Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 3-year-old child with minimal change nephrotic syndrome (MCNS) developed an acute hypertensive encephalopathy characterized by coma, focal seizures, right hemiparesis, global aphasia and cortical blindness. Episodic hypertension and seizures persisted for 24 h despite intervention with antihypertensive and anticonvulsant therapy. Clinical suspicion of cortical blindness was confirmed by visual-evoked potential studies. CT scans performed 14 and 21 days after the acute episode demonstrated symmetric occipital white matter lucencies compatible with ischemia and/or associated edema. Hypertensive encephalopathy with cortical blindness and symmetric white matter hypodense lesions visualized on CT scan have recently also been described in eclampsia of pregnancy. This report documents an unusual acute hypertensive encephalopathy in childhood MCNS, unassociated with membranoproliferative glomerulonephritis, or progressive focal glomerulosclerosis.
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PMID:Acute hypertensive encephalopathy in minimal change nephrotic syndrome. 225 60

A patient with eclampsia and severe but reversible neurological disorders is presented. Initial magnetic resonance imaging (MRI) revealed multiple hyperintense areas throughout the brain and brainstem that were consistent with ischemia and/or edema. Despite these diffuse lesions extending to the brainstem, the patient made a progressive neurological recovery and a follow-up MRI on day 21 demonstrated complete resolution of the hyperintense foci. MRI abnormalities were found to correlate more closely with clinical and electrophysiological data than CT findings.
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PMID:Magnetic resonance evaluation of severe neurological disorders in eclampsia. 233 33

Recent evidence supports the concept that cerebral vasospasm is involved in the pathogenesis of eclampsia. Magnesium, which has a beneficial effect in eclampsia, may act by opposing calcium-dependent arterial constriction, thereby relieving vasospasm. Magnesium may also antagonize the increase in intracellular calcium concentration caused by ischemia and thus prevent cell damage and death. Magnesium might have a role in the treatment of cerebral vasospasm and ischemia, such as occurs in subarachnoid hemorrhage, ischemic stroke, and brain trauma.
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PMID:Action of magnesium sulfate in the treatment of preeclampsia-eclampsia. 267 28

Cerebral infarction and hemorrhage are well-known cerebrovascular complications of eclampsia. A 30-year-old woman with eclampsia developed bilateral posterior parietal and occipital hemorrhages 4 hours after computed tomography demonstrated lucencies indicative of ischemia or infarction within the same regions. The association between infarction and hemorrhage has not been previously documented by computed tomography in eclampsia. Review of the pathophysiological mechanisms and associated risk factors has prompted a more aggressive prophylactic therapeutic approach.
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PMID:Relationships among cortical ischemia, infarction, and hemorrhage in eclampsia. 335 91

We describe a patient who experienced focal cerebral and brainstem ischemia in the setting of postpartum eclampsia. Cerebral angiography showed spasm of large- and medium-caliber arteries. This case provides rare documentation that vasospasm may account for cerebral ischemia in eclamptic women with focal signs. This observation suggests that in such patients cerebral angiography may be informative and useful.
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PMID:Cerebral vasospasm and eclampsia. 335 16

Cortical blindness is defined as a loss of vision due to bilateral retrogeniculate lesions (geniculocalcarine blindness). Gerstmann's syndrome is a combination of disorientation for left and right, finger agnosia, and profound agraphia, alexia, and acalculia. It is due to a lesion in the left angular gyrus, situated at the confluence of the temporal, parietal, and occipital lobes. We report on a patient who suffered from severe underdiagnosed eclampsia and who developed bilateral extensive medial temporal, parietal, and calcarine ischemic infarctions during an eclamptic fit. In addition, ischemia destroyed the left angular gyrus. The combination of these lesions led to Gerstmann's syndrome with additional cortical agnosia and cortical diplopia. For the first few months following the ischemic insult, the patient had been cortically blind. Thereafter, the patient slowly regained a visual acuity of 0.1 in both eyes. She then experienced monocular and binocular diplopia. Her ocular motility was normal; there was no phoria or tropia. Monocular and binocular diplopia slowly became less severe over the following year. Now, 2 years after the incident, the patient has a visual acuity of 0.2 in both eyes and no double vision. However, the handicapping symptoms of Gerstmann's syndrome, which make leading a normal life impossible, have persisted--the patient still cannot cope alone, mainly due to the severe disorientation for left and right. The picture of cortical agnosia, cortical diplopia, and Gerstmann's syndrome is a very rare combination. Visual recovery and rehabilitation in cortical blindness are severely affected and made difficult by the symptoms of Gerstmann's syndrome. In our case the reason for such a dramatic clinical picture was eclampsia, whose prodomes had not been diagnosed in time.
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PMID:Eclamptogenic Gerstmann's syndrome in combination with cortical agnosia and cortical diplopia. 749 36

Retinal detachment is a rare complication of preeclampsia, eclampsia and abruptio placentae. We report a case of bilateral retinal detachment in association with severe preeclampsia complicated with abruptio placentae, intrauterine fetal death and disseminated intravascular coagulation. In obstetric complications, placental thromboplastin may release into maternal circulation and activate the extrinsic coagulation system with resultant disseminated intravascular coagulation. This may be responsible for choroidal ischemia and consequent serous retinal detachment.
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PMID:Retinal detachment in association with preeclampsia and abruptio placentae. 763 40

To examine the possible role of endothelin and vasospasm in eclamptic seizures, we studied and analyzed the electroencephalograms (EEG) of endothelin-1 (ET-1)-treated pregnant, nonpregnant and sham control (dextrose-treated) rabbits. After multiple intravenous bolus injections of ET-1 (500 pmol/kg) or 5% dextrose in the rabbits, we recorded EEG directly from the brain cortex and analyzed by Fast Fourier Transform (FFT). Water content was measured in the brain of all groups (n = 7). Repeated seizures occurred in all of the pregnant and 2 of the nonpregnant rabbits by variable doses of ET-1. FFT analysis showed remarkable changes in frequency and power arrays characterized by mild to severe form of dysrhythmia, high-voltage spikes, high-voltage fast and slow waves after ET-1 injections. Water content was increased in brain mass in ET-1-treated rabbits (p = 0.001) suggesting an ET-1-induced edema. Histologically we confirmed that ET-1 caused ischemic changes in brain tissues. However, ET-1 induced more pronounced changes in behavior, EEG, brain edema or ischemia in pregnant than in nonpregnant groups. The injections of exogenous ET-1 into the brain substances were strongly suggested by immunohistochemical study with polyclonal antiendothelin antibody in brain tissue sections. Therefore, we assume that endothelin along with other vasoactive substances causes acute cerebral vasospasm and ischemia inducing EEG changes leading to ultimate clinical convulsions in eclampsia.
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PMID:Eclampsia-like seizures and electroencephalographic changes in pregnant rabbits with endothelin-1 injections. 789 Feb 45

Among 61 patients with severe pregnancy induced hypertension, cerebral lesions were detected on CT scans in 23 cases (37.7%). The positive rates were 5/25 cases in preeclampsia and 18/36 cases in eclampsia. The incidence rate of cerebral lesions in eclampsia was significantly higher than that in preeclampsia (chi 2 test, P < 0.05). Furthermore, it showed that patients with renal impairment and retinal changes were more susceptible to cerebral lesions (P < 0.05), through comparative study of the relationships between either the function of liver and kidney or retinal changes and cerebral lesions. Main manifestations of cerebral lesions were ischemia, edema and infarction. The represented the different pathological stage of cerebral lesions. The cerebral lesions were mainly involved at cortical or subcortical area of bilateral parietal or occipital lobe (60%), secondly at the deep basal ganglia and the superior sagittal sinus. The pathological process of cerebral lesions and the management of pregnancy induced hypertension were analysed.
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PMID:[Cerebral lesions in the severe pregnancy induced hypertension: 61 cases of X-ray computed tomography of the brain]. 824 45

Intracranial pressure (ICP) monitoring has been shown to improve clinical-pharmacological treatment of intracranial hypertension (ICH) in a rising number of situations, assuring effective cerebral perfusion pressure (CPP) and, concomitantly, reducing the risk of brain ischemia. Although its use in entities such as eclampsia have been reported, the continuous use of ICP monitoring is restricted. We report the case of an eclampsic woman in whom ICP was monitored. Recordings allowed CPP to be correctly stabilized, with strict correlation between ICP and tomographic measurements of density. We also review the pathophysiologic mechanisms that have been proposed to cause ICH in eclampsia and emphasize the usefulness of ICP monitoring to manage this complication.
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PMID:[Intracranial pressure monitoring and eclampsia]. 900 49


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