Kronik infarkt sonrası ensefalomalazi

Özet

Ensefalomalazi, geçirilmiş iskemi, travma veya başka doku hasarı sonrasında gelişen kalıcı parankim kaybını anlatır; kronik enfarkt en sık karşılaşılan nedenlerdendir. Kontrastsız BT'de lezyon beyin-omurilik sıvısına yakın düşük dansiteli kavite, çevresinde gliotik hipodensite ve komşu hacim kaybı olarak görünür. Ensefalomalazi beyin dokusu kaybını ifade eder ve BT'de hipodens alan olarak görülebilir; çevresinde gliosis bulunabilir. BT'de hipodens alan ve doku kaybı ensefalomalaziyle uyumlu olabilir; tek başına kronik süreci kesin olarak göstermez.

Faz ve pencere

Kontrastsız tanısal

Kronik hasarlı alanda parankim yoğunluğu BOS'a yaklaşan hipodensiteye döner; kavitasyon, kama biçimli hacim kaybı ve lezyona komşu sulkal genişleme görülebilir. BT'de güvenilir, evrensel bir HU eşiği yoktur; morfoloji ve çevre parankim etkisi esas alınır.

Önerilen pencereler: Beyin (G 80 / M 40), Subdural (G 200 / M 75).

BT bulguları

• BOS yoğunluğunda parankimal kavite — eski infarkt yatağında düzensiz veya kama biçimli hipodens alan oluşur.
• Damar alanı dağılımı — kortikal kama geniş tabanıyla yüzeye, tepesi derin beyaz cevhere uzanabilir.
• Fokal sulkal genişleme — lezyon üzerindeki konveksite sulkusları çevre doku kaybıyla birlikte açılır.
• Ex-vacuo komşu ventrikül değişikliği — derin infarkt yatağına yakın ventrikül konturu hacim kaybına doğru çekilebilir.
• Gliotik çevre hipodensitesi — kavitenin kenarında daha az belirgin, düzensiz düşük dansiteli doku kalabilir.
• Kronik ensefalomalazide kistik değişiklikler ve çevresel gliosis görülebilir.
• Bilateral ya da çok odaklı kronik hasar — farklı damar alanlarındaki eski kavite ve lakünler eşlik edebilir.

Normalde

Lezyonun kontralateral sağlam parankime göre hacim kaybı yarattığı ve hipodens olduğu görülür. Etkilenen düzeyde damar alanına uyan ensefalomalaziyi ve ipsilateral lateral ventrikülde ex-vacuo genişlemeyi değerlendirin.

Ayırıcı tanı

İskemik beyin hasarı hücre ölümüne ve gliozis ya da kavitasyona yol açabilir; kronik ensefalomalazi beyin dokusu kaybıyla karakterizedir.

Porensefalik kavite

BOS sinyalli/yoğunluklu boşluk ventriküle veya subaraknoid aralığa uzanabilir; neden ve dağılımı değişkendir.

Araknoid kist

ekstraaksiyel BOS dansiteli oluşum komşu beyni iter; parankim içinde damar alanına uyan doku kaybı oluşturmaz.

Kistik neoplazi

kavite çevresinde nodüler yumuşak doku, ödem veya kontrast tutulumu bulunabilir; kontrastlı MR ile açıklık kazanır.

Eski travmatik kontüzyon

inferior frontal ve anterior temporal yüzeylerde düzensiz, bazen hemorajik kalıntılı ensefalomalazi yapabilir.

Tuzaklar

• BT'de hipodens alan ve beyin dokusu kaybı, eski hasara bağlı ensefalomalaziyle uyumlu olabilir.
• Başlangıç BT'si normal olan erken akut iskemide ensefalomalazi beklenmez; yeni nörolojik defisit varsa eski kronik bulgu akut hastalığı dışlamaz.
• Parankim kenarında kitle etkisi, yeni kanama veya belirgin ödem varsa yalnızca eski ensefalomalazi olarak yorumlamayın; üstüne eklenen yeni süreç olabilir.

Kendini dene

1. Önceki MCA enfarktı bulunan hastada kortikal kama biçimli hipodensite, geniş sulkuslar ve kitle etkisi yok. Tanı nedir?

   • Kronik ensefalomalazi
   • Akut MCA enfarktı
   • Araknoid kist
   • Kistik gliom
   Cevabı göster

   Kronik ensefalomalazi. Kavite ve çevre hacim kaybı kronik hasarı gösterir. Akut enfarkt sulkusları silebilir; araknoid kist ekstraaksiyeldir, kistik gliomda çevresel doku veya ödem beklenebilir.

2. Bu DDMS olgusunda sol frontoparietal ensefalomalaziye eşlik eden ventriküler bulgu hangisidir?

   • Eks vakuo dilatasyon
   • Obstrüktif hidrosefali
   • Bilateral ventriküler simetri
   • Kompresif deformasyon
   Cevabı göster

   Eks vakuo dilatasyon. S85 kaynağında, sol beyin yarım küresi atrofisine ve ensefalomalaziye bağlı eks vakuo dilatasyonun izlendiği belirtilmektedir.

İlgili konular

• Lobar ve bölgesel atrofi örüntüsü

Kaynaklar

Bu sayfadaki 35 cümle ve 2 quiz sorusu aşağıdaki kaynaklardan alıntılarla otomatik olarak karşılaştırıldı; 11 cümle bu karşılaştırmada düzeltildi (2026-10-09).

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