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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since the causes of toxemia of pregnancy are unknown, therapy is still symptomatic and is now determined by the most recent knowledge of the pathophysiology of the disease. Rest, a balanced, predominantly protein-rich diet and avoidance of stress are recommended as prophylactic treatment of toxemia of pregnancy in patients with a predisposition of the condition. Early recognition of the symptoms of toxemia of pregnancy is of great importance. Treatment of mild cases consists of bed rest, possibly supplemented by sedatives and a preponderantly proteinrich diet. Administration of diuretics is obsolete and sodium restriction is no longer recommended. Antihypertensives are seldom indicated. Overweight women are no longer maintained on specially low calorie diets. Severe cases of toxemia of pregnancy must be trated as inpatients under intensive care. Principles of treatment are: 1. Prevention of seizures (by sedation). 2. Improvement of the general condition of the women (especially circulation and renal function). 3. Delivery at an opportune time for mother and child. Treatment of eclampsia follows largely the same principles. In these cases, immediate delivery is required regardless of the condition of the fetus.
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PMID:[Present day status in therapy of toxemia of pregnancy (author's transl)]. 47 58

Subcutaneous fat necrosis of the newborn (SFNN) developed in a 1-week-old black boy. His mother had received numerous medications for eclampsia. Birth was by Caesarean section and complicated by meconium aspiration. There were numerous nodules over the back, buttocks and extremities that yielded a caseous-like material. Microscopically, these nodules showed crystallization and necrosis of the fat. Hypoglycemia, pneumonia, oliguria, thrombocytopenia, seizures and urinary infection were associated with the cutaneous problem and led to a fatal outcome 2 weeks after birth.
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PMID:Subcutaneous fat necrosis of the newborn. 70 34

Clinical and neuroimaging studies were made in twenty-one patients during the attack of eclampsia. Most frequent neurological signs and symptoms were the impairment of consciousness, headache, seizure and visual disturbance. Mean arterial blood pressure increased by 46 mmHg (n = 21) during the attacks. Eight of 9 patients studied by CT and/or MRI showed transient abnormalities on brain images during the attack in the occipital cortex, basal ganglia, and internal and external capsule. The findings were compatible with brain edema and were seen mainly in the white matter. Cerebral blood flow measured by SPECT method in one patient during an attack with visual disturbance showed increased blood flow in the occipital cortex. Acute increase in blood pressure, cerebral hyperperfusion and edema, similar to the pathophysiology of hypertensive encephalopathy, were considered to play an important role in the pathogenesis of eclampsia.
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PMID:[Neurological and neuroimaging studies of eclampsia]. 129 Nov 59

Magnesium is an essential cofactor for many enzymatic reactions, especially those involved in energy metabolism. Deficits of magnesium are prevalent due to inadequate intake or malabsorption and due to the renal loss of magnesium that occurs in certain disease states (alcoholism, diabetes) and with drug therapy (diuretics, aminoglycosides, cisplatin, digoxin, cyclosporin, amphotericin B). Protracted deficits of magnesium in humans and animals result in neurological disturbances, including hyperexcitability, convulsions and various psychiatric symptoms ranging from apathy to psychosis, some of which can be reversed with magnesium supplementation, others requiring correction of the dysregulation mechanism. Although the role of magnesium in neuronal function is not completely understood, a lowering of CSF or brain magnesium can induce epileptiform activity and there is an association between decreased CSF magnesium and the development of seizures. CSF concentrations of magnesium are normally higher than magnesium plasma ultrafiltrate (diffusible) concentrations due to the active transport of magnesium across the blood-brain barrier. Under conditions of magnesium deficiency, CSF concentrations decline, although this decline lags behind and is less pronounced than the changes observed in plasma magnesium concentrations. Decreases in CSF magnesium concentrations correlate with the alterations observed in extracellular brain magnesium concentrations in animals following the dietary deprivation of magnesium. CSF magnesium concentrations can readily be repleted following magnesium supplementation, although high dose magnesium therapy, such as that used in the treatment of convulsions in eclampsia, will only increase CSF magnesium concentrations to a very limited degree (approximately 11-18 per cent) above physiological concentrations. Greater increases in CSF magnesium may occur in neonates since neonatal swine, following treatment with magnesium, have CSF magnesium concentrations that are similar to their plasma concentrations. There has been a recent resurgence of interest in magnesium deficiency and its neurological consequences due to the finding that magnesium, at physiological concentrations, blocks N-methyl-D-aspartate (NMDA) receptors in neurones. NMDA receptors are normally activated by glutamate and/or aspartate which represent the principal neurotransmitters for excitatory synaptic transmission in vertebrate CNS. Magnesium deficiency produces epileptiform activity in the CNS which can be blocked by NMDA receptor antagonists. Other mechanisms, including alterations in Na+/K(+)-ATPase activity, cAMP/cGMP concentrations and calcium currents in pre- and postsynaptic membranes, may also be at least partially responsible for the neuronal effects associated with low brain magnesium. Further studies are necessary to increase our understanding of the neurological implications of magnesium deficit in the central nervous system.
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PMID:Brain and CSF magnesium concentrations during magnesium deficit in animals and humans: neurological symptoms. 129 67

Three hundred forty-seven cases of eclampsia were managed at the University College Hospital (UCH), Ibadan, Nigeria from 1977 to 1986 (9.3 per 1000 deliveries). Thirty-one percent of seizures occurred antenatally, 46.2% during labor and 23.2% postnatally. Only 5% first occurred in the hospital. Seizures were controlled with diazepam, lytic cocktail (chlorpromazine, pethidine and phenergan), sodium amylobarbitone, paraldehyde and bromethol. Maternal mortality was 2.9%, and perinatal mortality 193 per 1000, respectively. Prevention of avoidable factors (absent or poor antenatal care and prolonged labor) by the provision of comprehensive antenatal care will reduce the incidence of eclampsia. Improvement in management facilities prior to transfer to referral centers, the use of magnesium sulfate or diazepam to control seizures and the avoidance of hypotonic solutions and 50% glucose during therapy will reduce morbidity and mortality.
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PMID:Presentation and management of eclampsia. 134 87

Seizures remain an important cause of maternal morbidity and mortality during pregnancy and the puerperium. Encouraged by some cases treated in our clinic (9 cases have been observed between 29. 12. 1989 and 22.5. 1991), the management of differential diagnosis in seizures are discussed in this article. Despite all possibilities of using technical apparatus for investigations, case history and clinical examination remain the basics of diagnosis with regard to paroxysm. EEG is an important, noninvasive method for judgement of cerebral function. It can be carried out continuously as a bedside-test and is extremely helpful in the differential diagnosis of eclampsia versus epilepsia. With a view to substantial defects as a possible convulsant factor, visualised examination procedures, e.g. cranial computed tomography (CCT) and magnetic resonance imaging (MRI) are available. Especially MRI has advantages in the diagnostic procedure. It could help to find the cause of cerebral structure defects and to clear the question of aetiology. Thus, a specific therapeutic procedure might become possible.
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PMID:[Differential diagnosis of seizures in the peripartal period]. 149 53

In their severest forms, pre-eclampsia and eclampsia may be life-threatening complications of pregnancy. We describe a patient with severe post-partum eclampsia characterized by seizures, deep coma, hypertension, renal insufficiency, coagulopathy, and microangiopathic hemolysis. The patient responded to treatment that included intensive plasma exchange, and she achieved full recovery. Our case supports the use of plasma exchange in patients with severe pre-eclampsia and eclampsia.
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PMID:Severe post-partum eclampsia: response to plasma exchange. 159 49

The characteristics and treatment of preeclampsia and eclampsia are reviewed. Risk factors for preeclampsia include (1) nulliparity, (2) a mother or sister(s) with a history of the disorder, (3) essential hypertension or renal disease, or (4) a twin or molar pregnancy. Preeclampsia is diagnosed when the systolic blood pressure (BP) increases by 30 mm Hg or the diastolic BP increases by 15 mm Hg after the 20th week of gestation and the BP rise is accompanied by edema, proteinuria, or both. Severe preeclampsia is diagnosed when the BP reaches or exceeds 160 mm Hg systolic or 110 mm Hg diastolic after bed rest. Eclampsia is the occurrence of seizures (in the preeclamptic patient) that cannot be attributed to other causes; it occurs in about 0.2% of preeclamptic patients. Magnesium sulfate (in the injectable, hydrated form) is the agent used most often for seizure prophylaxis in the preeclamptic patient in the United States. It is also used widely to control seizures once they develop. In the United States, diazepam is used to supplement magnesium sulfate if necessary to control seizures, but its use is not routine. Among antihypertensive agents, i.v. hydralazine is preferred in this country to control blood pressure in the severely preeclamptic or eclamptic patient. Several studies provide promising evidence that low-dose aspirin (60-150 mg daily beginning at 28-30 weeks of gestation) prevents preeclampsia in women who are at risk for its development. Until additional comparative studies are completed, magnesium sulfate and hydralazine will remain the standard of care for the treatment of preeclampsia in the United States.
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PMID:Treatment of preeclampsia and eclampsia. 161 13

Hypertensive encephalopathy is a syndrome consisting of headache, seizures, visual changes, and other neurologic disturbances in patients with elevated systemic blood pressure. The purpose of this study was to analyze the imaging findings in 14 patients with hypertensive encephalopathy. CT (n = 13), MR (n = 12), and single-photon emission computed tomography (n = 2) examinations performed in these patients before and after resolution of symptoms were reviewed. Eight had the preeclampsia-eclampsia syndrome, and six had hypertensive encephalopathy due to other causes. CT and MR findings in all patients having these examinations were indicative of edema in the cortex and subcortical white matter in the occipital lobes. Two of the 14 patients also had similar findings in the cerebellum and frontal lobes. Single-photon emission computed tomography showed increased vascular perfusion adjacent to areas that appeared abnormal on CT and MR. The findings on the imaging studies resolved on follow-up examinations performed after the hypertension was corrected. Our results suggest that the radiologic findings associated with hypertensive encephalopathy may be useful in establishing the diagnosis in the appropriate clinical setting.
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PMID:Hypertensive encephalopathy: findings on CT, MR imaging, and SPECT imaging in 14 cases. 163 61

Treatment of this pathophysiologically poorly understood disease is controversial. Despite this uncertainty, the goals of management of the patient with preeclampsia and eclampsia are diagnosis, stabilization, and delivery of the baby. Stabilization refers to both mother and fetus and should include the prevention of eclampsia or the recurrence of eclamptic seizures. There are empiric data supporting the use of magnesium sulfate for the management of preeclampsia and eclampsia in North America, but there are few data to support its efficacy as a classic anticonvulsant. Until controlled trials are completed, we suggest that magnesium sulfate continue to be used in preeclampsia, with the addition of established anticonvulsant medications when eclampsia occurs. Data on established antiepileptic drugs such as diazepam and phenytoin support their use in treating patients with eclamptic seizures. As stated in an earlier review, "in treating preeclampsia, magnesium sulfate therapy may have a role and may moderate factors leading to eclampsia. Whether magnesium sulfate therapy may have some as yet unproved effect on epileptogenic foci or seizure propagation is not the important issue for the physician caring for the eclamptic patient. Until adequately designed therapeutic trials are available, it is our opinion that treatment should be based on the use of anticonvulsant drugs of established efficacy in seizure control and prophylaxis (p. 1363)."
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PMID:Prophylaxis of eclamptic seizures: current controversies. 163 27


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