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

To determine what effect the addition of epinephrine has on bupivacaine toxicity, toxic doses of bupivacaine were administered to awake spontaneously breathing pigs. Twenty animals were randomized to one of two groups. One group received an infusion of bupivacaine with epinephrine (5 micrograms/ml) at a rate of 2 mg.kg-1.min-1; the other received an infusion of plain bupivacaine at the same rate. Bupivacaine infusion was continued until cardiovascular collapse. Following cardiovascular collapse we attempted to resuscitate the animals via open chest cardiac massage and a standardized resuscitation protocol. The addition of epinephrine to bupivacaine significantly increased blood pressure and systemic vascular resistance but not heart rate or cardiac output early in the bupivacaine infusion. Epinephrine had no effect on the dose of bupivacaine that caused cardiovascular collapse (P = 0.1), on the plasma concentration of bupivacaine at collapse (P = 0.9), or on the ability to resuscitate animals following cardiovascular collapse. The addition of epinephrine decreased the dose of bupivacaine required to initiate cardiac dysrhythmias (P = 0.003). The first dysrhythmia experienced by the epinephrine group was second degree heart block, which contrasts with the premature ventricular and atrial dysrhythmias experienced by the plain group. The dose of bupivacaine that produced seizures was also reduced by the addition of epinephrine (P = 0.006). The addition of epinephrine to bupivacaine did not alter the dose of bupivacaine that caused cardiovascular collapse in awake spontaneously breathing pigs but did decrease the dose of bupivacaine that caused seizures and dysrhythmias.
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PMID:Effect of epinephrine on central nervous system and cardiovascular system toxicity of bupivacaine in pigs. 281 65

During a one-month period, two cases of beta-adrenergic blocker overdose were treated by the emergency staff at our hospital. One case of propranolol intoxication demonstrated profound cardiovascular collapse and generalized tonic-clonic seizures. The condition failed to respond to high-dose intravenous pressor agents, but did improve significantly with IV glucagon infusion. The second overdose involved atenolol. Although the blood levels reported were very high, the patient showed no cardiovascular compromise and required only inhaled bronchodilators for an exacerbation of her asthma.
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PMID:Beta blocker overdose with propranolol and with atenolol. 285 42

Antihistamines are being increasingly administered in combination with various other agents, with adverse drug reactions the frequent result. The present study consisted of two experiments. Experiment 1 examined the toxicological response of rats to nicotine tartrate (0.0, 2.0, 4.0, and 8.0 mg/kg) in combination with either of two H1-histamine receptor antagonists, the ethylene diamine tripelennamine HCl (0.0, 16.0, 32.0, and 64.0 mg/kg) or the aminoethyl ether diphenhydramine HCl (0.0, 32.0, 64.0, and 96.0 mg/kg). Adult female rats received intraperitoneal injections when housed 12 per cage and toxicological response (number dead per group) was assessed 24 hours post-treatment. The results showed that over the dose ranges employed, and when given alone, nicotine was completely non-lethal, tripelennamine was virtually non-lethal and diphenhydramine was toxic only at the highest dose (5 of 12, at 96.0 mg/kg). However, when nicotine and the antihistamines were delivered in combinations, the toxicological response was markedly altered. Tripelennamine in combination with nicotine yielded supra-additive interaction, with the degree of potentiation being a simple linear function of nicotine within each dose of tripelennamine. The interaction between nicotine and diphenhydramine was more complicated, with certain dose combinations yielding supra-additivity, yet with others yielding antagonism. It was suggested that seizure-precipitated cardiopulmonary collapse was the immediate cause of death, plausibly mediated by central mechanisms. As such, Experiment 2 examined the influence of adding the proconvulsant pentylenetetrazole (PTZ) (0.0, 10.0, and 20.0 mg/kg) to nicotine (0.0, 2.0, 4.0, and 8.0 mg/kg)-tripelennamine (0.0 and 32.0 mg/kg) combination treatments. Effects were assessed both at 1.0 and 24.0 hours post-injection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Supra-additive toxic interaction of nicotine with antihistamines, and enhancement by the proconvulsant pentylenetetrazole. 285 8

In our previous studies, we hypothesized that activation and subsequent collapse of GABA-mediated inhibition during tetanus is an important seizure-triggering mechanism in the kindled epileptogenic focus. To examine this hypothesis, in the present study, we investigated the effects of pharmacological manipulations of the kindled amygdala with several drugs, and measured the kindled seizures as well as the EEG events during tetanus. The results obtained were: (i) The selective GABA-A agonist, muscimol (1 and 5 nM/1 microliter), suppressed kindled seizures in a dose-dependent fashion, and the 5 nM muscimol significantly prolonged EEG suppression and reduced the number of oscillations in the subsequent rhythmic synchronous discharge. Similar effects followed systemic injection of diazepam (2 mg/kg). (ii) The selective GABA-B agonist, baclofen (5 nM), had no effect on kindled seizures nor on the EEG events during tetanus. (iii) The NMDA antagonist, 2-amino-5-phosphonovaleric acid (80 nM), significantly reduced the afterdischarge duration and significantly delayed the appearance of the rhythmic synchronous discharge. However, these effects were not observed immediately, but 24 to 72 h after microinjection. (iv) The muscarinic cholinergic antagonist, atropine (40 and 80 nM), suppressed kindled seizures in a dose-dependent fashion, but the atropine caused marked synchronous discharge both in the awake resting EEG and during tetanic stimulation. We conclude that the GABA-A system, including the benzodiazepine system, is more involved in the seizure-triggering mechanism of amygdala kindling than the GABA-B system, that there is an interaction between the GABA-A and NMDA system, and that the cholinergic participation is independent of the primary seizure-triggering mechanisms.
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PMID:Kindling-induced changes in EEG recorded during stimulation from the site of stimulation. III. Direct pharmacological manipulations of the kindled amygdala. 288 27

To determine the effect of benzodiazepine premedication on central nervous system and cardiovascular effects of bupivacaine, the authors administered toxic doses of bupivacaine to awake spontaneously breathing pigs after intravenous premedication with midazolam (0.06 mg/kg), diazepam (0.15 mg/kg), or saline. Five minutes after administration of one of these solutions, they began an infusion of bupivacaine at 2 mg.kg-1.min-1. The bupivacaine infusion was continued until cardiovascular collapse. They then attempted to resuscitate the animals via open chest cardiac massage and a standard resuscitation protocol. Premedication with midazolam or diazepam significantly delayed the onset of ventricular dysrhythmias (P less than 0.05), decreased the incidence of seizures (P less than 0.05), and prevented the increase in blood pressure and heart rate following bupivacaine infusion (P less than 0.05). Benzodiazepine premedication did not affect the dose of bupivacaine or the blood concentration required to produce cardiovascular collapse. The ability to resuscitate animals premedicated with midazolam did not differ from control; however, significantly fewer animals premedicated with diazepam were resuscitated (P less than 0.05). A clinically relevant observation was that almost all animals premedicated with a benzodiazepine progressed directly to cardiovascular collapse without first manifesting seizures.
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PMID:Effect of midazolam and diazepam premedication on central nervous system and cardiovascular toxicity of bupivacaine in pigs. 291 66

Effects of brevetoxin were evaluated in cats anesthetized with pentobarbital under conditions of controlled end-expiratory pCO2 and constant body temperature. Recordings were made of arterial blood pressure, heart rate, respiratory pattern, diaphragm EMG, evoked tibialis muscle twitch and evoked contraction of the nictitating membrane. Electrical stimulation was employed for periodic excitation of the medullary respiratory center, the phrenic nerve, the peroneal nerve and the cervical sympathetic nerve. Brevetoxin was prepared at a concentration of 1.0 mg/ml in an aqueous medium of 2.5% ethanol plus 2.5% Emulphor 620 (General Aniline and Film Corp., New York). Small i.v. bolus injections of the toxin (40 micrograms/kg) evoked, without tachyphylaxis, the Bezold-Jarisch reflex triad of bradycardia, hypotension and bradypnea. This effect was essentially abolished by vagotomy. Continued injections then resulted in pressor reactions and tachycardia, along with the development of respiratory dysrhythmia. Large doses of brevetoxin (160 micrograms/kg i.v.) caused somatomotor seizures accompanied by severe hypertension, that occurred even after decerebration and cervical spinal cord transection. Cranial intra-arterial and intra-cerebroventricular injections of brevetoxin produced hypertension and respiratory depression more effectively than did i.v. injections. Systemic cumulation of the toxin, with the respiration supported artificially, caused death from cardiovascular collapse, without significant blockade of neuromuscular and ganglionic transmission. It is concluded that brevetoxin exerts its major toxic effects on the circulation and respiration through reflex and central actions, largely sparing peripheral motor mechanisms.
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PMID:Neurological analysis of respiratory, cardiovascular and neuromuscular effects of brevetoxin in cats. 299 23

A 1-year study of the etiology of acute diarrhea complicated by severe (10%) dehydration, active bleeding, shock and cardiovascular collapse, pneumonia, acute renal failure, or seizures in infants under 18 months of age was performed in Cairo, Egypt. Of 145 infants, 19 (13%) died or left the hospital moribund; the remaining 126 patients were classified as having potentially fatal illness. A variety of enteropathogens were identified with approximately equal frequency in the fatal and nonfatal complicated cases as well as in 135 controls with severe uncomplicated diarrhea. The agents most frequently detected in infants with severe diarrhea in this population which were felt to be etiologically important were rotavirus (33%), heat-stable enterotoxin-producing Escherichia coli (20%), heat-labile enterotoxin-producing E. coli (11%), enteropathogenic E. coli (8%), and Salmonella spp. (5%). The high rate of occurrence of Giardia lamblia (35%) probably represented the high carriage rate of the protozoan in this population. Complicated (fatal and potentially fatal) cases differed from control cases in a number of ways: the onset of diarrhea was more sudden, the course was progressive and of greater initial intensity, vomiting occurred more frequently, the patients more often had visited another physician before coming to the hospital, the patients more often had respiratory symptoms and pulmonary abnormalities on auscultation, hypoactive bowel sounds and abdominal distention were more common, as was oliguria, and the patients showed lower mean body weights.
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PMID:Detection of enteropathogens in fatal and potentially fatal diarrhea in Cairo, Egypt. 302 41

A review of 15 cases of pancreas transplantation at the Presbyterian University Hospital in Pittsburgh showed that all of the neurologic complications occurred outside of the pancreas transplantation surgery itself. Major CNS complications included hypoxic encephalopathy (20 per cent), cerebral and spinal-cord infarction (7 per cent), and seizures (13 per cent). These appeared to be closely associated with cardiovascular collapse or cardiac arrest that often occurred following septic, hemorrhagic, or additional surgical-anesthetic stresses, removed in time from the transplantation. When patients who died of sudden cardiorespiratory arrest were included, the overall frequency of global cerebral ischemia was 33 per cent. The occurrence of herpes zoster neuritis (13 per cent) was contrasted with the lack of CNS infections. The possible associations of visual hallucinations with cyclosporine therapy (7 per cent), CSF pleocytosis with OKT3 therapy (7 per cent), and compressive neuropathy with operative-anesthetic monitoring (7 per cent) were discussed in relation to previous reports in the literature. Randomized controlled clinical studies were suggested to distinguish more clearly the complications due to pancreas transplantation from those due to the natural history of the underlying diabetes and to distinguish the beneficial and adverse effects of pancreas transplants from those of coexisting renal transplants.
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PMID:Neurologic complications of pancreas transplants. 304 46

We report the neuropathologic findings in a 63-year-old white male with a history of birth asphyxia, cerebral palsy, seizures and mild mental retardation in conjunction with similar brain pathologic findings in animal models of perinatal asphyxia. The human case showed a left cerebral hemispheric hemiatrophy associated with an extensive ulegyria involving all cerebral lobes on that side and a single microscopic focus of cortical atrophy in the right hemisphere. Among a large number of experimental perinatal asphyctic exposures only an occasional animal, like the human case described, showed unilateral hemispheric injury with softening and necrosis if examined early and ulegyria with hemispheric hemiatrophy if examined late. The present paper suggests that perinatal asphyxia under specific pathophysiologic conditions may cause unilateral brain injury. Our experimental studies suggest the specific condition of perinatal asphyxia potentially causing unilateral or asymmetrical brain damage is marked hypoxemia combined with substantial reductions in blood pressure but without circulatory collapse. Given these conditions, the asymmetry of the brain damage likely reflects fetal head position within the gravitational field relative to the heart. With disturbed cerebral blood flow autoregulation from asphyxia, the gravitational field likely accentuates the ischemia of those brain areas most elevated above the level of the heart. Thus, we postulate head position may play a pivotal role in defining brain regions that are damaged in hypotensive perinatal asphyxia. This interpretation may affect the intensive care of hypoxemic, hypotensive newborns aimed at minimizing the risk of brain damage.
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PMID:Cerebral hemiatrophy--correlation of human with animal experimental data. 325 12

The authors report a retrospective study of 11 cases of malignant hyperthermia. The mean age of the patients was 5 months and 3 weeks. Clinical features included severe hyperthermia (greater than 41 degrees C), seizures, coma, collapse, rhabdomyolysis, acute renal failure and functional renal failure. Three infants died. Four patients presented neurological damages. Four recovered fully. The authors discuss the difficulties of diagnosis, the nosological position and the pathophysiology of this syndrome.
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PMID:[Severe hyperthermia syndrome in the infant. Apropos of 11 cases]. 367 Oct 30


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