Procyclidine is a muscarinic antagonist that crosses the blood-brain. Procyclidine hydrochloride (brand name Kemadrin) is a synthetic antispasmodic compound of relatively low toxicity. It has been shown to be useful for the symptomatic treatment of parkinsonism (paralysis agitans) and extrapyramidal dysfunction caused by tranquilizer therapy. Procyclidine hydrochloride was developed at The Wellcome Research Laboratories as the most promising of a series of antiparkinsonism compounds produced by chemical modification of antihistamines. Kemadrin is indicated in the treatment of parkinsonism including the postencephalitic, arteriosclerotic, and idiopathic types. Partial control of the parkinsonism symptoms is the usual therapeutic accomplishment. Procyclidine hydrochloride is usually more efficacious in the relief of rigidity than tremor; but tremor, fatigue, weakness, and sluggishness are frequently beneficially influenced. It can be substituted for all the previous medications in mild and moderate cases. For the control of more severe cases, other drugs may be added to procyclidine therapy as indications warrant. The mechanism of action is unknown. It is thought that procyclidine acts by blocking central cholinergic receptors, and thus balancing cholinergic and dopaminergic activity in the basal ganglia. Pharmacologic tests have shown that procyclidine hydrochloride has an atropine-like action and exerts an antispasmodic effect on smooth muscle. It is a potent mydriatic and inhibits salivation. It has no sympathetic ganglionblocking activity in doses as high as 4 mg/kg, as measured by the lack of inhibition of the response of the nictitating membrane to preganglionic electrical stimulation.

HEPTABARBITAL is an intermediate or short term barbiturate. It binds to the GABAA receptor at either the alpha or the beta subunit. This GABAA receptor binding decreases input resistance, depresses 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 increases both the amplitude and decay time of inhibitory postsynaptic currents. HEPTABARBITAL was formerly used as a sedative and hypnotic drug.

Talbutal is a short to intermediate-acting barbiturate, which had been used under brand name Latusate as a sedative and hypnotic, but then this usage was discontinued. It was found, that talbutal binds at a distinct binding site at the GABAA receptor, increasing the duration of time for which the Cl- ionopore is open. Thus, the post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged.

Phensuximide is an anticonvulsant in the succinimide class. For the treatment of epilepsy. Phensuximide suppresses the paroxysmal three cycle per second spike and wave EEG pattern associated with lapses of consciousness in absence (petit mal) seizures. The frequency of attacks is reduced by depression of nerve transmission in the motor cortex. Phensuximide's mechanism of action not understood, but may act in inhibitory neuronal systems that are important in the generation of the three per second rhythm. It's effects may be related to its ability to inhibit depolarization-induced accumulation of cyclic AMP and cyclic GMP in brain tissue.

Ethopropazine is an anticholinergic drug. Ethopropazine is an inhibitor of butyrylcholinesterase and non-selective muscarinic acetylcholine receptor antagonist. Ethopropazine has been used for the treatment of parkinsonism and drug-induced extrapyramidal reactions. Also It used for the symptomatic treatment of hepatolenticular degeneration and congenital athetosis.

Methbarbital is a barbiturate anticonvulsant, discovered by Merck in 1905. It was introduced to market for treatment of epolepsy by Abbott in 1952, and discontinued in 1990.

Beclamide (N-benzyl-B-chloropropionamide) is a drug that possesses anticonvulsant activity. It is no longer used. It has been used as a sedative and as an anticonvulsant. Beclamide has been used in the management of both epilepsy and behavioral disorders associated with epilepsy. It was introduced into clinical practice in 1952 under the brand names Hibicon, Lederle and later it was withdrawn. This agent was shown to be effective in grand mal but not absence seizures. Early claims emphasized its safety, and it is not entirely clear why it was withdrawn from therapy for epilepsy. Interest in the drug was rekindled in the 1990s as an adjunct in the treatment of schizophrenia.

Meparfynol is a tertiary hexanol and potent tranquilizer with hypnotic/sedative and anticonvulsant effects and exceptionally low therapeutic index. It was discovered by Bayer in 1913 and was used shortly thereafter for the treatment of insomnia, but its use was quickly phased out in response to newer drugs with far more favorable safety profiles. Meparfynol depresses monosynaptic and polysynaptic reflexes and exerted weak ganglion and neuromuscular blocking actions. Meparfynol also produces transitory hypotension, an increase of aortic blood flow. Perfusion of the coronary arteries with Meparfynol led to a slowing of the heart, diminished systolic amplitude, dysrhythmias, and increased coronary flow. Respiration was stimulated with small and depressed with larger doses of Meparfynol.

Phenacemide, also known as phenylacetylurea, is an anticonvulsant of the ureide (acetylurea) class. Phenacemide was introduced in 1949 for the treatment of epilepsy, but was eventually withdrawn from the market because of its severe side effects, which includes personality changes, blood, renal and skin disorders.

Metabutethamine hydrochloride was used as a local anesthetic.