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PubMed2003

Peripheral interactions between dextromethorphan, ketamine and amitriptyline on formalin-evoked behaviors and paw edema in rats.

The local, peripheral administration of antidepressants and excitatory amino acid receptor antagonists can cause analgesia in a number of conditions. The present study examined the effects of combinations of dextromethorphan and ketamine, two clinically used N-methyl-D-aspartate (NMDA) receptor antagonists, with amitriptyline on formalin-evoked behaviors and paw edema. Pretreatment with amitriptyline or dextromethorphan (10-300 nmol) resulted in suppression of flinching behaviors induced by 2.5% formalin, but ketamine had no intrinsic effect. Combination of an inactive dose of dextromethorphan with amitriptyline, and vice versa, resulted in an increase of analgesia so that previously inactive doses now caused significant analgesia. Combinations of multiple doses of ketamine with amitriptyline did not modify the response to amitriptyline. Both dextromethorphan and ketamine increased the paw edema induced by formalin, and this was blocked by low doses of amitriptyline. In the absence of formalin, amitriptyline (1-100 nmol) caused a dose-related suppression of the paw edema produced by dextromethorphan and ketamine. Amitriptyline also blocked paw edema produced by 5-hydroxytryptamine and compound 48/80. Each of the drugs used in this study exerts multiple pharmacological effects. Increased analgesia by drug combinations (amitriptyline/dextromethorphan) could show the involvement of a number of these mechanisms (e.g. NMDA receptor blockade, blockage of sodium channels, blockage of biogenic amine receptors), while a lack of intensification (amitriptyline/ketamine) could reflect occluded actions due to expression of similar actions by the other drug. Paw edema induced by dextromethorphan and ketamine involves inhibition of biogenic amine reuptake, and the ability of amitriptyline to block biogenic amine receptors likely accounts for its inhibiton of these actions. Combinations of these particular agents could represent a method for augmented analgesia and minimization of local adverse reactions.

Amitriptyline↗
PubMed1997

Highly sensitive high-performance liquid chromatographic-tandem mass spectrometric method for the analysis of dextromethorphan in human plasma.

A stable-isotope-dilution HPLC-tandem mass spectrometry-based method was developed for the determination of dextromethorphan in human plasma. Plasma samples were prepared for analysis by solid-phase extraction on octadecylsilane extraction cartridges. Dextromethorphan and the deuterium-labeled dextromethorphan internal standard were chromatographed on a short reversed-phase column and detected by a selected-reaction-monitoring scheme. Linear standard curves were obtained over three orders of magnitude and the limit of quantitation for dextromethorphan was 50 pg/ml, using a 1-ml plasma sample. The combination of HPLC and electrospray tandem mass spectrometry resulted in a rapid, selective and sensitive method for the analysis of dextromethorphan in plasma. The method was applied for the evaluation of the pharmacokinetic profile of dextromethorphan in human volunteers following peroral administration.

Adult↗
PubMed2000

Discrepancy between CYP2D6 phenotype and genotype derived from post-mortem dextromethorphan blood level.

OBJECTIVE: To describe the death of a toddler after a therapeutic dose of dextromethorphan and its investigation. STUDY DESIGN: Case report, cytochrome P450 phenotype and genotype determination in the victim and post-mortem drug redistribution study performed in rats. RESULTS: A 20-month Asian male who received 3 mg of dextromethorphan once at 09:00 h and again at 22:00 h was found dead at 04:35 h. Post-mortem examination showed signs of early bronchopneumonia (bacterial cultures were negative); dextromethorphan and dextrorphan blood concentrations taken from the heart cavity were 500 ng/ml (1. 84 micromol/l) and 200 ng/ml (0.78 micromol/l), respectively. Despite the dextromethorphan level being almost 100-fold higher than expected after therapeutic doses, intentional or unintentional overdose was extremely unlikely; other potential causes were investigated. Post-mortem drug redistribution study performed in rats showed that dextromethorphan does not undergo extensive redistribution after death (6+/-5-fold increase) and could not explain the observed dextromethorphan level. The dextromethorphan/dextrorphan concentration ratio of 2.5 found in this toddler was compatible with a slow CYP2D6 metabolizer phenotype. However, the toddler exhibited a fast metabolizer genotype. Potential reasons for this discrepancy are discussed. CONCLUSION: CYP450 phenotypes derived from post-mortem blood levels should be interpreted with caution and preferably confirmed by a genotype analysis.

Animals↗
PubMed1985

Polymorphic dextromethorphan metabolism: co-segregation of oxidative O-demethylation with debrisoquin hydroxylation.

Dextromethorphan hydrobromide, 25 mg po, was given to 268 unrelated Swiss subjects to study urinary drug and metabolite profiles. Rates of O-demethylation yielding the main metabolite dextrorphan were expressed by the urinary dextromethorphan/dextrorphan metabolic ratio. We found a bimodal distribution of this parameter in our population study, which indicates that there are two phenotypes for dextromethorphan O-demethylation. The antimode at a metabolic ratio of 0.3 separated the poor metabolizer (PM; n = 23; prevalence of 9%) from extensive metabolizer (EM) phenotypes. Urinary output of dextrorphan was less than 6% of the dose in all PMs and was 50% in the 245 EMs. Pedigree analysis of 14 family studies revealed an autosomal-recessive transmission of deficient dextromethorphan O-demethylation. In these families, 37 heterozygous genotypes could be identified; however, through use of the urinary drug and metabolite analysis it was not possible to identify the heterozygous genotypes within the EM phenotype group. Co-segregation of dextromethorphan O-demethylation with debrisoquin 4-hydroxylation was also studied. Complete concordance of the two phenotypic assignments was obtained, with a Spearman rank correlation coefficient of rs = 0.78 (n = 62; P less than 0.0001) for dextromethorphan and debrisoquin metabolic ratios. Presumably the two drug oxidation polymorphisms are under the same genetic control. Thus the innocuousness and ubiquitous availability of dextromethorphan render it attractive for worldwide pharmacogenetic investigations in man.

Administration, Oral↗
PubMed1997

An autoradiographic study of dextromethorphan high-affinity binding sites in rat brain: sodium-dependency and colocalization with paroxetine.

1. The distribution and some pharmacological properties of centrally located dextromethorphan high-affinity binding sites were investigated by in vitro autoradiography. 2. Sodium chloride (50 mM) induced a 7 to 12 fold increase in dextromethorphan binding to rat brain in all areas tested. The effect of sodium was concentration-dependent with a higher dose (120 mM) exerting a smaller effect on binding. 3. [3H]-dextromethorphan binding in the presence of sodium was inhibited in the presence of the anticonvulsant phenytoin at a concentration of 100 microM, while the sigma ligand (+)-3-(-3-hydroxyphenyl)-N-(1-propyl)pipendine ((+)-PPP) had no effect on the binding, suggesting an interaction with the DM2 site. 4. The distribution of the sodium-dependent binding identified in this study correlated significantly with the distribution of the selective 5-HT uptake inhibitor [3H]-paroxetine, and paroxetine and dextromethorphan mutually displaced their binding at concentrations in the low nanomolar range. 5. These data show that dextromethorphan and paroxetine share a sodium-dependent high affinity binding site in rat brain, and suggest that dextromethorphan might interact, in the presence of sodium, with the 5-HT uptake mechanism in rat brain.

Animals↗
PubMed2004

Phe120 contributes to the regiospecificity of cytochrome P450 2D6: mutation leads to the formation of a novel dextromethorphan metabolite.

Although the residues that determine the preference of CYP2D6 (cytochrome P450 2D6) for compounds containing a basic nitrogen are well characterized, the contribution of other active site residues to substrate binding and orientation is less well understood. Our structural model of CYP2D6 identifies the aromatic residue Phe120 as a likely major feature of the active site. To examine the role of Phe120, mutants of CYP2D6 in which this residue has been substituted by alanine, leucine, tyrosine, serine, histidine, tryptophan or methionine residues have been prepared in bacterial membranes co-expressing human cytochrome NADPH cytochrome P450 oxidoreductase. The mutants have been characterized using the prototypical bufuralol 1' hydroxylase and dextromethorphan O- and N-demethylase activities of CYP2D6. Larger effects on K(m) values are observed for dextromethorphan O-demethylation than for bufuralol 1' hydroxylation, indicating that the Phe120 side chain is more important in dextromethorphan than in bufuralol binding. A role for this side chain in determining the regiospecificity of substrate oxidation was indicated by changes in the relative rates of O- and N-demethylation of dextromethorphan and, notably, by the formation of 7-hydroxy dextromethrophan, a novel dextromethorphan metabolite, in mutants in which it had been substituted. Computational studies of dextromethorphan binding to the active site of the Phe120-->Ala mutant were carried out to throw light on the way in which the removal of this side chain leads to different modes of ligand binding.

Cytochrome P-450 CYP2D6↗
PubMed2001

Combined pre-incisional oral dextromethorphan and epidural lidocaine for postoperative pain reduction and morphine sparing: a randomised double-blind study on day-surgery patients.

The reduction in acute pain perception following dextromethorphan has previously been investigated in patients undergoing general anaesthesia. This random and double-blind study examined the effects of pre-incisional oral dextromethorphan on postoperative pain and intravenous patient-controlled morphine demand in 60 day-surgery patients undergoing lower body surgery under lidocaine (1.6%-16 ml) epidural anaesthesia after receiving placebo, 60 or 90 mg dextromethorphan, 90 min pre-operatively. Postoperative pain was scored on a visual analogue scale from 1 to 10. In-hospital observation continued for 6 h and for 3 days at home; diclofenac was available throughout. Dextromethorphan-treated patients reported significantly (p < 0.05) less pain and sedation, and felt better. Patients who received dextromethorphan 90 mg had significantly (p < 0.05) lower heart and respiratory rates than those who received 60 mg. Medicated patients required half the morphine and diclofenac of placebo patients: 38% of patients who received 90 mg and 21% who received dextromethorphan 60 mg used no morphine or diclofenac whatsoever, a previously unreported finding.

Aged↗
PubMed1999

Polymorphism of dextromethorphan oxidation in South Indian subjects.

One hundred fifty-six unrelated healthy South Indian subjects were phenotyped according to their ability to metabolize dextromethorphan to its O-demethylated metabolite dextrorphan. Each volunteer was administered 25 mg oral dextromethorphan hydrobromide (19.3 mg dextromethorphan). Urine was collected during an 8-hour period after drug administration and was analyzed for dextromethorphan and dextrorphan by HPLC with fluorescence detection. This analysis was performed with and without previous deconjugation. The log10 (metabolic ratio), calculated as the ratio of dextromethorphan to dextrorphan, was bimodally distributed, and it was inferred that the frequency of occurrence of poor metabolizers of dextromethorphan in South Indian subjects is 3.2%. Phenotype assignment remained the same with both methods of analysis. Furthermore, a fairly good correlation (Spearman rank order correlation coefficient [r(s)] = 0.61; P < .0001) was observed between the log-transformed metabolic ratio derived from both methods.

Adolescent↗
PubMed2003

Dextromethorphan and intrathecal morphine for analgesia after Caesarean section under spinal anaesthesia.

BACKGROUND: Dextromethorphan is an N-methyl-D-aspartic acid antagonist which can attenuate acute pain with few side-effects. In this prospective, randomized, double-blind study of dextromethorphan and intrathecal morphine, we investigated postoperative pain, pruritus, nausea and vomiting in women undergoing Caesarean section under spinal anaesthesia. METHODS: Women were allocated randomly to one of six groups, to receive intrathecal morphine 0.05, 0.1 or 0.2 mg plus oral dextromethorphan 60 mg or placebo. RESULTS: The addition of dextromethorphan did not reduce postoperative pain scores (P=0.83). Compared with women receiving intrathecal morphine 0.05 mg, women receiving higher doses had a significantly higher incidence of nausea and vomiting [odds ratio for intrathecal morphine 0.1 mg, 4.0 (95% confidence interval 1.2-14.1); for intrathecal morphine 0.2 mg, 7.9 (2.3-27.1)]. Compared with women receiving intrathecal morphine 0.05 mg, women receiving higher doses also had a significantly higher incidence of pruritus [odds ratio for intrathecal morphine 0.1 mg, 3.2 (95% confidence interval 1.3-8.2); for intrathecal morphine 0.2 mg, 3.7 (1.4-9.5)]. Women receiving dextromethorphan had a lower incidence of nausea and vomiting [odds ratio 2.6 (1.1-6.3)]. CONCLUSIONS: Postoperative pain after Caesarean section under spinal anaesthesia was not reduced by the addition of oral dextromethorphan to a multimodal approach including intrathecal morphine.

Adult↗
PubMed1988

High-pressure liquid chromatographic assay of dextromethorphan hydrobromide, guaifenesin, and sodium benzoate in an expectorant syrup.

An ion-pair reversed-phase high-pressure liquid chromatographic assay is developed that allows simultaneous quantitation of guaifenesin, dextromethorphan hydrobromide, and sodium benzoate in an expectorant syrup. The method is rapid and accurate. Average recoveries of 99.6, 99.8, and 99.7% with relative standard deviations of 0.5, 0.9, and 0.2% are obtained for guaifenesin, dextromethorphan hydrobromide, and sodium benzoate, respectively, from laboratory prepared samples. Chromatographic conditions are selected to afford a pH that provides adequate separation of guaifenesin, dextromethorphan hydrobromide, sodium benzoate, and sodium saccharin and a detection wavelength that effectively compensates for the great disparity in quantity between guaifenesin and dextromethorphan hydrobromide present in syrups. The relationships between the retention volume of dextromethorphan hydrobromide and the alkyl chain length as well as the concentration of the counterion are studied. The retention profiles for sodium saccharin, guaifenesin, sodium benzoate, and dextromethorphan hydrobromide in the apparent pH range of 2.5 to 6.6 are established.

Benzoates↗
PubMed1998

Comparison of ketamine and dextromethorphan in potentiating the antinociceptive effect of morphine in rats.

UNLABELLED: We compared the efficacy of two clinically available drugs with N-methyl-D-aspartate receptor antagonist properties, dextromethorphan and ketamine, in potentiating morphine-induced antinociception. Ketamine alone at 0.3-3 mg/kg had no effect on the hot plate test and at 10 mg/kg caused sedation/motor deficits. The antinociceptive effect of 5 mg/kg morphine was slightly enhanced by 1 mg/kg, but not 0.3 or 3 mg/kg, ketamine. Dextromethorphan alone at 45 mg/kg had no effect, but at 60 mg/kg caused sedation/motor deficit. At 15-45 mg/kg, dextromethorphan significantly and dose-dependently increased the magnitude and duration of morphine-induced antinociception. Dextromethorphan also potentiated morphine at doses that, by themselves, did not cause antinociception (1-2 mg/kg). IMPLICATIONS: Dextromethorphan was more effective than ketamine in potentiating morphine-induced antinociception. Dextromethorphan may thus be the drug of choice for testing the interactions between N-methyl-D-aspartate antagonists and morphine clinically.

Analgesia↗
PubMed1999

The preoperative administration of intravenous dextromethorphan reduces postoperative morphine consumption.

UNLABELLED: We evaluated the effect of dextromethorphan on postoperative pain management. Sixty ASA physical status I-III female patients undergoing major abdominal surgery underwent standardized general anesthesia. Thirty patients received an i.v. infusion of dextromethorphan 5 mg/kg before anesthetic induction (Pre group), whereas the remaining 30 patients received the same volume of isotonic sodium chloride solution, followed by a postoperative i.v. infusion of dextromethorphan 5 mg/kg (Post group). Patients in the Pre group received the same volume of isotonic sodium chloride solution postoperatively. All patients were then treated with patient-controlled i.v. analgesia, which administered a 0.6-mg bolus of morphine on demand (maximal 4 h dose 20 mg). The mean visual analog pain score during cough or movement and at rest were similar in the two groups in the first 3 days postoperatively. However, Post group patients consumed more morphine than Pre group patients during the first 2 days (P < 0.01). The sedation scores, patient satisfaction, and the incidence of morphine-related side effects were similar between the two groups. We conclude that the preoperative administration of dextromethorphan 5 mg/kg reduces postoperative morphine consumption compared with postoperative administration. IMPLICATIONS: In this double-blinded study, we found that the preoperative administration of i.v. dextromethorphan 5 mg/kg, compared with postoperative administration, reduces postoperative morphine consumption, which may provide clinical evidence of preemptive or preventive analgesic effects of dextromethorphan.

Adult↗
PubMed2001

Large-dose oral dextromethorphan as an adjunct to patient-controlled analgesia with morphine after knee surgery.

Dextromethorphan is a weak N-methyl-d-aspartate (NMDA) receptor antagonist that inhibits spinal cord sensitization in animal models of pain and also inhibits the development of cutaneous secondary hyperalgesia after tissue trauma. Perhaps coadministration of an NMDA antagonist with an opioid would lead to better pain relief, particularly with movement and an opioid-sparing effect. This has been shown for ketamine, but previous studies with dextromethorphan that have used small doses have shown only a modest reduction in morphine requirements with no or minimal changes in the postoperative pain experience. We sought to determine whether a large dose of this drug, just below the maximum tolerated dose, could potentiate morphine analgesia while simultaneously causing a significant improvement in the management of the postoperative pain experience. Sixty-six patients undergoing knee surgery were enrolled in the study. The study design was a prospective, randomized double-blinded comparison with placebo of 200 mg of dextromethorphan given eight hourly. Postoperative pain experiences were assessed by postoperative morphine usage. Visual analog and verbal rating scales were used to assess pain with movement as well as side effects. Dextromethorphan treatment led to a significant but modest reduction in morphine requirements (29.3% P < 0.05) but no reduction in postoperative pain levels. We conclude that increasing orally administered dextromethorphan to near maximum tolerated doses does not provide greater morphine sparing than 20-40 mg given 6-8 hourly as in previous studies. Furthermore we conclude that dextromethorphan does not improve pain scores in a manner expected of a drug with NMDA antagonist properties.

Administration, Oral↗
PubMed1990

Rapid screening for polymorphisms in dextromethorphan and mephenytoin metabolism.

1. The phenotyping parameters for dextromethorphan and mephenytoin were assessed in 48 normal male volunteers following administration of each metabolic probe drug on separate occasions and together according to a randomized 3-way crossover design. 2. Neither the urinary S-/R-mephenytoin ratio nor the dextromethorphan metabolic ratio were altered significantly by coadministration of the probe drugs. 3. Five-hundred and nineteen subjects were screened for expression of mephenytoin 4-hydroxylase and dextromethorphan O-demethylase activity following the coadministration of mephenytoin and dextromethorphan. The activity was determined in each case by methods not requiring any quantitative measurements. 4. Nineteen (3.7%) of the subjects were identified as poor metabolizers (PMs) of mephenytoin and 35 subjects (6.7%) as PMs of dextromethorphan. 5. All PMs of dextromethorphan were confirmed by more rigorous evaluation of the metabolic ratio.

Adolescent↗
PubMed2004

Comparison of the effects of dextromethorphan, dextrorphan, and levorphanol on the hypothalamo-pituitary-adrenal axis.

Dextromethorphan is a weak noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist. It is metabolized in vivo to dextrorphan, a more potent noncompetitive NMDA antagonist that is the dextrorotatory enantiomer of the opioid agonist levorphanol. The present study characterized the effects of the acute administration of dextromethorphan, dextrorphan, and levorphanol on the hypothalamo-pituitary-adrenal (HPA) axis in the rat and tested the involvement of opioid receptors in the responses produced by dextrorphan and levorphanol. Although both dextromethorphan and dextrorphan increased plasma levels of adrenocorticotropic hormone (ACTH) and corticosterone, the dextromethorphan-induced responses occurred more rapidly than the dextrorphan-induced responses. The analysis of plasma levels of dextrorphan produced after the administration of dextromethorphan indicates that the concentration of dextrorphan formed was too low to be pharmacologically relevant, suggesting that at least some of the effects on the HPA axis are due to the parent compound, and not the metabolite. Naloxone (2 mg/kg) had no effect on the dextrorphan-induced increases in plasma levels of ACTH and corticosterone, but it blocked the levorphanol-induced increases. These results support the hypothesis that dextromethorphan has pharmacological activity aside from its biotransformation to dextrorphan and demonstrate that the effects of dextrorphan are not mediated by opioid receptors.

Animals↗
PubMed1988

Dextromethorphan protects against cerebral injury following transient focal ischemia in rabbits.

We investigated dextromethorphan, both a dextrorotatory opioid derivative and a clinically tested N-methyl-D-aspartate (NMDA) receptor antagonist, in a rabbit model of transient focal cerebral ischemia. Fourteen rabbits were randomly assigned to treatment with a 20 mg/kg i.v. loading dose followed by a 10 mg/kg/hr infusion of 0.4% dextromethorphan in normal saline or with an equivalent volume of normal saline alone. One hour after treatment, the rabbits underwent a 1-hour occlusion of the left internal carotid and anterior cerebral arteries followed by 4 hours of reperfusion. The seven dextromethorphan-treated rabbits showed a significant decrease in the area of neocortical severe ischemic neuronal damage (10.5%) compared with the seven normal saline-treated controls (49.6%, p less than 0.001). The dextromethorphan-treated rabbits also demonstrated significantly smaller areas of cortical edema (10.2%) on magnetic resonance imaging than the controls (38.6%, p less than 0.01). Analysis of somatosensory evoked potentials revealed recovery of the ipsilateral amplitude to contralateral values within 5 minutes of reperfusion in the dextromethorphan-treated rabbits but not in the controls (p less than 0.01). In our rabbit model of transient focal cerebral ischemia, dextromethorphan appears to protect the brain against ischemic neuronal damage and edema, as well as to promote neurophysiologic recovery. This clinically available drug should be further investigated as having potential therapeutic value in the treatment of stroke.

Animals↗
PubMed2005

Adolescent abuse of dextromethorphan.

Dextromethorphan hydrobromide (DXM), a constituent of more than 125 patent cough/cold remedies, is the most popular antitussive medication in the United States. Cough syrups or capsules also contain additional ingredients such as acetaminophen, chlorpheniramine maleate, guaifenesin, and/or pseudoephedrine, and toxicity with overdosage is additive to that of dextromethorphan alone. An unknown number of adolescents in the United States and Europe intoxicate themselves with acute megadoses of dextromethorphan. A megadose of DXM is defined as 5 to 10 times the dose recommended for control of annoying nonproductive coughs. Although a moderate overdose of pure DXM hydrobromide is free of serious adverse effects, approximately 5% of persons of European ethnicity lack the ability to metabolize the drug normally, leading to rapid acute toxic levels. Variable quantities of pure dextromethorphan powder in multiples of 1 gram are easily available from the worldwide web, including e-Bay. Recipe-like extraction procedures are quickly available on the Internet for seemingly simple and inexpensive home manufacture of concentrated dextromethorphan powder from Coricidin HBP Cough & Cold tablets (street name triple C). Adolescents intoxicate themselves at parties and even before or after school since the drug is legal, relatively inexpensive, and easily purchased or shoplifted at drug or convenient stores. Acute megadoses of the drug have profound psychological and physiological effects similar to those of phencyclidine (PCP). Megadoses of dextromethorphan used to self-intoxicate, can produce a false-positive screening test for phencyclidine in a urine specimen.

Acetaminophen↗
PubMed2000

A randomized, controlled trial of high-dose dextromethorphan in facial neuralgias.

BACKGROUND: NMDA glutamate receptor antagonists such as ketamine and dextromethorphan reduce pain in certain neuropathic pain conditions. However, there have been no controlled trials of NMDA antagonists in facial neuralgias. METHODS: A randomized, double-blind, crossover trial compared 6 weeks of oral dextromethorphan with active placebo (low-dose lorazepam) in 19 patients, stratified into three groups: 11 with facial pain and possible trigeminal neuropathy, five with anesthesia dolorosa, and three with idiopathic trigeminal neuralgia. Dosage was titrated in each patient to the highest level reached without disrupting normal activities. RESULTS: Patients completing the trial included 10 with possible trigeminal neuropathy, four with anesthesia dolorosa, and two with trigeminal neuralgia. In patients with possible trigeminal neuropathy and anesthesia dolorosa, dextromethorphan decreased pain by a mean of only 2 to 4%, and these estimates were not significant. Both patients with trigeminal neuralgia had more pain during dextromethorphan treatment than during placebo treatment. Of three patients who demonstrated an analgesic response to dextromethorphan during the main trial, only one repeatedly responded in four subsequent confirmatory drug-placebo crossovers. CONCLUSIONS: Dextromethorphan shows little or no analgesic efficacy in pain due to possible trigeminal neuropathy and anesthesia dolorosa. Additional trials are necessary to conclusively evaluate the efficacy of NMDA-receptor antagonists in trigeminal neuralgia.

Adult↗