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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Administration of imipramine plus serotonin (5-HT) to rats has been proposed as an animal model of Duchenne muscular dystrophy. We studied the skeletal muscle necrosis produced in male rats given 5-HT after pretreatment with imipramine, other tricyclic antidepressants, or antihistamines, which like the tricyclic antidepressants, can block neuronal reuptake of 5-HT. Following one of these agents plus 5-HT, 20 mg/kg subcutaneously (s.c.), necrosis was more severe in the soleus muscle than the quadriceps. There was no significant difference in the incidence of necrosis in the soleus and quadriceps muscles following one of these agents plus 5-HT, 100 mg/kg, intraperitoneally (i.p.). After one of these agents plus 5-HT i.p., but not 5-HT s.c., extensive necrosis was significantly more frequent and severe in the quadriceps muscle than after 5-HT s.c. Chlorpheniramine (CP) plus 5-HT, 2.5 mg/kg intravenously, produced less muscle necrosis than CP plus 5-HT s.c. or i.p. The necrosis produced by CP plus 5-HT s.c. was comparable ipsilateral and contralateral to the injection site. The necrosis following CP plus 5-HT i.p. was maximal at 24 hr and remained fairly constant until 5 days. Regeneration was prominent by 7 days. The muscle necrosis produced by CP plus 5-HT is blocked by some 5-HT blockers, e.g., methiotepin and methysergide. It is also partially blocked by denervation. The capacity of tricyclic antidepressants and antihistamines to block neuronal 5-HT reuptake tended to be negatively correlated with the capacity to potentiate the muscle necrosis they produced with 5-HT, which suggests that blockade of 5-HT uptake is not the mechanism of the pathology produced by the combined treatment. The tricyclic antidepressants and the antihistamines are "membrane stabilizers-labilizers". Other drugs which are "membrane stabilizers-labilizers" such as trihexyphenidyl and procaine also promoted skeletal muscle necrosis when given prior to 5-HT. It is proposed that the effects of imipramine plus 5-HT on skeletal muscle are not due to the blockade of neuronal uptake of 5-HT and subsequent vascular-induced ischemia, but reflect direct toxic effects of these agents on skeletal muscle.
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An operant food-related conditioned reflex was developed in six cats by the "active choice" protocol: short-latency pedal presses were followed by presentation of low-quality reinforcement (bread-meat mix), while long-latency pedal presses were followed by presentation of high-quality reinforcement (meat). Animals differed in terms of their food-procuring strategies, displaying "self-control," "ambivalence," or "impulsivity." Multineuron activity was recorded from the frontal cortex and hippocampus (field CA3). Cross-correlation analysis of interneuronal interactions within (local networks) and between (distributed networks) study structures showed that the numbers of interneuronal interactions in both local and distributed networks were maximal in animals with "self-control." On the background of systemic administration of the muscarinic cholinoreceptor blockers scopolamine and trihexyphenidyl, the numbers of interneuronal interactions decreased, while "common source" influences increased. This correlated with impairment of the reproduction of the selected strategy, primarily affecting the animals' self-controlled behavior. These results show that the "self-control" strategy is determined by the organization of local and distributed networks in the frontal cortex and hippocampus.
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Atropine (AT) induces a dose-dependent increase in rate of rise of core temperature (heating rate) in sedentary heat-stressed rats, a muscarinic anticholinergic (MA) effect which is quantitatively similar to the increase in heating rate seen in heat-exposed men after equivalent atropine dose. In the heat-stressed rat, scopolamine (S) was found to have 16 x the MA effect of AT and, in the present study, aprophen (AP) and trihexyphenidyl (THP) manifested 0.067 x 0.061 x the MA effect of AT. In rats exercising on a treadmill (11 m/min, 6 degrees incline, 26 degrees C), physostigmine (PH) administration resulted in reduced endurance and increased heating rate, both of which were attenuated following AT administration-hypothesized to be a nicotinic anticholinergic (NA) effect. Optimum doses of anticholinergics to reverse the PH-induced decrements were: AT-200 micrograms/kg, S-8-16 micrograms/kg, AP-3000 micrograms/kg, and THP-800 micrograms/kg. These optimum NA doses for AT, S, and AP were the same as those predicted from their MA potency relative to AT in heat-stressed rats. However, it should be noted that 800 micrograms/kg of THP is only 1/4 of the expected 3200 micrograms/kg dose of THP based on MA equivalence to AT. Relative MA activities and optimum doses in PH-treated exercising rats appear to be due to differential MA and NA activities. Thus, a combination of both sedentary heat-stressed and exercising rat models may be useful in predicting relative cholinergic effects of new drugs with both MA and NA effects in man.
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After treatment, the frequency of average urination of 24 hours, frequency of incontinence of 24 hours and average urine volume at a time were obviously improved (all P < 0. 01), of which, the above items in group A were superior to those in group B (all P < 0. 05) the UPDRSIII score in group A was superior to that in group B (P < 0.05). The adverse reactions in group A were less than those in group B.
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In an inbred line of Syrian hamsters, attacks of sustained dystonic postures of the limbs and trunk can be initiated by handling or mild environmental stimuli (e.g. new cage). The severity of the dystonic syndrome in these mutant hamsters (gene symbol dtSZ) is age-dependent, with a peak at about 30-40 days of age. A scoring system for grading the type and severity of the dystonic attacks can be used to study the activity of drugs against dystonic movements with individual pre- and post-drug vehicle trials as control. The effects of drugs which alter dopaminergic or cholinergic functions in the brain were studied in selectively bred dystonic hamsters and age-matched non-dystonic controls. The dopamine precursor levodopa (injected together with carbidopa) and the dopamine receptor agonist apomorphine increased the severity of dystonia in hamsters when administered prior to the age of maximum severity of dystonia. A very similar effect was observed with the cholinomimetic pilocarpine. In contrast, the dopamine receptor antagonist haloperidol caused a marked overall reduction in dystonic movements. Anticholinergic drugs, i.e. trihexyphenidyl and biperiden, increased the latency to onset of the dystonic attack, but did not reduce its severity. No differences were observed between dystonic and non-dystonic hamsters with respect to extent and duration of stereotypies induced by dopaminergic and cholinergic drugs or hypolocomotion and catalepsy produced by haloperidol. The data suggest that dopaminergic hyperactivity might be involved in the pathophysiology of dystonia in dtSZ mutant hamsters.
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Status dystonicus (SD) is a medical emergency weighed by a relevant morbidity and mortality. It mainly affects patients with primary or secondary dystonia and is often triggered by events such as fever, infections, exposure medications or their abrupt cessation. We report on three patients presenting with SD. Two of them were affected by a static encephalopathy and the other one by a neurodegenerative disorder such as megalencephalic leukoencephalopathy with subcortical cysts (MLC). To our knowledge this is the first patient affected by MLC presenting with SD. All our patients underwent continuous infusion of midazolam, in association with pimozide and trihexyphenidyl, which led to complete resolution of muscular spasms in two patients. In the other one a complete cessation of dystonic spasms was obtained after intrathecal baclofen. From a therapeutic point of view there are no evidence-based management guidelines in SD. The approach is empiric and based on very limited anecdotal reports. On the basis of our observations and an extensive review of the literature we delineated a possible therapeutic strategy of SD in children.
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The effects of timiperone, its metabolites and related compounds on specific 3H-spiroperidol binding to dopamine receptors in the rat corpus striatum were studied to clarify the affinity of timiperone, a new butyrophenone, for the receptors and whether timiperone itself was active in vivo. Timiperone had an approx. 0.6, 5 and 30 times greater affinity for the receptors than did spiroperidol, haloperidol and chlorpromazine, respectively. This affinity was observed specifically for antipsychotic drugs but not for diazepam and trihexyphenidyl. Timiperone metabolites had little or no affinity for the receptors. Radioreceptor assay values agreed well with the radiochemical assay for timiperone in the plasma and brain of rats after i.v. injection of the 14C-labeled drug. Thus, it is conceivable that timiperone itself exerts its potent antipsychotic activity by blockade of cerebral dopamine receptors.
A 64-year-old woman with blepharospasm, sustained clenching of the jaw, antecollis, and a strained, high-pitched phonation continued chronic trihexyphenidyl therapy despite the lack of any obvious benefit. Abrupt, accidental withdrawal of trihexyphenidyl triggered severe exacerbation of the cranial dystonia associated with inspiratory stridor and acute respiratory difficulties, prompting emergency admission. On indirect laryngoscopy, hyperadduction of the vocal folds was not the cause of the upper airway obstruction. A more likely cause of the inspiratory obstruction appeared to be forward bending of the neck combined with mouth-clenching spasms. Reinstitution of intravenous anticholinergic medication provided relatively prompt relief. We caution against abrupt interruption of anticholinergics in patients with severe segmental cranial dystonia, even in those cases in which no benefit is apparent to observers.
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To study the effects of Qing-Xuan tablets (QXT) on behavior pattern and striatal TNF-alpha in mice model of Parkinson's disease (PD).
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Relief of blepharospasm was achieved with clonazepan (CNZ, 1 mg i.v.) and benzhexol (BH, 5 mg i.m.) by acute parenteral administration in 5 cases of Meige's syndrome. Improvement was greater with CNZ, mean value on a quantitative scale 100%, than for BH (84.1%). Both drugs were less effective on the associated oromandibular dystonia (OMD) observed in 3 of the cases, relief again being greater when using CNZ (87.3%) compared to BH (58.3%). Intravenous administration of CNZ predicted the response to prolonged oral medication (6 mg/day) in 3 of the cases. Though both blepharospasm and OMD are thought to represent focal dystonia at different body sites, the extent of improvement achieved with these drugs at the dosage employed differed markedly.
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.
Although trihexyphenidyl is used clinically to treat both primary and secondary dystonia in children, limited evidence exists to support its effectiveness, particularly in dystonia secondary to disorders such as cerebral palsy. A prospective, open-label, multicenter pilot trial of high-dose trihexyphenidyl was conducted in 23 children aged 4 to 15 years with cerebral palsy judged to have secondary dystonia impairing function in the dominant upper extremity. All children were given trihexyphenidyl at increasing doses over a 9-week period up to a maximum of 0.75 mg/kg/d. Trihexyphenidyl was subsequently tapered off over the next 5 weeks. Objective motor assessments were performed at baseline, 9 weeks, and 15 weeks. The primary outcome measure was the Melbourne Assessment of Unilateral Upper Limb Function, tested in the dominant arm. Tolerability and safety were monitored closely throughout the trial. Of the 31 children who agreed to participate in the study, 5 failed to meet entry criteria and 3 withdrew due to nonserious adverse events (chorea, drug rash, and hyperactivity). Three children required a dosage reduction because of nonserious adverse events but continued to participate. The 23 children who completed the study showed a significant improvement in arm function at 15 weeks (P = .045) but not at 9 weeks (P = .985). Post hoc analysis showed that a subgroup (n = 10) with hyperkinetic dystonia (excess involuntary movements) worsened at 9 weeks (P = .04) but subsequently returned to baseline following taper of the medicine. The authors conclude that scientific evidence for the clinical use of trihexyphenidyl in cerebral palsy remains equivocal. Trihexyphenidyl may be a safe and effective for treatment for arm dystonia in some children with cerebral palsy if given sufficient time to respond to the medication. Post hoc analyses based on the type of movement disorder suggested that children with hyperkinetic forms of dystonia may worsen. A larger, randomized prospective trial stratified by the presence or absence of hyperkinetic movements is needed to confirm these results.
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For the treatment of 42 patients with different forms of atherosclerotic and postencephalitic parkinsonism the author used levopa drugs, medantane, cyclodol and parkopan in combination and separately. The most stable improvement was obtained from a combination of levopa with cyclodol in patient with rigid-akynetic-trembling manifestations of parkinsonism. The treatment by medantane increased the therapeutical effect in the patients with postencephalitic parkinsonism. Methyl-dopa and pyridoxine served as a corrector of levopa. The studies on the blood content of acetylcholine and cholinesterase showed a growth of cholinolytic and cholinesterase activity in the blood.
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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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Fifty patients attending a neurological outpatient clinic for Parkinson's disease were assessed by standardized methods for both physical and psychiatric symptoms. The patients then received treatment with L-dopa with carbidopa or anticholinergic drugs and/or amantadine. During the following six-month period the subjects were assessed at intervals, both physically and psychiatrically. Forty patients were followed up for the full six-month period. The severity of physical signs and affective symptoms was shown to be significantly related at several stages of the investigation. Initially, the patients showed a high psychiatric morbidity. During treatment, 22 patients developed a depressive disorder, 12 or which had a history of previous depressive episodes. By contrast, of the 11 patients who showed very few affective symptoms during follow-up, none had a history of depression. Of the 22 patients with a depressive disorder, only two were in the anticholinergic/amantadine group, compared with nine and 11 in the other groups. L-dopa was not an effective antidepressant agent. The probable relevance of the findings of the study to the management of patients with Parkinson's disease is outlined.
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To assess the effect and adverse reaction of Qufeng Zhidong Recipe (QZR) in treating children's tic disorder (TD).
We present a case of long-term trihexyphenidyl (THP) abuse in which memory and cognitive impairments were observed 23 years after the commencement of medication. This case showed a dramatic improvement after withdrawal of THP. Clinical course during admission was followed with psychometric testing and laboratory examinations. The fact that the patient showed no evidence of lowered alertness during the clinical course raises the possibility that THP can primarily induce impairment of memory and cognitive functions. This is supported by the findings on the resting EEG of the patient. This case emphasizes the need to exercise caution in prescribing high doses of anticholinergic agents for long periods, particularly in elderly patients with underlying brain pathology.
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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.
Trihexyphenidyl (Tri) inhibited the contraction of rabbit basilar artery due to high K+ (45.6 mmol/L). IC50 was 2.9 +/- 0.7 mumol/L. The contractions of basilar and mesenteric arteries due to calcium and those of basilar artery and saphenous vein due to serotonin were noncompetitively. Tri inhibited myogenic activities of the portal vein strips of rats and increased the normal cerebral blood flow of rats to 19 +/- 7 ml/(min.100 g).
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A retrospective study of 13 patients (4 males/9 females) with acquired hemidystonia in childhood is reported. The mean age of onset of hemidystonia was 6.4 years (range 1-13.4 years); the mean duration of dystonia at the time of last follow-up was 11.4 years (range 3.6-23 years). Hemidystonia was caused by ischemic infarction in 9 patients and was attributed to perinatal trauma in 1; in 4 of the 9 patients with stroke and in the remaining 3 patients laboratory investigations were suggestive of primary antiphospholipid syndrome. Eleven of the 13 patients had delayed onset of dystonia: between 1 month and 8.9 years (mean 3.4 years). Ten patients had neuroradiological evidence of contralateral basal ganglia damage. A history of hemiparesis and evidence of striatal damage on CT or MRI were important risk factors for the development of dystonia. Response to medical treatment (trihexyphenidyl dose as high as 40 mg daily) in 5 patients was disappointing; 4 of the 5 patients who underwent functional stereotaxic operations were improved, but dystonia was still present at the end of the follow-up. Our study provides additional evidence that lesions of the striatum may induce dystonia, supporting the theory of striatopallido-thalamic disconnection. Furthermore, our results indicate that the occurrence of delayed dystonia must be considered in the diagnostic approach to childhood-onset dystonia.
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