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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Pretreatment of rats with agents with strong antimuscarinic activity in the CNS (scopolamine, benztropine, trihexyphenidyl, amitriptyline, and thioridazine) but not their inactive congeners (desipramine, fluphenazine, or haloperidol) led to significant increases in the maximum apparent density of binding sites for 3H-QNB in cerebral cortical or striatal membranes. The dopamine agonist bromocriptine induced a similar effect that was blocked by haloperidol in striatum. None of these treatments altered the apparent affinity of the test ligand. Tolerance to the behavioral activating action of scopolamine developed over two weeks of daily treatment. This change was paralleled by an increase in 3H-QNB binding in cerebral cortex which was dependent on the dose and duration of treatment with scopolamine and persisted for a week following two weeks of treatment. Scopolamine pretreatment led to a significant increase in basal, spontaneous motor activity in the rat, but also to a marked increase in the motor-inhibitory actions of the centrally active muscarinic agonist pilocarpine. These results add to the impression that decreased availability of ACh agonists can significantly increase the availability and functional activity of central muscarinic ACh receptors to reflect "disuse supersensitivity."
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To develop a method to measure trihexyphenidyl, chlorpromazine and clozapine in human blood with GC-MS.
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We report a 56-year-old woman with progressive gait disturbance. Her mother had Parkinson's disease with onset at age 70. She died at age 74 and the post-mortem examination confirmed the diagnosis of Lewy body positive Parkinson's disease. The patient was well until the age of 50(1995) when she noted an onset of resting tremor and difficulty of gait. She also developed delusional ideation and was admitted to a psychiatric service of another hospital, where a major tranquilizer was given. The delusion disappeared but she developed marked rigidity. The major tranquilizer was discontinued and an anticholinergic and amantadine HCl were given. She showed marked improvement to Hoehn and Yahr stage II and was discharged. In 1995, when she was 52 years of the age, she developed delusion again and a major tranquilizer was given. She developed marked parkinsonism again and became Hoehn and Yahr stage V. The major tranquilizer was discontinued and she was treated with levodopa/carbidopa, trihexyphenidyl, bromocriptine, and dops. She improved remarkably to stage II. She was admitted to our service on October 8, 1996 for drug adjustment. She was alert and not demented. She was anxious but delusion or hallucination was noted. Higher cerebral functions were intact. Cranial nerve functions were also intact except for masked face and small voice. Her posture was stooped and steps were small. She showed retropulsion and moderate bradykinesia. Resting tremor was noted in her left hand. Rigidity was noted in both legs. No cerebellar ataxia or weakness was noted. Deep tendon reflexes were within normal range and sensation was intact. Her cranial MRI revealed some atrophic changes in the putamen, in which a T 2-high signal linear lesion was seen along the lateral border of the putamen bilaterally. In addition, posterior part of the putamen showed T 2-low signal intensity change. She was treated with 1.6 mg of talipexole, 6 mg of trihexyphenidyl, and 100 mg of L-dops. She was in stage III of Hoehn and Yahr. She developed neurogenic bladder with a large amount of residual urine for which she required catheterization. She was transferred to another hospital. Despite drug adjustment, she lost response to levodopa and her parkinsonism deteriorated gradually. She also developed syncope orthostatic hypotension. In April of 1998, she developed intracerebral hemorrhage and was admitted again on April 19, 1998. She was unable to stand and showed marked akinesia and rigidity. She was in stage V of Hoehn and Yahr. Her cranial CT scan revealed bilateral high-density lesions in the posterior parietal lobes. She developed dysphagia for which she required gastrostomy. She was transferred to another hospital but her clinical condition deteriorated further. On December 22, 1999, she developed fever and dyspnea and was admitted to our service again. She developed cardial arrest at the emergency room from hypoxia. She was resuscitated; however, she was comatose with loss of brain stem reflexes. Later on she developed generalized myoclonus. She developed cardiac arrest and pronounced dead on December 28, 1999. The patient was discussed in a neurological CPC. The chief discussant arrived at the conclusion that the patient had striatonigral degeneration because of poor response to levodopa in the later course, autonomic failures, and MRI changes. Some other participants thought that the patient had a form of familial Parkinson's disease. Opinions were divided into these two possibilities. Post-mortem examination revealed that the substantia nigra showed intense neuronal loss and gliosis, however, no Lewy bodies were seen. In addition, intracytoplasmic inclusions were seen in oligodendrocytes. The putamen was markedly atrophic in its posterior part with marked gliosis and neuronal loss. The ventromedial part of the pontine nucleus also showed neuronal loss and intracytoplasmic glial inclusions. Pathologic diagnosis was multiple system atrophy. In the parietal lobe, an arteriovenous malformation with bleeding was noted. This is very unique case. Although her mother had Lewy body-positive Parkinson's disease, the patient had Lewy body-negative multiple system atrophy with a-synuclein-positive glial inclusions. Whether this is just a coincidental occurrence or the presence of a genetic load for Parkinson's disease might triggered her multiple system atrophy is an interesting question to be answered in future.
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The authors report a new case of Shy and Drager syndrome characterized by the severity of the extrapyramidal signs as well as that of orthostatic hypotension and urinary dysfunction. Peripheral adrenergic disturbance was proven, associated with an abnormality of the renin-angiotensin system. The authors describe the various drugs tried experimentally in treatment of the three main symptoms of the disease. A combination of Trihexyphenidyl and Dibenzepine finally appeared to be the most effective. Six months later, there remained a marked improvement in extrapyramidal signs and orthostatic hypotension. By contrast there was no improvement in urological symptoms.
The possible interactions between a fungicide, thiram, and some drugs acting on the central nervous system were investigated in rats by means of behavioral methods. Potentiation was found after combined treatment with thiram and promethazine, and after thiram and meprobamate. In the case of trihexyphenidyl, an additive interaction was observed. It is presumed that these observations will be of practical toxicological significance.
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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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The co-occurrence of tics and dystonia as an idiopathic condition has only rarely been reported. We report a series of patients with tics and persistent dystonia, with the aim of determining the prevalence and clinical characteristics of this syndrome.
artane medication classification
The main objective in the treatment of blepharospasm is to decrease or cease the unwanted, repeated forced closure of the eyelids. This is best achieved by the use of botulinum toxin. In a minority of patients, botulinum toxin is either ineffective or poorly tolerated. In this group of patients, a trial with oral medication in the following order is warranted: trihexyphenidyl, baclofen, clonazepam, and tetrabenazine. Before going to the next medication, each of these drugs should be administered at the highest tolerated dosage for a period of 1 or 2 months. If, as often happens, all pharmacologic treatment attempts fail, and the patient is too disabled to remain untreated, he or she can be referred to an experienced plastic surgeon for a myectomy of the eyelid protractors. For treatment of apraxia of eyelid opening, botulinum toxin should be administered as the first treatment. If this fails, and vision is significantly impaired, the patient may be referred to a plastic surgeon for a frontalis suspension of the eyelid. Treatments of hemifacial spasm are aimed at decreasing or ending the annoying twitches of one side of the face. In this disorder, interference with vision is not a problem unless the contralateral eye is amblyopic. Despite isolated reports of spasm relief by drugs such as carbamazepine, oral medication is unlikely to be helpful. Botulinum toxin is the preferred treatment in hemifacial spasm patients. In some patients, relief from spasms can only be obtained at the cost of an ipsilateral upper lip droop of varying severity. Patients who are dissatisfied with the results of treatment with botulinum toxin, and are not willing to tolerate their condition, can be referred to an experienced neurosurgeon for microvascular decompression of the facial nerve. Pending success of ongoing attempts to reduce adverse effects, we believe that doxorubicin chemomyectomy, a recent treatment that has been used for both facial spasm and blepharospasm, is best administered in a research setting.
AIMS To assess the prescribing pattern and to measure some specific aspects of the behaviour of the prescribers (psychiatrists) before and after educational interventions using core drug use indicators. METHODS In the present randomized retrospective controlled pre-post intervention prescription survey of schizophrenia and depression, 100 prescriptions each for schizophrenia and depression were obtained before and after each intervention. The prescriptions were analyzed for the following prescriber-specific indicators: number of drugs prescribed, prescribing by generic names, prescriptions for essential drugs, antiparkinsonian and benzodiazepines, nature of drugs and number of combinations prescribed. Based on the results of pre-intervention data, two interactional workshops were conducted 1 and 6 months after pre-intervention data collection. The first workshop focused on the results of the prescription audit feedback and reasons thereof. The second workshop focused, in addition, on appropriate management of schizophrenia and depression using consensus treatment guidelines with the aim of evolving a consensus on the treatment in a given hospital setting. RESULTS Before intervention, the essential drugs accounted for 80.95 and 96.91% of the total number of drugs prescribed in depression and schizophrenia, respectively. Prescription for essential drugs improved further significantly in the post intervention period to 95.26% (P<0.04) for depression; whereas, in schizophrenia, prescriptions for essential drugs declined to 80.95%. The average number of drugs prescribed per encounter marginally declined in both schizophrenia (2.46±0.94 to 2.34±0.65) and depression (2.09±0.79 to 2.00±0.65) after the second intervention. The patients receiving two or more drugs from the same group together declined from 12 to 9% in schizophrenia, but increased from 5 to 10% in depression after intervention. Trihexyphenidyl, an antiparkinsonian drug, was co-prescribed (90%) with antipsychotic agents (98%) in schizophrenia; however, use of benzodiazepines declined significantly after intervention to 28% compared to 48% in the pre-intervention period. Also, benzodiazepine use was high (68%) and remained so (70%) after interventions in depression cases. CONCLUSION The present study demonstrates excessive use of antiparkinsonian agents in schizophrenia and benzodiazepines in depression. Monitoring for the use of antiparkinsonian and benzodiazepines can form an important component for measuring specific aspects of prescriber's behaviour, which can be used as an indicator for comparisons at different time intervals and between health facilities.
To study the effects of Qing-Xuan tablets (QXT) on behavior pattern and striatal TNF-alpha in mice model of Parkinson's disease (PD).
artane drug classification
Musician's dystonia is characterized by loss of voluntary motor control in extensively trained movements on an instrument. The condition is difficult to treat. This retrospective study reports on the interventions received by a homogeneous cohort of pianists with musician's dystonia and the subjective and objective changes reported in task performance.
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The study provides some evidence that a large number of the patients may not be well informed about the specific role of BenzhexoI in their treatment and that that some of their assumptions may portend danger for their health and outcome. Health workers may also have neglected to educate them. There is a need to intensify patient education in our clinics.
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1. Activation of muscarinic receptors in rat olfactory bulb stimulates adenylyl cyclase activity. This response was competitively antagonized by the (R)- and (S)-enantiomers of trihexyphenidyl with pA2 values of 8.84 and 6.09, respectively. 2. Similarly, in rat striatal homogenates, muscarinic inhibition of adenylyl cyclase activity was antagonized by the (R)- and (S)-enantiomers with pA2 values of 8.75 and 6.12, respectively. 3. In contrast, in rat myocardium the muscarinic inhibition of the adenosine 3':5'-cyclic monophosphate (cyclic AMP) formation was more weakly antagonized by trihexyphenidyl, with a particularly marked loss (15 fold) in activity of the (R)-enantiomer. The (R)- and (S)-enantiomers had pA2 values of 7.64 and 5.72, respectively. 4. Each muscarinic response was completely antagonized by increasing concentrations of (R)-trihexyphenidyl with a Hill coefficient not significantly different from unity. 5. The present study shows that the muscarinic receptors coupled to stimulation of adenylyl cyclase in the olfactory bulb display high stereoselectivity for the enantiomers of trihexyphenidyl. The affinities of these receptors for the antagonists are similar to those shown by the striatal receptors. This finding supports the hypothesis that both the muscarinic stimulation of adenylyl cyclase in the olfactory bulb and the muscarinic inhibition of the enzyme in striatum are mediated by activation of a receptor subtype pharmacologically equivalent to the m4 gene product. On the other hand, the weaker affinities and the lower stereoselectivity for the trihexyphenidyl enantiomers exhibited by the muscarinic inhibition of adenylyl cyclase in the heart are consistent with the involvement of M2 receptors in this response.
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Intraventricular administration of 1,6-aminosuberyl-arginine8-vasopressin or somatostatin in rats barrel rotation, a peculiar rotation along the sagittal body axis. The vasopressin-induced barrel rotation was markedly enhanced by fluphenazine, haloperidol, 6-hydroxydopamine or alpha-methyl-p-tyrosine but was unaffected by (D-Ala2, MePhe4, Met(O)5-ol)-enkephalin. The enhancement of the rotation behavior of fluphenazine was prevented by pretreatment with trihexy-phenidyl a muscarinic receptor blocker. These observations clearly show that vasopressin can elicit barrel rotation and that dopaminergic inhibition and cholinergic activation are concomitantly involved.
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Isolated dystonia of trunk and neck muscles without involvement elsewhere has been termed segmental axial dystonia--a rare disorder. We report a 31-year-old man who developed marked dystonia of paraspinal muscles and progressive scoliosis 6 months after a closed head injury. Computed tomography (CT) disclosed three small areas of encephalomalacia, one involving the head of the caudate nucleus. Treatment with trihexyphenidyl resulted in significant improvement of the dystonia and scoliosis.
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We studied the functional role of individual subtypes of muscarinic cholinoceptors in the pathogenesis of neuroleptic parkinsonism in rats. Blockade of M4 receptors prevented the development of extrapyramidal disorders, which was abolished by simultaneous blockade of M2 receptors. The data suggest that various subtypes of muscarinic receptors are involved in the regulation of dopamine concentration.
Cholinergic muscarinic systems have been shown to influence dopaminergic function in the central nervous system. In addition, previous studies of benztropine analogs that inhibit dopamine uptake and show antagonism at muscarinic receptors show these drugs to be less effective than cocaine in producing its various prototypic effects such as locomotor stimulation. Because previous pharmacological studies on these topics have used nonselective M1 antagonists, we examined the interactions of preferential M1 muscarinic antagonists and cocaine. Dose-dependent increases in extracellular levels of dopamine in selected brain areas, the nucleus accumbens (NAc) shell and core, and the prefrontal cortex, were produced by cocaine but not by the preferential M1 antagonists telenzepine and trihexyphenidyl. When administered with cocaine, however, both M1 antagonists dose-dependently increased the effects of cocaine on dopamine in the NAc shell, and these effects were selective in that they were not obtained in the NAc core or in the prefrontal cortex. Telenzepine also increased locomotor activity, although the effect was small compared with that of cocaine. The locomotor stimulant effects of trihexyphenidyl, in contrast, approached those of cocaine. Telenzepine attenuated, whereas trihexyphenidyl enhanced the locomotor stimulant effects of cocaine, with neither drug facilitating cocaine-induced stereotypy. The present results indicate that preferential antagonist effects at muscarinic M1 receptors do not uniformly alter all of the effects of cocaine, nor do they explain the differences in effects of cocaine and benztropine analogs, and that the alterations in dopamine levels in the NAc shell do not predict the behavioral effects of the interactions with cocaine.
Central nervous system involvement in Kikuchi-Fujimoto disease is a very rare clinical manifestation. We report a 15-year-old girl who presented to us with fever, drowsiness, neck swellings, and involuntary closure of both eyelids of 2 days duration. Magnetic resonance imaging brain showed T2-weighted and fluid-attenuated inversion recovery hyperintensities in dorsal midbrain and pons. Cervical lymph node fine-needle aspiration cytology was suggestive of Kikuchi-Fujimoto disease. Blepharospasm secondary to infectious etiology is rare. Positron emission computed tomography brain showed increased focal uptake in anterior cingulate gyrus which can be the site of origin of blepharospasm. The patient was managed with steroids and trihexyphenidyl with significant recovery. Kikuchi-Fujimoto disease is a rare disease which has to be considered as one of the differential diagnosis in a case of acute encephalopathy with cervical lymphadenopathy.
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A retrospective case-control study was undertaken with 252 adults selected from the hospital endoscopy database between January 2006 and July 2008. Cases were selected if they had 'capacious', 'megacolon', 'redundant' and/or 'featureless' colonic architecture reported in their first completed colonoscopy (n = 63). Demographic information and medication records were collected for both cases and controls. Logistic regression analysis was performed for each of the medication groups.
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Various hallucinations are unpleasant for patients with Parkinson's disease (PD). Hallucinations are often related to anti-parkinsonian drugs. Tactile hallucinations rarely occur in patients with PD. In contrast to other types of hallucinations, tactile hallucinations often make physicians wonder if a physical abnormality is the underlying cause. However, the relation of tactile hallucinations to anti-parkinsonian drugs remains uncertain because studies are scant. We describe three patients with PD who had tactile hallucinations that were triggered by dopamine agonists. In our patients, tactile hallucinations occurred in a clear sensorium and persisted for a prolonged time. Two patients had clear visual hallucinations such as of insects, which were associated with tactile hallucinations such as of insects tied to the body. Clear tactile sensoria were unpleasant. Dopamine agonists were initiated or the doses were increased during several periods immediately before the onset of tactile hallucinations. Although the other anti-parkinsonian drugs used, such as amantadine, zonisamide, or trihexyphenidyl, were likely to be partly responsible for the tactile hallucinations, our observations suggest that an increase in the dose of dopamine agonists can trigger tactile hallucinations.
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The effects of slow withdrawal of anticholinergic medication and addition of benzhexol (8 mg/day) have been studied in patients with Parkinson's disease on stable levodopa therapy. Withdrawal of anticholinergic drugs led to measurable and often severe deterioration in about two-thirds of patients. Addition of benzhexol produced a slight but definite additional improvement in those patients in whom anticholinergics were withdrawn before the trial. Anticholinergic drugs thus still have a part to play in the treatment of Parkinson's disease, for they produce benefit in addition to that provided by levodopa.
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