Scopolamine mechanism of action in a nutshell:
Scopolamine inhibits signals originating from the vestibular system before they reach the vomiting center by blocking activity of muscarinic receptors.
In motion sickness, a sensory mismatch occurs due to a disconnect between visual, vestibular (balance), and proprioceptive (muscle) inputs received by the brain. This discrepancy is interpreted as a potential toxic exposure, triggering the body’s defense mechanisms, including activation of the vomiting center.
From Mandrake to Motion Patch A Brief History of Scopolamine
When I came across advertisement of a motion sickness patch, claiming it is “100% natural, herbal based”, I always remind myself that most of our today’s effective pharmaceuticals had herbal ancestors. Scopolamine, which is now commonly used for seasickness and became the first ever medication with transdermal application (aka dermal patch) is excellent example of it.
Scopolamine, M-acetilcholine blocker also know as hyoscine is common remedy for motion sickness first isolated in 1880 from Scopolia carniolica by German chemist Albert Ladenburg. Like its pharmacological buddy atropine, scopolamine is abundantly found in mandrake—a legendary “screaming plant” said to drive anyone who hears its cries to madness.
Before being approved by FDA in 1979 for the prevention of nausea and vomiting associated with motion sickness and surgical procedures, scopolamine was known for decades as poison and “truth serum” drug. In the WWII movie “The guns of Navarone” the German general demands that scopolamine be used to interrogate the prisoner left behind by the group.
Criminals have exploited his ability to induce “anesthetic amnesia” for more nefarious purposes, using it to facilitate robbery or sexual assault. The toxicity and potential side effects are far benign when scopolamine used in therapeutic doses of a transdermal patch and usually limited to:
- Blurred vision (due to pupil dilation)
- Increased intraocular pressure (risk in glaucoma)
- Tachycardia (increased heart rate)
- Dry mouth (xerostomia)
- Constipation (due to reduced gut motility)
- Urinary retention
- Difficulty urinating (especially in benign prostatic hyperplasia)
- Decreased sweating (anhidrosis)
- Risk of hyperthermia (especially in hot environments)
How scopolamine helps in motion sickness
Scopolamine blocks signals from the vestibular system before they are transmitted to the vomiting center.
Motion sickness arises due to sensory conflict, where signals from the eyes, inner ear (vestibular system), and somatosensory system do not align. The brain is getting suspicious “there is something wrong with them”, interpreting the disarray of stimuli as neurotoxin poisoning with the sequential reaction “Hey, empty the stomach, we are getting poisoned!”
The chain of command goes as follows:
- Balance organ (semicircular channels of an inner ear) and cerebellum start bombarding vestibular nuclei
- Overstimulation of the vestibular nuclei results in activation of the chemoreceptor trigger zone (CTZ) and vomiting center in the medulla.
- Vomiting center sends a signal “to empty the stomach”
While the whole interplay is described in the separate article, as well as pharmaceutical management of a motion sickness, scopolamine only targets a step in preventing the transmission of a signal from vestibular nuclei to vomiting centers and CTZ.
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