By Jason Luo
As human beings, we have taken advantage of a wide variety of substances found in our natural world. Some of these include the most well-known poisons such as cyanide, a common ingredient in gold processing. Another infamous example of one of these poisons is strychnine. After being brought over to the United States from Asia, the substance has been used in many products but has also taken thousands of lives of those unaware of its potency. This article will discuss the origins and effects of strychnine as well as how people have used the substance in their own lives.
Strychnine is an alkaloid poison found in Strychnos Nux-Vomica, a tree native to the East Indies, India, and Northern Australia. When extracted, the toxin appears colorless and is described to taste slightly bitter. The toxin is found mainly in the seeds and bark of the tree but is present throughout the entire plant. Strychnine is considered one of the most deadly poisons in the world, with doses of 30–100mg being lethal to adults and 15–30mg being lethal to children.
When ingested into the body, strychnine acts as a competitive inhibitor of the postsynaptic glycine receptors in the spinal cord. Glycine receptors (GlyR) function as a mediator for fast inhibitory neurotransmission and are primarily involved in motor movements, motor control, and pain perception. In other words, they are responsible for checking and regulating the muscle movements in the body.
The binding of the amino acid glycine to the receptors inhibits neuronal firing by causing hyperpolarization — the change in a cell’s interior membrane that makes it more negatively charged — of the postsynaptic neuron. Glycine serves many functions in regulating muscle control, preventing seizure activity, hyperactivity, and even bipolar depression. If GlyR is blocked by strychnine, the result is unchecked reflex stimulation, exaggerated reflex effects, and involuntary muscle contractions on the muscle groups that are affected.
The lack of inhibition from glycine can cause a multitude of symptoms that appear 15–30 minutes after oral ingestion and even quicker if injected or inhaled. Convulsions are one of the first symptoms that occur along with the appearance of an extremely arched back or clenched jaws. Convulsions may be followed by a condition called risus sardonicus, in which the person may start to feel muscle contractions in the face, leading to a fixated and stiff smiling appearance. If not treated quickly, muscle contractions caused by strychnine spread throughout the entire body and can lead to other conditions, including an extremely stiff neck, kidney failure, and seizures. Death by strychnine poisoning is ultimately caused by respiratory failure and asphyxiation due to muscle spasms in the respiratory system and the inability to take in air properly.
Symptoms of strychnine poisoning have been shown in several case reports. One report featured a 39-year-old man who accidentally ingested the leaves of the strychnos plant. Hours after consumption, the man started to experience twitching movements in his arms and forearm muscles as he was asleep. The man’s pulse rate also began to decline, initially starting at 60 beats/min and dropping to 48 beats/min. Another case involved an 87-year-old man who was suspected of ingesting strychnine powder. Under inspection, the man started experiencing repetitive tonic muscle contractions and respiratory arrest. As the man was being transferred to an immediate care unit, he became increasingly restless and showed signs of hyperreflexia — overactive or spastic reflexes shown by uncontrollable motor movements. Treatments using 750 mg of sodium valproate lessened the excessive muscle contractions, but unfortunately, the patient was pronounced dead two days after he was initially diagnosed.
Since strychnine is readily available in a plant and can be easily grown, many people have found a variety of uses for the toxin. The most common use of strychnine today is in pesticides, specifically for killing rodents. Given the potent nature of the toxin, laws have been enforced that put restrictions on using pesticides containing strychnine. More uncommon uses of strychnine include combinations with street drugs such as LSD, cocaine, and heroin to create a stronger “high” feeling. Many side effects associated with these stimulants may be due to the drug being mixed with small amounts of strychnine.
In the mid-1800s to early 1900s, strychnine was administered as medicine due to its ability to induce muscle contractions. It was particularly used for patients who had paralyzed limbs and was even used to treat those with impaired vision by forcing muscle contractions in particular areas of the eyes. At one point, the spastic side effects of strychnine have been compared to those of caffeine and the substance soon became an ingredient in performance-enhancing drugs for competitive sports. For instance, Kenyan marathon runner Felix Kirwa was banned from racing for nine months after he was tested positive for having strychnine in his system after a race.
Strychnine was previously a widely controversial substance used by many for its neurological effects on the body and its easy reproducibility. Although it is not nearly as talked about now, future uses for the toxin may arise as we continue to exploit our planet's resources and become a more technologically advanced society.
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