Description: Scopolamine, also known as l-hyoscine, is a naturally occurring tertiary antimuscarinic. It is one of the major active alkaloids found in belladonna leaf. Compared with atropine, scopolamine is more potent in its anticholinergic effects on the iris; ciliary body; and salivary, bronchial, and sweat glands, however, scopolamine is less potent than atropine on the heart and on bronchial and GI smooth muscle. In contrast to atropine and other antimuscarinics, scopolamine at therapeutic doses produces CNS depression (drowsiness, euphoria, amnesia, fatigue, and dreamless sleep characterized by a decrease in the REM cycle). Even so, paradoxical CNS excitation (restlessness, hallucinations, or delirium) can occur, especially when the patient is experiencing severe pain. Scopolamine is very effective for the prevention of motion sickness and this indication represents the most common clinical use. Other uses for scopolamine include treatment of iritis, uveitis, and parkinsonism. Scopolamine was known and was available for many years prior to its approval by the FDA in 1939. Under the General Agreement on Tariffs and Trade (GATT), the patent for Transderm-Scop® expired on December 8, 1995. In June 1997, the FDA approved scopolamine soluble tablets.

Mechanism of Action: Scopolamine antagonizes acetylcholine at muscarinic receptors (e.g., skin, GI tract, respiratory tract, heart, CNS, and the eye), although, in high doses, antagonism at nicotinic receptors (e.g., skeletal muscle, ganglia) can occur. Because scopolamine is a tertiary amine like atropine, it can cross into the CNS. Clinically, scopolamine is used to prevent nausea and vomiting associated with motion sickness, to reduce salivation and excess bronchial secretions prior to surgery, to reduce spastic states in parkinsonism, and to produce cycloplegic refraction and pupil dilation to treat pre- and postoperative iridocyclitis.

As an antiemetic, scopolamine probably blocks neural pathways from the vestibular nuclei in the inner ear to the brain stem and from the reticular formation to the vomiting center. Because acetylcholine mediates impulses from the inner ear, scopolamine is an effective antiemetic in motion sickness. Scopolamine is a poor choice, however, for treating nausea/vomiting in other settings since neural pathways not mediated by acetylcholine are involved. High doses of scopolamine produce symptoms of antimuscarinic toxicity such as restlessness, disorientation, irritability, and hallucinations.

Reduction of secretions occurs by competitive blockade of acetylcholine and other cholinergic stimuli at cholinergic receptor sites on salivary and bronchial glands. In the treatment of spastic states in parkinsonism, scopolamine blocks excess cholinergic activity in the basal ganglia. Antagonism of acetylcholine on the sphincter and ciliary body in the eye, produces mydriasis and cycloplegia.

Pharmacokinetics: Scopolamine is well absorbed after oral, topical, and IM or SC injection. Effects occur 15—30 minutes after oral, IM, or SC administration. The antiemetic effects of the transdermal system occur within 4 hours and last up to 72 hours. After ophthalmic administration, the drug can produce systemic effects; the mydriatic effect peaks at 20—30 minutes, and the cycloplegic effects peak at 30—60 minutes. After absorption, scopolamine is distributed throughout the body and crosses the placenta and the blood-brain barrier. The metabolism of scopolamine is not completely known, but the drug is believed to be almost completely metabolized in the liver and excreted renally as metabolites. The elimination half-life is about 8 hours.

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Gold Standard, Inc. � 2007