Background: Disease processes causing increased neural compartment pressure may induce transient or permanent neural dysfunction. Surgical decompression can prevent and reverse such nerve damage. Owing to insufficient evidence from controlled studies, the efficacy and optimal timing of decompression surgery remains poorly characterized for several entrapment syndromes.
New method: We describe the design, manufacture, and validation of a device for study of entrapment neuropathy in a small animal model. This device applies graded extrinsic pressure to a peripheral nerve and wirelessly transmits applied pressure levels in real-time. We implanted the device in rats applying low (under 100 mmHg), intermediate (200-300 mmHg) and high (above 300 mmHg) pressures to induce entrapment neuropathy of the facial nerve to mimic Bell's palsy. Facial nerve function was quantitatively assessed by tracking whisker displacements before, during, and after compression.
Results: At low pressure, no functional loss was observed. At intermediate pressure, partial functional loss developed with return of normal function several days after decompression. High pressure demonstrated complete functional loss with incomplete recovery following decompression. Histology demonstrated uninjured, Sunderland grade III, and Sunderland grade V injury in nerves exposed to low, medium, and high pressure, respectively.
Comparison with existing methods: Existing animal models of entrapment neuropathy are limited by inability to measure and titrate applied pressure over time.
Conclusions: Described is a miniaturized, wireless, fully implantable device for study of entrapment neuropathy in a murine model, which may be broadly employed to induce various degrees of neural dysfunction and functional recovery in live animal models.
Keywords: Bell’s Palsy; Bioimplantable device; Compression neuropathy; Entrapment neuropathy; Surgical decompression.
Published by Elsevier B.V.