Neurological aspects of eclampsia

The difficult types of preeclampsia and eclampsia are presented with the neurological symptoms. The break of cerebral autoregulation mechanism plays the most important role in pathogenesis of cerebral vasospasm. Nevertheless eclampsia isn’t just an ordinary hypertensive encephalopathy because other pathogenic mechanisms are involved in its appearance. The main neuropathologic changes are multifocal vasogenic edema, perivascular multiple microinfarctions and petechial hemorrhages. Neurological clinical manifestations are convulsions, headache, visual disturbances and rarely other discrete focal neurological symptoms. Eclampsia is a high-risk factor for onset of hemorrhagic or ischemic stroke. This is a reason why neurological diagnostic tests are sometimes needed. The method of choice for evaluation of complicated eclampsia is computerized brain topography that shows multiple areas of hypodensity in occipitoparietal regions. These changes are focal vasogenic cerebral edema. For differential diagnosis of eclampsia and stroke other diagnostic methods can be used - fundoscopic exam, magnetic resonance brain imaging, cerebral angiography and cerebrospinal fluid exam. The therapy of eclampsia considers using of magnesium sulfate, antihypertensive, anticonvulsive and antiedematous drugs

Plasminogen activator inhibitor-1 in the evolution of stroke

Fibrinolytic activity in the acute stroke was examined by monitoring the level of plasminogen activator inhibitor-1 (PAI-1), as one of the indicators of fibrinolytic activity. Given the role of PAI-1 in the processes of atherogenesis and thrombogenesis, plasma PAI-1 level was measured in 59 patients (up to 50 years of age) with atherothrombotic stroke (verified by computed tomography scanning or magnetic resonance imaging of brain) in the period from 12 to 24 hours (I analysis) and 30 days after the onset of stroke (II analysis); then, it was correlated with plasma PAI-1 level in the control group (57 healthy subjects), which was 2.86±0.70 U/ml. It was found that PAI-1 level was significantly higher in the acute stroke (I analysis: PAI-1 =4.10±1.40 U/ml, p<0.001; II analysis: PAI-1 =3.64+0.90 U/ml, p<0.001), while fibrinolytic activity was lower, especially on the first day from the stroke that was not completely increased even after 30 days. There was no difference in PAI-1 levels between the subgroups of patients with infarction and lacunar cerebral ischemia (p>0.05), as well as between females and males (p>0.05). Along with significantly increased fibrinogen level (4.65±1 g/l, in the controls - 2.83±0.64 g/l, p<0.001), significantly higher triglycerides (2.04±0.76 mmol/l, in the controls - 1.38+0.54 mmol/l, p<0.001) and lipoproteins(a) (0.405±0.29 g/l, in the controls -0.172±0.14 g/l, p<0.001) were found, correlating with higher plasma PAI-1 level in these patients. The increased plasma level of PAI-1 pointed to possibility of decreased fibrinolytic activity in pathogenesis of ischemie stroke, as well as, risk of reinsult, which had been the greatest after the onset of stroke and declined gradually within several weeks