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

Sodium cyanide was infused intravenously in 11 lightly anaesthetised and spontaneously breathing M. mulatta. In most, the EEG, ECG, respiratory rate, blood pressure, cerebral venous sinus pressure, end-tidal pCO2 and body temperature were recorded. Blood gases, pH, lactate and pyruvate were estimated in arterial and venous sinus blood samples. There was an initial hyperventilation with tetany in all animals. A rapid rate of cyanide infusion led to apnoea. An isoelectric or near-isoelectric EEG was usually precipitated by bradycardia often with additional hypotension. Neither epileptic seizures nor their EEG concomitants were seen at any stage. Three animals died of early heart failure. Brain damage was seen in 4 animals surviving up to 98 hr. White matter was involved in all. Ischaemic neuronal alterations, restricted to the striatum of one animal, were attributed to major circulatory complications. It was concluded that under these experimental conditions there is no evidence for hypoxic neuronal damage of purely histotoxic type.
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PMID:Cyanide intoxication in Macaca mulatta. Physiological and neuropathological aspects. 1 59

Only 6 patients with intracranial hypertension associated with unruptured cerebral arteriovenous malformations have been reported. We report 6 additional patients seen at the Cleveland Clinic during the past 10 years. The average age was 28 years (range, 19-44 years); 4 were women. Symptoms and signs included papilledema (6 patients), headache (6), transient nonepileptic focal symptoms (4), visual obscurations (3), ipsilateral carotid or ocular bruits (3), abnormal visual fields (3), focal seizures (2), and progressive visual loss (1). Enhanced computed tomography (CT) or magnetic resonance imaging (MRI) demonstrated the malformations in all 6 patients. The malformations were large, supplied by the branches of the middle and anterior cerebral arteries, with the posterior cerebral artery contributing in 3 patients, and all drained into the superior sagittal sinus. Associated venous obstruction was seen in 2 patients. Four patients underwent excision of the arteriovenous malformation, with resolution of papilledema in all 4. Measurements of cortical arterial and venous pressures during surgery in 3 patients showed decreased feeding artery pressures and elevated draining vein pressures, which normalized after removal of the malformation. Treatment in the 2 remaining patients consisted of medical therapy (acetazolamide, furosemide, steroids) alone in 1 patient, and in conjunction with proton beam radiation in the other. Papilledema resolved in the former patient, but the patient receiving proton beam radiation still had papilledema 2 years later. Intracranial hypertension associated with unruptured cerebral arteriovenous malformations occurs in young patients with high flow malformations that drain into the superior sagittal sinus, and is likely the result of increased cortical venous and superior sagittal sinus pressure. Excision of the malformation effectively reduces the intracranial pressure.
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PMID:Intracranial hypertension associated with unruptured cerebral arteriovenous malformations. 219 10

A case of unruptured arteriovenous malformations (AVMs) presenting benign intracranial hypertension is reported. A 14-year-old male suffered from headache and papilledema. Intracranial pressure was 260 mmH2O. Unenhanced CT demonstrated no evidence of hemorrhage or hydrocephalus. Angiogram demonstrated a large AVM in the left temporal lobe supplied by the left posterior cerebral artery and left middle cerebral artery. It drained into the transverse sinus. Surgical excision of the AVM eliminated the headache and papilledema. AVM causes hemorrhage in 50% of cases, seizure in 30%, and other focal neurological deficits in 20%. Benign intracranial hypertension is an uncommon effect of unruptured AVMs. Only 13 cases have been reported in the literature. Benign intracranial hypertension associated with unruptured AVMs occurs in young patients with high flow AVMs that drain into the major sinus. The mechanism of intracranial hypertension associated with unruptured AVM is unknown. However, there are several possible mechanisms of intracranial hypertension associated with unruptured AVMs. The arterial blood shunting into a major sinus impedes venous return from the surrounding brain. That causes the increase of cerebral blood volume and the elevation of sinus pressure. This mechanism would reduce CSF absorption and would increase intracranial pressure. Pharmacological therapy is ineffective in controlling intracranial hypertension. Surgical excision of AVM effectively reduced intracranial hypertension. Thus, surgical excision of AVMs, if it can be done with low risk, is the treatment of choice to decrease intracranial hypertension in patients with unruptured cerebral AVMs.
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PMID:[A case of intracranial arteriovenous malformation presenting with intracranial hypertension]. 819 38