Patofisiologi Kejang dan Perubahan Susunan Saraf Pusat pada Eklampsia

Abstract

Eklampsia merupakan komplikasi serius kehamilan yang menimbulkan berbagai komplikasi neurologis seperti nyeri kepala, gangguan penglihatan, mual, muntah, koma, dan kejang. Patofisiologi/ Patogenesis kejang serta perubahan sitim saraf pusat eclampsia belum diketahui secara pasti dan merupakan pokok bahasan yang terus diteliti secara ekstensif. Beberapa mekanisme etiologi yang berimplikasi terhadap patofisiologi /pathogenesis kejangeklampsiadan berbagai perubahan sistem saraf pusat meliputi vasospasme hipertensis ensefalopati, edema serebral (terutama edema vasogenik), iskemia uteroplasental, dan kerusakan/ disfungsi endotel. Komplikasi neurologic eklampsia mirip dengan hipertensi ensefalopati yang ditandai dengan peningkatan tekanan darah secara akut dan ekstrim sehingga menyebakan kerusakan sawar darah otak, berkuranganya aliran darah ke otak, gangguan autoregulasi, hiperperfusi, dan edema. Edema otak pada pasien peeklampsia-eklampsia juga berhubungan dengan abnormalitas penanda kerusakan endotel.

Pathophysiology of Convulsion and Central Nervous System Changes in Eclampsia

Eclampsia is a serious complication of pregnancy due to some neurologic complications, including convulsion and central nervous system changes in eclampsia remains unknown and contionues to be the subject of extensive investigation. Some of etiologic mechanisms that are implicated in the pathophysiology/pathogenesis of eclamptic convulsion and other central nervous system change have included vasopasm hypertensive, encephalopathy, cerebral edema (mostly vaspgenic edema), the uteroplacental ischemia, and endothelial damage/endothel dysfunction. Neurologic complication of eclampsia are thought to be similar to hypertensive encephalopathy in which an acute, excessive elevation in blood pressure causes blood-brain barrier disruption, lossof cerebral blood flow autoregulation, hyperperfusion, and edema formation, Brain edema in patients with preeclampsia-eclampsia also was associated with abnormalities in endhotelial damage markers.