Search Results

You are looking at 1 - 8 of 8 items for

  • Author or Editor: Amy M. Moore x
  • All content x
Clear All Modify Search
Full access

Amy M. Moore, Emily M. Krauss, Rajiv P. Parikh, Michael J. Franco, and Thomas H. Tung

Sciatic nerve injuries cause debilitating functional impairment, particularly when the injury mechanism and level preclude reconstruction with primary grafting. The purpose of this study was to demonstrate the anatomical feasibility of nerve transfers from the distal femoral nerve terminal branches to the tibial nerve and to detail the successful restoration of tibial function using the described nerve transfers.

Six cadaveric legs were dissected for anatomical analysis and the development of tension-free nerve transfers from femoral nerve branches to the tibial nerve. In 2 patients with complete tibial and common peroneal nerve palsies following sciatic nerve injury, terminal branches of the femoral nerve supplying the vastus medialis and vastus lateralis muscles were transferred to the medial and lateral gastrocnemius branches of the tibial nerve. Distal sensory transfer of the saphenous nerve to the sural nerve was also performed. Patients were followed up for lower-extremity motor and sensory recovery up to 18 months postoperatively.

Consistent branching patterns and anatomical landmarks were present in all dissection specimens, allowing for reliable identification, neurolysis, and coaptation of donor femoral and saphenous nerve branches to the recipients. Clinically, the patients obtained Medical Research Council Grade 3 and 3+ plantar flexion by 18 months postoperatively. Improved strength was accompanied by improved ambulation in both patients and by a return to competitive sports in 1 patient. Sensory recovery was demonstrated by an advancing Tinel sign in both patients.

This study illustrates the clinical success and anatomical feasibility of femoral nerve to tibial nerve transfers after proximal sciatic nerve injury.

Restricted access

Colin W. McInnes, Austin Y. Ha, Hollie A. Power, Thomas H. Tung, and Amy M. Moore

OBJECTIVE

Partial femoral nerve injuries cause significant disability with ambulation. Due to their more proximal and superficial location, sartorius branches are often spared in femoral nerve injuries. In this article, the authors report the benefits of femoral nerve decompression, demonstrate the feasibility of sartorius-to-quadriceps nerve transfers in a cadaveric study, describe the surgical technique, and report clinical results.

METHODS

Four fresh-frozen cadaveric lower limbs were dissected for anatomical analysis of the sartorius nerve. In addition, a retrospective review of patients with partial femoral nerve injuries treated with femoral nerve decompression and sartorius-to-quadriceps nerve transfers was conducted. Pre- and postoperative knee extension Medical Research Council (MRC) grades and pain scores (visual analog scale) were collected.

RESULTS

Up to 6 superficial femoral branches innervate the sartorius muscle just distal to the inguinal ligament. Each branch yielded an average of 672 nerve fibers (range 99–1850). Six patients underwent femoral nerve decompression and sartorius-to-quadriceps nerve transfers. Four patients also had concomitant obturator-to-quadriceps nerve transfers. At final follow-up (average 13.4 months), all patients achieved MRC grade 4−/5 or greater knee extension. The average preoperative pain score was 5.2, which decreased to 2.2 postoperatively (p = 0.03).

CONCLUSIONS

Femoral nerve decompression and nerve transfer using sartorius branches are a viable tool for restoring function in partial femoral nerve injuries. Sartorius branches serve as ideal donors in quadriceps nerve transfers because they are expendable, are close to their recipients, and have an adequate supply of nerve fibers.

Restricted access

Wilson Z. Ray, Rahul Kasukurthi, Esther M. Papp, Amy M. Moore, Andrew Yee, Daniel A. Hunter, Nancy L. Solowski, Thalachallour Mohanakumar, Susan E. Mackinnon, and Thomas H. Tung

Object

Peripheral nerve allografts provide a temporary scaffold for host nerve regeneration and allow for the repair of significant segmental nerve injuries. Despite this potential, nerve allograft transplantation requires temporary systemic immunosuppression. Characterization of the immunological mechanisms involved in the induction of immune hyporesponsiveness to prevent nerve allograft rejection will help provide a basis for optimizing immunomodulation regimens or manipulating donor nerve allografts to minimize or eliminate the need for global immunosuppression.

Methods

The authors used C57Bl/6 mice and STAT4 and STAT6 gene BALB/c knockout mice. A nonvascularized nerve allograft was used to reconstruct a 1-cm sciatic nerve gap in the murine model. A triple costimulatory blockade of the CD40, CD28/B7, and inducible costimulatory (ICOS) pathways was used. Quantitative assessment was performed at 3 weeks with nerve histomorphometry, walking track analysis, and the enzyme-linked immunospot assay.

Results

The STAT6 −/− mice received 3 doses of costimulation-blocking antibodies and had axonal regeneration equivalent to nerve isografts, while treated STAT4 −/− mice demonstrated moderate axonal regeneration but inferior to the T helper cell Type 2–deficient animals. Enzyme-linked immunospot assay analysis demonstrated a minimal immune response in both STAT4 −/− and STAT6 −/− mice treated with a costimulatory blockade.

Conclusions

The authors' findings suggest that Type 1 T helper cells may play a more significant role in costimulatory blockade–induced immune hyporesponsiveness in the nerve allograft model, and that Type 2 T helper differentation may represent a potential target for directed immunosuppression.

Restricted access

Christina K. Magill, Amy M. Moore, Ying Yan, Alice Y. Tong, Matthew R. MacEwan, Andrew Yee, Ayato Hayashi, Daniel A. Hunter, Wilson Z. Ray, Philip J. Johnson, Alexander Parsadanian, Terence M. Myckatyn, and Susan E. Mackinnon

Object

Glial cell line–derived neurotrophic factor (GDNF) has potent survival effects on central and peripheral nerve populations. The authors examined the differential effects of GDNF following either a sciatic nerve crush injury in mice that overexpressed GDNF in the central or peripheral nervous systems (glial fibrillary acidic protein [GFAP]–GDNF) or in the muscle target (Myo-GDNF).

Methods

Adult mice (GFAP-GDNF, Myo-GDNF, or wild-type [WT] animals) underwent sciatic nerve crush and were evaluated using histomorphometry and muscle force and power testing. Uninjured WT animals served as controls.

Results

In the sciatic nerve crush, the Myo-GDNF mice demonstrated a higher number of nerve fibers, fiber density, and nerve percentage (p < 0.05) at 2 weeks. The early regenerative response did not result in superlative functional recovery. At 3 weeks, GFAP-GDNF animals exhibit fewer nerve fibers, decreased fiber width, and decreased nerve percentage compared with WT and Myo-GDNF mice (p < 0.05). By 6 weeks, there were no significant differences between groups.

Conclusions

Peripheral delivery of GDNF resulted in earlier regeneration following sciatic nerve crush injuries than that with central GDNF delivery. Treatment with neurotrophic factors such as GDNF may offer new possibilities for the treatment of peripheral nerve injury.