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.
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To clarify the factors determining the amelioration of Meige's syndrome, changes of involuntary movements (IVMs) and functional disability, we examined 60 patients with Meige's syndrome during 5 years after the onset. On average, they showed gradual worsening of IVMs for approximately 2.1 years, then the IVMs ameliorated slowly. In many patients, blepharospasm appeared as the first symptom. Subsequent IVMs were seen in vicinity of the muscles of orbicularis oculi. Phasic involuntary contractions changed to tonic ones in some patients. Asynchrony of the IVMs in various facial or neck muscles may be originated from extensive pathological changes and high excitability in the brainstem. The factors determining the amelioration of functional disability are: (1) younger onset, (2) shorter duration from the onset to the period showing the worst symptoms, (3) mild IVMs when the symptoms were the worst, (4) shorter duration from the onset to the beginning of therapy, (5) synchrony of the IVMs between the muscles of orbicularis oculi and other muscles. Methylphenidate, trihexyphenidyl, and ceruletide showed a higher efficiency for IVMs than the other drugs. The drug therapy in Meige's syndrome should be started as early as possible.
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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.
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Treatment of manifestations: Intramuscular botulinum toxin, intrathecal or oral baclofen, ablative pallidotomy or thalmotomy, oral trihexyphenidyl, deep brain stimulation for dystonia; services for the blind, educational programs; physical therapy and occupational therapy to maintain normal joint mobility; adaptive aids (walker, wheelchair) for gait abnormalities; speech therapy and/or assistive communication devices. Prevention of secondary complications: Full-mouth dental extraction when severe orobuccolingual dystonia results in recurrent tongue-biting; adequate nutrition through swallowing evaluation, dietary assessment, gastrostomy tube feeding as needed. Surveillance: Evaluation for treatable causes of pain during episodes of extreme distress; monitoring of height and weight; routine ophthalmologic assessment; regular assessments of ambulation and speech abilities.
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In a developing country like Nigeria where prohibitive cost and availability limits the use of atypical antipsychotics, a large number of patients on antipsychotics are expected to be on conventional antipsychotics. Studies have shown that more than half of patients on conventional antipsychotics are also prescribed anti-cholinergic drugs. There are reports that psychiatric patients may not know important aspects of their treatments. Such audits of psychiatric services are uncommon in Nigeria.
In this double-blind, randomized study, indices of central (memory, sedation) and peripheral (salivation, ratio of R-R interval on electrocardiogram) muscarinic function were evaluated in 14 healthy volunteers who received trihexyphenidyl, biperiden, and placebo. Additionally, serum drug levels were obtained 2 hours after oral administration. All subjects participated in three study sessions. During each session, subjects received two doses of biperiden (4 mg), trihexyphenidyl (5 mg), or placebo, and four series of tests were administered. The tests included the determination of cardiac response to standing (R-R ratio), mouth salivation, finger-tapping speed, digit span (forward and backward), a selective reminding task, and visual analog scales (VAS). On the VAS, subjects rated biperiden as significantly more sedating than either trihexyphenidyl or placebo, and both biperiden and trihexyphenidyl were associated with more dizziness than was placebo. Saliva production was significantly reduced by both trihexyphenidyl and biperiden compared with placebo. Digit span performance was significantly decreased in only the backward direction. The selective reminding task revealed highly significant decrements in the number of words recalled and consistent long-term retrieval after both biperiden and trihexyphenidyl. Delayed recall was significantly decreased by both active drugs. Both trihexyphenidyl and biperiden caused a significant increase in the R-R ratio comparison with placebo. With the exception of the VAS measurement of sedation, the effects caused by biperiden and trihexyphenidyl did not differ. The results of this study do not support the hypothesis that the side effect profile of biperiden is significantly different from that of trihexyphenidyl.
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We identified two phenotypes, generalised dystonia and dystonia-parkinsonism non-responsive to levo-dopa, with three patients belonging to each of the groups. There was inter-individual and intra-family phenotypic heterogeneity.
1. The effects of a potential anti-Parkinson drug, benapryzine, have been compared with those of benzhexol, atropine and procaine on the excitatory responses induced by acetylcholine and L-glutamate on feline cortical neurones using the microiontophoretic technique.2. All the drugs tested reduced the excitatory responses evoked by acetylcholine and L-glutamate. However, benapryzine, benzhexol and procaine more effectively reduced the excitatory responses to L-glutamate than those to acetylcholine whereas atropine was more effective against acetylcholine-induced excitation.3. In the presence of procaine the amplitude of the extracellular spikes was decreased. This effect was also observed during applications of benapryzine and benzhexol.4. Tests on the isolated frog sciatic nerve indicated that benapryzine and benzhexol had local anaesthetic actions respectively greater than and equivalent to those of procaine.5. It was concluded that the effects of benapryzine and benzhexol on cortical neurones were probably related to their local anaesthetic properties. The possibility that a local anaesthetic action may account for the effects of these drugs and of many other commonly used anti-Parkinson drugs in Parkinson's disease is discussed.
These findings suggest that NDMC produces discriminative stimulus effects that are different from those elicited by its parent drug CLZ. This difference may be due to the agonist properties of NDMC at M(1) muscarinic cholinergic receptors.
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Medications with anticholinergic properties, when taken at therapeutic doses, are known to adversely affect memory functioning in young adults and the elderly. However, their impact at lower doses in geriatric persons has been less thoroughly studied. We investigated the impact of a single 2-mg dose of trihexyphenidyl on memory functioning in 20 healthy elderly subjects using a within-subjects, double-blind comparison with a placebo. Memory functioning was evaluated using subtests of the Wechsler Memory Scale. Subjects also rated the perceived impact of medication on their performance following memory testing. Results indicated that the single 2-mg dose of trihexyphenidyl produced impaired performance on measures of immediate and half-hour delayed recall of complex verbal and visual material when compared to the placebo condition. However, differences were not found on several other memory measures, including general orientation, attention-concentration, and learning of word associations. The significance of these selective memory deficits and suggestions regarding future research are discussed.
Antiparkinson agents possess excellent anticonvulsant properties against nerve agent-induced seizures by exerting both cholinergic and glutamatergic antagonisms. It is important, however, that drugs used as prophylactics not by themselves cause impairment of cognitive capability. The purpose of the present study was to make a comparative assessment of potential cognitive effects of benactyzine (0.3 mg/kg), biperiden (0.11 mg/kg), caramiphen (10 mg/kg), procyclidine (3 mg/kg), and trihexyphenidyl (0.12 mg/kg) separately and each in combination with physostigmine (0.1 mg/kg). The results showed that benactyzine, caramiphen, and trihexyphenidyl reduced rats' innate preference for novelty, whereas biperiden and procyclidine did not. When benactyzine, caramiphen, and trihexyphenidyl were combined with physostigmine the cognitive impairment disappeared. This counteracting effect, however, caused changes in locomotor and rearing activities not seen by each drug alone. Acetylcholinesterase inhibitors and anticholinergics used as prophylactics can offset each other, but exceptions are observed in a previous study when a very potent anticholinergic (scopolamine) or a high dose of procyclidine still results in cognitive deficits in spite of coadministration with physostigmine. Among the present drugs tested, procyclidine appears to be a robust anticonvulsant with few cognitive side effects.
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Cerebral palsy is the main cause of immobility in children. This motor dysfunction is caused by several motor components such as weakness, lack of motor control and muscle hypertonia. Drug treatment, delineated in this review, mainly addresses the latter. Recently, new definitions for clinical features of hypertonia in children were published, assisting the distinction between the two common motor symptoms in cerebral palsy, spasticity and dystonia. The main functional symptoms disrupt functional daily life, dictating the overall approach and the specific drug treatment. There are an increasing number of treatments for this distressing disorder. For general spasticity, treatments provided include Baclofen. If symptoms are local, either dystonia, or spasticity, Botulinum toxin is the revolutionary drug used with significant success and relatively few side effects. For generalized dystonia, a trial of both Dopamine and Trihexyphenidyl should be considered. Cerebral palsy, like other complex disorders, requires individualized decision-making and a team approach. Drug therapy is only one aspect of treatment, yet sometimes it may serve as a window of opportunity to facilitate better motor control.
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After resumption of ECT, there was marked improvement in psychopathology across the ECT course. There was no recurrence of visual symptoms.
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Experiments on cats showed that lesions affecting retrieval of an operant food-procuring reflex. occurring on a background of systemic administration of the centrally-acting muscarinic cholinoceptor blocker scopolamine (a non-selective M-cholinoceptor blocker) and trihexyphenidyl (a relatively selective M1-cholinoceptor blocker), might be associated with the central and peripheral side effects of these blockers, preventing performance of the conditioned reflex. It was established that when no side effects were present (low doses of trihexyphenidyl, 1 mg/kg), blockade of M1-cholinoceptors led to selective loss of the motor operant reflex while contextual behavior and other conditioned responses were retained or led to errors in performance of the reflex: this appears to be evidence that derangement of launching and performing the motor program is the most important component of the conditioned reflex. Systemic administration of trihexyphenidyl at a dose of 10 mg/kg, scopolamine at doses of 0.03 and 0.06 mg/kg, and the peripherally-acting non-selective blocker methylscopolamine at a dose of 0.03 mg/kg led to changes in the general functional state (disturbances in the emotional-motivational sphere), the extent of which depended on the individual sensitivity of the animal to the anticholinergic agents. The presence of side effects led to complete cessation of conditioned reflex activity, though this appeared not to be associated with memory impairment.
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Treatment of schizophrenia depends heavily on neuroleptic drugs. Hypersalivation is a common side effect when people with schizophrenia are treated with neuroleptic drugs. Hypersalivation can be an embarrassing and stigmatising problem, can affect quality of life and can result in discontinuation of neuroleptic treatment. It can also be difficult to treat.
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A group of antiparkinson drugs (benactyzine, biperiden, caramiphen, procyclidine, and trihexyphenidyl) has been shown to possess both anticholinergic and antiglutamatergic properties, making these agents very well suited as anticonvulsants against nerve agents. The first purpose of this study was to make a comparative assessment of the anticonvulsant potencies of the antiparkinson agents when microinfused (1 microl) into the seizure controlling area tempestas (AT) of rats 20 min before subcutaneous injection of soman (100 microg/kg). The second purpose was to determine whether cholinergic and/or glutamatergic antagonism was the effective property. The results showed that only procyclidine (6 microg) and caramiphen (10 microg) antagonized soman-induced seizures. Cholinergic, and not glutamatergic, antagonism was likely the active property, since atropine (100 microg), and scopolamine (1 microg) caused anticonvulsant effects, whereas MK-801 (1 microg), and ketamine (50 microg) did not. Soman (11 nmol) injected into AT resulted more frequently in clonic convulsions than full tonic-clonic convulsions. AT may serve as both a trigger site for soman-evoked seizures and a site for screening anticonvulsant potencies of future countermeasures.
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It was shown previously that peripherally administered antagonists of the central 1 M-cholinoreceptors led to a selective impairment of bar-pressing response in a food-reinforced operant conditioned task but did not alter contextual behavior and functions such as motivation, perception, and locomotion. To obtain information about the central mechanisms of the conditioning impairment, we recorded simultaneously the extracellular multiunit activity from the frontal and motor neocortical areas of five cats trained to acquisition criteria in a food-reinforced operant conditioning task. Multiunit recordings were performed drur 1) normal conditioning; 2) conditioning during subcutaneous administration of muscarinic antagonists scopolamine (0.03 mg/kg), trihexyphenidyl (1 mg/kg), and methylscopolamine (0.03 mg/kg). Autocorrelation analysis showed that scopolamine and trihexyphenidyl but not methylscopolamine led to a significant increase in the tendency of cortical cells to fire in a cyclic way (i.e., the shift of the firing pattern from a single-spike discharge to burst, rhythmic, or rhythmic-burst discharge) both in the motor and frontal areas. Cross-correlation analysis showed that the bursting and rhythmic-bursting cells synchronized their activity within and (in a number of cases) between the cortical areas. These changes in the neuronal activity within the motor cortex and frontal cortex were accompanied by a significant decrease in the functional connectivity both inside and between the cortical areas in parallel with selective impairment of the conditioned response.
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The effects of the enantiomers of structurally related chiral M3 antagonists (trihexyphenidyl, p-fluorohexahydrodifenidol, hexahydrodifenidol and p-fluorohexbutinol) were studied at the presynaptic M2 and postsynaptic M3 receptor level in the rabbit trachea. All isomers were M3- over M2-selective as they did not increase the release of acetylcholine (an M2 effect) at concentrations that significantly inhibited smooth muscle contraction (an M3 effect). At the smooth muscle receptor, the R-enantiomers were consistently more potent than the S-enantiomers. The potency ratios (IC50(S)/IC50(R)) varied from 6 for p-fluorohexbutinol to 288 for trihexyphenidyl, and increased with higher eutomer potencies, in accordance to Pfeiffer's rule. Furthermore, we found that the potency of the racemic mixture of hexahydrodifenidol was significantly lower than that of the eutomer R-hexahydrodifenidol. To exclude that this difference was due to the lower concentration of the more active isomer, present in a racemic mixture, we calculated the potencies (-log IC50 values) of mixtures of the isomers of hexahydrodifenidol with varying amounts of S-hexahydrodifenidol and a constant amount of R-hexahydrodifenidol. We found that the presence of the distomer altered the potency of the eutomer in a dose-related manner. In conclusion, we have shown that the muscarinic smooth muscle receptor can be blocked differentially by the isomers of muscarinic antagonists and that the presence of the less active compound alters the potency of the most active isomer. We, therefore, suggest that, in bronchodilating therapy, the use of the pure eutomer might have advantages.
In patients with cervical dystonia, the early part of HFOs showed a significant decrease in amplitude, and the amplitude ratios of both early and late parts of HFOs/N20 potential were also significantly decreased. The amplitudes of HFOs and N20 potential were linearly correlated in the control subjects but not in dystonia patients.
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Parkinson's disease (PD) is characterized by the degeneration of nigrostriatal dopaminergic neurons. Its primary clinical symptoms are akinesia, tremor, and rigidity, which usually start from one side, resembling the lateralization in hemiparkinsonian rats having 6-hydroxydopamine-induced unilateral lesion of the medial forebrain bundle. A novel exploratory Y-maze was designed to detect the lateralization of hemiparkinsonian rats in terms of biased turns in the maze. Dopamine agonists levodopa (L-3,4-dihydroxyphenylalanine, 10-30 mg/kg) and apomorphine (0.1-0.3 mg/kg), but not methamphetamine (0.5-2 mg/kg), improved the lateralization in the rat model. However, high doses of the dopamine agonists, 30 and 0.3 mg/kg, respectively, caused small movements in the arms that seemed to parallel the increase in counts per turn in the Y-maze. Interestingly, the muscarinic antagonists trihexyphenidyl and scopolamine improved lateralization moderately, while increasing total turns, an index of locomotive activity. (-)-5-Methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801) (0.3 mg/kg), an N-methyl-D-aspartate (NMDA) glutamate receptor antagonist, increased total counts, but did not alleviate the lateralization. The alpha2-adrenoceptor antagonist idazoxan (1 and 10 mg/kg) and 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo(f)quinoxaline (1 and 3 mg/kg), a non-NMDA glutamate receptor antagonist, did not affect any of the indices. These findings suggest that the clinical action of drugs on unbalanced movement in PD could be predicted by measuring their effects on lateralization of the 6-hydroxydopamine-lesioned rat model in this exploratory Y-maze.
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We included 23 professional musicians (4 female, 19 male; mean age 51.5 ± 11.4 years) with a TSTM. During anamnesis, clinical examination, by mail or via telephone patients were asked for epidemiological, phenomenological information, risk factors and treatments. We then compared our findings to primary writing tremor, the most common task specific tremor.
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Effects of antiparkinsonian medication on the rabbit syndrome (RS) and accompanying parkinsonian symptoms were studied in 5 schizophrenic inpatients receiving long-term antipsychotic medication. All patients showed early improvement of RS following additional treatment with trihexyphenidyl or biperiden, with a significant reduction in the RS score also observed. The improvement of RS paralleled improvement of the parkinsonian symptoms, with the score of the Simpson-Angus rating scale significantly reduced. Our data provide further evidence that the underlying mechanism of RS is similar to that of acute forms of drug-induced parkinsonism.
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To investigate the hypothesis that GTP cyclohydrolase I (GCH1) mutations are responsible for the phenotype of highly anticholinergic responsive dystonia in patients with apparent primary torsion dystonia.
The myenteric plexus-longitudinal muscle preparation of the guinea-pig ileum was preincubated with [3H]choline, then superfused and stimulated electrically (1 Hz 120 pulses). Oxotremorine reduced the evoked outflow of [3H]acetylcholine in a concentration-dependent manner. Each of the six antagonists (scopolamine, methylatropine, trihexyphenidyl, 4-DAMP, clozapine, pirenzipine) produced parallel shifts of the concentration-response curves for the prejunctional effects of oxotremorine. Similarly, in contraction experiments, the antagonists competitively antagonized the postjunctional responses to oxotremorine. The pre- and postjunctional pA2 values did not differ significantly for any of the antagonists. It is concluded that pre- and postjunctional muscarinic receptors in the guinea-pig ileum are pharmacologically similar.
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Groups of patients with Parkinson's disease, either medicated, or unmedicated and early in the course, together with age- and IQ-matched control subjects were tested in two paradigms measuring different aspects of selective attention. The first set of tests compared visual discrimination learning following intra- and extra-dimensional shifts, using a "total change" design in which each shift was made in the presence of novel exemplars of the compound stimuli used as discriminanda. The second test consisted of a visual search task in which the number of alternatives was varied. The results of the first experiment showed a selective deficit in both groups of Parkinsonian subjects in their ability to perform an extra-dimensional shift. In the visual search task, the patients were less accurate, but responded with equivalent choice reaction times to those of controls. The results are discussed in terms of the nature of the attentional dysfunction that occurs in Parkinson's disease.
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1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) produces a parkinsonian state in monkeys and humans and a marked 3,4-dihydroxyphenylethylamine (dopamine) depletion in mouse striatum. In this study, we found that pretreatment with 3-(10,11,-dihydro-5H-dibenzo-[a,d]-cycloheptan-5-ylidene)-1-ethyl- 2- methylpyrrolidine (piroheptine), an anticholinergic drug which also inhibits dopamine uptake completely prevented loss of striatal dopamine in MPTP-treated mice. Trihexyphenidyl partially protected against the neurotoxicity of MPTP. However, clomipramine, a selective 5-hydroxytryptamine uptake inhibitor, did not prevent the loss of striatal dopamine. Piroheptine is another agent which was found to prevent MPTP neurotoxicity.
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Myoclonic dystonia is a rare disorder that occurs in an hereditary and a sporadic form. The autosomal-dominantly inherited form is responsive to alcohol but not to other drugs. The sporadic form has been relatively resistant to drug treatment. We report a young man with myoclonic dystonia who displayed only little response to alcohol but improved significantly with a combination of sodium valproate for myoclonus and trihexiphenidyl hydrochloride for dystonia. His rehabilitation, however, was confounded by public authorities who thought the patient's appearance was indicative of drug use.
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The effects of a combination of trihexyphenidyl and L-DOPA methyl ester given i.m. were studied 3-5 years after MPTP induced hemiparkinsonism in five female adult Macaca nemistrina monkeys. Three years later, these studies were repeated to determine if the drug combination was equally effective. Although the combination of trihexyphenidyl and L-DOPA produced potentiation in both studies, 3 years later it was quantitatively less. This was due primarily to the reduced effectiveness of L-DOPA methyl ester in a dose of 12.5 mg/kg i.m. Even though the combination was less effective in subsequent years, the animals continued to show the same clinical signs of hemiparkinsonism. Reduced effectiveness of the drug combination does not appear to be due to a lessening of MPTP-induced hemiparkinsonism, but rather to the reduced effectiveness of L-DOPA.
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Twelve parkinsonian patients on long-term levodopa therapy developed intermittent, myoclonic body jerks. The movements consisted of single unilateral or bilateral abrupt jerks of the extremities and occurred most frequently during sleep. Although directly related to daily dosage of levodopa, the myoclonus was specifically blocked by the serotonin antagonist, methysergide. Levodopa-induced myoclonus may be related to intermittent increases of activity of serotonin in the brain and results from levodopa-induced dysregulation of serotonin activity.
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