Paramethadione is an anticonvulsant in the oxazolidinedione class developed by the Abbott Laboratories, approved by the Food and Drug Administration in 1949 for the treatment of absence seizures, also called partial seizures. Paramethadione acts to reduce T-type calcium currents in thalamic neurons which has been proposed to underlie the 3-Hz spike-and-wave discharge seen on electroencephalogram (EEG) during absence seizures.

Pyrithyldione is a sedative and hypnotic drug. It was demonstrated that drug has certain advantages over the barbiturates. It was indicated in mild cases of insomnia and in small doses as a sedative agent during the day. Pyrithyldione was withdrawn from the marked due to several cases of agranulocytosis.

Mephenytoin is an antiepileptic drug which can be useful in the treatment of epilepsy. The primary site of action appears to be the motor cortex where spread of seizure activity is inhibited. Possibly by promoting sodium efflux from neurons, mephenytoin tends to stabilize the threshold against hyperexcitability caused by excessive stimulation or environmental changes capable of reducing membrane sodium gradient. This includes the reduction of posttetanic potentiation at synapses. Loss of posttetanic potentiation prevents cortical seizure foci from detonating adjacent cortical areas. Mephenytoin reduces the maximal activity of brain stem centers responsible for the tonic phase of tonic-clonic (grand mal) seizures. The mechanism of action of mephenytoin is not definitely known, but extensive research strongly suggests that its main mechanism is to block frequency-, use- and voltage-dependent neuronal sodium channels, and therefore limit repetitive firing of action potentials. Mephenytoin is no longer available in the US or the UK. It is still studied largely because of its interesting hydroxylation polymorphism.

Trimethadione (brand name is TRIDIONE) is an oxazolidinedione compound that was developed as an antiepileptic agent for control of petit mal seizures that are refractory to treatment with other drugs. Tridione does not modify the maximal seizure pattern in patients undergoing electroconvulsive therapy and has a sedative effect that may increase to the point of ataxia when excessive doses are used. Trimethadione acts as a voltage-activated T-type Ca2+ channel blocker. Trimethadione is rapidly absorbed from the gastrointestinal tract. It is demethylated by liver microsomes to the active metabolite, dimethadione. Approximately 3% of a daily dose of tridione is recovered in the urine as the unchanged drug. The majority of trimethadione is excreted slowly by the kidney in the form of dimethadione.

Salicylamide is a non-prescription drug with analgesic and antipyretic properties (NSAID). It is used in combination with aspirin and caffeine in the over-the-counter pain remedies (such as EXAPRIN). Salicylamide can produce sedation and sleep in humans and animals. Has been used as model drug in pharmacokinetic and metabolic studies as a dophamine 2 receptor ligand. Salicylamide is a white or light pink crystals or powder. Organic compound it is a carboxamide derivative of salicylic acid.

Trichloroethylene (or TCE), a synthetic chemical that does not occur naturally in the environment. TCE is used to make chemicals. Additionally, it is used for spot removal in dry cleaning operations. TCE is the most common organic contaminant in groundwater. It was revealed that the compound was a human carcinogen that caused liver cancer, kidney cancer, and non-Hodgkin's lymphoma (NHL).

Sodium thiopental (also known as Sodium Pentothal, thiopental) was discovered in 1930s by investigators working for Abbott Laboratories. Thiopental sodium was used for the induction of general anesthesia and is used as an adjunct to provide hypnosis during balanced anesthesia with other anesthetic agents, including analgesics and muscle relaxants. Thiopental sodium was also used as an adjunct for control of convulsive disorders of various etiology, including those caused by local anesthetics. Finally, thiopental sodium had been used to reduce the intracranial pressure in patients with increased intracranial pressure, if controlled ventilation is provided. Nevertheless, these prescriptions of drug were discontinued. In addition, this drug was banned for use in US executions. Thiopental sodium acts through the CNS with particular activity in the mesencephalic reticular activating system. It was shown, that mechanism of action of sodium thiopental via GABAA receptor. Thiopental binds at a distinct binding site associated with a Cl- ionopore at the GABAA receptor, increasing the duration of time for which the Cl- ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged.

Vinyl ether (divinyl ether) is a clear colorless liquid with a characteristic odor. Less dense than water. Vapors heavier than air. Toxic by inhalation. Leake and Chen in 1930 demonstrated that vinyl ether possessed anaesthetic properties, and in 1931 a purer and more stable product was prepared in the research laboratories of Merck and Co. by Ruigh and Major and was used as ananaesthetic on dogs by Knoefel, Guedel, and Leake. These investigators found that dogs were more easily anaesthetized by vinyl ether than by chloroform. They also found that the period of recovery was rapid and free from vomiting; moreover, they did not notice any significant pathological effect on the various organs.The first experiments on human beings were conducted in 1933 by Gelfan and Bell. The first extensive account of vinyl ether anaesthesia in man was published in 1934, when Goldschmidt et al. reported having used it in operations in 461 mixed cases. In all these cases vinyl ether appeared to have no undesirable effect on respiration, the circulation, the liver, or the kidneys. Vinyl ether was widely used in Europe and North America for at least 30 years, until it was replaced by halothane. Vinyl ether was marketed under the name of Vinethine in the United States, Vinesthine in the United Kingdom, and Vinydan in continental Europe. Vinyl ether outlasted many of the inhalation agents introduced in recent years, and served a very useful purpose until safer, non-flammable agents, became available in the mid1960s.

AMOBARBITAL is a barbiturate derivative with hypnotic and sedative properties. In an in vitro study in rat thalamic slices amobarbital worked by activating GABAA receptors, which decreased input resistance, depressed burst and tonic firing, especially in ventrobasal and intralaminar neurons, while at the same time increasing burst duration and mean conductance at individual chloride channels; this increased both the amplitude and decay time of inhibitory postsynaptic currents. Adverse effects are mainly a consequence of dose-related CNS depression and the risk of dependence with continued use is high.

Butethal is a sedative and a hypnotic drug indicated for the treatment of severe intractable insomnia. It acts on receptors in the brain (GABA A receptors) causing the release of the chemical GABA. This chemical inhibits certain areas of the brain resulting in sleepiness. Common side effects are: drowsiness, sedation, unsteadiness, vertigo and inco- ordination. Also, hangover effect, paradoxical excitement, confusion, memory defects and skin rashes. Interactions may occur with the following: adrenocorticoids (cortisone-like medicine), anticoagulants (blood thinners), carbamazepine, corticotropin (barbiturates may decrease the effects of these medicines), central nervous system (CNS) depressants (using these medicines with barbiturates may result in increased CNS depressant effects), divalproex sodium, valproic acid (using these medicines with barbiturates may change the amount of either medicine that you need to take), and oral contraceptives containing estrogens (barbiturates may decrease the effectiveness of these oral contraceptives, and you may need to change to a different type of birth control).