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

The history, clinical signs and radiographic and ultrasonographic findings in 16 dogs with pancreatic neoplasia were reviewed retrospectively. Thirteen of the dogs had islet cell carcinoma compatible with insulinoma, one had a pancreatic adenocarcinoma and two had secondary invasion of the pancreas, one by a gastric carcinoma and one by an intestinal lymphoma. The clinical signs in the 13 dogs with insulinoma included collapse in 10 dogs, ataxia in seven, weakness in five, and seizures in two. Two of the 16 dogs had jaundice due to biliary obstruction by the primary tumour or metastases. The sensitivities for pancreatic neoplasia were three of 16 (19 per cent) for radiography and 12 of 16 (75 per cent) for ultrasonography; the sensitivities for metastasis were two of 11 (18 per cent) for radiography and six of 11 (55 per cent) for ultrasonography. Biliary obstruction was detected by ultrasonography in both affected dogs.
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PMID:Ultrasonography of pancreatic neoplasia in the dog: a retrospective review of 16 cases. 853 34

Four women were admitted over three years because of anemia and renal failure. They had evidence of hemolytic uremic syndrome (HUS) with severe vascular involvement and glomerular collapse. Despite intensive plasma exchange, all patients developed neurologic signs (with seizures and coma in 2) and papilledema. Three developed refractory hypertension and three required dialysis. All patients had abnormal von Willebrand factor (vWF) fragmentation as reflected by decreased high molecular weight and increased low molecular weight vWF multimers in the circulation. Assuming that the disease was sustained by shear stress-induced abnormal vWF fragmentation in damaged renal microvasculature, bilateral nephrectomy was done. Surgery was followed within two weeks by complete hematologic and clinical remission consistently associated with the restoring of vWF fragmentation pathway to normal. We speculate that in HUS resistant to plasma exchange or infusion, removing the kidneys eliminates a major site of vWF fragmentation, which would limit platelet activation and protect patients from the further spreading of microvascular lesions.
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PMID:Bilateral nephrectomy stopped disease progression in plasma-resistant hemolytic uremic syndrome with neurological signs and coma. 877 Sep 81

We present a case of acute lethal poisoning by oil of "epazote" (oil of chenopodium), in a 2 y 9 m female. The volatile oil was administered according to the advice of a "curandera" (female healer), in a total quantity of 40 ml. Clinical features of the poisoning were: vomiting, deep coma, seizures, mydriasis, apnea, metabolic acidosis, neurogenic shock and death. The EEG suggested a diffuse encephalopathy, the CT scan with an image of severe brain edema and ventricular collapse. Relevant postmortem findings were brain edema and neuronal necrosis, pneumonia, enteritis, pericholangitis, mild pancreatitis and tubular necrosis. The phytochemical analysis of volatile oil identified ascaridol, the main active compound of the chenopodium herbs, in a quantity of 39 mg/ml (1,560 mg in the dose administered), and Chenopodium graveolens as the plant employed to prepare it. According to the age of the patient, 60 mg of ascaridol would be the recommended dose formerly used in the treatment of parasitic disease. Thus 1,560 mg was 26 times higher than the recommended dose, and exceeded by 56% the dose of 1,000 mg reported as lethal in humans.
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PMID:[Fatal poisoning caused by oil of epazote, Chenopodium graveolens]. 896 84

A 39-year-old man, with no history of alcohol intake, who had had an esophago-ileo-colo-gastroplasty with ileotransversostomy, developed diplopia, seizures, metabolic acidosis, and cardiac failure and finally refractory hyperdynamic shock. He died 20 h after admission to our intensive care unit from cardiocirculatory collapse. Postmortem results revealed low erythrocyte transketolase activity, which was increased by 22% by in vitro addition of thiamine diphosphate (TDP effect). Cerebral pathology showed the alterations of Wernicke's encephalopathy. We discuss the possible mechanisms of fatal cardiovascular collapse and the unusual presentation of a case without a history of alcoholic intake or clinical malnutrition.
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PMID:Neurological disturbances and hyperdynamic shock in a patient with esophagocoloplasty. 920 34

In this study, seizures in the dentate gyrus were triggered by 2 Hz electrical stimulation while, at the same time, serial changes in paired-pulse depression was measured in free-moving rats. The perforant path was stimulated by paired pulses 25 ms apart and recordings were made in the dentate gyrus. We also observed the effect of kindling procedure on this change of evoked field potential. Paired-pulse depression started to fail following the onset of epileptic afterdischarge, both before and after kindling. As kindling progressed, paired-pulse depression increased in the initial part of the stimulus train, and also the time delay from the start of the stimulation to when paired-pulse depression started to fail increased significantly. These findings suggest that the collapse of local early, presumably GABAA-mediated, inhibition may occur after the dentate gyrus seizure onset and development of kindling epileptogenesis does not weaken but, on the contrary, enhances this local inhibitory function. Finally we propose that seizures triggered by 2 Hz electrical stimulation constitutes a useful model for examining physiological or biochemical changes during seizure initiation of awake, free-moving animals since it provides long (usually several seconds or more) latency from the start of stimulation to seizure onset.
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PMID:Changes in paired-pulse depression during the triggering of seizures by 2 Hz dentate gyrus stimulation: effect of the kindling. 943 20

A dysmorphic infant is described who presented with laryngeal collapse leading to intubation and respiratory problems that were assigned clinically to the Sussman syndrome. The baby had repeated episodes of respiratory distress necessitating assisted ventilation. At 6 months old, uvulopharyngopalatotomy was done to enlarge the supraglottic airway without any benefit. Surgical reduction of the tongue and cricoid splitting did not ameliorate the respiratory distress; repeated extubation attempts failed with the baby developing stridor, respiratory distress, and episodes of cardiac arrest. At 10 months old he developed seizures and computed tomography showed diffuse cerebral atrophy consisted with hypoxic-ischaemic damage. He died at 17 months old. Western blots using antibodies against collagen alpha 1 (II) showed an absence of collagen type II in laryngeal tissue, which may explain the laryngeal collapse and impaired respiratory functions.
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PMID:Deficiency of laryngeal collagen type II in an infant with respiratory problems. 971 15

It seems clear that the abundance of potential treatment options reflects the dearth of proved, effective options. Thus, although we appear to be on the brink of many potentially major breakthroughs in treatment, there currently remains a multitude of unanswered questions and the need for further study. At this point clinical recommendations must be limited to supportive care with moderation: oxygenation without hyperoxia; ventilation without hypocarbia; avoiding extremes of blood pressure, hematocrit, blood glucose, and body temperature. Unfortunately, data from human trials are extremely limited and often poorly controlled. Furthermore, even those few existing human studies have rarely--if ever--dealt with newborns infants (Table 2). In addition, many of the existing studies do not relate to generalized asphyxia but rather to single-organ reperfusion insults. Finally, there is the critical issue of timing. Unfortunately, much of the existing experimental data relate to prophylaxis rather than treatment, severely limiting their potential for clinical applicability. Interventions may have quite different effects when administered at different phases of this most intricate process. Hyperglycemia, for example, may be neuroprotective before an insult but detrimental if induced after an asphyxial episode. Conversely, the NMDA blocker MK-801 can adversely affect outcome when given before a global asphyxial insult but can reduce seizure-related damage when given during the hyperexcitability phase. Insulin-like growth factor is also neuroprotective only when given after an insult, but it is not helpful if given before. An intimate understanding of the pathophysiologic processes involved is essential before any attempts at applying the diverse data derived from numerous animal studies to the human situation in an intelligent manner. Future studies may focus on cocktails of different mixtures of the compounds discussed or on single multipotential drugs, which would make possible a multipronged approach. However, it is essential to investigate fully the potential for toxic drug interactions, as some combinations may be produce serious consequences. For example, Gluckman and Williams evaluated the potential of combining calcium channel blockers with NMDA receptor antagonists in hypoxic-ischemic rats and found that this combination led to rapid cardiovascular collapse. Other enticing approaches for future investigations will probably include some genetic-engineering-related studies in attempt to enhance endogenous antioxidant defenses with regulon stimulation or the administration of neurotrophic growth factors. Unavoidably, the trip from the laboratory to the bedside must of necessity be an arduous and rigorous one.
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PMID:Ischemia and reperfusion injury. The ultimate pathophysiologic paradox. 977 46

Convulsive status epilepticus (SE) is convincingly related to serious morbidity and mortality and well recognized as a medical emergency, but prompt diagnosis and treatment of patients with nonconvulsive status epilepticus (NCSE) is often not emphasized because its consequences are thought to be benign. Nonconvulsive status epilepticus has been considered a relatively benign entity because it does not produce the adverse systemic consequences of convulsive status epilepticus, such as hyperthermia, acidosis, hyperkalemia, pulmonary compromise, or cardiovascular collapse. However, recent reports indicate that NCSE is not so benign. There are two major forms of NCSE, absence status epilepticus and complex partial status epilepticus. Typical absence status epilepticus does not appear to have very serious consequences and may be a type of "inhibitory" seizure, but complex partial status epilepticus has been associated with serious morbidity and mortality. Despite not causing the systemic physiologic or metabolic derangements seen with convulsive SE, complex partial status epilepticus is still associated with the two other major factors correlated with poor outcomes in convulsive SE: 1) neuronal damage from abnormal electrical activity and 2) the interaction of acute neurologic disorders, such as stroke, that may precipitate SE. Other similar epileptiform encephalopathies such as "subclinical," "electroencephalographic," "nontonic-clonic," and "subtle" SE have not been as well studied as NCSE but pose similar issues. Early diagnosis and aggressive intervention have proven the best means of averting adverse outcomes in patients with convulsive SE. The diagnosis and treatment of NCSE, particularly complex partial status epilepticus, merit similar emphasis and attention.
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PMID:Epidemiology and evidence for morbidity of nonconvulsive status epilepticus. 1047 4

A series of 54 patients with lateral ventricle tumors diagnosed and surgically treated from 1988 to 1998 was reviewed. Neoplasms invading ventricles and originating beyond their walls were excluded. There were 35 male and 19 female patients. Their ages ranged from 15 days to 20 years, and two frequency peaks were observed, one at 2 and one at 11 years. The most frequent signs and symptoms were attributed to increased intracranial pressure. The 54 patients included 41 who developed hydrocephalus, but only 15 of these required shunting. The trigonal region and frontal horn were the most common sites of origin. Surgery was planned with due consideration for the localization of the tumor, its presumptive histology, its main feeding vessels, the parenchymal functionality, and the presence or absence of hydrocephalus. The most frequent tumor types were subependymal giant cell astrocytoma, choroid plexus tumors, ependymoma, and astrocytoma. The most common complications were intraventricular hemorrhage, cortical collapse, subdural collection and seizures. To conclude, tumors located within the lateral ventricles are often very voluminous and are predominantly benign, and the treatment of choice is total resection. In the case of malignancy, postsurgical radiotherapy and/or chemotherapy should be given.
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PMID:Lateral ventricle tumors in children: a series of 54 cases. 1060 22

A 75-year-old man with a recent history of pulmonary embolism, presented with collapse followed by a gran mal seizure and right-sided non-pulsatile proptosis. On recovery, he had diplopia on lateral and upward gaze and signs of congestive cardiac failure. Further pulmonary embolism was proven by lung scintigraphy. Computed tomography of his orbits confirmed a contrast-enhancing space-occupying lesion of the medial wall of the right orbit, with no intracranial abnormality. The patient was investigated for metastatic tumour as a possible cause of the space-occupying lesion and the unprovoked thromboembolic event, but no evidence of malignancy was found. The orbital lesion was not biopsied because of the risk of bleeding from anticoagulation. Three weeks later, the patient represented with recurrent cardiac failure, proptosis, and diplopia. A transorbital ultrasound confirmed an encapsulated, well-defined vascular lesion, with typical appearances and Doppler flow characteristics of a cavernous haemangioma. Diuretic therapy abolished the proptosis and diplopia in tandem with relief of the cardiac failure. This is the first description of recurrent proptosis with diplopia due to recurrent congestive expansion of an orbital cavernous haemangioma.
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PMID:Recurrent proptotic diplopia due to congestive expansion of cavernous haemangioma with relapsing right-sided cardiac failure. 1062 2


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