Compound Motor Action Potentials During a Modest Nerve Crush.

Nerve crush injury results in axonotmesis, characterized by disruption of axons and their myelin sheaths with relative sparing of the nerve's connective tissue. Despite the widespread use of crush injury models, no standardized method for producing these lesions has been established. We characterize a crush model in which a narrow forceps is used to induce a modest and controlled compressive injury. The instantaneous compound motor action potential (CMAP) is monitored in situ and in real-time, allowing the characterization of neuromuscular response during and after injury. The tibial nerves of 11 anesthetized rats were surgically isolated. After the placement of electrodes, CMAPs were elicited and registered using a modular-data-acquisition system. Dumont-#5 micro-forceps were instrumented with a force transducer allowing force measurement via a digital sensor. Baseline CMAPs were recorded prior to crush and continued for the duration of the experiment. Nerve crushing commenced by gradually increasing the force applied to the forceps. At a target decrease in CMAP amplitude of 70%-90%, crushing was halted. CMAPs were continually recorded for 5-20 min after the termination of the crushing event. Nerves were then fixed for histological assessment. The following post-crush mean values from 19 trials were reported: peak CMAP amplitude decreased by 81.6% from baseline, duration of crush was 17 sec, rate of applied force was 0.03 N/sec, and maximal applied force was 0.5 N. A variety of agonal phenomena were evident post-lesion. Following the initial decrease in CMAP, 8 of 19 trials demonstrated a partial and transient recovery, followed by a further decline. Thirteen trials exhibited a CMAP amplitude near zero at the end of the recording. Twelve trials demonstrated a superimposed EMG background response during and after the crush event, with disappearance occurring within 4-8 min. Qualitative histology assessment at the lesion site demonstrated a correspondence between CMAP response and partial sparing of nerve fibers. By using a targeted decline in CMAP amplitude as the endpoint, researchers may be able to produce controlled, brief, and reproducible crush injuries. This model can also be used to test interventions aimed at enhancing subsequent regeneration and behavioral recovery.

Consequences of Progressive Full-Thickness Focal Chondral Defects Involving the Medial and Lateral Femoral Condyles After Meniscectomy: A Biomechanical Study Using a Goat Model.

Background: Full-thickness chondral defects alter tibiofemoral joint homeostasis and, if left untreated, have the potential to progress to osteoarthritis. Purpose: To assess the effects of isolated and dual full-thickness chondral defect size and location on the biomechanical properties of the lateral femoral condyle (LFC) and medial femoral condyle (MFC) during dynamic knee flexion in goat knees without menisci. Methods: In 12 goat knees, we created progressively increasing full-thickness circular chondral defects (3-, 5-, and 7.5-mm diameter) in the weightbearing contact area of flexion and extension in the MFC, the LFC, or both. Each knee was fixed into a custom steel frame and attached to a motor with sensors inserted intra-articularly. For each testing condition, the knee was loaded to 100 N and underwent a dynamic range of motion between 90° of flexion and 30° of extension. The following parameters were collected: contact area, contact pressure, contact force, peak area, and peak pressure. Study Design: Controlled laboratory study. Results: The peak pressure at the defect rim of the MFC at full extension increased by 51.51% from no defect (1.887 MPa) to a 7.5-mm defect (2.859 MPa) (P < .001), and the peak pressure at the defect rim of the LFC at full extension increased by 139.14% from no defect (1.704 MPa) to a 7.5-mm defect (4.075 MPa) (P < .001). The peak pressures for LFC defects at all 3 diameters were significantly greater when compared with dual defects consisting of increasing LFC defect diameter and constant MFC defect diameter (P < .001 for all). Conclusion: Extremely large increases in peak pressure were seen at the rim of articular cartilage defects when evaluated under dynamic loading conditions. Isolated LFC defects experienced a greater increase in defect rim stress concentrations when compared with isolated MFC defects for equivalent increases in defect size. Defect size played a significant role independent of location for peak pressures on the MFC and LFC. Clinical Relevance: Significant rim-loading effects increase with defect size under dynamic loading and may result in increasingly rapid progression of articular cartilage lesions. Within the context of this goat model, findings suggest that lateral compartment chondral lesions are more likely to progress than medial compartment lesions of equivalent size.

Histological Assessment of Wallerian Degeneration of the Rat Tibial Nerve Following Crush and Transection Injuries.

BACKGROUND: Wallerian degeneration (WD) following peripheral nerve injury (PNI) is an area of growing focus for pharmacological developments. Clinically, WD presents challenges in achieving full functional recovery following PNI, as prolonged denervation of distal tissues for an extended period of time can irreversibly destabilize sensory and motor targets with secondary tissue atrophy. Our objective is to improve upon histological assessments of WD. METHODS: Conventional methods utilize a qualitative system simply describing the presence or absence of WD in nerve fibers. We propose a three-category assessment that allows more quantification: A fibers appear normal, B fibers have moderate WD (altered axoplasm), and C fibers have extensive WD (myelin figures). Analysis was by light microscopy (LM) on semithin sections stained with toluidine blue in three rat tibial nerve lesion models (crush, partial transection, and complete transection) at 5 days postop and 5 mm distal to the injury site. The LM criteria were verified at the ultrastructural level. This early outcome measure was compared with the loss of extensor postural thrust and the absence of muscle atrophy. RESULTS: The results showed good to excellent internal consistency among counters, demonstrating a significant difference between the crush and transection lesion models. A significant decrease in fiber density in the injured nerves due to inflammation/edema was observed. The growth cones of regenerating axons were evident in the crush lesion group. CONCLUSION: The ABC method of histological assessment is a consistent and reliable method that will be useful to quantify the effects of different interventions on the WD process.

Spinal Compression Fracture Management: A Review of Current Treatment Strategies and Possible Future Avenues.

STUDY DESIGN: Narrative review. OBJECTIVE: Despite the numerous treatment options for vertebral compression fractures, a consensus opinion for the management of patients with these factures has not been established. This review is meant to provide an up-to-date overview of the most common treatment strategies for compression fractures and to suggest possible routes for the development of clearer treatment guidelines. METHODS: A comprehensive database search of PubMed was performed. All results from the past 30 years were obtained and evaluated based on title and abstract. The full length of relevant studies was analyzed for level of evidence, and the strongest studies were used in this review. RESULTS: The major treatment strategies for patients with compression fractures are conservative pain management and vertebral augmentation. Despite potential adverse effects, medical management, including nonsteroidal anti-inflammatory drugs, calcitonin, teriparatide, and bisphosphonates, remains the first-line therapy for patients. Evidence suggests that vertebral augmentation, especially some of the newer procedures, have the potential to dramatically reduce pain and improve quality of life. At this time, balloon-assisted kyphoplasty is the procedure with the most evidence of support. CONCLUSIONS: Based on current literature, it is evident that there is a lack of standard of care for patients with vertebral compression fractures, which is either due to lack of evidence that a procedure is successful or due to serious adverse effects encountered with prolonged treatment. For a consensus to be reached, prospective clinical trials need to be formulated with potential new biomarkers to assess efficacy of treatment strategies.