The Inflammatory Effect of Nucleus Pulposus: A Possible Element in the Pathogenesis of Low-back Pain

  title={The Inflammatory Effect of Nucleus Pulposus: A Possible Element in the Pathogenesis of Low-back Pain},
  author={Robert F. McCarron and Marc W. Wimpee and Philip G. Hudkins and Gerald S. Laros},
Homogenized autogenous nucleus pulposus was injected into the lumbar epidural space of four dogs through an indwelling catheter. After daily injections of the material over 5 to 7 days, the dogs were killed at 5,7,14, or 21 days after the first injection. In four dogs that served as controls, normal saline was injected on an identical schedule and the dogs were killed at times identical to the experimental group. Evaluation of the dural sac, the spinal cord and its roots was performed by gross… 

The experimental basis of sciatica

It is to be hoped that the results of research into basic pathophysiologic mechanisms of sciatica will provide resources to diagnose and treat patients earlier and more specifically, and that the number of chronic cases should be dramatically reduced.

Early effects of nucleus pulposus application on spinal nerve root morphology and function

Morphological changes in terms of an epidural inflammatory reaction and minor axonal and Schwann cell damage may be demonstrated within 3 h of NP application, with or without compression, however, there is no functional deterioration of the nerve roots detectable within this time period.

Methylprednisolone reduces the early vascular permeability increase in spinal nerve roots induced by epidural nucleus pulposus application

It is demonstrated that nucleus pulposus can induce a rapid increase in endoneural vascular permeability in spinal nerve roots after epidural application and this increase can be partially prevented by pretreatment with high‐dose methylprednisolone.

Cytokine Expression in the Epidural Space: A Model of Noncompressive Disc Herniation-Induced Inflammation

In this model of acute noncompressive disc herniation, NP caused the elevation of epidural IL-6, TNF-&agr;, and IFN-&ggr;—all attenuated by IFN+anti-IFN; blockade.

Pathomechanisms of Nerve Root Injury Caused by Disc Herniation: An Experimental Study of Mechanical Compression and Chemical Irritation

It was shown that each of the assessed factors induces nerve dysfunction, however, the combination of mechanical compression (mass effect of herniated NP) and chemical irritation (inflammation around nerve root) may induce more nerve root injury than each factor per se.

Nucleus pulposus-induced nerve root injury: effects of diclofenac and ketoprofen

This study of two potent NSAIDs indicates that nucleus pulposus-induced nerve root dysfunction may be reduced by diclofenac but not by ketoprofen, and the reason for this difference is not known, but it might be related to the fact that keto-oxygenases COX-1 andCOX-2 belong to different NSAID subgroups and have a different selectivity for the two cyclo- oxygengenases.

Possible Mechanism of Painful Radiculopathy in Lumbar Disc Herniation

The authors suggest that chemical mediators such as phospholipase A, and nitric oxide, induced by extruded or sequestrated intervertebral discs, are involved in the pathophysiologic mechanisms of painful radiculopathy in lumbar disc herniations.

Indomethacin blocks the nucleus pulposus-induced effects on nerve root function

Indomethacin efficiently blocked the negative effects on both blood flow and nerve conduction but had no effects per se in the pathophysiology of nucleus pulposus-induced nerve root injury and thereby also for sciatica.

Role of Leukocytes in Radicular Pain Secondary to Herniated Nucleus Pulposus

WhetherLeukocytes play a role in the mechanical hyperalgesia induced by the nucleus pulposus and to characterize the role of leukocytes in radicular pain attributable to lumbar disc herniation are determined.