Research and Clinical Trials on Alprazolam (Xanax)
This list of current clinical research trials on Alprazolam (Xanax) is followed by a short set of abstracts from the most recent research articles published on the drug.
Alprazolam (Xanax) Clinical Research Trials
From our searchable database at ClinicalTrialsFeeds.org, this list includes all the latest information about clinical trials involving Alprazolam (Xanax).
- PharmacofMRI (Functional Magnetic Resonance Imaging) of Anxiolytic Medications (Alprazolam)
Status: Completed, Condition Summary: Anxiety Disorders
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Current Research Literature on Alprazolam (Xanax)
Here are abstracts for some of the latest research articles to have appeared on Alprazolam (Xanax):
J Anal Toxicol. 2012 Jan; 36(1): 12-8
Jones AW, Holmgren A, Ahlner J
Concentrations of d,l-methadone were determined in blood samples from people arrested for driving under the influence of drugs (DUID), users of illicit drugs, and methadone-related deaths. In drug overdose deaths (N = 346), mean (median) and highest concentrations of methadone in femoral blood were 0.53 mg/L (0.40 mg/L) and 6.7 mg/L, compared with 0.46 mg/L (0.30 mg/L) and 3.7 mg/L in non-poisoning deaths (N = 157) (p < 0.05). In DUID suspects and users of illicit drugs (N = 909), the blood-methadone concentrations were much lower, 0.23 mg/L (0.20 mg/L) and 1.1 mg/L (p < 0.001). The median concentration of methadone in blood decreased as the number of coingested drugs increased in the overdose deaths: 0.5 mg/L with methadone the only drug compared with 0.2 mg/L with 6-9 other drugs present (p < 0.001). These coingested drugs were mainly benzodiazepines (diazepam, alprazolam, flunitrazepam) and amphetamines; THC and morphine (from heroin) were the major illicit drugs. The overlap in blood-methadone concentrations in living cases and autopsy cases makes it difficult to conclude that methadone overdose was the cause of death. Adverse drug-drug interactions and varying degrees of tolerance to opiates complicate the interpretation.
Psychopathological dimensions of tinnitus and psychopharmacologic approaches in its treatment.
Gen Hosp Psychiatry. 2012 Jan 26;
Belli H, Belli S, Oktay MF, Ural C
BACKGROUND: The aim of this review to investigate presence of psychopathological states and efficacy of psychopharmacological drugs in the treatment of tinnitus. MATERIALS AND METHODS: An extensive Internet search has been performed for this aim through PubMed by using related key words in English. RESULTS: Higher anxiety and depression levels and somatoform disorder clusters are defined in patients with tinnitus. Additionally, impulsivity, hostility, demanding, physical discomfort, anxiety for health, emotionality and suicidal tendency are also defined in these people. Personality characteristics in these patients are depression, hysteria and hypochondriac features. Besides these symptom clusters, more severe psychopathologies like personality disorders may be encountered in these patients. Sertraline, paroxetine and nortriptyline can be considered as the first-line antidepressants in the psychopharmacological treatment of tinnitus. There are studies which have reported the efficacy of sulpiride. Carbamazepine, valproate and gabapentin can be effective as mood stabilizers. Short-acting benzodiazepines like alprazolam and midazolam are effective in signs of anxiety. Clonazepam and diazepam can be evaluated as other options. However, some glutamate receptor antagonists also can be used in the treatment of tinnitus. Disturbed sleep is frequently associated with tinnitus. Sleep disturbance can disrupt the quality of life in the patients with tinnitus. These patients might benefit from cognitive-behavioral therapy, which offers the promise of relief from tinnitus-related distress and insomnia. CONCLUSION: When pathophysiologic reasons are excluded, it should be at least considered that tinnitus is exaggerated by psychopathological symptoms. Life quality of patients can be increased by treating these symptoms.
Evaluation of postmortem redistribution phenomena for commonly encountered drugs.
Forensic Sci Int. 2012 Jan 25;
Han E, Kim E, Hong H, Jeong S, Kim J, In S, Chung H, Lee S
We described the findings of a study into the post-mortem redistribution (PMR) of 76 drugs found in 129 drug-related cases between 2006 and 2009. Seventy six drugs (psychotropic drugs (n=14), antidepressants (n=9), sedatives (n=6) and so on) were simultaneously quantified in cardiac and peripheral blood by gas chromatography-mass spectrometry (GC/MS) or liquid chromatography-tandem mass spectrometry (LC/MS/MS). The absence, possibility or presence of PMR of drugs was determined according to the ratios of cardiac to femoral blood concentrations (C/P ratios). Proxyphylline (C/P ratio: 0.85) showed no PMR; carbamazepine was not subject to PMR; a potential for PMR of lorazepam and mirtrazapine cannot be excluded; chlordiazepoxide is subject to PMR; acetaminophen and alprazolam exhibit minimal PMR; amitriptyline and benztropine exhibit PMR. Codeine (C/P ratio: 4.9), zolpidem (C/P ratio: 3.74), chlorpromazine (C/P ratio: 2.97), fluoxetine (C/P ratio: 2.83) and propranolol (C/P ratio: 2.72) had the largest C/P ratios. Postmortem drug concentrations showed variations depending on sampling sites and characteristics of the drugs. It is continuously necessary to analyze commonly used or abused drugs in simultaneously collected cardiac and peripheral blood to establish significant reference values for PMR. These findings can be used to reach a conclusion about the cause and manner of death.
Experimental panic provocation in healthy man-a translational role in anti-panic drug development?
Dialogues Clin Neurosci. 2011; 13(4): 485-93
Kellner M
Experimental neurochemical provocation of panic attacks in susceptible human subjects has considerably expanded our knowledge of the pathophysiology and psychopharmacology of panic disorder. Some panicogens also elicit short-lived panic-like states in healthy man. This offers the opportunity to assess the anti-panic action of drugs in proof-of-concept studies. However, from current data it is still unclear whether experimental panic in healthy man is a valid translational model. Most such studies in healthy volunteers have been performed using a cholecystokinin tetrapeptide (CCK-4) challenge. While CCK-4 panic was blocked by alprazolam pretreatment, escitalopram showed negative results in healthy man. Preliminary findings on novel investigational drugs and a few problematic results will be reviewed. Small sample sizes in many panic provocation studies, lack of dose-response aspects, and still-insufficient knowledge about the biological underpinning of experimental and spontaneous panic limit the interpretation of existing findings and should inspire further research.
Muscle relaxants for pain management in rheumatoid arthritis.
Cochrane Database Syst Rev. 2012; 1: CD008922
Richards BL, Whittle SL, Buchbinder R
Pain management is a high priority for patients with rheumatoid arthritis (RA). Muscle relaxants include drugs that reduce muscle spasm (for example benzodiazepines such as diazepam (Valium), alprazolam (Xanax), lorazepam (Ativan) and non-benzodiazepines such as metaxalone (Skelaxin) or a combination of paracetamol and orphenadrine (Muscol)) and drugs that prevent increased muscle tone (baclofen and dantrolene). Despite a paucity of evidence supporting their use, antispasmodic and antispasticity muscle relaxants have gained widespread clinical acceptance as adjuvants in the management of patients with chronic musculoskeletal pain.The aim of this review was to determine the efficacy and safety of muscle relaxants in pain management in patients with RA. The muscle relaxants that were included in this review are the antispasmodic benzodiazepines (alprazolam, bromazepam, chlordiazepoxide,cinolazepam, clonazepam, cloxazolam, clorazepate, diazepam, estazolam, flunitrazepam, flurazepam, flutoprazepam, halazepam, ketazolam, loprazolam, lorazepam, lormetazepam, medazepam, midazolam, nimetazepam, nitrazepam, nordazepam, oxazepam, pinazepam, prazepam, quazepam, temazepam, tetrazepam, triazolam), antispasmodic non-benzodiazepines (cyclobenzaprine, carisoprodol, chlorzoxazone, meprobamate, methocarbamol, metaxalone, orphenadrine, tizanidine and zopiclone), and antispasticity drugs (baclofen and dantrolene sodium).We performed a search of the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library, 4th quarter 2010), MEDLINE (1950 to week 1 November 2010), EMBASE (Week 44 2010), and PsycINFO (1806 to week 2 November 2010). We also searched the 2008 to 2009 American College of Rheumatology (ACR) and European League Against Rheumatism (EULAR) abstracts and performed a handsearch of reference lists of relevant articles.We included randomised controlled trials which compared a muscle relaxant to another therapy (active, including non-pharmacological therapies, or placebo) in adult patients with RA and that reported at least one clinically relevant outcome.Two blinded review authors independently extracted data and assessed the risk of bias in the trials. Meta-analyses were used to examine the efficacy of muscle relaxants on pain, depression, sleep and function, as well as their safety.Six trials (126 participants) were included in this review. All trials were rated at high risk of bias. Five cross-over trials evaluated a benzodiazepine, four assessed diazepam (n = 71) and one assessed triazolam (n = 15). The sixth trial assessed zopiclone (a non-benzodiazepine) (n = 40) and was a parallel group study. No trial duration was longer than two weeks while three single dose trials assessed outcomes at 24 hours only. Overall the included trials failed to find evidence of a beneficial effect of muscle relaxants over placebo, alone (at 24 hrs, 1 or 2 weeks) or in addition to non-steroidal anti-inflammatory drugs (NSAIDs) (at 24 hrs), on pain intensity, function, or quality of life. Data from two trials of longer than 24 hours duration (n = 74) (diazepam and zopiclone) found that participants who received a muscle relaxant had significantly more adverse events compared with those who received placebo (number needed to harm (NNTH) 3, 95% CI 2 to 7). These were predominantly central nervous system side effects, including dizziness and drowsiness (NNTH 3, 95% CI 2 to 11). Based upon the currently available evidence in patients with RA, benzodiazepines (diazepam and triazolam) do not appear to be beneficial in improving pain over 24 hours or one week. The non-benzodiazepine agent zopiclone also did not significantly reduce pain over two weeks. However, even short term muscle relaxant use (24 hours to 2 weeks) is associated with significant adverse events, predominantly drowsiness and dizziness.
