtle thickening and oedema of the conus medullaris with associated myelopathic changes (\u003cem\u003earrowhead\u003c/em\u003e); no evidence of spinal cord compression. (B) Two weeks after symptom onset: Visible swelling of the conus medullaris lesion. The evolution is most consistent with a spinal cord infarction (\u003cem\u003earrowhead\u003c/em\u003e); an inflammatory aetiology is considered less likely. (C) Ten weeks after symptom onset: Resolution of oedema with volume loss (atrophy) and persistent T2 hyperintensity (\u003cem\u003earrowhead\u003c/em\u003e), consistent with chronic myelomalacia.\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-7398122/v1/79a5b19b50ed052808b4ba3e.png"},{"id":92252076,"identity":"4705b772-ec8b-4c3c-abf7-22000053e6af","added_by":"auto","created_at":"2025-09-26 10:48:59","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1817601,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-7398122/v1/46f87149-fd2c-4a03-ba8e-4d3d09f3adcb.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"A rare clinical presentation of acute ischaemic myelopathy of the conus medullaris: a case report","fulltext":[{"header":"Background","content":"\u003cp\u003eSpinal cord infarction is an uncommon neurological emergency, representing a small fraction of all strokes and acute myelopathies. Infarction of the conus medullaris is particularly rare and often under-recognised in clinical practice [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e, \u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. The conus, located at the T12\u0026ndash;L1 vertebral levels, contains both upper and lower motor neuron structures and is supplied by a terminal vascular network, making it susceptible to ischaemic injury when perfusion is impaired [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e].\u003c/p\u003e\u003cp\u003eClinical presentation can be abrupt, with motor, sensory, and sphincter deficits that may mimic peripheral nervous system disorders. Such overlap often leads to diagnostic delay, especially in the absence of significant vascular risk factors. Magnetic resonance imaging (MRI) plays a key role in excluding compressive or inflammatory causes, though early ischaemic changes in the spinal cord may be subtle or absent [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e].\u003c/p\u003e\u003cp\u003eWe present a case of acute ischaemic myelopathy involving the conus medullaris in an older adult lacking major cardiovascular risk factors such as hypertension, dyslipidaemia, obesity, or a current smoking habit. This report illustrates the unusual clinical presentation, details the diagnostic reasoning, and describes functional outcomes following neurorehabilitation, adding to the sparse literature on this rare condition.\u003c/p\u003e"},{"header":"Case Description and Findings","content":"\u003cp\u003eA 68-year-old man with a history of smoking and resolved Pott's disease developed acute-onset paraesthesia in his left foot after waking up asymptomatic. Four hours after onset, lower limb ischaemia was ruled out in the emergency department. Over the subsequent hours, sensory and then motor symptoms progressed bilaterally, ascending to T10, with severe lumbar pain and urinary retention. Neurological examination revealed flaccid paraplegia. The Lower Extremity Motor Score (LEMS) for the right/left sides was as follows: L3: 4/3, L4: 4/3, L5 and S1: 0/0. He demonstrated hypoesthesia and areflexia in the lower limbs, with preserved upper limb function.\u003c/p\u003e\u003cp\u003eGuillain-Barr\u0026eacute; Syndrome (GBS) was initially suspected, and cerebrospinal fluid (CSF) analysis was performed, which was unremarkable\u0026mdash;showing no pleocytosis or albuminocytological dissociation. Empirical treatment with high-dose methylprednisolone (1 g/day for 5 days), however, yielded no improvement. MRI showed oedema at T12\u0026ndash;L1 without compression. Serological tests were negative for autoimmune markers (anti-MOG, anti-NMO) and infectious panels. Within 24 hours, the condition progressed to complete paraplegia (LEMS: L3 0/0, L4 0/1, L5-S1 0/0), anaesthesia and analgesia with a neurological level at T10 and classified as American Spinal Injury Association Impairment Scale (AIS) A.\u003c/p\u003e\u003cp\u003eThoracoabdominal CT and cardiac evaluation showed only mild aortoiliac atheromatosis, with no embolic source identified. Under suspicion of ischaemia of the conus medullaris, prophylaxis with acetylsalicylic acid and statin therapy was initiated.\u003c/p\u003e\u003cp\u003eFollow-up MRI at two weeks showed involution of the conus and decreased signal abnormality, consistent with evolving ischaemia (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e).\u003c/p\u003e\u003cp\u003e\u003c/p\u003e\u003cp\u003e(Placeholder for Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e)\u003c/p\u003e\u003cp\u003eSeven weeks post-onset, the individual was admitted to rehabilitation with paraplegia at the L1 level (AIS A). Initial rehabilitation assessment revealed mild motor strength at the L2\u0026ndash;L3 myotomes (psoas and quadriceps strength: 1 on the right, 2 on the left) and absent sphincter control. Sensation was preserved up to L1. A 10-week MRI demonstrated resolution of the swelling and new atrophy of the T11\u0026ndash;L1 segment, with necrotic-malacic changes.\u003c/p\u003e\u003cp\u003eAt 12 weeks, motor strength improved to grade 2 (right) and grade 3 (left) in the psoas and quadriceps (L2\u0026ndash;L3), with no improvement at L4\u0026ndash;S1 bilaterally. Intermittent catheterisation was required due to persistent urinary incontinence. He experienced neuropathic pain below the knees, which was controlled with gabapentin. Although non-ambulatory, he achieved independence in basic activities of daily living using a self-propelled wheelchair and was able to take a few steps with an orthosis and a walker.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eOur case, characterised by abrupt unilateral sensory onset that rapidly progressed to bilateral deficits with early urinary incontinence, a normal CSF analysis that excluded inflammatory or infectious aetiologies, and compatible sequential MRI changes, is most consistent with ischaemic injury of the conus medullaris.\u003c/p\u003e\n\u003ch3\u003eEpidemiological, Clinical and Diagnostic Features\u003c/h3\u003e\n\u003cp\u003eIschaemic myelopathy represents 6\u0026ndash;8% of acute myelopathies and 0.3-1% of strokes. Conus medullaris infarctions (T12-L1) are exceptionally rare [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e, \u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e], and their clinical presentation can mimic Guillain-Barr\u0026eacute; syndrome [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e], delaying diagnosis. However, acute urinary retention, T10 sensory level, and normal cerebrospinal fluid distinguished this central process from peripheral mimics, supporting spinal ischaemia.\u003c/p\u003e\u003cp\u003eSpinal cord infarction typically affects younger individuals and women more than cerebral stroke. Lower thoracic segments are most often involved [\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]. Classic features include abrupt-onset pain in 60\u0026ndash;70% of cases, localised on the affected dermatomal level [\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e], followed by weakness, sensory loss, and sphincter dysfunction, peaking within 12\u0026ndash;24 hours. Novy et al. report 59% of segmental back pain and over 80% of radicular radiation [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e]. Our patient\u0026rsquo;s evolution\u0026mdash;from unilateral paraesthesia to bilateral symptoms with lumbar pain and peaking within 12\u0026ndash;24 hours\u0026mdash;fits this pattern. Additionally, the absence of inflammatory markers (normal CSF, negative serologies), combined with MRI showing evolving oedema without compression, helped exclude other aetiologies such as compressive myelopathies, tumours/metastases, vascular malformations, demyelinating disorders [\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e], or mimics like GBS.\u003c/p\u003e\n\u003ch3\u003eAetiological Insights and Diagnostic Pitfalls\u003c/h3\u003e\n\u003cp\u003eSpinal cord infarctions can result from various conditions, such as aortic disease, embolism, vertebral dissection, disc-induced radicular artery compression, or hypercoagulable states, including antiphospholipid syndrome and malignancy. Up to 30% remain cryptogenic [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]; our individual had only mild atheromatosis, which suggests this category. Involvement of the conus medullaris may reflect vulnerability of the terminal supply zone of the artery of Adamkiewicz, which typically arises between T8\u0026ndash;L1 [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e].\u003c/p\u003e\u003cp\u003eMRI is not very sensitive in detecting acute spinal cord ischaemia but remains essential to rule out other causes. Conus infarctions lack specific MRI markers, often delaying diagnosis. The \"snake-eyes sign\"\u0026mdash;bilateral symmetric T2 hyperintensities on axial sequences\u0026mdash;may suggest poor prognosis when present [\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e]. In atypical presentations, integrating clinical features with imaging evolution, including diffusion-weighted sequences\u0026ndash;which may support the diagnosis despite common susceptibility artifacts\u0026ndash;, and CSF analysis remains essential, particularly when no clear aetiology is found.\u003c/p\u003e\n\u003ch3\u003ePrognostic Implications and Rehabilitation\u003c/h3\u003e\n\u003cp\u003ePredicting outcomes in spinal cord infarction is challenging. Poor prognostic indicators include AIS classification, bladder dysfunction, proprioceptive loss, older age, female sex, and lack of improvement within the first 24 hours [\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e, \u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]. Additionally, delayed admission to rehabilitation has been associated with increased complication risk [\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]. Functional recovery tends to favour motor over sensory or sphincter domains, with 70% showing some improvement but persistent gait impairment or bladder dysfunction remaining common [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e].\u003c/p\u003e\u003cp\u003eOur individual's presentation with complete paraplegia (AIS A), concomitant urinary and faecal incontinence, and minimal early recovery would, therefore, typically indicate a poor functional outcome based on these established parameters. However, longitudinal studies have demonstrated that meaningful late recovery can occur even in severe cases, with 41% of initially wheelchair-dependent patients eventually regaining ambulatory capacity [\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e, \u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e], and 33% recovering bladder function [\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e]. Our patient's partial motor recovery at the L2-L3 myotomes after 12 weeks, though modest, aligns with these observations and supports the need for sustained rehabilitation effort.\u003c/p\u003e"},{"header":"Conclusions","content":"\u003cp\u003eAcute ischaemic myelopathy of the conus medullaris represents a rare neurological emergency requiring prompt recognition. The rarity of this condition should not rule out its consideration in the differential diagnosis of acute paraplegia. It is important to maintain suspicion for spinal cord infarction when patients present with sudden-onset paraesthesia rapidly progressing to bilateral deficits, particularly with early sphincter dysfunction and severe segmental pain. The clinical presentation can closely mimic conditions such as GBS or other conus medullaris affectation aetiologies, making careful neurological examination and appropriate imaging essential for accurate diagnosis.\u003c/p\u003e\u003cp\u003eWhile prognosis remains reserved in cases with complete paraplegia and sphincter involvement, the potential for significant functional improvement should not be underestimated. Early rehabilitation and continuous therapeutic efforts may lead to significant benefits, as demonstrated by the partial motor recovery observed in this patient. Clinicians should maintain awareness of conus medullaris ischaemic myelopathy as a potential cause of acute spinal cord dysfunction, even without major vascular risk factors.\u003c/p\u003e"},{"header":"Declarations","content":"\u003ch2\u003eEthics approval and consent to participate\u003c/h2\u003e\n\u003cp\u003eNot applicable.\u0026nbsp;\u003c/p\u003e\n\u003ch2\u003eConsent for publication\u003c/h2\u003e\n\u003cp\u003eWritten informed consent was obtained from the patient for publication of this case report and accompanying images.\u003c/p\u003e\n\u003ch2\u003eAvailability of data and materials\u003c/h2\u003e\n\u003cp\u003eNo datasets were generated or analysed during the current study.\u003c/p\u003e\n\u003ch2\u003eCompeting interests\u003c/h2\u003e\n\u003cp\u003eThe authors declare that they have no competing interests.\u003c/p\u003e\n\u003ch2\u003eFunding\u003c/h2\u003e\n\u003cp\u003eThis research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.\u003c/p\u003e\n\u003ch2\u003eAuthors’ contributions\u003c/h2\u003e\n\u003cp\u003eFMB extracted the clinical data and drafted the manuscript. JP contributed to the development of the discussion section. HK reviewed and critically revised the manuscript. All authors read and approved the final manuscript.\u003c/p\u003e\n\u003ch2\u003eAcknowledgements\u003c/h2\u003e\n\u003cp\u003eWork performed at XXXX.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eWeng YC, Chin SC, Wu YY, Kuo HC. Clinical, neuroimaging, and nerve conduction characteristics of spontaneous Conus Medullaris infarction. BMC Neurol. 2019 Dec;19(1):328. \u003c/li\u003e\n\u003cli\u003eTan YJ, Manohararaj N. Isolated Infarctions of the Conus Medullaris: Clinical Features and Outcomes. Journal of Stroke and Cerebrovascular Diseases. 2021 Oct;30(10):106055. \u003c/li\u003e\n\u003cli\u003eAlektoroff K, Kettner M, Papanagiotou P. Spinale Isch\u0026auml;mie. Radiologe. 2021 Mar;61(3):263\u0026ndash;6. \u003c/li\u003e\n\u003cli\u003eTham SL, Prasad K, Umapathi T. Guillain\u0026ndash;Barr\u0026eacute; syndrome mimics. Brain and Behavior. 2018 May;8(5):e00960. \u003c/li\u003e\n\u003cli\u003eNasr DM, Rabinstein A. Spinal Cord Infarcts: Risk Factors, Management, and Prognosis. Curr Treat Options Neurol. 2017 Aug;19(8):28. \u003c/li\u003e\n\u003cli\u003eVargas MI, Gariani J, Sztajzel R, Barnaure-Nachbar I, Delattre BM, Lovblad KO, et al. Spinal Cord Ischemia: Practical Imaging Tips, Pearls, and Pitfalls. AJNR Am J Neuroradiol. 2015 May;36(5):825\u0026ndash;30. \u003c/li\u003e\n\u003cli\u003eNovy J, Carruzzo A, Maeder P, Bogousslavsky J. Spinal Cord Ischemia: Clinical and Imaging Patterns, Pathogenesis, and Outcomes in 27 Patients. Arch Neurol. 2006 Aug 1;63(8):1113. \u003c/li\u003e\n\u003cli\u003eYadav N, Pendharkar H, Kulkarni GB. Spinal Cord Infarction: Clinical and Radiological Features. Journal of Stroke and Cerebrovascular Diseases. 2018 Oct;27(10):2810\u0026ndash;21. \u003c/li\u003e\n\u003cli\u003eZhang QY, Xu LY, Wang ML, Cao H, Ji XF. Spontaneous conus infarction with \u0026lsquo;snake-eye appearance\u0026rsquo; on magnetic resonance imaging: A case report and literature review. World J Clin Cases. 2023 Mar 26;11(9):2074\u0026ndash;83. \u003c/li\u003e\n\u003cli\u003eBonavita J, Torre M, Capirossi R, Baroncini I, Brunelli E, Chiarottini G, et al. Outcomes Following Ischemic Myelopathies and Traumatic Spinal Injury. Topics in Spinal Cord Injury Rehabilitation. 2017 Oct;23(4):368\u0026ndash;76. \u003c/li\u003e\n\u003cli\u003eNedeltchev K, Loher TJ, Stepper F, Arnold M, Schroth G, Mattle HP, et al. Long-Term Outcome of Acute Spinal Cord Ischemia Syndrome. Stroke. 2004 Feb;35(2):560\u0026ndash;5. \u003c/li\u003e\n\u003cli\u003eRobertson CE, Brown RD, Wijdicks EFM, Rabinstein AA. Recovery after spinal cord infarcts: Long-term outcome in 115 patients. Neurology. 2012 Jan 10;78(2):114\u0026ndash;21. \u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":true,"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":"spinal cord injury, ischaemic SCI, conus medullaris, differential diagnoses, acute myelopathy","lastPublishedDoi":"10.21203/rs.3.rs-7398122/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-7398122/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eBackground:\u003c/strong\u003e Conus medullaris infarction is a rare cause of acute spinal cord injury that can mimic Guillain-Barré syndrome (GBS) or cauda equina syndrome. Early diagnosis is important for management and prognosis. We report a case in a patient without major vascular risk factors.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCase presentation:\u003c/strong\u003e A 68-year-old man with a history of Pott's disease and smoking presented with sudden left foot numbness that progressed within hours to bilateral leg weakness, back pain, urinary retention, and a T10 sensory level. Examination showed complete flaccid paraplegia (American Spinal Injury Association Impairment Scale, AIS, Grade A) with normal upper limb function. MRI revealed T12–L1 conus medullaris oedema without evidence of compression. Cerebrospinal fluid analysis and autoimmune/infectious workup were unremarkable. High-dose methylprednisolone was administered for suspected Guillain–Barré syndrome, with minimal clinical improvement. CT angiography showed only mild aortoiliac atherosclerosis. Acute ischaemic myelopathy of the conus medullaris was diagnosed. Rehabilitation started at 7 weeks led to partial recovery of strength in the hip flexors and quadriceps, as well as independent wheelchair mobility at 12 weeks.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConclusions:\u003c/strong\u003e This case demonstrates the diagnostic challenges of conus medullaris infarction. Clinicians should consider spinal cord ischaemia in acute paraplegia with early urinary retention and normal CSF, even in individuals without significant vascular risk factors. Rehabilitation can produce significant recovery despite poor initial presentation.\u003c/p\u003e","manuscriptTitle":"A rare clinical presentation of acute ischaemic myelopathy of the conus medullaris: a case report","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-09-26 10:48:50","doi":"10.21203/rs.3.rs-7398122/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"
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