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

The biochemical and behavioral effects of the anticonvulsant amino-oxyacetic acid (AOAA) have been studied in a model of focal penicillin seizures in rats. At 20 mg/Kg AOAA treatment results in a progressive 11 fold increase in GABA levels in cortex over three hours. There is a decrease in aspartate, ketoglutarate, alanine and glutamine, and an initial decrease followed by an increase in pyruvate and glutamate. These results reflect a functional inhibition of several B-6 dependent aminotransferase enzymes. When rats are pretreated 30 min before the onset of focal penicillin seizures there is a 60% reduction in the number of discharges and a 34% reduction in seizure duration. Pretreatment beyond 75 min results in progressively less anticonvulsant effect, such that seizures eventually become more severe than control. There is an increase in the number and duration of discharges, seizure spikes become complex, and tonic-clonic events develop. Penicillin seizures do not cause a change in levels of GABA, but result in a decrease in glutamate within the focus. AOAA pretreatment initially prevents this decrease in glutamate but later accentuates it. The biochemical effects of AOAA are complex, but biphasic anticonvulsant properties coincide in time with a change in the balance of excitatory and inhibitory amino acids in the seizure focus.
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PMID:Effect of amino-oxyacetic acid (AOAA) on focal penicillin seizures. 10 8

The purpose of this series of experiments was to understand how Clonazepam changes the mechanisms of synchronization in seizures. Penicillin was applied to the rabbits cortex. Interictal spikes and seizures were recorded with multiple electrodes from both the cortical surface and intracortically. The spatio-temporal relationships during these electrical events were studied by topographical methods. Moreover, power spectrum and coherence estimates were performed. A most characteristic feature seen with low doses of Clonazepam is a regularization of the spatio-temporal behaviour of both spikes and seizures. The number of tonic phases considerably increases at the cost of clonic phases. The seizures take more time to become generalized. The generator-zones become larger. This is explained by a decrease of the number of neurones--by Clonazepam--which are still left to produce "paroxysmal depolarization shifts". The findings confirm the increase of postsynaptic cortical inhibition under Clonazepam, as demonstrated by various authors.
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PMID:[The phenomenon of synchronization in the status epilepticus produced by penicillin and its changes after Clonazepam (author's transl)]. 40 96

Penicillin-induced epileptogenic foci in the cat hippocampus show a marked tendency for brief but periodic seizure discharges known as 'interictal spikes' (IS). Here, each IS is shown to be followed by a marked elevation and subsequent slow fall-off of the focal seizure threshold. The time constant of this process approximates the spontaneous inter-IS interval and these two parameters appear to vary in concert. The timing of the IS train is always reset by interjected ISs but not by stimuli that are subthreshold for the IS. In sum, this modulation of focal excitability does not appear to be imposed by local or projected rhythmic activity other than that initiated by the IS itself. The firing patterns of the majority of observed hippocampal single units in the vicinity of the focus show a prolonged suppression of spontaneous firing for from 2 to 10 sec or more after each IS, independent of whether the IS was spontaneous or elicited. A smaller number of units show delayed, intense activation following each IS. Both of these forms of response appear to originate from large cells in and near the pyramidal cell body layer. Assuming that these single unit data represent a sampling of pyramidal cell discharge, then the prevalence of a prolonged post-IS pause suggests that the rhythmicity of spontaneous penicillin foci derives from an inhibitory phasing of the population based paroxysmal activity. The periodic spontaneous IS discharge can be viewed, therefore, as a locally regulated, autorhythmic process impressed upon the activity of the neuronal population by the development of a functional suppression of unit activity following each IS.
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PMID:Autorhythmicity of spontaneous interictal spike discharge at hippocampal penicillin foci. 46 66

(1) Neurologic complications remain a significant problem in bacterial endocarditis. Of 218 patients with endocarditis, 84 (39%) had a neurologic complication and 58% of these 84 patients died. In contrast, the mortality rate was only 20% among those endocarditis patients without neurologic complications. (2) Of the neurologic complications, cerebral embolism is the most frequent and important. An embolic stroke occurred in 37 (17%) of our patients, with 30 of these patients dying. Emboli are important not only in terms of the direct morbidity and mortality they cause via cerebral infarction, but also because of their role in the causation of mycotic aneurysms, brain abscesses, and abnormal CSF formulae. (3) Cerebral emboli are particularly common in patients with mitral valve infection, and in patients with infection due to virulent organisms, particularly S. aureus and enteric gram-negative bacilli. (4) Mycotic aneurysms occur more frequently in the course of acute endocarditis rather than late in the course of subacute disease. Management of angiographically demonstrated mycotic aneurysms is dependent upon the presence or absence of hemorrhage, the anatomic location of the aneurysm, and the clinical course of the patient. Healing of mycotic aneurysms can occur during the course of effective antimicrobial therapy, thus obviating the need for neurosurgical intervention in all such patients. (5) Macroscopic brain abscess is a rare complication of bacterial endocarditis. Miliary microscopic abscesses are more common than larger abscesses, particularly in patients with acute disease and miliary infection in other organs of the body. (6) Focal seizures occur most commonly in endocarditis patients with acute embolic disease; generalized seizures are of diverse etiologies, with metabolic factors being most important. Penicillin neurotoxicity should be considered in patients with impaired renal function who are receiving high dose penicillin. (7) With the exception of hemorrhagic complications, lumbar puncture results tend to reflect the nature of the infecting organism rather than the nature of the neurologic complication. Endocarditis due to virulent organisms such as S. aureus is usually associated with a purulent CSF formula while nonvirulent organisms, such as viridans streptococci, susually have aseptic or normal CSF formulae.
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PMID:Neurologic complications of bacterial endocarditis. 58 Jul 94

Cases of penicillin-resistant pneumococcal meningitis have been reported in other countries since 1977, but never before reported in Taiwan. In 1990, two cases of the disease were diagnosed here. Case one was a two-year-old boy who had had fever and vomiting for several days prior to admission. Under the impression of meningitis, a spinal tap was done. The CSF yielded pneumococcus, which was misinterpreted as sensitive to penicillin. Penicillin (400,000 units/kg/day) was given parenterally without effect. On the 12th day after admission, another spinal tap still yielded pneumococcus. This time the sensitivity test was reread with great care, and then reported to be penicillin-resistant pneumococcus. Minimal inhibitory concentration (MIC) of penicillin was performed simultaneously and it revealed 0.1 microgram/ml. Vancomycin (60 mg/kg/day) was substituted for penicillin. The patient became afebrile two days later, and was discharged ten days later without sequelae. Case two, a five-month-old girl, was diagnosed to have meningitis because of fever, vomiting, tense fontanel and seizure on admission. After a spinal tap was done, she was put on ampicillin and cefotaxime. The fever subsided two days later. At that time, the CSF was reported to grow pneumococcus, again misread as sensitive to penicillin. The antibiotics was switched to penicillin, but fever recurred. The second spinal tap still yielded pneumococcus which was sensitive to penicillin but resitstant to oxacillin. Based on experience with the first case, penicillin was changed to vancomycin, and performed MIC immediately. The MIC was 1.0 microgram/ml. The patient became afebrile two days later, and was discharged in good condition after ten days of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Penicillin-resistant pneumococcal meningitis: report of two cases]. 177 62

We conducted a prospective, double-blind, placebo-controlled study in adult patients to determine whether prophylactic penicillin prevents infection in intraoral lacerations secondary to minor trauma or seizures. Uninfected full-thickness, mucosal-only, or through-and-through wounds presenting within 24 hours of injury were considered. Management consisted of cleansing, irrigation, debridement, and closure as indicated: no topical antibiotics were applied. Patients were randomly assigned to receive penicillin VK 500 mg or identically appearing placebo four times daily for five days. Home wound care was standardized and patients were followed for a minimum of four or five days. Infection was assessed clinically. Seventy-six patients were enrolled and 62 completed the study. Penicillin (30) and placebo (32) groups were similar in all parameters except wound etiology; assault was more common in the placebo group (P = .02). Two infections occurred in patients receiving penicillin, and six infections were seen among placebo-treated patients (P = .05, beta = 0.17). When patients poorly compliant with therapy were eliminated from analysis, none of the penicillin-treated patients and five of the placebo-treated patients developed infections (P = .027). Our data suggest that patients with intraoral wounds may benefit from prophylactic penicillin if compliant with their therapy. More studies are needed to further delineate the usefulness of prophylactic antibiotics for these wounds.
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PMID:Prophylactic penicillin for intraoral wounds. 250 38

Penicillin is well known as a potent convulsive agent. A cortical topical, intracerebral or systemic administration of penicillin produces abnormal and paroxysmal activity which may lead to seizure, and has been used in the investigation of the mechanisms of epilepsy. This is a report on the studies of an acute effect of potassium penicillin G on two models of experimental focal epilepsy: a) amygdaloid kindling model, and b) kainic acid-induced limbic seizure model. Twelve adult cats for amygdaloid kindling model (kindling group), six for KA-induced limbic seizure model (KA group) and four for a control group were prepared for this study. In kindling group, after completion of kindling procedure, 40-60 X 10(4) unit/kg of potassium penicillin G (PC), dissolved in sterilized normal saline, was injected intraperitoneally during an interictal period. In KA group, 1 micrograms of KA was injected into the left amygdala. Limbic seizures occurred frequently during the initial 5 hours but subsided completely within 3 days. After a latent period, spontaneous secondarily generalized convulsion occurred from 30 to 60 days after KA injection. The cats were completely normal in their behavior during the interictal period. During the interictal stage after the first generalized convulsion has been observed, 15-20 X 10(4) unit/kg of PC was injected intraperitoneally. In the control group, 40-60 X 10(4) unit/kg was injected intraperitoneally. Electroclinical observations were continued until 5 hours after PC injection in three groups. In the control group, no cats developed generalized convulsion. In the kindling group, 4 of 12 cats developed focal amygdaloid seizures with secondary generalization by nearly the identical doses required in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute effect of penicillin G on feline models of focal epilepsy]. 250 15

Five patients with seizures related to imipenem administration are described. The potential of imipenem therapy to cause seizure was further studied in a mouse model and compared with the potential for seizure with penicillin and cefotaxime therapy. Penicillin caused ataxia and seizure at a mean mouse serum level of 5800 microns/mL, cefotaxime at 3400 microns/mL, and imipenem at a much lower serum concentration of 1900 microns/mL. The potent activity of imipenem therapy against bacteria, allowing for a clinical dose of only 2 g/d, is unfortunately offset by its higher propensity to induce neurologic symptoms in humans and mice at much smaller doses than would therapy with penicillin G or the cephalosporins, such as cefotaxime.
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PMID:Seizure propensity with imipenem. 236 61

The objective of the study was to determine whether contemporary feline models of petit mal (systemic penicillin epilepsy) or temporal lobe epilepsy (amygdala kindling) resemble human seizure disorders with respect to disturbances of sleep and waking states, the state dependency of seizures, and transference of seizure susceptibility. These variables were examined in 6-h polygraphic recordings before and during exposure to both seizure models in 24 cats; 12 cats had intramuscular (i.m.) injections of 300,000 or 400,000 IU/kg of penicillin prior to kindling, and 12 were kindled before penicillin challenge. Results were as follows. First, penicillin increased light slow wave sleep (SWS) and drowsiness, during which spike-wave (SW) activity was maximal. Generalized tonic-clonic convulsions (GTCs) occurred predominantly in drowsiness after awakening from SWS. Second, kindling produced more deep SWS than did penicillin; susceptibility to kindled GTCs peaked during deep SWS, especially in transition to rapid eye movement sleep (REM). Third, penicillin did not influence subsequent sleep disorders or seizure susceptibility during kindling; kindling interfered with penicillin-induced GTCs, SW activity, and sleep disorders. Collectively, the findings suggest distinct state disorders and state-dependent seizure profiles in the two models. These differences parallel human analogues and may have contributed to the transference results. Kindling is a chronic model with persistent sleep and seizure abnormalities that differ from and may have discouraged penicillin epilepsy. Penicillin is an acute model with transient state and seizure disorders, a fact that may account for the absence of penicillin transference to kindling.
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PMID:Differences between two feline epilepsy models in sleep and waking state disorders, state dependency of seizures and seizure susceptibility: amygdala kindling interferes with systemic penicillin epilepsy. 311 27

gamma-Hydroxybutyrate (GHB) produces a constellation of EEG and behavioral events that respond selectively to antiabsence antiepileptic drugs. The GHB-induced seizure was quantitated in the presence of three other absence seizure models: pentylenetetrazole, systemic penicillin, and the flash evoked afterdischarge (FEAD). Penicillin and pentylenetetrazole produced a significant prolongation of GHB-induced seizure in a dose-dependent fashion. This potentiation of GHB seizure was observed when these compounds were given either before administration of gamma-butyrolactone (GBL), the prodrug of GHB, or at the onset of GHB-induced seizure. Photic stimulation given in a manner to produce FEAD also resulted in a significant prolongation of GHB-induced seizure. All of these maneuvers lowered the threshold to GHB seizure, but none interfered with the brain kinetics of GHB in the animals treated with GBL. Ethosuximide pretreatment significantly shortened the GHB seizure and overcame the potentiating effect of penicillin and pentylenetetrazole in this model. These data confirm the GHB-treated animal as a model of generalized absence seizure. The GHB model meets appropriate criteria for an absence seizure model and compares favorably with other models of absence currently in use.
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PMID:gamma-Hydroxybutyrate model of generalized absence seizures: further characterization and comparison with other absence models. 339 Nov 42


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