BACKGROUND: An in vivo animal model for carpal tunnel syndrome (CTS) is presented which allows for graded application of pressure to the median nerve within the carpal canal. We hypothesized that such pressure would cause electrophysiologic changes in the median nerve in a dose-related manner, with NCS/EMG changes consistent with CTS in humans. METHODS: In 40 New Zealand white rabbits, ranging from 2 to 2.5 kg, angioplasty catheters were placed in the carpal tunnel in the forepaws and pressures ranging from 50 to 80 mmHg applied to one side while the contralateral side served as the control and remained uninflated. Pressure was applied until a 15% increase in distal motor latency was obtained for 2 consecutive weeks by nerve conduction studies. RESULTS: All the experimental limbs exhibited a 15% increase in distal motor latency. None of the control limbs showed a significant increase in distal motor latency. In the experimental animals the 15% delay was achieved in approximately 4-5 weeks in the 50-70 mmHg groups and in approximately 1 week in the 80 mmHg group. CONCLUSION: This new animal model for CTS demonstrates a direct cause and effect relationship between carpal tunnel pressure and median nerve dysfunction. We anticipate that this in vivo model with clinically relevant outcomes will facilitate identification of injury mechanisms, and will serve as a basis for future development of novel interventions and treatments.
BACKGROUND: An in vivo animal model for carpal tunnel syndrome (CTS) is presented which allows for graded application of pressure to the median nerve within the carpal canal. We hypothesized that such pressure would cause electrophysiologic changes in the median nerve in a dose-related manner, with NCS/EMG changes consistent with CTS in humans. METHODS: In 40 New Zealand white rabbits, ranging from 2 to 2.5 kg, angioplasty catheters were placed in the carpal tunnel in the forepaws and pressures ranging from 50 to 80 mmHg applied to one side while the contralateral side served as the control and remained uninflated. Pressure was applied until a 15% increase in distal motor latency was obtained for 2 consecutive weeks by nerve conduction studies. RESULTS: All the experimental limbs exhibited a 15% increase in distal motor latency. None of the control limbs showed a significant increase in distal motor latency. In the experimental animals the 15% delay was achieved in approximately 4-5 weeks in the 50-70 mmHg groups and in approximately 1 week in the 80 mmHg group. CONCLUSION: This new animal model for CTS demonstrates a direct cause and effect relationship between carpal tunnel pressure and median nerve dysfunction. We anticipate that this in vivo model with clinically relevant outcomes will facilitate identification of injury mechanisms, and will serve as a basis for future development of novel interventions and treatments.