Research and Clinical Trials on Clonazepam (Klonopin, Rivotril)

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This list of current clinical research trials on Clonazepam (Klonopin, Rivotril) is followed by a short set of abstracts from the most recent research articles published on the drug.

Clonazepam (Klonopin, Rivotril) Clinical Research Trials

From our searchable database at ClinicalTrialsFeeds.org, this list includes all the latest information about clinical trials involving Clonazepam (Klonopin, Rivotril).

 

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Current Research Literature on Clonazepam (Klonopin, Rivotril)

Here are abstracts for some of the latest research articles to have appeared on Clonazepam (Klonopin, Rivotril):

Quantitation of Benzodiazepines in Urine, Serum, Plasma, and Meconium by LC-MS-MS.

J Anal Toxicol. 2008 Sep; 32(7): 491-8
Marin SJ, Coles R, Merrell M, McMillin GA
A single method for confirmation and quantitation of a panel of commonly prescribed benzodiazepines and metabolites, alpha-hydroxyalprazolam, alpha-hydroxyethylflurazepam, alpha-hydroxytriazolam, alprazolam, desalkylflurazepam, diazepam, lorazepam, midazolam, nordiazepam, oxazepam, temazepam, clonazepam, and 7-aminoclonazepam, was developed for three specimen types, urine, serum/plasma, and meconium. Quantitation was by liquid chromatography tandem-mass spectrometry (LC-MS-MS) using a Waters Alliance-Quattro Micro system. The instrument was operated in multiple reaction monitoring mode with an electrospray ionization source in positive ionization mode. The method was evaluated for recovery, imprecision, linearity, analytical measurement range, specificity, and carryover. Average recovery and imprecision (within-run, between-run, and total % CV) were within +/- 15% of the target concentrations for urine (10 to 5000 ng/mL) and serum/plasma (10 to 2500 ng/mL) and within +/- 20% for meconium (10 to 5000 ng/g). In all, 205 patient specimens were analyzed, and the results compared to a previous in-house gas chromatography-MS method or LC-MS-MS results from an outside laboratory. Oxazepam glucuronide was evaluated as a hydrolysis control for the urine and meconium specimens.

Gabapentin for refractory idiopathic trigeminal neuralgia.

J Indian Med Assoc. 2008 Feb; 106(2): 124-5
Pandey CK, Singh N, Singh PK
Trigeminal neuralgia is sudden, usually unilateral, severe, stabbing, brief recurrent pain in the distribution area of one or more of the branches of trigeminal nerve. Various pharmacological agents including carbamazepine, oxcarbazepine, phenytoin, lamotrigine, baclofen and clonazepam have been tried with variable success rate. Here a case of idiopathic trigeminal neuralgia is presented. The patient presented in the emergency room with severe pain in the distribution area of maxillary branch of trigeminal nerve, resistant to conventional pharmacotherapy, managed successfully with gabapentin without untoward side-effects.

Effect of antiepileptic drug polytherapy on urinary pH in children and young adults.

Childs Nerv Syst. 2008 Aug 14;
Go T
OBJECTS: The relationship between antiepileptic drugs (AEDs) polytherapy and urinary pH was studied to demonstrate the effect and difference of AED polytherapy compared to monotherapy. MATERIALS AND METHODS: A total of 271 urine samples from patients receiving AED polytherapy aged from 7 months to 35 years were enrolled. Two AEDs were co-administered to 215 patients, three AEDs to 45 patients, four AEDs to ten patients, and five AEDs to one patient. RESULTS: The distribution of urinary pH shifted to the alkaline range with increasing numbers of co-administered AEDs (p < 0.0001). The distribution of urinary pH shifted to the alkaline side with AED polytherapy that included valproate (p < 0.05) or acetazolamide (p < 0.03). The distribution of urinary pH did not change with or without zonisamide, carbamazepine, phenobarbital, phenytoin, or clonazepam. CONCLUSIONS: Urinary pH should be monitored in patients receiving AED polytherapy, particularly those receiving valproate, acetazolamide, or various AEDs in combination.

Effects of Various Combinations of Benzodiazepines with Buprenorphine on Arterial Blood Gases in Rats.

Basic Clin Pharmacol Toxicol. 2008 Jul 18;
Pirnay SO, Mégarbane B, Borron SW, Risède P, Monier C, Ricordel I, Baud FJ
Fatalities have been attributed to combinations of high-dose buprenorphine with benzodiazepines. In rats, high-dose buprenorphine combined with midazolam was shown to induce sustained respiratory acidosis, while buprenorphine alone did not. However, the effects of buprenorphine combined with pharmacological doses of benzodiazepines remain unknown. Our objective was to compare the acute effects of four selected benzodiazepines used intravenously at equi-efficacious doses in rats, alone and in combination with buprenorphine on sedation, respiratory rate and arterial blood gases. Buprenorphine (30 mg/kg) did not significantly modify sedation level or respiratory rate, but induced mild and transient effects on pH and PaCO(2) (P < 0.05). Similarly, despite having no effects on respiratory rate, nordiazepam (10 mg/kg), bromazepam (1 mg/kg) and oxazepam (12 mg/kg) mildly and transiently altered pH and PaCO(2) (P < 0.05), whereas clonazepam (5 mg/kg) did not. Buprenorphine combined with each benzodiazepine induced no significant effects on respiratory rate or blood gases, in comparison with buprenorphine alone. However, combinations of oxazepam or nordiazepam with buprenorphine significantly deepened sedation. While both combinations reduced respiratory rate, buprenorphine + 30 mg/kg clonazepam significantly increased PaCO(2) and buprenorphine + 30 mg/kg nordiazepam decreased PaO(2). In conclusion, not all benzodiazepines induce significant respiratory depression at therapeutic doses. We were unable to demonstrate significant effects on rat ventilatory parameters of buprenorphine combined with equi-efficacious pharmacological doses of benzodiazepines in comparison with buprenorphine alone. Our results may suggest that effects of these combinations are rather mild. Respiratory failure may, however, result from the association of buprenorphine with elevated doses of benzodiazepines.

Tremor associated with chronic inflammatory demyelinating peripheral neuropathy: treatment with pregabalin.

Clin Neuropharmacol. 2008 Jul-Aug; 31(4): 241-4
Alonso-Navarro H, Fernández-Díaz A, Martín-Prieto M, Ruiz-Ezquerro JJ, López-Alburquerque T, Jiménez-Jiménez FJ
OBJECTIVE: To report a case of a patient with tremor associated with chronic inflammatory demyelinating neuropathy (CIDP) that improved after treatment with pregabalin. CASE REPORT: A 68-year-old man diagnosed as having CIDP at age 63 years developed postural and kinetic tremor in both hands at age 64 years. Tremor did not improve with propranolol, primidone, phenobarbital, clonazepam, alprazolam, gabapentin, and topiramate, but improved markedly with pregabalin. Tremor worsened after pregabalin withdrawal and improved again after its reintroduction. CONCLUSIONS: Pregabalin could be useful in the treatment of postural tremor associated with CIDP resistant to other therapies.

 

This page was last reviewed by Dr Greg Mulhauser, Friday, 4 July 2008.

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