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At least 127 records · Page 7Linked to original sources
PubMed1975

A preliminary evaluation of pipothiazine palmitate in schizophrenia.

A preliminary evaluation of pipothiazine palmitate by injection was carried out in 25 schizophrenic patients to assess the therapeutic effectiveness of the drug, probable dosage schedules and intervals between doses, and to observ any undesirable side-effects. A good overall response was obtained in 64% of the patients. The authors suggest that the optimum maintenance dosage is between 50 and 100 mg. given at 4-weekly intervals. Although extra-pyramidal side-effects were high, only 1 patient had to be withdrawn on this account; the symptoms being well-controlled in mostly by procyclidine. Other adverse side-effects were negligible and there was no evidence of adverse biological effects. It is concluded that pipthiazine palmitate has considerable potential in the treatment of schizophrenia and a longer-term study is being conducted.

Adult↗
PubMedDate not supplied

Administration of PRN medication by mental health nurses.

The administration of PRN medication by mental health nurses is an important, yet poorly explored aspect of psychiatric inpatient care. An examination of nurses' reasons for administering PRN medication is essential in ensuring its appropriate and effective use. Data were gathered from the drug charts of 44 inpatients on two acute psychiatric wards. Most PRN medication was given orally and the most frequently administered drugs were procyclidine, lorazepam, ibuprofen, diazepam and droperidol. The main reason for administering PRN medication was because patients had 'requested' it. Results were broadly consistent with previous research. It is recommended that nurses should give clear and specific reasons for administering PRN medication based on a valid assessment. Implications for clinical practice and further research are also discussed.

Adult↗
PubMedDate not supplied

Anticholinergic drugs used in Parkinson's disease: An overlooked class of drugs from a pharmacokinetic perspective.

Anticholinergic drugs were the first pharmacological agents used in the treatment of Parkinson"s disease. Although levodopa and other centrally acting dopaminergic agonists have largely supplanted their use, they still have a place in treatment of the disease. As a therapeutic class, there is little pharmacokinetic information available for these drugs, which is inclusive of benztropine, biperiden, diphenhydramine, ethopropazine, orphenadrine, procyclidine and trihexyphenidyl. Pharmacokinetic information is largely restricted to studies involving young health volunteers given single doses. In general, this class of drugs is rapidly absorbed after oral administration to humans. Oral bioavailability is variable between the different drugs, ranging from 30% to over 70%. Each of the drugs appears to possess a large Vd in humans and animals, and distribution to tissues is rapid. The drugs are all characterized by relatively low clearance relative to hepatic blood flow, and appear to be extensively metabolized, primarily to N-dealkylated and hydroxylated metabolites. The available information suggests that excretion of parent drug and metabolite is via the urine and bile. Although the existence of a plasma concentration vs. therapeutic effect relationship has not been explored, there is some evidence suggesting a relationship between concentration and peripheral side effects. Elderly tolerate the drugs less well than do younger patients. There is a notable lack of pharmacokinetic information for these drugs in the elderly. The lack of pharmacokinetic information for multiple dose administration and in the elderly may be a possible hindrance in the safe and effective use of these drugs in patients with Parkinson"s disease.

Animals↗
PubMed1988

[3H]MK801 binding to the N-methyl-D-aspartate receptor reveals drug interactions with the zinc and magnesium binding sites.

We examined the ability of a range of tricyclic antidepressants (TCADs) and phenothiazine derivatives and their metabolites to inhibit the N-methyl-D-aspartate (NMDA) receptor complex using a [3H]MK801 binding assay. Desmethylation of the side chain of both TCADs and phenothiazines increased their potency against [3H]MK801 binding, as did removal of Cl substituted on the conjugated ring. Other side chain modifications further increased the potency of phenothiazines such as in the case of ethopropazine. Generally, the increase in potency of drugs at the NMDA receptor complex was associated with a decrease in the potency at other sites of action of these compounds. This finding suggests that it may be possible to separate the established actions of these compounds from their NMDA inhibitory effects. We also examined the mechanism of action of a number of compounds by monitoring drug effects on the dissociation rate of [3H]MK801 in the presence of Mg++. Phenothiazines and TCADs generally slow the dissociation of [3H]MK801, although to differing extents. Drugs such as 9-aminoacridine, cyproheptadine and ethopropazine also slowed the dissociation rate. These findings suggest a Zn++-like action of these compounds. In contrast, mecamylamine, methapyrilene and procyclidine had very little effect on the dissociation rate, suggesting a competitive action at the [3H]MK801/phencyclidine binding site. Chlorpromazine at low concentrations slowed the dissociation rate, while increasing it at higher concentrations. Thus, chlorpromazine demonstrated both Zn++ and Mg++-like effects. These studies demonstrate novel inhibitory actions of TCAD and phenothiazine derivatives at the NMDA receptor complex that are apparently mediated by the Zn++ binding site.

Animals↗
PubMed1980

[Modification of schizophrenia by intensive neuroleptic therapy and the course of the disease after withdrawal of neuroleptic drugs].

Since 1976 a group of 229 patients with schizophrenic or other paranoid illness (9 patients) were treated for about 14 weeks with intramuscular or intravenous injections of fluphenazinedecanoate. During the first 2 weeks, three injections of 250 mg were given after which time the injections were given at three weekly intervals with slowly decreasing dosage. The patients also received tablets of procyclidine and 100-150 mg of amitriptyline per os. After the initial intensive phase the patients received an average of 145 mg i.m. every 3 weeks. A total of 209 patients could be followed up. Of those, 127 had for various reasons not continued with oral medication. The course of their illnesses was compared with that of the patients who had complied. The present report which represents a 3-year follow-up study confirms the findings of an earlier paper which showed the rapid onset and stability of remission, the absence of relapses among the patients who were under continued treatment, and the relative freedom from relapses among the patients who did not continue to have further neuroleptic medication. The anticipation that the initial high-dosage medication would have deleterious effects on the personality, producing robots or zombies, was shown to be groundless.

Adolescent↗
PubMed1995

Classification of the presynaptic muscarinic receptor subtype that regulates 3H-acetylcholine secretion in the guinea pig urinary bladder in vitro.

The experiments were done to investigate the presence and subtype of functionally presynaptic muscarinic receptors in cholinergic nerves of the guinea pig urinary bladder. Bladder strips were incubated with 3H-choline and superfused with Tyrode's solution containing eserine. Secreted 3H-acetylcholine was separated from 3H-choline. The electrically evoked 3H-acetylcholine secretion increased with the stimulation frequency. 3H-Acetylcholine secretion was enhanced by muscarinic antagonists, was depressed by carbachol and by alpha adrenoceptor agonists but was not influenced by drugs acting at beta adrenoceptors or purinoceptors. The rank order for the enhancing effect of muscarinic antagonist EC50 values was propantheline < atropine < methylatropine < N-desethyloxybutynin < UH-AH 37 < benzhexol < AQ-RA 741 < 4-DAMP < procyclidine < emepronium < secoverine < oxybutynin < tropicamide < promethazine < himbacine < hexahydrosiladifenidol < methoctramine = pirenzepine < dicyclomine < AF-DX 116, and the EC50 values correlated best with constants for the M4/m4 muscarinic receptor subtype. The enhancing effect of atropine was counteracted by carbachol; the effects of atropine and emepronium were not additive. The 3H-acetylcholine secretion was also enhanced by forskolin, 3-isobutyl-1-methylxanthine, 8-bromo cyclic AMP and dibutyryl cyclic AMP. The combined effects of atropine and forskolin were additive. These results suggest that the 3H-acetylcholine secretion in the guinea pig urinary bladder is regulated by a presynaptic muscarinic autoreceptor of the M4 subtype that is not coupled to adenylate cyclase.

Acetylcholine↗
PubMedDate not supplied

Excitatory amino acid antagonists and the anticonvulsive activity of conventional antiepileptic drugs.

There is a great body of evidence, that excitatory amino acid antagonists, apart from their anticonvulsive properties per se, potentiate the protective activity of conventional antiepileptics against maximal electroshock-induced seizures in mice. It is worth stressing, that combinations of valproate with either CGP 37849 (a competitive NMDA antagonist) or dizocilpine (MK-801, a non-competitive NMDA antagonist), providing a 50% protection against maximal electroshock, resulted in no adverse effects, as measured in the chimney test (motor coordination) or passive avoidance task (long-term memory). On the other hand, valproate administered alone at its ED50, to protect against maximal electroshock, produced profound adverse effects. However, some NMDA antagonists (D-CPP-ene, memantine, procyclidine or trihexyphenidyl) did enhance the protection offered by common antiepileptics but these combined treatments were associated with considerable side-effects on motor coordination and long-term memory. Interestingly, ifenprodil (an antagonist of the polyamine site within the NMDA receptor complex) possessed some anticonvulsive activity against electroconvulsions but failed to enhance the antielectroshock efficacy of conventional antiepileptics. AMPA/KA receptor antagonists (NBQX and GYKI 52466), similarly to NMDA antagonists, potentiated the protective action of antiepileptic drugs against maximal electroshock and these combinations were generally devoid of unwanted effects.

Anticonvulsants↗
PubMed1977

Influence of the antiparkinsonian drugs on the plasma level of neuroleptics.

The interaction between various neuroleptics and antiparkinsonian drugs was analyzed by measuring the neuroleptic plasma level before and after withdrawal of antiparkinsonian drugs. The population completing the study consisted of 32 chronic schizophrenics treated with chlorpromazine (8), levomepromazine (14), thioridazine (6), or haloperidol (4). Twenty-five were also receiving benztropine; 4, trihexyphenidyl; and 3, procyclidine. During the first 4 weeks patients remained on neuroleptics and antiparkinsonians, the latter being withdrawn during the 5th week, and the neuroleptics alone being administered during 16 following weeks. The plasma level of neuroleptics was assayed by gas liquid chromatography, once weekly in the morning at two different times. The analysis of variance showed a significant difference in neuroleptic plasma level when patients took neuroleptics only versus the period they had received neuroleptics and antiparkinsonians. The multiple comparison based on Studentized range Q0-05 revealed a significant progressive increase of neuroleptic plasma level during 12 weeks after withdrawal of antiparkinsonian drugs after which a plateau was reached. The hypothetical mechanisms of action of antiparkinsonians on neuroleptic plasma level are discussed.

Adult↗
PubMed1998

[Fatalities caused by anticholinergic antiparkinsonian drugs. Analysis of findings in a 11-year national material].

All autopsy samples received at the National Institute of Forensic Toxicology during the years 1986-1996 which contained anticholinergic antiparkinsonian drugs were reviewed. Of a total of 69 cases, orphenadrine was present in 57 (83%), biperiden in 8 (12%), procyclidine in 3 (4%), and trihexyphenidyl/benzhexol in 1 (1%) of the subjects. The measured concentrations were assessed in light of previously published data. Of 21 cases where causality between drug ingestion and death was classified as either highly probable (18/21) or possible (3/21), all subjects tested positive for orphenadrine. In the autopsy samples from these patients, orphenadrine concentrations in the 4.5-600 mumol/l range (mean 62.5 mumol/l, SD 126.5 mumol/l) were determined. Because of a low national autopsy rate, there is reason to believe that the actual numbers of drug-related deaths in this period may have been significantly higher. It is concluded that orphenadrine is responsible for a disproportionally high number of overdose deaths.

Adolescent↗
PubMed1987

Muscle pathology in the neuroleptic malignant syndrome.

In a fatal case of neuroleptic malignant syndrome, a muscle sample taken within 1 h of death showed acute myopathic features with absence of muscle glycogen and neutral lipid. These features suggest that hyperpyrexia in this syndrome may be caused by heat production from uncoupled phosphorylation in muscle and imply that the primary biochemical abnormality responsible for this uncontrolled heat production might be muscular rather than hypothalamic.

Adult↗