The In Vivo Metabolic Pattern of Low-grade Brain Gliomas: A Positron Emission Tomographic Study Using f-18-fluorodeoxyglucose and c-11-L-Methylmethionine

Deep brain stimulation (DBS) is a neurosurgery technique widely used in movement disorders, although its mechanism of action remains unclear. In fact, apart from the stimulation itself, the mechanical insertion of the electrode may play a crucial role. Here we aimed to distinguish between the insertional and the DBS effects on brain glucose metabolism. To this end, electrodes were implanted targeting the medial prefrontal cortex in five adult male Wistar rats. Positron Emission Tomography (PET) studies were performed before surgery (D0) and seven (D7) and nine days (D9) after that. DBS was applied during the 18FDG uptake of the D9 study. PET data were analysed with statistical parametric mapping. We found an electrode insertional effect in cortical areas, while DBS resulted in a more widespread metabolic pattern. The consequences of simultaneous electrode and DBS factors revealed a combination of both effects. Therefore, the insertion metabolic effects differed from the stimulation ones, which should be considered when assessing DBS protocols.

Download Full-text

In Vivo Evaluation of 1-O-(4-(2-Fluoroethyl-Carbamoyloxymethyl)-2-Nitrophenyl)-O-β-D-Glucopyronuronate: A Positron Emission Tomographic Tracer for Imaging β-Glucuronidase Activity in a Tumor/Inflammation Rodent Model

Molecular Imaging ◽

10.2310/7290.2011.00029 ◽

2012 ◽

Vol 11 (1) ◽

pp. 7290.2011.00029 ◽

Cited By ~ 8

Author(s):

Iněs F. Antunes ◽

Hidde J. Haisma ◽

Philip H. Elsinga ◽

Aren van Waarde ◽

Antoon T.M. Willemsen ◽

...

Keyword(s):

Rodent Model ◽

Positron Emission Tomographic ◽

In Vivo Evaluation ◽

Glucuronidase Activity ◽

Positron Emission ◽

Tumor Inflammation

Download Full-text

Cerebral Metabolism during Propofol Anesthesia in Humans Studied with Positron Emission Tomography

Anesthesiology ◽

10.1097/00000542-199502000-00010 ◽

1995 ◽

Vol 82 (2) ◽

pp. 393-403 ◽

Cited By ~ 214

Author(s):

Michael T. Alkire ◽

Richard J. Haier ◽

Steven J. Barker ◽

Nitin K. Shah ◽

Joseph C. Wu ◽

...

Keyword(s):

Positron Emission Tomography ◽

Animal Studies ◽

Cerebral Metabolism ◽

Anterior Cingulate ◽

Emission Tomography ◽

Whole Brain ◽

Metabolic Pattern ◽

Positron Emission ◽

Cortical Regions

Background Although the effects of propofol on cerebral metabolism have been studied in animals, these effects have yet to be directly examined in humans. Consequently, we used positron emission tomography (PET) to demonstrate in vivo the regional cerebral metabolic changes that occur in humans during propofol anesthesia. Methods Six volunteers each underwent two PET scans; one scan assessed awake-baseline metabolism, and the other assessed metabolism during anesthesia with a propofol infusion titrated to the point of unresponsiveness (mean rate +/- SD = 7.8 +/- 1.5 mg.kg-1.h-1). Scans were obtained using the 18fluorodeoxyglucose technique. Results Awake whole-brain glucose metabolic rates (GMR) averaged 29 +/- 8 mumoles.100 g-1.min-1 (mean +/- SD). Anesthetized whole-brain GMR averaged 13 +/- 4 mumoles.100 g-1.min-1 (paired t test, P < or = 0.007). GMR decreased in all measured areas during anesthesia. However, the decrease in GMR was not uniform. Cortical metabolism was depressed 58%, whereas subcortical metabolism was depressed 48% (P < or = 0.001). Marked differences within cortical regions also occurred. In the medial and subcortical regions, the largest percent decreases occurred in the left anterior cingulate and the inferior colliculus. Conclusion Propofol produced a global metabolic depression on the human central nervous system. The metabolic pattern evident during anesthesia was reproducible and differed from that seen in the awake condition. These findings are consistent with those from previous animal studies and suggest PET may be useful for investigating the mechanisms of anesthesia in humans.

Download Full-text

In Vivo Evaluation of 1-O-(4-(2-Fluoroethyl-Carbamoyloxymethyl)-2-Nitrophenyl)-O-β-D-Glucopyronuronate: A Positron Emission Tomographic Tracer for Imaging β-Glucuronidase Activity in a Tumor/Inflammation Rodent Model

Molecular Imaging ◽

10.2310/7290.2011.00029s1 ◽

2012 ◽

Vol 11 (1) ◽

pp. 7290.2011.00029

Author(s):

Iněs F. Antunes ◽

Hidde J. Haisma ◽

Philip H. Elsinga ◽

Aren van Waarde ◽

Antoon T.M. Willemsen ◽

...

Keyword(s):

Rodent Model ◽

Positron Emission Tomographic ◽

In Vivo Evaluation ◽

Glucuronidase Activity ◽

Positron Emission ◽

Tumor Inflammation

Download Full-text

The in vivo Metabolic Investigation of Brain Gliomas with Positron Emission Tomography

Advances and Technical Standards in Neurosurgery ◽

10.1007/978-3-7091-6504-1_2 ◽

1998 ◽

pp. 41-76 ◽

Cited By ~ 3

Author(s):

J. M. Derlon

Keyword(s):

Positron Emission Tomography ◽

Emission Tomography ◽

Positron Emission ◽

Metabolic Investigation ◽

Brain Gliomas

Download Full-text

Imaging, Cognition, and Parkinson’s Disease—An Overview

US Neurology ◽

10.17925/usn.2010.05.02.26 ◽

2010 ◽

Vol 05 (02) ◽

pp. 26 ◽

Cited By ~ 1

Author(s):

Paul Mattis ◽

David Eidelberg ◽

◽

Keyword(s):

Cognitive Dysfunction ◽

Functional Disability ◽

Functional Brain Imaging ◽

Positron Emission Tomographic ◽

Disease Manifestation ◽

Positron Emission ◽

Imaging Methodology ◽

Common Manifestation ◽

Cholinergic Neurotransmitter

Although the clinical diagnosis of Parkinsons disease (PD) is defined by motor symptoms, cognitive dysfunction is a common manifestation of this disease and an important contributor to functional disability. Functional brain imaging tools have proved valuable in the study of cognitive impairment in PD. Recent advances in imaging methodology and analysis have provided novel insights into the pathophysiology of cognitive decline in these patients. This review summarizes how positron emission tomographic (PET) imaging of metabolic activity in the rest state has enhanced understanding of cognitive dysfunction in PD. This tool has also created the basis for an objective biomarker for use in clinical trials of new therapeutic agents for this disease manifestation. Moreover, insights gained from the use of specific radiotracers targeting the dopaminergic and cholinergic neurotransmitter systems will be discussed, as well as findings fromin vivodetection of amyloid-beta.

Download Full-text