Nöropatik Ağrıda Antikonvülzanlar

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Author NameUniversity of AuthorFaculty of AuthorDepartment of Author
Anticonvulsants in Neuropathic Pain
2004
Volume: 
11
Number: 
2
Sayfa Aralığı:: 
121-125
Publication Language: 
Turkish
Abstract (Original Language): 
Bu çalışmada nöropatik ağrının patogenezi değerlendirilmiş ve tedavide kullanılan antikonvülzanlar gözden geçirilmiştir. Periferik veya santral kökenli olsun, nöropatik ağrı sinir sisteminin hasarlanmış bölgesinde varolan nöronal hipereksitabilite ile karakterizedir. Periferik nöropatik ağrıda, hasarlı sinir sonlanmalarında bulunan sayısı kısmen artmış ve yeni sodyum kanalları nedeniyle anormal spontan ve artmış uyarılmış aktivite sergilerler. Santral ağrıda, spontan ve uyarılmış ağrı en iyi nöronal hipereksitabilite ile açıklanır. Periferik hipereksitabilite periferik nosiseptör, dorsal kök gangliyonlar, spinal kord arka boynuzu, ve beyin seviyesindeki bir seri moleküler değişikliğe bağlıdır. Bu değişiklikler arasında sodyum kanallarının anormal ekspresyonu, glutamat reseptörlerinde artmış aktivite, y-aminobütirik asid ( GABA-erjik ) inhibisyondaki değişiklikler, ve hücreye kalsiyum girişindeki değişim vardır. Nöropatik ağrıdaki nöronal hipereksitabilite ve benzer moleküler değişiklikler bazı epilepsi tiplerindeki hücre değişimleriyle ortak özelliklere sahiptir. Bu durum, nöropatik ağrıda antiepileptik kullanımına yol açmıştır.
Abstract (2. Language): 
Pathogenesis of neuropathic pain was overwieved and anticonvulsants used for alleviation were reviewed. Neuropathic pain, whether of peripheral or central origin, is characterized by a neuronal hyperexcitability in damaged nerve endings Neuropathic pain of peripheral origin exhibit abnormal spontaneous and increased evoked activity, partly due to an increased and novel expression of sodium channels. In central pain, the spontaneous pain and evoked pain are also best explained by a neuronal hyperexcitability in dorsal root ganglia, in the dorsal horn of spinal cord, and in the brain. These changes include abnormal expression of sodium channels, increased activity at glutamate receptor sites, changes in y-amynobutiric acid (GABA ergic) inhibition, and alteration of calcium influx into cells. The neuronal hyperexcitability and corresponding molecular changes in neuropathic pain have many features in common with cellular changes in certain forms of epilepsy. This has led to the use of anticonvulsant drugs for the treatment of neuropathic pain.
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