For convulsions

Extensive brain damage or lesions are certainly not essential for convulsions. These merely require appropriate conditions. Everyone is capable of having a convulsion, indeed their induction has been a common treatment for depression. The convulsive threshold of an epileptic, or more precisely that of some of their neurons, is just lower than normal. 

Information on the latency of this class of agents is unavailable. However, based on animal studies, there does not appear to be a significant latent period for convulsive effects. However, effects from subconvulsive doses may not be immediately obvious. 

The chronic oral MRL was based on a NOAEL of 0.025 mg/kg/day for convulsions in dogs administered endrin in the diet for 2 years (Kettering 1969). Concentrations of 0.05 and 0.1 mg/kg/day were associated with convulsive activity, slight to moderate vacuolization of hepatic cells, and occasional slight increases in liver weights. Other studies have reported hepatotoxicity in animals treated orally with endrin (Hassan etal. 1991 Treon et al. 1955). 

Human and animal evidence suggests there is a health risk for neurological effects only when exposures are high. There remains uncertainty in predicting dose levels for neurobehavioral effects, but 0.2 mg/kg body weight has been proposed as a threshold for convulsions in humans (Hayes 1963). 

No aeute-duration oral MRL was ealeulated for 3,3 -diehlorobenzidine because the available studies did not identify appropriate NOAELs or LOAELs (Ashby and Mohammed 1988 Bimer et al. 1990 Cihak and Vontorkova 1987 Ghosal and Iba 1990). No intermediate-duration oral MRL was calculated for 3,3 -dichlorobenzidine beeause the available studies did not identify relevant noncancer effects (Ito et al. 1983 Osanai 1976 Pliss 1959, 1963). No ehronie-duration oral MRL was ealeulated for 3,3 -diehloro-benzidine because there were no NOAELs identified below the lowest available serious LOAEL for convulsions and slight neuronal degeneration in dogs (Stula et al. 1978). 

The oral LDso in rats was 22mg/kg, and the expected dose for convulsions was 32mg/kg. Phenobarbital pretreatment prevented the convulsions and pulmonary damage ordinarily caused by a 50mg/kg intraperitoneal dose of MCT. 

Phenytoin, introduced as an anticonvulsant drug in 1938, remains one of the drugs most frequently prescribed for convulsive disorders. The precise mode of action is unknown, but it appears to inhibit the accumulation of sodium in nerve cells, thus stabilizing hyperexcitable cell membranes (A13)—a property also utilized in the treatment of cardiac arrhythmias. 

The Development of Effective Drug Treatment for Convulsive Disorders... 

General supportive care should be provided. Aggressive gut decontamination should be carried out using repeated doses of activated charcoal and whole bowel irrigation. Propranolol or other blockers (eg, esmolol) are useful antidotes for B-mediated hypotension and tachycardia. Phenobarbital is preferred over phenytoin for convulsions most anticonvulsants are ineffective. Hemodialysis is indicated for serum concentrations greater than 100 mg/L and for intractable seizures in patients with lower levels. 

Zephyranthes Candida Herbert Cong Lan (White zephyrlily) (aerial part) Lycorine, haemanthidien, nerinine, taxettin.50 For convulsion, hepatitis. 

The therapeutic plasma level of phenytoin for most patients is between 10 and 20 g/mL. A loading dose can be given either orally or intravenously the latter, using fosphenytoin, is the method of choice for convulsive status epilepticus (discussed later). When oral therapy is started, it is common... 

Figure 1 The convulsive (a) and antidepressant-like (b) effects of SNC80 administered by intravenous injection infused in 20 sec. During and immediately after the infusion, rats were observed for 20 min to watch for convulsive activity (a). Thirty minutes after the SNC80 infusion, rats were evaluated in the forced swim test (b). Counts of immobility were recorded as previously described [62]. P <. 01 as compared to vehicle by Dunnett s post hoc test.

The results are represented as the mean intensity administered and as percent change from control. The number of deaths is also recorded approximately 30 minutes after the animal has been tested for convulsions. 

There is no specific antidote for strychnine but recovery from strychnine exposure is possible with early hospital treatment. Treatment consists of removing the drug from the body (decontamination) and getting supportive medical care in a hospital setting. Supportive care includes intravenous fluids, medications for convulsions and spasms, and cooling measures for high temperature. 

Tenamfetamine ( ecstasy, MDMA methylenedioxymethamphetamine) is structurally related to mescaline as well as to amphetamine. It was originally patented in 1914 as an appetite suppressant and has recently achieved widespread popularity as a dance drug at rave parties (where it is deemed necessary to keep pace with the beat and duration of the music popular names reflect the appearance of the tablets and capsules and include White Dove, White Burger, Red and Black, Denis the Menace). Tenamfetamine stimulates central and peripheral a-and p-adrenoceptors thus the pharmacological effects are compounded by those of physical exertion, dehydration and heat. In susceptible individuals (poor metabolisers who exhibit the CYP450 2D6 polymorphism) a severe and fatal idiosyncratic reaction may occur with fulminant hyperthermia, convulsioirs, disseminated intravascular coagulation, rhabdomyolysis, and acute renal and hepatic failure. Treatment includes activated charcoal, diazepam for convulsions, P-blockade (atenolol) for tachycardia, a-blockade (phentolamine) for hypertension, and dantrolene if the rectal temperature exceeds 39°C. 

Overdose is common amongst users (up to 22% of heavy users report losing consciousness). The desired euphoria and excitement turns to acute fear, with psychotic symptoms, convulsions, hypertension, haemorrhagic storke, tachycardia, arrhythmias, hyperthermia coronary vasospasm (sufficient to present as the acute coronary syndrome with chest pain and myocardial infarction) may occur, and acute left ventricular dysfunction. Treatment is chosen according to the clinical picture (and the known mode of action), from amongst, e.g. haloperidol (rather than chlorpromazine) for mental disturbance diazepam for convulsions a vasodilator, e.g. a calcium channel blocker, for hypertension glyceryl trinitrate for myocardial ischaemia (but not a p-... 

Nagataki S. Hippocampus and frontal cortex are the potential mediatory sites for convulsions induced by new quinolones and non-steroidal anti-inflammatory drugs. Int J Qin Pharmacol Ther Toxicol 1991 29(6) 223-7. 

In 1976, the US Food and Drug Administration (FDA) published a Gamma Benzene Hexachloride (Kwell) Alert, based in part on several poorly documented cases of convulsions after topical treatment with lindane (6). Indeed, several authors have reported convulsions (7-9), but in most cases lindane had been inappropriately used (4,7), while another case took place in unusual therapeutic circumstances (prematurity, marasmus, pneumonia, congestive heart failure, ventricular septal defect) (8). A child with convulsions after the application of lindane had tuberous sclerosis and may therefore have had a reduced threshold for convulsions (9). 

Phenytoin (diphenylhydantoin) 5-10 mg/kg for convulsing foals and digoxin-induced arrhythmias 1 -5 mg/kg, every 4 h for maintenance 10 mg/kg, once daily for digoxin-induced arrhythmias 10mg/kg, once daily for chronic myositis or intermittent arrhythmias i.v. i.v., i.m., p.o. p.o, p.o. 

More recently Brochot et al. [89] reported an extension of the isobolographic approach to interaction studies for convulsant interaction among pelloxacin, norfloxacin, and theophylline in rats. Their contribution is unique in that they started out by explaining pharmacodynamic interactions for two drugs, but then extended the approach to derive an isobol for three drug interaction. In addition they included Bayesian analysis and developed a population model with Markov chain Monte Carlo methods. 

Yehuda and co-workers were the first to demonstrate that PUFAs can have an anticonvulsant effect in vivo (Yehuda, Carasso Mostofsky, 1994). They administered a mixture of a-linolenic/linoleic acid in a ratio of 1 4 to rats for 3 wk and assessed the protection against acute convulsant doses of pentylenetetrazole (PTZ), repeated subconvulsive doses of PTZ (chemical kindling), in rats made epileptic by a TeCI, injection in the amygdala and in rats made seizure-prone to acoustic stimulation by repeated injection with p-cresol. In all epilepsy models, the treatment either prevented the occurrence of seizures or increased the threshold for convulsions and diminished the severity and duration. 

Voskuyl RA, Dingemanse J, Danhof M. Determination of the threshold for convulsions by direct cortical stimulation. Epilepsy Res 1989 3 120-129. 

Treatment - inhaling of aerosol mixtures with sodium bicarbonate - 3% solution and Novphyllin - stomach washing and intestine cleaning - in peroral intake of the poison - 10% Calcium gluconicum amp. 10 ml venally 3-4 times daily - benzodiazepine preparations - Diazepam ampoule 10 mg muscularly for convulsion incidents - oxygentherapy, respiratory reanimation and antishock preparations - applied by the established methods. 

For convulsions and spasms due to high fever, add Cornu Antelopis (Ling Yang Jiao), Lumbricus (Di Long), and Ramulus Uncariae Cum Uncis (Gou Teng). 

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