Federica Agosta1, Daniele Altomare2,3, Cristina Festari2,3, Stefania Orini4, Federica Gandolfo4, Marina Boccardi5,6, Javier Arbizu7, Femke Bouwman8, Alexander Drzezga9, Peter Nestor10,11, Flavio Nobili12, Zuzana Walker13, Marco Pagani14,15. 1. Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, San Raffaele Scientific Institute, Vita-Salute San Raffaele University, Milan, Italy. agosta.federica@hsr.it. 2. LANE - Laboratory of Alzheimer's Neuroimaging & Epidemiology, IRCCS S. Giovanni di Dio, Fatebenefratelli, Brescia, Italy. 3. Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy. 4. Alzheimer Operative Unit, IRCCS S. Giovanni di Dio, Fatebenefratelli, Brescia, Italy. 5. LANE - Laboratory of Alzheimer's Neuroimaging & Epidemiology, IRCCS S. Giovanni di Dio, Fatebenefratelli, Brescia, Italy. marina.boccardi@unige.ch. 6. LANVIE (Laboratoire de Neuroimagerie du Vieillissement), Department of Psychiatry, University of Geneva, Geneva, Switzerland. marina.boccardi@unige.ch. 7. Department of Nuclear Medicine, Clinica Universidad de Navarra, University of Navarra, Pamplona, Spain. 8. Department of Neurology & Alzheimer Center, Amsterdam Neuroscience, VU University Medical Center, Amsterdam, the Netherlands. 9. Department of Nuclear Medicine, University Hospital of Cologne, University of Cologne and German Center for Neurodegenerative Diseases (DZNE), Cologne, Germany. 10. German Center for Neurodegenerative Diseases (DZNE), Magdeburg, Germany. 11. Queensland Brain Institute, University of Queensland and at the Mater Hospital Brisbane, Brisbane, Australia. 12. Department of Neuroscience (DINOGMI), University of Genoa and Polyclinic San Martino Hospital, Genoa, Italy. 13. Division of Psychiatry & Essex Partnership University NHS Foundation Trust, University College London, London, UK. 14. Institute of Cognitive Sciences and Technologies, CNR, Rome, Italy. 15. Department of Nuclear Medicine, Karolinska Hospital Stockholm, Stockholm, Sweden.
Abstract
AIM: To evaluate the incremental value of FDG-PET over clinical tests in: (i) diagnosis of amyotrophic lateral sclerosis (ALS); (ii) picking early signs of neurodegeneration in patients with a genetic risk of Huntington's disease (HD); and detecting metabolic changes related to cognitive impairment in (iii) ALS and (iv) HD patients. METHODS: Four comprehensive literature searches were conducted using the PICO model to extract evidence from relevant studies. An expert panel then voted using the Delphi method on these four diagnostic scenarios. RESULTS: The availability of evidence was good for FDG-PET utility to support the diagnosis of ALS, poor for identifying presymptomatic subjects carrying HD mutation who will convert to HD, and lacking for identifying cognitive-related metabolic changes in both ALS and HD. After the Delphi consensual procedure, the panel did not support the clinical use of FDG-PET for any of the four scenarios. CONCLUSION: Relative to other neurodegenerative diseases, the clinical use of FDG-PET in ALS and HD is still in its infancy. Once validated by disease-control studies, FDG-PET might represent a potentially useful biomarker for ALS diagnosis. FDG-PET is presently not justified as a routine investigation to predict conversion to HD, nor to detect evidence of brain dysfunction justifying cognitive decline in ALS and HD.
AIM: To evaluate the incremental value of FDG-PET over clinical tests in: (i) diagnosis of amyotrophic lateral sclerosis (ALS); (ii) picking early signs of neurodegeneration in patients with a genetic risk of Huntington's disease (HD); and detecting metabolic changes related to cognitive impairment in (iii) ALS and (iv) HDpatients. METHODS: Four comprehensive literature searches were conducted using the PICO model to extract evidence from relevant studies. An expert panel then voted using the Delphi method on these four diagnostic scenarios. RESULTS: The availability of evidence was good for FDG-PET utility to support the diagnosis of ALS, poor for identifying presymptomatic subjects carrying HD mutation who will convert to HD, and lacking for identifying cognitive-related metabolic changes in both ALS and HD. After the Delphi consensual procedure, the panel did not support the clinical use of FDG-PET for any of the four scenarios. CONCLUSION: Relative to other neurodegenerative diseases, the clinical use of FDG-PET in ALS and HD is still in its infancy. Once validated by disease-control studies, FDG-PET might represent a potentially useful biomarker for ALS diagnosis. FDG-PET is presently not justified as a routine investigation to predict conversion to HD, nor to detect evidence of brain dysfunction justifying cognitive decline in ALS and HD.
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