The motor nerve to the masseter muscle: an anatomic and histomorphometric study to facilitate its use in facial reanimation.

INTRODUCTION: The motor nerve to the masseter muscle is increasingly being used for facial reanimation procedures. However, many surgeons have been reluctant to use this versatile source of axons because of difficulty in locating it intraoperatively. In this study we conducted a detailed assessment of its gross and microscopic anatomy and develop a simple, reliable method for locating this nerve. METHODS: We defined the anatomy of the nerve to the masseter, in particular its relationship to common surgical landmarks such as the auricular tragus and the zygomatic arch, and determined its intramuscular anatomy. We also performed a histomorphometric analysis. RESULTS: The anatomy of the motor nerve to the masseter was consistent. A convenient starting point for its dissection was found 3.16 ± 0.30 cm anterior to the tragus at a level 1.08 ± 0.18 cm inferior to the zygomatic arch. The nerve was located 1.48 ± 0.19 cm deep to the superficial muscular aponeurotic system (SMAS) at this point. Relative to the zygomatic arch, the nerve formed an angle of 50 ± 7.6° as it coursed distally into the masseter muscle. The distance from the arch to the first branch of the motor nerve to the masseter was 1.33 ± 0.20 cm. The histomorphometric analysis demonstrated that the motor nerve to the masseter contained an average of 2775 ± 470 myelinated fibers. CONCLUSIONS: Successful intraoperative location of the motor nerve to the masseter is facilitated by knowledge of its anatomy relative to standard surgical landmarks. A consistent and convenient starting point for dissection of this nerve is found 3 cm anterior to the tragus and 1 cm inferior to the zygomatic arch. The nerve contains over 2700 myelinated fibers, demonstrating its usefulness as a source of motor innervation for facial reanimation.

Matching of motor-sensory modality in the rodent femoral nerve model shows no enhanced effect on peripheral nerve regeneration.

The treatment of peripheral nerve injuries with nerve gaps largely consists of autologous nerve grafting utilizing sensory nerve donors. Underlying this clinical practice is the assumption that sensory autografts provide a suitable substrate for motoneuron regeneration, thereby facilitating motor endplate reinnervation and functional recovery. This study examined the role of nerve graft modality on axonal regeneration, comparing motor nerve regeneration through motor, sensory, and mixed nerve isografts in the Lewis rat. A total of 100 rats underwent grafting of the motor or sensory branch of the femoral nerve with histomorphometric analysis performed after 5, 6, or 7 weeks. Analysis demonstrated similar nerve regeneration in motor, sensory, and mixed nerve grafts at all three time points. These data indicate that matching of motor-sensory modality in the rat femoral nerve does not confer improved axonal regeneration through nerve isografts.

Retrograde labeling in peripheral nerve research: it is not all black and white.

Retrograde labeling has become an important method of evaluation for peripheral nerve regeneration after injury. We review the features of the commonly used retrograde tracers Fast Blue, Fluoro-Gold, and Fluoro Ruby in addition to the various application methods (conduit reservoir, intramuscular injection, and crystal powder application) and the techniques used to count stained neurons. Upon application of the staining techniques and dyes in a rat and mouse nerve injury model, Fluoro-Gold was found to stain the greatest number of neurons with all application methods. However, due to variability of staining intensity, neuron size, and background staining, it is difficult to count the stained neurons accurately. Fast Blue stains consistently using intramuscular injection in the mouse but fails to provide adequate staining using the muscle injection method in the rat model and shows high failure rates using the conduit reservoir technique. However, crystal dye application with Fast Blue to the cut nerve end provides excellent results. We believe that it is imperative to use the various tracers and application methods prior to their experimental use to develop a consistent standardized approach to retrograde labeling.

Regeneration through nerve isografts is independent of nerve geometry.

Investigators have theorized that tortuosity in nerve grafts may adversely affect nerve regeneration. This study investigated the effect of graft configuration and redundancy on regeneration across 2.5-cm rat sciatic nerve isografts. Thirty-two Lewis rats were randomized to four nerve grafting groups defined by gap distance and isograft conformation. In Group 1, grafts were interposed into a 2-cm gap, resulting in mild graft redundancy. In Groups 2 and 3, grafts were tacked in sinusoidal or omega-shaped configurations, respectively, to bridge a 0.5-cm gap. In Group 4, grafts were interposed after 1 cm of native sciatic nerve was resected, resulting in no graft redundancy and an interstump distance of 2.5 cm. At 6 weeks, nerve tissue was harvested; subsequent histomorphometric analysis revealed no significant differences in regeneration between groups. These data suggest that regeneration through isografts is independent of the graft geometry and redundancy.

Delayed nerve repair is associated with diminished neuroenhancement by FK506.

OBJECTIVES/HYPOTHESIS: The immunosuppressive agent FK506 has been shown in many studies to enhance nerve regeneration and to accelerate functional recovery after immediate nerve repair. However, in clinical practice the diagnosis and treatment of patients with peripheral nerve injuries is often delayed. The study investigated whether FK506 would retain its neuroregenerative properties when nerve repair and initiation of FK506 therapy were delayed for 7 days. STUDY DESIGN: In vivo laboratory study. METHODS: Thirty-two Lewis rats underwent tibial nerve transection and were randomly assigned to four experimental groups: immediate repair with FK506 treatment, immediate repair without FK506 treatment, 7-day delayed repair with FK506 treatment, and 7-day delayed repair without FK506 treatment. Treated animals received daily subcutaneous injections of 2 mg/kg FK506. Serial walking track measurements were performed at 14, 16, and 18 days after nerve repair. On day 18 after repair, peripheral nerves were injected with a fluorescent tracer for retrograde labeling. On day 21, peripheral nerves and spinal cords were harvested for histomorphometric analysis and motor neuron cell body counts, respectively. RESULTS: Animals that underwent immediate repair with FK506 had significantly higher fiber counts and percentages of nerve than the other three groups (P <.05) but did not show statistically significant earlier functional recovery. The remaining three groups had intermediate levels of nerve regeneration that were not significantly different. Retrograde abled motor neurons counts were decreased in animals with delayed nerve repair that received no FK506 (P <.05). CONCLUSION: In a rat tibial nerve transection model, the neuroregenerative effects of FK506 diminished markedly when repair and initiation of FK506 therapy were delayed by 7 days.