Shigeru Kobayashi1, Yoshihiko Suzuki2, Adam Meir3, Naji Al-Khudairi3, Takashi Nakane4, Katsuhiko Hayakawa4. 1. Department of Orthopaedics and Rehabilitation Medicine, Faculty of Medicine, University of Fukui, 23-3, Shimoaizuki, Matsuoka, Eiheiji, Fukui 910-1193, Japan; Research and Education Program for Life Science, University of Fukui, Fukui, Japan. Electronic address: kshigeru@u-fukui.ac.jp. 2. Suzuki Orthopaedic Clinic, 5-1, Tokiguchi, Nakamati, Toki, Gifu, 509-5124, Japan. 3. Victor Horsley Department of Neurosurgery, The National Hospital for Neurology and Neurosurgery, Queen Square, London, WC1N 3BG, UK. 4. Department of Radiology and Orthopaedics, Aiko Orthopaedic Hospital, 1221, Sinmei, Okehazama, Midori, Aichi, 458-0911, Japan.
Abstract
BACKGROUND CONTEXT: There has been no study regarding the cauda equina circulation of patients with neurogenic intermittent claudication (NIC) in lumbar spinal canal stenosis (LSCS) using dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI). PURPOSE: The mechanism responsible for the onset of NIC was investigated using DCE-MRI to examine changes in cauda equina blood flow in patients with LSCS. STUDY DESIGN: This was a retrospective longitudinal registry and magnetic resonance imaging study. PATIENT SAMPLE: The subjects consisted of 23 patients who had LSCS associated with NIC (stenosis group). Ten asymptomatic volunteers who did not have NIC served as controls (control group). In the LSCS group, the cross-sectional area of the dural sac was <75 mm2 at the site of most severe stenosis. These patients were further divided into single and double stenosis subgroups. OUTCOME MEASURES: The main measures we used were the signal intensity (S-I) ratio and the shape and size of the time intensity (T-I) curves. We compared these between the stenosis and control groups. METHODS: At first, plain T1-weighted MR images were obtained and the lumbar dural sac cross-sectional area was measured using a digitizer. For DCE-MRI, sagittal T1-weighted images of the same slice were acquired continuously for 10 minutes after administration of gadolinium as an intravenous bolus to observe the distribution of contrast medium (gadolinium) in the cauda equina. To objectively evaluate changes in contrast enhancement of the cauda equina at the site of canal stenosis, regions of interest were established. The signal intensity (SI) ratio was calculated to compare the signal intensities before and after contrast enhancement, and time-intensity curves were prepared to investigate changes over time. RESULTS: The static imaging findings and the changes of gadolinium uptake showed striking differences between the study and control patients. In the stenosis group, abnormal intrathecal enhancement showed around the site of stenosis on enhanced MR imaging. The SI ratio at the site of canal stenosis had a slower increase in the arterial phase when compared with that in the control group and remained high in the venous phase for up to 10 minutes. Finally, abnormal intrathecal enhancement was visible around the site of stenosis on enhanced MR imaging in all patients. CONCLUSIONS: These clinical data indicate that cauda equina nerve roots in the LSCS patients are pathologic even when symptoms are not elicited in the supine position, suggesting that intraradicular venous congestion and edema themselves do not influence the existence of radicular symptoms.
BACKGROUND CONTEXT: There has been no study regarding the cauda equina circulation of patients with neurogenic intermittent claudication (NIC) in lumbar spinal canal stenosis (LSCS) using dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI). PURPOSE: The mechanism responsible for the onset of NIC was investigated using DCE-MRI to examine changes in cauda equina blood flow in patients with LSCS. STUDY DESIGN: This was a retrospective longitudinal registry and magnetic resonance imaging study. PATIENT SAMPLE: The subjects consisted of 23 patients who had LSCS associated with NIC (stenosis group). Ten asymptomatic volunteers who did not have NIC served as controls (control group). In the LSCS group, the cross-sectional area of the dural sac was <75 mm2 at the site of most severe stenosis. These patients were further divided into single and double stenosis subgroups. OUTCOME MEASURES: The main measures we used were the signal intensity (S-I) ratio and the shape and size of the time intensity (T-I) curves. We compared these between the stenosis and control groups. METHODS: At first, plain T1-weighted MR images were obtained and the lumbar dural sac cross-sectional area was measured using a digitizer. For DCE-MRI, sagittal T1-weighted images of the same slice were acquired continuously for 10 minutes after administration of gadolinium as an intravenous bolus to observe the distribution of contrast medium (gadolinium) in the cauda equina. To objectively evaluate changes in contrast enhancement of the cauda equina at the site of canal stenosis, regions of interest were established. The signal intensity (SI) ratio was calculated to compare the signal intensities before and after contrast enhancement, and time-intensity curves were prepared to investigate changes over time. RESULTS: The static imaging findings and the changes of gadolinium uptake showed striking differences between the study and control patients. In the stenosis group, abnormal intrathecal enhancement showed around the site of stenosis on enhanced MR imaging. The SI ratio at the site of canal stenosis had a slower increase in the arterial phase when compared with that in the control group and remained high in the venous phase for up to 10 minutes. Finally, abnormal intrathecal enhancement was visible around the site of stenosis on enhanced MR imaging in all patients. CONCLUSIONS: These clinical data indicate that cauda equina nerve roots in the LSCS patients are pathologic even when symptoms are not elicited in the supine position, suggesting that intraradicular venous congestion and edema themselves do not influence the existence of radicular symptoms.
Authors: Carlo Ammendolia; Pierre Côté; Y Raja Rampersaud; Danielle Southerst; Michael Schneider; Aksa Ahmed; Claire Bombardier; Gillian Hawker; Brian Budgell Journal: Chiropr Man Therap Date: 2019-06-19
Authors: Carlo Ammendolia; Pierre Côté; Y Raja Rampersaud; Danielle Southerst; Brian Budgell; Claire Bombardier; Gillian Hawker Journal: J Chiropr Med Date: 2016-06-20