dextromethorphan and Nervous-System-Diseases
dextromethorphan has been researched along with Nervous-System-Diseases* in 11 studies
Reviews
4 review(s) available for dextromethorphan and Nervous-System-Diseases
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Dextromethorphan/quinidine: a review of its use in adults with pseudobulbar affect.
Fixed-dose dextromethorphan/quinidine capsules (Nuedexta(®)) utilize quinidine to inhibit the metabolism of dextromethorphan, enabling high plasma dextromethorphan concentrations to be reached without using a larger dose of the drug. The drug combination is the first treatment to be approved for pseudobulbar affect (PBA), a condition of contextually inappropriate/exaggerated emotional expression that often occurs in adults with neurological damage conditions, such as amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), stroke, traumatic brain injury, Alzheimer's disease or Parkinson's disease. Dextromethorphan/quinidine at the recommended dosages of 20/10 or 30/10 mg twice daily reduced the rate of PBA episodes and improved PBA severity in a 12-week, double-blind, placebo-controlled trial in adults with ALS or MS (STAR), with further improvements in the severity of the condition observed in a 12-week open-label extension phase. Dextromethorphan/quinidine 20/10 mg twice daily also improved PBA secondary to dementia in a cohort of a 12-week noncomparative trial (PRISM II). The drug combination was generally well tolerated in these studies, with no particular safety or tolerability concerns. Although longer-term efficacy and tolerability data for dextromethorphan/quinidine 20/10 or 30/10 mg twice daily would be beneficial, current evidence indicates that it is a useful option in the treatment of adults with PBA. Topics: Adult; Dextromethorphan; Drug Combinations; Humans; Mood Disorders; Nervous System Diseases; Quinidine | 2015 |
Pharmacology and pharmacogenomics of neurological medications used in pregnancy.
Pregnancy increases the pharmacological management challenge of numerous neurological diseases as a result of complex physiological changes. Understanding pregnancy-induced changes in pharmacokinetic and pharmacodynamic parameters can lead to better outcomes for both the mother and baby. Although the application of pharmacogenomics in maternal-fetal medicine is in its infancy, further research and developments will provide important new developments for managing the efficacy of drug treatments during pregnancy and improving maternal-fetal safety. Although a wide variety of neurological medications are used during pregnancy, this article will focus on the drugs with currently known pharmacogenomic implications. Topics: Anticonvulsants; Codeine; Dextromethorphan; Female; Humans; Nervous System Diseases; Pharmacogenetics; Pregnancy; Pregnancy Complications; Teratogens; Tetrabenazine | 2013 |
Dextromethorphan as a potential neuroprotective agent with unique mechanisms of action.
Dextromethorphan (DM) is a widely-used antitussive. DM's complex central nervous system (CNS) pharmacology became of interest when it was discovered to be neuroprotective due to its low-affinity, uncompetitive N-methyl-D-aspartate (NMDA) receptor antagonism.. Mounting preclinical evidence has proven that DM has important neuroprotective properties in various CNS injury models, including focal and global ischemia, seizure, and traumatic brain injury paradigms. Many of these protective actions seem functionally related to its inhibitory effects on glutamate-induced neurotoxicity via NMDA receptor antagonist, sigma-1 receptor agonist, and voltage-gated calcium channel antagonist actions. DM's protection of dopamine neurons in parkinsonian models may be due to inhibition of neurodegenerative inflammatory responses. Clinical findings are limited, with preliminary evidence indicating that DM protects against neuronal damage. Negative findings seem to relate to attainment of inadequate DM brain concentrations. Small studies have shown some promise for treatment of perioperative brain injury, amyotrophic lateral sclerosis, and symptoms of methotrexate neurotoxicity. DM safety/tolerability trials in stroke, neurosurgery, and amyotrophic lateral sclerosis patients demonstrated a favorable safety profile. DM's limited clinical benefit is proposed to be associated with its rapid metabolism to dextrorphan, which restricts its central bioavailability and therapeutic utility. Systemic concentrations of DM can be increased via coadministration of low-dose quinidine (Q), which reversibly inhibits its first-pass elimination. Potential drug interactions with DM/Q are discussed.. Given the compelling preclinical evidence for neuroprotective properties of DM, initial clinical neuroprotective findings, and clinical demonstrations that the DM/Q combination is well tolerated, this strategy may hold promise for the treatment of various acute and degenerative neurologic disorders. Topics: Animals; Clinical Trials as Topic; Dextromethorphan; Humans; Nervous System Diseases; Neuroprotective Agents; Receptors, N-Methyl-D-Aspartate; Trauma, Nervous System | 2007 |
NMDA-receptor antagonists in neuropathic pain: experimental methods to clinical trials.
Recent clinical data suggest that chronic pain due to nerve or soft tissue injury may result in the sensitization of the central nervous system, mediated in part by the excitatory amino acids, glutamate and aspartate. Only a handful of N-methyl-D-aspartate antagonists are clinically available. These include ketamine, dextromethorphan, memantine, and amantadine, as well as three clinically used opioids (methadone, dextropropoxyphene, and ketobemidone). This review summarizes the single-dose efficacy of the first two compounds in the treatment of experimental and neuropathic pain. In all examples presented here, NMDA-receptor antagonists with affinity at the phencyclidine site have been shown to modulate pain and hyperalgesia but are limited by dose-limiting side effects. Thus, provided their therapeutic ratio is favorable, NMDA-receptor antagonists may be effective in the treatment of some types of chronic pain. Topics: Analgesics; Clinical Trials as Topic; Dextromethorphan; Excitatory Amino Acid Antagonists; Humans; Ketamine; Nervous System Diseases; Pain; Receptors, N-Methyl-D-Aspartate; Research Design | 2000 |
Trials
1 trial(s) available for dextromethorphan and Nervous-System-Diseases
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Multimodal prevention of pain, nausea and vomiting after breast cancer surgery.
Despite many one- or two-modal attempts to relieve postoperative nausea and vomiting (PONV) and pain, postoperative issues following breast cancer surgery remain a substantial problem. Therefore, the aim of this explorative, hypothesis-generating study was to evaluate the effect of a multimodal, opiate-sparing, evidence-based regimen for prevention of PONV and pain.. Two hundred consecutive patients scheduled for breast cancer surgery were included. The prevention regimen included a package consisting of preoperative paracetamol, dextromethorphan, celecoxib, gabapentin, dexamethasone, total intravenous anaesthesia and intraoperative ondansetron. The patients were prospectively scored according to PONV, pain during rest and mobilization and major side effects.. Of 200 consecutive breast cancer patients, 191 received the full package. During the first 36 postoperative hours, 79.1% reported no PONV at all and only 3.7% reported severe PONV. At rest, 69.6% reported no or light pain and 3.1% reported severe pain, with corresponding values of 59.7% and 8.9% during arm mobilization. Mean postoperative morphine consumption was 2.2 mg. The only significant side effect was transient dizziness.. A multimodal, opiate-sparing regimen to prevent pain and PONV seems to be more effective than one- or two-component regimens on PONV and pain after breast cancer surgery, a result which calls for large-scale multi-center or randomized studies. Topics: Acetaminophen; Aged; Amines; Analgesics, Non-Narcotic; Anesthesia Recovery Period; Anesthesia, Intravenous; Antiemetics; Breast Neoplasms; Celecoxib; Combined Modality Therapy; Cyclohexanecarboxylic Acids; Dexamethasone; Dextromethorphan; Female; Fentanyl; Gabapentin; gamma-Aminobutyric Acid; Humans; Intraoperative Care; Lymph Node Excision; Mastectomy; Middle Aged; Morphine; Narcotics; Nervous System Diseases; Ondansetron; Pain, Postoperative; Pilot Projects; Postoperative Nausea and Vomiting; Preanesthetic Medication; Pyrazoles; Sentinel Lymph Node Biopsy; Sulfonamides | 2010 |
Other Studies
6 other study(ies) available for dextromethorphan and Nervous-System-Diseases
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Cough mixture abuse as a novel cause of folate deficiency: a prospective, community-based, controlled study.
Cough mixture abuse has been reported to cause severe folate deficiency and neurological defects. We carried out a prospective case-controlled survey to confirm this association and define the incidence and severity of the problem. A total of 57 cough mixture abusers and 47 other substance abusers (controls) were studied. When compared with controls, cough mixture abusers had a high incidence of low folate levels that could only be detected by screening. Topics: Adult; Antitussive Agents; Case-Control Studies; Codeine; Data Collection; Dental Caries; Dextromethorphan; Erythrocyte Indices; Female; Folic Acid Deficiency; Hemoglobins; Hong Kong; Humans; Incidence; Male; Mass Screening; Nervous System Diseases; Platelet Count; Prospective Studies; Substance-Related Disorders; Vitamin B 12 Deficiency | 2007 |
Dextromethorphan-induced neurologic illness in a patient with negative toxicology findings.
Topics: Adult; Dextromethorphan; Diagnosis, Differential; False Negative Reactions; Humans; Male; Mental Disorders; Nervous System Diseases; Substance Abuse Detection; Substance-Related Disorders; Toxicology | 2006 |
Side effects of dextromethorphan abuse, a case series.
The aim of this study was to investigate the Dextromethorphan (DXM) abuse side effects. Subjects were 53 volunteers who had consumed DXM with mean age 23.4 years. The mean of side effects during first day was 12.49 and during first week was 5.57. The causes of repeated DXM abuse were psychological dependency 46.5%, recreational abuse in 32.6%. Neurological and psychological symptoms were the most common of side effects in DXM abusers. Topics: Adolescent; Adult; Analgesics, Opioid; Dextromethorphan; Female; Gastrointestinal Diseases; Humans; Male; Mental Disorders; Nervous System Diseases; Opioid-Related Disorders | 2005 |
4-Hydroxybutyric aciduria.
The clinical findings in six patients from three families with 4-hydroxybutyric aciduria are described. The onset of disease was in early infancy in all cases. All infants presented with severe global delay and severe hypotonia, and all patients had seizure disorder. Eye findings included optic atrophy in two patients, and retinitis pigmentosa in one. Three patients had choreoathetosis, two had myoclonus and one had severe dystonia. The urine 4-hydroxybutyric acid was 300-1000 times that of normal, and other organic acids related to its further metabolism or to its inhibitory effect on beta-oxidation were also increased. The administration of vigabatrine rapidly reduced the excretion of 4-hydroxybutyric acid promptly, and in the long-term its excretion could be kept at 80-200 times that of normal. However, the clinical course of the disease improved in only two, remained the same in two, and worsened in the remaining two patients. Topics: Adult; Anticonvulsants; Brain; Child; Child, Preschool; Dextromethorphan; Female; gamma-Aminobutyric Acid; Humans; Hydroxybutyrates; Infant; Magnetic Resonance Imaging; Male; Metabolism, Inborn Errors; Nervous System Diseases; Seizures; Vigabatrin | 1994 |
The neuroprotective effects of dextromethorphan on guinea pig-derived hippocampal slices during hypoxia.
The purpose of this study was to determine whether dextromethorphan, an opioid class antitussive, prevents hypoxia-induced loss of nerve function in an in vitro hippocampal slice preparation. The evoked population spike (PS) was recorded from CA1 pyramidal cells of guinea pig-derived hippocampal slices. Hippocampal slices were superfused with O2 (95%)/CO2 (5%) gassed artificial cerebral spinal fluid (ACSF) at 37 degrees C. The PS did not recover during reoxygenation in slices that were made hypoxic for 30 min by exposure to N2 (95%)/CO2 (5%) gassed ACSF in place of oxygenated ACSF. The PS recovered during reoxygenation, following 30 min of hypoxia, in 9 of 10 slices treated with dextromethorphan (100 microM) and in 4 of 6 slices treated with D,L-2-amino-5-phosphono-valerate (AP-5) (100 microM), an NMDA receptor antagonist. The mean PS amplitudes, one hour after perfusion with oxygenated ACSF, were 42% and 51%, respectively, of the pre-hypoxia amplitude. The PS recovered during reoxygenation in all of seven slices superfused with lowered temperature ACSF (25 degrees C) during 30 min of hypoxia. The results show that dextromethorphan, like the NMDA antagonist AP-5 and lowered temperature, protected neurons from hypoxia-induced injury in the hippocampus. Topics: 2-Amino-5-phosphonovalerate; Animals; Cold Temperature; Dextromethorphan; Guinea Pigs; Hippocampus; Hypoxia; In Vitro Techniques; Male; Nervous System Diseases; Receptors, N-Methyl-D-Aspartate; Synaptic Transmission | 1992 |
Prevention of soman neurotoxicity by non-opioid antitussives.
The antitussives dextromethorphan (DM), carbetapentane (CBP), and caramiphen (CM) are known to have anti-convulsant properties. They were given individually to guinea pigs prior to poisoning with 2 x LD50 soman to test their efficacy against organophosphorus-induced convulsions, brain damage, and lethality. All subjects received an injection of pyridostigmine coincident with the antitussive, and were treated with atropine methylnitrate and pralidoxime chloride 30 sec after soman administration. CM, in a dose-dependent manner, protected against lethality and either prevented or reduced the intensity of convulsions, electrographic seizure activity (EGSA), and brain damage. CBP delayed the onset of EGSA and reduced its intensity. DM prevented EGSA at higher doses, but neither DM nor CBP protected against the lethal effects of soman. CM is known to possess relatively stronger anticholinergic properties than the other antitussives used in this experiment, which may have contributed to its relatively superior efficacy against soman. Topics: Animals; Anticonvulsants; Antitussive Agents; Cyclopentanes; Dextromethorphan; Guinea Pigs; Male; Necrosis; Nervous System Diseases; Neurons; Soman | 1990 |