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

Deaths from tricyclic antidepressant (TCA) overdose are usually due to arrhythmias and/or hypotension. Tricyclic antidepressant toxicity is due mainly to the quinidine-like actions of these drugs on cardiac tissues. Slowing of phase 0 depolarisation of the action potential results in slowing of conduction through the His-Purkinje system and myocardium. Slowed impulse conduction is responsible for QRS prolongation and atrioventricular block, and contributes to ventricular arrhythmias and hypotension. Therapies that improve conduction, e.g. hypertonic sodium bicarbonate, are useful in treating these toxic effects. Other mechanisms contributing to arrhythmias include abnormal repolarisation, impaired automaticity, cholinergic blockade and inhibition of neuronal catecholamine uptake. Toxicity may be worsened by acidaemia, hypotension or hyperthermia. Sinus tachycardia is due to the anticholinergic effects of the tricyclic antidepressants as well as blockade of neuronal catecholamine reuptake. Sinus tachycardia is generally well-tolerated and requires no therapy. Sinus tachycardia with QRS prolongation may be difficult to distinguish from ventricular tachycardia. Electrocardiograms obtained using oesophageal or atrial electrodes may be useful in determining the relationship of atrial and ventricular activity. Although QRS prolongation alone is not compromising, it is a marker for patients at highest risk of developing seizures, arrhythmias or hypotension. Ventricular tachycardia (monomorphic) is a consequence of impaired myocardial depolarisation and impulse conduction. Hypertonic sodium bicarbonate may partially correct impaired conduction and be of benefit in treating ventricular tachycardia. Since hypertonic sodium bicarbonate appears to act by increasing the extracellular sodium concentration as well as by increasing extracellular pH, hyperventilation may be less effective. Hypertonic sodium bicarbonate is of particular benefit in patients who are acidotic, since acidosis aggravates cardiac toxicity. However, administration of hypertonic sodium bicarbonate is beneficial even when blood pH is normal. Lignocaine (lidocaine) may be useful in treating ventricular tachycardia but should be administered cautiously to avoid precipitating seizures. Ventricular bradyarrhythmias are due to impaired automaticity or depressed atrioventricular conduction and can be treated by placement of a temporary pacemaker, or with a chronotropic agent, e.g. isoprenaline (isoproterenol), with or without concomitant vasoconstrictors.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Tricyclic antidepressant poisoning. Management of arrhythmias. 378 39

Lidocaine is absorbed from mucous membranes of the oropharynx, gastrointestinal tract, and tracheobronchial tree. First-pass hepatic metabolism of the drug greatly reduces the amount reaching the general systemic circulation in the normal individual. In patients whose hepatic metabolism is reduced by disease or drugs, or in whom liver blood flow is reduced, this first-pass effect is decreased and lidocaine concentrations may be higher than those produced by the same dose in normal patients. We report an elderly man taking cimetidine with congestive heart failure in whom the accidental ingestion of lidocaine solution for esophageal anesthesia was followed by seizures and elevated serum lidocaine concentrations.
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PMID:Seizures following oral lidocaine for esophageal anesthesia. 397 59

A 30-month-old female infant had a cardiopulmonary arrest due to viscous lidocaine. The protective airway mechanisms were blunted by this drug, resulting in aspiration, hypoxia, seizures, and death. Lidocaine has also been associated with respiratory depression, psychosis, methemoglobinemia, and toxic cardiovascular reactions. We do not recommend the use of viscous lidocaine for minor oral irritation in infants and young children.
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PMID:Cardiopulmonary arrest due to misuse of viscous lidocaine. 405 69

All adult cardiopulmonary resuscitations attended by the pharmacy department at a 486-bed tertiary-care institution were analyzed over a 24-month period. Data describing patient demographics, drug and equipment use, and patient survival were collected on 516 consecutive adult arrests. These data were recorded on a report form by a pharmacy technician and were classified as cardiac, respiratory, trauma, or other. Trauma included arrests caused by motor-vehicle accidents and gunshot wounds, and other included arrests caused by anaphylaxis or seizures. The majority of arrests (70%) were classified as cardiac, 24% as respiratory, and 6% as other. Overall, 54.5% of the patients suffering from arrests were resuscitated successfully. There was an equal distribution of arrests throughout the day. The mean duration of the resuscitation efforts was 38 minutes with a trend toward greater patient survival when resuscitation efforts lasted less than 15 minutes. Arterial blood-gas determinations were made in 81% of the arrests, defibrillations in 40%, and pacemaker or chest tube insertion in less than 10%. Sodium bicarbonate was the most frequently administered medication, followed by calcium salts and atropine sulfate. Lidocaine was used in 83% of the cases requiring antiarrhythmic therapy. Pressor support was required in 44.6% of the cases; norepinephrine bitartrate was the first-line pressor agent. Drugs not categorized as essential according to the American Heart Association's Advanced Cardiac Life Support (ACLS) standards were administered infrequently. Hospitals may benefit from arrest data in assessing their equipment and supply needs, staffing patterns, and personnel training programs.
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PMID:Evaluation of 516 cardiopulmonary resuscitation attempts. 407 65

Lidocaine and procaine seizure thresholds were studied. The i.p. median convulsant dose (CD50) of lidocaine and procaine with saline pre-treatment was 95 and 240 mg/kg, respectively. Dopamine depletion by pre-treatment with d1-alpha-methyl-p-tyrosine plus dihydroxyphenylserine resulted in a significant drop of CD50 to 69 and 175 mg/kg for lidocaine and procaine, respectively. Serotonin depletion by pre-treatment with p-chlorophenylalanine resulted in a significant drop of CD50 to 68 mg/kg for lidocaine, but no significant change for procaine.
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PMID:Alteration of lidocaine- or procaine-induced convulsions by manipulation of brain amines. 645 Jul 81

Daily administration of lidocaine results in progressive increases in frequency and duration of convulsions in response to a dose of drug which was previously subconvulsive--a pharmacological kindling phenomenon. The effects of such lidocaine-kindling on local cerebral glucose utilization were determined by the 2-[14C]deoxyglucose method. Lidocaine-treated animals, in the absence of convulsions, exhibited decreased glucose utilization in most brain structures compared to saline-treated animals and showed no increase in aggressive behavior. In animals displaying lidocaine-kindled convulsions there were marked increases in glucose utilization in either the hippocampus and amygdala or in perirhinal cortical areas during the seizure administration; these animals also displayed long-lasting increases in irritable behavior. Seizure duration was positively correlated with the rate of glucose utilization in the hippocampus, amygdala and septum, but inversely correlated in several non-limbic areas. These data suggest that lidocaine-kindled seizures are highly localized to limbic and perirhinal structures and are associated with important behavioral consequences.
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PMID:Metabolic and behavioral consequences of lidocaine-kindled seizures. 654 25

The authors investigated the value of high-dose thiopental (TH) therapy after 16-min complete global brain ischemia (GBI) in three groups of pigtailed monkeys, using a neck cuff model of GBI with 96 h intensive care postischemia (PI). Control group (n18): Normotension was restored within 2 min PI; paralysis/controlled ventilation was maintained for 48 h PI with 50% N2O/O2. Thiopental loading group (n13): Control treatment plus TH-loading with 90 mg/kg iv given from 5 to 65 min PI (mean peak TH plasma level 130 micrograms/ml). Thiopental anesthesia group (n14): Control treatment plus TH anesthesia with 90 mg/kg iv given over 12 h PI (sustained TH plasma levels of 25-35 micrograms/ml and EEG burst suppression). Norepinephrine requirement for blood pressure control PI was greater in the TH groups than in the control group (P less than 0.05). Lidocaine was needed for control of arrhythmias in the TH loading group. There was no significant difference in mortality or neurologic outcome between the groups. At 96 h PI seven of 11 animals were awake in the control group, compared with seven of 12 and six of 12 in the two TH groups. Neurologic deficit scores (NDS) for the survivors at 96 h PI were 23 +/- 6% (mean +/- SD) (n10) in the control group, compared with 25 +/- 9% (n11) and 26 +/- 12% (n10) in the two TH groups (NDS 100% = brain death, 0% = normal). Seizures PI (in 1-2 of each group) were associated with worse neurologic deficits.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thiopental treatment after global brain ischemia in pigtailed monkeys. 669 50

A case is reported of an infant who experienced seizures while being treated with a topical lidocaine 2% solution (Xylocaine 2% Viscous) for teething. The pharmacology of lidocaine is reviewed to alert physicians to the potential dangers of topical mucosal application of these preparations.
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PMID:Lidocaine toxicity from topical mucosal application. With a review of the clinical pharmacology of lidocaine. 682 63

The effects of several excitant-convulsants, cataleptic anesthetics, and gamma-acetylenic gamma-aminobutyric acid (GABA) were tested on seizures kindled by repetitive electrical stimulation of the motor cortex in the rat. A dose response was determined for each drug. For most of the drugs, the doses tested ranged from those causing some signs of behavioral excitation to those inducing epileptoid activity. None of the excitant-convulsants, including strychnine, physostigmine, amphetamine, bicuculline, or pentylenetetrazol, increased the afterdischarge duration (AD) or behavioral response (BR) of the partially developed (PD-KCS) or generalized fully developed (KCS) kindled cortical seizures. Whereas pentylenetetrazol had no effect on the PD-KCS, it has been previously shown to increase significantly the AD and BR of the developing or partially developed amygdaloid kindled seizures. Lidocaine, gamma-butyrolactone, gamma-acetylenic GABA, phencyclidine, and ketamine inhibited the AD of the KCS by greater than or equal to 80%. Lidocaine, phencyclidine, and ketamine decreased whereas gamma-butyrolactone and gamma-acetylenic GABA increased the AD of the PD-KCS. The ability of gamma-butyrolactone and gamma-acetylenic GABA to potentiate the PD-KCS while inhibiting the KCS presents a paradox not readily explained. Our results combined with previous reports of the effects of gamma-butyrolactone and gamma-acetylenic GABA on amygdaloid kindled seizures indicate that the KCS is more susceptible to GABAnergic and cataleptic inhibition than is the fully developed amygdaloid kindled seizures. The differences between the response of cortical kindled and that of amygdaloid kindled seizures to some of the drugs tested may indicate differences in the physiological and biochemical mechanisms involved in producing these seizures.
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PMID:Cortical kindled seizures: modification by excitant and depressant drugs. 685 67

Lidocaine was infused at a fixed zero-order rate to eight healthy mongrel dogs until tonic extension (n = 5) and cortical seizures (n = 7) were produced. Lidocaine concentrations determined at 5-min intervals were used to calculate concentrations at which these effects occurred. The tonic extension phase occurred at a mean lidocaine concentration of 8.21 +/- 1.69 micrograms/ml. After a 1-month rest period, the same dogs were anaesthetized and ventricular tachycardia was produced by administering ouabain. Lidocaine was again infused at a fixed zero-order rate until all beats of ventricular origin were abolished. This occurred at a mean lidocaine concentration of 6.25 +/- 1.49 micrograms/ml.
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PMID:Determination of lidocaine concentrations producing therapeutic and toxic effects in dogs. 688 36


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