Tolga DÖLEN, İRFAN KAYGUSUZ, NUSRET AKPOLAT, Hayrettin Cengiz ALPAY, EROL KELEŞ, TURGUT KARLIDAĞ, ŞİNASİ YALÇIN, Koray YÜKSEL

Nimodipin ve prednizolonun travmatik fasiyalsinir hasarı üzerine etkisi

Amaç: Çalışmanın amacı klempleme ile periferik fasiyal paralizi oluşturulmuş hayvan modelinde nimodipin ve prednizolon tedavisininhistopatolojik etkisini araştırmaktır. Yöntem:Bukkal sinir dalları klemplenerek fasiyal sinir felci oluşturulmuş 28 Yeni Zelanda orijinli tavşan, yedişerlik 4 gruba ayrıldı veher bir gruba 21 gün boyunca nimodipin, metilprednizolon ve nimodipin-metilprednizolon kombinasyonu uygulandı. Tedavi sonrasındahasarlı nöral dokular histopatolojik olarak perinöral fibrozis, kollajendejenerasyonu, aksonal dejenerasyon, miyelin dejenerasyonu,Schwann hücre proliferasyonu, normal miyelin yapısı ve ödem açısından incelendi. Gruplar birbirleriyle ve kontrol grubuyla karşılaştırıldı. Bulgular:Kollajen liflerde artış, miyelin dejenerasyonu, aksonal dejenerasyon ve miyelin yapısı açısından nimodipin grubu ile kontrolgrubu arasında; nimodipin grubu ile metilprednizolon grubu arasındave nimodipin grubu ile nimodipin-metilprednizolon kombinasyongrubu arasında ise ödem oluşumu açısından istatistiksel olarak anlamlı farklılık belirlendi (p

The effect of nimodipine and prednisolone on traumatic facial nerve injury treatment

Objective:To investigate the histopathological effect of nimodipineand prednisolone treatment on an animal model with peripheral facialnerve paralysis generated by clamping. Methods:Twenty-eight New Zealand originated rabbits with facialnerve paralysis of the buccal branches generated by clamping weredivided into four groups of seven each, administered with nimodipine,methylprednisolone and nimodipine-methylprednisolone combinationthroughout 21 days. The injured neural tissues were investigatedhistopathologically after treatment regarding perineural fibrosis, collagen degeneration, axonal degeneration, myelin degeneration, Schwanncell proliferation, normal myelin structure, and edema. The groupswere compared with each other and with the control group. Results: Statistically significant difference was determined betweennimodipine and control groups regarding increased number of collagenfibers, myelin degeneration, axonal degeneration and myelin structure;between nimodipine and methylprednisolone groups, and betweennimodipine and nimodipine-methylprednisolone combination groupsregarding edema (p<0.05). Statistically significant data were also foundbetween methylprednisolone and control groups in terms of increasednumber of collagen fibers, myelin degeneration, axonal degenerationand edema; between nimodipine-methylprednisolone combination andthe control groups in terms of increased number of collagen fibers,myelin degeneration, axonal degeneration, normal myelin structure andedema (p<0.05). Conclusion:Nimodipine and methylprednisolone both have positiveeffects on traumatic peripheral nerve paralysis with nerve integrity preserved whereas advantage of nimodipine over methylprednisolone cannot be suggested.

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