Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tricyclic antidepressant overdose is the most common cause of death from prescription drugs. Clinical presentation of overdose from the tricyclic agents includes cardiac arrhythmias, hypotension, seizures, coma and anticholinergic signs such as hyperthermia, flushing and intestinal ileus. The highly toxic/lethal level (greater than 1,000 ng per mL) is manifested on electrocardiograms as prolongation of the QRS interval to 100 milliseconds or more. Treatment includes establishment of an airway, proper oxygenation and ventilation, fluid replacement at maintenance levels, cardiac monitoring, gastric lavage and charcoal administration, alkalinization to a blood pH of 7.5 with intravenous sodium bicarbonate, supportive therapy and continued cardiac monitoring after clinical recovery.
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PMID:Managing tricyclic antidepressant overdose. 162 27

To determine the rate and factors that affect carbamazepine absorption, six patients being treated in the pediatric intensive care unit for frequent seizures received loading doses (7.4 to 10.4 mg/kg) of carbamazepine suspension by either nasogastric or nasoduodenal tube. Carbamazepine serum concentrations were determined 15, 30, 60, 120, and 480 minutes after administration by fluorescence polarization immunoassay. One patient who had an ileus did not attain therapeutic concentrations (greater than 4.0 mg/L). The other five patients with normal gastrointestinal function achieved mean serum concentrations at 1 hour and 2 hours of 4.3 mg/L and 7.3 mg/L, respectively. Delayed gastric emptying and concurrent enteral feedings appear to slow the absorption of carbamazepine. No adverse effects were observed. Rapid loading with carbamazepine suspension appears to be a useful alternative for the management of critically ill pediatric patients who are experienced frequent seizures.
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PMID:Rapid loading of critically ill patients with carbamazepine suspension. 237 Nov

Thirty-four nonambulatory patients with progressive neuromuscular spinal deformity were surgically managed using a 1/4" U-shaped double rod construct with segmental instrumentation from T2 to the pelvis accompanied by posterior spinal fusion. Diagnoses included 17 patients with cerebral palsy, six with spinal bifida, and 11 with other diseases (spinal muscular atrophy, Friedreich's ataxia, polyneuropathy, nemaline myopathy, and polio). Twenty-three patients had single uncompensated thoracolumbar curves, and 11 had a double curve pattern. The mean preoperative major curve was 66 degrees (range, 22-132 degrees), the secondary curve 58 degrees (range, 23-84 degrees). No postoperative spinal support was used. Mean curve correction was 36 degrees or 54.6%. There were four major complications, including two implant failures requiring revision and two patients sustaining excessive intraoperative blood loss necessitating completion of the procedure in a second stage. There were two neurologic complications including one case of postoperative seizures and an L4 monoradicular neuropathy in a spina bifida patient. Four patients had temporary postoperative ileus, one gastroesophageal reflex, and four had urinary tract infections. There were no significant postoperative pulmonary complications. Excluding the patients with rod failure, mean loss of correction at mean follow-up of 21.3 months was 6.5%. The stability and curve correction obtained using this system supports its continued use in patients with progressive neuromuscular scoliosis.
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PMID:Unit rod segmental spinal instrumentation in the management of patients with progressive neuromuscular spinal deformity. 261 59

A boy suffering from epileptic seizures experienced five episodes of a twilight state. His twilight states continued for at least two weeks, and were characterized by behavioral disorders and severe autonomic symptoms. Sometimes functional ileus was present. The electroencephalographic finding in the first episode was 6-per-second phantom spike and wave complex (PSW). For treatment, a combination of carbamazepine and sodium valproate was useful in preventing the reappearance of the episode of the twilight state and in suppressing PSW. From the clinical and electroencephalographic findings and therapeutic response to antiepileptics, the episodes were considered to have originated in localized epileptic discharges in the hippocampal, amygdaloidal and hypothalamic regions.
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PMID:Episodic twilight state with severe autonomic symptoms in an epileptic patient. 315 Apr 76

Two patients with mitochondrial encephalomyopathy (MEP) serve to emphasize the variability of this group of diseases. Cerebral insults, mitochondrial cardiopathy, relapsing ileus, cerebral angioma, ataxia, and myoclonic seizures characterized the first case of an adult man with similar diseases in his family, interpreted as transitional form between mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) and myoclonus epilepsy associated with ragged red fibers (MERRF). The second patient, a floppy infant with cardiomyopathy and myoclonism, statomotoric and mental retardation showed combined defects in mitochondrial respiratory chain at NADH-CoQ reductase and cytochrome c oxidase and a deficiency of carnitine. In both patients neuropathologically criteria of Leigh's syndrome could be demonstrated in the cerebral cortex, in case 2 also clinically. The classificatory problems of the relationships between KSS, MELAS, MERRF, Leigh's as well as Alpers' syndromes are discussed.
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PMID:Mitochondrial myopathies with necrotizing encephalopathy of the Leigh type. 322 73

A severely hypocalcaemic, hypomagnesaemic lactating bitch exhibited clinical signs of pulmonary oedema, paresis, dementia, gastrointestinal ileus and urinary bladder atony. The total calcium, ionised calcium and magnesium levels were extremely low. The clinical picture was very different from the one typically encountered in canine lactation tetany, and instead resembled bovine postparturient paresis. Muscle tremors, rigidity and seizures were not part of the acute clinical picture, but rather atony, weakness and paresis. General muscle dysfunction probably resulted from the extremely low ionised calcium levels in combination with very low levels of magnesium and possibly potassium. Heart failure and atony of the urinary bladder and intestines were probably a result of the severe hypocalcaemia. The alteration in calcium to magnesium ratio may have depressed neuromuscular transmission, leading to paresis and atony. The unusual electrocardiogram possibly also resulted from abnormal magnesium and calcium cation levels.
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PMID:Paresis and unusual electrocardiographic signs in a severely hypomagnesaemic, hypocalcaemic lactating bitch. 967 8

We experienced a case of convulsion following the combination of single oral administration of enoxacine before an emergency operation and single postoperative intravenous administration of flurbiprofen axetil. The patient was an 87-year-old female referred to our hospital for severe abdominal pain. She was diagnosed as having the strangulation ileus, then underwent the emergent operation of partial resection of the necrotic small intestine under general anesthesia. Unfortunately we did not know that she had temporarily received oral enoxacine 200 mg, a new quinolone, administered by the previous doctor on the day before the operation. After the operation, flurbiprofen axetil 50 mg, a nonsteroidal anti-inflammatory drug, was given intravenously in thirty seconds due to postoperative pain. One minute after administration of the drug, she immediately developed a convulsive fit, severe disturbance of consciousness and apnea. We then administered at once, a single dose of diazepam intravenously for convulsion treatment, kept her airway open and controlled her ventilation. Convulsion disappeared in a minute and her condition improved gradually. We suspect that convulsive seizure may have been induced by the drug interaction between single oral dose of enoxacine before the operation and single intravenous dose of flurbiprofen axetil after the operation. We also suspect that the serum concentration of enoxacine was kept high because of metabolic disturbance and renal dysfunction resulting from her old age and dehydration. This case suggests that medication before the emergency operation must be considered in anesthetic management because of the possible side effect such as convulsion induced by the drug interaction between neuquinolones and anti-inflammatory drugs.
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PMID:[Convulsion following the combination of single preoperative oral administration of enoxacine and single postoperative intravenous administration of flurbiprofen axetil]. 1134 61

Acetylcholinesterase (AChE, EC3.1.1.7) functions in nerve impulse transmission, and possibly as a cell adhesion factor during neurite outgrowth. These functions predicted that a mouse with zero AChE activity would be unable to live. It was a surprise to find that AChE -/- mice were born alive and survived an average of 14 days. The emaciated appearance of AChE -/- mice suggested an inability to obtain sufficient nutrition and experiments were undertaken to increase caloric intake. Pregnant and lactating dams (+/-) were fed 11% high fat chow supplemented with liquid Ensure. AChE -/- pups were weaned early, on day 15, and fed liquid Ensure. Although nullizygous animals showed slow but steady weight gain with survival over 1 year (average 100 days), they remained small at all ages compared to littermates. They demonstrated delays in temperature regulation (day 22 vs. 15), eye opening (day 13 vs. 12), righting reflex (day 18 vs. 12), descent of testes (week 7-8 vs. 4), and estrous (week 15-16 vs. 6-7). Significant physical findings in adult AChE -/- mice included body tremors, abnormal gait and posture, absent grip strength, inability to eat solid food, pinpoint pupils, decreased pain response, vocalization, and early death caused by seizures or gastrointestinal tract ileus. Behavioral deficits included urination and defecation in the nest, lack of aggression, reduced pain perception, and sexual dysfunction. These findings support the classical role for AChE in nerve impulse conduction and further suggest that AChE is essential for timely physical development and higher brain function.
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PMID:Rescue of the acetylcholinesterase knockout mouse by feeding a liquid diet; phenotype of the adult acetylcholinesterase deficient mouse. 1212 53

Classically described antimuscarinic poisoning signs and symptoms include mydriasis, decreased secretions, ileus, urinary retention, hyperthermia, tachycardia, and altered mental status. These features may be used clinically to assist in the diagnosis of patients with unknown poisonings. We sought to analyze the prevalence of antimuscarinic physical examination findings in evaluating patients presenting with acute poisoning from antimuscarinic agents. We conducted a retrospective, medical record review at two urban tertiary care teaching hospitals. The study population consisted of patients presenting to the Emergency Department with a diagnosis of acute poisoning secondary to medications with known antimuscarinic side effects during a 78-month period between January 1994 and July 2001. Cases were excluded for incomplete medical records or unreliable histories of ingestion, and when concomitant ethanol intoxication was present on laboratory analysis. Clinical information obtained from each patient included vital signs, pupillary size, electrocardiogram abnormalities, the presence of mucous membrane and axillary secretions, initial urine output after bladder catheterization, quality of bowel sounds, mental status changes, the occurrence of seizures and coma, need for orotracheal intubation, and time required for clinical resolution. Diagnostic and therapeutic information including laboratory tests, administration of sodium bicarbonate, and usage of physostigmine was also collected. We identified a total of 345 cases, 213 of which met inclusion criteria. Of these cases, the most common documented findings included decreased secretions in 75.1%, tachycardia in 68.1%, confusion in 49.3%, drowsiness in 48.2%, and hypoactive or absent bowel sounds in 44.6%. Combining signs and symptoms to predict this toxic syndrome was not very reliable. Tachycardia, decreased oral or axillary secretions, and mydriasis proved to be the most predictive trio of clinical signs, but were found in only 28.2% of cases. At least one of these three signs was documented in 94% of our patients. The combination of tachycardia and decreased secretions was the most common pair of findings, recorded in 55.4% of cases. We conclude that the clinical presentation of antimuscarinic syndrome is variable.
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PMID:Prevalence of autonomic signs and symptoms in antimuscarinic drug poisonings. 1475 84

Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) is most commonly associated with a mitochondrial DNA A to G point mutation at nucleotide 3243 (A3243G) and individuals with the disorder present a wide range of multisystemic symptoms. Seizures in MELAS patients are often intractable and require multiple antiepileptic drugs. Here we report a MELAS patient who presented with acute intestinal pseudo-obstruction following the administration of phenytoin (PHT) as an antiepileptic treatment. She presented with the first stroke-like episode at the age of 6 years and mitochondrial DNA analysis revealed A3243G with 94% mutation load in skeletal muscle. Despite treatment with phenobarbital and clobazam at the age of 16 years, she developed status epilepticus which ceased following PHT infusion. Thereafter, she was started on PHT treatment. One month later, however, she was readmitted because of remarkable abdominal distention. Although abdominal CT showed acute ileus with hepatic portal venous gas mimicking surgical emergency, the abdominal distention gradually recovered over several days following the discontinuation of PHT. Our clinical observations suggest the possibility that intestinal pseudo-obstruction in this patient related to PHT therapy. Careful clinical observation including gastrointestinal symptoms is required in the management of epilepsy in MELAS patients.
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PMID:Intestinal pseudo-obstruction in a patient with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) associated with phenytoin therapy. 1822 64


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