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)

Strychnine poisoning results in a predictable and treatable sequence of events involving blockade of the inhibitory neurotransmitter, extensor muscle spasms, seizures, and respiratory paralysis. These spasms may lead to hyperthermia, profound lactic acidosis, and rhabdomyolysis. Acidosis is primarily attributable to lactate, as indicated by the correlation between arterial pH and log of lactic acid concentration (r = -0.878). Interruption of the strychnine blockade is the primary therapy for strychnine poisoning. Phenobarbital in moderate doses should be the first intervention and anesthetic doses should be used if necessary. Suppression of convulsions will permit successful management of the complications of strychnine poisoning. Our patient survived, even though at one point he had a pH of 6.55, a lactate level of 32 mM/liter, a temperature of 43 degrees C, and rhabdomyolysis with an increased creatine phosphokinase level of 359,000 mU/ml (5,983 mumol/s/liter).
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PMID:Strychnine poisoning. Recovery from profound lactic acidosis, hyperthermia, and rhabdomyolysis. 682 97

Serial serum creatine kinase (CK) level determinations were performed on selected patients for six days following tonic-clonic or focal motor seizures in a prospective study. The time course and magnitude of serum CK elevation was correlated with seizure CK level was observed in all patients. Isoenzyme determinations revealed that CK was derived from skeletal muscle. Our data demonstrate that profound elevations of serum CK level may occur postictally and appear to be related to the intensity of muscular activity. patients with seizures associated with alcohol abuse had the greatest postictal serum CK level increases.
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PMID:Postictal elevation of serum creatine kinase level. 684 27

Systemic arterial pressure was markedly increased in the early phase of cerebral ischemia induced by bilateral carotid artery occlusion (BCAO) in stroke-prone spontaneously hypertensive rats (SHRSP). The elevated level of arterial pressure was gradually returned to the initial level, and hypotension followed in the late phase. Severe neurological symptoms such as "ischemic seizure", dyspnea and coma were developed in the late phase. All SHRSP died within 6 hr after BCAO. The heart rate continued to increase during the brain ischemia. Cardiac arrhythmias, significant increases in plasma levels of creatine phosphokinase (CPK) and CPK-MB isozyme and disruption of myofibrils were observed after BCAO, particularly after the development of ischemic seizure. In contrast, in stroke-resistant SHR (SHRSR) and Wistar-Kyoto rats (WKY), ischemic seizure did not develop, yet all died within 8 hr after BCAO. Arterial pressures were moderately increased and never decreased to below the initial levels during the observation periods. Increases in CPK-MB isozyme activities in plasma from SHRSR and WKY were not detected. Pretreatments with propranolol and reserpine inhibited the increases in heart rate, reduced the frequency of arrhythmias and prolonged the survival time following BCAO in SHRSP. Our results indicate that cardiac dysfunction, which is a consequence of the cerebral ischemia, may be one of the causes of death following BCAO in SHRSP.
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PMID:Cardiovascular responses to cerebral ischemia following bilateral carotid artery occlusion in SHRSP, SHRSR and WKY rats. 687 14

Brain-type isoenzyme of creatine kinase was measured serially in 45 healthy and 22 severely asphyxiated term infants. The enzyme was measured in cord blood and in venous, capillary, or arterial blood at six to eight hours, 24 to 30 hours, and 72 to 80 hours after birth. In the healthy infants a brief rise of CK-BB occurred at six to eight hours; CK-BB activities were greater than 2.5 log-transformed standard deviations above the mean of the control values in ten of the asphyxiated infants and in none of the control infants. When normal CK-BB activity was used as a predictor of good neurologic outcome and elevated CK-BB as a predictor of subsequent neurologic abnormality, the outcome was predictable from the CK-BB activity in 17 of 22 cases (77%) and in 11 of the 12 survivors (92%). Eight of the 12 surviving infants had neonatal seizures and outcome was predictable from CK-BB activity in all cases. We conclude that serum CK-BB activity, especially when measured in cord blood and at six to 12 hours of life, correlates with neurologic outcome after severe asphyxia, and that measurement of CK-BB compares favorably with radionuclide and computerized tomographic scanning as a method of predicting neurologic outcome after asphyxia.
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PMID:Assessment of neurologic outcome in asphyxiated term infants by use of serial CK-BB isoenzyme measurement. 714 80

Decreased brain ATP and phosphocreatine (PCr) concentrations and intracellular pH were compared in hypoxic 4-, 10-11, and 24-25-day-old rats. Surface coil 31P-nuclear magnetic resonance (NMR) spectra were acquired in vivo every minute before, during, and after 7 min of breathing 4% O2. At all ages PCr decreased rapidly. At the two younger ages, the nucleoside triphosphate signal was still 80-85% of pre-hypoxic values, indicating 20-30% decrease in ATP, when PCr was almost fully depleted. At 24-25 days, PCr initially decreased 40-50% with an ATP loss of about 30%. Then, PCr and ATP decreased simultaneously. The decrease in brain pH was greatest at 24-25 days. More electrocortical seizure activity during hypoxia was seen at 10-11 days than at other ages. Seizure activity was seen only when ATP was less than 20% depleted and was not associated with more rapid decreases in ATP or PCr. At all ages, loss of electrocortical activity occurred when ATP was about 30% depleted. Brain creatine kinase catalyzed flux, measured by the NMR saturation transfer experiment before the hypoxic period, was 4-fold higher at 24-25 days than at 4- or 10-11 days. In conclusion, the temporally coupled depletion of PCr and ATP during hypoxia, which is characteristic of the mature brain, is seen only after the maturational increase in brain CK activity.
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PMID:Phosphocreatine and ATP regulation in the hypoxic developing rat brain. 760 Jun 67

An aqueous solution of norfloxacin nicotinate (NFN) was administered to donkeys (Aquus asinus) intravenously (once at 10 mg/kg), intramuscularly and orally (both routes once at 10 and 20 mg/kg, and for 5 days at 20 mg/kg/day). Blood samples were collected at predetermined times after each treatment and urine was sampled after intravenous drug administration. Serum NFN concentrations were determined by microbiological assay. Intravenous injection of NFN over 45-60 s resulted in seizures, profuse sweating and tachycardia. The intravenous half-life (t1/2 beta) was 209 +/- 36 min, the apparent volume of distribution (Vd(area)) was 3.34 +/- 0.58 L/kg, the total body clearance (ClB) was 1.092 +/- 0.123 x 10(-2) mL/min/kg and the renal clearance (C1R) was 0.411 +/- 0.057 x 10(-2) mL/min/kg. Oral bioavailability was rather poor (9.6% and 6.4% for the 10 and 20 mg/kg doses respectively). Multiple oral treatments did not result in any clinical gastrointestinal disturbances. After intramuscular administration (20 mg/kg), serum NFN concentrations > 0.25 microgram/mL (necessary to inhibit the majority of gram-negative bacteria isolated from horses) were maintained for 12 h. The intramuscular bioavailability was 31.5% and 18.8% for the 10 and 20 mg/kg doses respectively. After multiple dosing some local swelling was observed at the injection site. About 40% of the intravenous dose was recovered in the urine as parent drug. The results of comprehensive haematological and blood biochemistry tests indicated no abnormal findings except elevation in serum CPK (creatine phosphokinase) values after multiple intramuscular dosing.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intravenous disposition kinetics, oral and intramuscular bioavailability and urinary excretion of norfloxacin nicotinate in donkeys. 762 23

We report a 46-year-old man with bacterial endocarditis and cardiac failure, who developed status epileptics. The patient was apparently well until July of 1991 when there was a gradual onset of fever and general fatigue. He was hospitalized to the cardiology service of our hospital where diagnosis of bacterial endocarditis and aortic insufficiency was made. On October 9, 1991, he suddenly developed cardiogenic shock, and emergency replacement of the aortic valve was made; at the operation, the main trunk of the left coronary artery showed embolic occlusion, and the myocardial movement was markedly diminished; serum creatine kinase was 3.150 IU/l. His cardiac failure did not resolve, and renal failure developed in December 1991, for which peritoneal dialysis was necessary. On February 2, 1992, he suddenly developed a clonic seizure which started from his face with a transient post-ictal left hemiparesis; a cranial CT scan was unremarkable. He was treated with phenytoin and glycerol, however, he developed status epileptics on February 3; he developed cardiac arrest after the injection of phenytoin 750 mg. He was resuscitated, however, his status did not resolve. Neurological consultation was asked on February 4. On physical examination, his blood pressure was 80/40 mmHg heart rate 77/min and regular, and body temperature 39.1 degrees C. The palpebral conjunctiva were slightly anemic, however, the bulbar conjunctiva were not icteric. No cervical adenopathy was noted. Glade II systolic murmur was heard in the apex; the lungs were clear. The abdomen was flat and soft without organomegaly. No edema was present in the legs. On neurologic examination, he was comatose without response to painful stimuli. He repeatedly had convulsion lasting for 30 seconds every 2 to 3 minutes; his convulsions started with the conjugate deviation of the eyes to the left followed by turning of the head toward left, and then clonic convulsions started in this left upper limb extending to other extremities. The optic fundi were unable to visualize because of corneal clouding; light reflex was sluggish on the right side; no oculocephalic response was elicited; corneal reflex was also lost bilaterally. Extremities were hypotonic, and no automatic movement was seen. The triceps brachii reflex was diminished, but all the other deep reflexes were lost; no plantar response was elicited. Meningeal sign was absent. He was treated with intravenous diazepam; the interval of convulsions prolonged, however, blood pressure dropped to 40 to 40 mmHg. On February 4, intravenous thiopental anesthesia was instituted, and assisted respiration was started.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 46-year-old man with cardiac failure and statues epileptics]. 794 26

Both clinical and laboratory studies are being undertaken to investigate the deleterious neurologic and developmental effects associated with cardiopulmonary bypass, hypothermia, and circulatory arrest in the neonate and infant. A prospective, randomized clinical study of 171 neonates and young infants compared circulatory arrest with low-flow bypass (50 mL.kg-1.min-1). Circulatory arrest was associated with a higher incidence of early postoperative seizures as well as greater release of creatine kinase-BB. There was a strong correlation between duration of circulatory arrest and seizures (p = 0.004). The late consequences of these findings will be known at the completion of developmental assessment of all patients at 1 and 4 years of age. Laboratory studies have used a miniature piglet model that closely replicates clinical circulatory arrest. High-energy phosphate stores determined by magnetic resonance spectroscopy were maintained in animals undergoing 1 hour of low-flow bypass but became undetectable after 32 minutes of a 1-hour period of circulatory arrest. However, they returned to baseline within 3 hours of reperfusion as did cerebral blood flow and metabolism determined by microsphere studies. Piglets undergoing 1 hour of circulatory arrest showed more rapid recovery of cerebral adenosine triphosphate content and intracellular pH when managed with the pH-stat strategy during hypothermic bypass than with the more alkaline alpha-stat strategy. Other laboratory studies have examined pharmacologic methods of reducing cerebral injury associated with circulatory arrest including aprotinin, anti-CD18, neuronal receptor antagonists (MK801, NBQX), and blockade of glutamate release with adenosine in a cerebroplegia solution. These studies have suggested a number of promising approaches to improving the technique of circulatory arrest.
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PMID:Review of current research at Boston Children's Hospital. 826 70

Three cases with distinct clinical manifestations associated with rhabdomyolysis syndrome were encountered in this hospital's pediatric intensive care unit. Elevation of serum creatine phosphokinase, uric acid, potassium, inorganic phosphate and hypocalcemia with seizure were noted. The three patients all had signs of acute renal failure. One died of respiratory failure, and autopsy revealed multiple intrathoracic anomalies. The remaining two recovered completely from rhabdomyolysis. It is of importance to early recognize any acutely ill patient as having rhabdomyolysis syndrome when there is elevation of muscle enzymes, hypocalcemic seizure, positive orthotolidine reaction of urine strip while negative finding of red blood cell. The syndrome may damage the kidneys. Appropriate management to induce diuresis usually can salvage this potentially life-threatening condition.
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PMID:Rhabdomyolysis syndrome in children: report of three cases. 836 67

Clinical signs that included lethargy, inappetence, diarrhea, and vomiting and that progressed to seizures were observed in 40 feeder pigs that were approximately 70 days old. The pigs were fed ground red wheat and whole milk and were housed in a barn that did not allow exposure to direct sunlight. Analysis of samples of feed obtained from the farm indicated inadequate quantities of calcium and phosphorus as well as a low ratio of these 2 nutrients. Serum and tissue concentrations of vitamin A were less than normal. Low serum calcium concentrations, high serum phosphorus concentrations, and high alkaline phosphatase and creatine kinase activities were compatible with low vitamin D concentrations.
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PMID:Seizures and acute death attributable to hypovitaminosis A and suspected hypovitaminosis D in feeder pigs. 849 85


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