STUDY DESIGN: Laminectomy was performed on cats to destroy the posterior epidural ligament. Evoked potentials and spinal cord blood flows quantified the spinal cord function before and after cervical flexion. OBJECTIVES: This work describes a relationship between the loss of the posterior epidural ligaments and cervical spinal cord injury. SUMMARY OF BACKGROUND DATA: The posterior epidural ligaments of the human cervical spine have been recently described. These ligaments theoretically prevent injury to the spinal cord by resisting collapse of the dura during cervical flexion. METHODS: The animals were divided into three experimental groups: 1) control: no laminectomy and standard position, 2) flexion control: no laminectomy and known imposed flexion, 3) laminectomy (C3-C7) and flexion. Motor-evoked potentials and evoked spinal cord potentials were recorded to quantify the spinal cord functions. Radioactive microspheres were used to quantify ischemia in the spinal cord. RESULTS: Control subjects showed blood flows of 36 mL/100 g/min (C3-C4) to 46 mL/100 g/min (C7-C8). Flexion control subjects did not experience significant reductions in blood flows or substantial change in evoked potentials. The laminectomy plus flexion group experienced reduced blood flows and substantial motor-evoked potentials and slight evoked spinal cord potential changes with 50 degrees, 60 degrees, and 70 degrees flexion. Blood flow reduction was greater in the anterior half of the C7-C8 segments compared with the posterior half at 60 degrees flexion. Evoked spinal cord potentials were less vulnerable than motor-evoked potentials. CONCLUSIONS: The role of the posterior cervical epidural ligaments is to anchor the posterior dura mater to the ligamentum flavum. Loss of the ligaments allows anterior displacement of the posterior dura mater in flexion. Abnormal distribution of or lack of the cervical posterior epidural ligaments may lead to flexion myelopathy.
STUDY DESIGN: Laminectomy was performed on cats to destroy the posterior epidural ligament. Evoked potentials and spinal cord blood flows quantified the spinal cord function before and after cervical flexion. OBJECTIVES: This work describes a relationship between the loss of the posterior epidural ligaments and cervical spinal cord injury. SUMMARY OF BACKGROUND DATA: The posterior epidural ligaments of the human cervical spine have been recently described. These ligaments theoretically prevent injury to the spinal cord by resisting collapse of the dura during cervical flexion. METHODS: The animals were divided into three experimental groups: 1) control: no laminectomy and standard position, 2) flexion control: no laminectomy and known imposed flexion, 3) laminectomy (C3-C7) and flexion. Motor-evoked potentials and evoked spinal cord potentials were recorded to quantify the spinal cord functions. Radioactive microspheres were used to quantify ischemia in the spinal cord. RESULTS: Control subjects showed blood flows of 36 mL/100 g/min (C3-C4) to 46 mL/100 g/min (C7-C8). Flexion control subjects did not experience significant reductions in blood flows or substantial change in evoked potentials. The laminectomy plus flexion group experienced reduced blood flows and substantial motor-evoked potentials and slight evoked spinal cord potential changes with 50 degrees, 60 degrees, and 70 degrees flexion. Blood flow reduction was greater in the anterior half of the C7-C8 segments compared with the posterior half at 60 degrees flexion. Evoked spinal cord potentials were less vulnerable than motor-evoked potentials. CONCLUSIONS: The role of the posterior cervical epidural ligaments is to anchor the posterior dura mater to the ligamentum flavum. Loss of the ligaments allows anterior displacement of the posterior dura mater in flexion. Abnormal distribution of or lack of the cervical posterior epidural ligaments may lead to flexion myelopathy.