Artane alters unusual nerve impulses and relaxes stiff muscles.
Other names for this medication:
Also known as: Trihexyphenidyl.
Artane is used to treat the stiffness, tremors, spasms, and poor muscle control of Parkinson's disease. It is also used to treat and prevent the same muscular conditions when they are caused by drugs such as chlorpromazine (Thorazine), fluphenazine (Prolixin), perphenazine (Trilafon), haloperidol (Haldol), thiothixene (Navane), and others.
name of Artane is Trihexyphenidyl.
Artane is also known as Trihexyphenidyl, Triphen.
Brand name of Artane is Artane.
Take Artane by mouth before or after meals.
If Artane tends to dry your mouth excessively, it may be better to take it before meals, unless it causes nausea. If taken after meals, thirst can be improved by sucking hard sugarless candy, chewing gum, or drinking water.
If you want to achieve most effective results do not stop taking Artane suddenly.
If you overdose Artane and you don't feel good you should visit your doctor or health care provider immediately.
Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of reach of children.
The most common side effects associated with Artane are:
Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.
Do not take Artane if you are allergic to Artane components.
Be very careful with Artane if you are pregnant, planning to become pregnant or breast-feeding.
Artane may cause dizziness, lightheadedness, or fainting. Alcohol, hot weather, exercise, or fever may increase these effects. To prevent them, sit up or stand slowly, especially in the morning. Sit or lie down at the first sign of any of these effects.
Do not become overheated in hot weather or while you are being active. Heatstroke may occur.
Lab tests, including eye exams, may be performed while you use Artane. These tests may be used to monitor your condition or check for side effects. Be sure to keep all doctor and lab appointments.
Avoid driving machine.
It can be dangerous to stop Artane taking suddenly.
artane medication classification
Pantothenate kinase-associated neurodegeneration (PKAN) is a form of neurodegeneration with brain iron accumulation, or NBIA (formerly called Hallervorden-Spatz syndrome). PKAN is characterized by progressive dystonia and basal ganglia iron deposition with onset that usually occurs before age ten years. Commonly associated features include dysarthria, rigidity, and pigmentary retinopathy. Approximately 25% of affected individuals have an 'atypical' presentation with later onset (age >10 years), prominent speech defects, psychiatric disturbances, and more gradual progression of disease.
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The discriminative stimulus properties of scopolamine, a potent antagonist at muscarinic receptors, were used for testing the discriminative effects of drugs known to act on cholinergic transmission. Rats were trained in a standard two-bar operant conditioning procedure with food as the reinforcer, according to a FR10 schedule. The training dose of scopolamine was progressively reduced from 0.25 mg/kg SC to the low dose of 0.062 mg/kg SC. Scopolamine yielded an accurate discrimination in all the six rats tested. The generalization gradient resulted in an ED50 of 0.027 mg/kg. The scopolamine cue lasted for 1 h and was of central origin, since it was not mimicked by scopolamine methylbromide. The scopolamine stimulus generalized to atropine and trihexyphenidyl (respective ED50 values 2.20 and 0.21 mg/kg SC). Atropine depressed rate of responding, while trihexyphenidyl did not. Antagonism experiments with both direct agonists at the muscarinic receptor (arecoline and oxotremorine) and indirect agonists, i.e., inhibitors of the acetylcholine esterase [physostigmine and tetrahydroaminoacridine (THA)], led to inconsistent results. Increasing the doses of the agonists in order to block the scopolamine cue may be limited by their rate suppressant effect on responding. Based upon previously published results, it is suggested that the muscarinic agonist cue is more useful than the antagonist cue for investigating muscarinic transmission.
1. [3H]quinuclidinyl benzilate ([3H]QNB) binding in rat cerebral and cerebellar synaptosomes had different Bmax values, but similar Kd values. 2. These bindings could be displaced by classic muscarinic agents: pilocarpine (partial agonist), and atropine (antagonist), which both had similar binding affinities in rat cerebral and cerebellar synaptosomes. 3. The new muscarinic M1 selective agents: McN-A-343 (agonist), pirenzepine and trihexyphenidyl (antagonists) and higher affinities for receptor sites in the cerebrum than in the cerebellum. 4. The muscarinic M2 selective agents: carbachol, oxotremorine (agonists), and AF-DX-116 (antagonist) had higher affinities for receptor sites in the cerebellum than in the cerebrum. 5. GPP(NH)p (40 microM) decreased the binding affinities of carbachol and oxotremorine in the cerebellum, but not in the cerebrum. However, it did not decrease the binding affinities of all the antagonists studied in both brain regions. 6. These results reveal that more muscarinic M1 sites are present in the cerebrum than in the cerebellum, while the opposite is true for M2 sites. Furthermore, the regulatory role of G-protein on these muscarinic receptor subtypes in the brain is different.
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1. Benzhexol and three of its metabolites excreted in urine in man have been investigated by g.l.c.--mass spectrometry. 2. Three isomeric hydroxylated metabolites were identified as the 1-(hydroxycyclohexyl)-1-phenyl-3-piperidinopropan-1-ols. 3. The amounts of benzhexol and its identified metabolites have been semiquantitatively determined after a single oral dose in two healthy adults. Approx. 56% of the dose was excreted as the hydroxylated metabolites. The levels of benzhexol excreted were too low to be measured by the techniques used.
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We describe a 46-year-old woman who presented with lingual dystonia induced only by speaking, which responded well to anticholinergic treatment.
92 PD outpatients were enrolled in, including 48 males and 44 females, from 43 to 86 years old (mean 65.6 +/- 17.1) with duration of the disease from 0.2 to 27.8 years (mean 4.4 +/- 9.4). The preference of the drug use from the patients were: 40 (43.5%) preferred taking levodopa, 25 (27.2%) with amantadine and/or trihexyphenidyl, 14 (15.2%) with levodopa and others, 4 (4.4%) with dopamine agonist and others, 2 (2.2%) with other drugs, 7 (7.6%) with no treatment. There were 69 (75.0%) patients onset with resting tremor, 15 (16.3%) with bradykinesia, 6 (6.5%) with rigidity, and 2 (2.2%) with unknown symptoms. There was no startically significant difference in anti-PD drugs among the patients onset with different symptoms (P > 0.05). 45 patients appeared the onset of disease before 65 years old and with no dementia, 47 onset after 65 with or without dementia. There was no significant difference of anti-PD drugs between the two groups (P > 0.05). Most patients initiated anti-PD treatment with levodopa but few of them chose dopamine agonist. According to the classification of Hoehn & Yahr, 25(27.2%)belonged to Grade I, 53 (57.6%) to Grade II, 8 (8.7%) to Grade III, 3 (3.3%) to Grade IV and 3 (3.3%) to Grade V. There was no significant differences of anti-PD drugs between different grades of the disease (P > 0.05). 55.3% of the patients changed their anti-PD drugs randomly during the therapy, but with no relation to their gender, age, educational level, dementia, the number of family members, course of diseases, or the degree of Hoehn & Yahr, frequency and categories of medicine.
The goal of medical therapy for primary dystonia is conservative. While botulinum toxin (BTX) therapy is a first choice for blepharospasm and cervical dystonia, medical therapy is selected as such for other types of dystonia. As oral medications, trihexyphenidyl and benzodiazepines are most frequently used. Muscle relaxants are also commonly used, but dopamine antagonists are not recommended because of the risk of inducing tardive dyskinesia. For childhood-onset generalized dystonia, levodopa should be considered to rule out levodopa-responsive dystonia. Mexiletine is reported to be effective not only for bleharospasm and cervical dystonia but for focal limb dystonia. To improve the therapeutic performance of BTX therapy for blepharospasm, it is recommended that corrugator supercilii and procerus muscles, as well as orbicularis oculi muscle, be added as target muscles. To improve the therapeutic performance of BTX therapy for cervical dystonia, it is recommended that this therapy be started as early as possible, especially within one year of illness, and that levator scapulae muscle be added as target if necessary. To improve usefulness of medical therapy for dystonia, its strategy must be standardized, and more useful therapies must be positively adopted. Algorithm for treatment of dystonia must also be established and generalized.
artane pediatric dosing
To determine the most adequate strategies for the prevention and treatment of the acute adverse effects of the use of antipsychotics.
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The effects of the "atypical" antipsychotic olanzapine and several other antipsychotics were examined using a conflict schedule. Rats were trained to respond for food on a three-component schedule, comprising variable-interval 30s (food, VI30) and fixed-ratio 10s (food + shock, FR10) components separated by time-out (TO). Olanzapine (0.3125-1.25mg/kg), clozapine (1.25-5mg/kg) and chlordiazepoxide (2.5-5mg/kg) decreased or had no effect on VI30 responding, whereas responding in the FR10 component increased. Chlordiazepoxide (5mg/kg) also increased TO responding. The antipsychotic agents haloperidol (0.125 and 0.25mg/kg), trifluoperazine (0.0625-0.25mg/kg), remoxipride (1.25-5mg/kg) and risperidone (0.0625-0.5mg/kg) decreased V130 responding and either had no effect, or decreased TO and FR10 rates. The anticholinergic agent scopolamine (0.03125-0.25mg/kg) decreased VI30 responding. The 5-HT(2) antagonist ritanserin (2.5 and 5mg/kg) and the anticholinergic agent trihexyphenidyl (2.5 and 5mg/kg) had no effect on responding. Flumezanil (10mg/kg) reduced the anticonflict effect of chlordiazepoxide but not olanzapine. These results further emphasize the unusual profile of olanzapine.
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The biochemical linking event between the activation of muscarinic receptors and the inhibition of adenylate cyclase was studied with rat heart ventrical membranes. The muscarinic M2 selective antagonists were more potent than the M1 selective antagonists in the displacement of non-selective labeled 3H-QNB binding to the membranes. This was also true for the M2 selective agonists, with respect to the M1 selective agonists, in the reaction medium without Gpp(NH)p. With the same preparation, the muscarinic M2 selective agents were also more potent than the M1 selective agents in the inhibition of adenylate cyclase activity. The order of potencies of these agents in the displacement of 3H-QNB binding correlated well with their order of potencies in inhibiting adenylate cyclase activity. Gpp(NH)p reduced the binding affinities of M2 selective agonists (i.e. carbachol and oxotremorine), while it did not affect the binding affinities of non-selective agonist pilocarpine, M1 selective agonist McN-A-343 and antagonists (i.e. pirenzepine, trihexyphenidyl, AF-DX-116 and methoctramine). These results suggest that in the rat heart, the inhibition of adenylate cyclase by muscarinic agonists is through activation of the M2 subtype receptor and G-protein is likely to be involved in the coupling.
artane drug information
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.
The behavioral effects of a variety of advanced candidate anticonvulsants for organophosphate-induced seizures were evaluated under two rodent 'counting' models. Rats pressed the left of two levers a number of times (a 'run') before pressing the right lever. The targeted performance was a run of 12. The training contingency was a targeted percentile schedule, which provided food if the current run was closer to 12 than two-thirds of the most recent runs. Baseline performance was well controlled by the target, with mean run lengths slightly less than 12. Once this performance was acquired, half the subjects were switched to a procedure providing food following runs of different lengths with a probability yoked to previous percentile schedule performance. The two procedures generate comparable baseline performances, but behavioral disruptions generate reinforcement loss only under the yoked procedure. Atropine, scopolamine, azaprophen, aprophen, trihexyphenidyl, procyclidine, benactyzine, biperiden and diazepam were tested. All produced dose-related decreases in overall run length and response rate. Responding was disrupted more readily under the yoked procedure than under the percentile procedure. Only atropine affected responding at doses below those effective against soman-induced seizures. Of the present candidates, trihexyphenidyl, procyclidine, benactyzine and biperiden appear most promising for further development.
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The absolute configuration of the more active (-)-enantiomer of the anticholinergic trihexyphenidyl hydrochloride has been established as (R) by syntheses of (S)-(+)-procyclidine hydrochloride, whose absolute configuration has been established previously, and (S)-(+)-trihexyphenidyl hydrochloride from the same chiral building block, viz. (S)-(-)-cyclohexyl-3-hydroxy-3-phenylpropanoic acid. Both enantiomers of this chiral synthon were prepared by optical resolution of the corresponding racemate, employing (R)- and (S)-1-phenylethylamine, respectively, as resolving agents.
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In France, the observation and evaluation of drug abuse and dependence associated with pychoactive medications are the responsibility of the National Commission for Narcotics and Psychotropic Drugs. In order to assist this commission, several centres for evaluation and information on pharmacodependence (CEIP) were created throughout in France. Recently, in order to complete their epidemiological tools, several centres have developed another pharmacoepidemiological approach using data for refunded prescriptions obtained from the local and regional French Health Insurance database. This article underlines the potential contribution of the Health Insurance database to improving knowledge of drug use in the real-life conditions based on studies performed by the CEIP. Several examples are given showing the extent of the possibilities (population-based studies, cohort studies, development of misuse indicators). In spite of their limitations (e.g. the difference between consumption and delivery), these examples confirm that these database may be a novel tool for CEIP to assess a potential abuse of a medication.
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The limitations of antiparkinsonian treatment strategy when using anticholinergic drugs are determined by their side effects induced through excessive inhibition of parasympathetic functions. In the present study we have investigated the peripheral effects of antiparkinsonian agents on blood levels of concomitantly administered neuroleptic drugs. We have compared the anticholinergic and a dopamine mimetic antiparkinsonian agent in their effects on serum neuroleptic activity (SNA) and serum anticholinergic activity (SAA). Sixteen schizophrenic patients on chronic neuroleptic therapy with steady state neuroleptic levels were receiving either amantadine, 200 mg/day, or anticholinergic drugs (trihexyphenidyl, 10 mg/day, or benztropine, 6 mg/day) for the first 2 weeks, after which the amantadine group was crossed over to anticholinergic and the anticholinergic group to amantadine for the following 2 weeks. Blood samples were obtained once a week along with clinical testing. The results indicate that SAA was fivefold higher with benztropine than with trihexyphenidyl and that amantadine had no effect on SAA. Moreover, SNA was not altered either by anticholinergics or amantadine coadministration, indicating that the therapeutic blood neuroleptic levels are not compromised by antiparkinsonian administration.
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A group of 22 patients selected as a result of follow-up examinations of 104 patients with juvenile psychopathlike heboid schizophrenia is described. A specific feature of the disease course in the patients observed consisted in appearance of atypical protracted psychoses after a long-time period of psychopathlike heboid disorders. Peculiarities differentiating this form from the slow-progressive variant of psychopathlike heboid schizophrenia and from paroxysmal schizophrenia with heboid initial stage are presented. The group described occupies an intermediate place between these forms of schizophrenia. A question on the role of aggravation of the disease course with various exogenous adverse factors (noted in all the cases described) is discussed.
This preliminary study done by abstracting relevant data from different testing material and using multiple rating scales, describes the sociodemographic variables, psychopathological correlates, and features of trihexyphenidyl (artane) abuse in a sample of 14 Saudi psychiatric patients and, as a result of this research, various relevant issues have been discussed.
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The selectivity profiles of the muscarinic receptor antagonists dicyclomine and trihexyphenidyl have been examined in binding and functional studies and compared with those of pirenzepine and atropine. Dicyclomine, trihexyphenidyl and pirenzepine demonstrated the highest affinity for the M1 muscarinic receptor subtype as revealed in competition experiments against [3H]-pirenzepine labelling of cortical membranes. Their affinity values lay in a narrow range (3.7-14 nM) approaching that of atropine (1.6 nM). Competition experiments against [3H]-N-methylscopolamine in cardiac and glandular (salivary) membranes revealed differences between the drugs examined. Dicyclomine, trihexyphenidyl and pirenzepine displayed low affinity for the cardiac and intermediate affinity for the glandular receptors. Thus, the drugs appeared to discriminate between the M1 (cortical) and the peripheral muscarinic subtypes (cardiac and glandular). However, atropine displayed similar affinities for either subtype with IC50s varying only slightly (1.6-4.6 nM). The rank order of selectivity was: pirenzepine greater than dicyclomine greater than trihexyphenidyl greater than atropine. Mirroring the binding data, pirenzepine, dicyclomine and trihexyphenidyl showed a tenfold greater ability at inhibiting M1-receptor mediated ganglionic responses (McN A-343 pressor effect in pithed rats and nictitating membrane contraction in cats) than at inhibiting peripheral muscarinic responses in the heart and cardiovascular smooth muscle (vagal bradycardia in rats and cats and vagally-induced vasodilatation in cats). The muscarinic antagonists so far examined can be categorized into two groups. Trihexyphenidyl, dicyclomine and pirenzepine, included in one group, are characterized by a higher affinity for the neuronal (M1) muscarinic receptor, hence they antagonize functional responses mediated by the M1 subtype. Atropine, a member of the other group, shows essentially no selectivity. 6 Differentiation of M1 and peripheral muscarinic receptor subtypes appears to be a property not confined to tricyclics such as pirenzepine but shared by diverse chemical structures. Both trihexyphenidyl and dicyclomine appear to be useful pharmacological tools in the classification of muscarinic receptor subtypes.
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Dopa-responsive dystonias are rare. We report a 14-year-old male who was diagnosed as a case of limb girdle dystrophy and had features suggestive of dopa-responsive dystonia.
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The effect of three different M1 muscarinic antagonists, pirenzepine, biperiden, and trihexyphenidyl on memory consolidation was investigated. Rats were trained in a one-trial step-through inhibitory avoidance task and injected intraperitoneally immediately afterwards, either with pirenzepine, biperiden, or trihexyphenidyl (dose range from 0 to 16 mg/kg). The non-selective antimuscarinic compound scopolamine, was also administered for comparison. One day later, rats were tested for retention. Results show that biperiden, trihexyphenidyl and scopolamine produced a dose-dependent impairment of inhibitory avoidance consolidation, while pirenzepine had no effect. The amnestic state produced by biperiden and trihexyphenidyl was comparable to that observed after the administration of scopolamine. These results indicate that the selective blockade of the central M1 muscarinic receptors interfere with memory consolidation of inhibitory avoidance and suggest that this receptor subtype is critically involved in mnemonic functions.
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The combination of haloperidol and trihexyphenidyl is a dosage form to be used as antidyskinetic agent. Literature revealed that there is no single method for the simultaneous estimation of these drugs in tablet dosage form, which prompted us to develop a simple, rapid, accurate, economical and sensitive spectrophotometric method. The simultaneous estimation method is based on the principle of additivity of absorbance, for the determination of haloperidol and trihexyphenidyl in tablet formulation. The absorption maxima of the drugs were found to be at 245.0 nm and 206.0 nm respectively for haloperidol and trihexyphenidyl in methanol and 0.1N HCl (90:10). The obeyance of Beer Lambert's law was observed in the concentration range of 2.5-12.5 µg/ml for haloperidol and 1.0-5.0 µg/ml for trihexyphenidyl. The accuracy and reproducibility of the proposed method was statistically validated by recovery studies.
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Physical examination had a low predictive value in the detection of involved muscles. There was a significant correlation between changes in EMG total scores and changes in clinical measurements. We observed increased EMG activity in 20% of noninjected muscles after BTA treatment and in 27% of noninjected muscles after trihexyphenidyl treatment. A switch from one most active muscle to another was seen equally in both groups and had no influence on clinical response.
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We conducted a prospective study of 20 consecutive patients treated with the anti-cholinergic agent trihexyphenidyl after bilateral STN-DBS and assessed the effect of anti-cholinergic therapy on parkinsonism 1 month after its initiation using the Unified Parkinson's Disease Rating Scale (UPDRS).
artane medication dystonia
Fragile X syndrome (FXS) is a leading cause of intellectual disability. FXS is caused by loss of function of the FMR1 gene, and mice in which Fmr1 has been inactivated have been used extensively as a preclinical model for FXS. We investigated the behavioral pharmacology of drugs acting through dopaminergic, glutamatergic, and cholinergic systems in fragile X (Fmr1 (-/Y)) mice with intracranial self-stimulation (ICSS) and locomotor activity measurements. We also measured brain expression of tyrosine hydroxylase (TH), the rate-limiting enzyme in dopamine biosynthesis. Fmr1 (-/Y) mice were more sensitive than wild type mice to the rewarding effects of cocaine, but less sensitive to its locomotor stimulating effects. Anhedonic but not motor depressant effects of the atypical neuroleptic, aripiprazole, were reduced in Fmr1 (-/Y) mice. The mGluR5-selective antagonist, 6-methyl-2-(phenylethynyl)pyridine (MPEP), was more rewarding and the preferential M1 antagonist, trihexyphenidyl, was less rewarding in Fmr1 (-/Y) than wild type mice. Motor stimulation by MPEP was unchanged, but stimulation by trihexyphenidyl was markedly increased, in Fmr1 (-/Y) mice. Numbers of midbrain TH+ neurons in the ventral tegmental area were unchanged, but were lower in the substantia nigra of Fmr1 (-/Y) mice, although no changes in TH levels were found in their forebrain targets. The data are discussed in the context of known changes in the synaptic physiology and pharmacology of limbic motor systems in the Fmr1 (-/Y) mouse model. Preclinical findings suggest that drugs acting through multiple neurotransmitter systems may be necessary to fully address abnormal behaviors in individuals with FXS.
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1. The influence of two anticholinergic drugs (atropine, trihexyphenidyle) on the effectiveness of antidotal treatment to eliminate soman-induced lethal effects and convulsions was studied in rats. 2. The oxime HI-6 when combined with centrally acting anticholinergic drug trihexyphenidyle seems to be more efficacious in the elimination of acute toxic effects of soman than its combination with atropine. 3. The findings support the hypothesis that the choice of the anticholinergic drug is important for the effectiveness of antidotal mixture in the case of antidotal treatment of soman-induced acute poisoning.
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The interactions of various unlabelled antimuscarinic drugs with the muscarinic receptors in the cerebral cortex, heart and urinary bladder were studied by a receptor binding technique, using (-)[3H]QNB as radioligand. In contrast to the other drugs examined, dicyclomine, benzhexol, oxybutynine and pirenzepine were bound with a significantly higher affinity in the cortex than in the heart and bladder. Furthermore, not only pirenzepine, but also dicyclomine and benzhexol were capable of distinguishing between two populations of muscarinic binding sites in the cortex. The low affinity sites for these drugs in the cortex were characterised by dissociation constants which were similar to those determined in the heart and the bladder, respectively. It was concluded that dicyclomine and benzhexol, like pirenzepine, are selective antagonists at the putative M1-receptor. Oxybutynine exhibited the same affinity profile but the tissue selectivity of this drug was less pronounced.
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We inspected the results of the search to identify relevant studies. We were to extract data onto standard, simple forms. Disagreements were resolved through discussion. The risk of bias was to be assessed using the Cochrane risk assessment tool. For binary outcomes, we were to calculate a standard estimation of the risk ratio (RR) and its 95% confidence interval (CI). For continuous outcomes, we were to estimate the mean difference between groups.
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A patient with Meige syndrome associated with spasmodic torticollis was treated with benztropine mesylate (Cogentin) at doses of 12-16 mg daily. Marked suppression of both oromandibular dystonia and the torticollis was obtained. Mild impairment of recent memory was the major side effect. Peripheral anticholinergic side effects were controlled by the concomitant administration of ambenonium chloride (Mytelase) 15 mg daily.
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There are few reports in the literature and scarce research on the topic and the treatment of antipsychotic medication-induced urinary incontinence or nocturnal enuresis (NE) despite the significant frequency of these adverse effects.Treatment for antipsychotic medication-induced urinary incontinence has been reported in relation to clozapine with response to numerous pharmacological strategies such as ephedrine, oxybutynin, intranasal desmopressin, trihexyphenidyl, and amitriptyline.We report a case of NE induced by risperidone which has been successfully treated with reboxetine.To the best of our knowledge, this article is the first report of an atypical antipsychotic medication-induced NE treated with reboxetine.Reboxetine may be an effective treatment for risperidone-induced NE. Further research is required to confirm our finding and apply this treatment for NE caused by other neuroleptics.
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The subcellular distribution of biperiden (BP), trihexyphenidyl (TP) and (-)-quinuclidinyl benzylate (QNB) in brain, heart and lung following high dose (3.2 mg/kg) i.v. administration was investigated in rats. The subcellular distribution of BP or TP used clinically conformed with that of QNB, a typical potent central muscarinic antagonist. The concentration-time courses of the brain subcellular fractions for these drugs were of two types which decreased slowly and in parallel to the plasma concentration. The subcellular distribution in the brain and heart was dependent on the protein amount of each fraction. The percent post-nuclear fraction (P2) of the total concentration in the lung was characteristically about 3-5 times larger than that in the heart. It was elucidated that the distribution in the lung differs from that in the brain and heart, with high affinity which is not dependent on the protein amount in the P2 fraction containing lysosomes. On the other hand, at a low dose (650 ng/kg) of 3H-QNB, each fraction as a percentage of the total concentration in the brain increased in synaptic membrane and synaptic vesicles and decreased in nuclei and cytosol as compared with the high dose. These results show that although the tissue concentration-time courses of anticholinergic drugs appear to decrease simply in parallel to plasma concentration, the subcellular distribution exhibits a variety of patterns among various tissues.
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