Abstract

Chronic low back pain with sciatica complicating post laminectomy surgery is poorly understood. It is likely that some aspects of persistent pain of the syndrome results from spinal facilitation in which there is lowering of pain excitation levels. A small animal preclinical model is needed that mimics the clinical condition to permit detailed studies of the underlying altered neurochemistry of the sensory pathways. We propose herein a rat laminectomy model containing the elements required for study of the neurobiology of the condition. The model consists of a surgical laminectomy that includes L5 spinal nerve manipulation and disc injury, elements necessarily employed in human disc herniation surgery. At 8 weeks post laminectomy the proposed model demonstrates paraspinous muscle spasm, tail contracture, behavioral pain behavior, tactile allodynia, epidural and nerve root scarring, and nerve root adherence by scar to the underlying disc and adjacent pedicle. Two underlying pain facilitation states are invoked in the clinical condition: (1) an inflammatory state required to achieve wound healing; and (2) a nerve injury state resulting from nerve manipulation and subsequent epidural scarring, spinal nerve scarring, and spinal nerve tethering to the adjacent disc and pedicle. Both pain facilitation states are active in the model.

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