Aconitum (A-co-ní-tum), known as aconite, monkshood, wolfsbane, leopard's bane, women's bane, Devil's helmet or blue rocket, is a genus of flowering plant belonging to the buttercup family (Ranunculaceae). There are over 250 species of Aconitum.
These are handsome plants, the tall, erect stem being crowned by racemes of large and eye-catching blue, purple, white, yellow or pink zygomorphic flowers with numerous stamens. They are distinguishable by having one of the five petaloid sepals (the posterior one), called the galea, in the form of a cylindrical helmet; hence the English name monkshood. There are 2–10 petals, in the form of nectaries. The two upper petals are large. They are placed under the hood of the calyx and are supported on long stalks. They have a hollow spur at their apex, containing the nectar. The other petals are small and scale like or non forming. The 3–5 carpels are partially fused at the base.
The fruit is a follicle. It was said in former times that wolfsbane was the only way to tell a werewolf: if the flower cast a yellow shadow on the suspected shape-shifter's chin, the werewolf test was positive.
The roots of Aconitum ferox supply the Nepalese 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.
Several species of Aconitum have been used as arrow poisons. The Minaro in Ladakh use A. napellus on their arrows to hunt ibex, while the Ainus in Japan used a species of Aconitum to hunt bear. The Chinese also used Aconitum poisons both for hunting, and for warfare.
Many species of Aconitum are cultivated in gardens, having either blue or 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 perennial plants. 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 their poisonous character.
In Western medicine preparations of aconite were used until just after the middle of the 20th century, but it is no longer employed as it has been replaced by safer and more effective drugs and treatments. The 1911 British Pharmaceutical Codex regarded the medical uses and toxicity of aconite root or leaves to be virtually identical to that of purified aconitine. Aconite first stimulates and later paralyses the nerves of pain, touch, and temperature if applied to the skin or to a mucous membrane; the initial tingling therefore gives place to a long-continued anaesthetic action. Great caution was required, as abraded skin could absorb a dangerous dose of the drug, and merely tasting some of the concentrated preparations available could be fatal. The local anaesthesia of peripheral nerves can be attributed to at least eleven alkaloids with varying potency and stability.
Internal uses were also pursued, to slow the pulse, as a sedative in pericarditis and heart palpitations, and well diluted as a mild diaphoretic, or to reduce feverishness in treatment of colds, pneumonia, quinsy, laryngitis, croup, and asthma due to exposure. 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 is 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.
The above description of poisoning is characteristic of an oral administration. However, poisoning may occur simply by picking the leaves without wearing gloves; the aconitine toxin is absorbed easily 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 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.
Aconitine is a potent neurotoxin that blocks tetrodotoxin-sensitive sodium channels. Pretreatment with barakol 10 mg/kg IV reduces the incidence of aconitine-induced ventricular fibrillation and ventricular tachycardia, as well as mortality. Five μg/kg IV of tetrodotoxin has the same effect. The protective effects of barakol are probably due to the prevention of intracellular sodium ion accumulation.
Aconite was reported by the Sunday Mirror to have been used as poison in the murder of Pakistan cricket coach Bob Woolmer during the 2007 Cricket World Cup. However there is now evidence that Bob Woolmer was not murdered but died of natural causes.
According to an article by the Indian scientists Thorat and Dahanukar, "Crude aconite is an extremely lethal substance. However, the science of Ayurveda looks upon aconite as a therapeutic entity. Crude aconite is always processed i.e. it undergoes 'samskaras' before being utilized in the Ayurvedic formulations. This study was undertaken in mice, to ascertain whether 'processed' aconite is less toxic as compared to the crude or unprocessed one. It was seen that crude aconite was significantly toxic to mice (100% mortality at a dose of 2.6 mg/mouse) whereas the fully processed aconite was absolutely non-toxic (no mortality at a dose even 8 times as high as that of crude aconite). Further, all the steps in the processing were essential for complete detoxification"
Aconitum features in literature in a number of instances:
No, no, go not to Lethe, neither twist Wolf's bane, tight-rooted, for its poisonous wine Nor suffer thy pale forehead to be kissed By nightshade, ruby grape of Proserpine…
Widdershins go when the Moon doth wane, An’ the Werewolf howls by the dread Wolfsbane.
Even those who are pure of heart, and say their prayers at night, can become a wolf, when the wolfsbane blooms and the autumn moon is bright.
Rudolph Bloom died... in consequence of an overdose of monkshood (aconite) selfadministered in the form of a neuralgic liniment...