Cerebral glucose metabolism in adults with neurofibromatosis type 1.
Previous studies with positron emission tomography (PET) and the glucose analog F-18-fluorodeoxyglucose (FDG) in patients with neurofibromatosis type 1 (NF1) suggest reduced cerebral glucose metabolism in NF1 specifically in the thalamus. The latter is distinguished by extensive neural circuitry connections which makes thalamic hypoactivity in NF1 an interesting finding. Yet it is not very well confirmed, since previous studies were limited by small sample size and/or poorly matched control groups. Primary aim of the present study therefore was to compare brain FDG PET between a large sample of NF1 patients and a well-matched control group. Secondary aim was to test for an NF1-associated FDG effect in the amygdala, as increased blood flow in the amygdala has recently been detected in a mouse model of NF1. Fifty adult NF1 patients and 50 gender- and age-matched control subjects were included retrospectively. Voxel-wise comparison of brain FDG uptake was performed using the statistical parametric mapping (SPM8). Additional region-of-interest (ROI) analysis was performed using standard ROI templates. Voxel-based testing revealed a single 11.2 ml cluster of reduced FDG uptake in the thalamus of NF1 patients. There was no further significant cluster throughout the whole brain including the amygdala, neither hypo nor hyper. ROI-analysis confirmed reduction of thalamic FDG uptake in the NF1 group (p<0.0005) with a magnitude of 7.6%. In conclusion, adults with NF1 show reduced brain activity specifically in thalamus. There is no indication of abnormal brain activity in the amygdala in humans with NF1.
Department of Radiology and Nuclear Medicine, University Hospital Magdeburg, Magdeburg, Germany. Electronic address: ivayla.apostolova@med.ovgu.de.
Ivayla
I
Apostolova
Department of Nuclear Medicine, Medical University Hannover, Hannover, Germany.
Thorsten
T
Derlin
Department of Radiology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Johannes
J
Salamon
Department of Radiology and Nuclear Medicine, University Hospital Magdeburg, Magdeburg, Germany.
Holger
H
Amthauer
Department of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Sofia
S
Granström
Department of Nuclear Medicine, University Medicine Charité Berlin, Berlin, Germany.
Winfried
W
Brenner
Department of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Victor-Felix
VF
Mautner
Department of Nuclear Medicine, University Medicine Charité Berlin, Berlin, Germany.
Ralph
R
Buchert
D000328:Adult; D001931:Brain Mapping; D016022:Case-Control Studies; D002540:Cerebral Cortex / Q000000981:diagnostic imaging / Q000378:metabolism*; D005260:Female; D019788:Fluorodeoxyglucose F18 / Q000378:metabolism; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D007091:Image Processing, Computer-Assisted; D008297:Male; D008875:Middle Aged; D009456:Neurofibromatosis 1 / Q000000981:diagnostic imaging / Q000473:pathology*; D049268:Positron-Emission Tomography; D019275:Radiopharmaceuticals / Q000378:metabolism; D013788:Thalamus / Q000000981:diagnostic imaging / Q000378:metabolism; D015898:Tomography Scanners, X-Ray Computed; D055815:Young Adult
D019275:Radiopharmaceuticals; D019788:Fluorodeoxyglucose F18; D005947:Glucose
Amygdala; Cerebral glucose metabolism; FDG PET; Neurofibromatosis type 1; Thalamus