CONIUM

The common or spotted hemlock, Conium maculatum (N. O. Umbelliferæ), is indigenous. It must be distinguished from the Myrrhis temulenta, another indigenous, umbelliferous plant, which has also a spotted stem, but which is covered with hairs—the stem of the hemlock being smooth. Several cases of poisoning have occurred, hemlock having been mistaken for parsley, fennel, asparagus, and parsnip. The leaves of the plant have a peculiar mousy odour, which is intensified when they are rubbed in a mortar with some caustic potash. The poisonous properties reside in an alkaloid, conine. The activity of the plant appears to depend upon the time of the year when it is gathered, being most powerful in May. The ready decomposition of the alkaloid by heat or age renders the extract of conium a very uncertain preparation, the conine being converted into an inert resinoid matter.

Conine the alkaloid is a colourless volatile oil, lighter than water, with an odour of mice. It is strongly alkaline, soluble in diluted acid, but its salts have not yet been crystallised. It has been suggested that a ptomaine not unlike conine may be formed in the body by the combination of one molecule of butyric acid and one molecule of ammonia with separation of water, thus:

Butyric Acid. Ammonia. Conine.
2C₄H₈O₂ + NH₃ -  2H₂O = C₈H₁₅N

Conine is a deadly poison, killing all animals, death resulting from asphyxia. Neutralised with an acid, its activity is increased, and it becomes more soluble in water. Almost instant death resulted in a dog from injecting two grains of conine, neutralised with hydrochloric acid, into the femoral vein.

Symptoms in Man.—The symptoms in some cases resemble those of poisoning with opium; in others, the patient complains of dryness and constriction of the throat, and drowsiness. There is dilatation of the pupil, with closure of the eyes or ptosis, and loss of power in the muscles of the extremities, so that the patient falls on attempting to walk. The paralysis does not appear to be due to any direct influence upon the muscles, but upon the motor nerves, and especially on their extreme peripheral ends, and in this differs from Calabar bean, which acts on the spinal cord. Gradual loss of power in the respiratory muscles is the cause of death. Giddiness, coma, and convulsions were the typical symptoms of two cases of accidental poisoning recorded by Dr. Watson.

Symptoms in Animals.—“Palsy, first of the voluntary muscles, next of the chest, lastly of the diaphragm—asphyxia, in short, from paralysis, without insensibility, and with slight occasional twitches only of the limbs; and the heart was always found contracting vigorously for a long time after death” (Christison).

Post-mortem Appearances.—Congestion of the vessels of the brain and lungs. The blood is very fluid, and of a dark colour, the fluidity due probably to the mode of death—slowly induced asphyxia. There may be some redness of the mucous membrane of the alimentary canal.

Fatal Period.—The symptoms may come on in from ten minutes to an hour, or more, after the poison has been taken. Death usually takes place in about four hours.

Fatal Dose.—Uncertain. Thirty grains of the extract carefully prepared killed a rabbit in five minutes. A single drop of conine dropped into the eye of a rabbit killed it in nine minutes.

Chemical Analysis.—Conine may be extracted from organic mixture by the general process for extracting alkaloids. The following tests may then be applied:

1. The odour of conine, when diluted with water, resembles that of mice. Harley states that a mixture of caustic potash with organic substances may evolve a similar odour even when conine is absent.

2. On warming conine with sulphuric acid and potassium bichromate butyric acid is produced, and can be recognised by its peculiar odour.

3. If conine be added to a solution of alloxan a reddish-purple colour is produced in a few minutes, and white needle-shaped crystals form on standing. These crystals if dissolved in caustic potash solution produce a purple colour, and the odour of conine is given off.

Treatment.—Emetics, stomach pump, castor-oil, followed by ammonia and other diffusible stimulants. Artificial respiration should be resorted to and kept up for a long time.