Monkshood

(Aconitum napellus)

Monkshood

Aconitum napellus L.
Ranunculaceae

Other significant names: Wolf’s bane

Parts used: Radix

Common forms of prescription: Tincture for cream

Restriction: The Human Medicines Regulations 2012, Schedule 20, Part II


If you think you’ve swallowed Aconitum napellus (monkshood):

  • Call emergency services immediately (UK: 999 or 112). Do not wait for symptoms.

  • Do not induce vomiting. Rinse your mouth and spit out the water.

  • Do not eat or drink anything unless a medical professional tells you to.

  • Keep any plant material/packaging and take it with you.

  • Watch for tingling or numbness (mouth/face/hands), dizziness, nausea/vomiting, palpitations, chest pain, weakness, or confusion.

  • If symptoms are mild and you’re unsure, call NHS 111 for urgent advice, but if any symptoms are present or ingestion is likely, treat it as an emergency (999/112).

This website is for educational purposes only and is not medical advice. Aconitum species are highly toxic.

Monkshood (Aconitum napellus) - Clinical Snapshot

(Educational purposes only)

Primary Actions

Analgesic

Primary Indications

Topical use only.

For tingling or numbing sensations associated with pain, such as:
• Arthritic and rheumatic pain
• Sciatica
• Neuralgia (including facial neuralgia)
• Gout

Qualities: Hot, dry,

Cautions / Contraindications

External use only.
• Do not apply to broken skin.
• Avoid use during pregnancy and lactation.
• Always handle with gloves, absorption through skin can cause toxicity.

Do not use on children

Signs of Toxicity

Highly toxic. Internal ingestion leads rapidly to:
• Tingling and numbness of the tongue and mouth spreading over the body
• Crawling or prickling sensations
• Respiratory paralysis
• Tachyarrhythmia
• Cardiac arrest and death

The first sign of poisoning is tingling or numbness, followed by increasing motor paralysis and a strangling sensation due to respiratory failure.

Herbal Glossary

Chemical Constituents

Aconitum napellus

Because aconite’s active alkaloids have an extremely narrow therapeutic index, the dose at which analgesic effects might occur is very close to the dose that can cause serious or fatal toxicity.

Aconitum napellus (monkshood) is infamous for a reason: its main pharmacologically active and dangerous components are diterpenoid alkaloids, especially aconitine, mesaconitine, hypaconitine, and jesaconitine. These alkaloids are highly lipophilic, which means they can cross skin and mucous membranes easily; even handling fresh plant material and then touching your mouth can allow enough to be absorbed to cause symptoms. Once inside the body, the problem is what aconitine does at a cellular level.

Aconitine targets voltage-gated sodium channels in excitable tissues, such as nerves, cardiac muscle, and skeletal muscle. Under normal circumstances, these channels open briefly and then inactivate, allowing the cell to reset. Aconitine prevents that inactivation, so the channel stays open, sodium keeps rushing in, and the cell remains persistently depolarised. The clinical picture follows logically from that mechanism: first, increased excitability (tingling, burning, paraesthesia around the mouth and fingers); then cardiac irritability and arrhythmias; and, with higher exposure, paralysis and cardiac arrest. That’s why aconitine is recognised as the most toxic of the plant’s constituents.

Interestingly, the same effect underpins earlier reports of its use for pain: at very small, controlled external doses, partial interference with nerve firing can desensitise local pain receptors and reduce nerve excitability, giving an analgesic or antineuralgic effect. But that therapeutic window is vanishingly small, as Bone & Mills note, the therapeutic and lethal doses overlap sharply, giving Aconitum “one of the narrowest therapeutic indices of any plant” (Bone & Mills, 2013). That’s why modern Western herbal practice treats internal use as unsafe.

Alongside the major alkaloids, A. napellus also contains benzoylaconine, aconine, flavonoids and resins. These have minimal direct pharmacological activity in the context of poisoning, but they can influence the dissolution and absorption of toxic alkaloids. Traditional processing: heating, drying, or otherwise treating the root can hydrolyse aconitine into less toxic derivatives such as benzoylaconine and aconine, which is the rationale behind some historical and East Asian preparations. However, even after processing, preparations remain highly poisonous, so this doesn’t translate into safe DIY use (Hoffmann, 2003; Grieve, 1931/1971).

In short, Aconitum napellus contains potent, easily absorbed diterpenoid alkaloids that lock sodium channels open, causing a predictable but very dangerous cascade of neurological and cardiac effects. Any potential therapeutic action sits uncomfortably close to toxicity, which is why, in contemporary practice, it’s a plant to understand, respect, and teach about, rather than to give.

Traditional Use

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 before 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 intense caution. Later, in the 18th and 19th centuries, the plant was studied by homoeopaths 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.

Clinical Discussion

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. Prolonged depolarisation disrupts nerve conduction and desensitises sensory neurons, leading to local numbness and tingling —the same sensations that precede paralysis at 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 under any circumstance due to its extremely 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.

  • 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).

References

Bone, K., & Mills, S. (2013). Principles and Practice of Phytotherapy (2nd ed.). Churchill Livingstone.
Botanical Society of Britain and Ireland (BSBI). (2014). A vascular plant Red List for England.

https://bsbi.org/wp-content/uploads/dlm_uploads/England_Red_List_1.pdf
Grieve, M. (1971). A modern herbal (Vols. 1–2). Dover Publications. (Original work published 1931)
Hoffman, D. (2003). Medical Herbalism. Healing Arts Press.
NatMed (2018). Aconitum napellus [Monograph]. Natural Medicines Database. https://naturalmedicines.therapeuticresearch.com/databases/food,-herbs-supplements/professional.aspx?productid=609
Rose, F., & O’Reilly, C. (2006). The Wild Flower Key. Penguin Books Ltd.

Back to Schedule 20 Home