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At least 19 recordsLinked to original sources
PubMed1994

Anticonvulsant tolerance to clonazepam in amygdala kindled rats: clonazepam concentrations and benzodiazepine receptor binding.

The relationship between anticonvulsant tolerance to clonazepam and benzodiazepine receptor changes was studied in amygdala kindled rats. Fully kindled rats were given 1 mg/kg clonazepam (clonazepam treated) or vehicle (kindled control) orally three times per day for 4 weeks. During chronic treatment, amygdala stimulation was given twice per week, 30 min after a single protective dose of clonazepam (0.5 mg/kg, i.p.) was injected to both groups of rats. As measured by seizure stage, clonazepam treated rats showed a greater degree of tolerance than kindled control rats; contingent tolerance to the anticonvulsant effects of clonazepam developed in kindled control rats, while clonazepam treated rats shows contingent plus pharmacologic tolerance. There were no significant differences between clonazepam treated and kindled control rats in "peak" plasma clonazepam concentrations 40 min after clonazepam injections. Benzodiazepine receptor assays showed no significant difference in maximal binding capacity (Bmax), dissociation constant (Kd) or gamma-aminobutyric acid (100 microM) enhancement of benzodiazepine receptor binding between clonazepam treated and kindled control rats. These data suggest that pharmacologic tolerance to anticonvulsant action of clonazepam is not related to either plasma clonazepam concentrations or benzodiazepine receptor changes.

Amygdala↗
PubMed1997

Clonazepam in the treatment of panic disorder with or without agoraphobia: a dose-response study of efficacy, safety, and discontinuance. Clonazepam Panic Disorder Dose-Response Study Group.

In this multicenter, parallel-group, placebo-controlled, fixed-dose study, the efficacy, safety, dosing characteristics, and discontinuation of clonazepam were analyzed in patients with panic disorder. Four hundred thirteen patients were randomly assigned to receive placebo or one of five fixed daily doses of clonazepam (0.5 mg, 1.0 mg, 2.0 mg, 3.0 mg, and 4.0 mg). After 3 weeks of dose escalation, the fixed dose was given for 6 weeks (the dose-maintenance phase) and then was tapered during a 7-week discontinuance phase. The completion rates for the dose-maintenance phase ranged from 59 to 85% for the clonazepam groups (74% for the placebo group). Efficacy measurements at the end of the dose-maintenance phase indicated clinical improvement in all treatment groups but with a clear differentiation of the four higher doses of clonazepam from the 0.5-mg dose and placebo. The minimum effective dosage, as determined by the Williams' test, was 1.0 mg daily. Dose-response analysis showed that daily dosages of 1.0 mg and higher were equally efficacious in reducing the number of panic attacks. All treatments were well tolerated. Somnolence and ataxia were reported more often by patients in the 3.0- and 4.0-mg groups; depression, dizziness, fatigue, and irritability, although not showing dose-relatedness, were reported by more patients taking clonazepam than placebo. During the discontinuance phase, most patients worsened from their condition at the end of the dose-maintenance phase but did not revert to that at baseline. In addition, with the tapering schedule chosen for this study, patients in all treatment groups tolerated the discontinuance of clonazepam. Daily doses of 1.0 to 2.0 mg of clonazepam offered the best balance of therapeutic benefit and tolerability.

Adolescent↗
PubMed1994

Clonazepam in the treatment of panic disorder: a double-blind, placebo-controlled trial investigating the correlation between clonazepam concentrations in plasma and clinical response.

Thirty-two outpatients with a DSM-III diagnosis of panic disorder or agoraphobia with panic attacks were randomly assigned to 4 weeks of treatment with clonazepam or placebo, after a 1-week placebo washout period. Twenty-nine patients entered the double-blind phase of the study and were eligible for intent-to-treat analysis. Clonazepam-treated patients experienced significantly fewer panic attacks, and these were of lesser intensity and short duration than those in placebo-treated patients (p < 0.001). Clonazepam was also superior to placebo with respect to symptoms of anxiety and depression (p < 0.001). The mean dose of clonazepam at week 4 was 2.2 mg (standard deviation, 0.7 mg). There was significant (p < 0.05) correlation between drug concentration in plasma and decrease in the global measure of the severity of panic disorder (r = 0.68); similar trends were seen for the decreases in frequency (r = 0.60) and severity (r = 0.55) of panic attacks, but not between concentration in plasma and decline in generalized anxiety. The most common adverse event was drowsiness, which occurred in 9 of 13 clonazepam-treated patients.

Adult↗
PubMed1996

Treatment of manic episodes: zuclopenthixol and clonazepam versus lithium and clonazepam.

For the treatment of acute mania, no single drug is sufficiently effective in daily clinical routine for all patients. Drug combinations are often prescribed but poorly investigated. The present study examined whether a treatment with a neuroleptic drug (zuclopenthixol) combined with a benzodiazepine (clonazepam) was superior to a treatment with lithium and the same benzodiazepine (lithium citrate and clonazepam). Twenty-eight hospitalized patients with a DSM-III-R manic episode were included, randomized to fixed drug doses and observed up to 28 days. Degree of mania, side effects and patients satisfaction with the treatment were registered. Approximately two thirds of the patients improved fully or partially on both drug combinations. Furthermore no statistically significant differences were found regarding acceptance and tolerance of the two drug combinations. The present drug combination are only two among several which deserve a thorough examination in order to prevent a random polypharmacy for treatment of mania.

Administration, Oral↗
PubMed1979

[Direct determination of clonazepam (Rivotril) and 7-amino clonazepam in plasma by gas-chromatography (author's transl)].

A method is developed for direct gas-chromatographic determination of clonazepam (Rivotril) and its main metabolite, 7-amino clonazepam, in plasma, using desmethylflunitrazepam as internal standard. Following selective extraction, the benzodiazepines are analyzed by gas-chromatography, with a glass column filled with 3% OV17 on Gas Chrom Q and 63Ni electron capture detector. The procedure, which requires neither hydrolysis nor derivatisation, has a good selectivity. The sensitivity is 5 ng/ml of plasma for a valid quantitative determination. We have to improve this limit for fine pharmacokinetic studies, but the method is already available for therapeutic and pharmacovigilance controls. It is also suitable for diagnostic of eventual overdosing or poisoning, based on plasma or urine analysis.

Benzodiazepinones↗
PubMed2002

Pharmacoepidemiologic investigation of clonazepam relative clearance by mixed-effect modeling using routine clinical pharmacokinetic data in Japanese patients.

The effects of drug-drug interactions on clonazepam clearance were examined through a retrospective analysis of serum concentration data from pediatric and adult epileptic patients. Patients received clonazepam as monotherapy or in combination with other antiepileptic drugs. A total of 259 serum clonazepam concentrations gathered from 137 patients were used in a population analysis of drug-drug interactions on clonazepam clearance. Data were analyzed using a nonlinear mixed-effects modeling (NONMEM) technique. The final model describing clonazepam clearance was CL = 152 x TBW(-0.181) x DIF, where CL is clearance (ml/kg/h), TBWis total body weight (kg), and DIF (drug interaction factor) is a scaling factor for concomitant medication with a value of 1 for patients on clonazepam monotherapy, 1.18 for those patients receiving concomitant administration of clonazepam and one antiepileptic drug (carbamazepine or valproic acid), and 2.12 x TBW(-0.119) for those patients receiving concomitant administration of clonazepam and more than two antiepileptic drugs. Clonazepam clearance decreased in a weight-related fashion in children, with minimal changes observed in adults. Concomitant administration of clonazepam and carbamazepine resulted in a 22% increase in clonazepam clearance. Concomitant administration of clonazepam and valproic acid resulted in a 12% increase in clonazepam clearance. Concomitant administration of clonazepam with two or more antiepileptic drugs resulted in a 23% to 75% increase in clonazepam clearance.

Adolescent↗
PubMed1999

Efficacy and safety of clonazepam in refractory neurally mediated syncope.

Neurally mediated syncope is a complex syndrome that is often difficult to manage using currently available treatment strategies. The efficacy and safety of clonazepam was evaluated in 35 patients with refractory neurally mediated syncope. All patients had syncope (n = 33) or disabling presyncope (n = 2) and a positive head-up tilt table test (HUTT) despite treatment with one or more of the following therapies: beta-blocker, high-salt diet, fludrocortisone, elastic compression stockings, and disopyramide. Clonazepam was initiated at 0.5 mg/day and titrated in 0.25-0.5 mg/day increments for symptom control. Early (first 8 weeks) symptomatic response was achieved in 31 of 35 (89%) patients. Early HUTT reverted to negative in 29 of 35 (83%) patients. Two patients discontinued clonazepam during early follow-up due to side effects. Thirty-three patients received long-term clonazepam therapy. Twenty-five patients had late HUTT with 21 remaining negative. Of the eight patients who did not have late HUTT, one patient discontinued clonazepam prior to HUTT due to side effects. Seven patients refused late HUTT. All seven patients achieved symptomatic control on clonazepam with two requiring dose titration. Of the 21 patients with a negative late HUTT, 18 achieved symptomatic control with two of these patients requiring dose titration. Two patients who had only partial symptom control despite dose titration achieved total symptomatic control with the addition of disopyramide and beta-blockers. Two patients with a negative late HUTT discontinued clonazepam due to side effects. One patient had been symptomatically controlled while the other had recurrent symptoms with dose limiting side effects occurring after clonazepam dose titration. In the 4 patients with a positive late HUTT, 2 patients were symptomatically controlled, 1 patients required combination therapy with a beta-blocker to achieve symptomatic control, and 1 patient discontinued therapy due to side effects. Overall, 29 of 35 (83%) patients continue to receive clonazepam with symptom control. Based on intention-to-treat HUTT results, 21 of 35 (60%) patients were responders. Four patients required clonazepam dose titration and three required combination therapy with clonazepam plus disopyramide and/or a beta-blocker to achieve control. Clonazepam was discontinued in 6 patients, 5 for side effects and 1 following a transient ischemic attack. Clonazepam appears to be an effective therapeutic alternative in patients with refractory neurally mediated syncope. Based on our preliminary findings, a placebo controlled evaluation of clonazepam in neurally mediated syncope is warranted.

Adrenergic beta-Antagonists↗
PubMed1976

[Central effects of clonazepam].

The effects of oral administration of clonazepam, a new benzodiazepine derivative (F. Hoffmann-La Roche), on the central nervous system were compared with those of diazepam and several anticonvulsants in mice and rats. 1) Clonazepam exhibited a moderate inhibitory effect on the locomotor activity observed with open-field situation in mice and no effect in rats, while it inhibited markedly the rearing behavior in both animals, the duration of action being approximately six hours. 2) Clonazepam potentiated the methamphetamine-induced hyper-locomotor activity in mice whereas trimethadione had no effect. 3) Clonazepam inhibited with a moderate potency the conditioned avoidance response and response to a fixed-ratio (FR 20) schedule of food reinforcement in rats, the potency being a little weaker than that of diazepam. 4) The muscle relaxant effect of clonazepam determined by the traction test was slightly more potent as compared with that of diazepam. Thiopental hypnosis was markedly potentiated after clonazepam. 5) The clonic (CL), tonic-flexor (TF) and extensor convulsions (TE) induced by pentetrazol were strongly inhibited after clonazepam in mice, anticonvulsant potency against CL and TE of clonazepam being approximately 23 and 21 times stronger than that of diazepam, 3333 and 3846 times that of trimethadione, and over 3047 and 178 times that of phenytoin, respectively. Clonazepam reduced markedly CL and TE elicited by bemegride with about 12 to 14 times stronger potency than diazepam. On the contrary, the anticonvulsant effect of clonazepam against TE of maximal electroshock seizure evoked by supramaximal current was weak, the potency being 0.71 times weaker than that of phenacemide, 0.14 times than phenytoin and 0.24 times than phenobarbital. By the combined administration of clonazepam with other anticonvulsants such as trimethadione and phenytoin against pentetrazol convulsion, and phenacemide, phenytoin and phenobarbital against maximal electroshock seizure, the antagonistic effect of these anticonvulsants was potentiated by 4 to 5 times. 6) The acute toxicity (LD50) of clonazepam was weak but that of phenacemide or phenytoin was potentiated to a certain degree by combined administration with clonazepam. The results suggest that clonazepam has a psychopharmacological profile similar to that of benzodiazepines with a particularly potent anticonvulsant effect on pentetrazol and bemegride convulsions, and the anticonvulsant effect is synergic with that of other anticonvulsants.

Animals↗
PubMed2000

Clonazepam open clinical treatment trial for myofascial syndrome associated chronic pain.

OBJECTIVE: A number of case reports and nonplacebo controlled studies have documented the efficacy of clonazepam (Klonopin) in the treatment of a number of chronic pain syndromes including lancinating and neuropathic/deafferentation pain. There are, however, no data on the efficacy of clonazepam for chronic pain (CP) associated with myofascial pain syndrome (MFPS). Therefore, we wish to report the results of an open clinical treatment trial of clonazepam for CP associated with MFPS. DESIGN: Forty-six patients with chronic pain (PWCP) and a diagnosis of MFPS were recruited into a clonazepam pain treatment open clinical trial. At entrance and completion of the study the patients completed a 10-cm visual analog scale (VAS) requesting them to rate their pain over the last 24 hours. Clonazepam was titrated upwards from 0.5 mg per day, at 0.5 mg increments, every 2 days. These patients rated their perceived pain relief daily on a 3-point rating scale: none, partial, total. Once a patient claimed partial pain relief clonazepam increases were stopped. Patients who complained of intolerable side effects before partial pain relief were withdrawn from the study. For a subgroup of patients claiming partial pain relief, clonazepam serum levels were determined. Because of the reported efficacy of clonazepam for neuropathic/deafferentation type of pain, patients with this diagnosis were withdrawn from the partial response group. Statistical analyses were performed on this remaining patient group with myofascial pain syndrome without a secondary diagnosis of neuropathic/deafferentation pain and partially responsive to clonazepam. Descriptive statistics were calculated for this group. Drop in pain level from entrance to partial response was tested for statistical significance via t test. In addition, 17 independent variables such as presence of trigger points, presence of burning pain etc, were utilized in a regression analysis, with drop in pain level as the dependent variable. A Pearson correlation analysis was first performed in order to determine which of the independent variables significantly correlated with decrease in pain level. Independent variables having a Pearson r of.3687 or greater were selected for the regression procedure. SETTING: Multidisciplinary pain facility. PATIENTS: Patients with chronic pain with a diagnosis of MFPS and without neuropathic/deafferentation pain. RESULTS: Of the 46 patients entered into the study, 9 were not titrated to partial pain relief because of intolerable sedation and 9 had a diagnosis of neuropathic/deafferentation pain. For the remaining group (n = 28), mean drop in VAS pain level from beginning of the study to partial response was 2.78 (SD = 1.94). This was statistically significant (t = 5.49, P <.001). Mean clonazepam dosage to reach partial response was 2.41 (SD = 1.62) mg/day and the mean dosage per kilogram body weight per day was 0.04 (SD = 0.03) mg. Mean clonazepam serum level was 30.58 (SD = 24.53) microg/L. Decrease in pain level was associated with the presence of the following independent variables: trigger points (r =.451); range of motion restriction (r =.653); non anatomical sensory abnormalities (r =.370); chronic low back pain (r =.451); and burning pain (r =.482). In the regression analysis, restricted range of motion and presence of burning pain accounted for 42% and 16% of the variance respectfully. CONCLUSION: Clonazepam may have an antinociceptive effect for pain associated with myofascial pain syndrome.

Journal Article↗
PubMed1991

Chronic benzodiazepine administration. VII. Behavioral tolerance and withdrawal and receptor alterations associated with clonazepam administration.

Clonazepam administration may lead to tolerance and "withdrawal" syndromes in clinical use. To assess the effects of this drug in a mouse model, we administered clonazepam (1.5 mg/kg/day) for 1-14 days and evaluated open-field activity, cortical clonazepam concentrations, and binding and function at the GABAA receptor. We also evaluated the same parameters at 1, 2, 4 and 7 days after discontinuation of 7 days of clonazepam administration. During chronic treatment, tolerance developed to the effects of clonazepam on motor activity at 7 days and persisted to 14 days. Cortical clonazepam concentrations did not change significantly during this period. Benzodiazepine receptor binding in vivo was decreased in cortex at days 7 and 14 of clonazepam, but was unchanged in other regions. Binding determined in vitro was also decreased at these points. TBPS (t-butylbicyclophosphorothionate) binding in cortex was slightly, but not significantly, decreased. Muscimol-stimulated chloride uptake was also decreased at days 7 and 14. After clonazepam discontinuation, open-field activity returned to control values at 1 day but was increased above baseline at 4 days. Benzodiazepine binding in vivo and in vitro, as well as TBPS binding, were increased at 4 days. Muscimol-stimulated chloride uptake was also increased at this point. These results indicate that chronic clonazepam administration is associated with tolerance to motoric effects, with discontinuation effects, and with receptor alterations in a mouse model. Clonazepam is similar to other benzodiazepines in this regard.

Animals↗
PubMed2003

Comparative single-dose pharmacokinetics of clonazepam following intravenous, intramuscular and oral administration to healthy volunteers.

The objective was to assess the single-dose pharmacokinetics of clonazepam following i.m., p.o. and i.v. administration. In an open-label, three-way crossover study, 12 healthy volunteers were randomized to receive a single dose of 2 mg clonazepam either by the i.m., p.o. or i.v. route. Serial blood samples were collected up to 120 h after drug administration. Plasma concentrations of clonazepam were determined by electron-capture gas-liquid chromatography. The absorption rates of clonazepam after i.m. and p.o. administration of clonazepam were significantly different from each other, as reflected by the respective mean values of maximum plasma concentration (C(max) 11.0 vs. 14.9 ng.ml(-1)) and time to reach maximum concentration (t(max) 3.1 vs. 1.7 h). Secondary plasma peaks of clonazepam were observed in 9 volunteers after i.m. injection (C(max) 9.9 ng.ml(-1); t(max) 10.4 h). A comparison of the area under the plasma concentration-time curves (AUC) shows that the i.m. route is equivalent to the oral route (AUC(0- infinity ) 620 vs. 561 ng.h.ml(-1)). Clonazepam was almost completely absorbed after i.m. and p.o. administration, as shown by the mean absolute bioavailability of 93 and 90%, respectively. No significant differences existed between the elimination half-lives (i.v. 38.0 h; i.m. 43.6 h; p.o. 39.0 h). The average clearance and volume of distribution (V(Z)) were 55 ml.min(-1) and 180 liters, respectively. In conclusion, the observed differences in C(max) and t(max) after i.m. and p.o. administration were consistent with a slower absorption rate of clonazepam after i.m. injection. The systemic exposure to clonazepam was not affected by the route of extravascular administration. Statistical evaluation of these kinetic data showed differences in the absorption rate, so that clonazepam given by the i.m. route is not bioequivalent to the oral route. On the basis of the results of this study, we would recommend the same i.m. and p.o. dose in epileptic patients, but therapeutic response would be expected to be less predictable and to occur later in the case of i.m. administration.

Administration, Oral↗
PubMed2007

Possible predictors of response to clonazepam augmentation therapy in patients with protracted depression.

INTRODUCTION: Clonazepam has been shown to be an effective supplementary treatment for depression. Thus, it would be useful to determine which patient characteristics are associated with response to clonazepam. AIMS: The purpose of this study was to examine the possible predictors of response to clonazepam in the treatment of depression. METHOD: A retrospective cohort analysis was carried out in 120 patients with protracted depression who were being treated with clonazepam. RESULTS: A variety of clinical factors, including age, gender, type of depression, frequency of episodes, family history; and daily dose of clonazepam, were analyzed as possible predictors of response to clonazepam. A Weibull regression analysis showed that the factors that best predicted improvement with clonazepam augmentation were negative family history of psychiatric illness (e(coef) = 0.378), daily clonazepam dose of 2.5-4.0 mg (e(coef) = 0.160), and unipolar depression (e(coef) = 0.147). CONCLUSIONS: These factors should be considered when clonazepam augmentation therapy is selected for protracted depression.

Adult↗
PubMed1993

Clonazepam-induced intestinal motor disturbances are linked to central nervous system release of cholecystokinin in rats.

The central and peripheral effects of clonazepam (central benzodiazepine receptor agonist) on intestinal myoelectrical activity and the origin of the effects were evaluated in conscious rats, chronically fitted with Nichrome electrodes implanted on the jejunum and with an intracerebroventricular (i.c.v.) cannula. Administered intraperitoneally (i.p.) in 12-h fasted rats, clonazepam (0.05 to 0.5 mg/kg) dose dependently disrupted jejunal cyclic migrating myoelectric complexes, characterizing the fasted state, which were replaced by a permanent irregular spiking activity, lasting 259 +/- 37 min for clonazepam at the dose of 0.5 mg/kg. This disruption of migrating myoelectric complexes occurred after a delay which increased with increasing clonazepam doses. In contrast, injected i.c.v. at doses from 1 microgram/kg to 1 mg/kg, clonazepam did not alter the migrating myoelectric complexes pattern of the small intestine. Injected i.p., flumazenil (central benzodiazepine receptor antagonist) (1 mg/kg) but not PK 11-195 (peripheral benzodiazepine receptor antagonist) (5 mg/kg) suppressed the effects of i.p. clonazepam (0.1 mg/kg). Administered i.c.v., 10 min prior to clonazepam (0.1 mg/kg i.p.), devazepide (CCKA receptor antagonist) at a dose as low as 10 ng/kg reduced the migrating myoelectric complex disruption induced by clonazepam. L365-260 (CCKB receptor antagonist) administered i.c.v reduced the migrating myoelectric complex disruption at 10-fold higher doses and loxiglumide (CCKA receptor antagonist) injected i.c.v, at 100-fold higher doses. When administered i.p. neither devazepide nor L365-260 affected the duration of migrating myoelectric complex disruption induced by clonazepam (0.1 mg/kg i.p.) or its delay of occurrence at doses lower than 0.1 mg/kg.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Absence of tolerance to the excitatory effects of benzodiazepines: clonazepam-evoked shaking behavior in the rat.

Select benzodiazepine (BDZ) agonists, such as clonazepam, evoke wet-dog shakes (WDS) in the rat, a behavior which may be influenced by serotonergic drugs. To further study the role of serotonin (5-HT) and BDZ receptors in BDZ-induced WDS, we injected adult rats daily for 21 days with clonazepam and measured WDS and 5-HT1, 5-HT2, and BDZ receptors. Clonazepam 5 mg/kg upregulated 5-HT1 and 5-HT2 receptors in frontal cortex, but not in brainstem or spinal cord, compared to vehicle controls, without a change in BDZ receptors. A 10 mg/kg dose of the same drugs, however, did not alter 5-HT receptors. Chronic treatment with clonazepam failed to decrease clonazepam-induced WDS, resulting instead in a significant increase. The increase was prevented by chronic cotreatment with the 5-HT2 antagonist ketanserin, which significantly down-regulated 5-HT2 and BDZ sites. In vitro, clonazepam did not inhibit radioligand binding at 5-HT1 or 5-HT2 receptors in frontal cortex, brainstem, or spinal cord. Lack of tolerance to WDS evoked by clonazepam suggests different mechanisms for the excitatory and inhibitory effects of BDZs. The dose-independent effects of chronic clonazepam administration on 5-HT receptors are not mediated by activity of clonazepam at 5-HT receptor recognition sites.

Animals↗
PubMed2006

Effect of tubing on loss of clonazepam administered by continuous subcutaneous infusion.

Previous studies have reported loss of clonazepam from solutions administered intravenously from plastic infusion bags and administration sets. In palliative care, clonazepam is sometimes administered through syringe drivers using polyvinyl chloride (PVC) infusion tubing. No data currently exist to show whether use of PVC tubing affects the amount of clonazepam actually received by the patient. This study compared the use of two different types of PVC tubing with a non-PVC tubing. Solutions containing clonazepam or clonazepam and morphine were prepared with either normal saline or water for injection as diluent. Concentrations of morphine and clonazepam were determined using high-performance liquid chromatography. Significant loss of clonazepam (up to 50%) was observed in all solutions infused through PVC tubing. Solutions infused through non-PVC tubing retained greater than 90% of the initial concentration of clonazepam. It is recommended that when administering clonazepam using a syringe driver, non-PVC tubing be used.

Adsorption↗
PubMed1998

An open-label, dose escalation pilot study of the effect of clonazepam in burning mouth syndrome.

OBJECTIVE: Current treatment for burning mouth syndrome is usually directed at correction of detected organic causes or is empiric, and it often involves the use of tricyclic antidepressants. Recently, there has been renewed interest in the use of benzodiazepines for burning mouth syndrome. The present study was designed to assess the effect of clonazepam in burning mouth syndrome. STUDY DESIGN: Thirty patients, each with a chief complaint of mouth burning without oral mucosal lesions, were entered into the study. All patients underwent routine blood screens. Identified abnormalities were corrected, when possible, before clonazepam was prescribed. The starting dose was 0.25 mg daily, with an increase in dose of 0.25 mg on a weekly basis if symptoms continued. RESULTS: The subject population consisted of 29 women and 1 man. All subjects had been symptomatic (average premorbid burning intensity, 7.0 +/- 1.9 on 10-point scale) for 1 month to 12 years (mean, 3.9 +/- 3.4 years; median, 2.75 years), and 16% had had burning for more than 2 years. Three groups of patients were identified: those who experienced partial to complete relief with clonazepam and who were using the medication at the last follow-up (group 1; 43%); those who found the clonazepam helpful but withdrew from the medication because of side effects--usually drowsiness (group 2; 27%); and those who did not benefit from clonazepam (group 3; 30%). Among the 3 groups, age was found to be significantly lower for group 1 than for group 2 but not significantly lower for group 1 than for group 3. Although the difference did not reach significance, the mean dose of clonazepam appeared lower for group 1 patients than for the other 2 patient groups. The number of patients with burning for less than 2 years was larger in group 1 than in the other groups. CONCLUSIONS: The results suggest that clonazepam may be helpful in burning mouth syndrome, inasmuch as 70% of patients (groups 1 and 2) experienced pain reduction with effects at low doses. These findings suggest that the mechanism of action of clonazepam may be specific and separate from the anxiolytic effect of the benzodiazepines and that clonazepam may represent a useful therapy in a subset of patients with burning mouth syndrome. Double-blind, placebo-controlled trials are warranted.

Aged↗
PubMed2006

Clonazepam in the treatment of psychiatric disorders: an update.

An updated overview over the past decade is provided with respect to the use of clonazepam in a variety of psychiatric disorders. The efficacy of clonazepam monotherapy for the short-term treatment of panic disorder (PD) was fully established in two large pivotal multicentre studies in the late 1990s in a total of >800 patients. Other studies support a role for clonazepam, in association with selective serotonin reuptake inhibitors (SSRIs), to accelerate treatment response in PD. Although some longitudinal data suggest an ability to maintain improvement without tolerance for up to 3 years, long-term controlled studies of clonazepam in PD are lacking. Studies have shown that clonazepam can also block CO2-induced panic and improve certain aspects of quality of life in PD. Clonazepam has shown some efficacy in social phobia; however, because this evidence is based on few studies, further studies are warranted before definitive conclusions can be drawn. Finally, evidence for the use of clonazepam in acute mania and as augmentation therapy with SSRIs to accelerate response in depression is examined. The long half-life and higher potency of clonazepam may allow easier discontinuation with fewer withdrawal symptoms compared to other benzodiazepines and studies using a slow clonazepam taper appear promising.

Anti-Anxiety Agents↗