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

The central nervous system toxicity of cyclosporine, which is known to be neurotoxic clinically, was investigated in a rat model. Munich-Wistar rats were divided into 3 groups for a 2-week protocol. After baseline EEG and behavioral testing, group 1 (control) received a weight-adjusted volume of parenteral cyclosporine vehicle i.p., group 2 (low-dose) received 5 or 10 mg/kg/day i.p., and group 3 (high-dose) received 20 mg/kg/day i.p. Spontaneous behavior was observed, simple sensorimotor testing performed daily, and awake EEG's recorded 3 times per week. Four of 12 high-dose animals died during study, one after a witnessed tonic-clonic seizure, and two after recording of frankly epileptiform EEG's; there were no deaths in control or low-dose animals. Significant EEG abnormalities developed only at high-dose, with frankly epileptiform EEG's and/or seizures seen in 58 +/- 15% of these rats (P = 0.005, different from controls by life-table analysis). Although some high-dose animals demonstrated hyperirritability and dystonic posturing, behavioral changes were subtle, and animals were often still or rocking slightly during recording of frankly epileptiform EEG's. Walking latency and alley escape behaviors were delayed in high-dose rats, the latter correlating with abnormal EEG's. Serum urea nitrogens were mildly elevated in high-dose animals, but serum creatinine, electrolytes, bilirubin, body magnesium stores, and blood pressure remained normal in all groups. Kidneys showed only mild vacuolation histologically. The brain showed only very focal cortical injury sites related to electrode placement, which did not correlate with EEG changes or mortality. These results suggest that there may be a direct effect of cyclosporine on the central nervous system. This model system should prove useful in defining mechanisms of cyclosporine-related neurotoxicity.
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PMID:Central nervous system toxicity of cyclosporine in a rat model. 275 57

The etiology, pathophysiology, clinical features, diagnosis, and medical treatment of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) are reviewed. SIADH is a common cause of hyponatremia in hospitalized patients. Increased concentrations of antidiuretic hormone (ADH) result in retention of free water, increased excretion of sodium, and hyponatremia. Symptoms generally occur only when hyponatremia is severe (less than or equal to 125 meq/L) and may include anorexia, vomiting, and confusion, followed by seizures, coma, and death. SIADH may result from a variety of diseases, as well as from the use of drugs such as chlorpropamide, carbamazepine, diuretics, and some antineoplastic agents. Diagnosis of SIADH is confirmed by demonstration of a high urine osmolality with a low plasma osmolality, in the absence of diuretic use. Immediate treatment of the symptomatic patient with SIADH includes intravenous furosemide and 3% sodium chloride injection to produce a negative free-water balance. If the underlying cause of SIADH cannot be corrected, the treatment of choice for chronic SIADH is fluid restriction. If this is not tolerated by the patient, demeclocycline can be used to induce a negative free-water balance. Urea, lithium, phenytoin, and loop diuretics have been reported to be effective, but there are few data to support their use. Future research into the treatment of SIADH must be directed at developing effective antagonists of ADH. Treatment of SIADH consists of elimination of underlying causes and restriction of fluid intake; if these measures are unsuccessful or poorly tolerated, long-term drug therapy may be indicated.
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PMID:Management of the syndrome of inappropriate secretion of antidiuretic hormone. 312 Dec 40

This study examined the descriptive epidemiology of seizure disorder in 129 male residents of a Veterans Administration Nursing Home. Eighty-seven of the residents were institutionalized because of nonpsychiatric disorders (60 for chronic neurologic diseases, and 27 for other medical conditions). Forty-two were institutionalized because of a chronic psychosis (39 for schizophrenia, three for affective disorders). We determined for each resident an extensive clinical data base of 54 items including measures of hematologic, nutritional, metabolic and endocrine status, as well as continuing medications. In the nonpsychiatric group, 16 of the 87 men had a seizure disorder. In the psychiatric group, this proportion was only three of 42. The prevalence of epilepsy in the nonpsychiatric group was 20-40 times greater than in the aged-matched general population of men. In the nonpsychiatric group, the onset of seizures followed the onset of organic brain disease. Forty-five percent of seizure disorders occurred in men who had experienced a cerebrovascular accident, and 23% in men with other types of chronic brain disease. The seizures of the nonpsychiatric men had been observed to be generalized clonic-tonic in 45%, and partial complex in 22%. Ninety-four percent of the nonpsychiatric men with epilepsy received anticonvulsants, and none had experienced more than one seizure during the preceding year. Univariate statistical analysis of the 54 item data base showed that the occurrence of seizure disorder correlated inversely with age, blood urea nitrogen, serum creatinine and serum bilirubin, and directly with plasma testosterone, hemoglobin, use of anticonvulsants, and use of psychotherapeutic agents.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Seizure disorder in the men of a Veterans Administration nursing home. 328 Jul 35

Seizures in renal transplant recipients may be due to a variety of causes. Although intravenous pulse methylprednisolone used to treat acute rejection episodes has been reported to be associated with acute central nervous system (CNS) manifestations in adult renal transplant patients, this complication has not previously been described in pediatric patients. We report a 12 year old renal transplant recipient who developed transient blindness and focal seizures 72 hours following intravenous pulse methylprednisolone. Serum creatinine and urea nitrogen were 1.5 and 31 mg/dl respectively; serum electrolytes, calcium, magnesium, phosphate, and glucose were normal. Although usually due to other etiologies, seizures in the pediatric transplant recipient may be secondary to acute CNS toxicity resulting from intravenous glucocorticoid infusion.
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PMID:Seizures and blindness following intravenous pulse methylprednisolone in a renal transplant patient. 330 30

A girl, ultimately diagnosed as having profound ornithine transcarbamylase (OTC) deficiency, presented as a neonate with feeding intolerance, irritability, and seizures without concurrent hyperammonemia. Developing normally until ten months of age, the girl subsequently experienced two episodes of hyperammonemia, which were associated with focal seizures and residual hemiparesis. She continued to have profound neurologic impairment and seizures and died at 26 months of age, despite appropriate dietary protein restriction, sodium benzoate, and arginine supplementation. Symptomatic OTC deficiency has not been previously reported unassociated with hyperammonemia. The recurrent cerebrovascular episodes are distinctly uncommon in patients with urea cycle enzymopathies.
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PMID:Unusual biochemical and clinical features in a girl with ornithine transcarbamylase deficiency. 350 74

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

We reviewed the natural history and differential diagnosis of ornithine transcarbamylase deficiency (an X-linked inborn error of urea synthesis) in 13 symptomatic female heterozygotes. The patients presented as early as the first week of life or as late as the sixth year. The most common symptoms before diagnosis were nonspecific: episodic extreme irritability (100 percent), episodic vomiting and lethargy (100 percent), protein avoidance (92 percent), ataxia (77 percent), Stage II coma (46 percent), delayed physical growth (38 percent), developmental delay (38 percent), and seizures (23 percent). Including the proband, 42 percent of the female members of the 13 families studied had symptoms. The median interval between the onset of major symptoms (vomiting and lethargy, seizures, and coma) and diagnosis was 16 months (range, 1 to 142). Five patients had IQ scores below 70 at the time of diagnosis. We suggest that careful evaluation of the family history, the dietary history, the episodic nature of the nonspecific symptoms, the response of these symptoms to the withdrawal of protein, and their frequent onset at the time of weaning from breast milk will permit early diagnosis and might thereby reduce the risk of death or neurologic impairment in female patients with partial ornithine transcarbamylase deficiency.
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PMID:Natural history of symptomatic partial ornithine transcarbamylase deficiency. 394 92

Three adolescent patients with severe seizure disorders were treated with phenacemide. All three patients showed elevated serum creatinine and normal blood urea nitrogen values while on phenacemide. Simultaneous urea and creatinine clearance studies performed on each patient demonstrated normal urea clearances and decreased creatinine clearances. Inulin clearance performed in one patient was normal. The medication was discontinued in two of the patients because of co-existing neutropenia. Serum creatinine values returned to normal after phenacemide treatment was terminated. The elevation in serum creatinine values with phenacemide appears to be dose related, reversible, and unrelated to impairment of glomerular filtration.
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PMID:Elevated serum creatinine levels in three patients treated with phenacemide. 395 82

We reviewed clinical data in 33 patients with transient hyperammonemia of the newborn (THAN): six previously unreported cases and 27 from the literature. Thirteen neonates with urea cycle enzyme deficiencies (UCED) served for comparison. No differences were found in the incidence of perinatal complications, route of delivery, Apgar scores, sex, or incidence or time of onset of seizures. On the other hand, neonates with THAN had significantly lower birth weights (mean +/- SEM 2282 +/- 78 gm vs 3336 +/- 222 gm, P less than 0.001) and gestational ages (35.1 +/- 0.5 weeks vs 39.6 +/- 0.5 weeks, P less than 0.001). Mean time of onset of respiratory distress (3.9 +/- 1.4 hours vs 71.5 +/- 26.1 hours, P less than 0.001), ventilatory support (P less than 0.001), lethargy (P less than 0.005), and coma (P less than 0.005) occurred earlier in THAN. Distinctive laboratory findings in patients with THAN included abnormal chest radiographic findings and plasma ammonium concentrations that were higher (1871 +/- 209 microM vs 973 +/- 169 microM, P less than 0.02) at an earlier age. Respiratory distress occurred in all but one patient with THAN before 24 hours; in contrast, only 62% of infants with UCED had respiratory symptoms, and none before 30 hours. In this retrospective study, the clinical presentation alone differentiated THAN from UCED.
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PMID:Differentiation of transient hyperammonemia of the newborn and urea cycle enzyme defects by clinical presentation. 405 69

Eleven electroencephalograms in 4 infants with urea-cycle disorders were reviewed. All infants had one or more abnormal EEGs. The abnormalities consisted mainly of multiareal spikes, spike-waves, or sharp-and-slow-wave activity. In addition, one patient, a term infant, exhibited exaggerated spindle-delta bursts. This infant, and also one other at a similar age, had monorhythmic paroxysmal theta activity. Clinically, all patients had seizures shortly preceding abnormal EEGs. EEG alterations were encountered over a wide range of elevated serum ammonia levels. Normal EEGs occurred in the face of slightly elevated levels. It is concluded that epileptiform EEG alterations may be a characteristic manifestation of urea-cycle disorders.
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PMID:Electroencephalographic findings in urea-cycle disorders. 619 50


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