Prematüre Bebeklerde Nörolojik Sorunlar ve İzlemi

ÖzNörogelişimsel sekeller prematüre bebeklerde görülen uzun dönem morbiditelerin en önemlisidir. Yenidoğan yoğun bakımındaki ilerlemelere bağlı olarak prematüre bebeklerin mortalitesi giderek azalmakta ancak serebral palsi gibi ağır motor sekeller ve belirgin bilişsel, davranışsal ve duyusal bozukluklar gibi ciddi nörogelişimsel bozukluklar görülmeye devam etmektedir. Germinal matriks kanaması-İntraventriküler kanama (GMK-İVK) ve beyaz cevher hasarı, prematüre bebeklerde sık görülen ve beyin hasarının en önemli nedenlerini oluşturan nörolojik komplikasyonlardır. Prematüre bebeklerde son yıllarda ağır destrüktif beyin hasarından çoke nöronal ve glial hücre ölümüne yol açmayan daha hafif beyin hasarının olduğu, bununbeyin büyümesini olumsuz etkilediği, bozulmuş beyin büyümesinin hücre ölümünden ziyade nöron ve glial hücrelerin anormal maturasyonu ile ilişkili olabileceği gösterilmiştir. Serebral gri ve beyaz cevher dismaturasyonunun daha iyi anlaşılmasıyla gelecekte engellenmesi ve uzun dönem nörolojik prognozun düzeltilmesi ile ilgili yeni yaklaşımlar gündeme gelebilecektir.

Neurological in premature infants Problems and Watch

AbstractNeurodevelopmental disabilities continue to be a leading cause of morbidity insurvivors of premature birth. Although improved neonatal intensive care has reduced the mortality of preterm neonates, many preterm survivors continue to have major motor deficits, including cerebral palsy and significant cognitive, behavioral orsensory deficits.Germinal matrixintraventricular hemorrhage and white matter injury are common patterns of brain injury in premature newborns.  Whereas preterm infants werepreviously at high risk for destructive white and gray matter degeneration, now lesssevere injury that does not appear to involve pronounced glial or neuronal loss is com-mon. These milder forms of injury are associated with reduced cerebral growth. Recent studies support that this impaired cerebral growth involves abnormal maturation of neurons and glia rather than cell death. These recently recognized forms ofcerebral gray and white matter dysmaturation raise new diagnostic challenges andmay suggest new therapeutic directions in future.

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