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

A review of a series of 56 patients with a giant intracranial aneurysm showed that 28 presented with signs related to the mass effect and 19 with subarachnoid hemorrhage (SAH). Additional clinical signs observed were seizures, ischemia, and endocrinological disturbances. Fourty-five aneurysms involved the carotid artery territory and eleven the vertebrobasilar system. On computed tomography (CT) images partially thrombosed aneurysms (23 cases) showed 1) a marginal or central "target" appearance on contrast enhanced scans corresponding to the non-thrombosed lumen as demonstrated by angiography, 2) capsular enhancement in 16 cases and 3) calcifications in 9. SAH occurred in 13 and 6 cases of non-thrombosed and partially thrombosed aneurysms, respectively. Magnetic resonance imaging (MRI) in 6 cases showed several layers of thrombosis in 4 cases and a small signal void close to the parent artery. In one case of a non-thrombosed aneurysm, thrombosis was mimicked by flow artifacts of MRI.
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PMID:Clinico-radiological spectrum of giant intracranial aneurysms. 179 40

Strokes are the most common cause of epilepsy in the elderly. Seizures after an acute stroke have been estimated to occur in 5% to 10% of cases. A distinction between early and late seizures should be made. Early seizures are more common, occur very early in the evolution of the stroke, and tend to be focal motor, brief, and isolated. They are likely to be the result of an acute local brain metabolic alteration induced by the cerebrovascular event, and once these derangements are reversed, seizures disappear. Epilepsy usually does not follow early seizures, but the risk is probably increased. Late seizures occur months to years after the stroke and are probably due to structural brain abnormalities leading to the development of an epileptic focus. The majority of these cases develop epilepsy. The risk of seizures is markedly increased when the cerebrovascular event involves the cerebral cortex. Deep-seated hemispheric or infratentorial lesions rarely produce seizures or epilepsy. It is possible that hemorrhagic stroke carries a higher incidence of seizures, but the issue remains controversial. It has also been suggested that embolic infarction has a higher incidence of seizures that does thrombotic infarction, but definitive evidence is lacking. The presence of seizures in an acute stroke does not seem to correlate with the size of the lesion, functional outcome, or mortality. Prophylactic treatment with antiepileptic drugs is probably not indicated in most types of strokes, except for subarachnoid hemorrhage after a ruptured intracranial aneurysm. When early seizures develop, treatment is indicated but may not be necessary for a prolonged period of time. If late seizures develop, chronic anticonvulsant therapy is recommended.
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PMID:Poststroke seizures in the elderly. 186 6

This article describes a number of treatment strategies for the management of perforations that occur during neurointerventional procedures. During the past 5 years, we have performed over 1200 endovascular procedures to treat vascular disorders involving the brain and spinal cord (400 cerebral arteriovenous malformations, 230 tumors, 197 carotid cavernous fistulas, 183 aneurysms, 130 dural fistulas, 80 spinal arteriovenous malformations, 18 vein of Galen aneurysms, and 20 cases of vasospasm). Fifteen patients (1.1%) sustained a vascular perforation as a direct result of these procedures. Among these 15 patients, indications for endovascular treatment were six symptomatic arteriovenous malformations, two spinal cord arteriovenous malformations, two cavernous sinus dural fistulas, one transverse sinus fistula, one case of vasospasm following subarachnoid hemorrhage, one direct carotid cavernous fistula, one vein of Galen malformation, and one ruptured basilar artery aneurysm. The vascular perforations were grouped into three probable mechanisms: mechanical perforation of a normal vessel (six patients), mechanical disruption of a dysplastic vessel or aneurysm (five patients), and fluid overinjection (four patients). Treatment of the perforations included immediate reversal of anticoagulants (12 patients) and direct closure of the perforation site with coils (five patients). In addition, closure of the intravascular compartment adjacent to the perforation was achieved with coils (six patients), liquid adhesives (four patients), balloons (two patients), or particles (two patients). In two patients a detachable balloon was placed transiently across the perforation site for several minutes, deflated, and removed when no further extravasation was noted. Five patients were started on anticonvulsant therapy, two of whom have had a new onset seizure related to the perforation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Management of vascular perforations that occur during neurointerventional procedures. 190 36

Though there is a large body of knowledge regarding the management of pregnant women with arterial lesions in the central nervous system, little information is available on venous malformations. We report our experience with two pregnant patients with cerebral venous angiomas. These lesions are usually asymptomatic and only rarely cause seizures or subarachnoid hemorrhage. Based on our experience and literature review, we suggest that patients with venous angiomas without a history of hemorrhage can safely undergo labor and vaginal delivery.
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PMID:Management of the pregnant patient with a cerebral venous angioma: a report of two cases. 192 31

We studied the pattern and outcome of strokes in 200 Saudi patients. Cerebral infarction constituted 87% of strokes, subarachnoid hemorrhage 4.5%, cerebral hemorrhage 6.5%, and venous infarction 2%. The vessel most commonly involved was part or all of the middle cerebral artery, constituting 52% (90) of the 174 arterial infarcts. Lacunar infarcts were seen in 21% (37) of the patients with arterial infarcts. Among all 200 patients, 8% died and 8% had secondary generalized seizures. Hypertension occurred in 41% of the 174 patients with arterial infarcts and 62% of the 13 with cerebral hemorrhages. The highest incidence of hypertension as a risk factor was among those with lacunar infarcts (81%), ganglionic cerebral hemorrhages (80%), and infarcts of deep branches of the middle cerebral artery (57%). Embolic infarcts due to rheumatic heart disease constituted 11% of all arterial infarcts. We conclude that our pattern of strokes is similar to that of the west rather than that of the Japanese, but with less frequent arteriovenous malformations and aneurysms.
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PMID:Cerebrovascular disease in Saudi Arabia. 192 60

Despite increases in survival beyond the initial hemorrhage, the devastating consequences of subarachnoid hemorrhage persist. Ruptured intracranial aneurysms are the most likely cause of subarachnoid hemorrhage, with morbidity and mortality rates approaching 75%. Complications arising from aneurysmal subarachnoid hemorrhage include rebleeding, delayed cerebral ischemia, hydrocephalus, hypothalamic dysfunction, and seizure activity. In order to positively influence outcome after subarachnoid hemorrhage, preservation of an adequate cerebral blood flow and prevention of secondary aneurysmal rupture is essential. This article reviews aneurysmal subarachnoid hemorrhage, relating the management of complications to currently accepted treatment strategies.
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PMID:Aneurysmal subarachnoid hemorrhage: neurosurgical frontiers and nursing challenges. 195 55

Creatine kinase brain isoenzyme (CK-BB) was determined in cerebrospinal fluid of 150 neonates by a newly developed immunoenzymatic assay. Newborns with a documented neurologic disorder (intraventricular hemorrhage, postasphyxial encephalopathy, central nervous system infection, or persistent periventricular intraparenchymal echodensities) showed markedly higher concentrations of immunoreactive CK-BB than did the normal newborns or those with subarachnoid hemorrhage. In neonates with seizures the data suggest that the underlying neurologic disorder accounts for the higher CK-BB values and not the seizures per se. High concentrations of CK-BB in the neonatal period were followed by poor short-term outcome.
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PMID:Creatine kinase isoenzyme BB concentrations in the cerebrospinal fluid of newborns: relationship to short-term outcome. 195 38

The authors retrospectively reviewed the charts of 31 alcoholic patients admitted with fever without a defined source. In our population 58% of patients were subsequently found to have an infectious cause for their fever. Pneumonia was the most common infection, but occult urinary tract infections were seen surprisingly often. Noninfectious but serious disorders, such as delirium tremens, prolonged postictal state, and subarachnoid hemorrhage, were also common. Infectious and noninfectious causes commonly coexisted. The most common noninfectious cause was alcohol withdrawal, with or without seizures. The authors believe that indigent, malnourished, chronic alcoholics with fever for which a source cannot be readily identified, should usually be admitted to the hospital for observation and to await culture results.
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PMID:The febrile alcoholic in the emergency department. 198 54

Leukotrienes and prostaglandins are formed from arachidonic acid by activation of local phospholipases in pathological conditions such as cerebral ischemia, subarachnoid hemorrhage, cerebral tumors and seizures. These mediators, especially leukotrienes have a very potent vasoconstrictor effect on cerebral arteries. Experimental studies have shown that this effect, by increasing vascular permeability causes vasogenic edema that contributes to the ischemic penumbra. In this study, after developing an experimental animal model simulating the concept of ischemic penumbra in the rat, the levels of leukotriene C and prostaglandin E2 produced in the forebrain were measured and the effects of these mediators in prolonged ischemia were investigated. The results, in the first 4 min of ischemia, showed that the arachidonic acid metabolites, particularly, leukotriene C4, reached a peak in the ischemic cerebral tissue in association with leukocyte accumulation. Later in the 15th min, significant decreases in leukotriene C4 and prostaglandin E2 levels were seen. In the 1st and 4th h, probably due to the stimulation of the relevant enzymes by free oxygen radicals in the ischemic tissue; the levels increase again, returning to control values by the 12th h. It is concluded that the use of lipoxygenase inhibitors and free radical scavengers may be helpful to limit the infarct area in the first 4 h of ischemia.
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PMID:The alterations of leukotriene C4 and prostaglandin E2 levels following different ischemic periods in rat brain tissue. 201 13

We reported a 39-year-old man with punch drunk syndrome who had cerebellar ataxia, seizure and dementia. CT scan of the brain revealed remarkable atrophy and enlargement of the ventricular system. MRI of the brain showed severe atrophy which was especially evident in the frontal base. On RI cisternography both early ventricular reflux at 3 hours and delayed ventricular stasis at 52 hours were found, which resembled the findings of the normal pressure hydrocephalus. The MRI and RI cisternographic findings suggested that the remarkable brain atrophy and enlargement of the ventricular system were caused by repeated KARATE traumas including minor brain contusion or subarachnoid hemorrhage in the base of the brain, since traumatic brain contusions affect particularly the orbital surfaces of the frontal lobes and the lateral and inferior surfaces of the temporal lobes. Communicating hydrocephalus may be one of the pathogenesis of punch drunk syndrome.
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PMID:[Punch drunk syndrome due to repeated karate kicks and punches]. 208 30


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