{"title":"Isolated Pancerebellar Syndrome With anti-GQ1b IgG Positivity: A Case Report.","authors":"Iyas Daghlas, Liza Solovey, Vanja C Douglas","doi":"10.1177/19418744251367176","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Ataxia is a hallmark of the anti-GQ1b antibody syndrome, though it is unclear whether this symptom arises primarily from sensory nerve injury or from cerebellar involvement. We report a case of a patient with a clinically isolated post-infectious pancerebellar syndrome with anti-GQ1b antibody positivity.</p><p><strong>Case presentation: </strong>A 22-year-old previously healthy woman presented with acute-onset, progressive imbalance, limb ataxia, and dysarthria following an upper respiratory tract infection. She had no paresthesias, numbness, or diplopia. Neurological examination revealed an isolated pancerebellar syndrome including ocular and limb dysmetria, intention tremor, and gait ataxia. All sensory modalities were unaffected, reflex testing was normal, and there was no ophthalmoplegia. In-hospital serum and CSF testing was unremarkable, and brain magnetic resonance imaging was normal. The patient was empirically treated with intravenous immunoglobulin. Her symptoms were moderately improved by discharge (hospital day 5), and fully resolved several months later. Serological testing sent during the hospitalization subsequently revealed anti-GQ1b IgG positivity.</p><p><strong>Conclusions: </strong>This case expands the spectrum of anti-GQ1b syndrome to include isolated cerebellar ataxia, suggesting that ataxia in this syndrome can have cerebellar origin. Clinicians should consider anti-GQ1b testing in cases of acute cerebellar ataxia following infection.</p>","PeriodicalId":46355,"journal":{"name":"Neurohospitalist","volume":" ","pages":"19418744251367176"},"PeriodicalIF":0.7000,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12328339/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neurohospitalist","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1177/19418744251367176","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Ataxia is a hallmark of the anti-GQ1b antibody syndrome, though it is unclear whether this symptom arises primarily from sensory nerve injury or from cerebellar involvement. We report a case of a patient with a clinically isolated post-infectious pancerebellar syndrome with anti-GQ1b antibody positivity.
Case presentation: A 22-year-old previously healthy woman presented with acute-onset, progressive imbalance, limb ataxia, and dysarthria following an upper respiratory tract infection. She had no paresthesias, numbness, or diplopia. Neurological examination revealed an isolated pancerebellar syndrome including ocular and limb dysmetria, intention tremor, and gait ataxia. All sensory modalities were unaffected, reflex testing was normal, and there was no ophthalmoplegia. In-hospital serum and CSF testing was unremarkable, and brain magnetic resonance imaging was normal. The patient was empirically treated with intravenous immunoglobulin. Her symptoms were moderately improved by discharge (hospital day 5), and fully resolved several months later. Serological testing sent during the hospitalization subsequently revealed anti-GQ1b IgG positivity.
Conclusions: This case expands the spectrum of anti-GQ1b syndrome to include isolated cerebellar ataxia, suggesting that ataxia in this syndrome can have cerebellar origin. Clinicians should consider anti-GQ1b testing in cases of acute cerebellar ataxia following infection.