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Salla Lamusuo, MD; Leena Jutila, MD; Aarne Ylinen, MD, PhD; Reetta Kälviäinen, MD, PhD; Esa Mervaala, MD, PhD; Merja Haaparanta, PhD; Satu Jääskeläinen, MD, PhD; Kaarina Partanen, MD, PhD; Matti Vapalahti, MD, PhD; Juha Rinne, MD, PhD

Arch Neurol. 2001;58:933-939.

Background  The relationship between reduced glucose metabolism in positron emission tomography with fludeoxyglucose F 18 ([¹⁸F]FDG-PET) and hippocampal damage (HD) in patients with temporal lobe epilepsy is still unclear.

Objective  To determine whether the presence and severity of HD verified by quantitative magnetic resonance imaging (QMRI) and histopathological analysis affect the degree of hypometabolism.

Patients and Methods  Sixteen patients with drug-resistant temporal lobe epilepsy underwent [¹⁸F]FDG-PET and QMRI (hippocampal volumetry and T2 relaxometry) before surgery. Histopathological analysis of the hippocampus included measurements of neuronal loss, proliferation of glial cells, and mossy fiber sprouting. The asymmetry in glucose metabolism described the degree of hypometabolism.

Results  Temporal hypometabolism was not related to severity of HD as measured by QMRI or histopathological analysis. The degree of hypometabolism did not differ in patients with mild, moderate, or severe HD. In addition, [¹⁸F]FDG-PET revealed significant temporal hypometabolism even though hippocampal QMRI findings were normal or showed only mild HD. Thus, glucose consumption was reduced over and above the histopathological changes.

Conclusions  [¹⁸F]FDG-PET is sensitive for localizing the epileptogenic region in patients with temporal lobe epilepsy. However, it is insensitive to reflect the severity of HD.

From the Departments of Neurology (Drs Lamusuo and Rinne) and Neurophysiology (Dr Jääskeläinen) and the Turku PET Centre, Radiopharmaceutical Chemistry Laboratory (Dr Haaparanta) and PET Unit (Dr Rinne), University of Turku, Turku, Finland; the Departments of Neurology (Drs Jutila, Ylinen, and Kälviäinen), Neurophysiology (Dr Mervaala), and Radiology, MRI Unit (Dr Partanen), Kuopio University Hospital, Kuopio, Finland; and the Departments of Neuroscience and Neurology (Dr Ylinen) and Neurosurgery (Dr Vapalahti), University of Kuopio.

Corresponding author and reprints: Juha Rinne, MD, PhD, Department of Neurology, University of Turku, PO Box 52, FIN-20521 Turku, Finland (e-mail: juha.rinne{at}pet.tyks.fi).

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