Acute Disseminated Encephalomyelitis following Thoracic Endovascular Aortic Repair: An unusual presentation

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This paper reports the case of a patient who developed acute disseminated encephalomyelitis with hemorrhagic white matter abnormalities after thoracic endovascular aortic repair.

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This paper reports an imaging-focused fatal case of acute disseminated encephalomyelitis (ADEM) in a 62-year-old patient after thoracic endovascular aortic repair (TEVAR) for type B aortic dissection, with onset about 2 weeks after intubation/sedation and no recent infection or immunization history. MRI showed multifocal, patchy confluent T2/FLAIR hyperintense white matter lesions with diffusion restriction and some contrast enhancement, plus susceptibility-weighted evidence of hemosiderin deposition; cerebrospinal fluid had lymphocytic pleocytosis with mildly elevated protein and no oligoclonal bands, and EEG showed generalized slowing. The authors emphasize that critical-care neurological assessment and timing can be challenging and note that unlike children, adult ADEM often lacks an identified trigger. Relevance to endometriosis: this paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index, though it is not about pelvic inflammatory disease.

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Abstract

Abstract Acute disseminated encephalomyelitis (ADEM) is a central nervous system demyelinating condition caused by viral or bacterial infections or immunizations. The postulated aetiology is an autoimmune reaction against myelin components; however, the mechanistic details are yet unknown. We present the imaging findings of a patient who passed away due to the manifestations of acute disseminated encephalomyelitis. The patient initially underwent surgical repair for type B aortic dissection. 2 weeks after he had poor GCS and no motor response following multiple attempts at sedation hold in the intensive care unit. On magnetic resonance imaging, haemorrhagic white matter abnormalities were noted throughout the cerebral hemisphere indicative of an inflammatory demyelinating process. Our case emphasizes the challenges involved in evaluating emerging neurological problems following a period of intubation /sedation amongst these patients. In addition, unlike children, 50% of adult patients do not have illness or immunisation as a trigger event for this condition.
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Acute Disseminated Encephalomyelitis following Thoracic Endovascular Aortic Repair: An unusual presentation | 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 Acute Disseminated Encephalomyelitis following Thoracic Endovascular Aortic Repair: An unusual presentation Dr. Cleofina Furtado, Dr. Changrez Jadun, Dr. Sachin Srivastava, and 2 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-2082527/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 Acute disseminated encephalomyelitis (ADEM) is a central nervous system demyelinating condition caused by viral or bacterial infections or immunizations. The postulated aetiology is an autoimmune reaction against myelin components; however, the mechanistic details are yet unknown. We present the imaging findings of a patient who passed away due to the manifestations of acute disseminated encephalomyelitis. The patient initially underwent surgical repair for type B aortic dissection. 2 weeks after he had poor GCS and no motor response following multiple attempts at sedation hold in the intensive care unit. On magnetic resonance imaging, haemorrhagic white matter abnormalities were noted throughout the cerebral hemisphere indicative of an inflammatory demyelinating process. Our case emphasizes the challenges involved in evaluating emerging neurological problems following a period of intubation /sedation amongst these patients. In addition, unlike children, 50% of adult patients do not have illness or immunisation as a trigger event for this condition. Neurology Acute Disseminated Encephalomyelitis (ADEM) thoracic endovascular aortic repair (TEVAR) Computed tomography (CT) magnetic resonance imaging (MRI) Figures Figure 1 Figure 2 Figure 3 Figure 4 Background Acute Disseminated Encephalomyelitis (ADEM) is a virus or vaccine-induced monophasic inflammatory myelinating autoimmune reaction against myelin (1). ADEM often occurs relatively late after the beginning of infection and is distinguished by increased white matter damage (2). Encephalopathy with rapid neurologic impairments and brain magnetic resonance imaging (MRI) findings consistent with multifocal demyelination describe this condition (3). It is more common in children and young adults, while occurrence in middle age or elderly individuals are uncommon (4,5). SARS-CoV-2, varicella-zoster, Measles, rubella, mumps, Epstein Barr virus, coxsackievirus, cytomegalovirus, hepatitis A, and herpes simplex virus are all viral diseases linked to ADEM (6–9). Mycoplasma pneumonia is the most common, with leptospira, Borrelia borgdorgeri, and group-A beta-hemolytic streptococci being the other bacterial illnesses (7,9). Anti-rabies, Pertussis, diphtheria, measles, mumps, rubella, and influenza immunizations are also linked to ADEM with growing cases also noted post-COVID-19 vaccination in the recent era (9,10). We present this unique case of ADEM which occurred following thoracic endovascular aortic repair. Because of its unique occurrence, presentation of the disease and prognosis, it was found worthy to be mentioned. Case Description A 62-year-old patient was hospitalised in the intensive care unit following an elective thoracic endovascular aortic repair of type B aortic dissection. He was intubated and ventilated subsequently due to worsening breathing and requirement for oxygen. Chest radiographs (Fig 1 a) and computed tomography did not reveal any untoward. There was no history of immunization, infectious or vaccination in recent days. He had no known chronic illness or drug use. Magnetic resonance imaging (MRI) was performed, as he had poor GCS and no motor response following multiple attempts at sedation hold with no recovery of consciousness which was 2 weeks following the TEVAR. It showed multiple patchy confluent T2WI and FLAIR hyperintense lesions (Fig 2) involving cerebral white matter (callosal, pericallosal, deep, periventricular, basal ganglia), brainstem and bilateral cerebellar peduncles. These lesions demonstrated diffusion restriction (Fig 3) with some showing avid contrast enhancement. Susceptibility weighted imaging sequence (Fig 4) demonstrated multiple foci of hemosiderin deposition in the cerebral cortices bilaterally, thalamus and cerebellar hemispheres. Findings were concluded to be characteristic of demyelination such as acute disseminated encephalomyelitis (ADEM). Lumber punction revealed lymphocytic pleocytosis with slightly raised protein and absence of oligoclonal bands. The EEG demonstrated generalised slowing of sleep activity. He also developed multi-organ failure with anuria requiring continuous hemodiafiltration. Over the next few days, he remained critically unwell with a high level of inflammatory markers and no signs of neurological improvement. Following a discussion with his family, it was decided to withdraw support following which he passed away. Discussion TEVAR has enabled a less invasive method to treat a variety of thoracic aortic diseases and is generally performed in surgically repaired type A dissection and those with a complicated type B dissection (11). ADEM after TEVAR has not yet been documented. Radiopaque contrast medium might have triggered an immune-mediated response, resulting in ADEM. ADEM is known to occur as a result of an inflammatory response to a foreign antigen that causes vascular congestion and increased permeability of the vasculature of the central nervous system (12). This is expected to set off an inflammatory cascade including oedema, inflammatory cell infiltration and perivenous haemorrhage leading to gliosis, demyelination and necrosis (13). Neurologic symptoms are variable, with the majority exhibiting encephalopathy, which includes confusion, and lethargy, with difficulty awakening from sedation as the most common presentation (14). These characteristics have the potential to hide an underlying inflammatory central nervous system condition in the critical care setting, where clinical neurological assessment is particularly difficult (6). In addition, para infectious neuropathological processes often manifest after a latent time following an infection, raising the clinical challenge of when to evaluate emerging neurological problems following a period of intubation along with challenges involved in transporting the patient for more complex imaging studies (15). Histology is characterised by tiny (5mm) white matter lesions with macrophage clusters and a variety of related axonal damage (15). The widespread haemorrhagic white matter lesions identified have some of the characteristic features of acute haemorrhagic necrotizing encephalitis which is known to have a fulminant (16) . MRI imaging lesions show lesions with high sensitivity and may help rule out other entities that look similar, such as multiple sclerosis, which displays lesions around the deep white matter, near the corpus callosum or calloso septal junction (17). FLAIR hyper-intensities in deep white matter and at the grey/white matter interface with diffusion restriction are typical MRI lesions. Punctate or rim enhancing lesions are seen on post-contrast enhancement (18). Conclusion Whilst infection and vaccination are the most common associations for ADEM, we suspect that radiopaque contrast material might have been a possible immunological trigger element in this case. The patient's clinical course demonstrates that during lengthy hospitalizations, neurological manifestations of ADEM might arise which are especially difficult to assess and recognize in critically unwell patients. Declarations Conflict of interest: None declared. I/We confirm that written informed consent for the case to be published (including radiological images and case history) was obtained from the patient’s next of kin for publication of this case report. References Baum PA, Barkovich AJ, Koch TK, Berg BO. Deep gray matter involvement in children with acute disseminated encephalomyelitis. American Journal of Neuroradiology. 1994;15(7):1275–83. Hartung HP, Grossman RI. Adem: Distinct disease or part of the MS spectrum? Vol. 56, Neurology. 2001. p. 1257–60. Akç Ay N, Bektaş G, Menentoǧ Lu ME, Oǧ Ur M, Sofuoǧ Lu AEİR, Palabiyik FB, et al. COVID-19-associated Acute Disseminated Encephalomyelitis-like Disease in 2 Children. Pediatric Infectious Disease Journal. 2021;40(11):e445–50. Wang PN, Fuh JL, Liu HC, Wang SJ. Acute disseminated encephalomyelitis in middle-aged or elderly patients. Eur Neurol. 1996;36(4):219–23. Stonehouse M, Gupte G, Wassmer E, Whitehouse WP. Acute disseminated encephalomyelitis: Recognition in the hands of general paediatricians. Vol. 88, Archives of Disease in Childhood. 2003. p. 122–4. Langley L, Zeicu C, Whitton L, Pauls M. Acute disseminated encephalomyelitis (ADEM) associated with COVID-19. BMJ Case Rep. 2020;13(12):e239597. Noorbakhsh F, Johnson RT, Emery D, Power C. Acute Disseminated Encephalomyelitis: Clinical and Pathogenesis Features. Vol. 26, Neurologic Clinics. 2008. Torisu H. Epidemiology of acute disseminated encephalomyelitis. In: Acute Encephalopathy and Encephalitis in Infancy and Its Related Disorders. 2018. Zelada-Ríos L, Pacheco-Barrios K, Galecio-Castillo M, Yamunaqué-Chunga C, Álvarez-Toledo K, Otiniano-Sifuentes R. Acute disseminated encephalomyelitis and COVID-19: A systematic synthesis of worldwide cases. Vol. 359, Journal of Neuroimmunology. 2021. p. 577674. Permezel F, Borojevic B, Lau S, de Boer HH. Acute disseminated encephalomyelitis (ADEM) following recent Oxford/AstraZeneca COVID-19 vaccination. Forensic Sci Med Pathol. 2022;18(1):74–9. Nation DA, Wang GJ. TEVAR: Endovascular Repair of the Thoracic Aorta. Semin Intervent Radiol. 2015;32(3):265–71. McMahon EJ, Bailey SL, Castenada CV, Waldner H, Miller SD. Epitope spreading initiates in the CNS in two mouse models of multiple sclerosis. Nat Med. 2005;11(3):335–9. LD W, LK W, DF B, TM M. Adult Onset Acute Disseminated Encephalomyelitis Following Appendicitis: A Case Report. J Neurol Neurosci. 2016;7:S3. Manzano GS, McEntire CRS, Martinez-Lage M, Mateen FJ, Hutto SK. Acute Disseminated Encephalomyelitis and Acute Hemorrhagic Leukoencephalitis Following COVID-19: Systematic Review and Meta-synthesis. Neurology(R) neuroimmunology & neuroinflammation. 2021;8(6):e1080. Reichard RR, Kashani KB, Boire NA, Constantopoulos E, Guo Y, Lucchinetti CF. Neuropathology of COVID-19: a spectrum of vascular and acute disseminated encephalomyelitis (ADEM)-like pathology. Acta Neuropathol. 2020;140(1):1–6. Xu J, Zhong S, Liu J, Li L, Li Y, Wu X, et al. Detection of severe acute respiratory syndrome coronavirus in the brain: Potential role of the chemokine mig in pathogenesis. Clinical Infectious Diseases. 2005;41(8):1089–96. Singh S, Alexander M, Korah IP. Acute disseminated encephalomyelitis: MR imaging features. American Journal of Roentgenology. 1999;173(4). Marin SE, Callen DJA. The Magnetic Resonance Imaging Appearance of Monophasic Acute Disseminated Encephalomyelitis. An Update Post Application of the 2007 Consensus Criteria. Vol. 23, Neuroimaging Clinics of North America. 2013. p. 245–66. 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. 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ADEM often occurs relatively late after the beginning of infection and is distinguished by increased white matter damage (2). \u0026nbsp;Encephalopathy with rapid neurologic impairments and brain magnetic resonance imaging (MRI) findings consistent with multifocal demyelination describe this condition (3). \u0026nbsp;It is more common in children and young adults, while occurrence in middle age or elderly individuals are uncommon (4,5).\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eSARS-CoV-2, varicella-zoster, Measles, rubella, mumps, Epstein Barr virus, coxsackievirus, cytomegalovirus, hepatitis A, and herpes simplex virus are all viral diseases linked to ADEM (6\u0026ndash;9). Mycoplasma pneumonia is the most common, with leptospira, Borrelia borgdorgeri, and group-A beta-hemolytic streptococci being the other bacterial illnesses (7,9).\u0026nbsp;Anti-rabies, Pertussis, diphtheria, measles, mumps, rubella, and influenza immunizations are also linked to ADEM with growing cases also noted post-COVID-19 vaccination in the recent era (9,10).\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eWe present this unique case of ADEM which occurred following thoracic endovascular aortic repair. Because of its unique occurrence, presentation of the disease and prognosis, it was found worthy to be mentioned.\u0026nbsp;\u003c/p\u003e"},{"header":"Case Description","content":"\u003cp\u003eA 62-year-old patient was hospitalised in the intensive care unit following an elective thoracic endovascular aortic repair of type B aortic dissection. He was intubated and ventilated subsequently due to worsening breathing and requirement for oxygen. Chest radiographs (Fig 1 a) and computed tomography did not reveal any untoward. There was no history of immunization, infectious or vaccination in recent days. He had no known chronic illness or drug use. Magnetic resonance imaging (MRI) was performed, as he had poor GCS and no motor response following multiple attempts at sedation hold with no recovery of consciousness which was 2 weeks following the TEVAR. It showed multiple patchy confluent T2WI and FLAIR hyperintense lesions (Fig 2) involving cerebral white matter (callosal, pericallosal, deep, periventricular, basal ganglia), brainstem and bilateral cerebellar peduncles. These lesions demonstrated diffusion restriction (Fig 3) with some showing avid contrast enhancement. \u0026nbsp;Susceptibility weighted imaging sequence (Fig 4) demonstrated multiple foci of hemosiderin deposition in the cerebral cortices bilaterally, thalamus and cerebellar hemispheres. Findings were concluded to be characteristic of demyelination such as acute disseminated encephalomyelitis (ADEM). Lumber punction revealed lymphocytic pleocytosis with slightly raised protein and absence of oligoclonal bands.\u0026nbsp;The EEG demonstrated generalised slowing of sleep activity.\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eHe also developed multi-organ failure with anuria requiring continuous hemodiafiltration. Over the next few days, he remained critically unwell with a high level of inflammatory markers and no signs of neurological improvement. Following a discussion with his family, it was decided to withdraw support following which he passed away.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eTEVAR has enabled a less invasive method to treat a variety of thoracic aortic diseases and is generally performed in surgically repaired type A dissection and those with a complicated type B dissection (11). ADEM after TEVAR has not yet been documented. Radiopaque contrast medium might have triggered an immune-mediated response, resulting in ADEM.\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eADEM is known to occur as a result of an inflammatory response to a foreign antigen that causes vascular congestion and increased permeability of the vasculature of the central nervous system (12). This is expected to set off an inflammatory cascade including oedema, inflammatory cell infiltration and perivenous haemorrhage leading to gliosis, demyelination and necrosis (13).\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eNeurologic symptoms are variable, with the majority exhibiting encephalopathy, which includes confusion, and lethargy, with difficulty awakening from sedation as the most common presentation (14). These characteristics have the potential to hide an underlying inflammatory central nervous system condition in the critical care setting, where clinical neurological assessment is particularly difficult (6). \u0026nbsp;In addition, para infectious neuropathological processes often manifest after a latent time following an infection, raising the clinical challenge of when to evaluate emerging neurological problems following a period of intubation along with challenges involved in transporting the patient for more complex imaging studies (15). \u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eHistology is characterised by tiny (5mm) white matter lesions with macrophage clusters and a variety of related axonal damage (15). The widespread haemorrhagic white matter lesions identified have some of the characteristic features of acute haemorrhagic necrotizing encephalitis which is known to have a fulminant (16) .\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eMRI imaging lesions show lesions with high sensitivity and may help rule out other entities that look similar, such as multiple sclerosis, which displays lesions around the deep white matter, near the corpus callosum or calloso septal junction (17). FLAIR hyper-intensities in deep white matter and at the grey/white matter interface with diffusion restriction are typical MRI lesions. Punctate or rim enhancing lesions are seen on post-contrast enhancement (18).\u0026nbsp;\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eWhilst infection and vaccination are the most common associations for ADEM, we suspect that radiopaque contrast material might have been a possible immunological trigger element in this case. The patient\u0026apos;s clinical course demonstrates that during lengthy hospitalizations, neurological manifestations of ADEM might arise which are especially difficult to assess and recognize in critically unwell patients.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eConflict of interest:\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNone declared.\u003c/p\u003e\nI/We confirm that written informed consent for the case to be published (including radiological images and case history) was obtained from the patient’s next of kin for publication of this case report."},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eBaum PA, Barkovich AJ, Koch TK, Berg BO. Deep gray matter involvement in children with acute disseminated encephalomyelitis. American Journal of Neuroradiology. 1994;15(7):1275\u0026ndash;83.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHartung HP, Grossman RI. Adem: Distinct disease or part of the MS spectrum? Vol.\u0026nbsp;56, Neurology. 2001. p.\u0026nbsp;1257\u0026ndash;60.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eAk\u0026ccedil; Ay N, Bektaş G, Menentoǧ Lu ME, Oǧ Ur M, Sofuoǧ Lu AEİR, Palabiyik FB, et al. COVID-19-associated Acute Disseminated Encephalomyelitis-like Disease in 2 Children. Pediatric Infectious Disease Journal. 2021;40(11):e445\u0026ndash;50.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWang PN, Fuh JL, Liu HC, Wang SJ. Acute disseminated encephalomyelitis in middle-aged or elderly patients. Eur Neurol. 1996;36(4):219\u0026ndash;23.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eStonehouse M, Gupte G, Wassmer E, Whitehouse WP. Acute disseminated encephalomyelitis: Recognition in the hands of general paediatricians. Vol.\u0026nbsp;88, Archives of Disease in Childhood. 2003. p.\u0026nbsp;122\u0026ndash;4.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLangley L, Zeicu C, Whitton L, Pauls M. Acute disseminated encephalomyelitis (ADEM) associated with COVID-19. BMJ Case Rep. 2020;13(12):e239597.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eNoorbakhsh F, Johnson RT, Emery D, Power C. Acute Disseminated Encephalomyelitis: Clinical and Pathogenesis Features. Vol.\u0026nbsp;26, Neurologic Clinics. 2008.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eTorisu H. Epidemiology of acute disseminated encephalomyelitis. In: Acute Encephalopathy and Encephalitis in Infancy and Its Related Disorders. 2018.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eZelada-R\u0026iacute;os L, Pacheco-Barrios K, Galecio-Castillo M, Yamunaqu\u0026eacute;-Chunga C, \u0026Aacute;lvarez-Toledo K, Otiniano-Sifuentes R. Acute disseminated encephalomyelitis and COVID-19: A systematic synthesis of worldwide cases. Vol.\u0026nbsp;359, Journal of Neuroimmunology. 2021. p.\u0026nbsp;577674.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003ePermezel F, Borojevic B, Lau S, de Boer HH. Acute disseminated encephalomyelitis (ADEM) following recent Oxford/AstraZeneca COVID-19 vaccination. Forensic Sci Med Pathol. 2022;18(1):74\u0026ndash;9.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eNation DA, Wang GJ. TEVAR: Endovascular Repair of the Thoracic Aorta. Semin Intervent Radiol. 2015;32(3):265\u0026ndash;71.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMcMahon EJ, Bailey SL, Castenada CV, Waldner H, Miller SD. Epitope spreading initiates in the CNS in two mouse models of multiple sclerosis. Nat Med. 2005;11(3):335\u0026ndash;9.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLD W, LK W, DF B, TM M. Adult Onset Acute Disseminated Encephalomyelitis Following Appendicitis: A Case Report. J Neurol Neurosci. 2016;7:S3.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eManzano GS, McEntire CRS, Martinez-Lage M, Mateen FJ, Hutto SK. Acute Disseminated Encephalomyelitis and Acute Hemorrhagic Leukoencephalitis Following COVID-19: Systematic Review and Meta-synthesis. Neurology(R) neuroimmunology \u0026amp; neuroinflammation. 2021;8(6):e1080.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eReichard RR, Kashani KB, Boire NA, Constantopoulos E, Guo Y, Lucchinetti CF. Neuropathology of COVID-19: a spectrum of vascular and acute disseminated encephalomyelitis (ADEM)-like pathology. Acta Neuropathol. 2020;140(1):1\u0026ndash;6.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eXu J, Zhong S, Liu J, Li L, Li Y, Wu X, et al. Detection of severe acute respiratory syndrome coronavirus in the brain: Potential role of the chemokine mig in pathogenesis. Clinical Infectious Diseases. 2005;41(8):1089\u0026ndash;96.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSingh S, Alexander M, Korah IP. Acute disseminated encephalomyelitis: MR imaging features. American Journal of Roentgenology. 1999;173(4).\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMarin SE, Callen DJA. The Magnetic Resonance Imaging Appearance of Monophasic Acute Disseminated Encephalomyelitis. An Update Post Application of the 2007 Consensus Criteria. Vol.\u0026nbsp;23, Neuroimaging Clinics of North America. 2013. p.\u0026nbsp;245\u0026ndash;66.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":true,"hideJournal":true,"highlight":"","institution":"University Hospitals of North Midlands NHS Trust","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":"Acute Disseminated Encephalomyelitis (ADEM), thoracic endovascular aortic repair (TEVAR), Computed tomography (CT), magnetic resonance imaging (MRI)","lastPublishedDoi":"10.21203/rs.3.rs-2082527/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-2082527/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003eAcute disseminated encephalomyelitis (ADEM) is a central nervous system demyelinating condition caused by viral or bacterial infections or immunizations. The postulated aetiology is an autoimmune reaction against myelin components; however, the mechanistic details are yet unknown. We present the imaging findings of a patient who passed away due to the manifestations of acute disseminated encephalomyelitis. The patient initially underwent surgical repair for type B aortic dissection. 2 weeks after he had poor GCS and no motor response following multiple attempts at sedation hold in the intensive care unit. On magnetic resonance imaging, haemorrhagic white matter abnormalities were noted throughout the cerebral hemisphere indicative of an inflammatory demyelinating process.\u003c/p\u003e \u003cp\u003eOur case emphasizes the challenges involved in evaluating emerging neurological problems following a period of intubation /sedation amongst these patients. In addition, unlike children, 50% of adult patients do not have illness or immunisation as a trigger event for this condition.\u003c/p\u003e","manuscriptTitle":"Acute Disseminated Encephalomyelitis following Thoracic Endovascular Aortic Repair: An unusual presentation","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2022-09-22 01:35:21","doi":"10.21203/rs.3.rs-2082527/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":"f6add77c-80ff-4698-811b-08c364acdeac","owner":[],"postedDate":"September 22nd, 2022","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[{"id":15642497,"name":"Neurology"}],"tags":[],"updatedAt":"2022-09-22T01:35:22+00:00","versionOfRecord":[],"versionCreatedAt":"2022-09-22 01:35:21","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-2082527","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-2082527","identity":"rs-2082527","version":["v1"]},"buildId":"cBFmMYwuxLRRLfASyISRj","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}

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