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Glucose metabolism in small subcortical structures in Parkinson’s disease
Author(s) -
Borghammer Per,
Hansen Søren B.,
Eggers Carsten,
Chakravarty Mallar,
Vang Kim,
Aanerud Joel,
Hilker Rüdiger,
Heiss WolfDieter,
Rodell Anders,
Munk Ole L.,
Keator David,
Gjedde Albert
Publication year - 2012
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.2011.01556.x
Subject(s) - hypermetabolism , putamen , white matter , basal ganglia , positron emission tomography , deoxyglucose , pathology , neuroscience , spatial normalization , atrophy , neuroradiology , neurology , nuclear medicine , voxel , medicine , psychology , magnetic resonance imaging , radiology , central nervous system
Objectives – Evidence from experimental animal models of Parkinson’s disease (PD) suggests a characteristic pattern of metabolic perturbation in discrete, very small basal ganglia structures. These structures are generally too small to allow valid investigation by conventional positron emission tomography (PET) cameras. However, the high‐resolution research tomograph (HRRT) PET system has a resolution of 2 mm, sufficient for the investigation of important structures such as the pallidum and thalamic subnuclei. Materials and methods – Using the HRRT, we performed [ 18 F]‐fluorodeoxyglucose (FDG) scans on 21 patients with PD and 11 age‐matched controls. We employed three types of normalization: white matter, global mean, and data‐driven normalization. We performed volume‐of‐interest analyses of small subcortical gray matter structures. Voxel‐based comparisons were performed to investigate the extent of cortical hypometabolism. Results – The most significant level of relative subcortical hypermetabolism was detected in the external pallidum (GPe), irrespective of normalization strategy. Hypermetabolism was suggested also in the internal pallidum, thalamic subnuclei, and the putamen. Widespread cortical hypometabolism was seen in a pattern very similar to previously reported patterns in patients with PD. Conclusion – The presence and extent of subcortical hypermetabolism in PD is dependent on type of normalization. However, the present findings suggest that PD, in addition to widespread cortical hypometabolism, is probably characterized by true hypermetabolism in the GPe. This finding was predicted by the animal 2‐deoxyglucose autoradiography literature, in which high‐magnitude hypermetabolism was also most robustly detected in the GPe.