DOI: 10.1007/s00259-018-4033-0Pages: 1546-1556

Clinical utility of FDG-PET in amyotrophic lateral sclerosis and Huntington’s disease

1. Vita-Salute San Raffaele University, Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, San Raffaele Scientific Institute

2. IRCCS S. Giovanni di Dio, Fatebenefratelli, LANE – Laboratory of Alzheimer’s Neuroimaging & Epidemiology

3. University of Brescia, Department of Molecular and Translational Medicine

4. IRCCS S. Giovanni di Dio, Fatebenefratelli, Alzheimer Operative Unit

5. University of Geneva, LANVIE (Laboratoire de Neuroimagerie du Vieillissement), Department of Psychiatry

6. University of Navarra, Department of Nuclear Medicine, Clinica Universidad de Navarra

7. VU University Medical Center, Department of Neurology & Alzheimer Center, Amsterdam Neuroscience

8. University Hospital of Cologne, University of Cologne and German Center for Neurodegenerative Diseases (DZNE), Department of Nuclear Medicine

9. German Center for Neurodegenerative Diseases (DZNE)

10. University of Queensland and at the Mater Hospital Brisbane, Queensland Brain Institute

11. University of Genoa and Polyclinic San Martino Hospital, Department of Neuroscience (DINOGMI)

12. University College London, Division of Psychiatry & Essex Partnership University NHS Foundation Trust

13. Institute of Cognitive Sciences and Technologies, CNR

14. Karolinska Hospital Stockholm, Department of Nuclear Medicine

Correspondence to:
Marina Boccardi
Tel: 0041.(0)22.3055764




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.


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.


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.


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.

To access the full text, please Sign in

If you have institutional access, please click here

  • Accepted: Apr 16, 2018
  • Online: May 1, 2018

Article Tools