Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although hypercalcemia may cause drowsiness, lethargy, weakness, confusion and coma it rarely causes seizures or cerebral infarction. The patient presented had a clinical evolution from hallucinosis to a generalized tonic-clonic seizure, and subsequent cortical blindness with occipital cerebral ischemia as evidenced by SPECT and MRI scans. EEG revealed occipital PLEDs. With reversal of hypercalcemia, there was a return of vision, resolution of EEG epileptiform activity, although with some residual occipital infarction. This case, in concert with a literature review of hypercalcemia, reveals examples of occipital and watershed ischemia, blindness, seizures and hypertension, a pattern markedly similar to that of eclampsia. Furthermore, medications such as magnesium sulfate, believed to reverse cerebrovasospasm responsible for the eclamptic neurologic findings, may counter the effects of hypercalcemia at a cellular level, lending support to a calcium-mediated injury in eclampsia.
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PMID:Reversible hypercalcemic cerebral vasoconstriction with seizures and blindness: a paradigm for eclampsia? 966 11

Seizures are common after severe cerebral ischemia. To examine the mechanisms underlying these seizures, we determined the impact of prior forebrain ischemia on the seizure thresholds of four convulsants with differing modes of action: lidocaine, pentylenetetrazol (PTZ), N-methyl-D-aspartate (NMDA), and picrotoxin. Anesthetized Sprague-Dawley rats were chronically instrumented with screw electrodes and vascular catheters, and then subjected to 10 min of forebrain ischemia, produced by carotid occlusion and hypotension (mean arterial pressure to 30 mmHg). Animals were then awakened. 6, 24 or 48 h later, groups of awake animals received intravenous infusions of the four drugs. The total dose of drug infused prior to either electrical seizures (lidocaine, PTZ, and picrotoxin) or tonic-clonic convulsions (all drugs) were noted. For each drug, a group of Sham animals (no ischemia) served as controls. There were markedly different patterns of changes in the convulsant thresholds for the drugs. For example, at 6 h post-ischemia, rats treated with lidocaine died before convulsing, while the threshold for PTZ increased by 86%. There was no change in the picrotoxin threshold at 6 h, but the dose of NMDA needed to induce tonic-clonic seizure activity was reduced by 70%. By 48 h, lidocaine and PTZ thresholds had returned to values similar to those in Shams, but the NMDA threshold had now increased to a value 62% greater than Sham. Ten minutes of cerebral ischemia is followed by a complex and changing pattern of susceptibility to chemical convulsants. Finding suggests that early post-ischemic seizures may be related to increased NMDA receptor sensitivity.
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PMID:Forebrain ischemia: effect on pharmacologically induced seizure thresholds in the rat. 1041 92

Reversible cerebrovascular vasoconstriction syndrome is an uncommon condition that presents as severe headache and hypertension. Recent literature suggests a 1% incidence in postpartum headache cases. It can cause subarachnoid hemorrhages, cerebral ischemia, and seizures. It is often misdiagnosed as postdural puncture headache or preeclampsia. In this case, a postpartum woman, who had received epidural anesthesia for labor, presented 5 days postpartum with severe headache that did not resolve with an epidural blood patch. She then became more hypertensive and suffered a grand mal seizure. When treatment for eclampsia failed to resolve her symptoms, magnetic resonance angiography was performed. It demonstrated the pathognomic signs of reversible cerebrovascular vasoconstriction syndrome. Her symptoms resolved with nimodipine.
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PMID:Severe Postpartum Headache and Hypertension Caused by Reversible Cerebral Vasoconstriction Syndrome: A Case Report. 2869 30