MCP arthrodesis using an intramedullary interlocking device.

BACKGROUND: A variety of metacarpophalangeal joint (MCPJ) arthrodesis techniques have been described for the treatment of symptomatic arthritis and instability of the thumb MCPJ including K wire fixation, tension-band arthrodesis, plate fixation, intramedullary screw, and other intramedullary devices. This study presents a retrospective review of one surgeon's initial series of patients undergoing thumb MCP arthrodesis using an intramedullary compression device with a fixed angle of 25°. METHODS: A retrospective chart and radiographic review of patients treated for thumb MCP arthrodesis using the intramedullary device was performed. Final radiographs were evaluated for arthrodesis angle, bony fusion, and implant fixation. Any complication found during surgery or the follow-up period was noted. RESULTS: In this study, 17 patients were reviewed. Indications for surgery were osteoarthritis (five patients), rheumatoid arthritis (three patients), MCP instability alone (seven patients), and post-traumatic conditions (two patients). Of these, 12 patients had a simultaneous trapeziometacarpal (TMC) soft tissue arthroplasty. Mean follow-up was 4.9 months. All 17 patients had clinical and radiographic evidence of fusion at an average of 7.9 weeks, with an average fusion angle of 24.4°. There were no hardware complications, no infections, no revisions, and no indications for hardware removal. DISCUSSION: Our study results indicate the technique promotes rapid union at a precise angle, provides strong fixation that does not require prolonged immobilization, does not cause hardware irritation, and can be used in conjunction with other procedures including TMC arthroplasty when MCP arthrodesis is indicated for joint instability.

Changes in mumps virus gene sequence associated with variability in neurovirulent phenotype.

Mumps virus is highly neurotropic and, prior to widespread vaccination programs, was the major cause of viral meningitis in the United States. Nonetheless, the genetic basis of mumps virus neurotropism and neurovirulence was until recently not understood, largely due to the lack of an animal model. Here, nonneurovirulent (Jeryl Lynn vaccine) and highly neurovirulent (88-1961 wild type) mumps virus strains were passaged in human neural cells or in chicken fibroblast cells with the goal of neuroadapting or neuroattenuating the viruses, respectively. When tested in our rat neurovirulence assay against the respective parental strains, a Jeryl Lynn virus variant with an enhanced propensity for replication (neurotropism) and damage (neurovirulence) in the brain and an 88-1961 wild-type virus variant with decreased neurotropic and neurovirulent properties were recovered. To determine the molecular basis for the observed differences in neurovirulence and neuroattenuation, the complete genomes of the parental strains and their variants were fully sequenced. A comparison at the nucleotide level associated three amino acid changes with enhanced neurovirulence of the neuroadapted vaccine strain: one each in the nucleoprotein, matrix protein, and polymerase and three amino acid changes with reduced neurovirulence of the neuroattenuated wild-type strain: one each in the fusion protein, hemagglutinin-neuraminidase protein, and polymerase. The potential role of these amino acid changes in neurotropism, neurovirulence, and neuroattenuation is discussed.