Miller Fisher Syndrome and Bickerstaff Encephalitis as Manifestations of an Anti-gq1b Antibody Syndrome: Case Report

Miller Fisher Syndrome and Bickerstaff Encephalitis as Manifestations of an Anti-gq1b Antibody Syndrome: 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 Miller Fisher Syndrome and Bickerstaff Encephalitis as Manifestations of an Anti-gq1b Antibody Syndrome: Case Report Oscar Arturo Amaro Vazquez, Valeria Estefania Aguilar Mercado, and 2 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8865140/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 Miller Fisher syndrome (MFS) and Bickerstaff brainstem encephalitis (BBE) represent two clinical entities within the anti-GQ1b antibody spectrum, both characterized by acute onset and immune-mediated pathophysiology. We report the case of a 22-year-old woman who presented with dorsal pain, visual disturbances, ophthalmoplegia, and ataxia, showing a progressive neurological decline. Neuroimaging and cerebrospinal fluid analyses revealed no structural or cytochemical abnormalities. Despite this, the patient tested positive for anti-GQ1b antibodies, confirming the diagnosis of an atypical Miller Fisher syndrome associated with brainstem involvement. Early initiation of intravenous immunoglobulin and corticosteroid therapy led to a rapid and almost complete recovery of neurological function. This case highlights the diagnostic challenges of anti-GQ1b antibody syndromes, emphasizing the need for high clinical suspicion and early immunotherapy to prevent irreversible neurological damage. Miller Fisher syndrome Bickerstaff brainstem encephalitis Anti-GQ1b antibodies Autoimmune neuropathy Figures Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 Figure 6 Figure 7 INTRODUCTION Miller Fisher syndrome (MFS) represents one of the least common acute inflammatory polyneuropathies of unknown etiology worldwide. Reported cases are rare, and therefore few clinical manifestations—beyond the classic triad—are well known within this entity. Guillain himself recognized the existence of a form of acute polyradiculoneuritis with mesencephalic presentation. The classic triad—ophthalmoparesis, ataxia, and areflexia—constitutes the pathognomonic clinical picture of this disease. However, in some cases, a constellation of brainstem-related symptoms coexists, corresponding to Bickerstaff encephalitis. Clinical and neurophysiological findings tend to be variable, and confirmation of the disease generally involves detecting anti-GQ1b antibodies. CASE REPORT A 29-year-old male patient, previously healthy and with no relevant medical history, was admitted to the emergency department complaining of a 4-day history of rapidly progressive neurological symptoms. The clinical course was characterized by the acute onset of horizontal diplopia and significant gait instability, preceded two days prior by a self-limited diarrheal illness. The patient also reported ascending paresthesia in both lower extremities, although no motor weakness was initially described. Upon a rigorous neurological examination at admission, the patient was found to be alert and oriented but exhibited complex ocular motility disturbances, including marked bilateral horizontal and vertical ophthalmoplegia associated with bilateral ptosis. The evaluation of coordination revealed a severe ataxic gait, and the examination of muscle stretch reflexes demonstrated generalized areflexia in all four limbs. At this stage, the clinical triad of ophthalmoplegia, ataxia, and areflexia strongly suggested a diagnosis of Miller Fisher Syndrome (MFS), a localized variant of Guillain-Barré Syndrome [ 3 , 5 , 12 ]. However, the clinical phenotype evolved significantly during the second day of hospitalization. The patient developed fluctuating levels of consciousness, transitioning into states of somnolence and disorientation. Concomitantly, a shift in upper motor neuron signs was observed, characterized by the emergence of hyperreflexia in the lower limbs and the presence of a bilateral Babinski sign. This progression from peripheral signs to central nervous system involvement provided clinical evidence of a transition or overlap toward Bickerstaff Brainstem Encephalitis (BBE) [ 2 , 6 , 14 ]. To confirm the diagnosis and assess the extent of the lesions, a comprehensive diagnostic workup was initiated. A lumbar puncture was performed, revealing albuminocytologic dissociation, with an elevated protein level of 85 mg/dL and a normal white cell count (2/mm³). Magnetic resonance imaging (MRI) of the brain was crucial, demonstrating distinct T2-weighted and Fluid-Attenuated Inversion Recovery (FLAIR) hyperintense signals localized in the midbrain and the pons (Figs. 1 –4). These radiological findings confirmed the inflammatory involvement of the brainstem, consistent with the BBE diagnosis [ 13 , 14 ]. Electrophysiological studies were carried out to further characterize the neuropathy. Nerve conduction studies (NCS) showed a significant reduction in the amplitudes of sensory nerve action potentials (SNAPs) (Fig. 7 ), while motor terminal latencies and conduction velocities remained within normal limits. These findings were diagnostic of a sensory ataxic neuropathy, a common feature within this clinical spectrum [ 12 , 16 ]. Finally, the immunological profile was definitive, showing high titers of serum anti-GQ1b IgG antibodies, which confirmed the diagnosis of anti-GQ1b antibody syndrome with an MFS/BBE overlap [ 1 , 9 ]. Therapeutic intervention was started immediately with intravenous immunoglobulin (IVIg) at a standard dose of 0.4 g/kg/day for five consecutive days [ 8 , 17 ]. The patient demonstrated a remarkable clinical response; his level of consciousness began to stabilize after the second dose of IVIg. By the end of the treatment course, both ophthalmoplegia and ataxia showed significant regression. A follow-up MRI performed ten days later revealed partial resolution of the previously identified brainstem lesions (Fig. 1 – 6 ). The patient was discharged after 14 days of hospitalization with only minor residual diplopia. At the 3-month follow-up visit, a complete clinical recovery was documented, with a total resolution of all neurological deficits. DISCUSSION Since their original identification, both Miller Fisher syndrome (MFS) and Bickerstaff brainstem encephalitis (BBE) have undergone substantial reinterpretation in terms of their pathophysiology and nosological classification. The recognition of serological coincidences—particularly the presence of specific immunoglobulin G antibodies against the ganglioside GQ1b (anti-GQ1b IgG)—along with preceding infectious processes, convergent electrophysiological findings, and neuroimaging abnormalities, have allowed the proposal of a shared autoimmune mechanism, displacing the previous notion of divergent etiologies (1). The detection of “incomplete” clinical forms with anti-GQ1b antibody positivity has led to the conceptualization of a unifying entity termed the anti-GQ1b antibody syndrome, which encompasses a continuous clinical spectrum defined by a homogeneous serological profile and variable degrees of involvement of both the peripheral nervous system (PNS) and the central nervous system (CNS) (4). In its initial descriptions, BBE was characterized by rapidly progressive bilateral ophthalmoparesis, cerebellar ataxia, and impaired consciousness, often accompanied by pyramidal signs. In parallel, a syndrome with nearly overlapping phenotypic features—MFS—was documented, which since Fisher’s characterization has been regarded as an uncommon variant of Guillain-Barré syndrome (GBS), a group of acute-onset immune-mediated neuropathies whose cardinal clinical triad includes ataxia, areflexia, and ophthalmoparesis (1,4). In 1951, Bickerstaff described in the British Medical Journal three patients with progressive onset of ataxia, external ophthalmoplegia, and drowsiness, all preceded by an infectious episode. He proposed the terms “mesencephalitis” and “rhombencephalitis” to differentiate this condition from classical viral encephalitides (5). Subsequently, he defined BBE as a “severe syndrome with a benign prognosis,” characterized by ophthalmoplegia, ataxia, and somnolence, suggesting its pathophysiological relationship with GBS, since both conditions presented areflexia and albuminocytologic dissociation in the cerebrospinal fluid (CSF). The main distinction lies in that altered consciousness was exclusive to BBE (4,5). Although the overall incidence of MFS remains imprecisely quantified, it is recognized that the incidence of GBS ranges between 1 and 2 cases per 100,000 inhabitants per year, of which MFS constitutes a minor fraction. There is a slight male predominance, and it may occur in any age group (1). The detection of anti-GQ1b antibodies in MFS patients, described by Chiba in 1991, and later in BBE cases by Yuki, provided conclusive evidence of a shared immune-mediated origin, usually triggered by a preceding infectious episode. This led to grouping both entities under the eponym “Fisher-Bickerstaff syndrome” (1). The GQ1b ganglioside, located in paranodal myelin—particularly in the oculomotor nerves (cranial nerves III, IV, and VI), dorsal root ganglia, and muscle spindle afferent fibers—constitutes the principal antigenic target. The recognition of anti-GQ1b antibodies in atypical phenotypes supported the delineation of a broader clinical spectrum with variable CNS and PNS involvement (4). The diagnosis of MFS is fundamentally clinical, supported by complementary findings. Albuminocytologic dissociation, a hallmark of GBS, may not be evident in the early stages of MFS, being reported in approximately 47% of cases and increasing progressively up to 82% by the third week of evolution. In contrast, anti-GQ1b antibody positivity is observed in about 85% of MFS patients, making this marker more sensitive than hyperproteinorrhachia in early stages (1). Additionally, anti-GD1a (28%) and anti-GM1 (15%) antibodies have been reported, although their pathogenic significance remains uncertain (1). The so-called “anti-GQ1b spectrum” includes overlapping forms with GBS, isolated acute ophthalmoplegia, and BBE itself (4). In most patients, a preceding infection is present, most frequently an upper respiratory tract infection (56–76% of cases), followed by gastrointestinal infection (4%) and isolated fever (2%). Associations with autoimmune diseases, neoplastic processes, exposure to certain drugs (heroin, isotretinoin, streptokinase), TNF-α antagonist therapy, bone marrow transplantation, and surgical procedures have also been reported (1). In a retrospective study of 92 patients, 28 received intravenous immunoglobulin (IVIG; 0.4 g/kg/day for 5 days), 23 were treated with plasma exchange (PLEX; 2–6 cycles, mean 4), and 41 received no specific therapy. Survival was approximately 100% across all groups, and IVIG showed a modest acceleration of recovery, attributed to its ability to block the binding of anti-GQ1b antibodies at motor nerve terminals and mitigate their pathogenic effects (3). CONCLUSIONS The present clinical case compellingly illustrates the diagnostic and therapeutic complexity inherent to the anti-GQ1b antibody syndrome, particularly in its clinical expressions corresponding to Miller Fisher syndrome (MFS) and Bickerstaff brainstem encephalitis (BBE). The symptomatic overlap and phenotypic variability demand a high index of clinical suspicion, especially in the early phases when albuminocytologic dissociation may be absent and conventional neuroimaging fails to reveal structural abnormalities. The serological detection of anti-GQ1b IgG antibodies stands as a biomarker of high sensitivity and specificity for early diagnostic confirmation, surpassing even the usefulness of hyperproteinorrhachia in the initial stages. The identification of this immunologic profile supports the concept of a unified neuroimmunologic spectrum, with shared pathophysiological mechanisms that differentially affect both the peripheral and central nervous systems through postinfectious autoimmune processes directed against gangliosides located in oculomotor nerves, dorsal root ganglia, and muscle spindles. The multimodal therapeutic approach, involving early administration of intravenous immunoglobulin and pulse corticosteroid therapy, demonstrated remarkable clinical efficacy in this case, promoting near-complete resolution of neurological deficits within a short time frame. These results reinforce the relevance of initiating early immunotherapy upon well-founded clinical suspicion, even in the absence of initial serological confirmation, with the aim of limiting axonal damage and preventing functional sequelae. From a neurosurgical and neuroscientific perspective, this case underscores the need for integrated diagnostic and therapeutic protocols that include interdisciplinary collaboration among neurology, neurosurgery, ophthalmology, and neuromotor rehabilitation. Furthermore, it highlights the importance of continued research into molecular characterization and the development of more specific immunomodulatory strategies to optimize functional outcomes in patients within this clinical spectrum. Declarations Acknowledgements: Not applicable. Funding: The authors received no financial support for the research, authorship, and/or publication of this article. Availability of data and materials: Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study. Ethics approval and consent to participate: This study was conducted in accordance with the Declaration of Helsinki. Ethical approval was obtained from the Hospital Espanol. Consent for publication: Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal. Competing interests: The authors declare that they have no competing interests. References Odaka M, Yuki N, Hirata K. Anti-GQ1b antibody syndrome: clinical relevance and biological significance. J Neurol Neurosurg Psychiatry. 2001;70(3):350-5. https://doi.org/10.1136/jnnp.70.3.350 Shahrizaila N, Yuki N. Bickerstaff brainstem encephalitis and Fisher syndrome: anti-GQ1b antibody syndrome. J Neurol Neurosurg Psychiatry. 2013;84(5):576-83. https://doi.org/10.1136/jnnp-2012-302824 Teener JW. Miller Fisher's syndrome. Semin Neurol. 2012;32(5):512-6. https://doi.org/10.1055/s-0033-1334470 Bukhari S, Taboada J. A Case of Bickerstaff Brainstem Encephalitis (BBE): A Rare Variant of Guillain-Barre Syndrome (GBS). Cureus. 2022;14(8):e28033. https://doi.org/10.7759/cureus.28033 Wakerley BR, Uncini A, Yuki N. Guillain-Barré and Miller Fisher syndromes—new diagnostic classification. Nat Rev Neurol. 2014;10(9):537-44. https://doi.org/10.1038/nrneurol.2014.138 Hardy TA, Reddel SW, Barnett MH, et al. Miller Fisher syndrome, Bickerstaff brainstem encephalitis and Guillain-Barré syndrome revisited: the unifying concept of anti-GQ1b antibody syndromes. J Clin Neurosci. 2011;18(11):1448-54. https://doi.org/10.1016/j.jocn.2011.02.043 Ito M, Kuwabara S, Odaka M, et al. Bickerstaff's brainstem encephalitis and Fisher syndrome form a continuous spectrum: clinical analysis of 581 cases. J Neurol. 2008;255(5):674-82. https://doi.org/10.1007/s00415-008-0675-y Overell JR, Hsieh ST, Odaka M, et al. Treatment for Miller Fisher syndrome, Bickerstaff's brainstem encephalitis and related disorders. Cochrane Database Syst Rev. 2007;2007(1):CD004730. https://doi.org/10.1002/14651858.CD004730.pub2 Paparounas K. Anti-GQ1b antibodies: are they pharmacological tools or biomarkers of clinical states? J Clin Neuromuscul Dis. 2004;5(4):167-74. https://doi.org/10.1097/00131402-200406000-00001 Yuki N. Fisher syndrome and Bickerstaff brainstem encephalitis (BBE). In: Islam MS, editor. Guillain-Barré Syndrome. Brisbane (AU): Exon Publications; 2021. Koga M, Gilbert M, Li J, et al. Antecedent infections in Fisher syndrome: a common pathogenesis of molecular mimicry. Neurology. 2005;64(9):1605-11. https://doi.org/10.1212/01.WNL.0000160399.08456.7C Lo YL. The Miller Fisher syndrome: a review. ISNR Neurol. 2011;2011:452503. https://doi.org/10.5402/2011/452503 Micheli C, Atzori M, Sola P, et al. Bickerstaff's brainstem encephalitis: a case report and review of the literature. J Neurol. 2011;258(11):2080-2. Odaka M, Yuki N, Yamada M, et al. Bickerstaff's brainstem encephalitis: clinical features of 62 cases and a comparison with Fisher syndrome. Brain. 2003;126(Pt 10):2279-90. https://doi.org/10.1093/brain/awg226 Yabuki S, Matsushita T, Kaneko S, et al. A case of Bickerstaff's brainstem encephalitis with overlapping Miller Fisher syndrome. Rinsho Shinkeigaku. 2016;56(5):345-9. Uncini A, Kuwabara S. The electrodiagnosis of Guillain-Barré syndrome: axonal or demyelinating? Clin Neurophysiol. 2012;123(11):2113-5. https://doi.org/10.1016/j.clinph.2012.07.001 Hughes RA, Swan AV, van Doorn PA. Intravenous immunoglobulin for Guillain-Barré syndrome. Cochrane Database Syst Rev. 2014;2014(9):CD002063. https://doi.org/10.1002/14651858.CD002063.pub6 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-8865140","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":592355317,"identity":"6fb5c232-97d9-4a26-97d6-c10cc4bc8926","order_by":0,"name":"Oscar Arturo Amaro Vazquez","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA20lEQVRIiWNgGAWjYHACZhiD8QGUYUC0FmaYUuK1sEkQpYWf//hjg5977KL5Zx8+Vs27wy6agb15mwQ+LZIzEpITe54l5844l5Z2m/dMcm4Dz7EyvFoMbjAcPsBzgDm34QyP2W3eNiBDIscMv5bzB5sP/jlQnzsfqKWYt60+t0H+DQEtB5KZk3kOHM7dANTCzNt2GGgLD34tkjPSmI1lDhzP3XiGLVlybtvx3DaetGILfFpAISb55kB17rwzzAc/vG2rzu1nP7zxBj4tmICNNOWjYBSMglEwCrABALS1SCMMZSmiAAAAAElFTkSuQmCC","orcid":"","institution":"National Autonomous University of Mexico","correspondingAuthor":true,"prefix":"","firstName":"Oscar","middleName":"Arturo Amaro","lastName":"Vazquez","suffix":""},{"id":592355320,"identity":"13e82ee6-6ae3-433b-a3fe-d71aba8e0e89","order_by":1,"name":"Valeria Estefania Aguilar Mercado","email":"","orcid":"","institution":"Hospital Español","correspondingAuthor":false,"prefix":"","firstName":"Valeria","middleName":"Estefania Aguilar","lastName":"Mercado","suffix":""},{"id":592355321,"identity":"73a98c41-5211-4cf8-a144-659e1d6cc661","order_by":2,"name":"Pedro Pablo De Juambelz Cisneros","email":"","orcid":"","institution":"Hospital Español","correspondingAuthor":false,"prefix":"","firstName":"Pedro","middleName":"Pablo De Juambelz","lastName":"Cisneros","suffix":""},{"id":592355323,"identity":"817ce834-f1a5-4ded-a6e4-dde1ed73739b","order_by":3,"name":"Fernando Pazos Gomez","email":"","orcid":"","institution":"Hospital Español","correspondingAuthor":false,"prefix":"","firstName":"Fernando","middleName":"Pazos","lastName":"Gomez","suffix":""}],"badges":[],"createdAt":"2026-02-12 19:24:21","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-8865140/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-8865140/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":102853491,"identity":"557114c6-9dec-4f95-aeee-491a72d4342e","added_by":"auto","created_at":"2026-02-17 14:42:04","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":80899,"visible":true,"origin":"","legend":"\u003cp\u003eMRI of the brain, T2/FLAIR sequence, axial section. Hyperintense signal is observed in the brainstem and cerebellum (arrows).\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-8865140/v1/4e60a57ae87672ea80ab90b4.png"},{"id":102853308,"identity":"a081af03-0d99-4ffa-bf12-fbbeb880027f","added_by":"auto","created_at":"2026-02-17 14:41:20","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":73901,"visible":true,"origin":"","legend":"\u003cp\u003eMRI of the brain, T2 sequence, axial section. (A) Midbrain level and (B) Pons level showing areas of signal abnormality.\u003c/p\u003e","description":"","filename":"2.png","url":"https://assets-eu.researchsquare.com/files/rs-8865140/v1/d2197143540f74d374109a35.png"},{"id":102853496,"identity":"e7462df0-e3c2-4156-8b91-132492141c75","added_by":"auto","created_at":"2026-02-17 14:42:07","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":84917,"visible":true,"origin":"","legend":"\u003cp\u003eMRI of the brain, T2 sequence, sagittal section. Extension of the hyperintense signal across the brainstem.\u003c/p\u003e","description":"","filename":"3.png","url":"https://assets-eu.researchsquare.com/files/rs-8865140/v1/b07054f099f9c5658876f163.png"},{"id":102853542,"identity":"f4f0d2fb-19ed-49c4-afe8-c5a1609cd293","added_by":"auto","created_at":"2026-02-17 14:42:21","extension":"png","order_by":4,"title":"Figure 4","display":"","copyAsset":false,"role":"figure","size":79362,"visible":true,"origin":"","legend":"\u003cp\u003eCoronal section of the brain MRI showing cerebellar involvement.\u003c/p\u003e","description":"","filename":"4.png","url":"https://assets-eu.researchsquare.com/files/rs-8865140/v1/76e54050ef020aa610852e47.png"},{"id":102853364,"identity":"a286ae4c-821a-4390-9aad-966fd087928c","added_by":"auto","created_at":"2026-02-17 14:41:37","extension":"png","order_by":5,"title":"Figure 5","display":"","copyAsset":false,"role":"figure","size":53266,"visible":true,"origin":"","legend":"\u003cp\u003eFollow-up MRI showing partial resolution of the initial lesions.\u003c/p\u003e","description":"","filename":"5.png","url":"https://assets-eu.researchsquare.com/files/rs-8865140/v1/62ef557bae6a551978328402.png"},{"id":102853352,"identity":"b53de1d4-e2f3-483b-b191-89c7dc9ff580","added_by":"auto","created_at":"2026-02-17 14:41:33","extension":"png","order_by":6,"title":"Figure 6","display":"","copyAsset":false,"role":"figure","size":85331,"visible":true,"origin":"","legend":"\u003cp\u003eClinical evolution: (A) At admission showing ophthalmoplegia, (B) Post-treatment recovery.\u003c/p\u003e","description":"","filename":"6.png","url":"https://assets-eu.researchsquare.com/files/rs-8865140/v1/5f2e2b890409c3bd1394b866.png"},{"id":102853499,"identity":"be978160-9397-4cab-bc90-dbbf680baf9c","added_by":"auto","created_at":"2026-02-17 14:42:08","extension":"png","order_by":7,"title":"Figure 7","display":"","copyAsset":false,"role":"figure","size":158481,"visible":true,"origin":"","legend":"\u003cp\u003eSchematic representation of the Anti-GQ1b antibody syndrome overlap.\u003c/p\u003e","description":"","filename":"7.png","url":"https://assets-eu.researchsquare.com/files/rs-8865140/v1/e2fcebc5b8f10d153252d2ab.png"},{"id":103504228,"identity":"9510c6f4-d183-4c5e-93ed-a95f36c0774d","added_by":"auto","created_at":"2026-02-26 13:18:35","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":922020,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8865140/v1/442b4378-b082-44d5-ab39-68eb3cd9bc88.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"\u003cp\u003eMiller Fisher Syndrome and Bickerstaff Encephalitis as Manifestations of an Anti-gq1b Antibody Syndrome: Case Report\u003c/p\u003e","fulltext":[{"header":"INTRODUCTION","content":"\u003cp\u003eMiller Fisher syndrome (MFS) represents one of the least common acute inflammatory polyneuropathies of unknown etiology worldwide. Reported cases are rare, and therefore few clinical manifestations\u0026mdash;beyond the classic triad\u0026mdash;are well known within this entity. Guillain himself recognized the existence of a form of acute polyradiculoneuritis with mesencephalic presentation. The classic triad\u0026mdash;ophthalmoparesis, ataxia, and areflexia\u0026mdash;constitutes the pathognomonic clinical picture of this disease. However, in some cases, a constellation of brainstem-related symptoms coexists, corresponding to Bickerstaff encephalitis. Clinical and neurophysiological findings tend to be variable, and confirmation of the disease generally involves detecting anti-GQ1b antibodies.\u003c/p\u003e"},{"header":"CASE REPORT","content":"\u003cp\u003eA 29-year-old male patient, previously healthy and with no relevant medical history, was admitted to the emergency department complaining of a 4-day history of rapidly progressive neurological symptoms. The clinical course was characterized by the acute onset of horizontal diplopia and significant gait instability, preceded two days prior by a self-limited diarrheal illness. The patient also reported ascending paresthesia in both lower extremities, although no motor weakness was initially described.\u003c/p\u003e \u003cp\u003eUpon a rigorous neurological examination at admission, the patient was found to be alert and oriented but exhibited complex ocular motility disturbances, including marked bilateral horizontal and vertical ophthalmoplegia associated with bilateral ptosis. The evaluation of coordination revealed a severe ataxic gait, and the examination of muscle stretch reflexes demonstrated generalized areflexia in all four limbs. At this stage, the clinical triad of ophthalmoplegia, ataxia, and areflexia strongly suggested a diagnosis of Miller Fisher Syndrome (MFS), a localized variant of Guillain-Barr\u0026eacute; Syndrome [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e, \u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eHowever, the clinical phenotype evolved significantly during the second day of hospitalization. The patient developed fluctuating levels of consciousness, transitioning into states of somnolence and disorientation. Concomitantly, a shift in upper motor neuron signs was observed, characterized by the emergence of hyperreflexia in the lower limbs and the presence of a bilateral Babinski sign. This progression from peripheral signs to central nervous system involvement provided clinical evidence of a transition or overlap toward Bickerstaff Brainstem Encephalitis (BBE) [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e, \u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e, \u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eTo confirm the diagnosis and assess the extent of the lesions, a comprehensive diagnostic workup was initiated. A lumbar puncture was performed, revealing albuminocytologic dissociation, with an elevated protein level of 85 mg/dL and a normal white cell count (2/mm\u0026sup3;). Magnetic resonance imaging (MRI) of the brain was crucial, demonstrating distinct T2-weighted and Fluid-Attenuated Inversion Recovery (FLAIR) hyperintense signals localized in the midbrain and the pons (Figs.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e\u0026ndash;4). These radiological findings confirmed the inflammatory involvement of the brainstem, consistent with the BBE diagnosis [\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e, \u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e].\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eElectrophysiological studies were carried out to further characterize the neuropathy. Nerve conduction studies (NCS) showed a significant reduction in the amplitudes of sensory nerve action potentials (SNAPs) (Fig.\u0026nbsp;\u003cspan refid=\"Fig5\" class=\"InternalRef\"\u003e7\u003c/span\u003e), while motor terminal latencies and conduction velocities remained within normal limits. These findings were diagnostic of a sensory ataxic neuropathy, a common feature within this clinical spectrum [\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e, \u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e]. Finally, the immunological profile was definitive, showing high titers of serum anti-GQ1b IgG antibodies, which confirmed the diagnosis of anti-GQ1b antibody syndrome with an MFS/BBE overlap [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e, \u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e].\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eTherapeutic intervention was started immediately with intravenous immunoglobulin (IVIg) at a standard dose of 0.4 g/kg/day for five consecutive days [\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e, \u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e]. The patient demonstrated a remarkable clinical response; his level of consciousness began to stabilize after the second dose of IVIg. By the end of the treatment course, both ophthalmoplegia and ataxia showed significant regression. A follow-up MRI performed ten days later revealed partial resolution of the previously identified brainstem lesions (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e\u0026ndash;\u003cspan refid=\"Fig6\" class=\"InternalRef\"\u003e6\u003c/span\u003e ). The patient was discharged after 14 days of hospitalization with only minor residual diplopia. At the 3-month follow-up visit, a complete clinical recovery was documented, with a total resolution of all neurological deficits.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e"},{"header":"DISCUSSION","content":"\u003cp\u003eSince their original identification, both Miller Fisher syndrome (MFS) and Bickerstaff brainstem encephalitis (BBE) have undergone substantial reinterpretation in terms of their pathophysiology and nosological classification. The recognition of serological coincidences\u0026mdash;particularly the presence of specific immunoglobulin G antibodies against the ganglioside GQ1b (anti-GQ1b IgG)\u0026mdash;along with preceding infectious processes, convergent electrophysiological findings, and neuroimaging abnormalities, have allowed the proposal of a shared autoimmune mechanism, displacing the previous notion of divergent etiologies (1). The detection of \u0026ldquo;incomplete\u0026rdquo; clinical forms with anti-GQ1b antibody positivity has led to the conceptualization of a unifying entity termed the anti-GQ1b antibody syndrome, which encompasses a continuous clinical spectrum defined by a homogeneous serological profile and variable degrees of involvement of both the peripheral nervous system (PNS) and the central nervous system (CNS) (4).\u003c/p\u003e \u003cp\u003eIn its initial descriptions, BBE was characterized by rapidly progressive bilateral ophthalmoparesis, cerebellar ataxia, and impaired consciousness, often accompanied by pyramidal signs. In parallel, a syndrome with nearly overlapping phenotypic features\u0026mdash;MFS\u0026mdash;was documented, which since Fisher\u0026rsquo;s characterization has been regarded as an uncommon variant of Guillain-Barr\u0026eacute; syndrome (GBS), a group of acute-onset immune-mediated neuropathies whose cardinal clinical triad includes ataxia, areflexia, and ophthalmoparesis (1,4).\u003c/p\u003e \u003cp\u003eIn 1951, Bickerstaff described in the \u003cem\u003eBritish Medical Journal\u003c/em\u003e three patients with progressive onset of ataxia, external ophthalmoplegia, and drowsiness, all preceded by an infectious episode. He proposed the terms \u0026ldquo;mesencephalitis\u0026rdquo; and \u0026ldquo;rhombencephalitis\u0026rdquo; to differentiate this condition from classical viral encephalitides (5). Subsequently, he defined BBE as a \u0026ldquo;severe syndrome with a benign prognosis,\u0026rdquo; characterized by ophthalmoplegia, ataxia, and somnolence, suggesting its pathophysiological relationship with GBS, since both conditions presented areflexia and albuminocytologic dissociation in the cerebrospinal fluid (CSF). The main distinction lies in that altered consciousness was exclusive to BBE (4,5).\u003c/p\u003e \u003cp\u003eAlthough the overall incidence of MFS remains imprecisely quantified, it is recognized that the incidence of GBS ranges between 1 and 2 cases per 100,000 inhabitants per year, of which MFS constitutes a minor fraction. There is a slight male predominance, and it may occur in any age group (1).\u003c/p\u003e \u003cp\u003eThe detection of anti-GQ1b antibodies in MFS patients, described by Chiba in 1991, and later in BBE cases by Yuki, provided conclusive evidence of a shared immune-mediated origin, usually triggered by a preceding infectious episode. This led to grouping both entities under the eponym \u0026ldquo;Fisher-Bickerstaff syndrome\u0026rdquo; (1). The GQ1b ganglioside, located in paranodal myelin\u0026mdash;particularly in the oculomotor nerves (cranial nerves III, IV, and VI), dorsal root ganglia, and muscle spindle afferent fibers\u0026mdash;constitutes the principal antigenic target. The recognition of anti-GQ1b antibodies in atypical phenotypes supported the delineation of a broader clinical spectrum with variable CNS and PNS involvement (4).\u003c/p\u003e \u003cp\u003eThe diagnosis of MFS is fundamentally clinical, supported by complementary findings. Albuminocytologic dissociation, a hallmark of GBS, may not be evident in the early stages of MFS, being reported in approximately 47% of cases and increasing progressively up to 82% by the third week of evolution. In contrast, anti-GQ1b antibody positivity is observed in about 85% of MFS patients, making this marker more sensitive than hyperproteinorrhachia in early stages (1). Additionally, anti-GD1a (28%) and anti-GM1 (15%) antibodies have been reported, although their pathogenic significance remains uncertain (1).\u003c/p\u003e \u003cp\u003eThe so-called \u0026ldquo;anti-GQ1b spectrum\u0026rdquo; includes overlapping forms with GBS, isolated acute ophthalmoplegia, and BBE itself (4). In most patients, a preceding infection is present, most frequently an upper respiratory tract infection (56\u0026ndash;76% of cases), followed by gastrointestinal infection (4%) and isolated fever (2%). Associations with autoimmune diseases, neoplastic processes, exposure to certain drugs (heroin, isotretinoin, streptokinase), TNF-α antagonist therapy, bone marrow transplantation, and surgical procedures have also been reported (1).\u003c/p\u003e \u003cp\u003eIn a retrospective study of 92 patients, 28 received intravenous immunoglobulin (IVIG; 0.4 g/kg/day for 5 days), 23 were treated with plasma exchange (PLEX; 2\u0026ndash;6 cycles, mean 4), and 41 received no specific therapy. Survival was approximately 100% across all groups, and IVIG showed a modest acceleration of recovery, attributed to its ability to block the binding of anti-GQ1b antibodies at motor nerve terminals and mitigate their pathogenic effects (3).\u003c/p\u003e"},{"header":"CONCLUSIONS","content":"\u003cp\u003eThe present clinical case compellingly illustrates the diagnostic and therapeutic complexity inherent to the anti-GQ1b antibody syndrome, particularly in its clinical expressions corresponding to Miller Fisher syndrome (MFS) and Bickerstaff brainstem encephalitis (BBE). The symptomatic overlap and phenotypic variability demand a high index of clinical suspicion, especially in the early phases when albuminocytologic dissociation may be absent and conventional neuroimaging fails to reveal structural abnormalities.\u003c/p\u003e \u003cp\u003eThe serological detection of anti-GQ1b IgG antibodies stands as a biomarker of high sensitivity and specificity for early diagnostic confirmation, surpassing even the usefulness of hyperproteinorrhachia in the initial stages. The identification of this immunologic profile supports the concept of a unified neuroimmunologic spectrum, with shared pathophysiological mechanisms that differentially affect both the peripheral and central nervous systems through postinfectious autoimmune processes directed against gangliosides located in oculomotor nerves, dorsal root ganglia, and muscle spindles.\u003c/p\u003e \u003cp\u003eThe multimodal therapeutic approach, involving early administration of intravenous immunoglobulin and pulse corticosteroid therapy, demonstrated remarkable clinical efficacy in this case, promoting near-complete resolution of neurological deficits within a short time frame. These results reinforce the relevance of initiating early immunotherapy upon well-founded clinical suspicion, even in the absence of initial serological confirmation, with the aim of limiting axonal damage and preventing functional sequelae.\u003c/p\u003e \u003cp\u003eFrom a neurosurgical and neuroscientific perspective, this case underscores the need for integrated diagnostic and therapeutic protocols that include interdisciplinary collaboration among neurology, neurosurgery, ophthalmology, and neuromotor rehabilitation. Furthermore, it highlights the importance of continued research into molecular characterization and the development of more specific immunomodulatory strategies to optimize functional outcomes in patients within this clinical spectrum.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003eAcknowledgements: Not applicable.\u003c/p\u003e\n\u003cp\u003eFunding: The authors received no financial support for the research, authorship, and/or publication of this article.\u003c/p\u003e\n\u003cp\u003eAvailability of data and materials: Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.\u003c/p\u003e\n\u003cp\u003eEthics approval and consent to participate: This study was conducted in accordance with the Declaration of Helsinki. Ethical approval was obtained from the Hospital Espanol.\u003c/p\u003e\n\u003cp\u003eConsent for publication: Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.\u003c/p\u003e\n\u003cp\u003eCompeting interests: The authors declare that they have no competing interests.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eOdaka M, Yuki N, Hirata K. Anti-GQ1b antibody syndrome: clinical relevance and biological significance. J Neurol Neurosurg Psychiatry. 2001;70(3):350-5. https://doi.org/10.1136/jnnp.70.3.350 \u003c/li\u003e\n\u003cli\u003eShahrizaila N, Yuki N. Bickerstaff brainstem encephalitis and Fisher syndrome: anti-GQ1b antibody syndrome. J Neurol Neurosurg Psychiatry. 2013;84(5):576-83. https://doi.org/10.1136/jnnp-2012-302824 \u003c/li\u003e\n\u003cli\u003eTeener JW. Miller Fisher\u0026apos;s syndrome. Semin Neurol. 2012;32(5):512-6. https://doi.org/10.1055/s-0033-1334470 \u003c/li\u003e\n\u003cli\u003eBukhari S, Taboada J. A Case of Bickerstaff Brainstem Encephalitis (BBE): A Rare Variant of Guillain-Barre Syndrome (GBS). Cureus. 2022;14(8):e28033. https://doi.org/10.7759/cureus.28033 \u003c/li\u003e\n\u003cli\u003eWakerley BR, Uncini A, Yuki N. Guillain-Barr\u0026eacute; and Miller Fisher syndromes\u0026mdash;new diagnostic classification. Nat Rev Neurol. 2014;10(9):537-44. https://doi.org/10.1038/nrneurol.2014.138 \u003c/li\u003e\n\u003cli\u003eHardy TA, Reddel SW, Barnett MH, et al. Miller Fisher syndrome, Bickerstaff brainstem encephalitis and Guillain-Barr\u0026eacute; syndrome revisited: the unifying concept of anti-GQ1b antibody syndromes. J Clin Neurosci. 2011;18(11):1448-54. https://doi.org/10.1016/j.jocn.2011.02.043 \u003c/li\u003e\n\u003cli\u003eIto M, Kuwabara S, Odaka M, et al. Bickerstaff\u0026apos;s brainstem encephalitis and Fisher syndrome form a continuous spectrum: clinical analysis of 581 cases. J Neurol. 2008;255(5):674-82. https://doi.org/10.1007/s00415-008-0675-y \u003c/li\u003e\n\u003cli\u003eOverell JR, Hsieh ST, Odaka M, et al. Treatment for Miller Fisher syndrome, Bickerstaff\u0026apos;s brainstem encephalitis and related disorders. Cochrane Database Syst Rev. 2007;2007(1):CD004730. https://doi.org/10.1002/14651858.CD004730.pub2 \u003c/li\u003e\n\u003cli\u003ePaparounas K. Anti-GQ1b antibodies: are they pharmacological tools or biomarkers of clinical states? J Clin Neuromuscul Dis. 2004;5(4):167-74. https://doi.org/10.1097/00131402-200406000-00001 \u003c/li\u003e\n\u003cli\u003eYuki N. Fisher syndrome and Bickerstaff brainstem encephalitis (BBE). In: Islam MS, editor. Guillain-Barr\u0026eacute; Syndrome. Brisbane (AU): Exon Publications; 2021. \u003c/li\u003e\n\u003cli\u003eKoga M, Gilbert M, Li J, et al. Antecedent infections in Fisher syndrome: a common pathogenesis of molecular mimicry. Neurology. 2005;64(9):1605-11. https://doi.org/10.1212/01.WNL.0000160399.08456.7C \u003c/li\u003e\n\u003cli\u003eLo YL. The Miller Fisher syndrome: a review. ISNR Neurol. 2011;2011:452503. https://doi.org/10.5402/2011/452503 \u003c/li\u003e\n\u003cli\u003eMicheli C, Atzori M, Sola P, et al. Bickerstaff\u0026apos;s brainstem encephalitis: a case report and review of the literature. J Neurol. 2011;258(11):2080-2. \u003c/li\u003e\n\u003cli\u003eOdaka M, Yuki N, Yamada M, et al. Bickerstaff\u0026apos;s brainstem encephalitis: clinical features of 62 cases and a comparison with Fisher syndrome. Brain. 2003;126(Pt 10):2279-90. https://doi.org/10.1093/brain/awg226 \u003c/li\u003e\n\u003cli\u003eYabuki S, Matsushita T, Kaneko S, et al. A case of Bickerstaff\u0026apos;s brainstem encephalitis with overlapping Miller Fisher syndrome. Rinsho Shinkeigaku. 2016;56(5):345-9. \u003c/li\u003e\n\u003cli\u003eUncini A, Kuwabara S. The electrodiagnosis of Guillain-Barr\u0026eacute; syndrome: axonal or demyelinating? Clin Neurophysiol. 2012;123(11):2113-5. https://doi.org/10.1016/j.clinph.2012.07.001 \u003c/li\u003e\n\u003cli\u003eHughes RA, Swan AV, van Doorn PA. Intravenous immunoglobulin for Guillain-Barr\u0026eacute; syndrome. Cochrane Database Syst Rev. 2014;2014(9):CD002063. https://doi.org/10.1002/14651858.CD002063.pub6\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":"Miller Fisher syndrome, Bickerstaff brainstem encephalitis, Anti-GQ1b antibodies, Autoimmune neuropathy","lastPublishedDoi":"10.21203/rs.3.rs-8865140/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8865140/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003eMiller Fisher syndrome (MFS) and Bickerstaff brainstem encephalitis (BBE) represent two clinical entities within the anti-GQ1b antibody spectrum, both characterized by acute onset and immune-mediated pathophysiology. We report the case of a 22-year-old woman who presented with dorsal pain, visual disturbances, ophthalmoplegia, and ataxia, showing a progressive neurological decline. Neuroimaging and cerebrospinal fluid analyses revealed no structural or cytochemical abnormalities. Despite this, the patient tested positive for anti-GQ1b antibodies, confirming the diagnosis of an atypical Miller Fisher syndrome associated with brainstem involvement. Early initiation of intravenous immunoglobulin and corticosteroid therapy led to a rapid and almost complete recovery of neurological function. This case highlights the diagnostic challenges of anti-GQ1b antibody syndromes, emphasizing the need for high clinical suspicion and early immunotherapy to prevent irreversible neurological damage.\u003c/p\u003e","manuscriptTitle":"Miller Fisher Syndrome and Bickerstaff Encephalitis as Manifestations of an Anti-gq1b Antibody Syndrome: Case Report","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-02-17 14:38:49","doi":"10.21203/rs.3.rs-8865140/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":"b668d355-814a-4945-9736-f25c6ae3cda8","owner":[],"postedDate":"February 17th, 2026","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2026-02-21T10:10:22+00:00","versionOfRecord":[],"versionCreatedAt":"2026-02-17 14:38:49","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-8865140","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8865140","identity":"rs-8865140","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}