Historically infamous as one of nature’s most lethal poisons, Aconitum carries a long and complex legacy in both medicine and myth. Its name derives from the Greek akóniton, thought to mean “without struggle”, an allusion to the swift and silent death it can cause. In ancient Greece, it was reputedly used for executions, assassinations, and warfare, admired and feared in equal measure for the calm, almost peaceful paralysis it induced prior to death.

According to legend, Aconitum first sprang from the foam of Cerberus, the three-headed hound of Hades, as Hercules dragged him from the underworld. The plant’s association with the realm of death and transformation continued throughout classical mythology and European folklore, where it became linked to witchcraft, sorcery, and shape-shifting. It was said to be one of the ingredients in witches’ “flying ointments,” along with Atropa and Hyoscyamus, used in hallucinogenic salves that blurred the line between the physical and spiritual worlds.

The common name “wolf’s bane” refers to its former use by hunters and shepherds who smeared Aconitum extract onto arrow tips or meat baits to kill wolves and large predators. Variants of this practice appear across Europe and Asia, where the plant was similarly used to poison arrows for hunting or warfare. In the Himalayas, Aconitum ferox was used for the same purpose and remains one of the most toxic species known.

Despite its deadly reputation, Aconitum also found a place in early medicine. Ancient physicians such as Dioscorides and Galen described its narcotic and pain-relieving effects, though always with strong caution. Later, in the 18th and 19th centuries, the plant was studied by homeopaths and early pharmacologists for its analgesic and antineuralgic potential, leading to its controlled external use in conditions involving severe pain, particularly neuralgia and rheumatism.

Thus, Aconitum napellus stands as one of the clearest examples of the poison–medicine duality in herbal history, a plant capable of easing suffering in minute doses yet causing certain death in slightly higher ones.

Aconitum napellus occupies a unique and cautionary position within the materia medica, a plant historically revered for its analgesic and antineuralgic power, yet feared for its extreme toxicity. Its therapeutic potential lies within a razor-thin margin between pain relief and fatal poisoning, making it a model example of the similia similibus curentur (“like cures like”) principle often referenced in historical medical philosophy.

The primary active alkaloid, aconitine, acts by modifying sodium channel kinetics in excitable membranes. By prolonging depolarisation, it disrupts nerve conduction and desensitises sensory neurons, leading to local numbness and tingling, the same sensations that precede paralysis in toxic doses. In extremely dilute topical preparations, this mechanism may contribute to pain reduction by dulling peripheral nerve excitability and interfering with pain signalling pathways.

Historically, external applications were used to alleviate neuralgic and rheumatic pain, particularly where the pain presented as sharp, burning, or tingling. 19th-century physicians such as Fleming and Turnbull explored Aconitum liniments and ointments for trigeminal neuralgia, sciatica, and facial neuralgia, noting a transient anaesthetic effect followed by relief of deep-seated pain. This topical action was considered especially valuable when pain was accompanied by cutaneous hyperaesthesia (hypersensitivity of the skin).

In modern herbalism, Aconitum is no longer used internally under any circumstance due to its extreme narrow therapeutic index and rapid systemic toxicity. However, its traditional reputation for numbing neural pain has persisted into cautious external applications in compounded creams at concentrations not exceeding 1.3% of a 1:1 tincture (13% 1:10). Such preparations may be used to treat localised neuralgic pain, sciatica, or arthritic inflammation under professional supervision.

Clinically, the herb’s toxic profile mirrors its pharmacodynamic actions: tingling, warmth, numbness, cardiac irregularity, hypotension, and respiratory depression. These same physiological responses underscore why it can only be justified for external use, and even then only in minute, measured, and localised doses.

Modern pharmacological reviews confirm that aconitine and its analogues exhibit both analgesic and anti-inflammatory potential via sodium channel blockade and modulation of calcium influx, supporting the historical observations of pain relief. However, due to its systemic danger, all internal therapeutic use is restricted to experimental pharmacology and homeopathic preparations.

The pharmacologically active and toxic constituents of Aconitum napellus are diterpenoid alkaloids, primarily aconitine, mesaconitine, hypaconitine, and jesaconitine. These alkaloids are highly lipophilic and can be absorbed through intact skin, producing systemic toxicity even with minimal exposure.

Aconitine, a Diterpenoid alkaloid, acts on voltage-gated sodium channels of excitable membranes (neurons, cardiac and skeletal muscle), preventing their inactivation. This causes persistent depolarisation, leading to increased excitability, paresthesia, arrhythmia, and ultimately paralysis and cardiac arrest. For this reason, aconitine is the most toxic constituent.

In very small, controlled external doses, the same action underlies its analgesic and antineuralgic properties by reducing nerve excitability and desensitising local pain receptors. However, the therapeutic and lethal doses overlap sharply, giving Aconitum one of the narrowest therapeutic indices of any plant (Bone & Mills, 2013).

Other constituents include benzoylaconine, aconine, flavonoids, and resins, which contribute minimally to pharmacological effects but significantly impact solubility and absorption. Heating, drying, or processing the root can hydrolyse aconitine to less toxic derivatives, though all remain highly poisonous (Hoffman, 2003; Grieve, 1931/1971).

Found on lower mountain slopes and rocky areas. Native to Europe and naturalised in parts of the UK, though uncommon

(BSBI, 2014; Grieve, 1931/1971; Rose & O’Reilly, 2006).

Of least concern (BSBI, 2014).

A hardy perennial herb reaching 1–1.5 m in height.

The flowers are a deep violet to blue-purple, arranged in tall, erect racemes; each flower has a distinctive hood-shaped upper sepal, giving rise to the name monkshood.

The leaves are deeply palmately divided with dark green, glossy surfaces and paler undersides.

The roots form a cluster of elongated, tuberous structures resembling small carrots or turnips; these are the most toxic part of the plant.

The stems are firm, green to purplish, and unbranched except near the top.

Flowering occurs midsummer to early autumn.

Handle with extreme care, use gloves.

Fatal cases from skin absorption have been recorded.

Propagate by root division in autumn, replanting side roots in December - January

(Grieve, 1931/1971).