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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A sensitive and rapid method for the simultaneous determination of three commonly abused anticholinergic drugs in Jordan; trihexyphenidyl, procyclidine, and biperiden in plasma and urine has been developed using solid phase extraction and GC-MS. Linearity was established from therapeutic to fatal concentrations of the three drugs; 5-300 ng/ml in plasma, with correlation coefficient r(2) > or = 0.9978 and 10-800 ng/ml in urine r(2) > or = 0.9993. Recoveries were in the range of 86-92% and intra-day and inter-day relative standard deviations (n = 6) were in the range of 6.6-10.3% for the three drugs at three different concentrations in plasma and urine. The base peak m/z 98 for trihexyphenidyl, m/z 84 for procyclidine, and m/z 98 and 218 for biperiden, and m/z 339 for papaverine (internal standard) were monitored at selective ion monitoring; their retention times were 8.10, 8.67 and 8.92 min, respectively, and 14.79 min for the internal standard with analysis time of 16.75 min. The limit of detection of 0.5 ng/ml was attained for trihexyphenidyl and procyclidine, while for biperiden 2.0 and 1.0 ng/ml in spiked plasma and urine, respectively. This method has been applied to forensic and authentic samples taken from abuser and patients using these drugs. The method will offer the clinicians and the legal authority the right diagnosis regarding the anticholinergic involved in any case of abuse with less than 1 h per sample (plasma or urine) from the time of receiving.
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This is a retrospective descriptive study. Fifty four pianists with musician's dystonia who had received care in a Movement Disorders Clinic completed a self report questionnaire regarding type and effectiveness of treatment received over the last 4 years. Pianists' fine motor control was assessed objectively by measuring the temporal regularity of their scale playing.
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Two cases of normal dose dependence on Trihexyphenidyl are reported. The literature on anti parkinsonian drug abuse and dependence is briefly reviewed.
Recent studies from our laboratory have provided evidence that multiple states of the phencyclidine (PCP) receptor exist. In addition, several compounds such as PCP and the novel anticonvulsant MK-801 were found to inhibit binding more potently in the presence of Mg2+ and L-glutamate (L-GLU) than when these agents were excluded from the binding assay. In the present study, a number of pharmacological compounds that have been suggested to interact within the N-methyl-D-aspartate (NMDA) receptor complex, including tricyclic antidepressants (TCAs), were examined for their ability to inhibit the binding of [3H]1-[1-(2-thienyl)cyclohexyl]piperidine [( 3H]TCP) in the absence or presence of Mg2+ and L-GLU. The TCAs imipramine, amitriptyline, and opipramol produced shallow inhibition curves in the absence of Mg2+ and L-GLU. Computer analysis of the binding data indicated that a two-component binding model described the data significantly better than a one-component model. In the presence of Mg2+ and L-GLU, the inhibition curves became steeper and were shifted to the right, and computer analysis of the binding data indicated that a one-component model adequately described the binding data. A series of other centrally active compounds, including several antipsychotics and antihistamines, the antiparkinsonian anticholinergic trihexyphenidyl and the antitussive dextromethorphan, were also found to be affected similarly by the inclusion of Mg2+ and L-GLU in the binding assay. Dextrorphan, in contrast to dextromethorphan, inhibited [3H]TCP binding more potently in the presence of Mg2+ and L-GLU. The present results suggest that the compounds that inhibit binding more potently in the absence of Mg2+ and L-GLU are interacting with the PCP receptor in a different manner from that of PCP and MK-801, because these open-channel blockers inhibit [3H]TCP binding more potently in the presence of Mg2+ and L-GLU. The data support previous findings that TCAs interact with the NMDA receptor complex and suggest that the compounds trihexyphenidyl and dextromethorphan, which have been shown to block NMDA-mediated neurotoxicity, may produce their effects through an interaction with the PCP receptor, albeit by a different mechanism from that of open-channel blockers.
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For assessment of the effect of trihexiphenidil on the excitability state of the alpha-motoneurons of the plantar flexor of the foot in patients with drug-induced parkinsonian rigidity curves of the excitability of motoneurons of the soleus muscle were plotted in two variants of experiments: I. with afferent stimulation of the Ia fibres of the soleus muscle as the conditioning and testing stimulus (tibial nerve in the popliteal fossa), II. with afferent stimulation of Ia fibres of the anterior tibial muscle (peroneal nerve behind the fibular capitulum) used as the conditioning stimulus and stimulation of the tibial nerve as the testing stimulus. These investigations were carried out on 12 psychiatric patients who received no drugs at the time of these investigations (control group), 13 similar patients treated with chlorpromazine, 12 treated with phenothiazine compounds with piperazine ring in the side chain. The investigations were repeated 30-50 min. after oral administration of trihexiphenidil 5 mg. In variant I typical excitability curves were obtained and 5 phases could be discerned in them. In patients treated with piperazine-containing phenothiazine derivatives inducting more significant parkinsonian effects phase III - depression - was significantly shortened, and the excitability was raised in phase IV. In variant II phases III and IV were reversed and in phase IV a rise in excitability was observed in place of depression. In variant II in the group of drug-induced parkinsonism as compared with controls the rise in exictability was greater in phase III and depression in phase IV was smaller. The effect of trihexiphenidil in variant I depended on the initial state. In controls and in patients treated with chlorpromazine trihexiphenidil reduced the duration of phase III of depression and decreased its intensity. In atients treated with phenothiazines containing the piperazine ring depression in phase III was weak but increased after trihexiphenidil administration and increased excitability in phase IV was decreased. The curves became similar to those obtained in controls. In variant II in the control group excitability in phase III increased after trihexiphenidil administration.
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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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KW-5338 (domperidone), a new dopamine antagonist, is considered to be an agent to cross the blood-brain barrier with difficulty. The antagonistic activities of KW-5338 against L-DOPA were investigated, KW-5338 showed a strong anti-emetic action against L-DOPA induced emesis in beagle dogs (ED50=0.056 mg/kg (p.o.)) and restored the L-DOPA induced depression of intestinal motility to some extent, while it did not antagonize anti-tremorine activities of L-DOPA and trihexyphenidyl in mice. These results suggest that KW-5338 prevents side effects of L-DOPA such as nausea, vomiting and constipation, without reduction in therapeutic effects of L-DOPA in Parkinson's disease.
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We report on a 47-year-old female patient with Sheehan's syndrome who developed delayed-onset dystonia following recovery from central pontine myelinolysis. The dystonia was observed in the head, neck and limbs during active movement. MRI scan demonstrated a discrete lesion in the central pons without involving the basal ganglia. The action dystonia was markedly improved by giving trihexyphenidyl. The patient showed that generalized dystonia can be induced by an isolated pontine myelinolysis. There have been four other cases reported in the literature. On reviewing all five cases, we conclude that delayed-onset dystonia following central pontine myelinolysis usually presents with generalized action dystonia and has a beneficial response to trihexyphenidyl.
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All autopsy samples received at the National Institute of Forensic Toxicology during the years 1986-1996 which contained anticholinergic antiparkinsonian drugs were reviewed. Of a total of 69 cases, orphenadrine was present in 57 (83%), biperiden in 8 (12%), procyclidine in 3 (4%), and trihexyphenidyl/benzhexol in 1 (1%) of the subjects. The measured concentrations were assessed in light of previously published data. Of 21 cases where causality between drug ingestion and death was classified as either highly probable (18/21) or possible (3/21), all subjects tested positive for orphenadrine. In the autopsy samples from these patients, orphenadrine concentrations in the 4.5-600 mumol/l range (mean 62.5 mumol/l, SD 126.5 mumol/l) were determined. Because of a low national autopsy rate, there is reason to believe that the actual numbers of drug-related deaths in this period may have been significantly higher. It is concluded that orphenadrine is responsible for a disproportionally high number of overdose deaths.
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Male Wistar rats were trained to press a lever with food reinforcement according to a continuously reinforced schedule (CRF). Afterwards, rats were subjected to three experimental sessions (30 min each) during which responding was rewarded according to a progressive ratio schedule (following an initial 2-min CRF period, the number of presses necessary for the pellet delivery was doubled every second minute). Responding during the first half of each session, i.e., pressing for food, was maintained at a significant level, whereas it was almost suppressed during the second part of the session. As compared to controls (200 +/- 20 presses/30 min) animals given amfonelic acid (0.5, 1 mg/kg IP), methylphenidate (4, 8 mg/kg IP), caffeine (16 mg/kg IP), cocaine (4 mg/kg IP), oxolinic acid (32 mg/kg IP), nomifensine (4 mg/kg IP), DR 250 (2, 4 mg/kg IP) and d-amphetamine (0.25, 0.5, 1 mg/kg IP) showed an increased rate of responding ranging from 400 to 950 presses/30 min. In contrast, apomorphine, MK 486 + L-dopa, trihexyphenidyl, imipramine, salbutamol and diazepam did not increase responding. These results suggested that this test is highly sensitive for psychomotor stimulants and perhaps for their ability to enhance the reinforcing value of the reward or stimuli associated with the reward. Such activity seemed related to a catecholaminergic substrate since the increase of responding induced by amphetamine was blocked by pimozide, d,l-propranolol and prazosin.
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Task specific tremors in musicians have been mainly described as primary bowing tremor in string instrumentalists in relatively small sample sizes. Our aim was to describe epidemiology, risk factors, phenomenology and treatment options of this disorder in 23 musicians of different instruments.
To clarify the role and mechanism of the 5-HT1A receptor in modulating extrapyramidal motor disorders, we studied the actions of 5-HT1A agonists in the mouse pole test, a valid model of parkinsonian bradykinesia. Haloperidol markedly delayed pole-descending behavior of mice in the pole test, and this effect was alleviated by the antiparkinsonian agent trihexyphenidyl (a muscarinic antagonist). The selective 5-HT1A agonists, 8-hydroxydipropylaminotetraline (8-OH-DPAT) and tandospirone, significantly attenuated haloperidol-induced bradykinesia in a dose-dependent manner. The alleviation of haloperidol-induced bradykinesia by 8-OH-DPAT was completely antagonized by WAY-100135 (a selective 5-HT1A antagonist), but was unaffected by cerebral 5-HT depletion with p-chlorophenylalanine (PCPA) treatment (300 mg/kg, i.p. for 3 days). These results suggest that 5-HT1A agonists improve extrapyramidal motor disorders associated with antipsychotic treatments by stimulating the postsynaptic 5-HT1A receptor.
Classical galactosemia is an autosomal recessive inborn error of metabolism leading to toxic accumulation of galactose and derived metabolites. It presents with acute systemic complications in the newborn. Galactose restriction resolves these symptoms, but long-term complications, such as premature ovarian failure and neurological problems including motor dysfunction, may occur despite adequate treatment. The objective of the current study was to determine the frequency and phenotype of motor problems in adult patients with classical galactosemia. In this cross-sectional study, adult patients with a biochemically confirmed diagnosis of galactosemia attending our clinic were assessed with an interview and neurological examination and their notes retrospectively reviewed. Patients were classified according to the presence/absence of motor dysfunction on examination. Patients with motor dysfunction were further categorized according to the presence/absence of reported motor symptoms. Forty-seven patients were included. Thirty-one patients showed evidence of motor dysfunction including: tremor (23 patients), dystonia (23 patients), cerebellar signs (6 patients), and pyramidal signs (4 patients). Tremor and dystonia were often combined (16 patients). Thirteen patients reported motor symptoms, with 8 describing progressive worsening. Symptomatic treatment was effective in 4 of 5 patients. Nonmotor neurological features (cognitive, psychiatric, and speech disorders) and premature ovarian failure were more frequent in patients with motor dysfunction. Motor dysfunction is a common complication of classical galactosemia, with tremor and dystonia the most frequent findings. Up to one third of patients report motor symptoms and may benefit from appropriate treatment. Progressive worsening is not uncommon and may suggest ongoing brain damage in a subset of patients.
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Cerebral calcifications are a cause of secondary dystonia and may be an uncommon complication of radiotherapy. We report a very severe case of generalized dystonia due to postradiotherapy basal ganglia calcifications.
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Studies were performed on 5 patients with idiopathic dystonia-parkinsonism, each of whom had minor dystonic movements and parkinsonian symptoms with marked diurnal fluctuation. Levels of homovanillic acid and 5-hydroxyindoleacetic acid were not different from those in controls. Considerable improvement in dystonic movements and parkinsonian symptoms was obtained with a small dose of L-dopa, trihexyphenidyl hydrochloride, amantadine, or bromocriptine hydrochloride. Electrophysiological investigation confirmed that the dystonic movements, which became remarkably worsened on attempted movement, contributed importantly to the diurnal fluctuation of symptoms.
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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1. The influence of pharmacological pretreatment (pyridostigmine, benactyzine and trihexyphenidyle), designated PANPAL, on soman-induced cholinergic and stressogenic effects as well as on the efficacy of antidotal treatment (HI-6 plus obidoxime) in rats was studied. 2. PANPAL prophylaxis significantly decreased soman-induced cholinesterase inhibition in blood, brain and diaphragm as well as stressogenic effects of soman (an increase in plasma corticosterone level and liver tyrosine aminotransferase activity). 3. PANPAL pretreatment did not improve the efficacy of HI-6 in combination with benactyzine on soman-induced anticholinesterase and stressogenic effects. 4. These findings confirm that PANPAL prophylaxis can improve prognosis of soman poisoning especially by protection of cholinesterases.
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1 The present study examined the role of muscarinic receptors in the modulation of noradrenaline (NA) release in the guinea-pig isolated distal colon. The spontaneous endogenous NA overflow assayed by HPLC-ED was taken as an index of NA release from enteric noradrenergic nerve terminals. 2 Physostigmine (10 microM) significantly enhanced spontaneous endogenous NA overflow. Hyoscine (muscarinic antagonist), (R)-(-)-trihexyphenidyl and telenzepine (M1-selective antagonists), and 11[[2-[(diethylamino)methyl]-1-piperydil]acetyl]-5,11 -dihydro-6H-pyrido[2,3-b][1,4]benzodiazepine-6-one (AF-DX 116, M2-selective antagonist) inhibited NA overflow in a concentration dependent manner, with the following EC50 values: 131.74 (18.19-953.96), 101.62 (58.83-175.60), 150 (60-330), 30 (5-170) nM, respectively. 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP, M1- and M3-selective antagonist) had no significant effect up to 100 microM. 3 The muscarinic agonist oxotremorine inhibited NA overflow in a concentration dependent manner, with an EC50 value of 0.67 (0.30-1.51) microM. The response to oxotremorine was inhibited by muscarinic antagonists with the following order of potency: hyoscine = (R)-(-)-trihexyphenidyl = telenzepine > 4-DAMP > AF-DX 116. 4 In the presence of 3 microM tetrodotoxin (TTX), the effect of oxotremorine and 4-DAMP was unchanged, while hyoscine, (R)-(-)-trihexyphenidyl, telenzepine and AF-DX 116, instead of inhibiting, significantly enhanced NA overflow. 5 The present results indicate that, in the guinea-pig colon, endogenous acetylcholine sustains spontaneous NA release by activating muscarinic receptors possibly located on interneurones. In addition, inhibitory muscarinic receptors may exist on adrenergic terminals.
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A double blind trial on the effects of 2 mg of benzhexol on memory was performed on thirteen elderly subjects without cognitive impairment. The tests given 90 minutes after the drug or placebo involved learning a list of ten words, a paired-associate learning task, learning a short story and a test of digit span. Subjects were asked to recall the word list one minute after an interfering task, and 6 items from the story directly. Digit span involved immediate recall and the paired learning was measured by the number of trials necessary to learn. All tests were significantly impaired by the benzhexol except for digit span. This suggests that muscarinic blocking drugs should be avoided in the elderly, as they mimic the memory deficits found in senile dementia of Alzheimer type.
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The two antiparkinsonian drugs procyclidine and benzhexol are presently finding considerable favor for their euphoric hallucinogenic effects among drug abusers in some countries. In anticipation of their possible scheduling in national drug laws, gas chromatography-mass spectrometry (GC-MS) methods for their detection in urine will be required. However, because of uncertainty of the metabolic fate of the two drugs in humans, the urinary target analytes for GC-MS detection were not well defined. The problem was addressed in the present study in which it was found that mono-hydroxy metabolites, where hydroxylation took place at the cyclohexane ring in both drugs, could be endorsed as the major target analytes. The metabolites could only be detected as the mono- and/or di-trimethylsilyl (TMS) derivatives. The predominance of either derivative depended on the temperature and time of heating with the derivatizing reagent. Because of the basic properties of the hydroxy metabolites, analytic method optimization was needed for their detection in urine included extraction under basic pH conditions. Urine hydrolysis with β-glucuronidase did not have an effect on the recovery of the metabolites, but was usually performed in search for other drugs. Because of the relative abundance of ions, the electron impact mass spectra of the mono-TMS derivatives and the chemical ionization (CI) mass spectra of the mono- and di-TMS derivatives of the hydroxy metabolites of both drugs were found to be more structurally informative. The CI mass spectra of the di- TMS derivatives have the additive advantage of being potentially useful for quantitative analysis.
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Finding about structural and functional relation between NMDA receptors specific binding and phencyclidine sites was very important for a possible modulation of NMDA receptors' function. We have therefore got interested what would happen with EEG and vegetative patterns of PS in the case when NMDA receptors function is modulated by blocking of phencyclidines' site. Consequently, we studied the effects of Trihexyphenydil, the structural analog of phencyclidine, on neocortical and hippocampal electrical activity in SWC. On cats (n=5) metallic electrodes were implanted under Nembutal anesthesia. EEG registration lasting 12 hr daily started after animals' recovery. Trihexyphenydil was administered intraperitoneally (0.5 mg/kg - 1 mg/kg). Statistical processing was made by Students' t-test. Trihexyphenydil resulted in dissociated triggering of PS. Rapid eye movements and PGO waves appeared on the face of active waking state. Therefore on the background of behavioral active waking according to electrical activity of the visual cortex and rapid eye movements, electrographic patterns of paradoxical sleep were recorded. Thus in our experiments it was shown firstly that the mechanism of hallucinogenic action of Trihexyphenydil is closely related to the disturbance of paradoxical sleep integrity. Blocking of NMDA receptors phencyclidines site and therefore functional modulation of these receptors produce the splitting of PS patterns and their intrusion in waking state. Such an effect never takes place in normal conditions since the waking system has the powerful inhibitory influence on the PS triggering system. Suggestion is make that NMDA glutamate receptors must be involved in mechanisms providing structural and functional integrity of PS and that fulfillment of such function is possible in the case when the NMDA receptors phencyclidine site isn't in blocked state. Normal functioning of NMDA receptors phencyclidine site represents the mechanism which inhibits and/or hampers appearance of hallucination. NMDA glutamate receptors, possessing phencyclidine site, are implicated in the mechanisms providing structural and functional integrity of PS.
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Our findings confirmed our hypothesis that primary bowing tremor is similar to primary writing tremor, with regard to phenomenology and epidemiology as well as tremor frequency. There was no difference in tremor frequency between conditions, suggesting that tremor is not influenced by bimanual coordination or bowing speed. Our findings thus provide new phenomenological aspects and may contribute to a better understanding of primary bowing tremor.
In view of the coincidence of antiviral and antiparkinsonism activities of amantadine four antiparkinsonism drugs, NorakinR (triperiden), ParkopanR (trihexyphenidyl), AntiparkinR (diethylbenzhydramine) and AkinetonR (biperiden) were tested for antiviral activity in various virus-cell systems. Norakin inhibited the replication of influenza A viruses in chick embryo fibroblast, MDCK and Ehrlich ascites tumour cells. It also inhibited the replication of measles virus in Vero cells, 50% inhibitory concentrations being 2-6 micrograms/ml. The drugs were also active against influenza B virus. Several representatives of other virus families, e.g. vaccinia, vesicular stomatitis, polio type 1 and herpes simplex type 1 viruses were insensitive to the compounds.
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Movement Disorder-Childhood Rating Scale (MD-CRS) is a new tool for assessment of movement disorders during developmental age.
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(2-Hydroxyethyl) methyldiethylammonium iodide (diethylcholine; DEC) was tested against trihexyphenidyl for its ability to block tremors in two animal models of Parkinsonism tremors. Both DEC (75 mg/kg) and trihexyphenidyl (10 mg/kg) antagonized physostigmine tremors in mice. Both drugs also blocked tremors in rats which received intracaudate injections of carbachol. DEC was more efficacious than trihexyphenidyl in the rat model. No dose-related inhibition of tremors was seen for trihexyphenidyl (5--20 mg/kg) but inhibition by DEC was dose-related (25--50 mg/kg). The ED50 for tremor inhibition in the rat model by DEC was 33 mg/kg. DEC was also shown to cross the blood-brain barrier in mice. The probable mechanism of action of DEC is discussed.
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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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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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Physical examination had a low predictive value in the detection of involved muscles. There was a significant correlation between changes in EMG total scores and changes in clinical measurements. We observed increased EMG activity in 20% of noninjected muscles after BTA treatment and in 27% of noninjected muscles after trihexyphenidyl treatment. A switch from one most active muscle to another was seen equally in both groups and had no influence on clinical response.
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ADR is commonly experienced by children with dystonia, regardless of dystonia severity or aetiology. A wide variation in drug management of dystonia was identified. Collectively these findings highlight the need for a rational approach to the pharmacological management of dystonia in childhood.
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Three novel GCH1 mutations were identified in two patients. One patient was a compound heterozygote with asymptomatic carrier parents. The clinical phenotype of patients with and without GCH1 mutations was similar.
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