Metallosis Presenting as a Progressive Neurologic Deficit Four Years After a Posterior Spinal Fusion for Adolescent Idiopathic Scoliosis: A Case Report.

STUDY DESIGN: A case report. OBJECTIVE: The aim of this study was to report a case of progressive pain and paraparesis secondary to metallosis four years after a pediatric posterior spinal fusion (PSF). SUMMARY OF BACKGROUND DATA: Metallosis as a late complication of pediatric spinal surgery is rarely reported. Myelographic computed tomography (CT) can be helpful in establishing the diagnosis. The use of serum chromium levels as a means of definitive diagnosis has been suggested, but has only been reported retrospectively. METHODS: A 19-year-old male presented four years after PSF for adolescent idiopathic scoliosis with sudden onset of pain and neurologic deficits. Radiographs and CT scan suggested infection. Intraoperatively, no purulent material was noted, but black and yellowish corrosive debris was found around the right L1 pedicle screw, so it was removed and the cavity packed with tobramycin impregnated calcium sulfate beads. After surgery, neurologic deficits worsened. CT myelogram showed irregular opacification of the thecal sac at the level of the conus. A posterior laminectomy and decompression was performed with removal of all debris and spinal instrumentation. Metallosis within the spinal canal was noted and serum chromium levels were obtained. RESULTS: The patient was discharged one week after admission with improvement of pain and gradual improvement in neurologic examination. Three years postdischarge, the patient is asymptomatic and examination shows bilateral clonus. Serum chromium levels declined from a high of 4.5 µg/L operatively to 0.8 at final follow-up (normal: 0.2-0.6 µg/L). CONCLUSION: Although uncommon, metallosis should be considered in the differential diagnosis of any late presenting case of pain, infection-like symptoms, or neurologic deficits after pediatric PSF. CT myelography and serum chromium levels may help guide diagnosis; however, surgical exploration is needed for definitive diagnosis and treatment. LEVEL OF EVIDENCE: 4.

The correlation between severity of paraparesis and reduced density of resident antigen-presenting cells implicates an unknown role for the spinal perivascular macrophages in experimental autoimmune encephalomyelitis in rats.

To study alterations in the morphology of spinal perivascular macrophages (SPM) during experimental allergic encephalomyelitis (EAE), we labelled SPM by intracerebroventricular (i.c.v.) injection of horseradish peroxidase (HRP). As earlier electron microscopical analysis had shown severely damaged SPM, we suspected that each inflammatory process is accompanied by the death of SPM. To prove this hypothesis, we compared the numerical density of resident SPM (i.c.v. labelled in red by Fluoro-Ruby) with that of monocytes/macrophages recruited to the perivascular space (i.c.v. labelled in green by Fluoro-Emerald). At the peak of paraparesis, the density of resident SPM was reduced by 33%. Since this reduction contrasted sharply with earlier data indicating a massive increase in the density of SPM during EAE, we checked our findings after general or selective suppression of the immune response to myelin autoantigens with the drugs dexamethasone and copaxone, respectively. Dexamethasone treatment commenced after evident paraparesis accelerated recovery, but did not influence SPM density. Immunisation with copaxone completely prevented the occurrence of EAE (monitored by video-based motion analysis of tail motility); the subsequent histological analysis revealed no reduction in SPM density. Based on this inverse correlation between the severity of EAE and the density of resident macrophages, we conclude that SPM plays an important role in the pathogenesis of EAE.