nach oben

European Journal of Nuclear Medicine and Molecular Imaging

Erschienen in:

01.05.2018 | Original Article

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

verfasst von: Federica Agosta, Daniele Altomare, Cristina Festari, Stefania Orini, Federica Gandolfo, Marina Boccardi, Javier Arbizu, Femke Bouwman, Alexander Drzezga, Peter Nestor, Flavio Nobili, Zuzana Walker, Marco Pagani, for the EANM-EAN Task Force for the Prescription of FDG-PET for Dementing Neurodegenerative Disorders

Erschienen in: European Journal of Nuclear Medicine and Molecular Imaging | Ausgabe 9/2018

Einloggen, um Zugang zu erhalten

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.

Nobili F, Arbizu J, Bouwman FH, Drzezga A, Agosta F, Nestor P, et al. EANM-EAN recommendations for the use of brain 18F-Fluorodeoxyglucose Positron Emission Tomography (FDG-PET) in neurodegenerative cognitive impairment and dementia: Delphi consensus. Eur J Neurol. 2018 (submitted, March 13, 2018; MS: EJoN-18-0310).

Boccardi M, Festari C, Altomare D, Gandolfo F, Orini S, Nobili F et al. Assessing FDG-PET diagnostic accuracy studies to develop recommendations for clinical use in dementia. Eur J Nucl Med Mol Imaging. 2018; https://doi.org/10.1007/s00259-018-4024-1.CrossRefPubMed

Leone MA, Brainin M, Boon P, Pugliatti M, Keindl M, Bassetti CL. Guidance for the preparation of neurological management guidelines by EFNS scientific task forces - revised recommendations 2012. Eur J Neurol. 2013;20(3):410–9. https://doi.org/10.1111/ene.12043.CrossRefPubMed

Moher D, Liberati A, Tetzlaff J, Altman DG. Preferred reporting items for systematic reviews and meta-analyses: the PRISMA statement. J Clin Epidemiol. 2009;62(10):1006–12. https://doi.org/10.1016/j.jclinepi.2009.06.005.CrossRefPubMed

Coon EA, Whitwell JL, Parisi JE, Dickson DW, Josephs KA. Right temporal variant frontotemporal dementia with motor neuron disease. J Clin Neurosci. 2012;19(1):85–91. https://doi.org/10.1016/j.jocn.2011.06.007.CrossRefPubMed

Garraux G, Salmon E, Degueldre C, Lemaire C, Franck G. Medial temporal lobe metabolic impairment in dementia associated with motor neuron disease. J Neurol Sci. 1999;168(2):145–50.CrossRefPubMed

Hoffman JM, Mazziotta JC, Hawk TC, Sumida R. Cerebral glucose utilization in motor neuron disease. Arch Neurol. 1992;49(8):849–54.CrossRefPubMed

Jeong Y, Park KC, Cho SS, Kim EJ, Kang SJ, Kim SE, et al. Pattern of glucose hypometabolism in frontotemporal dementia with motor neuron disease. Neurology. 2005;64(4):734–6. https://doi.org/10.1212/01.WNL.0000152047.58767.9D.CrossRefPubMed

Tanaka M, Kondo S, Hirai S, Sun X, Yamagishi T, Okamoto K. Cerebral blood flow and oxygen metabolism in progressive dementia associated with amyotrophic lateral sclerosis. J Neurol Sci. 1993;120(1):22–8.CrossRefPubMed

10.

Tanaka M, Ichiba T, Kondo S, Hirai S, Okamoto K. Cerebral blood flow and oxygen metabolism in patients with progressive dementia and amyotrophic lateral sclerosis. Neurol Res. 2003;25(4):351–6. https://doi.org/10.1179/016164103101201670.CrossRefPubMed

11.

Chio A, Calvo A, Moglia C, Restagno G, Ossola I, Brunetti M, et al. Amyotrophic lateral sclerosis-frontotemporal lobar dementia in 3 families with p.Ala382Thr TARDBP mutations. Arch Neurol. 2010;67(8):1002–9. https://doi.org/10.1001/archneurol.2010.173.CrossRefPubMedPubMedCentral

12.

Carluer L, Mondou A, Buhour MS, Laisney M, Pelerin A, Eustache F, et al. Neural substrate of cognitive theory of mind impairment in amyotrophic lateral sclerosis. Cortex. 2015;65:19–30. https://doi.org/10.1016/j.cortex.2014.12.010.CrossRefPubMed

13.

Pagani M, Chio A, Valentini MC, Oberg J, Nobili F, Calvo A, et al. Functional pattern of brain FDG-PET in amyotrophic lateral sclerosis. Neurology. 2014;83(12):1067–74. https://doi.org/10.1212/WNL.0000000000000792.CrossRefPubMed

14.

Van Laere K, Vanhee A, Verschueren J, De Coster L, Driesen A, Dupont P, et al. Value of 18fluorodeoxyglucose-positron-emission tomography in amyotrophic lateral sclerosis: a prospective study. JAMA Neurol. 2014;71(5):553–61. https://doi.org/10.1001/jamaneurol.2014.62.CrossRefPubMed

15.

Cistaro A, Pagani M, Montuschi A, Calvo A, Moglia C, Canosa A, et al. The metabolic signature of C9ORF72-related ALS: FDG PET comparison with nonmutated patients. Eur J Nucl Med Mol Imaging. 2014;41(5):844–52. https://doi.org/10.1007/s00259-013-2667-5.CrossRefPubMedPubMedCentral

16.

Cistaro A, Valentini MC, Chio A, Nobili F, Calvo A, Moglia C, et al. Brain hypermetabolism in amyotrophic lateral sclerosis: a FDG PET study in ALS of spinal and bulbar onset. Eur J Nucl Med Mol Imaging. 2012;39(2):251–9. https://doi.org/10.1007/s00259-011-1979-6.CrossRefPubMed

17.

Dalakas MC, Hatazawa J, Brooks RA, Di Chiro G. Lowered cerebral glucose utilization in amyotrophic lateral sclerosis. Ann Neurol. 1987;22(5):580–6. https://doi.org/10.1002/ana.410220504.CrossRefPubMed

18.

Hatazawa J, Brooks RA, Dalakas MC, Mansi L, Di Chiro G. Cortical motor-sensory hypometabolism in amyotrophic lateral sclerosis: a PET study. J Comput Assist Tomogr. 1988;12(4):630–6.CrossRefPubMed

19.

Ludolph AC, Langen KJ, Regard M, Herzog H, Kemper B, Kuwert T, et al. Frontal lobe function in amyotrophic lateral sclerosis: a neuropsychologic and positron emission tomography study. Acta Neurol Scand. 1992;85(2):81–9.CrossRefPubMed

20.

Rajagopalan V, Pioro EP. Comparing brain structural MRI and metabolic FDG-PET changes in patients with ALS-FTD: 'the chicken or the egg?' question. J Neurol Neurosurg Psychiatry. 2015;86(9):952–8. https://doi.org/10.1136/jnnp-2014-308239.CrossRefPubMed

21.

Solje E, Aaltokallio H, Koivumaa-Honkanen H, Suhonen NM, Moilanen V, Kiviharju A, et al. The phenotype of the C9ORF72 expansion carriers according to revised criteria for bvFTD. PLoS One. 2015;10(7):e0131817. https://doi.org/10.1371/journal.pone.0131817.CrossRefPubMedPubMedCentral

22.

Boeve BF, Boylan KB, Graff-Radford NR, DeJesus-Hernandez M, Knopman DS, Pedraza O, et al. Characterization of frontotemporal dementia and/or amyotrophic lateral sclerosis associated with the GGGGCC repeat expansion in C9ORF72. Brain. 2012;135(Pt 3):765–83. https://doi.org/10.1093/brain/aws004.CrossRefPubMedPubMedCentral

23.

Canosa A, Pagani M, Cistaro A, Montuschi A, Iazzolino B, Fania P, et al. 18F-FDG-PET correlates of cognitive impairment in ALS. Neurology. 2016;86(1):44–9. https://doi.org/10.1212/WNL.0000000000002242.CrossRefPubMed

24.

Matusch A, Saft C, Elmenhorst D, Kraus PH, Gold R, Hartung HP, et al. Cross sectional PET study of cerebral adenosine A(1) receptors in premanifest and manifest Huntington's disease. Eur J Nucl Med Mol Imaging. 2014;41(6):1210–20. https://doi.org/10.1007/s00259-014-2724-8.CrossRefPubMed

25.

Politis M, Pavese N, Tai YF, Tabrizi SJ, Barker RA, Piccini P. Hypothalamic involvement in Huntington's disease: an in vivo PET study. Brain. 2008;131(Pt 11):2860–9. https://doi.org/10.1093/brain/awn244.CrossRefPubMed

26.

Grafton ST, Mazziotta JC, Pahl JJ, St George-Hyslop P, Haines JL, Gusella J, et al. A comparison of neurological, metabolic, structural, and genetic evaluations in persons at risk for Huntington's disease. Ann Neurol. 1990;28(5):614–21. https://doi.org/10.1002/ana.410280503.CrossRefPubMed

27.

Grafton ST, Mazziotta JC, Pahl JJ, St George-Hyslop P, Haines JL, Gusella J, et al. Serial changes of cerebral glucose metabolism and caudate size in persons at risk for Huntington's disease. Arch Neurol. 1992;49(11):1161–7.CrossRefPubMed

28.

Boecker H, Kuwert T, Langen KJ, Lange HW, Czech N, Ziemons K, et al. SPECT with HMPAO compared to PET with FDG in Huntington disease. J Comput Assist Tomogr. 1994;18(4):542–8.CrossRefPubMed

29.

Hayden MR, Martin WR, Stoessl AJ, Clark C, Hollenberg S, Adam MJ, et al. Positron emission tomography in the early diagnosis of Huntington's disease. Neurology. 1986;36(7):888–94.CrossRefPubMed

30.

Kuwert T, Lange HW, Langen KJ, Herzog H, Aulich A, Feinendegen LE. Cortical and subcortical glucose consumption measured by PET in patients with Huntington's disease. Brain. 1990;113(Pt 5):1405–23.CrossRefPubMed

31.

Lee SJ, Lee WY, Kim YK, An YS, Cho JW, Choi JY, et al. Apparent relative hypermetabolism of selective brain areas in Huntington disease and importance of reference region for analysis. Clin Nucl Med. 2012;37(7):663–8. https://doi.org/10.1097/RLU.0b013e3182478bf2.CrossRefPubMed

32.

Martin WR, Clark C, Ammann W, Stoessl AJ, Shtybel W, Hayden MR. Cortical glucose metabolism in Huntington's disease. Neurology. 1992;42(1):223–9.CrossRefPubMed

33.

Powers WJ, Videen TO, Markham J, McGee-Minnich L, Antenor-Dorsey JV, Hershey T, et al. Selective defect of in vivo glycolysis in early Huntington's disease striatum. Proc Natl Acad Sci U S A. 2007;104(8):2945–9. https://doi.org/10.1073/pnas.0609833104.CrossRefPubMedPubMedCentral

34.

Young AB, Penney JB, Starosta-Rubinstein S, Markel DS, Berent S, Giordani B, et al. PET scan investigations of Huntington's disease: cerebral metabolic correlates of neurological features and functional decline. Ann Neurol. 1986;20(3):296–303. https://doi.org/10.1002/ana.410200305.CrossRefPubMed

35.

Kuhl DE, Metter EJ, Riege WH. Patterns of local cerebral glucose utilization determined in Parkinson's disease by the [18F]fluorodeoxyglucose method. Ann Neurol. 1984;15(5):419–24. https://doi.org/10.1002/ana.410150504.CrossRefPubMed

36.

Kuwert T, Lange HW, Boecker H, Titz H, Herzog H, Aulich A, et al. Striatal glucose consumption in chorea-free subjects at risk of Huntington's disease. J Neurol. 1993;241(1):31–6.CrossRefPubMed

37.

Mazziotta JC, Phelps ME, Pahl JJ, Huang SC, Baxter LR, Riege WH, et al. Reduced cerebral glucose metabolism in asymptomatic subjects at risk for Huntington's disease. N Engl J Med. 1987;316(7):357–62. https://doi.org/10.1056/NEJM198702123160701.CrossRefPubMed

38.

Otsuka M, Ichiya Y, Kuwabara Y, Hosokawa S, Sasaki M, Fukumura T, et al. Cerebral glucose metabolism and striatal 18F-dopa uptake by PET in cases of chorea with or without dementia. J Neurol Sci. 1993;115(2):153–7.CrossRefPubMed

39.

Young AB, Penney JB, Starosta-Rubinstein S, Markel D, Berent S, Rothley J, et al. Normal caudate glucose metabolism in persons at risk for Huntington's disease. Arch Neurol. 1987;44(3):254–7.CrossRefPubMed

40.

Kuwert T, Noth J, Scholz D, Schwarz M, Lange HW, Topper R, et al. Comparison of somatosensory evoked potentials with striatal glucose consumption measured by positron emission tomography in the early diagnosis of Huntington's disease. Mov Disord. 1993;8(1):98–106. https://doi.org/10.1002/mds.870080118.CrossRefPubMed

41.

van Oostrom JC, Dekker M, Willemsen AT, de Jong BM, Roos RA, Leenders KL. Changes in striatal dopamine D2 receptor binding in pre-clinical Huntington's disease. Eur J Neurol. 2009;16(2):226–31. https://doi.org/10.1111/j.1468-1331.2008.02390.x.CrossRefPubMed

42.

Ciarmiello A, Giovacchini G, Orobello S, Bruselli L, Elifani F, Squitieri F. 18F-FDG PET uptake in the pre-Huntington disease caudate affects the time-to-onset independently of CAG expansion size. Eur J Nucl Med Mol Imaging. 2012;39(6):1030–6. https://doi.org/10.1007/s00259-012-2114-z.CrossRefPubMed

43.

Feigin A, Tang C, Ma Y, Mattis P, Zgaljardic D, Guttman M, et al. Thalamic metabolism and symptom onset in preclinical Huntington's disease. Brain. 2007;130(Pt 11):2858–67. https://doi.org/10.1093/brain/awm217.CrossRefPubMed

44.

Herben-Dekker M, van Oostrom JC, Roos RA, Jurgens CK, Witjes-Ane MN, Kremer HP, et al. Striatal metabolism and psychomotor speed as predictors of motor onset in Huntington's disease. J Neurol. 2014;261(7):1387–97. https://doi.org/10.1007/s00415-014-7350-7.CrossRefPubMed

45.

Tang CC, Feigin A, Ma Y, Habeck C, Paulsen JS, Leenders KL, et al. Metabolic network as a progression biomarker of premanifest Huntington's disease. J Clin Invest. 2013;123(9):4076–88. https://doi.org/10.1172/JCI69411.CrossRefPubMedPubMedCentral

46.

Antonini A, Leenders KL, Spiegel R, Meier D, Vontobel P, Weigell-Weber M, et al. Striatal glucose metabolism and dopamine D2 receptor binding in asymptomatic gene carriers and patients with Huntington's disease. Brain. 1996;119(Pt 6):2085–95.CrossRefPubMed

47.

Ciarmiello A, Cannella M, Lastoria S, Simonelli M, Frati L, Rubinsztein DC, et al. Brain white-matter volume loss and glucose hypometabolism precede the clinical symptoms of Huntington's disease. J Nucl Med. 2006;47(2):215–22.PubMed

48.

Feigin A, Leenders KL, Moeller JR, Missimer J, Kuenig G, Spetsieris P, et al. Metabolic network abnormalities in early Huntington's disease: an [(18)F]FDG PET study. J Nucl Med. 2001;42(11):1591–5.PubMed

49.

van Oostrom JC, Maguire RP, Verschuuren-Bemelmans CC. Veenma-van der Duin L, Pruim J, Roos RA et al. striatal dopamine D2 receptors, metabolism, and volume in preclinical Huntington disease. Neurology. 2005;65(6):941–3. https://doi.org/10.1212/01.wnl.0000176071.08694.cc.CrossRefPubMed

50.

Allain P, Gaura V, Fasotti L, Chauvire V, Prundean A, Sherer-Gagou C, et al. The neural substrates of script knowledge deficits as revealed by a PET study in Huntington's disease. Neuropsychologia. 2011;49(9):2673–84. https://doi.org/10.1016/j.neuropsychologia.2011.05.015.CrossRefPubMed

51.

Berent S, Giordani B, Lehtinen S, Markel D, Penney JB, Buchtel HA, et al. Positron emission tomographic scan investigations of Huntington's disease: cerebral metabolic correlates of cognitive function. Ann Neurol. 1988;23(6):541–6. https://doi.org/10.1002/ana.410230603.CrossRefPubMed

52.

Pagani M, Oberg J, De Carli F, Calvo A, Moglia C, Canosa A, et al. Metabolic spatial connectivity in amyotrophic lateral sclerosis as revealed by independent component analysis. Hum Brain Mapp. 2016;37(3):942–53. https://doi.org/10.1002/hbm.23078.CrossRefPubMed

53.

Van Weehaeghe D, Ceccarini J, Delva A, Robberecht W, Van Damme P, Van Laere K. Prospective validation of 18F-FDG brain PET discriminant analysis methods in the diagnosis of amyotrophic lateral sclerosis. J Nucl Med. 2016;57(8):1238–43. https://doi.org/10.2967/jnumed.115.166272.CrossRefPubMed

54.

Strong MJ, Abrahams S, Goldstein LH, Woolley S, McLaughlin P, Snowden J, et al. Amyotrophic lateral sclerosis - frontotemporal spectrum disorder (ALS-FTSD): revised diagnostic criteria. Amyotroph Lateral Scler Frontotemporal Degener. 2017;18(3-4):153–74. https://doi.org/10.1080/21678421.2016.1267768.CrossRefPubMedPubMedCentral

55.

Chio A, Ilardi A, Cammarosano S, Moglia C, Montuschi A, Calvo A. Neurobehavioral dysfunction in ALS has a negative effect on outcome and use of PEG and NIV. Neurology. 2012;78(14):1085–9. https://doi.org/10.1212/WNL.0b013e31824e8f53.CrossRefPubMed

56.

Rascovsky K, Hodges JR, Knopman D, Mendez MF, Kramer JH, Neuhaus J, et al. Sensitivity of revised diagnostic criteria for the behavioural variant of frontotemporal dementia. Brain. 2011;134(Pt 9):2456–77. https://doi.org/10.1093/brain/awr179.CrossRefPubMedPubMedCentral

57.

Lopez-Mora DA, Camacho V, Perez-Perez J, Martinez-Horta S, Fernandez A, Sampedro F, et al. Striatal hypometabolism in premanifest and manifest Huntington's disease patients. Eur J Nucl Med Mol Imaging. 2016;43(12):2183–9. https://doi.org/10.1007/s00259-016-3445-y.CrossRefPubMed

Titel: Clinical utility of FDG-PET in amyotrophic lateral sclerosis and Huntington’s disease
verfasst von: Federica Agosta
Daniele Altomare
Cristina Festari
Stefania Orini
Federica Gandolfo
Marina Boccardi
Javier Arbizu
Femke Bouwman
Alexander Drzezga
Peter Nestor
Flavio Nobili
Zuzana Walker
Marco Pagani
for the EANM-EAN Task Force for the Prescription of FDG-PET for Dementing Neurodegenerative Disorders
Publikationsdatum: 01.05.2018
Verlag: Springer Berlin Heidelberg
Erschienen in: European Journal of Nuclear Medicine and Molecular Imaging / Ausgabe 9/2018
Print ISSN: 1619-7070
Elektronische ISSN: 1619-7089
DOI: https://doi.org/10.1007/s00259-018-4033-0

Springer Medizin

Abstract

Aim

Methods

Results

Conclusion

Bitte loggen Sie sich ein, um Zugang zu diesem Inhalt zu erhalten

Weitere Artikel der Ausgabe 9/2018

Noradrenaline transporter availability on [11C]MRB PET predicts weight loss success in highly obese adults

18F-FDG PET and high-resolution MRI co-registration for pre-surgical evaluation of patients with conventional MRI-negative refractory extra-temporal lobe epilepsy

Use of FET PET in glioblastoma patients undergoing neurooncological treatment including tumour-treating fields: initial experience

Assessing FDG-PET diagnostic accuracy studies to develop recommendations for clinical use in dementia

Diagnostic utility of 18F-Fluorodeoxyglucose positron emission tomography (FDG-PET) in asymptomatic subjects at increased risk for Alzheimer’s disease

Clinical utility of FDG-PET for the differential diagnosis among the main forms of dementia