# 1911 Encyclopædia Britannica/Strychnine

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​STRYCHNINE, C$_{21}$H$_{22}$N$_2$O$_2$, an alkaloid discovered in 1818 by Pelletier and Caventou in St Ignatius's beans (Strychnos Igpatii) ; it also occurs in other species of Strychnos, e.g. S. Nux vomica, S. colubrina, S. Tieuté, and is generally accompanied by another alkaloid brucine, C$_{23}$H$_{26}$N$_2$O$_2$·4H$_2$O, which was isolated by Pelletier and Caventou in 1819. Strychnine crystallizes from alcohol in colourless prisms, which are practically insoluble in water, and with difficulty soluble in the common organic solvents. Its taste is exceptionally bitter. It has an alkaline reaction, and is a tertiary monacid base. It is optically active, the natural form being laevorotatory. Brucine closely resembles strychnine, and is its dimethoxy derivative. The constitutions are unknown (see J. Schmidt, Die Alkaloidchemie, 1904; 1909).
Medicine.–The B.P. dose of strychnine is 1/60 to 1/15 gr. in solution or in pill form. A preparation is syrupus ferri phosphatis cum quinina et strychnina, containing 1/32 gr. of strychnine in each fluid drachm. Strychninae hydrochloridum is also used; it is much more soluble than strychnine. From it is prepared liquor strychninae hydrochloridi, containing 1 gr. of hydrochloride in no minims. The United States pharmacopoeia also contains strychninae nitras and strychninae sulphas. Strychnine is incompatible with liquor arsenicalis and potassium iodide.
Physiological Action.—Applied externally strychnine is a powerful antiseptic, but its poisonous nature prevents it from being used for this purpose. Brucine is a local anaesthetic. Strychnine enters the blood as such, being freely absorbed from mucous surfaces or when given hypodermically. Internally strychnine acts as a bitter, increasing the secretion of gastric juice and the intestinal peristalsis, being a direct stimulant to the muscular coat; in this manner it has a purgative action. The specific effects of the drug, however, are upon the central nervous system. It excites the motor areas of the spinal cord and increases their reflex irritability. Small doses increase the sensibility of touch, sight and hearing; large doses cause twitching of the muscles and difficulty in swallowing; while in overdose violent convulsions are produced. The cerebral convolutions remain unaffected, but the important centres of the medulla oblongata are stimulated. Not only is the respiratory centre stimulated but the cardiac centre is acted upon both directly by the drug and indirectly for a time by the enormous rise in blood pressure due to the contraction of the arterioles all over the body. Ordinary doses have no effect upon the temperature but in overdose the temperature rises during a convulsion. Strychnine is eliminated by the kidneys as strychnine and strychnic acid. It is excreted very slowly and therefore accumulates in the system.
Therapeutics.—Strychnine is chiefly used as a stimulant. It is indicated in paralyses (chiefly functional), and is most valuable in the treatment of post-diphtheritic paralysis. In progressive lead palsy, beri-beri, and the paralysis following acute alcoholism, fairly large doses are useful. In pneumonia and other acute disease, where the patient is liable to sudden collapse, a hypodermic injection of strychnine will often save the patient's life. In collapse following severe haemorrhage and in sudden and accidental arrest of the heart or respiration during chloroform narcosis an intra-muscular injection of 1/12 gr. of the hydrochloride may stimulate the cardiac action. In acute opium poisoning strychnine is very valuable. It is a physiological antagonist of chloral hydrate, morphine and physostigmine, and may be given in poisoning by these drugs. In dyspnoea due to emphysema, phthisis and asthma, strychnine is of service, given internally in doses of 1 to 3 minims of the liquor. The syrup of iron, quinine and strychnine is used as a tonic.
Toxicology.—The symptoms of strychnine poisoning usually appear within twenty minutes of the ingestion of a poisonous dose, starting with an uneasy sensation, stiffness at the back of the neck, twitching of the muscles and a feeling of impending suffocation. The patient is then seized with violent convulsions of a tetanic character; the arms are stretched out, respiration impeded, the muscles are rigid, the body is thrown into opisthotonos, i.e. it rests bow-form on the head and the heels (occasionally the body is flexed forward [emprosthotonos], the eyes remain wide open and fixed, and the mouth is drawn aside (risus sardonicus). After a minute the muscles relax, and the patient sinks back exhausted, consciousness being preserved throughout. Any noise, a draught of air or a touch may cause a convulsion. If the case is about to terminate fatally the spasms rapidly succeed each other and death usually occurs within two hours, either from asphyxia produced by spasm of the respiratory muscles or more rarely from exhaustion. After death the position of the body may or may not be flexed; usually rigor mortis develops rapidly. In cases which recover the convulsions diminish in severity, leaving the patient exhausted. Complications are infrequent. The average fatal dose for an adult is 11/2 grs., but death has resulted in twenty minutes from 1/2 grain. On the other hand, recovery has taken place after 5 and 10 and even 20 grains have been swallowed, but in the latter case an emetic was at once administered. Idiosyncrasy plays a considerable part in determining the effects, some people being particularly susceptible; death has occurred in five minutes from the appearance of the first symptoms, but when a narcotic has been administered at the same time as the poison the development is proportionately slow. Tetanus resembles strychnine poisoning, but the development of the, symptoms in tetanus is usually much slower, death rarely occurring within 24 hours. In strychnine poisoning trismus or lockjaw is generally secondary to spasm of the other muscles, while in tetanus it is usually the first symptom, no relaxation taking place between the spasms.
The treatment of strychnine poisoning is to immediately evacuate the stomach with a stomach-pump or emetic, chloroform being administered to allay the spasms. If the patient can swallow, draughts of water containing tannic acid may be given. Nitrite of amyl inhalations are useful in the early stages when the respiratory muscles are freely movable. Chloral and potassium bromide may be given as physiological antidotes. If death from asphyxia appears imminent artificial respiration may be resorted to.