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

A 12-year-old girl presented with weakness, diplopia, and lethargy after a prodrome of gastroenteritis. Laboratory studies were compatible with a diagnosis of hemolytic uremic syndrome. She developed seizures that were controlled by diphenylhydantoin and valium. In spite of peritoneal dialysis and fresh frozen plasma infusions, she progressed to a left hemiplegia associated with a brain scan finding of decreased blood flow in the right middle cerebral artery perfusion area. A 5 liter whole blood exchange transfusion did not improve the neurological status or low platelet count. Daily plasma exchanges with fresh frozen plasma replacement resulted in normal platelet count within 48 hours and was followed by progressive improvement in neurological status. Platelet agglutinating factor decreased to control levels. A repeat brain scan was normal.
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PMID:Reversal of central nervous system involvement in hemolytic uremic syndrome by use of plasma exchanges. 311 70

Magnesium is an important element for health and disease. Magnesium, the second most abundant intracellular cation, has been identified as a cofactor in over 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Approximately half of the total magnesium in the body is present in soft tissue, and the other half in bone. Less than 1% of the total body magnesium is present in blood. Nonetheless, the majority of our experimental information comes from determination of magnesium in serum and red blood cells. At present, we have little information about equilibrium among and state of magnesium within body pools. Magnesium is absorbed uniformly from the small intestine and the serum concentration controlled by excretion from the kidney. The clinical laboratory evaluation of magnesium status is primarily limited to the serum magnesium concentration, 24-hour urinary excretion, and percent retention following parenteral magnesium. However, results for these tests do not necessarily correlate with intracellular magnesium. Thus, there is no readily available test to determine intracellular/total body magnesium status. Magnesium deficiency may cause weakness, tremors, seizures, cardiac arrhythmias, hypokalemia, and hypocalcemia. The causes of hypomagnesemia are reduced intake (poor nutrition or IV fluids without magnesium), reduced absorption (chronic diarrhea, malabsorption, or bypass/resection of bowel), redistribution (exchange transfusion or acute pancreatitis), and increased excretion (medication, alcoholism, diabetes mellitus, renal tubular disorders, hypercalcemia, hyperthyroidism, aldosteronism, stress, or excessive lactation). A large segment of the U.S. population may have an inadequate intake of magnesium and may have a chronic latent magnesium deficiency that has been linked to atherosclerosis, myocardial infarction, hypertension, cancer, kidney stones, premenstrual syndrome, and psychiatric disorders. Hypermagnesemia is primarily seen in acute and chronic renal failure, and is treated effectively by dialysis.
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PMID:Magnesium metabolism in health and disease. 328 51

Patients with agammaglobulinemia are particularly susceptible to chronic enteroviral infections of the central nervous system. Data on 42 patients were obtained by literature review, communications with other physicians, and personal experiences. Thirty-eight patients had congenital immunodeficiencies, most frequently X-linked agammaglobulinemia. Most patients who could be assessed were receiving maintenance therapy with intramuscular gamma-globulin before their enteroviral infection. Seven patients had not been recognized as hypogammaglobulinemic before the onset of infection. The commonest pathogens were echoviruses (37 of 41 cases), especially type 11 (11 cases). Thus far, four patients have had sequential or simultaneous infections with a second enteroviral serotype. Other features of the disease have included weakness, lethargy or coma, headaches, hearing loss, seizures, ataxia, and paresthesias. Some patients have also had nonneurologic manifestations of chronic enteroviral infection, including fever, the dermatomyositis-like syndrome, edema, rashes, and hepatitis. Treatment has consisted primarily of antibody administration, either in intravenous immunoglobulin preparations or in immune plasma. Twelve patients have received intraventricular immunoglobulin through reservoir devices; six of these 12 have improved substantially, as judged by clinical criteria.
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PMID:Chronic enteroviral meningoencephalitis in agammaglobulinemic patients. 329

Three cases of nocardial brain abscess are presented. All three patients were receiving immunosuppressive therapy at the time of diagnosis. Two patients had cardiac transplantation and the third had periarteritis nodosa. The patients presented with generalized seizures or focal weakness. Accurate localization of the intracerebral mass lesion was obtained from computed tomography (CT) scans, but CT-guided stereotactic aspiration was required for diagnosis and treatment in every case. After Nocardia asteroides was seen on Gram's stain and subsequently identified by culture, appropriate antibiotic therapy was initiated. Both heart transplant patients survived in good neurological condition. We believe that stereotactic aspiration followed by prolonged antibiotic therapy may significantly improve the outcome of patients with nocardial brain abscess.
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PMID:Nocardial brain abscess: diagnostic and therapeutic use of stereotactic aspiration. 329 25

The clinical and laboratory features of moderate to severe organophosphate and carbamate toxicity in 37 infants and children are presented. Ingestion of an improperly stored liquid pesticide was the most common route of intoxication (76% of patients); five (14%) children became intoxicated after playing on carpets and floors of homes that had been sprayed or fogged by unlicensed exterminators. The transfer diagnoses were incorrect for 16 or 20 patients who were transferred to our center from another institution. Miosis (73%), excessive salivation (70%), muscle weakness (68%), and lethargy (54%) were the most common abnormal signs; 49% and 22% of patients had tachycardia and seizures, respectively, and 38% of children had respiratory insufficiency that required endotracheal intubation and mechanical ventilation. The results of erythrocyte and serum cholinesterase activity assays were concordant in 83% of patients. Thirty-four (92%) patients were treated with atropine and/or pralidoxime; three patients required only supportive care. Most patients had a prompt response to therapy; however, two patients with organophosphate toxicity required multiple doses of atropine during a 24-hour period; in both instances, the doses of atropine were subtherapeutic. There were no deaths. Pneumonitis and/or atelectasis developed in ten patients, including six who had ingested a petroleum distillate-containing insecticide.
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PMID:Organophosphate and carbamate poisoning in infants and children. 333 78

Poison hemlock (Conium maculatum) was toxic to pregnant ewes and their fetuses when fed during gestation days 30 through 60. Maternal effects included trembling, muscular weakness in the neck initially, then progressing to the limbs, ataxia, frequent urination and defecation, and death. Convulsive seizures were not observed. Fetotoxic effects included excessive flexure of the carpal joints with lateral deviation in the front limbs and kinked tails. At term, 7 of 11 lambs had varying degrees of the limb abnormalities, but all lambs appeared clinically normal at 8 weeks after parturition.
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PMID:Maternal and fetal toxicity of poison hemlock (Conium maculatum) in sheep. 334 38

Two dogs were examined because of anorexia, lethargy, muscle tremors, weakness, and seizures that were associated with an acute onset of hypocalcemia. Both dogs had histories of chronic hypercalcemia. Examination of the parathyroid glands revealed infarction of focal parathyroid adenomas, with atrophy of the remaining parathyroid glands. It was concluded that the acute onset of hypocalcemia was caused by infarction of functional parathyroid adenomas that were previously responsible for the cause of persistent hypercalcemia. Infarction of a parathyroid adenoma should be included in a list of differential diagnoses of acute hypocalcemia in the dog, especially if hypercalcemia has been diagnosed previously.
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PMID:Acute hypocalcemia associated with infarction of parathyroid gland adenomas in two dogs. 335 Jul 46

The clinical features of 33 patients with primary intracranial arachnoid cysts are reviewed. Magnetic resonance imaging was performed in 9 patients and was particularly useful in the multiplanar definition of complex cysts and in differentiating arachnoid cysts from other lesions that are hypodense on computed tomographic scans. Hydrocephalus, cranial nerve palsies, or symptomatic brain compression was considered an indication for surgical intervention in 21 patients. Outcome was uniformly good: mild focal weakness and seizure disorders constituted the sequelae.
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PMID:Clinical and magnetic resonance features of primary intracranial arachnoid cysts. 357 19

A 28-month-old male with generalized hypotonia and muscle weakness, a myopathic face, skeletal dysmorphism and delayed motor milestones from birth is reported. He gradually developed the ability of sitting and rolling over, but could not stand without support until 28 months. There was no intellectual impairment or seizures. Deep tendon reflexes were absent. The serum CK value, peripheral nerve conduction velocity and EMG were within normal limits. A muscle biopsy specimen showed mild variation in fiber size, and an increased number of type 2C fibers on histochemical examination, but no apparent abnormalities on electron microscopy. The baby was tentatively diagnosed as having minimal change myopathy or nonspecific congenital myopathy which is thought to be one of the congenital nonprogressive myopathies.
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PMID:Nonspecific congenital myopathy (minimal change myopathy): a case report. 360 41

Two siblings with hyperornithinemia, hyperammonemia, and homocitrullinuria are reported. The clinical picture included protein intolerance, mental retardation, seizures, and stuporous episodes. One patient had cerebellar ataxia, myoclonus, convulsive seizure, and muscular weakness in both legs. Isolated liver mitochondria in the patient revealed that ornithine transport and citrulline synthesis were decreased, but urea cycle enzymes and ornithine aminotransferase were normal. Ornithine metabolism was decreased in cultured skin fibroblasts.
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PMID:Hyperornithinemia, hyperammonemia, and homocitrullinuria: case report and biochemical study. 367 Jun 19


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