Author(s): Menovsky T, van Overbeeke JJ
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Abstract BACKGROUND: Transient cranial nerve deficit is a common postoperative complication after surgery at the cranial base. In this type of surgery, the cranial nerves are often not macroscopically damaged or transected, but more or less manipulated during surgery. In this article, the cellular mechanisms of postoperative cranial nerve deficit are reviewed. METHODS: Experimental and clinical papers concerning cranial and peripheral nerve damage during surgery were critically reviewed. RESULTS: There are definite differences in the anatomical and histological structure between peripheral and intracranial nerves, which make the latter much more prone to intraoperative damage. Several pathological mechanisms are responsible for postoperative deficit, such as segmental demyelination of the nerve, comprised microcirculation within the nerve, postoperative edema, and "synaptic stripping" around the cell bodies of the affected neurons, which can be regarded as a regenerative response of the nervous system. CONCLUSIONS: Several cellular mechanisms are responsible for postoperative cranial nerve deficit after skull base surgery. Understanding these mechanisms is important for all surgeons involved in the treatment of skull base lesions.
This article was published in Surg Neurol
and referenced in International Journal of Neurorehabilitation