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At least 19 recordsLinked to original sources
PubMed2000

Nimodipine for primary degenerative, mixed and vascular dementia.

BACKGROUND: Dementia is an age-related condition in which Alzheimer's disease (AD) and cerebrovascular disease account for the bulk of cases. The role played by calcium in regulating brain functions is well known - the calcium ion links membrane excitation to subsequent intracellular enzymatic response. Change in calcium homeostasis is one important effect of aging with repercussions on higher cortical functions. Nimodipine is an isopropyl calcium channel blocker which can easily cross the blood brain barrier. Its primary action is to reduce the number of open channels, thus restricting influx of calcium ions into the cell. The usefulness of nimodipine in patients with Alzheimer's disease and vascular dementia and unspecified dementia is still controversial with mixed results. In spite of the uncertainties about its efficacy in dementia, nimodipine is currently a frequently prescribed drug for cognitive impairment and dementia in several European countries. This review will be conducted in two phases; the current review is based on evidence from published data only. The second phase will be based on individual-patient data analysed centrally and added to this review in due course. OBJECTIVES: To determine the clinical efficacy of nimodipine for the symptoms of dementia, either unclassified or according to the major subtypes - Alzheimer's disease, vascular, or mixed Alzheimer's and vascular dementia. SEARCH STRATEGY: The Cochrane Dementia Group Register of Clinical Trials was searched using the terms 'nimodipine' and 'isopropyl (2-methoxy-ethyl) 1,4-dihydro-2, 6-dimethyl-4-(3-nitrophenyl)-3, 5-pyridinedicarboxylate'. SELECTION CRITERIA: All unconfounded, double-blind, randomised trials in which treatment with nimodipine was administered for more than a day and compared to placebo in patients with dementia, either unclassified or according to the major subtypes - Alzheimer's disease, vascular, or mixed Alzheimer's and vascular dementia. DATA COLLECTION AND ANALYSIS: Data were extracted independently by the reviewers and the odds ratio (95%CI) or the average difference (95%CI) were estimated. Both intention-to-treat and on-treatment results were extracted. MAIN RESULTS: This review produced no clear results. Many of the data published were not capable of being sensibly pooled. The data were compatible with nimodipine producing improvement, no change or even harm for those with Alzheimer's disease, vascular dementia, or mixed Alzheimer's and vascular dementia. It was not possible to use many of the published results in a combined analysis. For measures of overall clinical improvement, the intention-to-treat analysis, based on one study only, failed to detect any difference between nimodipine and placebo (OR 0.53; 95%CI 0.25 - 1.13). An on-treatment analysis, based on one study only, produced a statistically significant difference in favour of nimodipine (SMD 4.4; 95%CI 3.9 - 5.0). For cognitive function, the effect of nimodipine was statistically significantly different from placebo for the Mini Mental State Examination score (0-30; high =good) (SMD 0.9; 95%CI 0.59 - 1.22) and there was a statistically significant effect in favour of treatment for the Wechsler Memory Scale (SMD 0.47; 95%CI 0.17 - 0.77). These analyses were based only on those who completed the study and not intention-to-treat analyses. There were no results presented in a form suitable for pooling for functional autonomy, behaviour, quality of life dependency (eg institutionalization), effect on carer, death, acceptability of treatment (as measured by withdrawal rate, safety (as measured by the incidence of adverse effects, including side effects, leading to withdrawal). REVIEWER'S CONCLUSIONS: This review provides no convincing evidence that nimodipine is a useful treatment for the symptoms of dementia, either unclassified or according to the major subtypes - Alzheimer's disease, vascular, or mixed Alzheimer's and vascular dementia. (ABSTRACT TRUNCATED)

Alzheimer Disease↗
PubMed2006

Enhanced nimodipine bioavailability after oral administration of nimodipine with morin, a flavonoid, in rabbits.

The aim of this study was to investigate the effect of morin on the bioavailability of nimodipine after administering nimodipine (15 mg/kg) orally to rabbits either co-administered or pretreated with morin (2, 10 and 20 mg/kg). The plasma concentrations of nimodipine in the rabbits pretreated with morin were increased significantly (p < 0.05 at 10 mg/kg, p < 0.01 at 20 mg/kg) compared with the control, but the plasma concentrations of nimodipine co-administered with morin were not significant. The areas under the plasma concentration-time curve (AUC) and the peak concentrations (Cmax) of the nimodipine in the rabbits pretreated with morin were significantly higher (p < 0.05 at 10 mg/kg, p < 0.01 at 20 mg/kg), but only the Cmax of nimodipine coadministered with morin 10 mg/kg was increased significantly (p < 0.05). The absolute bioavailability (A.B%) of nimodipine in the rabbits pretreated with morin was significantly (p < 0.05 at 10 mg/kg, p < 0.01 at 20 mg/kg) higher (54.1-65.0%) than the control (36.7%). The increased bioavailability of nimodipine in the rabbits pretreated with morin might have been resulted from the morin, which inhibits the effiux pump P-glycoprotein and the first-pass metabolizing enzyme by cytochrome P-450 3A4 (CYP 3A4).

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2003

[Dissolution of nimodipine in an aqueous solution of hydroxyethyl-beta-cyclodextrin and a review of solubility of nimodipine with cyclodextrins].

The results of a comprehensive study of the dissolution of the calcium antagonist nimodipine in aqueous solutions of nine cyclodextrins are reported. The used cyclodextrins were native beta-cyclodextrin (beta-CD), its derivatives hydroxyethyl-beta-CD (HE-beta-CD), three hydroxypropyl-beta-CD (HP-beta-CD) with various degree of substitution and methyl-beta-CD (M-beta-CD), native alpha-cyclodextrin (alpha-CD), hydroxypropyl-alpha-CD (HP-alpha-CD) and hydroxypropyl-gamma-CD (HP-gamma-CD). The nimodipine dissolution was studied as a function of time (up to 14 days) and cyclodextrin concentration up to 0.07 mol/l, excepting the less soluble beta-CD. In this range of cyclodextrin concentration, linear phase diagrams of nimodipine solubility in the cyclodextrin solutions were observed. From them we derived the stability constants of the inclusions complexes nimodipine-cyclodextrin (1:1) as well as the empirical linear equations for the calculation of the saturated nimodipine concentration at a given cyclodextrin concentration. The most efficient solubiliser of nimodipine was M-beta-CD, a good solubilizing efficiency was also shown by HE-beta-CD and HP-beta-CDs (with a low degree of substitution), which may be acceptable for the preparation of parenteral nimodipine solutions.

Calcium Channel Blockers↗
PubMed1989

European multicenter trial of nimodipine in the prophylaxis of common migraine (migraine without aura). Migraine-Nimodipine European Study Group (MINES).

This double blind, randomized study of the calcium antagonist Nimodipine 40 mg t.i.d. vs placebo in the prophylaxis of common migraine (migraine without aura) included 192 patients. Patients with 2-8 migraine days/4 weeks, age 18-60, who had no other types of recurring headaches except up to 6 interval headaches/4 weeks were included. The study was carried out at 11 European centers. After a 4 week run-in period, patients were randomly allocated to Nimodipine or placebo for 12 weeks (parallel groups). There were 19 drop-outs, 12 on Nimodipine and 7 on placebo. A gradual and marked improvement was seen both with Nimodipine and with placebo amounting to approximately 60% during the last 4 weeks. Statistical analysis on all included patients (intention to treat) revealed no difference between Nimodipine and placebo for migraine days (P = 0.69) or migraine index (p = 0.91). In patients "valid for analysis of efficacy" there were also no significant differences. Due to a very marked placebo effect and use of the parallel groups design, the present trial was not very powerful despite the large number of patients and a satisfactory compliance. We cannot rule out that Nimodipine might have up to 30% effect on a single main outcome parameter, but the uniform lack of response in all tested parameters makes this unlikely. Therefore Nimodipine probably has only a small or no effect in common migraine (migraine without aura).

Adolescent↗
PubMed2000

Studies on concentration-time profiles of nimodipine enantiomers following intravenous and oral administration of nimodipine in patients with subarachnoid hemorrhage.

After i.v. and oral administration of nimodipine the concentration-time profiles of the drug and its enantiomers were studied in seven patients with subarachnoid hemorrhage. Concentrations of nimodipine, (+)-(R)-, and (-)-(S)-nimodipine were analyzed using a new stereoselective high-performance liquid chromatographic method. During the first 3 h after oral administration the concentrations of (+)-(R)- and (-)-(S)-nimodipine were significantly different, the (-)-(S)-enantiomer being found in much lesser concentrations compared to the (+)-(R)-enantiomer. The results indicate that if uptake from the gastrointestinal system is equal for the two enantiomers, then (-)-(S)-nimodipine is metabolized at a much faster rate compared to (+)-(R)-nimodipine after oral administration of the drug in patients with subarachnoid bleeding. After i.v. administration; no significant differences between the concentrations of the (-)-(S) and the (+)-(R) isomers were demonstrated.

Administration, Oral↗
PubMed1989

Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial.

OBJECTIVE: To determine the efficacy of oral nimodipine in reducing cerebral infarction and poor outcomes (death and severe disability) after subarachnoid haemorrhage. DESIGN: Double blind, placebo controlled, randomised trial with three months of follow up and intention to treat analysis. To have an 80% chance with a significance level of 0.05 of detecting a 50% reduction in an incidence of cerebral infarction of 15% a minimum of 540 patients was required. SETTING: Four regional neurosurgical units in the United Kingdom. PATIENTS: In all 554 patients were recruited between June 1985 and September 1987 out of a population of 1115 patients admitted with subarachnoid haemorrhage proved by the results of lumbar puncture or computed tomography, or both. The main exclusion criterion was admission to the neurosurgical units more than 96 hours after subarachnoid haemorrhage. There were four breaks of code and no exclusions after entry. One patient was withdrawn and in 130 treatment was discontinued early. All patients were followed up for three months and were included in the analysis, except the patient who had been withdrawn. INTERVENTIONS: Placebo or nimodipine 60 mg was given orally every four hours for 21 days to 276 and 278 patients, respectively. Treatment was started within 96 hours after subarachnoid haemorrhage. END POINTS: Incidence of cerebral infarction and ischaemic neurological deficits and outcome three months after entry. MEASUREMENTS: Demographic and clinical data, including age, sex, history of hypertension and subarachnoid haemorrhage, severity of haemorrhage according to an adaptation of the Glasgow coma scale, number and site of aneurysms on angiography, and initial findings on computed tomography were measured at entry. Deterioration, defined as development of a focal sign or fall of more than one point on the Glasgow coma scale for more than six hours, was investigated by using clinical criteria and by computed tomography, by lumbar puncture, or at necropsy when appropriate. All episodes of deterioration and all patients with a three month outcome other than a good recovery were assessed by a review committee. MAIN RESULTS: Demographic and clinical data at entry were similar in the two groups. In patients given nimodipine the incidence of cerebral infarction was 22% (61/278) compared with 33% (92/276) in those given placebo, a significant reduction of 34% (95% confidence interval 13 to 50%). Poor outcomes were also significantly reduced by 40% (95% confidence interval 20 to 55%) with nimodipine (20% (55/278) in patients given nimodipine v 33% (91/278) in those given placebo). CONCLUSIONS: Oral nimodipine 60 mg four hourly is well tolerated and reduces cerebral infarction snd improves outcome after subarachnoid haemorrhage.

Administration, Oral↗
PubMed1992

Clinical trial of nimodipine in acute ischemic stroke. The American Nimodipine Study Group.

BACKGROUND AND PURPOSE: A randomized, double-blind, multicenter clinical trial of placebo versus nimodipine was conducted to test the hypothesis that nimodipine would reduce the frequency of death and of worsening by 30% compared with placebo. METHODS: Nimodipine was used in doses of 60 mg, 120 mg, and 240 mg daily in 1,064 patients treated for 21 days. Treatment was begun within 48 hours of stroke due to infarction as inferred by initial computed tomographic scan findings. The Toronto and motor scales were analyzed by analysis of covariance, using covariance-adjusted means, the last-value-carried-forward, to compare the baseline value with the 3 assessment days (days 4, 10, and 21). RESULTS: No difference in mortality or neurological outcome was found with any of the rating scales for the overall cohort. Planned but post hoc subgroup analysis showed a reduction in worsening frequency of 30% compared with placebo and significantly better outcome scores with 120 mg nimodipine daily started within 18 hours of stroke as measured by the Toronto scale (p less than 0.005) and when the pretreatment computed tomographic scan was negative (p less than 0.003). CONCLUSIONS: Nimodipine had no overall effect when treatment was begun within 48 hours. Confirmation of the benefits suggested by post hoc analyses for the subgroup treated with 120 mg nimodipine within 18 hours, and who had negative computed tomographic scans, would require a separate trial.

Adult↗
PubMed1989

European multicenter trial of nimodipine in the prophylaxis of classic migraine (migraine with aura). Migraine-Nimodipine European Study Group (MINES).

This double-blind, randomized study of the Nimodipine 40 mg t.i.d. vs placebo in the prophylaxis of classic migraine (migraine with aura) included 89 patients. Required migraine frequency was 2-8 migraine days/4 weeks and at least two of the attacks within the last 6 months had to be with aura. The study was carried out at 11 European centers. After a 4 week run-in period, patients were randomly allocated to nimodipine or placebo for 12 weeks (parallel groups). There were 7 drop-outs, 3 on Nimodipine, and 4 on placebo. A gradual and very marked improvement was seen both with Nimodipine and placebo amounting to between 60 and 90 per cent during the last 4 weeks. Statistical analysis on all included patients (intention to treat) revealed no difference between Nimodipine and placebo for migraine days or migraine index. In patients "valid for analysis of efficacy" there were also no significant difference. Due to a very marked placebo effect and use of the parallel groups design, the present trial is relatively weak despite a fairly large sample size. It cannot rule out the possibility of an important effect of Nimodipine in classic migraine with a high degree of certainty.

Adult↗
PubMed1986

Prevention by nimodipine, a calcium entry blocker, of the effect of alpha 2-adrenoceptor blocking agents on noradrenaline release: differential effects of nimodipine, on [3H]noradrenaline and [14C]acetylcholine release measured concomitantly from the guinea-pig ileum.

The calcium channel blocker, nimodipine (Bay e 9736), inhibited the evoked (1 Hz, 1 msec, 180 pulses) release of [14C]acetylcholine ([14C]ACh) while it enhanced the release of [3H]noradrenaline ([3H]NA) measured concomitantly from the same longitudinal muscle strip of guinea-pig ileum loaded with [14C]choline and [3H]noradrenaline. These effects of nimodipine were concentration-dependent: in 0.1 microM concentration yielding maximal inhibition of [14C]ACh release and in 0.5 microM concentration yielding half maximal stimulation of [3H]NA-release. Enhancement of [3H]NA-release by nimodipine was strongly dependent on stimulation frequency while the inhibitory effect of nimodipine on release of [14C]ACh did not depend on stimulation frequency in the 0.5-10 Hz range. In addition, in the presence of nimodipine when the release of [3H]NA was enhanced, i.e. when a significant negative feedback operation could have been expected, alpha 2-adrenoceptor blocking agents (yohimbine and idazoxane) failed to enhance [3H]NA-release. It is proposed that nimodipine somehow exerts a presynaptic alpha 2-adrenoceptor blocking property at noradrenergic axon terminals through an effect on calcium entry, which may be an essential step in events linking alpha 2-adrenoceptor activation and inhibition of noradrenaline release.

Acetylcholine↗
PubMed1985

Pharmacokinetics of nimodipine. I. Communication: absorption, concentration in plasma and excretion after single administration of [14C]nimodipine in rat, dog and monkey.

Studies on absorption, plasma concentrations and excretion with (+/-)isopropyl-2-methoxyethyl-1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl) -3,5-pyridinedicarboxylate (nimodipine, Bay e 9736, Nimotop) have been conducted in rat, dog and monkey using the carbon-14-labelled substance and a wide range of doses (0.05-10 mg/kg) administered via different routes (intravenous, oral, intraduodenal). Nimodipine was well absorbed in all species. Peak plasma concentrations of radioactivity were determined 28-40 min (male rat), 60 min (female rat), about 3 h (dog) and 7 h (monkey) after administration. Dependent on the observation period (24-216 h) terminal half-lives for the elimination of radioactivity from plasma ranging between 4.6 h (female rat) and 157 h (dog) were observed. Comparing the AUC, the concentration of unchanged [14C]nimodipine in plasma represented only a small (maximally 37% in dogs after i.v. dose) to negligible (about 1%, monkey after oral dosing) part of the total radioactivity. Excretion of radioactivity via feces and urine was rapid in all species after both oral and intravenous dosing. Fecal (biliary) excretion was the major excretory route in rat and dog. The monkeys excreted about 40 to 50% via the urine. Residues in the body never exceeded 1.5% of the dose. [14C]nimodipine and/or its radiolabelled metabolites were secreted in milk of orally dosed lactating rats. Binding of [14C]nimodipine to plasma proteins of rat and dog was about 97%.

Animals↗
PubMed1994

A multicenter trial of the efficacy of nimodipine on outcome after severe head injury. The European Study Group on Nimodipine in Severe Head Injury.

Between January 1, 1989, and June 30, 1991, 852 severely head-injured patients were entered into a prospective placebo-controlled trial of the efficacy of nimodipine administration. The patients could not obey commands at the time of entry into the trial, which was within 12 hours after the start of the inability to obey commands and within 24 hours of injury. The main hypothesis that nimodipine would increase the percentage of patients with a favorable outcome (moderate disability or good recovery) from 50% to 60% was rejected. A trend toward a favorable effect was seen in patients who exhibited traumatic subarachnoid hemorrhage (SAH) on the computerized tomography (CT) scan obtained prior to entry into the study. The effect was statistically significant in those patients who complied with all protocol requirements. This finding is consistent with the effect of nimodipine on secondary ischemia following spontaneous SAH. The results of the study warrant a clinical trial of the efficacy of nimodipine in severely head-injured patients who show traumatic SAH on the initial CT scan.

Adult↗
PubMedDate not supplied

Mental deterioration in old age: results of two multicenter, clinical trials with nimodipine. The Nimodipine Study Group.

The efficacy and tolerability of nimodipine, a calcium antagonist selective for the central nervous system, was evaluated in old age dementias in two multicenter, clinical trials. A total of 755 elderly patients suffering from mental deterioration of degenerative or vascular origin were enrolled in the studies. In the first study, 352 patients received nimodipine 30 mg TID orally for 3 months; in the second study, 403 patients received the same treatment for 6 months. In both studies, psychobehavioral instruments showed a highly significant improvement of the global functional state. In hypertensive patients, nimodipine had a synergistic effect with the antihypertensive drugs. These results confirm the therapeutic efficacy and safety of nimodipine in the treatment of old age dementias.

Activities of Daily Living↗
PubMed1985

Pharmacokinetics of Nimodipine. II. Communication: distribution, elimination and placental transfer in rats following single and multiple doses of [14C]nimodipine.

(+/-)Isopropyl-2-methoxyethyl-1,4-dihydro-2,6-dimethyl-4- (3-nitrophenyl)-3,5-pyridinedicarboxylate (nimodipine, Bay e 9736, Nimotop) is a calcium antagonist from the 1,4-dihydropBridine group which influences the cerebral blood flow. The active substance labelled with carbon-14 was administered orally or intravenously to rats at doses ranging from 1 to 10 mg/kg. The objective of the study was to determine the course of the distribution of total radioactivity among organs and tissues, to investigate the extent and kinetics of diaplacental transfer and to study the influence of continuous treatment over three weeks on concentrations and elimination kinetics in organs and tissues. The radioactivity concentration was determined qualitatively by whole-body autoradiography or quantitatively after autopsy. Following intravenous administration the radioactivity of [14C]nimodipine is distributed rapidly and uniformly. Later, and also after oral administration, the distribution pattern is strongly differentiated with high concentrations in the liver, kidneys and fat and low concentrations in the brain and testes and subsequently in the plasma. Within one day the concentration in the animal excluding the gastrointestinal tract falls by a factor of 25 and a slow elimination phase then ensues. Only a little of the radioactivity of nimodipine passes through the placental barrier. The distribution patterns and excretion routes detected in the foetus are essentially the same. The radioactivity concentration in the foetus was a factor of 8-15 lower than in the dam.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Nimodipine and haloperidol attenuate behavioural sensitization to cocaine but only nimodipine blocks the establishment of conditioned locomotion induced by cocaine.

The classical conditioning of the behavioural effects of cocaine has been shown to contribute to behavioural sensitization. In the present experiments, it was demonstrated that the effects of cocaine in rats can be conditioned to contextual stimuli. Furthermore, sensitization to cocaine's locomotor effects were demonstrated, and shown to be context specific. Nimodipine (10 mg/kg, SC), an L-type dihydropyridine Ca2+ channel antagonist, appeared to completely block the establishment of conditioning of cocaine's effects, but only partially blocked sensitization to cocaine. Haloperidol (0.05 mg/kg, IP), a relatively specific D2 dopamine receptor antagonist, attenuated behavioral sensitization but had no influence on the establishment of the conditioned component of cocaine. These results indicate that the sensitization to, and the development of classical conditioning of, cocaine's behavioural effects can be pharmacologically dissociated, but that a non-associative process involved in sensitization is normally overridden by conditioning factors.

Animals↗
PubMedDate not supplied

The effect of nimodipine monotherapy and combined treatment with ketamine and lignocaine in aneurysmal subarachnoid haemorrhage.

The clinical effects of nimodipine monotherapy were compared with the effects of nimodipine combined with ketamine and lignocaine (combination therapy) in a single-centre, one investigator, open study in patients with proven aneurysmal subarachnoid haemorrhage (aSAH). After clipping of the aneurysm, nimodipine was administered intravenously until day 5-7 after clipping. Thereafter the intravenous nimodipine was substituted by oral doses of nimodipine. These were decreased gradually and then discontinued within the following 6 days. For combination therapy, nimodipine was given together with both a bolus injection of 1 microgram/kg ketamine followed by an infusion of the drug at a rate of 3 micrograms/kg/min and a bolus injection of 1.5 mg/kg lignocaine followed by an infusion of the drug at a rate of 12 micrograms/kg/min. During the study period, 173 patients were admitted to the hospital with subarachnoid haemorrhage (SAH). Of these patients, 115 with a proven aneurysm were operated on and evaluated: 66 patients received nimodipine monotherapy and 49 were given nimodipine combined with ketamine and lignocaine. These subgroups were comparable in terms of the baseline characteristics (age, Hunt and Hess score). The (baseline corrected) Hunt and Hess scores after surgery and a 0-5 clinical outcome score were applied as indices for clinical effects. Patients receiving nimodipine monotherapy and combined therapy showed a significant clinical improvement compared to baseline (P = 0.001 and P = 0.006, respectively). The beneficial effect of nimodipine monotherapy is in line with previous double-blind, placebo-controlled studies. Although nimodipine monotherapy seems to be more effective than combined treatment, this was not statistically significant. Our data indicate that combined treatment with ketamine and lignocaine is not more effective than nimodipine monotherapy in patients with mild aSAH, but this does not rule out an effect in severe cases. There was no indication of a pharmacodynamic interaction between nimodipine and co-medication. No serious or clinically relevant adverse reactions were noted during the study.

Adult↗
PubMed2006

Development and pharmacokinetics of nimodipine-loaded liposomes.

In order to improve the water solubility of nimodipine and prolong the time of the drug in the circulation, nimodipine-loaded liposomes with a small size and high entrapment efficiency were prepared by a method that was easy to scale up (the modified ethanol injection method). The nimodipine liposome dispersions were characterized with respect to particle size distribution, zeta potential and entrapment efficiency. Liposomal nimodipine and nimodipine solution were intravenously administered to mice as a single dose of 4 mg kg-1. The pharmacokinetic parameters of nimodipine changed significantly when encapsulated in liposomes. The clearance of nimodipine encapsulated in liposomes was reduced and the elimination half-life was prolonged. The ratios of the area under the curve values of nimodipine liposomes to nimodipine solution were 1.78 and 1.90 in plasma and cerebral tissue, respectively. The drug concentration in cerebral tissue and in plasma showed a good linear correlation, which showed that liposomes could efficiently deliver nimodipine into brain tissue. These findings suggest that intravenous administration of liposomal nimodipine produces higher and more stable plasma and cerebral drug concentrations compared with nimodipine solution. In conclusion, liposomal nimodipine is a promising alternative to the solution preparation.

Animals↗