What is dextromethorphan? |

History of Use

Familiar since the 1950s to people with coughs and colds, dextromethorphan (DXM) was originally developed as a safer alternative to the codeine cough syrups that were then common. DXM was long considered devoid of any potential for abuse, even though it is an opioid derivative. When taken at higher than recommended doses, however, DXM produces dissociative hallucinogenic effects. As a result, since the 1990s, abuse of over-the-counter (OTC) medications, including DXM, has grown. In 2011, only alcohol, tobacco, and cannabis were abused more frequently than OTC medications.

Effects and Potential Risks

DXM acts in the brain and spinal cord to inhibit receptors for N-methyl-d-aspartate (NMDA). As such, DXM—along with other NMDA antagonists—alters distribution of the neurotransmitter glutamate throughout the brain, in turn altering the user’s perception of pain, the user’s understanding of the environment, and the user’s memory. Subjective effects include euphoria, hallucinations, paranoid delusions, confusion, agitation, altered moods, difficulty concentrating, nightmares, catatonia, ataxia, and anesthesia. The typical clinical presentation of DXM intoxication involves hyperexcitability, lethargy, ataxia, slurred speech, sweating, hypertension, and nystagmus.

Abusers of DXM describe the following dose-dependent plateaus: mild stimulation at a dosage between 100 and 200 milligrams (mg); euphoria and hallucinations begin at a dosage of between 200 and 400 mg; between 300 and 600 mg, the user will experience distorted visual perception and loss of motor coordination; and between 500 and 1,500 mg, the user will experience dissociative sedation. These effects are experienced only when a person has consumed vastly more DXM than recommended for normal therapeutic use.

This consumptive practice is particularly dangerous when DXM is combined with other active ingredients, such as pseudoephedrine, acetaminophen, or guaifenesin. Health risks associated with abusing these latter substances include increased blood pressure (pseudoephedrine), potential liver damage (acetaminophen), and central nervous system toxicity, cardiovascular toxicity, and anticholinergic toxicity (antihistamines).

Bibliography

Cherkes, Joseph. “Dextromethorphan-Induced Neurological Illness in a Patient with Negative Toxicology Findings.” Neurology 66 (2006): 1952–53. Print.

"DrugFacts: Cough and Cold Medicine Abuse." National Institute on Drug Abuse. NIH, May 2014. Web. 27 Oct. 2015.

Heller, Jacob L. "Dextromethorphan Overdose." Medline Plus. US Nat'l. Lib. of Medicine, 18 Jan. 2014. Web 27 Oct. 2015.

Lachover, Leonard. “Deciphering a Psychosis: A Case of Dextromethorphan-Induced Symptoms.” Primary Psychiatry 14 (2007): 70–72. Print.

Zawertailo, Laurie A., et al. “Effect of Metabolic Blockade on the Psychoactive Effects of Dextromethorphan.” Human Psychopharmacology 25 (2010): 71–79. Print.