Benjamin M Ellingson1, Davis C Woodworth2, Kevin Leu3, Noriko Salamon3, Langston T Holly4. 1. Department of Radiological Sciences, David Geffen School of Medicine, University of California, Los Angeles, California, USA; Department of Physics and Biology in Medicine, David Geffen School of Medicine, University of California, Los Angeles, California, USA; Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, University of California, Los Angeles, California, USA. Electronic address: bellingson@mednet.ucla.edu. 2. Department of Radiological Sciences, David Geffen School of Medicine, University of California, Los Angeles, California, USA; Department of Physics and Biology in Medicine, David Geffen School of Medicine, University of California, Los Angeles, California, USA. 3. Department of Radiological Sciences, David Geffen School of Medicine, University of California, Los Angeles, California, USA. 4. Department of Neurosurgery, David Geffen School of Medicine, University of California, Los Angeles, California, USA.
Abstract
OBJECTIVES: Although a number of studies have implicated ischemia and hypoxia in the pathogenesis of cervical spondylosis, quantification remains difficult and the role of ischemia and hypoxia on disease progression and disease severity in human cervical spondylosis remains largely unknown. Therefore, the objective of this study was to assess spinal cord perfusion and oxygenation in human cervical spondylosis and examine the relationship between perfusion, degree of spinal cord compression, and neurological status. METHODS: Twenty-two patients with cervical spondylosis with or without myelopathy received a dynamic susceptibility contrast perfusion MRI exam consisting of a novel spin-and-gradient echo echoplanar acquisition before, during, and following gadolinium-based contrast injection. Estimation of relative spinal cord blood volume (rSCBV), the reversible relaxation rate (R2á), and relative oxygen extraction fraction (rOEF = R2á/rSCBV) was performed at the site of compression and compared with anterior-posterior spinal cord diameter and modified Japanese Orthopedic Association (mJOA) score, a measure of neurological impairment. RESULTS: rSCBV was linearly correlated with both anterior-posterior cord diameter (R2 = 0.4667, P = 0.0005) and mJOA (R2 = 0.2274, P = 0.0248). R2á was linearly correlated with mJOA (R2 = 0.3998, P = 0.0016) but not cord diameter (R2 = 0.055; P = 0.2950). Also, rOEF was correlated with both cord diameter (R2 = 0.3440, P = 0.0041) and mJOA (R2 = 0.4699, P = 0.0004). CONCLUSIONS: Results support the hypothesis that spinal cord compression results in ischemia and hypoxia, and the degree of ischemia and hypoxia is proportional to the degree of neurological impairment.
OBJECTIVES: Although a number of studies have implicated ischemia and hypoxia in the pathogenesis of cervical spondylosis, quantification remains difficult and the role of ischemia and hypoxia on disease progression and disease severity in human cervical spondylosis remains largely unknown. Therefore, the objective of this study was to assess spinal cord perfusion and oxygenation in human cervical spondylosis and examine the relationship between perfusion, degree of spinal cord compression, and neurological status. METHODS: Twenty-two patients with cervical spondylosis with or without myelopathy received a dynamic susceptibility contrast perfusion MRI exam consisting of a novel spin-and-gradient echo echoplanar acquisition before, during, and following gadolinium-based contrast injection. Estimation of relative spinal cord blood volume (rSCBV), the reversible relaxation rate (R2á), and relative oxygen extraction fraction (rOEF = R2á/rSCBV) was performed at the site of compression and compared with anterior-posterior spinal cord diameter and modified Japanese Orthopedic Association (mJOA) score, a measure of neurological impairment. RESULTS: rSCBV was linearly correlated with both anterior-posterior cord diameter (R2 = 0.4667, P = 0.0005) and mJOA (R2 = 0.2274, P = 0.0248). R2á was linearly correlated with mJOA (R2 = 0.3998, P = 0.0016) but not cord diameter (R2 = 0.055; P = 0.2950). Also, rOEF was correlated with both cord diameter (R2 = 0.3440, P = 0.0041) and mJOA (R2 = 0.4699, P = 0.0004). CONCLUSIONS: Results support the hypothesis that spinal cord compression results in ischemia and hypoxia, and the degree of ischemia and hypoxia is proportional to the degree of neurological impairment.
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