SUMMARY Forty-three women with neurological complications secondary to eclampsia or severe pre-eclampsia were studied by CT scanning and in six intracranial pressure (ICP) monitoring was carried out. In seven women who died, neuropathological findings were correlated with clinical features. Cerebral oedema was present in 27 of the patients studied and the severity of oedema correlated to the duration of intermittent seizures. In five of the six women who had ICP measured, this was found to be transiently high. Intracranial haemorrhage was demonstrated in four of the 43 women, all of whom died. Hypoxic-ischaemic cerebral damage and fibrinoid necrosis were the most important neuropathological lesions identified. The management of neurological complications of eclampsia may be placed upon a more rational basis by an understanding of the mechanisms responsible for these lesions.Neurological complications due to hypertensive disorders of pregnancy are the most common cause of maternal death from these disorders. -3 However, the pathogenesis of these complications, namely eclamptic seizures, coma, visual disturbances and localising neurological defects, remains poorly understood. The purpose of this report is to document the neuropathological findings of seven women dying from eclampsia or severe pre-eclampsia. These changes are related to clinical and CT observations in a larger series of 43 women with pregnancy-induced hypertension (PIH) and one or more of the above mentioned neurological complications. The pathophysiological mechanisms which may have led to these lesions are reviewed.

Of the many complications which may develop after eclamptic seizures, prolonged unconsciousness is one of the most difficult for obstetricians to manage as the pathophysiology of this condition remains largely unknown. Computed axial tomography (CT scan) was performed on 20 unconscious eclamptic patients, and autopsy was obtained on an additional two patients. Changes compatable with cerebral oedema were demonstrated in 75% of patients; cerebral haemorrhage occurred in 9%. A programme of intensive neurological management aimed at optimizing cerebral perfusion and controlling intracranial pressure is outlined. We have reduced the mortality rate for unconscious eclamptic patients from 50% to 17% in our institution.

Forty-three women with neurological complications secondary to eclampsia or severe pre-eclampsia were studied by CT scanning and in six intracranial pressure (ICP) monitoring was carried out. In seven women who died, neuropathological findings were correlated with clinical features. Cerebral oedema was present in 27 of the patients studied and the severity of oedema correlated to the duration of intermittent seizures. In five of the six women who had ICP measured, this was found to be transiently high. Intracranial haemorrhage was demonstrated in four of the 43 women, all of whom died. Hypoxic-ischaemic cerebral damage and fibrinoid necrosis were the most important neuropathological lesions identified. The management of neurological complications of eclampsia may be placed upon a more rational basis by an understanding of the mechanisms responsible for these lesions.

SummaryTwo groups of postmenopausal women were compared. One group of 13 was given the synthetic steroid Org OD14 to suppress climacteric symptoms and one group of 14 was given placebo. After a 2 week baseline period the subjects received daily for 12 weeks, either 2.5 mg Org OD14 or placebo. There were no significant differences between the groups pre-treatment. Compared with the placebo group, during treatment, the Org OD14 group showed the following significant differences: higher haemoglobin, haematocrit, platelet count, plasminogen, fibrinolytic activity on fibrin plates and antithrombin III and lower fibrinogen. No significant differences between the groups were found in α2 antiplasmin levels, total cholesterol, total triglycerides, bilirubin or transaminase levels but the Org OD14 group had significantly lower levels of HDL cholesterol. With the exception of the haemoglobin and haematocrit levels all of the differences had disappeared by 2 weeks post treatment.