Dextromethorphan (DXM) is a synthetic chemical used as an antitussive (cough suppressant) and dissociative drug. DXM is available in countless pharmaceuticals in many countries.

DXM was approved by the US Food and Drug Administration in 1958. It was quickly discovered that DXM has potential for recreational use when high doses are ingested.
After recreational use of DXM became popular, Romilar, the original cough medicine containing only DXM in pills, was removed from the market and replaced with DXM-containing cough syrup in order to discourage recreational use. However, recreational use of DXM continued, exploded by the year 2000, and is present today almost everywhere where DXM is available. DXM-containing preparations are usually inexpensive and sold over-the-counter, which makes DXM attractive for minors. Most DXM users are teenagers and young adults.
The effects of DXM usually include dissociation of mind and body, euphoria, and closed-eye visuals, but also itching, nausea and other adverse reactions.
DXM is the dextrorotary enantiomer of levomethorphan , (-)-3-methoxy-17-methylmorphinan, an opioid. DXM is a prodrug of dextrorphan (DXO), which is the dextroroatory enantiomer of levorphanol (-)-3-Hydroxy-N-methylmorphinan. DXO has much higher affinity for NMDA receptors and is responsible for most of its dissociative effects. [1]
Common terms used for dextromethorphan are DXM, Dex, and DM. Slang names for certain pharmaceuticals containing DXM are also common, for example Robo for DXM-containing varieties of Robitussin.

Using DXM

Pure DXM hydrobromide can be consumed by either administering the powder as such (for example in a capsule) or by dissolving a dose in water or other consumable liquid and drinking the solution.
If pure DXM HBr is consumed, each dose should be weighed with a scale of minimum 100 mg (0.1 g) accuracy, preferably of 10 mg accuracy.
Pure DXM (free base) can be consumed by dissolving it in a consumable acid first. Citrus juices, citric acid in water, vitamin C (ascorbic acid) in water, vinegar, etc are suitable. This procedure results in a solution of the respective salts of DXM, which can be consumed.
Each dose of DXM base should be weighed with a minimum 100 mg (0.1 g) accurate scale (preferably 10 mg accurate) prior to preparing it for consumption. Because all doses on this page (and generally everywhere) are given for DXM hydrobromide unless otherwise specified, the dose has to be adjusted when free base is to be used. 100 mg DXM base are equivalent to 130 mg DXM HBr; 100 mg DXM HBr are equivalent to 77 mg DXM base.
DXM-containing medicinal products are usually consumed as intended. Extractions can be performed on some types of products (syrup, lozenges, etc.) to yield a more palatable product. See extractions

Ways of Administration

Swallowing DXM

Oral administration is by far the most used and documented way of consuming DXM. As with most other drugs, DXM is most potent when consumed on an empty stomach – about 4 to 6 hours after the last meal.

Snorting DXM

DXM has also been reported to be used intranasally (insufflated, snorted). There is a published case report of an individual got addicted to snorting DXM powder he thought to be amphetamine.[2] Anecdotal reports often mention very unpleasant burning in sinuses after insufflating DXM.

Injecting DXM

In some human trials, low-dose DXM was administered by injection. However, injecting DXM should not be attempted for recreational use because of the unpredictability of the effects of high-dose DXM by this route.

Rectal administration of DXM

Anecdotal evidence suggests that DXM is also active rectally.

Vaporizing DXM

DXM (both as free base and as the hydrobromide) decomposes before vaporizing, which renders smoking DXM impracticable. Decombustion products include carbon oxides, nitrogen oxide and HBr gas.[3]

First time approach

Many persons can be oversensitive to DXM and develop serious adverse effects from it. For example, people who lack the enzyme cytochrome P450 2D6 (CYP2D6) can experience overpowering effects from common recreational doses, while others develop allergic reactions from therapeutic doses. Many persons who consume high doses for their first experience with DXM will have a very unpleasant time because the effects may be unexpected and overpowering.
To prevent problems caused by an unknown oversensitivity to DXM, a low screening dose (no more than 1 mg/kg) should be consumed in order to determine the individual response to DXM. If one has never before consumed DXM therapeutically, a 20-30 mg dose should be consumed before the screening dose.
Generally, neither therapeutic nor screening doses produce noticeable effects. If one is allergic to DXM, such doses can reveal this. Many people who become sedated or dizzy after such small doses are CYP2D6 deficient. Generally, any significant effect warrants extra caution when one proceeds to higher doses.
When experimenting with dose escalation, the previous dose should be increased by increments of no more than 1.5 mg/kg (milligrams per kilogram of body weight) on each occasion.
While the screening dose should be safe in virtually all cases, each dose escalation experiment should be done in a controlled and safe environment, preferably with a sober assistant (the response to a particular dose needs to be determined as safely as possible).

Controlling use

The major cause of serious health problems caused by DXM is excessive use over a long period of time (months or years). The chronic dangers of DXM can be prevented by keeping use frequency to occasional or rare.
Depending on the consumed doses, breaks of several weeks or months are recommended to avoid chronic adverse effects. If DXM is used repeatedly over several consecutive days, minor adverse effects (lethargy, some cognitive impairment, etc) may be noticeable upon cessation. Longer breaks are required if such patterns of use are present.
Frequent use of DXM is NOT recommended. Most users experience cognitive impairment which may be severe and long lasting. See chronic adverse effects

The effects of DXM

DXM has dissociative effects, somewhat similar to ketamine and PCP. The main effects are those of dissociation (separation of mind and body), which include:
Double vision and no perception of depth (eyes are not able to focus)
Altered kinesthetic sense (distorted perception of gravity and movements)
Overall reduction of external stimuli (loosens the connection between mind and body, can lead to out-of-body experiences)
Total loss of reality awareness (dissociative anaesthesia – at high doses)
Other effects include:
Emotion amplification
Hallucinations (closed-eye visuals, vision trails and increased awareness of color, flanging of sound)
Music appreciation
The effects of DXM usually start to become noticeable 30-60 minutes after consumption (on an empty stomach), peak at about 30-60 minutes after this, and generally last 4-8 hours in total, depending on dosage.
While hangovers are often reported, some users report a so-called afterglow which may be present the day (sometimes several days) after a DXM experience. This is usually characterized by a general mood lift.
Some features of the experience, mainly timing and potency, seem to vary between different forms of DXM. For example, Zicam Cough Mist is commonly reported to act faster and more potently than Robitussin Maximum Strength Cough syrup.
The presence, intensity and duration of the above effects depend greatly on dosage. The dose and effect ranges are generally divided into so-called plateaus. There are four dosage-related DXM plateaus, and one named 'Plateau Sigma', which is achieved by prolonging DXM intake.
Note that all doses are given for dextromethorphan hydrobromide (except when otherwise specified) and represent average doses. The exact amounts vary from individual to individual. The doses presented herein should be considered rough guidelines only. They do not replace careful titration of dosage (see first time approach).

The first plateau

The first DXM plateau is achieved at a dose of 1.5 – 2.5 mg/kg. A first plateau dose is somewhat similar to a medium dose of alcohol.
Mild effects are usually experienced. They include slightly altered kinesthetic sense, music euphoria, stimulation, general mood lift, slight intoxication, lowered inhibitions (may be positive or negative, depending on the situation) and some difficulties in talking (stuttering, not being able to find the right words). Memory effects are usually not noticeable, although some may have some difficulty with short-term memory and learning.
Dancing and listening to music are generally enjoyable. Dancing and other physical activities should not be overdone.

The second plateau

The second DXM plateau ranges between dosages of 2.5 and 7.5 mg/kg. It is similar to the first plateau and is characterized by more pronounced effects.
General effects include stronger intoxication, double vision, stronger alteration of kinesthetic sense, feelings of separation to reality (most users are still able to maintain constant contact to reality at this dosage), sensation of floating and closed-eye visuals. Short-term memory is impaired, often to a significant degree. Most users are still able to conduct conversations.

The third plateau

The dosage for the third DXM plateau ranges between 7.5 and 15 mg/kg. The effects of a third plateau experience mainly consist of stronger second plateau effects, with significantly more dissociation.
The effects include complete loss of stereoscopic vision (complete double vision), periods of total disconnection from reality, flanging of the perception of time and strong intoxication. Memory and other cognitive abilities are strongly impaired, reaction speed is greatly reduced. Self-awareness is heavily impaired (their own actions may seem distant to users). Panic attacks may happen, especially to inexperienced users.
The upper DXM plateaus (third, fourth and Sigma) are generally very intense and can be overpowering for many users, especially those inexperienced with dissociatives. Cognitive and motor skills are significantly impaired at upper plateau doses. Users should never be in public or engage in potentially dangerous activities. The presence of a trip sitter is essential, especially if the user has no experience with a particular dose.

The fourth plateau

The fourth DXM plateau (15-17 mg/kg) is marked by complete dissociation of the mind from the body.
The effects of the fourth plateau resemble those of full dissociative anaesthesia. Self-awareness may subside to zero; users don't have any contact to their own body.
These effects are likely to be too intense to many users. Having no or very little awareness of reality, users are generally unable to react to emergencies, which is why a sober assistant needs to be present.
Because users are usually not able to control their body and react to emergencies, a sober trip assistant needs to be present.

Plateau Sigma

Plateau Sigma is reached by prolonging DXM intake. Plateau Sigma can be achieved by taking a low second plateau dose, then one hour after the peak taking another second plateau dose, and one hour after the second peak taking a high second plateau or a low third plateau dose.
After the third plateau experience diminishes, one is left in plateau Sigma. Open-eye visual hallucinations and psychosis-like effects may be experienced. Thoughts become very abstract and users aren't capable of doing any intellectual task.
To most users, the plateau Sigma experience is very unpleasant or too powerful to be repeated. Again, the presence of a trip sitter is vital.

Side effects

The side effects listed here may or not be undesirable but do not usually pose a significant risk to users. For dangerous adverse effects see health risks of DXM.
Nausea, vomiting: Common. Vomiting may cause suffocation if the user is unconscious or asleep. Nausea can be partly attributed to other ingredients in some cough preparations, but pure DXM HBr also causes nausea [4][5][6]
Nausea and vomiting can be prevented by using antiemetics (antiemetic antihistamines such as diphenhydramine and meclizine are suitable). Other measures which may be useful to combat nausea from DXM include: ascorbic acid (vitamin C), bismuth subsalicylate (Pepto Bismol), citric acid, citrus juices (orange, lemon), ginger tea, etc.
Metoclopramide should not be used against nausea caused by DXM, because of the possibility of serotonin syndrome[7]
[8][9]and the availability of the aforementioned safer alternatives.
Itching: Common in anecdotal reports, also a reported side effect in trials.[10] Unpleasant but usually not serious; scratching does not usually help and is not recommended. Antihistamines may alleviate or prevent itching.
Impaired speech: Common. Usually consists of slurred speech and difficulties finding words and forming sentences, which is usually controllable at moderate doses of DXM. Slurred speech has been a reported side effect in several trials[11][12][13] and in a case report.[14]
Sedation, drowsiness: Common, has been reported in trials and case reports [15]
CYP2D6 activity seems to correlate negatively with levels of sedation: Zawerailo, Kaplan, Busto, Tyndale, and Sellers (1998) found that CYP2D6 poor metabolizers experience more sedation from DXM than extensive metabolizers.
Agitation, hyperactivity, insomnia: Occasional [1,7-8,15-17] (sedation is more common). Generally not dangerous, but DXM can also cause mania (see URL="https://drugs-forum.com/threads/39191#Short-term_%28acute%29_dangers"]acute adverse effects[/URL]).
Sweating: Occasional [7]. Usually not serious. May cause dehydration and electrolyte loss in extreme cases.
Nystagmus (rapid involuntary eye movements): Common but not serious [2,7,13,18].
Hot flashes: Occasional [4], can be very unpleasant in some cases. Hot flashes may be confused with hyperthermia (an actual increase in body temperature). As a precaution, temperature may be measured.
Dry skin, mouth and nose: Occasional [4,8,17]. Dry nose from DXM may cause nose bleeding in sensitive individuals [8].
Yawning: Mentioned in anecdotal reports and in medical literature [19].
Mydriasis (dilated pupils): Common but generally not serious [7,16-18]. Is a well-known indicator of possible drug use and may cause photophobia (unpleasantness of bright light).
Erectile dysfunction, difficulty achieving orgasm: Common in males. May persist for several days.
Urinary retention (difficulty urinating): Occasional [8]. May be very unpleasant but is usually not serious.
Hangover: Many users experience hangovers from DXM, especially after upper plateau doses. Symptoms usually consist of headache, dizziness, and lethargy [1]. Hangovers may last several days for some users (especially after high doses, redosing or binges).
Hangovers can be prevented respectably by sufficient high-quality sleep (not going to sleep until the effects of DXM have mostly worn off), good hydration (especially if fluids are lost through vomiting or excessive sweating), good physical condition, healthy eating habits, etc. Avoiding overexertion is also recommended.

Combining DXM with other drugs

This section needs to be expanded.
Small amounts are said to potentiate DXM and ‘take the edge off’ (reduce stimulation and anxiety). When DXM is consumed together with alcohol (prefferably dissolved in it), absorption takes place more quickly, resulting in a shorter onset, higher peak and overall shorter duration. Large amounts may aggravate nausea and respiratory depression. See dangerous combinations.
Smoking cannabis during a DXM trip can make the experience significantly stronger, while also combating nausea. This combination may result in very intense (often overwhelmingly so) experiences, especially when high doses of DXM are used. This is most likely not physically dangerous, but the risk of panic attacks and psychotic breaks increases. This combination should not be approached by persons that are inexperienced with either DXM or cannabis. It should be noted that combining cannabis with DXM to achieve a stronger experience is probably many times physically safer than taking a higher dose of DXM.
Nitrous oxide
This is a dissociative drug like DXM, although more intense and euphoric and with a much shorter duration. Inhaling nitrous oxide during a DXM trip can result in a very dissociative experience. This is likely to be too overwhelming for many users, especially if upper-plateau doses of DXM are consumed. Therefore, this combination should not be carried out unless one is experienced with both DXM and nitrous oxide.
See also dangerous combinations.

Potentiators and enhancers of DXM

Inhibitors of cytochrome P450 3A (CYP3A) potentiate DXM by letting less DXM be metabolized into the inactive 3-methoxymorphian and less dextrorphan (DXO) be metabolized into the inactive 3-hydroxymorphinan [20].
The most common CYP3A inhibitor used to potentiate DXM is grapefruit juice. Seville orange juice is a suitable substitute with similar potency [20]. These are well-researched and should be preferred over other CYP3A inhibitors.
Itching, facial edema, rash and other allergic reactions can be at least partially prevented by taking therapeutic doses of an antihistamine prior to DXM consumption.
Diphenhydramine (Benadryl, Tylenol PM) is known to be effective for alleviating these reactions, especially itching. Therapeutic doses of other common antihistamines such as chlorpheniramine, loratadine (Claritin), etc are also suitable.
Severe allergic reactions such as anaphylaxis are too dangerous to be self-medicated and may require medical care.
Inhibitors of the enzyme cytochrome P450 2D6 (CYP2D6) slow down the conversion of DXM to dextrorphan, resulting in more potent, although less subjectively pleasant, effects. It has been reported that CYP2D6 inhibitors can be used to potentiate the dissociative effects of DXM.
This method should not be used by persons inexperienced with dissociatives. In extreme cases (high-dose DXM with long-lasting CYP2D6 inhibitors), the effects may last for days, which is capable of causing severe psychological damage to inexperienced users.
Clonazepam (Klonopin) and chlordiazepoxide (Librium) are reported to potentiate DXM. The mechanism of this interaction is not yet fully understood.
Nootropics (cognition enhancers such as DMAE, choline, lecithin, piracetam, etc) are reported to reduce the excessive confusion and memory loss caused by DXM.

Other uses for DXM

DXM is most commonly used in doses up to 30 mg every 4 to 6 hours (maximum 120 mg/day) for its antitussive (cough suppressing) effects. DXM is usually psychologically inactive at this dose, although some persons may experience some sedation.
DXM may interact with certain drugs and should only be used for unproductive (dry) cough. See health risks of medicinal use of DXM.
Another important use of DXM is to determine the activity of the enzymes cytochrome P450 2D6 (CYP2D6) and 3A (CYP3A), which are responsible for the metabolism (breakdown) of DXM [20-21]. This procedure, generally referred to as phenotyping, consists of administering a small dose of DXM (20-30 mg) to the patient and later analyzing the ratio of unmetabolized DXM to its metabolites (dextrorphan, 3-methoxymorphinan and 3-hydroxymorphinan), generally in urine. Depending on the particular ratios, patients are generally classified as either poor or extensive metabolizers.
DXM has analgesic (pain relieving) qualities in some forms of pain. DXM has been found effective as an analgesic in painful diabetic neuropathy [10,22-23], neuropathic pain of traumatic origin [4], hyperalgesia (heightened pain sensitivity often unresponsive to opiates) [24], postoperative pain [25-26] and phantom pain [27].
DXM, generally in small doses, is investigated as a means of preventing the development of and reducing tolerance to opiates and opioids [28-30], both in the recreational drug scene and in medicine. However, some studies have not found DXM to be effective for this purpose [31-34].
Anecdotal reports and some animal studies suggest that DXM also potentiates other recreational drugs, including amphetamines and cocaine [35-37].
Scientific and anecdotal reports indicate that DXM may be useful to alleviate opiate withdrawal and cravings, thus helping opiate addicts quit [38-40]. However, in a trial using naloxone-initiated opiate withdrawal, DXM was not found to be effective in alleviating withdrawal [41].
DXM is being investigated as a treatment for pseudobulbar affect (uncontrolled laughing and crying) in persons suffering from amyotrophic lateral sclerosis or multiple sclerosis [42-43]. For this purpose, DXM is used orally in doses of 30 mg, together with 30 mg quinidine to inhibit metabolism.
DXM is also reported to counteract autistic behavior [44-45], alleviate dyskinesias caused by the Parkinson's treatment levodopa [46-47], and alleviate alcohol withdrawal in rats [48].

Pharmacology of DXM

needs to be expanded

Chemistry of DXM

Column 1 Column 2
Systematic (IUPAC) name: (4bS,8aR,9S)-3-methoxy-11-methyl-6,7,8,8a,9,10-hexahydro-5H-9,4b-(epiminoethano)phenanthrene
Synonyms: (9[alpha],13[alpha],14[alpha])-3-methoxyl-17-methylmorphinan, (+)-3-methoxy-N-methylmorphinan, d-methorphan; Ro-1-5470/5, Acodin, AquiTos, Balminil DM, Benylin, Dexir, Rodefex (hydrobromide); Nuedexa (combination of the hydrobromide with quinidine sulfate)
Molecular Formula: C18H25NO, C18H25NO.HBr (hydrobromide)
Molar mass: 271.40 g/mol, 352.31 g/mol (hydrobromide) [2]
CAS Registry Number: 125-71-3, 125-69-9 (hydrobromide)
Melting Point: 109-111°C, 122-124°C
Boiling Point: no data
Flash Point: no data
Solubility: Freebase freely soluble in chloroform; practically insoluble in water. Hydrobromide approximative solubility in water 1.5% (25°C), 5% (50°C), 25% (85°C); freely soluble in ethanol, chloroform; practically insoluble in ether.
Additionnal data: pH of 1% hydrobromide aqueous solution 5.2-6.5
Notes: Freebase aspect : white to slightly yellow, odorless, crystalline powder. Hydrobromide occurs as the monohydrate

Dangers of DXM

Recreational use of DXM has more or less dangerous side effects, especially if DXM is combined with other drugs (including many pharmaceuticals), if too much is taken or if DXM is used chronically. DXM can also cause psychological addiction (habituation).
The following information is based on anecdotal reports from DXM users and on articles, reviews, and letters published in the medical literature.

Short-term (acute) dangers

Short-term dangers and side effects of DXM occur during the DXM experience and usually wear off with it or shortly after it.
These may pose a serious risk to the user. Some may require medical care.
Dizziness, imbalance, ataxia, vertigo: Common [1-2,7,10-11]. In extreme cases, users may lose coordination and accidentally injure themselves. May induce nausea in persons with motion sickness.
Acute cognitive impairment (inattention, confusion; impaired memory, judgment, reflexes and reaction speed): Common [4,7-8,10-11,13-15]. May lead users to potentially dangerous activities and impair the ability to react and make decisions in critical situations.
Users should be in a controlled environment with few potential dangers. Driving or otherwise partaking in traffic, operating machinery, and any other activities which expose the user and others to danger should be avoided. DXM is known to impair driving abilities [13]. A fatal car accident in which DXM was involved has been recently reported [49].
Tachycardia (fast heart rate), hypertension (high blood pressure), hyperthermia (overheating): Common but not particularly serious in most cases [7,9,11-12,16-17]. May cause serious reactions (hypertensive crisis, myocardial infarction, cerebrovascular accident, etc.) in susceptible individuals (high blood pressure, cardiovascular disease, etc.), or when stimulants are concomitantly used with DXM Activities which raise blood pressure and heart rate (dancing, sex, sports, etc.) should not be overdone while on DXM (overexertion is possible).
These effects could be limited with low quantities of sedatives (benzodiazepines, kava, valerian, etc.). Because of the risk of increasing respiratory depression, these should not be used in high doses.
Respiratory depression (slow and shallow breathing): Common effect of high doses but not measurable with amounts up to 480 mg [8]. May be more pronounced and possibly life-threatening at high doses or when DXM is combined with other depressants.
Urticaria (hives), fixed drug eruption, rash: Rare [4,50-51]. While usually not serious by themselves, these and other cutaneous allergic reactions may predict a more serious allergic reaction and therefore warrant discontinuing DXM.
Facial edema (swelling of face through accumulation of fluids): Rare. May warrant discontinuing DXM. May be prevented by antihistamines.
Anxiety, paranoia: Occasional [8,11,52]. While usually not serious, may trigger panic attacks in certain individuals.
Unconsciousness: Being an effect of full dissociation, it is common at upper plateau doses, especially at fourth and Sigma plateaus. Usually not dangerous per se, but the unresponsive user needs to be watched by a sober trip assistant in order to prevent possible accidents (choking on vomit, etc).
Panic attacks, bad trips: Uncommon. May be caused by unfavorable set and setting. High doses of DXM may make the user believe he or she is going to die or become insane, which may lead to panic attacks, especially in inexperienced users. Read about preventing and controlling panic attacks and bad trips here.
Convulsions (seizures): Rare [18,53-54]. Seizures are more likely to develop in susceptible individuals such as epileptics or if the seizure threshold is reduced by other drugs or non-drug factors (see factors reducing the seizure threshold).
Data on this topic is conflicting. In most trials on rodents, DXM was shown to have anticonvulsant effects [55-58], although proconvulsant (seizure-potentiating) effects were observed in two trials (on rats) [59-60]. In another trial on rats, DXM was shown to be anticonvulsant at low doses, but induced seizures at high doses [61]. In humans, daily doses of 160-200 mg DXM were shown to have anticonvulsant effects which were more pronounced in intermediate and poor metabolizers at CYP2D6 [54]. However, a moderate amount of DXM (two doses of 300 mg, taken several hours apart) in a CYP2D6 poor metabolizer was reported to cause seizures [18]. In a human trial, DXM in daily doses of 120 mg increased the frequency of complex partial seizures by 25% [53]. In another trial on brain-damaged children suffering from seizures, doses of 20-42 mg/kg DXM (with assisted respiration) had anticonvulsant effects [62].
Psychotic break: Rare [63-64]. More likely to develop at very high doses of DXM, in individuals with underlying mental health disorders, in CYP2D6 poor metabolizers, etc.

Long-term (chronic) dangers and side effects

Chronic dangers of DXM generally become apparent after DXM is consumed regularly for more than several days. These can be more or less serious, greatly varying between individuals.

Chronic cognitive impairment

Excessive use of DXM can cause chronic cognitive impairment [7,15], ranging from slightly impaired memory and concentration to inability to form proper sentences or severe cognitive decline. This is not to be confused with the acute cognitive impairment during a DXM experience, which can be similar but is short-lived.
The intensity of chronic cognitive impairment caused by excessive DXM use can vary significantly, depending on frequency of use, the length of the period over which DXM was used, individual susceptibility, etc. In most cases, chronic cognitive impairment caused by DXM usually subsides if the user is abstinent. However, there have been reported confirmed and anecdotal cases of persisting cognitive impairment caused by long-term DXM abuse [15].


Chronic DXM abuse has been associated with depression [7]. Many anecdotal reports have also described depression following long-term DXM abuse. It is possible that depression may be a symptom of DXM withdrawal, although this is unproven.

Psychological and physical dependence

Several cases describing psychological addiction to DXM have been described in the medical literature [1,7,15,52]. Psychologically addicted users often experience dysphoria and craving after ceasing DXM use.
As it often happens with psychological addiction to other drugs, DXM addiction tends to cause the addict to become very self-centered and neglect relationships, school, work, etc [15,52].
Two cases of physical withdrawal following cessation of chronic DXM abuse have been described in the medical literature. The symptoms consisted of severe nausea and vomiting, night sweats, tremor, muscle aches, abdominal pain, diarrhea, anxiety, restlessness and insomnia. Most symptoms subsided after several days [12,52].
Anecdotal reports of DXM withdrawal also include severe lethargy and headache.
It should be pointed out that the withdrawal symptoms caused by DXM are generally very mild and not comparable in intensity with those caused by opiates, alcohol, benzodiazepines, etc.


Long-term use of DXM can cause significant tolerance to its effects, some individuals being reported to use daily doses as high as 2000-3600 mg [7,52] to achieve effects.
When DXM is used regularly, the nature of effects also changes – the ‘magic’ gets lost. The positive effects DXM tend to diminish in time, while tolerance builds up and adverse effects are more pronounced. Overall, the DXM experience loses its appeal for many users (although not all). While this may be interpreted as purely physical tolerance, raising the dose doesn’t usually bring the magic back and the loss of magic is permanent in many cases.
In extreme cases (if DXM use is continued for a long time despite loss of magic), only few effects remain, the experience degrading to a state of dizziness, confusion, and discomfort.
Loss of magic can be prevented by limiting the frequency of DXM use to occasionally or rare.

Hypothetical and unconfirmed chronic side effects

Because DXM is usually supplied in the form of its hydrobromide salt, its use elevates blood bromide (Br-). Long-term heavy use may raise bromide serum concentrations to toxic levels, causing bromism. The symptoms of bromism include fatigue, ataxia, cognitive impairment, psychosis, coma, bromoderma (an acne-like skin rash), etc. The threshold of bromide toxicity is a serum concentration of about 50 mg/dL.
In a human trial of DXM HBr in doses of 120/240/480 mg/day for 4 days each, consecutively, the mean bromide serum concentration was 3.2 mg/dL at the last day of administration. The total amount of consumed bromide was 740 mg [8].
An individual who consumed approximately 1500 mg DXM HBr per week for about one year had a bromide serum concentration of 27.2 mg/dL, which is still well below the threshold of toxicity [15].
In a controlled trial on humans, administration of 9 mg/kg/day bromide (the equivalent of about 2860 mg DXM HBr daily) for 12 weeks raised bromide concentrations to 34 mg/dL, whereas the threshold of bromide toxicity is 50 mg/dL. The recorded side effects consisted of slightly impaired concentration and drowsiness in males, and mild hyperthyroidism in females [65].
Although some effects of heavy DXM use certainly resemble bromism, it can be concluded the actual risk of bromism from DXM use is very low and that bromide has little to no role in the adverse effects of DXM.
In 1989, it was discovered that injecting very high doses of NMDA antagonists causes neuron death and chronic learning impairment in rats. These lesions are known as NMDA antagonist neurotoxicity (NAN) or Olney’s lesions (after their discoverer, John W. Olney).
Injected into rats, DXM and its metabolite dextrorphan induce heat-shock protein, which is related to NAN. Orally administered DXM, even in lethal doses or administered chronically, was shown not to cause NAN in rats [66].
Some have suggested that recreational use of DXM (and use of NMDA antagonists in general) causes these lesions in humans. However, this was never proven and there is circumstantial evidence that NAN does not have anything to do with the cognitive impairment caused by some NMDA antagonists in humans. See NMDA antagonist neurotoxicity.
Because DXM raises blood pressure [7-9,11-12,16,67], it should be expected that DXM increases the risk of heart attack, stroke and heart failure if used chronically. This should be considered especially if other risk factors (obesity, pre-existing high blood pressure, high cholesterol, caffeine dependence, etc.) are present.

Where caution or abstinence is warranted

Because DXM raises blood pressure [7-9,11-12,16,67], it should not be used recreationally by persons with atherosclerosis, cardiovascular disease, or other conditions which contraindicate use of stimulants. Caution is also advised to persons with a family history of aforementioned conditions.
Persons with psychological and neurological disorders should be very careful with DXM, due to possible exacerbation of the illness.
DXM has been reported to exacerbate schizophrenia [68]. It is believed that some depressives may self-medicate with DXM [69], which can cause addiction and exacerbate the depression in time.
Persons suffering from bipolar disorder should be cautious, because DXM can cause mania [70-71] and mood swings resembling bipolar disorder [1,15], as well as exacerbate existing bipolar disorder [71].
Because DXM can cause seizures in some individuals (see short-term dangers), extreme caution is also warranted in epileptics and persons with a history of seizures in general.
The only controlled study of the effects of DXM in pregnancy has failed to show any significant effect of therapeutic use of DXM in the first trimester of pregnancy on the rate of birth defects [72]. However, DXM was shown to be teratogenic (i.e. cause birth defects) on chicken embryos [73] and NMDA antagonists in general are possible teratogens.
DXM is most likely safe to use therapeutically in pregnancy, but due to few safety data, recreational use of DXM during pregnancy is not recommended.
Because DXM may suppress respiration, high doses may be problematic to persons suffering of conditions which impair respiration, such as COPD (emphysema, bronchitis), lung cancer, severe asthma, etc.
CYP2D6 poor metabolizers (individuals who lack the cytochrome P450 2D6 enzyme) metabolize DXM to dextrorphan at a much lower rate than normal [4,11,14]. For these persons, the effects of DXM are prolonged, psychomotor impairment is more intense, and the overall effects are significantly less enjoyable. In a published pilot study, CYP2D6 poor metabolizers could barely tolerate doses of 3 mg/kg (lower-end second plateau), while extensive metabolizers (the majority of the population) could tolerate 6 mg/kg, which was the highest tested dose [14].
People who know to be CYP2D6 deficient should be very cautious (see first time approach). 5-10% of caucasians are CYP2D6 poor metabolizers, but prevalence varies widely between different populations.
The metabolites of DXM are excreted through the kidneys. Persons with kidney failure are expected to clear DXM much more slowly than persons with normally functioning kidneys, which can cause effects of very long duration. Persons with kidney failure should not risk consuming DXM recreationally.

Dangerous and otherwise undesirable interactions with DXM

Because it inhibits serotonin reuptake [74-76] and stimulates its release [77], DXM may cause serotonin syndrome when combined with other serotonergic drugs (drugs which increase brain serotonin activity). Although serotonin syndrome is rare, it is a serious and potentially lethal condition. Cases of serotonin syndrome in which DXM played a role also involved:
Generally, serotonin reuptake inhibitors and releasers only cause death (due to serotonin syndrome) when combined with MAO inhibitors; therefore, combinations of DXM and MAO inhibitors should be avoided. Although generally not resulting in death, combining DXM with other serotonin reuptake inhibitors (SSRI antidepressants, venlafaxine, tramadol, pethidine, etc) and serotonin releasers (MDMA, MBDB, methylone, amphetamines, etc) can cause serotonin syndrome and should be avoided or approached with great caution (testing at low doses, etc). See serotonergic drugs.
Although data on DXM and seizures is conflicting (see acute adverse effects), caution is advised when combining DXM with seizure threshold-reducing drugs or when other seizure threshold-reducing factors are present (see seizure threshold-reducing factors).
Inhibitors of the enzyme cytochrome P450 2D6 (CYP2D6) slow down the conversion of DXM to dextrorphan. Commonly used CYP2D6 inhibitors include bupropion (Wellbutrin, Zyban), citalopram (Celexa), escitalopram (Lexapro), fluoxetine (Prozac), paroxetine (Paxil), etc.
Using DXM in combination with CYP2D6 inhibitors resembles the effects of DXM in CYP2D6 poor metabolizers, which are generally characterized by much more potent and less pleasant effects (see where caution or abstinence is warranted).
Note that after chronic use of a CYP2D6 inhibitor, some time is required for CYP2D6 activity to return to normal. Small amounts of DXM, such as low first plateau doses, may be used to determine individual response. See CYP2D6 inhibitors.
When combined with DXM, stimulants can amplify the tachycardia and hypertension caused by DXM and also increase the possibility of seizures (see acute adverse effects). Such combinations are capable of causing hypertensive crisis, hyperthermia, and possibly cerebrovascular addicent (stroke) and myocardial infarction (heart attack). The seriousness of such interactions is proportional with the intensity of the stimulant taken and the consumed doses of both substances (consuming large amounts of cocaine after third plateau DXM is likely much worse than first plateau DXM with a cup of coffee). Preexisting risk factors also play an important role – see where abstinence or caution is warranted.
Alcohol can significantly amplify the nausea and vomiting caused by DXM. Respiratory depression may also be a potentially lethal problem when both DXM and alcohol are consumed in large doses (see below). Large amounts of alcohol should not be combined with DXM.
Using depressant drugs (alcohol, benzodiazepines, barbiturates, opiates, kava, etc) with DXM may depress respiration to life-threatening levels.
DXM in large amounts (upper plateau doses) causes respiratory depression by itself, and other depressants add to this effect. Concomitantly consuming low doses of both DXM and a depressant is most likely safe. Three recorded deaths have been caused by DXM in combination with other depressants (two from DXM+diphenhydramine, one from DXM+diphenhydramine+alcohol).
Because DXM is a mild competitive cytochrome P450 3A (CYP3A) inhibitor in high doses, it should not be used with the antihistamines terfenadine and astemizole. These can cause cardiac arrhythmias (heart irregularities), especially when used with CYP3A inhibitors or when overdosed upon. One reported death has been attributed to a combination of high-dose DXM and terfenadine [83].
It should be noted that some internet sources warn against using DXM with nonsedating (non-drowsy) antihistamines in general. However, cardiotoxicity is not a class effect of nonsedating antihistamines but believed to be unique to terfenadine and astemizole. Both terfenadine and astemizole have been withdrawn from the market in most countries.
Recent reports indicate that massive doses of cetirizine (Zyrtec), another nonsedating antihistamine, can also cause arrhythmias. As a precaution, concomitant use of cetirizine and DXM should be avoided.

Because of being a competitive CYP2D6 inhibitor, DXM can cause potentially severe interactions with a number of medications:
  • Amitriptyline (Elavil), nortriptyline (Pamelor), desipramine (Norpramin), imipramine (Tofranil). CYP2D6 inhibitors increase the toxicity of these tricyclic antidepressants. Combination should be avoided.
  • Risperidone (Risperdal): CYP2D6 inhibitors increase extrapyramidal side effects. Combination should be avoided.
  • Codeine, tramadol (Ultram): CYP2D6 inhibitors decrease analgesic efficacy.
  • Flecainide, mexiletine (Mexitil), propafenone (Rythmol). CYP2D6 inhibitors increase the potential for arrhytmias. Combination should be avoided.
  • Haloperidol (Haldol): CYP2D6 inhibitors may increase side effects.
  • Propranolol: CYP2D6 inhibitors may increase hypotensive effects. Combination should be avoided.
  • Trazodone (Desyrel): CYP2D6 inhibitors increase side effects. Combination should be avoided.

Dangerous ingredients in DXM products

DXM is most commonly used in the form of a pharmaceutical. Depending on the product, this may pose a significant risk to the user.

Multiple active ingredients

Combination (multi-symptom) products which contain other active ingredients besides DXM are common in some countries. When consumed in recreational doses, combination products can be dangerous because of the toxicity of the other active substances.
Information on the most common active ingredients found in combination products containing DXM is listed below.


Guaifenesin is a mucolytic agent which aids in coughing up mucus. High amounts can cause nausea and vomiting. Chronic high-dose abuse can result in kidney stones.

Acetaminophen (paracetamol, APAP)

Acetaminophen is a drug commonly used to relieve minor pain and to reduce fever. In high doses, over 4000 mg/day, it can cause liver damage, which can be fatal. Products containing acetaminophen often contain 500-1000 mg per dose.


Anticholinergic antihistamines such as chlorpheniramine and diphenhydramine are often present in combination cold preparations. Overdose generally manifests itself in drowsiness, dry mucosa, blurred vision, urinary retention, tachycardia, dysphoria and delirium. Both can prolong the QT interval, raising the risk of cardiac arrythmias.
Chlorpheniramine maleate is an antihistamine used in combination with DXM in Coricidin HBP Cough & Cold and some generics. Besides the risks of overdose, chlorpheniramine is especially dangerous because it is a potent inhibitor of CYP2D6 (which potentiates DXM, prolongs toxicity and may cause toxic chlorpheniramine buildup when used repeatedly), a serotonin reuptake inhibitor (a case of serotonin syndrome has been reported [78]), and a respiratory depressant. Coricidin HBP Cough & Cold is notorious for causing adverse reactions and deaths at relatively low doses, having a significantly higher risk profile than DXM alone [84-85].
Diphenhydramine causes respiratory depression and is a serotonin receptor agonist (primarily 5-HT 2A and 2C) and CYP2D6 inhibitor. Products containing diphenhydramine and DXM should not be used recreationally.

Systemic nasal decongestants

Pseudoephedrine is a sympathomimetic and psychostimulant mostly used to relieve nasal congestion. High doses can cause tachycardia, hyperthermia, and hypertension. Products containing pseudoephedrine besides DXM should not be used recreationally.
Phenylephrine (neosynephrine) is growing increasingly popular as a decongestant due to the use of pseudoephedrine as a meth precursor and is found besides DXM in some combination products. Phenylephrine is a potent vasopressor (causes hypertension) even in single doses, being potentially dangerous or fatal when used in high doses with DXM. Products containing phenylephrine should never be used recreationally.

Potentially dangerous inactive ingredients

While generally posing a less significant health risk to users, some inactive ingredients (excipients) in certain pharmaceuticals may be dangerous for some persons or if they are consumed in high doses.
Sugars & other sweeteners
Most cough syrups contain sugars (sucrose, glucose, high-fructose corn syrup, etc.) and other sweeteners, mostly sugar alcohols (sorbitol, glycerine, mannitol, etc).
Sorbitol is commonly used as a sweetener in chewing gum, cough syrups, low-calorie foods, etc. In large amounts, it can cause abdominal pain, bloating and diarrhea.
Cough syrups containing large amounts of sugars should not be used chronically. Sugar is linked to tooth decay, obesity, insulin resistance, etc. Because sugar-containing cough syrup can have a very high caloric value, chronic abuse may also result in malnutrition, as it often occurs in alcoholics. For obvious reasons, diabetics should avoid any cough syrups containing sugar. Syrups formulated for diabetics are available, although these may contain sorbitol as a sweetener.
Food colorings such as tartrazine (E102, FD&C Yellow 5), Allura Red AC (E129, FD&C Red 40), Brilliant Blue FCF (E133, FD&C Blue 1) and others are often used in pharmaceuticals. These may cause allergic reactions in a minority of users, as well as hyperactivity. Effects of chronic high doses of these colorings are generally unknown in humans.

DXM deaths

Two deaths resulting from overdose on DXM alone have been reported in the medical literature. Both took place in Sweden. One case was a suicide of an 18-year-old girl who most likely ingested 3000 mg. The other case involved uncertain amounts of DXM and suspected chronic abuse, in a 27-year-old man [86].
Several other fatalities caused by DXM have been reported by the media and websites about DXM [dextromethorphan.ws, indexed 6 Feb 2006]. Most of these involved use of unknown amounts of DXM HBr powder. Most victims used or intended to use DXM recreationally, but at least two cases were intentional suicides. Most deaths occurred in the US, while one was reported from Sweden.
Several deaths have been caused by concomitant use of DXM and other drugs. One death thought to be caused by an interaction between DXM and terfenadine was reported in the medical literature [83]. Another case is thought to be caused by an interaction between DXM and the monoamine oxidase inhibitor phenelzine [81]. Two teenagers died in February 2005 after overdosing on DXM powder and diphenhydramine. Another reported death involved alcohol and a product containing DXM and diphenhydramine. From 1993 to 1996, nine deaths caused by concomitant recreational use of DXM and zipeprol (another opioid antitussive which is used recreationally) have been reported in Korea [87].
Most fatalities caused by DXM alone share a common point: consumption of very large amounts of pure DXM HBr in powder form, in most cases without weighing the doses.
Any purified form of DXM (hydrobromide or free base) should not be consumed without weighing each dose with a scale of at least 10 mg accuracy. Estimating (eyeballing) the right amount of powder is generally not possible, which can result in overdose.
Although chronic users can build up a massive tolerance to DXM and may be resistant to doses that would kill any beginner, continuing use with a high tolerance should be avoided.
Anything above the third plateau (doses higher than 15 mg/kg) should be considered very risky and preferably avoided.

DXM as an antitussive - side effects and risks

Medicinal use of DXM as an antitussive (in maximal doses of 30 mg every 4 hours, not exceeding 120 mg/day) is generally safe but may have side effects.
DXM should not be used to treat productive cough (accompanied by mucus). It should only be used to treat nonproductive (dry) or slightly productive cough.
DXM should be used for a limited period of time. If cough persists for more than several days, a health care professional should be contacted, as persistent cough may indicate serious underlying conditions.
Possible adverse effects include drowsiness, dizziness, nausea, vomiting, agitation, and allergic reactions (skin rash, bronchospasm, etc).
Using DXM in conjunction with central nervous system depressants (alcohol, sedative antihistamines, anxiolytics, hypnotics, etc) can increase drowsiness.
DXM should not be used with MAO inhibitors (nonselective MAO inhibitors and selective MAO-A inhibitors), because of the possibility of serotonin syndrome.
DXM can cause drowsiness and dizziness, which can impair the ability to drive and operate machinery. The individual response to therapeutic doses of DXM should be assessed before planning to drive or operate machinery.
Because of inconclusive data on its safety in pregnancy, DXM should be avoided during pregnancy and lactation unless necessary.
Therapeutic use of DXM in toddlers has repeatedly resulted in death. DXM should not be administered to anyone under 4 years of age unless directed by a physician.

Producing DXM

DXM can be extracted from different types of cough preparations. This can be useful for a number of reasons. First, the product will be very pure, which means it will be a smaller amount to consume, which helps in combating nausea (from drinking a bottle or more of cough syrup). Also, the Agent Lemon method will result in DXM as a hydrocitrate salt, which eliminates the danger of bromide poisoning (see hypothetical chronic side effects). Other extraction methods help separate DXM from other, potentially harmful ingredients of the cough preparation. If not stated otherwise, preparations containing DXM as the only active ingredient are used for extraction. Note that the procedures described might be illegal in some jurisdictions and should not be carried out without legal permission.

Agent Lemon extraction

This extraction starts from DXM cough syrup or soft gels and results in a solution of DXM hydrocitrate in water (or DXM free base). 3 mg/ml DXM syrup is used, with DXM as the only active ingredient.
If soft gels are used, they have to be opened, the contents dissolved in some water and poured into the 2 liter bottle. The concentration of the resulting liquid has to be adjusted to be approximately 3 mg DXM/ml (the same as the used syrup).
For each 8 oz of syrup, 1.5 tablespoons citric acid are dissolved in 4 fl. oz of water.
The syrup (or dissolved soft gels) is poured into a 2 liter plastic bottle.
An about equal amount of ammonia is added. Clear household ammonia (cleaning grade, 5% ammonia) is used, not scented/cloudy ammonia.
The solution is shaked for at least five minutes.
An about 1 cm thick layer of naphtha (Zippo lighter fluid) is added to the solution. Other non-polar solvents can also be used.
The solution is shaked again, for at least five minutes, after which the two layers are left to separate thoroughly.
The contents of the bottle are poured into a sealable plastic bag, which is then sealed. The layers are left to separate again, if needed.
The bag is held up by one (top) corner, so that a bottom corner faces down.
The bottom corner is held over a sink. The edge of the plastic bag is cut off. The smaller the hole is, the better.
The bottom layer (syrup) is left to drain into the sink, but the bag is quickly put over a clean jar after the syrup is gone, so the naphtha will get into the jar.
The citric acid solution is added to the naphtha. The liquids are shaked for at least five minutes.
The plastic bag method is used to separate the layers, but now the bottom (citric acid) layer is needed, not the naphtha.
The naphtha is discarded by letting it evaporate outdoors.
The citric acid solution is boiled for some time, so the volume gets smaller and remaining naphtha will evaporate. The liquid is an aqueous solution of DXM hydrocitrate, with some citric acid. This can be drunk or boiled down to obtain a water soluble powder.
It is a little easier to obtain DXM free base using this extraction. For this, the naphtha+DXM solution is left to evaporate (in a glass dish, in a ventilated area). The resulting crystals (DXM free base) are scraped off. See ways of using DXM for information about consumption.

Sucrets extraction

This method is designed to extract DXM HBr from Sucrets Four (TM) lozenges, which contain 10 mg DXM HBr each. Many variations of Sucrets lozenges are available, many of which don’t contain DXM at all (there is another variation which contains 15 mg DXM per lozenge). The active ingredients have to be checked prior to doing this extraction.
Lozenges are crushed until fine. If this is not possible for some reason, leaving them whole just makes the extraction take more time.
The crushed lozenges are covered withhot water.
The liquid is microwaved for one minute (high power), then stirred well.
The above step is repeated until the lozenges are dissolved. If a microwave is not available, the lozenges can be dissolved using a stove to heat the mixture.
When the lozenges are dissolved, the liquid is left to sit until the white powder (DXM HBr) settles. The liquid is removed, for example with a syringe. The less liquid+powder left, the better (but no powder has to be lost).
The resulting mixture can be mixed into a beverage and drunk.

Cold water extraction

This extraction starts from tablets containing DXM and results in a solution of DXM HBr in water. It is also capable of removing acetaminophen if present in the tablets. If the product does not contain acetaminophen, warm water can be used to improve DXM solubility.
The right amount of pills is crushed into fine powder.
The powder is stirred into an amount of water at room temperature (50-100 ml per 100 mg DXM HBr).
The solution is stirred and then left undisturbed for at least 30 minutes.
The solution is filtered with a coffee filter (filter paper is better). All liquid is squeezed out of the filter. Most of the fillers and binders (and, if present, the acetaminophen) are filtered out and don’t go into the solution.
The resulting solution consists of DXM hydrobromide, lactose , and eventually other water soluble fillers.

Forms of DXM

DXM can be found in the following forms :


Dextromethorphan hydrobromide (DXM.HBr) is available from many chemical suppliers. This salt occurs as the monohydrate form.

DXM cough preparations

More commonly, DXM is available in the form of several types of cough preparations, very often in combination with other active ingredients. The use of products containing other active ingredients besides DXM can be dangerous and has repeatedly been been fatal. Always check if DXM is the only active ingredient in your product.

DXM tablets
Tablets containing only DXM are very rare and usually found only in some countries. These tablets usually contain DXM HBr and some commonly used excipients (binders and fillers): lactose, magnesium stearate, talc, microcrystalline cellulose, etc. Tablets are, besides pure DXM, one of the best suited forms of DXM for ingestion. Some brand names of tablets containing only DXM are Tussin (available in Romania), Tussal, Acodin (available in Poland), etc.

DXM gelatin capsules
Gelatin capsules containing DXM are found more commonly. These usually contain DXM HBr and eventually some excipients, in a two-piece gelatin capsule. These are also a superior method of consuming DXM. DXM-containing capsules are available at head shops (these may contain high doses of DXM in each capsule), from internet suppliers, or as cough medicine (up to 30 mg per capsule), for example DexAlone.

DXM soft gels
Soft gels are a different form of gelatin capsules, but they are thicker and they cannot be opened without breaking them. DXM-only soft gels enclose a thick liquid, which contains DXM HBr. If ingested, soft gels take about an hour to dissolve in the stomach, which causes a longer duration of onset. Some brand names of DXM soft gels are Drixoral Cough Liquid Caps, Robitussin Cough Gels.

DXM lozenges
DXM-containing lozenges are pieces of small candy, which are intended to dissolve in the mouth. These can be either consumed normally, or dissolved in hot water and drunk. A brand name for DXM lozenges is Sucrets.

DXM cough syrup
DXM cough syrup is probably the most common form of medically-used DXM. DXM cough syrup is considered to have low abuse potential, mainly because of the unpleasantness of drinking large amounts of it, and because of some thickening, flavoring and sweetening agents present in the syrup, which can worsen the nausea caused by DXM. DXM from cough syrup is absorbed rapidly into the system. DXM cough syrup is found under many brand names, which include: Buckley’s Mixture, CVS Tussin Cough, Robitussin Cough Suppressant, Vicks 44 Cough, etc.

DXM throat spray
DXM is also available in the form of a throat spray, which has a high concentration of DXM. A brand name for DXM throat spray is Zicam Cough Mist Max, which contains 6 mg DXM HBr per spray. Throat spray is usually easier to ingest than DXM cough syrup, because of the smaller amount of liquid.

DXM long-release suspension
Another form of DXM is a long-release suspension, which contains DXM Polistirex. Polistirex is an edible plastic which gradually dissolves in the body, slowly releasing the DXM. This form of DXM is not recommended for recreational use. A brand name for this form of DXM is Delsym Extended-Release Suspension.

Legal status of DXM

This chapter needs to be written. See [[How to write an article]]

History of DXM

DXM was developed in Switzerland in the late 1940s. [16][17][18][19]
DXM was approved as a cough suppressant by the Food and Drug Administration, in 1958. DXM was the product of a long search for [[opiate]] antitussives and analgesics with no abuse and addiction potential. DXM replaced codeine, which was commonly used and abused at that time. DXM was found to be an effective cough suppressant, not psychoactive at normal doses, and not physically addictive.

DXM first appeared on the market in 1960, under the brand name Romilar, a product containing DXM as the only active ingredient. The abuse potential of DXM was soon discovered.

In 1973, Romilar was removed from the market. After a time, DXM was re-released, in the form of syrup, in order to discourage abuse.

Recreational use of DXM continued, but was never very pronounced, probably because of the US-led ‘war on drugs’ and the rising popularity of psychedelics like LSD, psilocybin, mescaline, etc. It is known that DXM use was popular in the hardcore punk subculture in the 1980s.

DXM was introduced as a cough suppressant in many parts of the world, but recreational use was never very pronounced, mainly because of lack of information.

When the internet started to take shape in the 1990s, more information about recreational DXM use started to spread. Websites dedicated to DXM appeared, which helped to provide factual information about recreational use of DXM. William E. White wrote his famous ‘[http://www.erowid.org/chemicals/dxm.faq DXM FAQ]’, which condensed most information on DXM available at that time. The DXM FAQ was updated several times and is constantly expanding. At this time, internet chemical suppliers and head shops started to sell pure DXM hydrobromide powder, which is still happening today.

By the year 2000, recreational DXM use already got major public attention, especially in the US, mainly because of some deaths linked to DXM abuse. This led to attempts to regulate the distribution of DXM-containing cough-medicines. The state of Illinois banned the distribution and possession of DXM which is not intended for human consumption (and FDA-approved). Most large chain-stores and pharmacies started to refuse sales of DXM-containing cough medicine to minors, and limited the maximum amount of containers of DXM cough medicine per customer to two or three. On January 11th, 2006, two men who sold DXM over the internet were convicted after 5 persons died ingesting their product.


  1. ^Zawertailo, L. A., Kaplan, H. L., Busto, U. E., Tyndale, R. F., & Sellers, E. M. (1998). Psychotropic effects of dextromethorphan are altered by the CYP2D6 polymorphism: a pilot study. Journal of clinical psychopharmacology, 18(4), 332-337.
  2. ^Fleming PM. Dependence on dextromethorphan hydrobromide (letter). British Medical Journal 1986;293:597.
  3. ^Sigma-Aldrich; Material Safety Data Sheet for Dextromethorphan hydrobromide, Product Number: D9684, Version 5.2
  4. ^Fleming PM. Dependence on dextromethorphan hydrobromide (letter). British Medical Journal 1986;293:597.
  5. ^Steinberg GK, Bell TE, Yenari MA. Dose escalation and safety study of the N-methyl-D-aspartate antagonist dextromethorphan in neurosurgery patients. Journal of Neurosurgery 1996 May;84(5):860-6.
  6. ^Wadhwa A, Clarke D, Goodchild GS, Young D. Large-dose oral dextromethorphan as an adjunct to patient-controlled analgesia with morphine after knee surgery. Anesthesia & Analgesia 2001 Feb;92(2):448-54.
  7. ^Fisher, A. A., & Davis, M. W. (2002). Serotonin syndrome caused by selective serotonin reuptake-inhibitors-metoclopramide interaction. The Annals of pharmacotherapy, 36(1), 67.
  8. ^Kung, S. W., & Ng, M. H. (2007). Serotonin syndrome with tramadol and dextromethorphan. Hong Kong Journal of Emergency Medicine, 14(1), 48-52.
  9. ^Carlsson, K. C., Hoem, N. O., Moberg, E. R., & Mathisen, L. C. (2004). Analgesic effect of dextromethorphan in neuropathic pain. Acta anaesthesiologica scandinavica, 48(3), 328-336.
  10. ^Wadhwa, A., Clarke, D., Goodchild, C. S., & Young, D. (2001). Large-dose oral dextromethorphan as an adjunct to patient-controlled analgesia with morphine after knee surgery. Anesthesia & Analgesia, 92(2), 448-454.
  11. ^Carlsson, K. C., Hoem, N. O., Moberg, E. R., & Mathisen, L. C. (2004). Analgesic effect of dextromethorphan in neuropathic pain. Acta anaesthesiologica scandinavica, 48(3), 328-336.
  12. ^Cornish, J. W., Herman, B. H., Ehrman, R. N., Robbins, S. J., Childress, A. R., Bead, V., ... & O'Brien, C. P. (2002). A randomized, double-blind, placebo-controlled safety study of high-dose dextromethorphan in methadone-maintained male inpatients. Drug & Alcohol Dependence, 67(2), 177-183.
  13. ^Steinberg, G. K., Bell, T. E., & Yenari, M. A. (1996). Dose escalation safety and tolerance study of the N-methyl-D-aspartate antagonist dextromethorphan in neurosurgery patients. Journal of neurosurgery, 84(5), 860-866.
  14. ^Wolfe, T. R., & Caravati, E. M. (1995). Massive dextromethorphan ingestion and abuse. The American journal of emergency medicine, 13(2), 174-176.
  15. ^Carlsson et al., 2004; Cochems, Harding, & Liddicoat, 2007; Desai, Aldea, Daneels, Soliman, Braksmajer, & Kopes-Kerr, 2006; Nelson, Park, Robinovitz, Tsigos, & Max, 1997; Schneider, 1991; Steubing, 2005
  16. ^Hellerbach J, Schnider 0, Besendorf H, Pellmont B. Synthetic Analgesics, part IIA: Morphinans. Pergamon Press Ltd, New York, 1966.
  17. ^Schnider O & Grüssner A. (1949). Synthese von Oxy‐morphinanen. Helvetica Chimica Acta, 32: 821-828.
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  19. ^Process for the preparation of optically active 3-methoxy-N-methylmorphinans and salts thereof. U.S. Patent No. 2,676,177. Washington, DC: U.S. Patent and Trademark Office.

1. Fleming PM. Dependence on dextromethorphan hydrobromide (letter). British Medical Journal 1986;293:597.

2. Steinberg GK, Bell TE, Yenari MA. Dose escalation and safety study of the N-methyl-D-aspartate antagonist dextromethorphan in neurosurgery patients. Journal of Neurosurgery 1996 May;84(5):860-6.

3. Wadhwa A, Clarke D, Goodchild GS, Young D. Large-dose oral dextromethorphan as an adjunct to patient-controlled analgesia with morphine after knee surgery. Anesthesia & Analgesia 2001 Feb;92(2):448-54.

4. Carlsson KC, Hoem NO, Moberg ER, Mathisen LC. Analgesic effect of dextromethorphan in neuropathic pain. Acta Anaesthesiologica Scandinavica 2004 Mar;48(3):328-36.

5. Fisher AA, Davis MW. Serotonin syndrome caused by selective serotonin reuptake-inhibitors-metoclopramide interaction. Annals of Pharmacotherapy 2002 Jan;36(1):67-71.

6. Kung SW, Ng MH. Serotonin syndrome with tramadol and dextromethorphan. Hong Kong Journal of Emergency Medicine 2007 Jan;14(1):48-52.

7. Wolfe TR, Caravati EM. Massive dextromethorphan ingestion and abuse. American Journal of Emergency Medicine 1995 Mar;13(2):174-6.

8. Cornish JW, Herman BH, Ehrman RN, Robbins SJ, Childress AR, Bead V, Esmonde CA, Martz K, Poole S, Caruso FS, O'Brien CP. A randomized, double-blind, placebo-controlled safety study of high-dose dextromethorphan in methadone-maintained male inpatients. Drug and Alcohol Dependence 2002 Jul 1;67(2):177-83.

9. Schneider SM. Dextromethorphan poisoning reversed by naloxone. American Journal of Emergency Medicine 1991;9:237-8.

10. Nelson KA, Park KM, Robinovitz E, Tsigos C, Max MB. High-dose oral dextromethorphan versus placebo in painful diabetic neuropathy and postherpetic neuralgia. Neurology 1997 May;48(5):1212-8.

11. Steubing D. Comparison of the induced subjective effects in alcoholics and healthy subjects after experimental challenge with the NMDA antagonist dextromethorphan. Dissertation of the Ludwig-Maximilians-University, München, 2005 (German).

12. Desai S, Aldea D, Daneels E, Soliman M, Braksmajer AS, Kopes-Kerr CP. Chronic addiction to dextromethorphan cough syrup: a case report. Journal of the American Board of Family Medicine 2006 May-Jun;19(3):320-3.

13. Cochems A, Harding P, Liddicoat L. Dextromethorphan in Wisconsin drivers. Journal of Analytical Toxicology 2007 May;31(4):227-342.

14. Zawertailo LA, Kaplan HL, Busto UE, Tyndale RF, Sellers EM. Psychotropic effects of dextromethorphan are altered by the CYP2D6 polymorphism: a pilot study. Journal of Clinical Psychopharmacology 1998 Aug;18(4):332-7.

15. Hinsberger A, Sharma V, Mazmanian D. Cognitive deterioration from long-term abuse of dextromethorphan: a case report. Journal of Psychiatry & Neuroscience 1994 Nov;19(5):375-7.

16. Budai B, Iskandar H. Dextromethorphan can produce false positive phencyclidine testing with HPLC (letter). American Journal of Emergency Medicine 2002 Jan;20(1):61-2.

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26. Avi A. Weinbroum, Benjamin Bender, Alexander Nirkin, Shoshana Chazan, Isaac Meller, and Yehuda Kollender, Dextromethorphan-associated epidural patient-controlled analgesia provides better pain- and analgesics-sparing effects than dextromethorphan-associated intravenous patient-controlled analgesia after bone-malignancy resection: a randomized, placebo-controlled, double-blinded study (2004), Anesthesia & Analgesia, March 2004, Vol. 98, Issue 3, Pages 714-722

27. Ben Abraham R, Marouani N, Weinbroum AA. Dextromethorphan mitigates phantom pain in cancer amputees. Annals of Surgical Oncology 2003 Apr;10(3):268-74.

28. Kathryn Elliott, Alexandra Hynansky, Charles E. Inturrisi, Dextromethorphan attenuates and reverses analgesic tolerance to morphine (1994), Pain, Vol. 59, Issue 3, December 1994, Pages 361–368

29. Barton H. Manning, Jianren Mao, Hanan Frenk, Donald D. Price, David J. Mayer, Continuous co-administration of dextromethorphan or MK-801 with morphine: attenuation of morphine dependence and naloxone-reversible attenuation of morphine tolerance (1996), PAIN, Vol. 67, Issue 1, September 1996, Pages 79–88

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32. Tarja Heiskanen, Brita Härtel, Marja-Liisa Dahl, Timo Seppälä, Eija Kalso, Analgesic effects of dextromethorphan and morphine in patients with chronic pain (2002), Pain, Vol. 96, Issue 3, April 2002, Pages 261–267

33. Bradley S. Galer, David Lee, Tina Ma, Barbara Nagle, Thomas G. Schlagheck, MorphiDex (morphine sulfate/dextromethorphan hydrobromide combination) in the treatment of chronic pain: three multicenter, randomized, double-blind, controlled clinical trials fail to demonstrate enhanced opioid analgesia or reduction in tolerance (2005) (abstract), Pain, Vol. 115, Issue 3, June 2005, Pages 284–295

34. Deborah J. Dudgeon, Eduardo Bruera, Bruno Gagnon, Sharon M. Watanabe, Sharon J. Allan, David G. Warr, Susan M. MacDonald, Colleen Savage, Dongsheng Tu, Joseph L. Pater, A phase III randomized, double-blind, placebo-controlled study evaluating dextromethorphan plus slow-release morphine for chronic cancer pain relief in terminally ill patients (2007), Journal of Pain and Symptom Management, Vol. 33, Issue 4, April 2007, Pages 365–371

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36. Kim HC, Park BK, Hong SY, Jhoo WK. Dextromethorphan alters the reinforcing effect of cocaine in the rat (abstract). Methods & Findings in Experimental & Clinical Pharmacology 1997 Nov;19(9):627-31.

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39. H. Koyuncuoǧlu, M. Güngör, H. Saǧduyu, F. Aricioǧlu, Suppression by ketamine and dextromethorphan of precipitated abstinence syndrome in rats (1990), Pharmacology Biochemistry and Behavior, Vol. 35, Issue 4, April 1990, Pages 829–832

40. Bisaga A, Gianelli P, Popik P. Opiate withdrawal with dextromethorphan. American Journal of Psychiatry 1997 Apr;154(4):584.

41. Rosen MI, McMahon TJ, Woods SW, Pearsall HR, Kosten TR. A pilot study of dextromethorphan in naloxone-precipitated opiate withdrawal. European Journal of Pharmacology 1996 Jul 4;307(3):251-7.

42. B. R. Brooks, R. A. Thisted, S. H. Appel, W. G. Bradley, R. K. Olney, J. E. Berg, L. E. Pope, R. A. Smith, Treatment of pseudobulbar affect in ALS with dextromethorphan/quinidine: a randomized trial (2004), Neurology, 2004/Oct/26, Vol. 63, No. 8, Pages 1364-1370

43. Panitch HS, Thisted RA, Smith RA, Wynn DR, Wymer JP, Achiron A, Vollmer TL, Mandler RN, Dietrich DW, Fletcher M, Pope LE, Berg JE, Miller A, Pseudobulbar Affect in Multiple Sclerosis Study Group. Randomized, controlled trial of dextromethorphan/quinidine for pseudobulbar affect in multiple sclerosis (abstract). Annals of Neurology 2006 May;59(5):780-7.

44. Woodard C, Groden J, Goodwin M, Shanower C, Bianco J. The treatment of the behavioral sequelae of autism with dextromethorphan: a case report. Journal of Autism & Developmental Disorders 2005 Aug;35(4):515-8.

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46. Verhagen Metman L, Blanchet PJ, van den Munckhof P, Del Dotto P, Natté R, Chase TN. A trial of dextromethorphan in parkinsonian patients with motor response complications (abstract). Movement Disorders 1998 May;13(3):414-7.

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49. Aiello T. Cops: Man Caused Fatal Accident By 'Robotripping': Westchester Resident Allegedly Drove Under The Influence Of Cough Syrup. WCBSTV.com Jul 31, 2007 <http://wcbstv.com/topstories/robotri....2.246127.html> Accessed Dec 2, 2007.

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51. Kawakami A, Nakayama H, Yamada Y, Hirosaki K, Yamashita T, Kondo S, Jimbow K. Dextromethorphan induces multifocal fixed drug eruption (letter). International Journal of Dermatology 2003 Jun;42(6):501-2.

52. Miller SC. Dextromethorphan psychosis, dependence and physical withdrawal. Addiction Biology 2005 Dec;10(4):325-7.

53. Fisher RS, Cysyk BJ, Lesser RP, Pontecorvo MJ, Ferkany JT, Schwerdt PR, Hart J, Gordon B. Dextromethorphan for the treatment of complex partial seizures (abstract). Neurology 1990 Mar;10(3 Pt 1):547-9.

54. Kimiskidis VK, Mirtsou-Fidani V, Papaioannidou PG, Niopas I, Georgiadis G, Constadinidis TC, Kazis AD. A phase I clinical trial of dextromethorphan in intractable partial epilepsy (abstract). Methods & Findings in Experimental & Clinical Pharmacology 1999 Dec;21(10):673-8.

55. Kim HC, Pennypacker KR, Bing G, Bronstein D, McMillian MK, Hong JS. The effects of dextromethorphan on kainic acid-induced seizures in the rat (abstract). Neurotoxicology 1996 Summer;17(2):375-85.

56. Stephen A Barat, Mohamed S Abdel-Rahman, Decreased cocaine- and lidocaine-induced seizure response by dextromethorphan and DNQX in rat (1997), Brain Research, Vol. 756, Issues 1–2, 9 May 1997, Pages 179–183

57. Nirupama Laroia, Laura McBride, Raymond Baggs, Ronnie Guillet, Dextromethorphan ameliorates effects of neonatal hypoxia on brain morphology and seizure threshold in rats (1997), Developmental Brain Research, Vol. 100, Issue 1, 20 May 1997, Pages 29–34

58. Hyoung-Chun Kim, Guoying Bing, Wang-Kee Jhoo, Won-Ki Kim, Eun-Joo Shin, Doo-Hyun Im, Kee-Seok Kang, Kwang Ho Ko, Metabolism to dextrorphan is not essential for dextromethorphan's anticonvulsant activity against kainate in mice (2003), Life Sciences, Vol. 72, Issue 7, 3 January 2003, Pages 769–783
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60. Thompson KW, Wasterlain CG. Dextromethorphan and its combination with phenytoin facilitate kindling (abstract). Neurology 1993 May;43(5):992-4.

61. Wolfgang Löscher, Dagmar Hönack, Differences in anticonvulsant potency and adverse effects between dextromethorphan and dextrorphan in amygdala-kindled and non-kindled rats (1993), European Journal of Pharmacology, Vol. 238, Issues 2–3, 20 July 1993, Pages 191–200

62. B Schmitt, R Netzer, S Fanconi, P Baumann, and E Boltshauser, Drug refractory epilepsy in brain damage: effect of dextromethorphan on EEG in four patients (1994), Journal of Neurology, Neurosurgery, and Psychiaty, 1994, 57, Pages 333-339

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65. B. Sangster, J.L. Blom, V.M. Sekhuis, J.G. Loeber, A.G. Rauws, J.C. Koedam, E.I. Krajnc, M.J. van Logten, The influence of sodium bromide in man: a study in human volunteers with special emphasis on the endocrine and the central nervous system (1983), Food and Chemical Toxicology, Vol. 21, Issue 4, August 1983, Pages 409–419

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71. Bostwick JM. Dextromethorphan-induced manic symptoms in a bipolar patient on lithium (letter). Psychosomatics 1996 Nov-Dec;37(6):571-3.

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74. Ahtee L. Dextromethorphan inhibits 5-hydroxytryptamine uptake by human blood platelets and decreases 5-hydroxyindoleacetic acid content in rat brain (abstract). Journal of Pharmacy & Pharmacology 1975 Mar;27(3):177-80.

75. Sinclair JG, Lo GF. The blockade of serotonin uptake into synaptosomes: relationship to an interaction with monoamine oxidase inhibitors (abstract). Canadian Journal of Physiology & Pharmacology 1977 Apr;55(2):180-7.

76. Henderson MG, Fuller RW. Dextromethorphan antagonizes the acute brain depletion of brain serotonin by p-chloroamphetamine and H75/12 in rats. Brain Research 1992;594:323-6.

77. Gaikwad RV, Gaonkar RK, Jadhav SA, Thorat VM, Jadhav JH, Balsara JJ. Involvement of central serotonergic systems in dextromethorphan-induced behavioral syndrome in rats (abstract). Indian Journal of Experimental Biology 2005 Jul;43(7):620-5.

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81. Rivers N, Horner B. Possible lethal interaction between Nardil and dextromethorphan (letter). Canadian Medical Association Journal 1970;103:85.

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83. Kintz P, Mangin P. Toxicological findings in a death involving dextromethorphan and terfenadine (abstract). American Journal of Forensic Medicine & Pathology 1992 Dec;13(4):351-2.

84. Banerji S, Anderson IB. Abuse of Coricidin HBP cough & cold tablets: episodes recorded by a poison center (abstract). American Journal of Health-System Pharmacy 2001 Oct 1;58(19):1811-4.

85. Baker SD, Borys DJ. A possible trend suggesting increased abuse from Coricidin exposures reported to the Texas Poison Network: comparing 1998 to 1999 (abstract). Veterinary & Human Toxicology 2002 Jun;44(3):169-71.

86. Rammer L, Holmgren P, Sandler H. Fatal intoxication by dextromethorphan: a report on two cases. Forensic Science International 1988 Jun;37(4):233-6.

87. Youngchan Yoo, Heesun Chung, Eunmi Kim, and Myungduck Kim, Fatal zipeprol and dextromethorphan poisonings in Korea (1996), Journal of Analytical Toxicology, Vol. 20, Issue 3, Pages 155-158

[1]Merck Index, fifteenth edition (2013)
[2] Calculated from Atomic Weights of the Elements, 2007

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