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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Intermittent high-frequency electrical stimulation of the caudate nucleus induces contralateralhead-turning in rats. The anti-Parkinson drugs, L-dopa, amantadine and apomorphine, raise the threshold for or completely inhibit head-turning. There was a high correlation between the predicted clinical potency and these drugs based on inhibition of head-turning and their respective clinical anti-Parkinson potency. The centrally acting anticholinergic drugs also antagonized head-turning but there was not a good correlation between the predicted and acutal anti-Parkinson doses used in man. In order to determine if these drugs blocked head-turning by acting on the caudate nucleus, a combination cannula and stimulating electrode was used to administer drugs directly into the same area of the caudate nucleus being stimulated electrically. Dopamine, amantadine and apomorphine each antagonized head-turning when infused into the same site, at doses which did not produce concurrent overt sterotyped behavior. Time- and dose-response data with all three drugs suggest a direct inhibitory action on the caudate nucleus consistent with their proposed mechanism for treatment of Parkinson symptomatology. Head-turning appears to be a useful animal model for the development of new, specific anti-Parkinson drugs and for the study of possible mechanism(s) of action of existing drugs.
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Rats with the Parkinsonian syndrome induced by administration of acetyl choline and proserine into the rostral part of both caudate nuclei manifest an increased electrical activity (EA) in this part. Tremor, oligokinesia and rigidity are characterized by the appearance of paroxysmal EA with high amplitude of slow and rapid waves. The data obtained allow to conclude that neuropathophysiological basis of the Parkinsonian syndrome is the formation of the generator of pathologically enhanced excitation (GPEE) in the caudate nuclei. Some peculiarities of the GPEE activity in tremor and akinetic rigidity syndromes were observed. Intrarostral administration of dopamine or intraperitoneal administration of cyclodol resulted in the inhibition of GPEE and disappearance of clinical manifestations of Parkinsonian syndrome.
This is a report on a 62-year-old Chinese woman with Parkinson's disease (PD) for 8 years who developed myasthenia gravis (MG) in the last year. In this case, there was no adverse effect of trihexyphenidyl on MG, whereas pyridostigmine worsened the PD.
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The clinical manifestations, differential diagnosis, and treatment of the neuroleptic malignant syndrome and neuroleptic-induced catatonia are discussed. A case is presented in which the catatonic-like behavior and extrapyramidal sequelae of the neuroleptic malignant syndrome responded to combined treatment with anticholinergics and levodopa/carbidopa. Differential diagnosis and theories regarding the development of these neuroleptic-induced disorders are reviewed.
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Drugs that act at the N-methyl-D-aspartate (NMDA) receptor complex have the ability to terminate nerve agent-induced seizures and modulate the neuropathologic consequences of agent exposure. Drugs with mixed anticholinergic and anti-NMDA properties potentially provide an ideal class of compounds for development as anticonvulsant treatments for nerve agent casualties. The present experiment evaluated the potential NMDA antagonist activity of 11 anticholinergic drugs by determining whether pretreatment with the compound was capable of protecting mice from the lethal effects of NMDA. The following anticholinergic drugs antagonized NMDA lethality and are ranked according to their potency: mecamylamine > procyclidine = benactyzine > biperiden > trihexyphenidyl. The anticholinergics atropine, aprophen, azaprophen, benztropine, 3-quinuclidinyl benzilate (QNB), and scopolamine failed to show NMDA antagonist properties. In addition, and unexpectedly, diazepam, ethanol, and pentobarbital were also shown to be capable of antagonizing NMDA lethality over a certain range of doses. The advantages and limitations of using antagonism of NMDA lethality in mice as a bioassay for determining the NMDA antagonist properties of drugs are also discussed.
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A 20-year-old psychiatric patient receiving haloperidol treatment developed acute-onset fever, rigidity, and mental changes. Subcutaneous apomorphine was given alone for treatment. The patient had rapid clinical improvement after the treatment. Serial blood examinations showed decline and subsequent normalization of the creatine phosphokinase levels.
Drooling is a common dysfunction in children with cerebral palsy and may also affect neurologically unimpaired children. It causes significant social handicap to both children and their families.
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The ultimate goal is to discover new treatments that can lead to measurable improvement in functional outcome for affected children. In order to accomplish this goal, we must have consistent definitions and accurate measurements to determine the diagnosis and severity for each child in a clinic or research trial. Recent progress in defining childhood movement disorders has led to consensus definitions of different types of hypertonia. There has also been progress in the development of outcome measures that relate to meaningful functional performance in a variety of skill areas. Most exciting is the prospect of new treatments, and we survey the current non-medical, medical, and surgical therapies for childhood motor disorders.
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.
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Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are severe cutaneous adverse reactions (SCAR) with high mortality and have a significant public health impact because of high mortality and morbidity.
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Extracellular single-cell recording techniques were employed to study the mechanism of action of repeated oral clozapine administration on the in vivo spontaneous activity of substantia nigra (A9) and ventral tegmental area (A10) dopamine (DA)-containing neurons in the rat. Clozapine was observed to affect DA neurons differentially within these two regions when compared to haloperidol. Acute treatment (1 hr) with both drugs increased the number of spontaneously firing neurons in both A9 and A10. Chronic (21 day) treatment with haloperidol decreased the number of cells encountered in both regions, whereas repeated treatment with clozapine reduced the number of DA cells per track only in A10. In all cases, the silent DA neurons were inferred to be in a state of depolarization inactivation since they could be induced to discharge normally by the microiontophoretic application of the inhibitory neurotransmitter gamma-aminobutyric acid. These effects were not due to an effect of chloral hydrate anesthesia since they were also observed in gallamine-paralyzed, artificially respired animals. Chronic co-administration with haloperidol of either an anticholinergic (trihexyphenidyl) or the alpha 1-norepinephrine (NE) receptor antagonist, prazosin, but not an alpha 2-NE antagonist, RX781094, resulted in a differential effect on A9 and A10 DA neurons identical to that observed with repeated clozapine administration alone. Thus, chronic treatment with these combinations of drugs resulted in the depolarization inactivation of only A10 cells. These data suggest that anticholinergic and/or alpha 1-NE-blocking properties of clozapine may, in part, mediate its differential effects on A9 and A10 midbrain DA neurons.
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We studied the effect of anti-cholinergic therapy on axial symptoms that show a tendency to worsen over time after deep brain stimulation of the subthalamic nucleus (STN-DBS) in patients with Parkinson's disease (PD).
We present a 20-year-old woman with previous treatment of risperidone 6-7 mg daily for approximately 4 years. She developed TD 2 years later after switching to paliperidone 9 mg daily. To the best of our knowledge, she is the first case report of having direct paliperidone-induced TD. Immediate treatments including paliperidone dose reduction to 6 mg daily, clonazepam 1.5 mg daily and trihexyphenidyl 2 mg daily were performed for 1 month, and her symptoms were relieved eventually after switching to clozapine 75 mg daily.
The phenomenon of delayed-onset dystonia following presumed "static" brain injuries was described after stroke and head trauma. Burke et al. described a different category of secondary dystonia, where perinatal injury (asphyxia) caused minimal or no immediate neurological deficit, with the delay of years before dystonia emerged. This type of dystonia following perinatal injury has been termed "delayed onset dystonia due to static encephalopathy of childhood". According to the definition of dystonia, we were able to select 5 patients with the aetiologic diagnosis of perinatal asphyxia from the group of 347 out- and inpatients (1.4%) treated for various types of dystonia at the Movement Disorders Department (Institute of Neurology, CCS, Belgrade) from November 1986 to November 1994. At onset of dystonia the mean age of patients was 13.2 years (range from 10 to 17), with combined initial involvement of the arm and neck in 3 patients. The period from the onset of the disease to the maximum severity lasted 8.2 years (range from 4 to 14), resulting in segmental brachial dystonia in 3, hemidystonia and generalized dystonia in one patient each (Table 1). The adverse perinatal events are described in Table 2. Three of our patients had delayed achievements of developmental milestones. All patients were regularly schooled and had preserved intellectual capacities, except the patient 3 whose achievements were below average (IQ = 86). Different drugs were administered (Table 3), but moderate effects were achieved only with trihexyphenidyl in two patients (daily doses of 24 mg and 30 mg, respectively), and baclofen (80 mg p.d.) in one patient. In this study we describe 5 new patients who fulfilled the criteria for the diagnosis of delayed-onset dystonia due to perinatal asphyxia (Tables 1 and 2). We accepted the approach of Saint-Hilaire et al. to suggest a relationship between perinatal asphyxia and later occurrence of dystonia in our 5 patients. However, coincident occurrence of a primary dystonia with a static encephalopathy of childhood due to perinatal asphyxia cannot be excluded. This phenomenon of delayed appearance of dystonia was also described in other forms of static cerebral injury; i.e. stroke, head trauma or anoxic brain damage. Interestingly enough, age at the time of anoxia or brain insults seemed to be crucial for the development of dystonia: those who suffer acute brain insults during childhood or early life are more likely to develop dystonia than the older patients. Therefore, the "static" nature of encephalopathy induced by perinatal asphyxia is questionable. Finally, this study strengthens the suggestion that perinatal asphyxia can lead to delayed-onset dystonia, and, since "some of these patients closely resemble cases of idiopathic torsion dystonia, the prior occurrence of asphyxia should be used as a criterion of exclusion for that diagnosis".
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In Rett syndrome (RS), acute life-threatening episodes (ALTEs) are usually attributed to epilepsy or autonomic dysfunction but they can represent a movement disorder (MD). We describe three girls with RS who experienced ALTEs from an early age. These were long considered epileptic until video-EEG in Patients 1 and 3 revealed their non-epileptic nature. A primary dystonic mechanism was suspected and Patients 1 and 2 were treated with Trihexyphenidyl with significantly reduced frequency of the ALTEs. Patient 3 died before Trihexyphenidyl was tried. Trihexyphenidyl in RS patients with similar presentations can modify the dystonia and prevent ALTEs.
The mainstay of the pharmacologic management of delirium remains typical antipsychotics, primarily haloperidol. Typical antipsychotics are associated with significant side effects, particularly in the elderly. This article reviews the literature on the use of both typical and atypical antipsychotics in the management of acute delirium, with a focus on the elderly. In this population, typical antipsychotics are associated with substantially more drug induce side effects--either extrapyramidal side effects or anticholinergic effects from the antipsychotics alone or in combination with benztropine or trihexyphenidyl. Anticholinergic toxicity is especially problematic in delirious, demented patients, because most dementias are associated with pre-existing deficiencies in cholinergic neurotransmission. These issues will be reviewed for typical antipsychotics as well as the emerging literature on the use of atypical antipsychotics-- risperidone, olanzapine, and quetiapine--for pharmacologic management of acute delirium. Data from two studies conducted at the Wesley Woods Center at Emory University will be briefly reviewed as they constitute the largest series to date investigating the pharmacologic management of delirious demented patients.
In patients with cranial dystonia, we compared the effects of central anticholinergic, peripheral anticholinergic, and placebo treatments in a double-blind crossover study. One of the nine patients who completed the study improved markedly with central anticholinergic therapy. The three treatments were indistinguishable in the other eight patients except for the higher incidence of central and peripheral anticholinergic side effects with trihexyphenidyl.
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A total of 250 patients were enrolled with mean age 40.36 ± 12.3 years. Most common diagnosis was major depressive disorder 101 (40.4%). A total of 980 drugs (mean 3.68 ± 1.42) were prescribed out of which 387 (39.5%) were off-label. Of 250 patients, 198 (79.2%) received at least one off-label drug. Psychopharmacological agents most frequently used in off-label manner were clonazepam 31 (12.4%), lorazepam 30 (12%), and trihexyphenidyl HCl 25 (10%). Prevalence of off-label use of these three drugs was significantly higher than other off-label drugs (P < 0.0001, P < 0.0001 and P < 0.0001 respectively). Inappropriate indication was the most common category of off-label use. There was positive and significant correlation between off-label prescribing and number of drugs (r = 0.722, P ≤ 0.000). Off-label prescribing was statistically significantly higher in 21-40 year age group, but no difference was seen in any co-morbid condition or in between any psychiatric disorder.
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Amantadine and biperiden have similar effects on neuroleptic-induced EPS and TD and may ameliorate mild TD.
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Paradigms of isometric force control allow study of the generation and release of movement in the absence of complications due to disordered visuomotor coordination. The onset and release of isometric force in Parkinson's disease (PD) was studied, using computerised determinants of latency of response and rate of force generation and release. Components of isometric force control were related to measures of cognitive, affective and clinical motor disability. The effects of treatment were determined by longitudinal study of de novo patients. Patients with PD showed impairment in latency and rate of force change for movement release as well as onset. Rate of force change correlated with depression, clinical motor disability and memory quotient but latency showed no correlation with any of these measures. Treatment improved rate of force release, in concert with clinical motor disability, but not latency. These results suggest dissociations between latency and rate of force change that may be linked to different neurochemical deficits. Further, they demonstrate akinetic deficits in force release that argue against the "neural energy hypothesis" of akinesia.
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We have previously proposed that the reciprocal hindlimb scratching (RHS) of mice elicited by intrathecal injection of muscarinic agents is mediated by M1 muscarinic receptors. In this study, benzhexol potently inhibited pilocarpine-induced RHS (ID50 = 0.5 ng), methoctramine did not fully block RHS and RS 86 neither produced nor blocked RHS. These data (1) differentiate the three muscarinic agents using this in vivo endpoint, (2) substantiate binding studies characterizing benzhexol and methoctramine as putative M2 and M2 antagonists, respectively, and (3) further support using RHS for studying muscarinic agents.
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Segmental craniocervical dystonia is characterized by blephalospasm and oromandibular dystonia and is also called Meige syndrome. The current treatment strategy including botulinum toxin (BTX) injections has not yet attained an acceptable level. We describe a long-term favorable response of a novel combination therapy with aripiprazole (ARP), trihexyphenidyl (THP), and BTX in three patients with segmental craniocervical dystonia. The symptoms of three patients responded promptly to the combination therapy with ARP 3-6 mg daily, THP 2-8 mg daily, and BTX. Although the patients were required to receive a BTX 50-100 IU injection every 3-6 months, their symptoms were kept in a satisfactory condition for up to 2 years without any adverse effects. ARP possesses the potential for dramatically improving dystonia. THP has the possibility to enhance the efficacy of ARP and prolong the effective period of BTX. It may be an important requisite to give all three agents together for a successful treatment. The combination therapy with ARP, THP, and BTX was well-tolerated and useful in controlling the symptoms of segmental craniocervical dystonia, however, the reason why this combination therapy succeeded is unknown. A further long-term follow-up is required to monitor the delayed neurological adverse effects.
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To better evaluate the non-medical use of anticholinergic substances in Brazil, a review of the local literature was performed. Synthetic compounds such as triexyphenidyl (Artane), benactizine (Asmosterona), dicyclomine (Bentyl) as well as Datura sp. tea were reported as being used by first and second grade students and by street children of several Brazilian cities. In several cases the percentage of youngsters indulging in such use was higher than the percentage found for cocaine, barbiturates, cough syrups and amphetamine-related drugs. Several cases of patients seeking treatment for dependence or for acute psychotic symptoms were also described.
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Patients in selegiline group had less severe disease (UPDRS score 24.11 +/- 14.07) as compared to controls (UPDRS score 40.53 +/- 18.52). There was significant improvement in UPDRS score (p < 0.05), WAIS (p < 0.001) and memory (p < 0.001) in selegiline group. In the control group there was a significant prolongation of P300 latency (p < 0.05).
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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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