Subcortical [ 18F]fluorodeoxyglucose uptake in lesional epilepsy in patients with intracranial tumour

Research output: Contribution to journalArticle

Abstract

Background: We hypothesized that in patients with intracerebral tumours a subcortical metabolical shift may be present when the underlying pathology can, itself, be the epileptogenic focus. We also assumed that by studying the alterations in glucose metabolism beyond the tumour's borders we could identify a modulator area. Methods: Sixty-seven patients with supratentorial brain tumour associated epilepsy were investigated interictally, in normoglycaemlc conditions, by using [ 18F]fluorodeoxyglucose positron emission tomography (FDG PET). The studies were analysed semiquantitatively by calculating standardized uptake values and asymmetry indices. Normal subjects and patients with non-epileptic brain lesions were used as controls. Results: Compared to normal controls frontal and temporal tumours showed significant changes in thalamic FDG uptake, which reflected hypometabolism of the affected side. It was noted in occipito-medial cortex in temporal tumours and in lentiform nucleus in frontal tumours as well. Comparison to lesional brains only proved that there was significant hypometabolism in lentiform nucleus in temporal tumours. Conclusions: The quantified values obviously reflect biological changes. The observed subcortical hypometabolism Is most likely secondary to underlying pathology. Although seizures in tumorous patients do not originate from subcortical structures their influence on cortical sites of seizure initiation could be explained by defective subcortical regulation of cortical excitability.

Original languageEnglish
Pages (from-to)123-128
Number of pages6
JournalNuclear Medicine Communications
Volume25
Issue number2
DOIs
Publication statusPublished - Feb 2004

Fingerprint

Fluorodeoxyglucose F18
Epilepsy
Corpus Striatum
Neoplasms
Seizures
Supratentorial Neoplasms
Pathology
Brain
Temporal Lobe
Brain Neoplasms
Positron-Emission Tomography
Glucose

Keywords

  • [ F]fluorodeoxyglucose pet
  • Brain tumour
  • Lesional epilepsy
  • Subcortical metabolic depression

ASJC Scopus subject areas

  • Radiology Nuclear Medicine and imaging
  • Radiological and Ultrasound Technology

Cite this

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title = "Subcortical [ 18F]fluorodeoxyglucose uptake in lesional epilepsy in patients with intracranial tumour",
abstract = "Background: We hypothesized that in patients with intracerebral tumours a subcortical metabolical shift may be present when the underlying pathology can, itself, be the epileptogenic focus. We also assumed that by studying the alterations in glucose metabolism beyond the tumour's borders we could identify a modulator area. Methods: Sixty-seven patients with supratentorial brain tumour associated epilepsy were investigated interictally, in normoglycaemlc conditions, by using [ 18F]fluorodeoxyglucose positron emission tomography (FDG PET). The studies were analysed semiquantitatively by calculating standardized uptake values and asymmetry indices. Normal subjects and patients with non-epileptic brain lesions were used as controls. Results: Compared to normal controls frontal and temporal tumours showed significant changes in thalamic FDG uptake, which reflected hypometabolism of the affected side. It was noted in occipito-medial cortex in temporal tumours and in lentiform nucleus in frontal tumours as well. Comparison to lesional brains only proved that there was significant hypometabolism in lentiform nucleus in temporal tumours. Conclusions: The quantified values obviously reflect biological changes. The observed subcortical hypometabolism Is most likely secondary to underlying pathology. Although seizures in tumorous patients do not originate from subcortical structures their influence on cortical sites of seizure initiation could be explained by defective subcortical regulation of cortical excitability.",
keywords = "[ F]fluorodeoxyglucose pet, Brain tumour, Lesional epilepsy, Subcortical metabolic depression",
author = "Laszlo Novak and M. Emri and P. Moln{\'a}r and L. Balkay and Z. Lengyel and L. Tr{\'o}n",
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T1 - Subcortical [ 18F]fluorodeoxyglucose uptake in lesional epilepsy in patients with intracranial tumour

AU - Novak, Laszlo

AU - Emri, M.

AU - Molnár, P.

AU - Balkay, L.

AU - Lengyel, Z.

AU - Trón, L.

PY - 2004/2

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N2 - Background: We hypothesized that in patients with intracerebral tumours a subcortical metabolical shift may be present when the underlying pathology can, itself, be the epileptogenic focus. We also assumed that by studying the alterations in glucose metabolism beyond the tumour's borders we could identify a modulator area. Methods: Sixty-seven patients with supratentorial brain tumour associated epilepsy were investigated interictally, in normoglycaemlc conditions, by using [ 18F]fluorodeoxyglucose positron emission tomography (FDG PET). The studies were analysed semiquantitatively by calculating standardized uptake values and asymmetry indices. Normal subjects and patients with non-epileptic brain lesions were used as controls. Results: Compared to normal controls frontal and temporal tumours showed significant changes in thalamic FDG uptake, which reflected hypometabolism of the affected side. It was noted in occipito-medial cortex in temporal tumours and in lentiform nucleus in frontal tumours as well. Comparison to lesional brains only proved that there was significant hypometabolism in lentiform nucleus in temporal tumours. Conclusions: The quantified values obviously reflect biological changes. The observed subcortical hypometabolism Is most likely secondary to underlying pathology. Although seizures in tumorous patients do not originate from subcortical structures their influence on cortical sites of seizure initiation could be explained by defective subcortical regulation of cortical excitability.

AB - Background: We hypothesized that in patients with intracerebral tumours a subcortical metabolical shift may be present when the underlying pathology can, itself, be the epileptogenic focus. We also assumed that by studying the alterations in glucose metabolism beyond the tumour's borders we could identify a modulator area. Methods: Sixty-seven patients with supratentorial brain tumour associated epilepsy were investigated interictally, in normoglycaemlc conditions, by using [ 18F]fluorodeoxyglucose positron emission tomography (FDG PET). The studies were analysed semiquantitatively by calculating standardized uptake values and asymmetry indices. Normal subjects and patients with non-epileptic brain lesions were used as controls. Results: Compared to normal controls frontal and temporal tumours showed significant changes in thalamic FDG uptake, which reflected hypometabolism of the affected side. It was noted in occipito-medial cortex in temporal tumours and in lentiform nucleus in frontal tumours as well. Comparison to lesional brains only proved that there was significant hypometabolism in lentiform nucleus in temporal tumours. Conclusions: The quantified values obviously reflect biological changes. The observed subcortical hypometabolism Is most likely secondary to underlying pathology. Although seizures in tumorous patients do not originate from subcortical structures their influence on cortical sites of seizure initiation could be explained by defective subcortical regulation of cortical excitability.

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