Abstract
Eclampsia is characterized by generalized convulsions in pregnant women with hypertension and proteinuria. Little is known about what triggers the convulsions in this syndrome. The prevailing view is that convulsions are caused by cerebral vasospasm and cerebral edema. However, many important clinical findings argue against cerebral edema or hypertensive encephalopathy as the sole causes of convulsions in eclampsia. The utero-placental ischemia causes the release of certain molecules such as neurokinin B, inflammatory cytokines, endothelins, and tissue plasminogen activator. These molecules stimulate excitatory neuronal receptors and alter neuronal excitability, synaptic transmission, and neuronal survival independent of any vascular effects. Highlighting the neuromodulatory and the convulsive effects of each of these molecules which are elevated in pre-eclampsia, offers a new perspective on the mechanisms of convulsions in eclampsia.
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