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

In experiments on albino mice with pentylenetetrazol convulsions it has been found that GABA, introduced intracerebroventricularly in a dose of 100 microgram/mouse, has a marked anticonvulsive effect. Scopolamine in doses of 1, 10 and 50 mg/kg i. p. does not influence significantly the convulsive-seizure reactions, while spasmolytin inhibits them only in large doses (80 mg/kg weight). The inhibitory effect of GABA does not change significantly on the background of scopolamine, while spasmolytin in a dose of 50 mg/kg (and to a lesser extent 80 mg/kg) antagonizes the inhibitory effect of GABA. Arecoline in doses of 1 and 10 mg/kg inhibits to a certain extent the convulsive-seizure reactions, and in doses of 10 mg/kg it potentiates the effect of GABA. Physostigmine in doses of 0.1 and 0.5 mg/kg has no significant effect, while in a dose of 0.3 mg/kg its effect is inhibitory. On the background of the two higher physostigmine doses, however, the anticonvulsive effect of GABA is markedly decreased. The results show that changes in the functional activity level of the brain cholinergic systems lead to changes in the inhibitory effect of GABA on the convulsive reactivity. The mechanisms of these correlations are complex. However, the results are in support of the view that the balance between the different neurotransmitter systems in the brain and not a separate specifically responsible neurotransmitter system, are of decisive significance for the convulsive excitability and reactivity.
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PMID:On some relationships between gamma-aminobutyric acid (GABA) and the cholinergic mechanisms in pentylenetetrazol convulsions. 61 63

A total of 103 cases of amitriptyline (AT) overdose (group 1) and 81 cases of overdose with a fixed combination of AT and chlordiazepoxide (CDE) (group 2), treated at our Intensive Care Unit or reported to our Poison Information Center between 1985-1990, were evaluated with respect to clinical course, symptoms and outcome, as well as efficacy of therapy. The mean amount of AT was considerably higher in group 1 compared to group 2 (13 mg kg-1 vs 7.7 mg kg-1). The most frequent symptoms in both groups were impaired consciousness, anticholinergic symptoms, seizures, arrhythmia and hypotension. Respiratory insufficiency necessitated respirator therapy in 63 of the patients. Two patients in group 1 and one patient in group 2 did not survive. Therapy included primary detoxification by gastric lavage and repeated administration of activated charcoal. In four of eight patients with cardiac conduction disturbances, hypertonic sodium bicarbonate led to a significant reduction in QRS duration and AV interval. Physostigmine was effective in eight of 14 patients with pronounced anticholinergic symptoms. No effect was observed in the other six patients. Haemoperfusion, which was performed in five patients, led to rapid improvement of coma after initiation of therapy in four patients. The clinical efficacy of haemoperfusion in AT overdose despite the high volume of distribution of AT deserves further investigation. The rather high average overdose of AT implies that large package sizes of AT were available to the patients. A major step towards prevention of serious AT overdose would be the prescription of package sizes containing a total of less than 500 mg AT.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical course, therapy, outcome and analytical data in amitriptyline and combined amitriptyline/chlordiazepoxide overdose. 136 Nov 33

Male Sprague-Dawley rats received LiCl (5 mEq/kg; sc) or saline 24 h prior to injection of cholinomimetics. Physostigmine (PHY, 0.54-0.80 mg/kg), diisopropylfluorophosphate (DFP, 1.3-2.5 mg/kg), pilocarpine (PIL, 23-30 mg/kg), or saline was injected subcutaneously at time 0. Rats were observed for seizure activity for 2 h, survivors were killed 24 h later and edema was measured in samples from parietal and piriform cortices, dorsal thalmus, and hippocampus. None of the rats pretreated with saline had seizures when given doses of cholinomimetics alone. However, rats pretreated with LiCl had the following incidence of seizures: PHY 68%, DFP 71% and PIL 100%. Rats given cholinomimetic agents alone did not have brain edema. In contrast, all LiCl-pretreated rats that seized had pronounced brain edema which was greatest in the piriform cortex. Thus, these studies demonstrate that LiCl pretreatment potentiates cholinomimetic-induced seizures. Further, cholinomimetic-induced seizures produce brain changes resulting in edema.
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PMID:Effect of LiCl pretreatment on cholinomimetic-induced seizures and seizure-induced brain edema in rats. 216 59

In order to clearing the influence of neurotransmitters in concussive unconsciousness, immediate convulsion and mortality, the following experiments were performed. Awake male mice of dd-strain were restrained and subjected to head injury using a bakelite weight of 30 gm dropped from a height of 20 cm on to the skull. This injury resulted in immediate loss of consciousness in 100%, convulsive seizure in 66% and death in 30% of animals. The severity of consciousness disturbance was evaluated by two parameters; (1) time interval required for the recovery of righting reflex (RR) and (2) time interval for the recovery of spontaneous movement (SM). Agonist or antagonist of various neurotransmitters was given intraperitoneally 0.5 or 2 hours before injury. The following results were obtained although some of them were statistically not significant. Physostigmine shortened both RR (p less than 0.1) and SM (p less than 0.01), whereas scopolamine did not change these intervals. Atropine sulfate shortened both of them. Nevertheless, atropine methylbromide, which dose not pass through blood-brain-barrier, also had same effects. Methamphetamine shortened both RR (p less than 0.1) and SM (p less than 0.05), whereas haloperidol prolonged these intervals. 5-HTP shortened RR (p less than 0.05), but prolonged SM (p less than 0.1). Methysergide shortened both RR (p less than 0.05) and SM (p less than 0.01). Convulsive seizure was suppressed by physostigmine (p less than 0.01) or 5-HTP (p less than 0.20). These results suggested that suppression of dopaminergic and cholinergic systems, and/or activation of serotonergic system contribute to concussive unconsciousness.
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PMID:[The influences of neurotransmitters on the traumatic unconsciousness, immediate convulsion and mortality in the experimental mice model]. 289 33

Enuresis is a common problem often treated effectively with imipramine hydrochloride. The usefulness of this therapy carries with it, however, the risk of accidental overdose by younger siblings of these enuretic patients. Traditional support measures are effective in the treatment of the mild to moderate overdose, while separate symptomatic treatment of seizures and cardiac arrhythmias is possible as outlined herein. Physostigmine offers a single alternate treatment which is effective in the full panorama of life-threatening manifestations of an imipramine overdose.
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PMID:Treatment of imipramine overdose in children. 626 68

Self poisoning with maprotiline was studied in 41 patients (43 episodes) consecutively admitted to an intensive care unit. Thirty five patients had taken more than one drug or alcohol. Fifteen patients were in coma grade III or IV; 17 patients were still not conscious after 24 hours in the intensive care unit. Among six patients given ventilation the mean duration of ventilation in the five who recovered was 36 hours. Three patients had a cardiorespiratory arrest, and one patient died. Twenty eight patients had a QRS interval of 100 ms or more, and 15 patients had seizures. In six patients seizures were precipitated by physostigmine. Cardiotoxicity after overdosage of maprotiline is equal to if not greater than that found after overdosage of conventional tricyclic antidepressants. Overdosage of maprotiline is more often associated with seizures than overdosage with tricyclic antidepressants. Physostigmine further increases the risk of seizures and should not be used in cases of overdosage of maprotiline.
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PMID:Effects of self poisoning with maprotiline. 642 94

Effects of intravenous cholinergic and dopaminergic agents on pre-cocaine olfactory bulb (OB) spindling and behavioral arousal, and on cocaine-induced OB-amygdala spindling and behavioral seizures were evaluated in seven cats with stereotaxically implanted electrodes. Spindle data were computer analyzed using a special program for spindle detection and averaging. The number, duration and amplitude of pre-cocaine OB spindles were increased by physostigmine and decreased by atropine. Physostigmine augmented pre-cocaine behavioral arousal levels and this effect was associated with the absence of cocaine seizures. Cocaine-induced amygdala spindle number was increased by physostigmine. Changes in seizure duration following cholinergic drugs suggest cholinergic inhibitory effects. These data, in accord with previous studies showing cholinergic effects on reticulocortical arousal and seizures, suggest a cholinergic mechanism which is excitatory on OB-amygdala arousal spindling and inhibitory on cocaine-induced seizures.
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PMID:Cholinergic effects on arousal and cocaine-induced olfactory-amygdala spindling and seizures in cats. 665 67

Physostigmine is a commonly used therapy for the anticholinergic manifestations of tricyclic antidepressant (TCA) overdose. We describe two patients with TCA toxicity who developed asystole following the administration of physostigmine to treat seizures.
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PMID:Asystole complicating physostigmine treatment of tricyclic antidepressant overdose. 700 62

The influence of some noradrenergic, 5-hydroxytryptaminergic and cholinergic agents on imipramine-induced seizures were investigated in mice. DL-threo-3,4-dihydroxyphenylserine (DOPS) and pargyline significantly potentiated imipramine-induced seizures. Phentolamine and prazosin significantly attenuated seizures elicited by imipramine and significantly attenuated the seizure-enhancing effect of DOPs. alpha-Methyl-p-tyrosine and reserpine significantly attenuated seizures induced by imipramine. Disulfiram significantly protected mice against imipramine-induced seizures. However, DOPS significantly potentiated seizures induced by imipramine in disulfiram-pretreated animals. Clonidine effectively protected mice against imipramine-induced seizures. Idazoxan, on the other hand, significantly potentiated seizures induced by imipramine and significantly antagonised the protective effect of clonidine against the seizures. 5-HTP, PCPA, cyproheptadine, mianserin, ketanserin and trazodone did not affect imipramine-induced seizures to any significant extent. Physostigmine antagonised seizures induced by imipramine while atropine significantly potentiated the seizures, and significantly attenuated the protective effect of physostigmine against the seizures. These data suggest that enhancement and attenuation of central noradrenergic and cholinergic neurotransmissions respectively, and not 5-HT mechanisms, may underlie imipramine-induced seizures in mice.
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PMID:The involvement of noradrenaline, 5-hydroxytryptamine and acetylcholine in imipramine-induced seizures in mice. 822 1

In modern anaesthesia various antagonists are used. They provide efficient tools to facilitate better control of pharmacological effects and side effects of drugs routinely used in anaesthesia. Naloxone is a competitive antagonist of opioids without any intrinsic activity. It counteracts respiratory depression, pruritus, sedation and analgesia caused by opioids. It is fast-acting with a duration of action of 45 to 90 min. Several investigators have reported severe side effects of naloxone including hypertension, tachyarrhythmias, left heart failure and cardiac arrest, and hence the use of naloxone must be carefully considered in every single patient. Flumazenil is a competitive antagonist of benzodiazepines. It is a remarkably safe drug and very effective to terminate all benzodiazepine effects in anaesthesia and intensive-care patients. Serious complications caused by flumazenil have been reported in patients receiving benzodiazepines in the treatment of seizure disorders and in patients with mixed intoxications. Neostigmine is one of several antagonists of neuromuscular blocking agents. Its side effects include bradycardia, increased bronchial secretions and increased peristalsis. Indication depends on the results of neuromuscular monitoring. Physostigmine is an unspecific antagonist of the central anticholinergic syndrome, an acute psychosis that may be caused by numerous drugs used in anaesthesia. Generally, antagonists should be carefully titrated. In emergency medicine the use of these antagonists is not recommended; the primary goal is to restore vital functions.
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PMID:[Antagonists in anesthesia]. 854 33


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