Ignite Creation Date:
2024-05-05 @ 12:00 PM
Last Modification Date:
2024-10-26 @ 9:18 AM
Study NCT ID:
NCT00205582
Status:
UNKNOWN
Last Update Posted:
2005-11-04
First Post:
2005-09-12
Brief Title:
Excitatory Amino Acids and Activated Microglia After Traumatic Brain Injury a R-11CPK11195 PET Study
Sponsor:
Amsterdam UMC location VUmc
Organization:
Amsterdam UMC location VUmc
Study Overview
Official Title:
The Role of Excitatory Amino Acids on Neuronal Damage and Outcome After Traumatic Brain Injury Assessment in Patients Using Microdialysis and R-11CPK11195 Positron Emission Tomography
Status:
UNKNOWN
Status Verified Date:
2001-05
Last Known Status:
ACTIVE_NOT_RECRUITING
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
Excitatory amino acids may be involved in secondary neuronal damage after traumatic brain injury The amount of microglia activation is an indirect measure of neuronal damage Micorglia activation will be measured R-11CPK11195 PET 1 week 1 month and 6 months after brain injury
Detailed Description:
Glutamate and aspartate have been identified as the major excitatory neurotransmitters in the central nervous system A massive increase in the release of these excitatory amino acids EEA has been described following traumatic brain injury The resulting overstimulation of neuronal EAA receptors particularly the N-Methyl-D-Aspartate NMDA receptors leads to excessive influx of calcium through receptor gated ion-channels causing metabolic derangement and finally cell death Although the exact role of EEA in patients who have suffered severe head injury remains to be established it has been shown that sustained high intracranial pressure ICP and poor outcome are significantly correlated to high levels of EEA using microdialysis Disadvantages of microdialysis are that it can only be used to evaluate a limited part of the brain and that it can only be applied in the acute phase following injury The same limits also apply to ICP measurements Therefore methods which evaluate both the extent and time course of damage in vivo are urgently needed
Peripheral type benzodiazepine binding sites are a potential candidate for monitoring neuronal damage They are not normally present in cerebral tissue but following neuronal damage the cells involved in the ensuing gliosis show marked expression of these sites
R-PK11195 is a ligand that selectively binds to peripheral type benzodiazepine receptors Labeled with carbon-11 its uptake can be measured with Positron Emission Tomography PET Thus R-11CPK11195 PET can be used to monitor in-vivo gliosis after brain injury
A maximum of twenty patients with traumatic brain injury will be included in this study A microdialysis probe will be placed in the brain parenchyma to continuously measure EEA until the first PET scan is performed Several cerebral and haemodynamic parameters such as ICP and mean arterial blood pressure will be registered All patients will receive two Magnetic Resonance Imaging MRI scans to evaluate the extent and anatomical localization of cerebral damage Three R-11CPK11195 PET scans will be performed 1 week 1 month and 6 months after the injury Outcome will be determined using several outcome scales including the Glasgow Outcome Scale at six months In addition patients will be investigated by repeated neuropsychological examinations
Peripheral type benzodiazepine binding sites are a potential candidate for monitoring neuronal damage They are not normally present in cerebral tissue but following neuronal damage the cells involved in the ensuing gliosis show marked expression of these sites
R-PK11195 is a ligand that selectively binds to peripheral type benzodiazepine receptors Labeled with carbon-11 its uptake can be measured with Positron Emission Tomography PET Thus R-11CPK11195 PET can be used to monitor in-vivo gliosis after brain injury
A maximum of twenty patients with traumatic brain injury will be included in this study A microdialysis probe will be placed in the brain parenchyma to continuously measure EEA until the first PET scan is performed Several cerebral and haemodynamic parameters such as ICP and mean arterial blood pressure will be registered All patients will receive two Magnetic Resonance Imaging MRI scans to evaluate the extent and anatomical localization of cerebral damage Three R-11CPK11195 PET scans will be performed 1 week 1 month and 6 months after the injury Outcome will be determined using several outcome scales including the Glasgow Outcome Scale at six months In addition patients will be investigated by repeated neuropsychological examinations
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None