Aconitum is a genus of plants belonging to the buttercup family Ranunculaceae. There are about 60 species, which are known as aconite, monkshood, or wolfsbane. They are chiefly natives of the mountainous parts of the northern hemisphere. They are distinguished by having one of the five blue or yellow coloured sepals (the posterior one) in the form of a helmet; hence the English name monkshood. Two of the petals placed under the hood of the calyx are supported on long stalks, and have a hollow spur at their apex, containing nectar. They are handsome plants, the tall stem being crowned by racemes of showy flowers.

Aconitum napellus, the Common monkshood, is a doubtful native of Britain, and is of therapeutic and toxicological importance. Its roots have occasionally been mistaken for horseradish. It has a short underground stem, from which dark-coloured tapering roots descend. The crown or upper portion of the root gives rise to new plants. When put to the lip, the juice of the aconite root produces a feeling of numbness and tingling.

The roots of Aconitum ferox supply the Indian (Nepal) poison called bikh, bish, or nabee. It contains large quantities of the alkaloid pseudaconitine, which is a deadly poison. Aconitum palmatum yields another of the bikh poisons. The root of Aconitum luridum, of the Himalaya, is said to be as virulent as that of A. ferox or A. napellus.

Many species of Aconitum are cultivated in gardens, some having blue and others yellow flowers. Aconitum lycoctonum, Alpine wolfsbane, is a yellow-flowered species common in the Alps of Switzerland. As garden plants the aconites are very ornamental, hardy perennials. They thrive well in any ordinary garden soil, and will grow beneath the shade of trees. They are easily propagated by divisions of the root or by seeds; care should be taken not to leave pieces of the root where livestock might eat them, owing to the poisonous character.

Aconite has been ascribed with supernatural powers relating to werewolves and other lycanthropes, either to repel them or in some way induce their lycanthropic condition.

Canadian film actor Andre Noble died of aconitine poisoning on July 30, 2004 after accidentally ingesting monkshood.

Chemistry

The active principle of Aconitum napellus is the alkaloid aconitine, first examined by P.L. Geiger. Hesse, Alder Wright & A.B. Luff obtained apoaconitine, aconine, and benzoic acid by hydrolysis; while, in 1802, C. Ehrenberg and A. Purfurst observed acetic acid as a hydrolytic product. This, and allied alkaloids, have formed the subject of many investigations by Wyndham Dunstan and his pupils in England, and by Martin Freund and Paul Beck in Berlin. But their constitution is not yet solved, there even being some divergence of opinion as to their empirical formulae. Aconitine (C₃₄H₄₇NO₁₁) is a crystalline base, soluble in alcohol, but very sparingly in water; its alcoholic solution is dextrorotatory, but its salts are levorotatory. When heated it loses water and forms pyraconitine. Hydrolysis gives acetic acid and benzaconine, the chief constituent of the alkaloids picraconitine and napelline; further hydrolysis gives aconine. Pseudaconitine, obtained from Aconitum ferox, gives on hydrolysis acetic acid and veratrylpseudaconine, the latter of which suffers further hydrolysis to veratric acid and pseudaconine. Japaconitine, obtained from the Japanese aconites, known locally as kuza-uzu, hydrolyses to japbenzaconine, which further breaks down to benzoic acid and japaconine. Other related alkaloids are lycaconitine and myoctonine which occur in wolfsbane, Aconitum lycoctonum.

The usual test for solutions of aconitine consists in slight acidification with acetic acid and addition of potassium permanganate, which causes the formation of a red crystalline precipitate. In 1905, Dunstan and his collaborators discovered two new aconite alkaloids, indaconitine in "mohri" (Aconitum chasmanthum), and bikhaconitine in "bikh" (Aconitum spicatum); he also proposes to classify these alkaloids according to whether they yield benzoic or veratric acid on hydrolysis.

A liniment and a tincture can be prepared from the root of Aconitum napellus. The dose of the tincture is of importance as being exceptionally small, for it is not advisable to give more than at most five drops at a time. The official preparation is an ointment which contains one part of the alkaloid in fifty. It must be used with extreme care, and in small quantities, and it must not be used at all where cuts or cracks are present in the skin.

Pharmacology of Aconite and Aconitine

Aconite first stimulates and later paralyses the nerves of pain, touch and temperature, if applied to the skin, broken or unbroken, or to a mucous membrane; the initial tingling therefore gives place to a long-continued anaesthetic action. Taken internally aconite acts very notably on the circulation, the respiration and the nervous system. The pulse is slowed, the number of beats per minute being actually reduced, under considerable doses, to forty, or even thirty, per minute. The blood-pressure synchronously falls, and the heart is arrested in diastole. Immediately before arrest the heart may beat much faster than normally, though with extreme irregularity, and in the lower animals the auricles may be observed occasionally to miss a beat, as in poisoning by veratrine and colchicum. The action of aconitine on the circulation is due to an initial stimulation of the cardio-inhibitory centre in the medulla oblongata (at the root of the vagus nerves), and later to a directly toxic influence on the nerve-ganglia and muscular fibres of the heart itself. The fall in blood-pressure is not due to any direct influence on the vessels. The respiration becomes slower owing to a paralytic action on the respiratory centre and, in warm-blooded animals, death is due to this action, the respiration being arrested before the action of the heart. Aconite further depresses the activity of all nerve-terminals, the sensory being affected before the motor. In small doses it therefore tends to relieve pain, if this be present. The activity of the spinal cord is similarly depressed. The pupil is at first contracted, and afterwards dilated. The cerebrum is totally unaffected by aconite, consciousness and the intelligence remaining normal to the last. The antipyretic action which considerable doses of aconite display is not specific, but is the result of its influence on the circulation and respiration and of its slight diaphoretic action.

Therapeutics

The indications for its employment are limited, but definite. It is of undoubted value as a local anodyne in sciatica and neuralgia, especially in ordinary facial or trigeminal neuralgia. The best method of application is by rubbing in a small quantity of the aconitine ointment until numbness is felt, but the costliness of this preparation causes the use of the aconite liniment to be commonly resorted to. This should be painted on the affected part with a camel hair brush dipped in chloroform, which facilitates the absorption of the alkaloid. Aconite is indicated for internal administration whenever it is desirable to depress the action of the heart in the course of a fever. Formerly used in every fever, and even in the septic states that constantly followed surgical operations in the pre-Listerian epoch, aconite is now employed only in the earliest stage of the less serious fevers, such as acute tonsilitis, bronchitis, and, notably, laryngitis. The extreme pain and rapid swelling of the vocal cords -- with threatened obstruction to the respiration that characterize acute laryngitis -- may often be relieved by the sedative action of this drug upon the circulation. In order to reduce the pulse to its normal rate in these cases, without at the same time lessening the power of the heart, the drug must be given in doses of about two minims of the tincture every half-hour and then every hour until the pulse falls to the normal rate. Thereafter the drug must be discontinued. It is probably never right to give aconite in doses much larger than that named. There is one condition of the heart itself in which aconite is sometimes useful. Whilst absolutely contra-indicated in all cases of valvular disease, it is of value in cases of cardiac hypertrophy with over-action. But the practitioner must be assured that neither valvular lesion nor degeneration of the myocardium is present.

Toxicology

In a few minutes after the introduction of a poisonous dose of aconite, marked symptoms supervene. The initial signs of poisoning are referable to the alimentary canal. There is a sensation of burning, tingling and numbness in the mouth, and of burning in the abdomen. Death usually supervenes before a numbing effect on the intestine can be observed. After about an hour there is severe vomiting. Much motor weakness and cutaneous sensations similar to those above described soon follow. The pulse and respiration steadily fail, death occurring from asphyxia. As in strychnine poisoning, the patient is conscious and clear-minded to the last. The only post-mortem signs are those of asphyxia. The treatment is to empty the stomach by tube or by a non-depressant emetic. The physiological antidotes are atropine and digitalin or strophanthin, which should be injected subcutaneously in maximal doses. Alcohol, strychnine, and warmth must also be employed.

The above description of poisoning is characteristic of an oral administration. It should however be noted that aconitine may be easily absorbed through the skin, and poisoning may occur through this route simply by picking the leaves without the use of gloves; the toxin in the sap is absorbed through the skin. From practical experience, the sap oozing from eleven picked leaves will cause cardiac symptoms for a couple of hours. In this event, there will be no gastrointestinal effects. Tingling will however start at the point of absorption, and extend up the arm to the shoulder, after which the heart will start to be affected. The tingling will be followed by numbness - it is fairly unpleasant. As remarked above, atropine is an antidote. Atropine is a constituent of Belladonna.

Aconitine is a potent neurotoxin that blocks tetrodotoxin-sensitive sodium channels. Pretreatment with barakol (10 mg/kg i.v. - that is intravenously - the compound is isolated from the leaves of Cassia siamea Lam) reduces the incidence of aconitine-induced ventricular fibrillation and ventricular tachycardia, as well as mortality. 5 micrograms/kg i.v. of tetrodotoxin also had the same effect. The protective effects of barakol are probably due to the prevention of intracellular sodium ion accumulation.

External links

Eclectic herbal information

• Aconitine (http://www.ibiblio.org/herbmed/eclectic/kings/aconitum_aconitine.html) King's American Dispensatory @ Henriette's Herbal
• Aconitum napellus (Aconite) (http://www.ibiblio.org/herbmed/eclectic/kings/aconitum-nape.html) King's American Dispensatory @ Henriette's Herbal
• Aconitum fischeri (American) (http://www.ibiblio.org/herbmed/eclectic/kings/aconitum-fisc.html) King's American Dispensatory @ Henriette's Herbal
• Aconite (http://www.botanical.com/botanical/mgmh/a/aconi007.html) Mrs. Grieve's "A Modern Herbal" @ Botanical.com

Homeopathic information

• Aconitum napellus (aconitin.) (http://www.homeoint.org/books3/kentmm/acon.htm) "Kent's Lectures on Homeopathic Materia Medica" by Dr Robert Séror
• Aconite (http://www.homeoint.org/books5/allenprimer/aco.htm) "A Primer of Materia Medica for practitioners of Homœopathy" by Timothy Allen

Miscellaneous

• Photographs of Aconite plants (http://plants.usda.gov/cgi_bin/gallery_page.cgi?earl=gallery.cgi&category=genus&classes=all&sort=scisort&txtparm=Aconitum&wetland=all&origin=all&results=thumbnails&pagenum=1)

This article incorporates text from the public domain 1911 Encyclopædia Britannica.