Modular Bioactive Scaffold for Facial Nerve Reconstruction

• Published in: Journal of Neurological Surgery Part A: Central European Neurosurgery
• Main Authors: Röthlisberger, M., Madduri, S., Marbacher, S., Schaefer, D. J., Kalbermatten, D., Mariani, L., Guzman, R.
• Format: Conference Proceeding
• Language: English
• Published: 07.09.2015
• DOI: 10.1055/s-0035-1564516
• ISSN: 2193-6315

Background: Tumorous lesions growing in the cerebellopontine angle (CPA) get into close contact with the brainstem and the root entry and exit zone of the cranial nerves (CNs), and affect those same in their intracranial extension, often by stretching and compression. While operating on these lesions, the CNs are at risk of surgical damage by manipulation of the lesion itself or the associated CNs, which may lead to postoperative nerve palsy. In case of the CPA, a facial nerve (CN VII) palsy is clinically relevant and, if complete, a heavy burden for a patient, as facial dysmorphy and ocular complications are the clinical consequences. Direct coaptation of nerve ends is the currently preferred treatment, which is often associated with poor functional recovery. Thus, there is a great need for innovative treatment options. We have developed a modular bioactive scaffold which has a high potential for treating both crush injury and denervation. Such bioactive scaffold will be tested in a rabbit CN VII injury model, and biological performance will be evaluated using anatomical and behavioral measures. Methods: In the line of establishing a CN VII injury model, perfusion-fixed rabbit heads were used for anatomical dissection and localization of CN VII in CPA. Surgical procedures for operating the rabbit CN VII were reviewed and key requirements were identified. For treating the CN VII damage, modular bioactive fibrin scaffold releasing glial cell line–derived neurotrophic factor (GDNF) was developed to adapt to narrow space of the CPA. Anatomical and functional readouts, that is, histological analysis of regenerated nerve, target muscle innervation, Wallerian degeneration of the facial colliculus, and electromyography (EMG), were considered to be potential end points for evaluating treatment outcome. Results: As shown in previous preclinical studies addressing the CNVII/CNVIII complex, anatomical dissection showed the feasibility for surgical manipulation of CN VII in CPA. We have developed bioactive fibrin scaffold to address the complex requirements of injured CN VII and to protect the regenerative axons from surround tissue constrictions. Conclusions: Establishment of a facial nerve injury model is an important prerequisite for testing and developing efficacious novel treatment modalities. Bioactive fibrin nerve conduits hold great promise for protecting facial nerve from crush injury and for promoting axonal regeneration.