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Kemadrin (Procyclidine)

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Generic Kemadrin is a synthetic antispasmodic compound of relatively low toxicity. In Parkinson's disease, the deficiency of dopamine causes overactivity of acetylcholine. This causes some of the symptoms of the disease. Generic Kemadrin works by blocking the receptors that acetylcholine acts on.

Other names for this medication:

Similar Products:
Sinemet, Requip


Also known as:  Procyclidine.


Generic Kemadrin is used to treat parkinsonism and extrapyramidal dysfunction caused by tranquilizer therapy.

In Parkinson's disease, the deficiency of dopamine causes overactivity of acetylcholine. This causes some of the symptoms of the disease. Generic Kemadrin works by blocking the receptors that acetylcholine acts on. This reduces the activity of the acetylcholine and helps restore the balance of acetylcholine and dopamine in the brain. In this way, Generic Kemadrin helps to control some of the symptoms of Parkinson's disease.

Generic name of Generic Kemadrin is Procyclidine.

Brand name of Generic Kemadrin is Kemadrin.


Take Generic Kemardin tablets orally.

Take Generic Kemadrin with or without food.

Do not drink alcohol during Generic Kemadrin usage.

Be careful if you drive or do anything that requires you to be awake and alert while using Generic Kemadrin.

The dosage and the kind of medicine depend on the disease and its prescribed treatment.

If you want to achieve most effective results do not stop taking Generic Kemadrin suddenly.


If you overdose Generic Kemadrin and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature 15 and 30 degrees C (59 and 86 degrees F) away from away from moisture, light and heat. Do not store in the bathroom. Throw away any unused medicine after the expiration date. Keep out of the reach of children in a container that small children cannot open.

Side effects

The most common side effects associated with Kemadrin are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Generic Kemadrin if you are allergic to Generic Kemadrin components.

Be careful with Generic Kemadrin if you are pregnant, planning to become pregnant or breast-feeding.

Do not take Generic Kemadrin if you have closed angle glaucoma, have obstruction of the stomach or intestines, have urinary retention.

Generic Kemardin is not recommended for children.

Be careful if you are elderly aged person.

Be careful with Generic Kemadrin if you have decreased kidney function, have decreased liver function; have the risk of glaucoma.

Be careful with Generic Kemadrin if you take amantadine; antihistamines, eg. brompheniramine, chlorphenamine; antispasmodics, eg. hyoscine; antipsychotics, eg. chlorpromazine, clozapine; certain antisickness medicines, eg. promethazine, prochlorperazine, meclozine, cyclizine; certain medicines for abnormal heartbeats (antiarrhythmics), eg. disopyramide, propafenone; MAOI antidepressants, eg. Phenelzine; medicines for urinary incontinence, eg. oxybutynin, flavoxate, tolterodine, propiverine, trospium; memantine; muscle relaxants, eg baclofen; nefopam; other anticholinergics, eg. trihexyphenidyl, orphenadrine; tricyclic or related antidepressants, eg. amitriptyline, maprotiline.

Avoid alcohol.

Be careful when you are driving machine.

It can be dangerous to stop Generic Kemadrin taking suddenly.

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A case of Gilles de la Tourette syndrome in a mildly mentally retarded adult female is described. The clinical features, natural history and response to treatment were typical of the condition but the association with mental retardation, epilepsy and psychotic phenomena were unusual.

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We examined the ability of a range of tricyclic antidepressants (TCADs) and phenothiazine derivatives and their metabolites to inhibit the N-methyl-D-aspartate (NMDA) receptor complex using a [3H]MK801 binding assay. Desmethylation of the side chain of both TCADs and phenothiazines increased their potency against [3H]MK801 binding, as did removal of Cl substituted on the conjugated ring. Other side chain modifications further increased the potency of phenothiazines such as in the case of ethopropazine. Generally, the increase in potency of drugs at the NMDA receptor complex was associated with a decrease in the potency at other sites of action of these compounds. This finding suggests that it may be possible to separate the established actions of these compounds from their NMDA inhibitory effects. We also examined the mechanism of action of a number of compounds by monitoring drug effects on the dissociation rate of [3H]MK801 in the presence of Mg++. Phenothiazines and TCADs generally slow the dissociation of [3H]MK801, although to differing extents. Drugs such as 9-aminoacridine, cyproheptadine and ethopropazine also slowed the dissociation rate. These findings suggest a Zn++-like action of these compounds. In contrast, mecamylamine, methapyrilene and procyclidine had very little effect on the dissociation rate, suggesting a competitive action at the [3H]MK801/phencyclidine binding site. Chlorpromazine at low concentrations slowed the dissociation rate, while increasing it at higher concentrations. Thus, chlorpromazine demonstrated both Zn++ and Mg++-like effects. These studies demonstrate novel inhibitory actions of TCAD and phenothiazine derivatives at the NMDA receptor complex that are apparently mediated by the Zn++ binding site.

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Oxyphenonium prevents FDM in chicks. The ineffectiveness or partial effectiveness of other compounds, coupled with the high concentrations of effective compounds required to prevent FDM, suggests that muscarinic antagonists act to prevent FDM, either at sites distant from the retina, or through a nonmuscarinic mechanism, on which only some of these drugs act.

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A transdermal patch system containing procyclidine, an N-methyl-d-aspartate receptor antagonist possessing anticholinergic action, and physostigmine, a reversible cholinesterase inhibitor, was developed, and its prophylactic efficacy against soman intoxication was investigated. Male rhesus monkeys were shaved on the dorsal area, attached with a matrix-type patch with various sizes (2×2 to 7×7 cm) for 24 or 72 h, and challenged with 2×LD₅₀ doses (13μg/kg) of soman. The smallest patch size for the protection against lethality induced by soman intoxication was 3×3cm, resulting in blood procyclidine concentration of 10.8 ng/ml, blood physostigmine concentration of 0.54 ng/ml, which are much lower concentrations than maximum sign-free doses, and blood cholinesterase inhibition of 42%. The drug concentrations and enzyme inhibition rate corresponding to a diverging point of survivability were presumably estimated to be around 7 ng/ml for procyclidine, 0.35 ng/ml for physostigmine, and 37% of enzyme inhibition. Separately, in combination with the patch treatment, the post treatment consisting of atropine (0.5 mg/kg) plus 1-[([4-(aminocarbonyl)pyridinio]methoxy)methyl]-2-[(hydroxyimino)methyl]pyridinium (HI-6, 50 mg/kg) exerted protection against 5×LD₅₀ challenge of soman, which means the posttreatment remarkably augmented the efficacy of the patch. Additionally, it was found that brain injuries induced by soman toxicity were effectively prevented by the patch treatment according to histopathological examinations. These results suggest that the patch system could be an effective alternative for diazepam, an anticonvulsant, and the current pyridostigmine pretreatment, and especially in combination with atropine plus HI-6, could be a choice for quality survival from nerve-agent poisoning.

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After pretreatment of adult male Wistar rats with phenobarbital, a well-known cytochrome P-450 inductor, the liver microsomal cytochrome P-450 content increased significantly compared to that of control rats. At the same time the amount of procyclidine, metabolized by the 9000 g supernatant fraction of rat liver homogenate fortified with a NADPH generating system, increased significantly as well. However when related to the liver microsomal cytochrome P-450 content, the amount of metabolized procyclidine does not differ anymore between phenobarbital treated and control rats. Therefore phenobarbital induces the in vitro metabolism of procyclidine.

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In study 1, baseline IL-6 (P= 0.003) and IL-8 levels (P= 0.001) were higher in IBS than in controls. Pyridostigmine stimulated the release of IL-6 and GH, but not IL-8 or IL-10; these responses were significantly augmented in IBS patients relative to controls. The IL-6 level following pyridostigmine administration correlated significantly with the symptom score (P < 0.01). In study 2, IL-6 rose following pyridostigmine in IBS but not depression and procyclidine blocked the rise. The GH response was abolished by procyclidine in all three groups.

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The purpose of the present study was to examine the efficacy of a triple combination of drugs with adequate anticonvulsant effects and a dual combination with inadequate anticonvulsant effects followed by adjunct therapy. The results showed that combined intramuscular injections of HI-6 (42 mg/kg), atropine (14 mg/kg), and avizafone (3 mg/kg) administered 1, 16, and 31 min. after exposure to a soman dose of 4 x LD(50) completely terminated seizures with a moderate mortality rate (25%). When the soman dose was lowered to 3 x LD(50) the anticonvulsant effect was complete, and no rats died within 24 hr. Rats challenged with 5 x LD(50) of soman all died within 10 min. Without avizafone in the combination, seizures induced by 3 or 4 x LD(50) of soman could not be terminated unless an adjunct therapy consisting of procyclidine (6 mg/kg), diazepam (10 mg/kg), and pentobarbital (30 kg/kg) was given, and the mortality rate was comparatively high (78%). Administration of the adjunct therapy alone 6-16 min. after 4 x LD(50) of soman stopped the seizure activity, but all the rats died within 24 hr. Marked neuropathology was found in the piriform cortex and amygdala, whereas the hippocampal CA1 field was effectively protected when both the triple combination and the dual combination plus adjuncts had stopped seizures 35-55 min. after onset. It is concluded that termination of soman-induced seizures at an early stage (<20 min.) is crucial to avoid neuronal pathology.

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A group of antiparkinson drugs (benactyzine, biperiden, caramiphen, procyclidine, and trihexyphenidyl) has been shown to possess both anticholinergic and antiglutamatergic properties, making these agents very well suited as anticonvulsants against nerve agents. The first purpose of this study was to make a comparative assessment of the anticonvulsant potencies of the antiparkinson agents when microinfused (1 microl) into the seizure controlling area tempestas (AT) of rats 20 min before subcutaneous injection of soman (100 microg/kg). The second purpose was to determine whether cholinergic and/or glutamatergic antagonism was the effective property. The results showed that only procyclidine (6 microg) and caramiphen (10 microg) antagonized soman-induced seizures. Cholinergic, and not glutamatergic, antagonism was likely the active property, since atropine (100 microg), and scopolamine (1 microg) caused anticonvulsant effects, whereas MK-801 (1 microg), and ketamine (50 microg) did not. Soman (11 nmol) injected into AT resulted more frequently in clonic convulsions than full tonic-clonic convulsions. AT may serve as both a trigger site for soman-evoked seizures and a site for screening anticonvulsant potencies of future countermeasures.

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Didepil seems to be an effective antiepileptic agent in maximal generalized seizures as well as in temporal lobe seizures.

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Prepulse inhibition (PPI) of the startle response refers to a reduction in response to a strong stimulus (pulse) if this is preceded shortly by a weak non-startling stimulus (prepulse). Consistent with theories of deficiencies in early stages of information processing, PPI is found to be reduced in patients with schizophrenia. Atypical antipsychotics are found to be more effective than typical antipsychotics in improving PPI in this population. Anticholinergic drugs are often used to control extrapyramidal symptoms induced by antipsychotic medication, especially by typical antipsychotics, in schizophrenic patients and are known to disrupt cognitive functions in both normal and schizophrenic populations. The effect of anticholinergics on PPI in schizophrenia has not yet been examined. This study determined the effects of procyclidine, an anticholinergic drug, on PPI in patients with schizophrenia given risperidone or quetiapine and not on any anticholinergic drugs, employing a placebo-controlled, cross-over design. Under double-blind conditions, subjects were administered oral 15 mg procyclidine and placebo on separate occasions, 2 weeks apart, and tested for acoustic PPI (prepulse 8 dB and 15 dB above the background and delivered with 30-ms, 60-ms and 120-ms prepulse-to-pulse intervals). Procyclidine significantly impaired PPI compared to placebo (assessed as percentage reduction) with 60-ms prepulse-to-pulse trials and increased the latencies to response peak across all trials. The use of anticholinergics needs to be carefully controlled/examined in investigations of information processing deficits using a PPI model and reduced to the minimum level in clinical care of schizophrenia.

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There is great interest in testing neuroprotectants which inhibit the neurodegeneration that results from excessive activation of N-methyl-D-aspartate (NMDA) receptors. As an alternative to in vivo testing in animal models, we demonstrate here the use of a complex in vitro model to compare the efficacy and toxicity of NMDA receptor inhibitors. Organotypic hippocampal slice cultures were used to compare the effectiveness of the Alzheimer's disease drug, memantine, the Parkinson's disease drug, procyclidine, and the novel neuroprotectant, gacyclidine (GK11), against NMDA-induced toxicity. All three drugs are non-competitive NMDA receptor open-channel blockers that inhibit excitotoxic injury, and their neuroprotective capacities have been extensively investigated in vivo in animal models. They have also been evaluated as potential countermeasure agents against organophosphate poisoning. Quantitative densitometric image analysis of propidium iodide uptake in hippocampal regions CA1, CA3 and DG, showed that, after exposure to 10microM NMDA for 24 hours, GK11 was the most potent of the three drugs, with an IC50 of about 50nM and complete protection at 250nM. When applied at high doses, GK11 was still the more potent neuroprotectant, and also the least cytotoxic. These findings are consistent with those from in vivo tests in rodents. We conclude that the slice culture model provides valuable pre-clinical data, and that applying the model to the screening of neuroprotectants might significantly limit the use of in vivo tests in animals.

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In an era when it is generally believed that the acute symptoms of schizophrenia can be controlled pharmacologically, the case of a young man who has remained almost continuously floridly psychotic for 13 years, despite treatment, is disquieting. Conventional psychiatric treatment appears to be rendered impotent. It is in this context that it may be of interest to report a summary of the proceedings of a Special Problems Conference held at the Institute of Psychiatry on 18 February 1985 to discuss such a case.

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The authors administered haloperidol 4.5 mg t.i.d. to 33 drug-free schizophrenic patients. Ten patients did not receive anything else (group HPL), while ten patients received procyclidine 5 mg t.i.d., and 13 patients were given promethazine 25 mg t.i.d. (groups HPRC and HPRM respectively) in addition. Seven patients dropped out of the HPL group and three out of the HPRM group, but none out of the HPRC group. These drop outs were due to the development of early extrapyramidal side effects, which were absent in the HPRC group. The findings suggest that antiparkinson prophylaxis is useful during commencement of therapy with high-potency neuroleptic agents.

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Compliance to the prescription of anticholinergic drugs in 274 consecutive schizophrenic outpatients has been assessed retrospectively from their clinical records. Ten point four percent of the sample (22 patients) took these drugs in amounts greater than those prescribed. Some possible explanations of this excessive use are discussed.

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Balamuthia mandrillaris is a free-living protist pathogen that can cause life-threatening granulomatous amoebic encephalitis. Given the lack of effective available drugs against B. mandrillaris encephalitis with a mortality rate of more than 90%, here we screened drugs, targeting vital cellular receptors and biochemical pathways, that are already in approved clinical use for their potential clinical usefulness. Amoebicidal assays were performed by incubating B. mandrillaris with drugs (3 × 10(5) cells/0.5 mL/well) in phosphate buffered saline for 24 h and viability was determined using Trypan blue exclusion staining. For controls, amoebae were incubated with the solvent alone. To determine whether effects are reversible, B. mandrillaris were pre-exposed to drugs for 24 h, washed twice, and incubated with human brain microvascular endothelial cells, which constitute the blood-brain barrier as food source, for up to 48 h. Of the ten drugs tested, amlodipine, apomorphine, demethoxycurcumin, haloperidol, loperamide, prochlorperazine, procyclidine, and resveratrol showed potent amoebicidal effects, while amiodarone and digoxin exhibited minimal effectiveness. When pre-treated with these drugs, no viable trophozoites re-emerged, suggesting that drugs destroyed parasite irreversibly. Based on the in vitro assay, amlodipine, apomorphine, demethoxycurcumin, haloperidol, loperamide, prochlorperazine, procyclidine, and resveratrol are potential antimicrobials for further testing against B. mandrillaris encephalitis. These findings may provide novel strategies for therapy but further research is needed to determine clinical usefulness of aforementioned drugs against granulomatous amoebic encephalitis caused by B. mandrillaris, and other free-living amoebae, such as Acanthamoeba spp., and Naegleria fowleri.

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On the basis of the hypothesis that there is a common structural basis for central nervous system (CNS) drug action consisting primarily of an aromatic group and a nitrogen atom, a four-point model for a common pharmacophore is defined with use of five semirigid CNS-active drug molecules: morphine, strychnine, LSD, apomorphine, and mianserin. Two of the points of the model represent possible hydrophobic interactions between the aromatic group and the receptor, while the other two represent hydrogen bonding between the nitrogen atom and the receptor. The model is then extended by the inclusion of nine additional CNS-active drug molecules: phenobarbitone, clonidine, diazepam, bicuculline, diphenylhydantoin, amphetamine, imipramine, chlorpromazine, and procyclidine, each being chosen as a key representative of a different CNS-active drug class or neurotransmitter system. Consideration of all phenyl group and nitrogen atom combinations, as well as all feasible conformations, shows that all nine molecules closely fit the common model in low-energy conformations. It is proposed that the model may eventually be used to design CNS-active drugs by mapping the relative locations of secondary binding sites. It can also be used to predict whether a given structure is likely to show CNS activity: a search over 1000 entries in the Merck Index shows a high probability of CNS activity in compounds fitting the common structural model.

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After intraperitoneal administration of procyclidine, eight metabolites were isolated from rat urine. They were identified as 1-(4-oxocyclohexyl)-1-phenyl-3-(1-pyrrolidinyl)-1-propanol, 1-(cis-4-hydroxycyclohexyl)-1-phenyl-3-(1-pyrrolidinyl)-1-propanol, 1-(trans-4-hydrocyclohexyl)-1-phenyl-3-(1-pyrrolidinyl)-1-propanol , (1R,3R,4S,7R)- and (1R,3R,4S,7S)-1-(cis-3,cis-4-dihydroxycyclohexyl)-1-phenyl-3-(1-py rrolidinyl)- 1-propanol, (1R,3R,4R,7R)- and (1R,3R,4R,7S)-1-(cis-3,trans-4-dihydroxycyclohexyl)-1-phenyl- 3-(1-pyrrolidinyl)-1-propanol, and one of both (1R,3S,4R,7R)- or (1R,3S,4R,7S)- 1-(trans-3,trans-4-dihydroxycyclohexyl)-1-phenyl-3-(1-pyrrolidinyl )-1-propanol by comparative TLC, GLC-MS and 13C-NMR spectroscopy.

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To determine whether the use or the withdrawal of anticholinergic drugs (benzhexol or benztropine or biperiden or orphenadrine or procyclidine or scopolamine or trihexylphenidyl) were clinically effective for the treatment of people with both neuroleptic-induced TD and schizophrenia or other chronic mental illnesses.

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Vomiting is one of the most distressing adverse effects of cancer chemotherapy. Metoclopramide by continuous infusion (400 micrograms/kg/h after a loading dose of 2.5 mg/kg) is a novel administration method for optimizing efficacy. A two-year-old boy developed urinary retention on three occasions, once accompanied by priapism and slurred speech, while receiving a continuous infusion. This was reversed by procyclidine, suggesting that it may have been a dystonic reaction.

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Trihexyphenidyl, biperiden and procyclidine are anticholinergic drugs produced as racemates for the treatment of Parkinson's disease. This paper describes a simple and sensitive LC-MS method for the simultaneous determination of these compounds in human serum. An on-line sample clean-up procedure was used, where serum samples were directly injected into a "restricted-access media" pre-column. After the exclusion of the serum proteins, the drug molecules were eluted to a beta-cyclodextrin analytical column for chiral separation. The quantitation was done by electrospray ionization MS using diphenidol as an internal standard. The method developed has limits of detection of 1 ng/ml, at least two-orders-of-magnitude linear dynamic ranges (r>0.999), and RSDs of less than 10%. The system can be completely automated for increased sample throughput and unattended analyses.

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A case is described in which a patient developed acute pancreatitis following an overdose of amoxapine and procyclidine. Pancreatitis is not at this time a recognized complication of the use or abuse of these two drugs. Other drugs were used in the medical management of the complications of the overdose, but none of these are drugs known to be associated with pancreatitis. Amoxapine is probably, but not certainly the cause of the pancreatitis. Possible mechanisms for this unusual and serious complication are described.

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A double-blind, placebo-controlled, crossover study with long-term follow-up of amantadien i- Parkinson's disease was performed on 26 patients. Other antiparkinsonian medications were discontinued in all but three patients. Amantadine resulted in a statistically significant 12 percent overall improvement over placebo. Twenty of 26 patients, without breaking the code, selected amantadine for long-term usage. Ten patients continued treatment for 10 to 12 months, and an overall statistically significant improvement was noted at 2 weeks and at 1, 2, 3, and 10 to 12 months. Improvements in tremor and rigidity remained relatively constant, while there was some apparent loss of efficacy in timed tests and quality of timed tests. Amantadine appears effective in the long-term treatment of some patients with Parkinson's disease.

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Serum anticholinergic levels were measured by radioreceptor assay (RRA) in schizophrenic patients treated for drug-induced Parkinsonism; 68 patients stabilized on a single neuroleptic and an anticholinergic antiparkinsonian agent (benzhexol, benztropine or procyclidine) were assessed using the extrapyramidal side effects (EPS) scale prior to each blood sampling. Serum anticholinergic levels showed a significant inverse correlation with EPS but did not appear to be dose-related in any of the three anticholinergic drug groups. Percentage binding to proteins was significantly less with benztropine than either benzhexol or procyclidine. Serum-free anticholinergic levels correlated significantly with total serum levels in the benzhexol and procyclidine groups but not in the benztropine group. At serum levels above 4.5 pmol/ml atropine equivalents, EPS was significantly less than at levels below that. We discuss the implications of this finding and suggest practical clinical applications of measurement of serum anticholinergic levels. Serum neuroleptic and serum prolactin levels did not correlate with either dose or serum level of anticholinergics.

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In a fatal case of neuroleptic malignant syndrome, a muscle sample taken within 1 h of death showed acute myopathic features with absence of muscle glycogen and neutral lipid. These features suggest that hyperpyrexia in this syndrome may be caused by heat production from uncoupled phosphorylation in muscle and imply that the primary biochemical abnormality responsible for this uncontrolled heat production might be muscular rather than hypothalamic.

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The case history presented illustrates that, following an overdose of 'Whizz' and alcohol, a protracted dystonic syndrome can develop, clinically indistinguishable from tetanus. A prolonged period of ventilation may be necessary, but, in this case, complete recovery eventually occurred.

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This is a study of 10 men presenting with priapism and a further 25 men with impotence following priapism. Recurrent episodes of prolonged erection were a common finding and the priapism was present in most men on waking. Abnormal nocturnal tumescence was observed in one patient. The role of medical and surgical treatment was assessed.

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The authors review the literature on fatal complications of clozapine-related constipation and bowel obstruction.

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Anticholinergic drugs were the first pharmacological agents used in the treatment of Parkinson"s disease. Although levodopa and other centrally acting dopaminergic agonists have largely supplanted their use, they still have a place in treatment of the disease. As a therapeutic class, there is little pharmacokinetic information available for these drugs, which is inclusive of benztropine, biperiden, diphenhydramine, ethopropazine, orphenadrine, procyclidine and trihexyphenidyl. Pharmacokinetic information is largely restricted to studies involving young health volunteers given single doses. In general, this class of drugs is rapidly absorbed after oral administration to humans. Oral bioavailability is variable between the different drugs, ranging from 30% to over 70%. Each of the drugs appears to possess a large Vd in humans and animals, and distribution to tissues is rapid. The drugs are all characterized by relatively low clearance relative to hepatic blood flow, and appear to be extensively metabolized, primarily to N-dealkylated and hydroxylated metabolites. The available information suggests that excretion of parent drug and metabolite is via the urine and bile. Although the existence of a plasma concentration vs. therapeutic effect relationship has not been explored, there is some evidence suggesting a relationship between concentration and peripheral side effects. Elderly tolerate the drugs less well than do younger patients. There is a notable lack of pharmacokinetic information for these drugs in the elderly. The lack of pharmacokinetic information for multiple dose administration and in the elderly may be a possible hindrance in the safe and effective use of these drugs in patients with Parkinson"s disease.

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Four schizophrenic patients are reported in whom the acute development of dystonic muscle spasms, usually involving gaze deviation, was accompanied by the exacerbation or appearance of psychotic symptoms. In all cases the relationship between the neurological and psychiatric phenomena was close, and sometimes the presentation was bizarre or dramatic. The similarity of these states to the complex neuropsychiatric disturbances seen in post-encephalitic Parkinsonism is emphasised.

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The protective effect of cholinolytics such as procyclidine and atropine, in combination with carbamate prophylactics, against diisopropylfluorophosphate poisoning was examined in mice. Doses of carbamates were optimized, based on the maximum sign-free dose, the time course of cholinesterase inhibition and the protective potential against diisopropylfluorophosphate poisoning. Centrally-active physostigmine was more toxic than centrally-inactive pyridostigmine and the toxic signs of carbamates appeared to be closely related to the level of inhibition of brain cholinesterase activity. In combination with atropine, physostigmine was more effective than pyridostigmine in protecting mice intoxicated with diisopropylfluorophosphate. Moreover, centrally-active atropine sulfate was a more effective co-antidote to carbamates than centrally-inactive atropine methylnitrate. The most prominent protection was achieved with the combination of carbamates and procyclidine, a centrally-active cholinolytic showing anticonvulsion, which was also observed to prevent diisopropylfluorophosphate-induced convulsions (Kim et al., 1997). Taken together, it is suggested that procyclidine could be a possible substitute for atropine as an antidote to diisopropylfluorophosphate poisoning.

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kemadrin maximum dose 2016-06-02

The tolerance of five central muscarinic receptor antagonists has been studied in experimental animals. According to the effect on orientation-exploratory reaction, drugs were arranged in the following order of increasing toxicity: procyclidine < trihexiphenidyl < benactizine < atropine < scopolamine. For the same therapeutic index, trihexiphenidyl and benactizine were characterized by the maximum tolerance (TD50/ED50 > 10) in mice. Scopolamine and atropine exhibited anticonvulsant activity at doses exceeding the threshold values by a factor of 6.3 and 3.9, respectively. For procyclidine, the average anticonvulsant dose was threefold lower than the threshold value. Benactizine and buy kemadrin procyclidine had maximum tolerance levels in rats. The TD50/ED50 ratio for these drugs was greater than 3 (against 0.5 - 0.7 in groups treated with trihexiphenidyl, atropine and scopolamine).

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The goals of the present study were: (1) to investigate the binding properties of (R)- and (S)-procyclidine and two achiral derivatives of muscarinic M1, M2 and M4 receptor subtypes and (2) to identify the interactions which allow these receptors to discriminate between the two stereoisomers. (R)-Procyclidine showed a higher affinity for human neuroblastoma NB-OK 1 muscarinic M1 and rat striatum muscarinic M4 receptors, as compared to rat cardiac M2 receptors. (S)-Procyclidine had a 130-fold lower affinity than (R)-procyclidine for M1 and M4 receptors, and a 40-fold lower affinity for M2 receptors. Pyrrinol, the achiral diphenyl derivative with the cyclohexyl group of (S)-procyclidine replaced by a phenyl group, has an eight-fold lower affinity for M1 and M4 receptors, as compared to (R)-procyclidine, and a three-fold lower affinity for M2 receptors. buy kemadrin Hexahydro-procyclidine, the corresponding achiral dicyclohexyl compound, had a 10- to 20-fold lower affinity than (R)-procyclidine for the three receptors. The increase in binding free energy, which is observed when the phenyl and cyclohexyl groups of procyclidine are separately replaced by cyclohexyl and phenyl groups, respectively, was additive in the case of M1, M2 and M4 receptors. This indicates that the muscarinic receptor stereoselectivity was based on the coexistence of two binding sites, one preferring a phenyl rather than cyclohexyl group and the second preferring a cyclohexyl rather than a phenyl group. In addition, there were also binding sites for the hydroxy moiety and the protonated amino group of the ligands. The greater affinity and stereoselectivity of M1 and M4 muscarinic receptors for (R)-procyclidine reflected the better fit of the cyclohexyl group of (R)-procyclidine to the subsite of M1 and M4 as compared to M2 receptors.

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After pretreatment of adult male Wistar rats with phenobarbital, a well-known cytochrome P-450 inductor, the liver microsomal cytochrome P-450 content buy kemadrin increased significantly compared to that of control rats. At the same time the amount of procyclidine, metabolized by the 9000 g supernatant fraction of rat liver homogenate fortified with a NADPH generating system, increased significantly as well. However when related to the liver microsomal cytochrome P-450 content, the amount of metabolized procyclidine does not differ anymore between phenobarbital treated and control rats. Therefore phenobarbital induces the in vitro metabolism of procyclidine.

kemadrin drug classification 2015-03-02

In a series of 36 patients with acute schizophrenia flupenthixol dosage was blindly adjusted to give a fixed level of sedation. Patients were than randomly allocated to procyclidine or placebo. The patients receiving procyclidine experienced more positive schizophrenic symptoms and less severe extrapyramidal features by comparison with placebo patients. Blood levels of prolactin and flupenthixol estimated by radioimmunoassay were not significantly changed by the addition of procyclidine. Flupenthixol buy kemadrin dosage and levels and prolactin levels were significantly related. There was no significant association between clinical and laboratory measures, with the exception that a curvilinear (inverted U) relationship was demonstrated between flupenthixol levels and antipsychotic and extrapyramidal effects. This relationship may be due to the fact that, in a study of this design, patients resistant to the effects of neuroleptic medication are likely to be given the highest doses. The findings support earlier claims that anticholinergic medication has adverse effects on schizophrenic symptoms.

kemadrin storage 2016-12-08

In study 1, baseline IL-6 (P= 0.003) and IL-8 levels (P= 0.001) were higher in IBS than in controls. Pyridostigmine stimulated the release of IL-6 and GH, but not IL-8 or IL-10; these responses were significantly augmented in IBS patients relative to controls. The IL-6 level following pyridostigmine administration correlated significantly with the symptom score buy kemadrin (P < 0.01). In study 2, IL-6 rose following pyridostigmine in IBS but not depression and procyclidine blocked the rise. The GH response was abolished by procyclidine in all three groups.

kemadrin alcohol 2017-07-22

Subjects underwent testing for PPI on two occasions: once after buy kemadrin the oral administration of a placebo and once after the oral administration of procyclidine in two separate experiments. Experiment 1 examined the effects of 10 mg procyclidine, whereas experiment 2 examined the effects of 15 mg procyclidine.

kemadrin tab 5mg 2017-10-23

Extrapyramidal symptoms developed a variable time after the start of treatment buy kemadrin with oral diazoxide in 15% of a series of 100 severely hypertensive patients. Six illustrative cases are described. Treatment with diazoxide could be continued in four of these. The symptoms are usually controllable either by dosage adjustment or by the use of diazepam or procyclidine. There was no evidence of irreversibility of the extrapyramidal syndromes observed.

kemadrin tablet 2015-10-14

IBS and major depression are characterized by a pro-inflammatory profile buy kemadrin , whereas IBS patients alone exhibit an exaggerated muscarinic receptor-mediated IL-6 response.

kemadrin overdose 2015-08-14

Clozapine is an atypical antipsychotic known for its efficacy in refractory schizophrenia. However, according to different epidemiological studies clozapine can induce neutropenia in less than 3% of patients and may represent a major problem for the management of treatment-resistant patients not responding to conventional or other atypical antipsychotics. Recently, a few case of neutropenia have been reported following the addition of other medications to clozapine, notably paroxetine, risperidone, trimethoprim-sulfamethoxazole and erythromycin. In our report we present the case of Mr A., a 40-year-old Caucasian patient with a 20-year history of paranoid schizophrenia. After numerous trials with conventional antipsychotics, partial remission of psychotic symptoms was obtained with clozapine. Over the past eight years during his treatment with clozapine, the patient presented 2 episodes of neutropenia. The first episode came five years after starting clozapine and was attributed to the addition 6 weeks earlier of haloperidol (2 mg/day) to clozapine (250 mg/day) and divalproex (1,500 mg/day). Recently, one week after the addition of risperidone (2 mg/day) to clozapine (550 mg/day), leukocytes count dropped from 12 100/mm(3) to 5 700/mm(3) and neutrophils from 7 400/mm(3) to 900/mm(3). The patient was also taking haloperidol (4 mg/day), methotrimeprazine (35 mg/day), procyclidine (5 mg/day) and valproic acid (1,500 mg/day). Twelve days after discontinuation of risperidone, leukocytes and neutrophils count increased to 11,100/mm(3) and 6,300/mm(3) respectively while the treatment with clozapine was continued. The first eighteen weeks of treatment represent the period where the risk of neutropenia is the highest. In our patient neutropenia occurred 5 and 7 buy kemadrin years after starting clozapine. It is proposed that the two neutropenic episode were precipitated by adding respectively haloperidol and risperidone to clozapine. Also, divalproex can potentially cause a decrease in white blood cell count and may have contributed to the two neutropenic episode. It is suggested that drug interactions may be responsible for neutropenia in clozapine treated patients and that clozapine should not necessarily be discontinued in the presence of neutropenia. Also we propose that hematological surveillance should be done on a weekly basis for 4 to 6 weeks following the addition of psychotropic drugs known for their potential to cause neutropenia when associated with clozapine. Therefore polypharmacy may contribute to cause neutropenia in clozapine treated patients and that discontinuation of an antipsychotic should be done before introducing another one.

kemadrin dosage 2016-06-10

The present study compared the effects of buy kemadrin aprophen hydrochloride, atropine sulfate, azaprophen hydrochloride, benactyzine hydrochloride, biperiden hydrochloride, diazepam, procyclidine hydrochloride, scopolamine hydrobromide, and trihexyphenidyl hydrochloride on activity levels in rats.

kemadrin tablet cost 2017-04-15

The study presented here shows that GC-MS with ion trap detection can be used for screening post mortem blood. The method described was used to simultaneously screen for unknowns, identify basic buy kemadrin drugs present and semi-quantitate 14 drugs commonly encountered in coroner's toxicology (i.e. was used to determine whether the drugs were present in sub-therapeutic, therapeutic or greater than therapeutic amounts). The equipment used included a Varian Saturn 2000 GC-MS operating in full scan mode, a CP-3800 GC, a CP-8400 autosampler and Saturn GC-MS workstation Version 5.5 software. Post mortem blood samples were extracted using a standard liquid-liquid procedure; diethylether followed by back extraction into 0.1 M HCl. Standard curves for the 14 drugs which were semi-quantitated (amitriptyline, citalopram, clozapine, cocaine, cyclizine, diazepam, dihydrocodeine, dothiepin, methadone, mirtazapine, procyclidine, sertraline, tramadol, venlafaxine) were prepared covering the concentration range 0-1.0 ug/mL. The procedure is in routine use for coroners toxicology; semi-quantitation has been used (i) to speed-up the through put of cases where drugs are an incidental finding and (ii) for cases where the amount of sample submitted for analysis was too small to allow for screening, identification and quantitation on separate sample volumes.

kemadrin medication 2015-11-01

During the establishment of a research branch, all relevant matters encountered will be of interest to study. After having acquired a body of basal knowledge, it becomes possible to derive ideas or hypotheses for further elaboration of information. The purpose of the present study buy kemadrin was to show that therapies for nerve agent poisoning based on specific neuropharmacological approaches can have greater probability for being successful than treatment regimens based on fragmental research or serendipitous discoveries. By following the guidelines for research in experimental epilepsy, neuronal target areas for nerve agents have been identified through lesion studies, and critical receptors for pharmacological treatment have been specified through microinfusion studies of rats. Subsequent experimentations have shown that the results achieved from microinfusion studies are transferable to systemic administration. It is demonstrated that a treatment regimen developed through the novel approach is more efficacious than regimens derived from conventional research on countermeasures. A therapy consisting of HI-6, levetiracetam, and procyclidine that has been worked out along the new lines, exerts powerful anticonvulsant capacity and appears to have universal utility as a stand-alone therapy against soman intoxication in rats. It would be of great interest to examine whether the latter findings can be expanded to other animal species than rats and other classical nerve agents than soman.

kemadrin generic 2015-04-20

Irritable bowel syndrome (IBS) is a functional disorder, which has recently been buy kemadrin linked to immune activation. We tested the hypothesis that the pro-inflammatory cytokine profile in IBS is driven by the cholinergic system and determined if the responses are mediated by muscarinic receptors.

kemadrin dose 2015-09-06

We conducted a systematic review and aimed to answer the following clinical questions: What are the effects of drug treatments, surgical treatments, and physical treatments for focal and generalised dystonia? We searched: Medline, Embase, The Cochrane Library, and other important databases up to September 2013 (Clinical Evidence reviews are updated periodically; please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration ( buy kemadrin FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA).

kemadrin medicine 2017-08-30

Analogs of the potent inhibitor of glucosylceramide (GlcCer) synthase, D-threo-1-phenyl-2-palmitoylamino-3-pyrrolidino-1-propanol (P4), based on substitutions in the palmitoyl group were made by means of a stereo-selective synthetic method in order to elucidate the role of the hydrophobic portion in both the inhibitory action toward the enzyme and the biological effects. While P4 strongly inhibited GlcCer synthase with an IC(50) of 0.5 microM in vitro, it also inhibited cell growth by 50% at the concentration of 7 microM. The shorter N-acyl chain analogs including decanoyl, octanoyl, and Arava Chemotherapy Drug hexanoyl groups showed similar IC(50) values for GlcCer synthase (around 2 microM) but the hexanoyl analog exhibited only a slight inhibitory effect on cell growth, showing the dissociation between GlcCer depletion and cell growth. Several compounds which exhibit similar hydrophobicity to the hexanoyl analog of P4 were subsequently designed. We found that D-threo-1-phenyl-2-benzyloxycarbonylamino-3-pyrrolidino-1-pr opanol (PBPP) was a most potent inhibitor, showing an IC50 of 0.3 microM. In cultured cells, PBPP was able to deplete glycosphingolipids without affecting cell growth or the ceramide level.

dose of kemadrin 2016-03-27

The method was validated by comparing with published data for the dose response to NMDA and Cytoxan Cancer Drug glycine and IC(50) values for ion-channel block by Mg(2+) and MK-801.

kemadrin tablets 5mg 2015-11-11

A total of eight anticholinergic drugs (aprophen, atropine, azaprophen, benactyzine, biperiden, procyclidine, scopolamine, trihexyphenidyl) were tested in parallel with diazepam for the ability to terminate seizure activity induced by the nerve agent soman. Guinea pigs, implanted with electrodes to record cortical electroencephalographic (EEG) activity, were pretreated with pyridostigmine Br (0.026 mg/kg, i.m.) and 30 min later challenged with 2 x LD50 soman (56 microg/kg, s.c.) followed 1 min later by treatment with atropine SO4 (2 mg/kg, i.m.) and pralidoxime chloride (2-PAM Cl; 25 mg/kg, i.m.). All guinea pigs developed sustained seizure activity following this Depakote Good Reviews treatment. Dose-effect curves were determined for the ability of each drug to terminate seizure activity when anticonvulsant treatment was given either 5 or 40 min after seizure onset. Body weight gain and recovery of behavioral performance of a previously trained one-way avoidance task were measured after exposure. With the exception of atropine, all anticholinergic drugs were effective at lower doses than diazepam in terminating seizures when given 5 min after seizure onset; benactyzine, procyclidine and aprophen terminated seizures most rapidly while scopolamine, trihexyphenidyl, biperiden, and diazepam were significantly slower. When given 40 min after seizure onset, diazepam was the most potent compound tested, followed by scopolamine, benactyzine and biperiden; atropine was not effective when tested 40 min after seizure onset. For diazepam, the time to terminate the seizure was the same whether it was given at the 5- or 40-min delay. In contrast, most anticholinergics were significantly slower in terminating seizure activity when

buy kemadrin 2016-02-16

A 56-year-old lady was admitted with complaint of involuntary muscle twitching around the eyes, face and neck for two days. She had a history of low grade non-hodgkin lymphoma with completion of the first cycle of chemotherapy. Her medication on presenting consisted of Ondansetron 8 mg two times a day and Metoclopramide 10 mg three times a day (TDS). She started taking these medications 24 hours before having the above symptoms. She was clinically diagnosed with acute dystonic reactions and was also secondarily treated with anti-emetic medications. She was given IV procyclidine 10 mg stat followed by per Motrin Pediatric Dosage oral (PO) procyclidine 2.5 mg TDS. Within an hour of administering IV procyclidine her symptoms began to gradually settle down. Acute dystonic reactions are not a very rare clinical presentation in the daily practice. The above case is a good example for the clinicians dealing with acute medical admissions.

kemadrin 5mg tab 2017-09-12

Oxyphenonium prevents Buspar Low Dose FDM in chicks. The ineffectiveness or partial effectiveness of other compounds, coupled with the high concentrations of effective compounds required to prevent FDM, suggests that muscarinic antagonists act to prevent FDM, either at sites distant from the retina, or through a nonmuscarinic mechanism, on which only some of these drugs act.

kemadrin reviews 2017-09-17

A simple, sensitive and precise gas-chromatographic method for simultaneous extraction, derivatization and determination of methsuximide, ethosuximide, diphenylhydantoin, carbamazepine, phenobarbital and primidone in the presence of other drugs has been described. The method is especially useful for drug monitoring in patients on multiple anticonvulsant therapy while also on combination therapy with psychotropic drugs. It overcomes the analytical interferences between mephenytoin and phenobarbital; methsuximide and primidone; kemadrin and primidone; cholesterol and primidone; prolixin, haldol and other drugs; encountered in other methods using underivatized, trimethylsilylated or methylated drugs. As little as 0.5 microgram/ml of a drug can be determined and if needed the method can be scaled Levitra Generic Reviews down to 0.3 ml plasma. The method yielded recoveries of 97-103% with standard deviations of 0.7-1.8. For a constant check of the precision, an internal quality control using daily analysis of a sample from a frozen plasma pool supplemented with known concentrations of the anticonvulsants was used. The method is suitable for use in routine clinical laboratory.

kemadrin generic name 2017-07-09

Neuroleptic medication is used extensively to treat people with chronic mental illnesses. However, it is associated with a wide range of adverse effects, including movement disorders. Because of this, many acutely psychotic patients being treated with neuroleptic medication also receive anticholinergic drugs in order to reduce some of Motrin Syrup the associated movement side-effects.

kemadrin tablets 2017-07-09

Procyclidine and ethopropazine, widely used as anti-parkinsonian agents because of their anti-cholinergic Zithromax 500 Mg action, are also known to have NMDA antagonist properties. Unlike other NMDA antagonists, these agents-because of their anti-cholinergic action-are devoid of neurotoxic side effects. In the present study, we used a sciatic nerve ligation model that produces a hyperalgesic (neuropathic pain) state in adult rats to evaluate the ability of procyclidine or ethopropazine, either alone or in combination with an alpha(2) adrenergic agonist, to ameliorate neuropathic pain. We found that both procyclidine and ethopropazine alleviated thermal hyperalgesia in a dose dependent manner; when a marginally effective dose of these agents was combined with an ineffective dose of an alpha(2) adrenergic agonist (clonidine or guanabenz), the combination therapy provided effective and long-lasting relief from neuropathic pain. In addition, the combination therapy was free from neurotoxic or behavioral side effects, and hyperactivity, a side effect associated with procyclidine monotherapy, was counteracted by clonidine.

kemadrin drug 2017-11-27

Physicians have prescribed anticholinergic agents such as benztropine, procyclidine, biperiden and trihexyphenidyl for treatment and prophylaxis of antipsychotic-induced extrapyramidal symptoms (EPS) for decades. Anticholinergic agents can however worsen tardive dyskinesia and cause many adverse effects, including cognitive impairment. Previous studies of anticholinergic discontinuation in patients with schizophrenia receiving antipsychotics have yielded a wide range of EPS relapse rates. Improvement in cognition after anticholinergic withdrawal was observed in some studies.

kemadrin maximum dose 2016-11-15

Compliance to the prescription of anticholinergic drugs in 274 consecutive schizophrenic outpatients has been assessed retrospectively from their clinical records. Ten point four percent of the sample (22 patients) took these drugs in amounts greater than those prescribed. Some possible explanations of this excessive use are discussed.

kemadrin 5 mg 2016-07-27

The absolute configuration of the more active (-)-enantiomer of the anticholinergic trihexyphenidyl hydrochloride has been established as (R) by syntheses of (S)-(+)-procyclidine hydrochloride, whose absolute configuration has been established previously, and (S)-(+)-trihexyphenidyl hydrochloride from the same chiral building block, viz. (S)-(-)-cyclohexyl-3-hydroxy-3-phenylpropanoic acid. Both enantiomers of this chiral synthon were prepared by optical resolution of the corresponding racemate, employing (R)- and (S)-1-phenylethylamine, respectively, as resolving agents.