The purpose of this study was to investigate the presence of any correlation between recurrent radicular pain during the first six months following first surgery for herniated lumbar intervertebral disc and the amount of lumbar peridural fibrosis as defined by MR imaging. 197 patients who underwent first-time single-level unilateral discectomy for lumbar disc herniation were evaluated in a randomized, double-blind, controlled multicenter clinical trial. Clinical assessments, performed by physicians blinded to patient treatment status, were conducted preoperatively and at one and six months postoperatively. The enhanced MR images of the operative site utilized in the analysis were obtained at six months postoperatively. Radicular pain was recorded by the patient using a validated visual analog pain scale in which 0 = no pain and 10 = excruciating pain. The data obtained at the 6 month time point were analyzed for an association between amount of peridural scars as measured by MR imaging and clinical failure as defined by the recurrence of radicular pain. The results showed that the probability of recurrent pain increases when scar score increases. Patients having extensive peridural scar were 3.2 times more likely to experience recurrent radicular pain than those patients with less extensive peridural scarring. In conclusion, this prospective, controlled, randomized, blinded, multicenter study has demonstrated that there is a significant association between the presence of extensive peridural scar and the occurrence of recurrent radicular pain.

The purpose of this study was to investigate the presence of any correlation between recurrent radicular pain during the first six months following first surgery for herniated lumbar intervertebral disc and the amount of lumbar peridural fibrosis as defined by MR imaging. 197 patients who underwent first-time single-level unilateral discectomy for lumbar disc herniation were evaluated in a randomized, double-blind, controlled multicenter clinical trial. Clinical assessments, performed by physicians blinded to patient treatment status, were conducted preoperatively and at one and six months postoperatively. The enhanced MR images of the operative site utilized in the analysis were obtained at six months postoperatively. Radicular pain was recorded by the patient using a validated visual analog pain scale in which 0 = no pain and 10 = excruciating pain. The data obtained at the 6 month time point were analyzed for an association between amount of peridural scars as measured by MR imaging and clinical failure as defined by the recurrence of radicular pain. The results showed that the probability of recurrent pain increases when scar score increases. Patients having extensive peridural scar were 3.2 times more likely to experience recurrent radicular pain than those patients with less extensive peridural scarring. In conclusion, this prospective, controlled, randomized, blinded, multicenter study has demonstrated that there is a significant association between the presence of extensive peridural scar and the occurrence of recurrent radicular pain.

The senile plaques found within the cerebral cortex and hippocampus of the Alzheimer disease brain contain beta-amyloid peptide (A beta) fibrils that are associated with a variety of macromolecular species, including dermatan sulfate proteoglycan and heparan sulfate proteoglycan. The latter has been shown recently to bind tightly to both amyloid precursor protein and A beta, and this binding has been attributed largely to the interaction of the core protein of heparan sulfate proteoglycan with A beta and its precursor. Here we have examined the ability of synthetic A beta s to bind to and interact with the glycosaminoglycan moieties of proteoglycans. A beta(1-28) associates with heparin, heparan sulfate, dermatan sulfate, and chondroitin sulfate. The interaction of these sulfated polysaccharides with the amyloid peptide results in the formation of large aggregates that are readily sedimented by centrifugation. The ability of both A beta(1-28) and A beta(1-40) to bind glycosaminoglycans is pH-dependent, with increasing interaction as the pH values fall below neutrality and very little binding at pH 8.0. The pH profile of heparin-induced aggregation of A beta(1-28) has a midpoint pH of approximately 6.5, suggesting that one or more histidine residues must be protonated for binding to occur. Analysis of the A beta sequence reveals a consensus heparin-binding domain at residues 12-17, and this motif contains histidines at positions 13 and 14 that may be involved in the interaction with glycosaminoglycans.(ABSTRACT TRUNCATED AT 250 WORDS)

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