926 Perineural Spread of Cutaneous Squamous Cell Carcinoma Manifesting as Ptosis and Ophthalmoplegia (Orbital Apex Syndrome). Alonso PE, Bescansa E, Salas J, et al. Br J Plast Surg 48564, 1995
CURRENT LITERATURE
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Some cases of trigeminal neuralgia have been found to be caused by vascular compression of the trigeminal nerve at the pans. Previous authors have described the insertion of a variety of materials (absorbable gelatin sponge, muscle, fascia, Teflon, and even vascular clips) to maintain separation of the vessel (usually the superior cerebellar artery) and the nerve. However, these prostheses can slip, resorb, and migrate. More recently, authors have described a retromastoid craniectomy approach for decompression of the vessel in the cerebellar-pontine angle. In this report, the authors describe a modification of the technique where a dural sling is fashioned from the inferior layer of the tentorium cerebelli (a folded meningeal layer) to suspend the vessel away from the nerve. A pedicle of tissue, approximately 1.5 mm in length and 3 to 4 mm in width, is obtained from the undersurface of the tentorium cerebilli, with attachment medially. The free end of the pedicle is passed medial to and beneath the artery, then looped backwards, forming a loop that contains the artery. A hemoclip holds the lateral tip of the pedicle, keeping the sling in position. The authors have used this technique on seven patients and six patients have reported complete resolution of their facial pain in follow-ups up to 8 months. The other patient, who had undergone several previous procedures, reported improvement. The authors encourage further evaluation of this technique in larger studies.
A Tentorial Sling in Microvascular Decompression for Trigeminal Neuralgia: Technical Note. Melvill RL, Baxter BL. J Neurosurg 84:127, 1996
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Squamous cell carcinoma (SCC) has been known to produce metastasis by perineural spread, a common way for it to enter the central nervous system. This paper presents two cases of orbital apex syndrome as the only sign of SCC recurrence. Both patients had been previously diagnosed and treated for SCC. Both lesions were excised with tumor-free margins. Within 1 to 2 years postoperatively, the patients sought treatment for dysesthesia and/or paresthesia of the first division of the trigeminal nerve, ptosis, and other signs of ophthalmoplegia on the same side as the original tumor. Neither showed any signs of local or other regional occurrence. When central nervous system spread of the SCC was subsequently diagnosed, the tumor was so advanced that surgical treatment was no longer an option. Both patients were treated satisfactorily with radiation. Awareness of perineural spread of SCC could allow the physician to diagnose these recurrences earlier and, thus, enhance treatment success by allowing for a combination of surgery and radiotherapy.-M.J. RISSER