The impact of spinal cord perfusion deficits and hypoxia on recovery
Funded in: 2020, 2021, 2022
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Problem: Neurodegeneration including complex hemodynamic impairments
Target: Study how the precise timing of these hemodynamic impairments evolves
Goal: Better understanding of changes in spinal hemodynamics
Traumatic cervical spinal cord injury (SCI) and degenerative cervical myelopathy (DCM) present with a focal cervical myelopathy. SCI and DCM both demonstrate similar degrees of neurodegeneration above the injury, including complex hemodynamic impairments at the epicentre of the injury. Cord hemodynamic impairments contribute to neuronal damage and consequently clinical impairments after SCI. However, how the precise timing of these hemodynamic impairments evolves beyond the level of lesion and its clinical relevance in human SCI, is understudied.
A quantitative technique measuring cord perfusion and tissue oxygenation would therefore allow characterizing the spatio-temporal dynamics of perfusion deficits. Quantitative MRI (qMRI) techniques, such as intravoxel incoherent motion (IVIM) MRI (estimates blood perfusion in tissue) and quantitative Blood Oxygenation Level Dependent (qBOLD) (estimates change of deoxyhaemoglobin molecules) allow quantifying in-vivo hemodynamics in spinal cord. These techniques benefit from ultra-high field (UHF) system (i.e. 7 Tesla scanner) which enables high image resolution and improved contrast. However, measuring at 7 Tesla is only possible in patients without metal implants.
The aim of this study is therefore to investigate SCI-induced changes of blood perfusion and oxygenation in the spinal cord using IVIM and qBOLD. For this purpose, the researchers will first develop blood perfusion sensitive MRI techniques and then apply these advanced methods in SCI and DCM patients using 3 Tesla and 7 Tesla MRI scanners, respectively. To address the spread of hemodynamic impairments, they will perform a longitudinal analysis to track perfusion and hemodynamic changes rostral to a cervical cord lesion in SCI patients at 3T during the first 6-months post-SCI.
Characterizing the hemodynamic impairments will result in better understanding of changes in spinal hemodynamics and their impact on neurological outcomes. The latter may inform therapeutic strategies that rely on appropriate interactions of the hemodynamic system and neural changes, like secondary degradation and beneficial neural plasticity.