Beheshti PET/CT Imaging in Tracers Beyond FDG, An Issue of PET Clinics

1. Auflage 2014
ISBN: 978-0-323-31187-8
Verlag: Elsevier HealthScience EN
Format: EPUB
Kopierschutz: Adobe DRM (»Systemvoraussetzungen)

E-Book, Englisch, 100 Seiten

This issue of PET Clinics examines PET/CT Imaging in Tracers Beyond FDG. Article include standardization and quantification in PET/CT imaging: tracers beyond FDG; 18F NaF PET/CT imaging; 18F NaF PET/CT imaging in pediatrics; choline PET/CT imaging for the head and neck, thorax, abdomen, and pelvis; DOPA PET/CT imaging for the head and neck, thorax, abdomen, and pelvis; 68 GaSSRTs PET/CT imaging for the head and neck, thorax, abdomen, and pelvis; FLT PET/CT imaging for the head and neck, thorax, abdomen, and pelvis; hypoxia tracers; PET/MRI tracers beyond FDG: current status and future aspects; PET/CT normal variations: effect of novel quantitative approaches; and more!

Autoren/Hrsg.

Beheshti, Mohsen

Leseproben

Brain
Positron Emission Tomography Tracers Beyond [18F]Fluorodeoxyglucose
Tarun Singhal, MDa, Abass Alavi, MDb and Chun K. Kim, MDa*[e-mail],     aDivision of Nuclear Medicine and Molecular Imaging, Department of Radiology, Brigham and Women’s Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA; bDivision of Nuclear Medicine, Department of Radiology, University of Pennsylvania School of Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania *Corresponding author. Division of Nuclear Medicine and Molecular Imaging, Department of Radiology, Brigham and Women’s Hospital, Harvard Medical School, 75 Francis Street, ASB1 L1-037, Boston, MA 02115. Several positron emission tomography (PET) radiopharmaceuticals beyond fluorodeoxyglucose (FDG) have been used to study the physiology and pathophysiology in neurosciences. This article provides a broad overview of some of the commonly studied radiopharmaceuticals for PET imaging in selected neurologic conditions, particularly attempting to study their clinical relevance. Future studies on the use of advanced PET imaging in delineating neural pathophysiology, drug development, and altering patient management and outcomes across the disciplines of neurosciences are needed. Keywords Positron emission tomography Brain Central nervous system Positron Dementia Parkinson disease Epilepsy Neuroinflammation Key points
• Positron emission tomography (PET) has led to significant insights into nervous system biology, physiology, and pathophysiology in health and disease. • Several PET radiopharmaceuticals beyond fluorodeoxyglucose (FDG) have been used to study the physiology and pathophysiology in neurosciences. • Future studies on the use of advanced PET imaging in delineating neural pathophysiology, drug development, and altering patient management and outcomes across the disciplines of neurosciences are needed. Introduction
Positron emission tomography (PET) is a molecular imaging technique used for generating maps of functional and biochemical activity in target tissues in vivo.1 PET has led to significant insights into nervous system biology, physiology, and pathophysiology in health and disease. Several of these insights and applications have a direct usefulness for the neurologist.2 Although fluorine 18 [18F]fluorodeoxyglucose (FDG) has remained a workhorse of clinical PET imaging, many other radiolabeled biomolecules have been studied using PET.3 In this article, brain PET ligands beyond FDG, across the spectrum of neurologic subspecialties, including dementias, movement disorders, epilepsy, brain tumors, and neuroinflammation, are reviewed. Of the numerous available PET radiopharmaceuticals, a few have been selected that have been extensively studied in common neurologic disorders. Dementia
There is widespread deposition of amyloid in the cerebral cortex in Alzheimer disease (AD). Carbon 11 (11C) Pittsburgh compound B (PiB) is a radiolabeled analogue of thioflavin dye, which has been established as a valid biomarker for amyloid deposition in the human brain.4 Given the short half-life of 11C, limiting its availability, several 18F-labeled amyloid-binding PET radiopharmaceuticals have been developed, including 18F-florbetapir, 18F-flutemetamol and 18F-florbetaben, which have recently been approved by the US Food and Drug Administration (FDA) for clinical use.5–7 However, no single diagnostic test or imaging is considered sufficient. Amyloid imaging and cerebrospinal fluid CSF Aß levels are considered markers of the neuropathologic process, whereas FDG-PET is considered a marker for neuronal damage, and their combined interpretation may aid a diagnosis of AD in the right clinical context.8 There has been a controversy regarding the overall and relative usefulness of these PET agents with respect to FDG-PET for diagnosing AD.9–11 18F-Florbetapir is a fluorine-labeled stilbene derivative. The recommended dose for 18F-florbetapir is 370 MBq (10 mCi). For routine clinical use, the scan is obtained as a 10-minute acquisition, starting 40 to 50 minutes after intravenous injection (Table 1). The effective radiation dose after a 10-mCi injection in an adult is 7.0 mSv.12 An excellent correlation between 18F-florbetapir and 11C-PiB uptake has been shown.13 Table 1 Imaging protocols 18F-Florbetapir 10-min acquisition starting 40–50 min after intravenous injection of 10 mCi 11C- or 18F-Flumazenil Dynamic list mode acquisition for 60–90 min after injection of 10 mCi 11C-Methionine or 18F-fluoroethyltyrosine Dynamic acquisition or 10-min acquisition performed 20 min after injection of 10 mCi 18F-Fluorothymidine Dynamic acquisition obtained for 60–90 min after injection of radiopharmaceutical or static imaging obtained for 10 min 60 min after injection of 5–10 mCi 18F-Fluorodopa Ki values obtained from dynamic imaging performed over 90 min. Static imaging performed 60–70 min after injection for striatal imaging in movement disorders but earlier (approximately 20 min) for brain tumor evaluation 18F-Fluoropropyl-(+)-dihydrotetrabenazine 10-min acquisition 90 min after intravenous injection of 10 mCi or dynamic acquisition 11C-PK11195 Dynamic acquisition over approximately 60 min Normal amyloid scans show a clear gray-white matter contrast, with more radioactivity concentration in white matter. In patients with AD, uptake is increased in the orbitofrontal cortex, anterior cingulate, precuneus, posterior cingulate, and lateral temporal cortex, consistent with autopsy findings in direct comparison studies (Fig. 1).2,14 According to some recommendations, the 18F-florbetapir scan is considered positive if either (1) 2 or more brain areas (each larger than a single cortical gyrus) show reduced or absent gray-white matter contrast, or (2) there are 1 or more areas in which gray matter uptake is intense and clearly exceeds the uptake in adjacent white matter. A potential pitfall of scan interpretation using these criteria is in cases with brain atrophy, in which the gray-white matter contrast may be lost because of atrophy rather than abnormal accumulation in the gray matter. Alternatively, the ratio of radiotracer concentration in the region of disease to either the whole brain or to pons has been proposed as a semiquantitative index of 18F-florbetapir uptake.15
Fig. 1 (Top row) Normal 18F-florbetapir amyloid scan showing clear gray-white matter contrast with higher uptake in white matter. (Bottom row) Positive 18F-florbetapir amyloid scan with extensive loss of gray-white matter contrast. On correlation with disease, a negative amyloid scan corresponded to a neuropathologic amyloid deposition rating (Consortium to Establish a Registry for Alzheimer’s Disease) of none to sparse, whereas a positive amyloid scan corresponded to a rating of moderate to frequent amyloid plaque deposition in the cortex. Amyloid imaging can be useful in differentiating AD from frontotemporal dementia. Patients with frontotemporal dementia do not show significant amyloid deposition. However, abnormal amyloid deposition may be seen in 50% to 70% of patients with dementia with Lewy bodies (DLB) (Table 2).16 Negative 18F-florbetapir PET scans have been reported for some clinically diagnosed patients with AD, consistent with literature reports that 10% to 20% of clinically diagnosed patients with AD do not have amyloid disease at autopsy.17 Table 2 Pearls, pitfalls, variants Amyloid agents 50%–70% of patients with DLB may have positive scans
10%–20% of patients with AD may have negative scans
False-positive results in 12%, 30%, and 50% of normal adults in 60s, 70s, 80s age group, respectively 11C- or 18F-Flumazenil Patients with coma and vegetative state, motor neuron disease, cerebral ischemia may have decreased flumazenil binding
Increased levels of flumazenil may be seen in white matter, reflecting microdysgenesis 11C-Methionine or 18F-fluoroethyltyrosine False-positive results may be seen in benign conditions such as demyelination, leukoencephalitis, or abscess
Major clinical usefulness in determination of tumor extent, treatment, and biopsy...