SAK sonrası Caudate Nucleus Degenerasyonu

Giriş: Kaudat çekirdek lateral ventriküllerin en yakın komşusu olmasına rağmen subaraknoid kanamalar sonrası gelişen pek çok psikomotor bozukluğun nedeni bilinmeyene yol açabilmektedir. Bu konu henüz yeterince çalışılmamıştır. Bu çalışma, subaraknoid kanama sonrası kaudat çekirdekte meydana gelen histopatolojik değişiklikleri incelemeyi amaçlamaktadır. Gereç ve Yöntemler: 25 adet yabani erkek sağlıklı tavşan kullanıldı. Ağırlıkları, kalp ve solunum hızları, tansiyon değerleri kaydedildi. Hayvanlar kontrol grubuna ayrıldı (GI, n=5); SHAM (1,2 cc salin enjekte edildi (GII, n=5) ve çalışma grubuna (GIII, n=15) Çalışma grubunda hayvanların sisterna magnalarına 1,2 cc otolog kan enjekte edildi.Hayvanlar takibe alındı. kaudat çekirdeğin dejenere nöron yoğunlukları stereolojik yöntemlerle tahmin edildi ve Mann-Witney U testi ile analiz edildi. Bulgular: Bir çalışma grubunda üç tavşan öldü. Bu hayvanlarda meningeal tahriş belirtileri ve bilinç kaybı kaydedildi. GIII hayvanlarında uzamış QT aralıkları, ST çöküntüleri ve düşük voltajlı QRS'ler gözlendi. Ortalama kalp-solunum hızlarının (n/dak), kaudat çekirdeğin dejenere nöron yoğunluklarının (n/mm3) sayısal değerleri aşağıdaki gibidir: GI'de 226±30/22±5/9±3; GII'de 211±18/16±4/13±4; ve 188±19/14±4/98±13 GIII. P değerleri: GI/GII'de p<0,005; GII/GIII'de p<0,0005 ve GI/GIII'de p<0,00001. Sonuç: Subaraknoid kanama kaudat çekirdeği besleyen arterlerde spazmlara neden olarak iskemik yaralanmaya neden olur.

Anahtar Kelimeler:

Subaraknoid kanama, kaudate çekirdek, dejenerasyon, komplikasyon

Exploration of Caudate Nucleus Degeneration following Subarachnoid Hemorrhage: An Experimental Study

Background: Although the caudate nucleus is the closest neighbor of the lateral ventricles, it can lead to the unknown cause of many psychomotor disorders that develop after subarachnoid hemorrhages. This subject has not been adequately studied yet. The study aims to examine the histopathological changes in the caudate nucleus after subarachnoid hemorrhage. Material and Methods: Twenty-five wild male healthy rabbits were used. Their weights, heart and respiration rates, and blood pressure values were recorded. Animals were divided into the control (GI, n=5); SHAM (1.2 ccs of saline injected (GII, n=5), and study group (GIII, n=15). N the study group, 1.2 ccs of autologous blood was injected into the cisterna magna of animals. The animals were followed up for three weeks and sacrificed under general anesthesia. Degenerated neuron densities of the caudate nucleus were estimated by the stereological methods and analyzed by the Mann-Witney U test. Results: Three rabbits dead in a study group. Meningeal irritation signs and unconsciousness were noted in those animals. Prolonged QT intervals, ST depressions, and low voltage QRSs were observed in GIII animals. Numerical values of mean heart-respiratory rates (n/min), degenerated neuron densities of the caudate nucleus (n/mm3) as follows: 226±30/22±5/9±3 in GI; 211±18/16±4/13±4 in GII; and 188±19/14±4/98±13 GIII. P values: p<0.005 in GI/GII; p<0.0005 in GII/GIII and p<0.00001 in GI/GIII. Conclusion: Subarachnoid hemorrhage causes spasms of the arteries supplying the caudate nucleus, leading to ischemic injury.

Keywords:

subarachnoid hemorrhage, caudat nucleus, dejeneration,

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