مروری بر اتیولوژی و پاتوژنز سندرم انسفالوپاتی خلفی برگشت‌پذیر (PRES) در بیماران با بیماری مولتیپل اسکلروزیس (MS) و بیماری طیف نورومیلیت اپتیکا (NMOSD)

نوع مقاله : Review Article

نویسندگان

1 استاد، گروه نورولوژی، دانشگاه علوم پزشکی اصفهان، اصفهان، ایران

2 کمیته تحقیقات و فناوری دانشجویی، دانشکده‌ی پزشکی، دانشگاه علوم پزشکی اصفهان، اصفهان، ایران

10.48305/jims.v43.i821.0770

چکیده

مقاله مروری




مقدمه: سندرم انسفالوپاتی خلفی برگشت‌پذیر (Posterior Reversible Encephalopathy Syndrome) PRES یک اختلال عصبی با پاتوفیزیولوژی چندوجهی است که معمولاً با ادم وازوژنیک در تصویربرداری مغز تظاهر می‌یابد. اگرچه بروز PRES در بیماران مبتلا به ام‌اس و NMOSD نادر است، اما شناسایی عوامل اتیولوژیک و مکانیسم‌های پاتوژنز در این بیماران برای تشخیص و مدیریت بهینه بسیار حائز اهمیت است.
روش‌ها: این مطالعه با جستجوی سیستماتیک در پایگاه‌های داده PubMed، Scopus، Web of Science و Google Scholar با استفاده از کلیدواژه‌های مرتبط انجام شد.
یافته‌ها: ۱۷ گزارش موردی مرتبط شناسایی و مرور شدند. در بیماران با  NMOSDپاتوژنز PRES به طور اولیه با اختلال عملکرد سد خونی- مغزی (blood-brain barrier) BBB ناشی از حمله آنتی‌بادی‌های anti-AQP4 IgG به آستروسیت‌ها مرتبط است. به علاوه، درمان‌های رایج این بیماری مانند ریتوکسیماب (با القای آسیب اندوتلیال)، کورتیکواستروئیدها و پلاسمافرز (با القای نوسانات فشارخون) به عنوان عوامل خطر مستعدکننده قابل توجهی برای PRES شناسایی شده‌اند.در بیماران با (Multiple sclerosis) MS، التهاب اطراف عروقی و اختلال جفت‌شدگی عروقی- عصبی در سد خونی‌- مغزی، بستر مناسبی برای ایجاد PRES فراهم می‌کند. داروهایی مانند فینگولیمود (با مکانیسم آسیب اندوتلیال) و اینترفرون-بتا (از طریق القای فشارخون یا اختلال در  سد خونی- مغزی و همچنین استفاده از کورتیکواستروئیدهای، از جمله عوامل محرک بروز PRES در این بیماران هستند.
نتیجه‌گیری: اگرچه PRES یک عارضه‌ی نادر در بیماران MS و NMOSD است، اما ماهیت این بیماری‌ها که با اختلال در سد خونی- مغزی همراه است، همراه با استفاده از درمان‌های خاص، این بیماران را در معرض خطر ابتلا به PRES قرار می‌دهد.

کلیدواژه‌ها

موضوعات


عنوان مقاله [English]

A Review of the Etiology and Pathogenesis of Posterior Reversible Encephalopathy Syndrome (PRES) in Patients with Multiple Sclerosis (MS) and Neuromyelitis Optica Spectrum Disorder (NMOSD)

نویسندگان [English]

  • Mohammadamin Najafi 1
  • Ali Abesi 2
1 Assistant Professor of Neurology, Isfahan University of Medical Sciences, Isfahan, Iran
2 Student Research Committee, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
چکیده [English]

Background: Posterior Reversible Encephalopathy Syndrome (PRES) is a neurological disorder with multifaceted pathophysiology, typically presenting with vasogenic edema on brain imaging. Although the occurrence of PRES in patients with MS and NMOSD is rare, identifying the etiological factors and pathogenesis mechanisms in these patients is crucial for optimal diagnosis and management.
Methods: This study was conducted through a literature search of PubMed, Scopus, Web of Science, and Google Scholar databases using relevant keywords.
Findings: Seventeen relevant case reports were identified and reviewed. In NMOSD patients, the pathogenesis of PRES is primarily associated with blood-brain barrier (BBB) dysfunction caused by the attack of anti-AQP4 IgG antibodies on astrocytes. Furthermore, common treatments for this disease, such as rituximab (which induces endothelial injury), corticosteroids, and plasmapheresis (which induces blood pressure fluctuations), have been identified as significant predisposing risk factors for PRES. In MS patients, perivascular inflammation and impaired neurovascular coupling at the blood-brain barrier provide a suitable basis for the development of PRES. Medications such as fingolimod (via an endothelial injury mechanism) and interferon-beta (through the induction of hypertension or disruption of the BBB), as well as the use of high-dose corticosteroids, are among the triggering factors for PRES in these patients.
Conclusion: Although PRES is a rare complication in MS and NMOSD patients, the nature of these diseases, which is associated with disruption of the blood-brain barrier, along with the use of specific treatments, places these patients at risk of developing PRES.

کلیدواژه‌ها [English]

  • Posterior Reversible Leukoencephalopathy Syndrome
  • Multiple Sclerosis
  • Neuromyelitis Optica Spectrum Disorder
  1. Fischer M, Schmutzhard E. Posterior reversible encephalopathy syndrome. J Neurol 2017; 264(8): 1608-16.
  2. Hinchey J, Chaves C, Appignani B, Breen J, Pao L, Wang A, et al. A reversible posterior leukoencephalopathy syndrome. N Engl J Med 1996; 334(8): 494-500.
  3. Shankar J, Banfield J. Posterior reversible encephalopathy syndrome: a review. Can Assoc Radiol J 2017; 68(2): 147-53.
  4. Fugate JE, Rabinstein AA. Posterior reversible encephalopathy syndrome: clinical and radiological manifestations, pathophysiology, and outstanding questions. Lancet Neurol 2015; 14(9): 914-25.
  5. Bartynski WS. Posterior reversible encephalopathy syndrome, part 1: fundamental imaging and clinical features. AJNR Am J Neuroradiol 2008; 29(6): 1036-42.
  6. Kozak OS, Wijdicks EF, Manno EM, Miley JT, Rabinstein AA. Status epilepticus as initial manifestation of posterior reversible encephalopathy syndrome. Neurology 2007; 69(9): 894-7.
  7. Lee VH, Wijdicks EF, Manno EM, Rabinstein AA. Clinical spectrum of reversible posterior leukoencephalopathy syndrome. Arch Neurol 2008; 65(2): 205-10.
  8. Derle E, Güneş HN, Konuşkan B, Tuncer-Kurne A. Neuromyelitis optica in children: a review of the

    Turk J Pediatr 2014; 56(6): 573-80.
  9. Zarei S, Eggert J, Franqui-Dominguez L, Carl Y, Boria F, Stukova M, et al. Comprehensive review of neuromyelitis optica and clinical characteristics of neuromyelitis optica patients in Puerto Rico. Surg Neurol Int 2018; 9: 242.
  10. Dobson R, Giovannoni G. Multiple sclerosis - a review. Eur J Neurol 2019; 26(1): 27-40.
  11. Strandgaard S, Olesen J, Skinhoj E, Lassen NA. Autoregulation of brain circulation in severe arterial hypertension. Br Med J 1973; 1(5852): 507-10.
  12. Feske SK. Posterior reversible encephalopathy syndrome: a review. Semin Neurol 2011; 31(2): 202-15.
  13. Bartynski WS. Posterior reversible encephalopathy syndrome, part 2: controversies surrounding pathophysiology of vasogenic edema. AJNR Am J Neuroradiol 2008; 29(6): 1043-9.
  14. Fugate JE, Claassen DO, Cloft HJ, Kallmes DF, Kozak OS, Rabinstein AA. Posterior reversible encephalopathy syndrome: associated clinical and radiologic findings. Mayo Clin Proc 2010; 85(5): 427-32.
  15. Vincent T, Saikali P, Cayrol R, Roth AD, Bar-Or A, Prat A, et al. Functional consequences of neuromyelitis optica-IgG astrocyte interactions on blood-brain barrier permeability and granulocyte

    J Immunol 2008; 181(8): 5730-7.
  16. Cazzaniga J, Jara Silva CE, Quinonez J, Ruxmohan S, Leyva MM, Fahs A. Neuromyelitis Optica Spectrum Disorder. Cureus 2023; 15(11): e48168.
  17. Kim HJ, Paul F, Lana-Peixoto MA, Tenembaum S, Asgari N, Palace J, et al. MRI characteristics of neuromyelitis optica spectrum disorder: an international update. Neurology 2015; 84(11): 1165-73.
  18. Wingerchuk DM, Banwell B, Bennett JL, Cabre P, Carroll W, Chitnis T, et al. International consensus diagnostic criteria for neuromyelitis optica spectrum disorders. Neurology 2015; 85(2): 177-89.
  19. Kim S-M, Waters P, Woodhall M, Kim J-Y, Kim J-E, Yang JW, et al. Utility of aquaporin-4 antibody assay in patients with neuromyelitis optica spectrum disorders. Mult Scler 2013; 19(8): 1060-7.
  20. Chan KH, Lee CY. Treatment of neuromyelitis optica spectrum disorders. Int J Mol Sci 2021; 22(16): 8636.
  21. Yang B, Guo L, Yang X, Yu N. The pathogenesis and treatment of posterior reversible encephalopathy syndrome after neuromyelitis optica spectrum disorder: a case report and literature review. BMC Neurol 2022; 22(1): 493.
  22. Yuan M, Ge M, Yin J, Dai Z, Xie L, Li Y, et al. Isoflurane post-conditioning down-regulates expression of aquaporin 4 in rats with cerebral ischemia/reperfusion injury and is possibly related to bone morphogenetic protein 4/Smad1/5/8 signaling pathway. Biomed Pharmacother 2018; 97: 429-38.
  23. Wu Y, Zhong L, Geng J. Neuromyelitis optica spectrum disorder: Pathogenesis, treatment, and experimental models. Mult Scler Relat Disord 2019; 27: 412-8.
  24. Magaña SM, Matiello M, Pittock SJ, McKeon A, Lennon VA, Rabinstein AA, et al. Posterior reversible encephalopathy syndrome in neuromyelitis optica spectrum disorders. Neurology 2009; 72(8): 712-7.
  25. McKinney AM, Short J, Truwit CL, McKinney ZJ, Kozak OS, SantaCruz KS, et al. Posterior reversible encephalopathy syndrome: incidence of atypical regions of involvement and imaging findings. AJR Am J Roentgenol 2007; 189(4): 904-12.
  26. Lamy C, Oppenheim C, Mas JL. Posterior reversible encephalopathy syndrome. Handb Clin Neurol 2014; 121: 1687-701.
  27. Berger JR, Neltner J, Smith C, Cambi F. Posterior reversible encephalopathy syndrome masquerading as progressive multifocal leukoencephalopathy in rituximab treated neuromyelitis optica. Mult Scler Relat Disord 2014; 3(6): 728-31.
  28. Etemadifar M, Alaei SA, Saffari E, Salari M. Rituximab-associated PRES in antibody-mediated kidney rejection: A case report. Transpl Immunol. 2023; 80: 101907.
  29. Mustafa KN, Qasem U, Al-Ryalat NT, Bsisu IK. Rituximab-associated posterior reversible encephalopathy syndrome. Int J Rheum Dis 2019; 22(1): 160-5.
  30. Igel C, Garretto D, Robbins MS, Swerdlow M, Judge N, Dayal A. Neuromyelitis optica in pregnancy complicated by posterior reversible encephalopathy syndrome, eclampsia and fetal death. J Clin Med Res 2015; 7(3): 193-5.
  31. Kontos HA, Wei EP, Navari RM, Levasseur JE,

    Rosenblum WI, Patterson JL, Jr. Responses of cerebral arteries and arterioles to acute hypotension and hypertension. Am J Physiol 1978; 234(4): H371-83.
  32. MacKenzie ET, Strandgaard S, Graham DI, Jones JV, Harper AM, Farrar JK. Effects of acutely induced hypertension in cats on pial arteriolar caliber, local cerebral blood flow, and the blood-brain barrier. Circ Res 1976; 39(1): 33-41.
  33. Kamo H, Ueno Y, Sugiyama M, Miyamoto N, Yamashiro K, Tanaka R, et al. Pontine hemorrhage accompanied by neuromyelitis optica spectrum disorder. J Neuroimmunol 2019;330: 19-22.
  34. Srichawla BS, Kaur T, Singh H. Corticosteroids in posterior reversible encephalopathy syndrome: Friend or foe? A systematic review. World J Clin Cases 2025; 13(12): 98768.
  35. Ge Y. Multiple sclerosis: the role of MR imaging. AJNR Am J Neuroradiol 2006; 27(6): 1165-76.
  36. Jain RS, Khan I, Ahmad R. Posterior Reversible Encephalopathy Syndrome (PRES) Associated with Papilledema Mimicking Multiple Sclerosis and Boomerang Sign on Imaging: Report of Two Cases. J Neurol Exp Neurosci 2017; 3(2): 48-50.
  37. Nelke C, Schulte-Mecklenbeck A, Pawlitzki M, Rolfes L, Räuber S, Gross CC, et al. The Innate Immune Response Characterizes Posterior Reversible Encephalopathy Syndrome. J Clin Immunol 2021; 41(6): 1229-40.
  38. Zierfuss B, Larochelle C, Prat A. Blood-brain barrier dysfunction in multiple sclerosis: causes, consequences, and potential effects of therapies. Lancet Neurol 2024; 23(1): 95-109.
  39. Adams CW, Abdulla YH, Torres EM, Poston RN. Periventricular lesions in multiple sclerosis: their perivenous origin and relationship to granular ependymitis. Neuropathol Appl Neurobiol 1987; 13(2): 141-52.
  40. Lindå H, von Heijne A. A Case of Posterior Reversible Encephalopathy Syndrome Associated with Gilenya® (Fingolimod) Treatment for Multiple Sclerosis. Front Neurol 2015; 6: 39.
  41. Morrow SA, Rana R, Lee D, Paul T, Mahon JL. Posterior reversible encephalopathy syndrome due to high dose corticosteroids for an MS relapse. Case Rep Neurol Med 2015; 2015: 325657.
  42. Mastorodemos VC, Ioannidis SG, Papadaki EZ, Mitsias PD. Posterior reversible encephalopathy syndrome, multiple sclerosis and interferon therapy: association, co-incidence or convoluted interplay? Mult Scler Relat Disord 2020; 45: 102356.
  43. Omoto S, Utsumi T, Matsuno H, Terasawa Y, Iguchi Y. Thrombotic Microangiopathy Presenting with Intestinal Involvement Following Long-term Interferon-β1b Treatment for Multiple Sclerosis. Intern Med 2018; 57(5): 741-4.
  44. Sánchez-Carteyron A, Alarcia R, Ara JR, Martín J. Posterior reversible encephalopathy syndrome after rituximab infusion in neuromyelitis optica. Neurology 2010; 74(18): 1471-3.
  45. Shima T, Tsujino S, Yamashita K, Hirayama T, Fukushima K, Kanamoto T, et al. Neuromyelitis Optica Spectrum Disorder Complicated by Posterior Reversible Encephalopathy Syndrome as an Initial Manifestation. Intern Med 2020; 59(15): 1887-90.