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PubMed1979

Analgesic combinations with orphenadrine in oral post-surgical pain.

Two hundred male and female patients underwent a variety of oral surgical procedures and were treated afterwards in four test groups. They took a combination of orphenadrine (25 mg) and acetaminophen (325 mg), either drug alone, or placebo. A double-blind study design was used. All patients had moderately severe baseline pain intensity; post-treatment pain relief was recorded at 30 minutes, one, two, four and six hours. A back-up analgesic (codeine-ASA) was made available if needed. Pain intensity difference (PID) and sums of pain intensity difference (SPID) were calculated using established analgesic study techniques. Statistical analyses indicated better analgesic efficacy in both PID and SPID scores for the orphenadrine-acetaminophen combination over the three other treatments. This was evident at 30 minutes and continued through the sixth hour. Each active drug, in turn, was also significantly better throughout than placebo for pain relief. Sub-groups in each treatment regimen required additional pain relief prior to six hours, with significantly more placebo than orphenadrine-acetaminophen patients needing remedication. Side-effect incidence was very low and randomly distributed among the four groups.

Acetaminophen↗
PubMed1982

The bioavailability of orphenadrine hydrochloride after intramuscular and oral administration.

The bioavailability of orphenadrine hydrochloride after a single intramuscular injection was compared to that after a single oral dose by following serial plasma concentration estimations of the unchanged drug. Eight subjects received 40 mg orphenadrine HCl intramuscularly and 50 mg orally on separate occasions 1 week apart. The bioavailability of orphenadrine from the intramuscular dosage form proved to be equal to or even greater than that from the tablet. The first hour plasma concentrations after intramuscular doses were significantly higher than those after oral doses, supporting the clinical use of the intramuscular route in those indications where rapid effects of the drug are required.

Administration, Oral↗
PubMed1975

A controlled clinical trial of chlormezanone, orphenadrine, orphenadrine/paracetamol and placebo in the treatment of painful skeletal muscle spasms.

Four hundred patients with painful muscle spasm caused by five common musculoskeletal diseases were included in a double-blind controlled trial of chlormezanone, orphenadrine, orphenadrine/paracetomol and placebo. Patients were treated for one week and then asked for their subjective assessment of the treatment. Fifty-three per cent improved on placebo, 57 percent on chlormezanone, 66 percent on orphenadrine and 71 percent on orphenadrine/paracetamol. There was no significant difference between chlormezanone and placebo, but orphenadrine appeared to have a beneficial effect, presumably because of its muscle relaxant activity.

Acetaminophen↗
PubMed1985

[Acute poisoning by orphenadrine].

From January 1974 to June 1983, the Paris Poison Control Centre collected 84 cases of overdosage with orphenadrine alone or in combination. Prior papers emphasized fatalities related to orphenadrine poisoning. This retrospective study suggests an underestimated incidence of anticholinergic drugs abuse in our country. The clinical picture of orphenadrine poisoning associates drowsiness, agitation, confusion, delirium and seizures. Anticholinergic symptoms are often noted: mydriasis, sinus tachycardia, dryness of the mouth and urinary retention. No severe cardiac disturbance was found in these patients.

Accidents, Home↗
PubMed1987

Simple and rapid GLC method for the determination of orphenadrine in human plasma.

A rapid and specific method has been developed for the determination of orphenadrine concentration in plasma. It involves a one-step sample preparation using n-hexane/isopropyl alcohol (98:2) extraction, and analysis by gas chromatography on a wide bore capillary column using nitrogen/phosphorus detection. This procedure considerably simplifies previously reported assays and is specific and sensitive enough for the determination of orphenadrine in plasma of patients on chronic therapy.

Chromatography, Gas↗
PubMed1984

Relationship between molecular structure and cytochrome P450-metabolic intermediate complex formation, studied with orphenadrine analogues.

Complexation of ferrous cytochrome P450 by metabolic intermediates formed during NADPH-catalyzed metabolism of compounds structurally related to orphenadrine was studied. This so-called metabolic intermediate complexation was determined in rat liver microsomes, obtained from phenobarbital-pretreated rats, at 455 nm using 33 microM of the orphenadrine derivatives. Using secondary amine derivatives with various N-alkyl substituents, a parabolic relationship between the logarithm of percentage of cytochrome P450 complexation and hydrophobic fragmental constant was observed. The derivative with a bulky tertiary butyl group, however, was devoid of metabolic intermediate-complexing activity. This indicates that steric factors besides lipid solubility may govern the complexing activity; also substitution at the phenyl group affects metabolic intermediate complex formation.

Animals↗
PubMed1980

Cardiotoxicity from orphenadrine intoxication in humans.

Eight cases of Orphenadrine intoxication were treated in the Resuscitation Centre of Rome's University Medical School. All these cases arrived in coma, after taking an overdose of Orphenadrine in an attempt at suicide. The clinical signs and therapy are reported in detail; the cardiovascular side-effects, in particular those involving arrhythmias are dangerous and life threatening. From the clinical data it is believed that these changes in rhythm are mostly due to the autonomic nervous system (A.N.S.). In fact all the 8 patients survived, without treatment never having been treated with cardiokinetic or antiarrhythmic drugs, but a few were given Diazepam as well as respiratory assistance, cardiovascular assistance, and forced diuresis.

Adolescent↗
PubMed2002

Nefopam, an analogue of orphenadrine, protects against both NMDA receptor-dependent and independent veratridine-induced neurotoxicity.

Nefopam hyghochloride is a potent analgesic compound commercialized in most Western Europe for 20 years, which possesses a profile distinct from that of opioids or anti-inflammatory drugs. Previous evidence suggested a central action of nefopam but the detailed mechanisms remain unclear. While, nefopam structure resembles that of orphenadrine, an uncompetitive NMDA receptor antagonist, here we report that differently from orphenadrine, nefopam (100 microM) failed to protect cultured cerebellar neurons from excitotoxicity following direct exposure of neurons to glutamate. Moreover, nefopam failed to displace MK-801 binding to hippocampal membranes. Nefopam effectively prevented NMDA receptor-mediated early appearance (30 min) of toxicity signs induced by the voltage sensitive sodium channel (VSSC) activator veratridine. The later phase (24 h) of neurotoxicity by veratridine occurring independently from NMDA receptor activation, was also prevented by nefopam. Nefopam effect was not mimicked by the GABA receptor agonist muscimol.

Analgesics, Non-Narcotic↗
PubMed1990

Evidence for complexation of P-450 IIC6 by an orphenadrine metabolite.

Removal of the orphenadrine metabolite from its complex with rat liver P-450 IIB1 is associated with a discrepancy in the reactivation of IIB1 activity. Two possible explanations are that either (1) NADPH-P-450-reductase is inaccessible to the restored IIB1, or (2) complexation of other P-450s may occur. Exogenous P-450 reductase increased all pathways of steroid hydroxylation (1.9 to 3.6-fold) but did not enhance reactivation of IIB1-dependent steroid 16 beta-hydroxylation. Instead, P-450 IIC6-dependent progesterone 21-hydroxylase activity was increased after dissociation to 122% of control. IIC6 activity was also inhibited in vitro in microsomes from phenobarbital-induced rats (ki = 151 microM). Thus, orphenadrine appears to complex P-450 IIC6 as well as IIB1 in rat liver.

Androstenedione↗
PubMedDate not supplied

A report on the analysis of orphenadrine in post mortem specimens.

A discussion of the methods reported for the analysis of orphenadrine is given. The drug levels in biological specimens and the methods reported vary widely. The stability and extractability of orphenadrine is investigated and a method suggested, which uses subtilisin digestion of tissue followed by extraction with 1-chlorobutane. Body fluids are extracted directly by 1-chlorobutane after pH adjustment. Analysis is performed by gas chromatography with a nitrogen selective detector and no interferences are observed from bland specimens. The following levels are results from a case of a 19-year-old male who was found dead 2.5 hours after last being seen alive. This laboratory analysed the case using diphenhydramine as an internal standard: blood 18.1 micrograms/mL, liver 242 micrograms/g, urine 7.0 micrograms/mL, stomach contents 1452 mg.

Adult↗
PubMed1990

5-HT2 antagonist ritanserin in neuroleptic-induced parkinsonism: a double-blind comparison with orphenadrine and placebo.

Several studies support the hypothesis of 5-HT (serotonin) involvement in the physiopathology of the extrapyramidal system. Ritanserin is a new compound with a high, selective, and long-lasting binding affinity for 5-HT2 receptors. A therapeutic effect of ritanserin has been reported in Parkinson's tremor and L-Dopa-induced dyskinesias but no effect was seen in essential tremor. In this double-blind comparative study with orphenadrine (150 mg daily p.o.) and placebo, ritanserin (30 mg daily p.o.) was administered to 36 schizophrenic outpatients who were being treated with neuroleptic drugs and who had parkinsonism. For a period of 3 weeks, the treatment was added to the antipsychotic therapy after a 7-day washout from previous antiparkinson medication. Psychopathology was rated weekly by the Brief Psychiatric Rating Scale and showed no significant changes during the trial. The Mindham Rating Scale was used to assess symptoms of parkinsonism; at week 3, ritanserin was superior to orphenadrine (p less than 0.03) and to placebo (p less than 0.01). The results confirm previous observations of the therapeutic efficacy of ritanserin on neuroleptic-induced parkinsonism, and support the hypothesis that serotonin influences extrapyramidal physiopathology.

Adolescent↗
PubMed1977

Antiparkinsonian agents and long-term neuroleptic treatment. Effect of G 31.406, orphenadrine, and placebo on parkinsonism, schizophrenic symptoms, depression and anxiety.

The need for medication with anticholinergic antiparkinsonian drugs was examined in 118 schizophrenic patients under long-term neuroleptic treatment. It was found that 1) none of 18 patients under treatment with low mg potency neuroleptics (chlorprothixene, clozapine, and thioridazine) had any need for anticholinergics; 2) of 60 patients under treatment with short-acting high mg potency neuroleptics (perphenazine greater than 16 mg daily and haloperidol greater than 2 mg daily) nine patients (15%) required medication with anticholinergics, whereas 3) of 40 patients under treatment with long-acting (depot) neuroleptics, 17 (43%) had a need for anticholinergic medication; and 4) no patient factors predisposing to the need for continued antiparkinsonian treatment could be identified. In an additional double-blind cross-over study of 12 patients presenting persisting neuroleptic-induced parkinsonism, it was found that G 31.406 (a new potentially antiparkinsonian drug), compared with placebo, had an antiparkinsonian effect (P less than 0.01) as well as an antidepressant effect (P less than 0.05). G 31.406 resulted in an improvement in anxiety and schizophrenia-score in some patients. Compared with placebo, orphenadrine had a more questionable effect on parkinsonism (0.05 less than P less than 0.01) and no significant effect on mental symptoms. There were no significant differences between the effects of G 31.406 and orphenadrine.

Administration, Oral↗
PubMed1983

A double-blind comparison in general practice of a combination tablet containing orphenadrine citrate and paracetamol ('Norgesic') with paracetamol alone.

A double-blind trial of a combination tablet containing orphenadrine and paracetamol, 'Norgesic', was carried out to assess the value of this product compared with paracetamol alone. All three symptomatic parameters which were measured: pain, spasm and impaired activity, showed a significantly quicker recovery when the combination product was used. Further studies are necessary to evaluate the combination product against orphenadrine citrate alone.

Acetaminophen↗
PubMed1993

Effects of placebo, orphenadrine, and rising doses of chlorpromazine, on PAT performance in chronic schizophrenia. A two year longitudinal study.

An earlier study (Study 1: 14 months duration) showed that the PAT (an auditory attention task) is sensitive to changes of clinical state in chronic schizophrenia and is able to predict hospital discharge. The newly presented study (Study 2: 12 months duration) investigated the effects of increasing the dose of chlorpromazine (CPZ) stepwise (double-blind) to between 900 mg and 1800 mg per day, in 10 of the original 20 patients. Measurements were made fortnightly throughout both studies and the data were depicted continuously for each patient. Study 2 showed that a 300% increase of CPZ dose neither improved nor impaired PAT performance. Also, the addition of orphenadrine 300 mg per day had no significant effect on performance. Four types of relapse were detected. The first was induced by placebo substitution for CPZ and recovered when the drug was reinstated. The remaining types of relapse were all resistant to CPZ and comprised: a long-period pattern with a spontaneous reversal; unremitting deterioration; and a short-period pattern of labile relapse and recovery.

Adult↗
PubMed2002

Spectrophotometric determination of phenylephrine HCl and orphenadrine citrate in pure and in dosage forms.

A simple and rapid spectrophotometric methods have been estimated for the microdetermination of phenylephrine HCl (I) and orphenadrine citrate (II). The proposed methods are based on the formation of ion-pair complexes between the examined drugs with alizarine (Aliz), alizarine red S (ARS), alizarine yellow G (AYG) or quinalizarine (Qaliz), which can be measured at the optimum lambda(max). The optimization of the reaction conditions is investigated. Beer's law is obeyed in the concentration ranges 2-36 microgram ml(-1), whereas optimum concentration as adopted from Ringbom plots was 3.5-33 microgram ml(-1). The molar absorptivity, Sandell sensitivity, and detection limit are also calculated. The correlation coefficient was >/=0.9988 (n=6) with a relative standard deviation of </=1.7, for six determinations of 20 microgram ml(-1). The proposed methods are successfully applied to the determination of drugs I and II in their dosage forms using the standard addition technique.

Chemistry, Pharmaceutical↗
PubMed2003

Upregulation of cytochromes P450 2B in rat liver by orphenadrine.

1 The alkylamine drug orphenadrine (ORPH) is an inducer and inhibitor of the microsomal cytochrome P450 (CYP) system in mammals. This study evaluated the selectivity of CYP induction by ORPH in rat liver. 2 Immunoblot analysis indicated that ORPH was a selective inducer of the phenobarbitone (PB)-inducible CYP2B in rat liver. CYP2B protein was increased to approximately 14-fold of levels in untreated rat liver. By comparison PB increased CYP2B expression 40-fold. Corresponding increases in the activity of CYP2B-dependent androstenedione 16beta-hydroxylation were measured in microsomes from ORPH and PB-induced rats. 3 Northern analysis indicated that CYP2B1/2 mRNA was increased in ORPH-induced rat liver. Consistent with this finding, ORPH was found to activate a PB-responsive enhancer module in constitutive androstane receptor (CAR)-transfected Hep G2 cells. 4 Other alkylamines like troleandomycin impair CYP turnover. We tested whether ORPH induction of CYP2B may include a post-translational component. In PB-pretreated animals ORPH administration delayed the loss of CYP2B after PB withdrawal, but no evidence for altered turnover was found. 5 These studies establish ORPH as a selective inducer of CYP2B in rat liver. Induction appears to be mediated pretranslationally by CAR activation of CYP2B gene transcription. Post-translational stabilisation by an ORPH metabolite does not elicit induction. Induction of CYP2B may influence pharmacokinetic interactions involving ORPH.

Animals↗
PubMed1989

Residual neuroleptic-induced parkinsonian symptoms in schizophrenia. A naturalistic study with orphenadrine.

A naturalistic study was performed on 44 schizophrenic outpatients diagnosed according to DSM III-R and presenting neuroleptic-induced extrapyramidal side-effects. All patients had been treated continuously for the previous 10-12 weeks with haloperidol (HL) combined with orphenadrine (ORD). The dosages of HL and ORD remained unchanged for at least four weeks before the evaluations. All patients were assessed for depressive features (HRS-D), extrapyramidal (EPSE) and anticholinergic (ACS check list) side-effects. The plasma levels of ORD and its metabolite tofenacine (TOF) were determined by gas chromatography. There was a positive relationship between HRS-D and EPSE total scores, while there was a negative relationship between age and EPSE total scores. No relationship between the administered dose and plasma levels of ORD was found. The HL daily dose (mg/kg), ORD plasma levels and the TOF/ORD plasma level ratio seem to influence significantly the severity of residual extrapyramidal side-effects.

Adult↗