A pilot trial for assessing early microvascular alterations after aneurysmal subarachnoid hemorrhage using dynamic 18F-FDG PET/CT. The primary endpoint will be the measure of early changes in cerebral glucose uptake reflecting microperfusion.
We hypothesize that an early irreversible microvascular deterioration following initial bleeding could contribute to DCI occurrence. More precisely, we suspect that DCI areas are somehow overlaps of regions in which microperfusion is precociously altered, shortening circulatory reserves, and territories of secondarily spasmed arteries further lowering blood flow, resulting in ischemia. We aim to explore the potential microvasculature alteration through cerebral glucose perfusion and metabolism assessment using early dynamic 18F-fluorodesoxyglucose Positron Emission Tomography/Computer Tomography (dynamic 18F-FDG PET/CT). If our hypothesis turned out to be valid, we would at the same time be able to determine risk factors for this unpredictable complication and gain remarkable insight into DCI pathophysiology. Thus, the purpose of this trial is to demonstrate, in patients affected by SAH, the correlation between early cerebral glucose uptake defects in 18F-FDG PET/CT and delayed cerebral infarction in magnetic resonance imaging (MRI).
Study Type
INTERVENTIONAL
Allocation
NA
Purpose
OTHER
Masking
NONE
Enrollment
35
The intervention will consist in a dynamic cerebral 18F-FDG PET study performed at D2+/-1. Kinetic modeling will be performed using in-house software at the global, regional, and voxel level. In addition, cerebral perfusion and blood-brain-barrier permeability will be assessed at D4+/- 1 using perfusion MRI and permeability MRI.
Département d'Anesthésie-Réanimation Gui de Chauliac 80 Av Augustin.Fliche
Montpellier, France
Quantification of K1 parameter.
A kinetic modeling for cerebral glucose uptake will be performed using in-house software in order to provide the K1 parameter (in min-1) in every voxel reflecting the cerebral blood flow (in mL/min).
Time frame: Day 2 +/- 1 day after the initial bleeding
Quantification of Ki parameter.
A kinetic modeling for cerebral glucose uptake will be performed using in-house software in order to provide the Ki parameter (in min-1) in every voxel reflecting the cerebral metabolic rate of glucose in µmol/100g/min.
Time frame: Day 2 +/- 1 day after the initial bleeding
Delayed cerebral ischemic regions.
Delayed cerebral ischemic lesions will be ascertained by routine MRI scans until the end of the period of time in which the subject may present DCI (D21+/-3).
Time frame: From day 2 to day 21 +/- 3 days after the initial bleeding
Delayed spasmed arteries territories.
Occurence of vasospasm will be determined on routine angiograms until the end of the period of time in which the subject may present vasospasm (D21+/-3).
Time frame: From day 2 to day 21 +/- 3 days after the initial bleeding
Quantification of cerebral blood flow using DSC-MRI
Cerebral blood flow in mL/100g/min will be measured using DSC-MRI (Dynamic Susceptibility Contrast Magnetic Resonance Imaging)
Time frame: At day 4 +/- 1 day after the initial bleeding
Quantification of cerebral blood flow using ASL-MRI
Cerebral blood flow in mL/100g/min will be measured using ASL-MRI (Arterial Spin Labelling Magnetic Resonance Imaging)
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Time frame: At day 4 +/- 1 day after the initial bleeding
Quantification of blood-brain-barrier permeability using DSC-MRI
The blood-brain barrier permeability will be measured using DSC-MRI. A kinetic modeling will be performed in order to provide the leakage parameter K2 (in min-1) in every voxel.
Time frame: At day 4 +/- 1 day after the initial bleeding
Quantification of blood-brain-barrier permeability using DCE-MRI
The blood-brain barrier permeability will be measured using DCE-MRI (Dynamic Contrast-Enhanced Magnetic Resonance Imaging). A kinetic modeling will be performed in order to provide the leakage parameter Ktrans (in min-1) in every voxel.
Time frame: At day 4 +/- 1 day after the initial bleeding