Striking Bilateral Cerebellar Hypermetabolism on 18F FDG-PET in a Patient of Sudden Onset Gait Ataxia with Absence of Paraneoplastic Antibody and Other Localizing Imaging Indicator.
IF 0.5 Q4 RADIOLOGY, NUCLEAR MEDICINE & MEDICAL IMAGING
{"title":"Striking Bilateral Cerebellar Hypermetabolism on <sup>18</sup>F FDG-PET in a Patient of Sudden Onset Gait Ataxia with Absence of Paraneoplastic Antibody and Other Localizing Imaging Indicator.","authors":"Parth Baberwal, Sunita Nitin Sonavane, Sandip Basu","doi":"10.4103/ijnm.ijnm_26_25","DOIUrl":null,"url":null,"abstract":"<p><p>A 69-year-old gentleman presented with complains of giddiness, gait ataxia, vomiting, and slurring of speech with clinical signs pointing to cerebellar etiology. The magnetic resonance imaging brain revealed no significant abnormality. <sup>18</sup>F-fluorodeoxyglucose (<sup>18</sup>F FDG) positron emission tomography (PET)/computed tomography showed hyper-metabolism in bilateral cerebellar hemispheres, pons, mid-brain and bilateral medial temporal cortices. Further quantitative NeuroQ analysis of <sup>18</sup>F FDG-PET showed similar findings. Paraneoplastic antibody panel (anti-Hu, anti-Yo, anti-Ri, NMDA, CASPR-2 etc.) was negative. Clinical suspicion and PET imaging correlation led the neurologist to suspicion of inflammatory/autoimmune etiology, and the patient was empirically started on four cycles of plasma exchange therapy and course of steroids, however, no significant clinical response was noted. At post-6 months of <sup>18</sup>F FDG-PET, he expired out of respiratory illness (pneumonia).</p>","PeriodicalId":45830,"journal":{"name":"Indian Journal of Nuclear Medicine","volume":"40 4","pages":"240-243"},"PeriodicalIF":0.5000,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12503172/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Indian Journal of Nuclear Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4103/ijnm.ijnm_26_25","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/9/19 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"RADIOLOGY, NUCLEAR MEDICINE & MEDICAL IMAGING","Score":null,"Total":0}
引用次数: 0
Abstract
A 69-year-old gentleman presented with complains of giddiness, gait ataxia, vomiting, and slurring of speech with clinical signs pointing to cerebellar etiology. The magnetic resonance imaging brain revealed no significant abnormality. 18F-fluorodeoxyglucose (18F FDG) positron emission tomography (PET)/computed tomography showed hyper-metabolism in bilateral cerebellar hemispheres, pons, mid-brain and bilateral medial temporal cortices. Further quantitative NeuroQ analysis of 18F FDG-PET showed similar findings. Paraneoplastic antibody panel (anti-Hu, anti-Yo, anti-Ri, NMDA, CASPR-2 etc.) was negative. Clinical suspicion and PET imaging correlation led the neurologist to suspicion of inflammatory/autoimmune etiology, and the patient was empirically started on four cycles of plasma exchange therapy and course of steroids, however, no significant clinical response was noted. At post-6 months of 18F FDG-PET, he expired out of respiratory illness (pneumonia).