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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 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 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

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Prepulse inhibition (PPI) of the startle response refers to an attenuation in response to a strong stimulus (pulse) if this is preceded shortly by a weak non-startling stimulus (prepulse). Patients with schizophrenia have repeatedly been found to show reduced PPI when compared to healthy people. Anticholinergic drugs are often used to control extrapyramidal symptoms induced by antipsychotic medication in schizophrenic patients. Antipsychotic medication, in particular with atypical drugs, has been shown to improve a range of cognitive functions and normalize PPI deficits in schizophrenia, whereas anticholinergic drugs disrupt cognitive functions in both normal and schizophrenic populations and also impair PPI in experimental animals. No previous study has investigated the effects of anticholinergic drugs on human PPI.

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Procyclidine was administered to 25 chronic psychotic inpatients, stabilised on chlorpromazine, haloperidol or fluphenazine decanoate injection. We observed a significant reduction in mean serum levels of all three neuroleptic drugs which was reversed on stopping procyclidine and was inversely correlated with mean serum procyclidine levels. No significant alterations occurred on the BPRS scores or in serum prolactin levels throughout the study in any of the three groups. Possible mechanisms of this interaction and its clinical relevance are discussed.

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We found 19 studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.

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Microinfusion of anticonvulsants into the perirhinal cortex through 1 guide cannula in each hemisphere only invades a small area of this seizure controlling site in rats exposed to soman. The purpose of the present study was to examine whether infusions made through 2 cannulas in each perirhinal cortex may produce more efficacious anticonvulsant action against soman intoxication than the use of 1 cannula only in rats infused with the ionotropic antagonists procyclidine and caramiphen or the metabotropic glutamate modulators DCG-IV and MPEP. The results showed that the mere presence of indwelling double cannulas caused proconvulsant effect in response to subsequent systemic administration of soman. Both the control and caramiphen groups with double cannulas had significantly shorter latencies to seizure onset than the corresponding groups with single cannula. Procyclidine resulted in anticonvulsant efficacy, even in rats with double cannulas. In rats that received twin infusions of DCG-IV or MPEP, the anticonvulsant impact was very high, inasmuch as a majority of the rats in each group was protected against seizure activity. Drugs possessing powerful anticonvulsant potency can apparently counteract the proconvulsant effect of double cannulas, and some can even gain enhanced anticonvulsant capacity when invading a larger area of the perirhinal cortex. Perirhinal EEG recordings (electrodes in indwelling cannulas) in a separate set of rats not exposed to soman or drugs showed no differences in basal electrical activity (total power 0.5-25Hz or the theta band 4-12Hz) between groups with single or double cannulas. The intrinsic excitability and synaptic connectivity of the perirhinal cortex may be associated with the proconvulsant impact observed in rats with double cannulas when exposed to soman.

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The effects of eight antiparkinsonian anticholinergic drugs on motor activity in mice were studied. Trihexyphenidyl, biperiden, benztropine, etybenztropine, procyclidine and tropacine clearly stimulated motor activity. Orphenadrine did not change motor activity, and profenamine had sedative properties. The classification of these drugs by order of their effect on this animal model does not agree with the classification proposed by Deniker et al (1980).

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The authors found a 31% incidence of tardive dyskinesia among 261 schizophrenic outpatients treated with neuroleptics. Multiple linear logistic regression analysis revealed a higher incidence of tardive dyskinesia among elderly patients, those with longer records of hospitalization, those for whom neuroleptic medication had little therapeutic effect, and those treated with fluphenazine. Patients manifesting tardive dyskinesia tended to have fewer parkinsonian symptoms than those without the disorder, especially when tremors and akathisia were excluded from consideration. Multiple linear regression analysis indicated that brain-damaged patients and male patients were more susceptible to severe forms of the disorder, even though these factors were not implicated in its initial appearance.

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A case is reported in which platelet monoamine oxidase (MAO) activity fluctuated in the course of a schizophreniform psychosis in a way which suggests a direct relationship between low levels of MAO activity and the psychosis.

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A sensitive (50-100 pg/ml) method is described for the analysis of the anticholinergic drugs cycrimine, procyclidine and trihexyphenidyl by capillary gas chromatography with flame thermionic detection. Since these anticholinergic drugs are frequently administered in combination with antipsychotic medication for the treatment of mental illness, the potential interference by antipsychotic drugs in this assay was examined. No interference was observed from a series of antipsychotic drugs in the quantitation of cycrimine, procyclidine or trihexyphenidyl. The use of this technique to study trihexyphenidyl pharmacokinetics in man is described.

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This study assessed misuse of anticholinergic drugs in a population of 50 patients with serious mental illness who were assertively managed by a community-based outreach team in Sydney, Australia. One-third of the subjects reported having misused anticholinergics over the previous month. All anticholinergics were misused, and trihexyphenidyl (benzhexol) was misused most frequently. Most subjects misused at least one other drug as well. On direct questioning, the reason given most frequently was "to get high"; on indirect questioning, reasons were related more to peer participation and feelings of futility. Marginalized patients living in the community are vulnerable to the misuse of anticholinergic drugs.

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A case of procyclidine abuse is described in which the clinical presentation was indistinguishable from mania. The patient was a long-standing poly-drug abuser and was obtaining the drugs from medical sources. Controlled exposure on the ward to drugs of abuse, including a double-blind comparison with placebo, confirmed that procyclidine caused a manic response in this patient.

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Atropine, azaprophen, biperiden, scopolamine, and trihexyphenidyl increased both ambulations and fine motor activity significantly during the first hour post-injection, but the increased activity levels returned to vehicle control levels within 2-6 h post-injection. Benactyzine and procyclidine only increased fine motor activity significantly above vehicle control levels and activity levels returned to vehicle control levels within 2-3 h. Finally, aprophen and diazepam generally did not increase measures of activity significantly above vehicle controls at the dose ranges examined.

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The authors present a setting for abrupt withdrawal treatment with the following targets: 1. To facilitate the addicts the voluntary use of medical and psychiatric service. 2. To develop methods for withdrawal treatment, as riskless and easy to handle as possible. 3. To use the time of inpatient treatment for building up confidence in psychiatric services to motivate the patients for a following therapy. Drugs and dosage of peroral and intravenous neuroleptic treatment and possible complications are discussed. Peroral treatment has the advantage of lower doses, easier handling and lower complication rates. The setting and the used drugs seem to be attractive enough for many addicts to contact the clinic on their own account.

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Reports identified in the search were included if they were controlled trials dealing with people with neuroleptic-induced TD and schizophrenia or other chronic mental illness who had been randomly allocated to either an anticholinergic agent or to a placebo (or no intervention).

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improvement was observed in cases of grand mal as well as temporal lobe seizures in 70% of patients, EEG improvement was found in 50% of patients. Side effects including oral dryness, accomodation disturbances developed in 17 patients but were usually slight and transient, in only 4 cases they were sufficiently severe as to justify reduction of dosage. Improvement of mood and contact with surroundings was noted in 60% of cases.

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The effects of clinically available drugs targeting muscarinic cholinergic, adrenergic, dopaminergic, and serotonergic receptors; intracellular calcium levels and/or the function of calcium-dependent biochemical pathways; ion channels; and cellular pumps were tested against a keratitis isolate of Acanthamoeba castellanii belonging to the T4 genotype. In vitro growth inhibition (amoebistatic) assays were performed by incubating A. castellanii with various concentrations of drugs in the growth medium for 48 h at 30°C. To determine amoebicidal effects, amoebae were incubated with drugs 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. Of the eight drugs tested, amlodipine, prochlorperazine, and loperamide showed potent amoebicidal effects, as no viable trophozoites were observed (>95% kill rate), while amiodarone, procyclidine, digoxin, and apomorphine exhibited up to 50% amoebicidal effects. In contrast, haloperidol did not affect viability, but all the drugs tested inhibited A. castellanii growth. Importantly, amlodipine, prochlorperazine, and loperamide showed compelling cysticidal effects. The cysticidal effects were irreversible, as cysts treated with the aforementioned drugs did not reemerge as viable amoebae upon inoculation in the growth medium. Except for apomorphine and haloperidol, all the tested drugs blocked trophozoite differentiation into cysts in encystation assays. Given the limited availability of effective drugs to treat amoebal infections, the clinically available drugs tested in this study represent potential agents for managing keratitis and granulomatous amoebic encephalitis caused by Acanthamoeba spp. and possibly against other meningoencephalitis-causing amoebae, such as Balamuthia mandrillaris and Naegleria fowleri.

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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.

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The administration of PRN medication by mental health nurses is an important, yet poorly explored aspect of psychiatric inpatient care. An examination of nurses' reasons for administering PRN medication is essential in ensuring its appropriate and effective use. Data were gathered from the drug charts of 44 inpatients on two acute psychiatric wards. Most PRN medication was given orally and the most frequently administered drugs were procyclidine, lorazepam, ibuprofen, diazepam and droperidol. The main reason for administering PRN medication was because patients had 'requested' it. Results were broadly consistent with previous research. It is recommended that nurses should give clear and specific reasons for administering PRN medication based on a valid assessment. Implications for clinical practice and further research are also discussed.

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

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The results of evaluating the therapeutic efficacy of the new psychotropic drugs adepren, didepil, anq tempalgin made by the "Farmakhim" plant (the People's Republic of Bulgaria) are presented. Clinical trials revealed new facts that allowed to expand the scope of the indications for use formulated in the "Farmakhim" recommendations. It was found that Adepren could be used with success (in addition to the indications suggested by "Farmakhim") in the treatment of patients with depressive-paranoid paroxysms of periodic schizophrenia taking its course in the presence of general depression, as well as patients with somatogenic lingering astheno-depressive states. The therapeutic efficacy of didepil (an antiepileptic) was found to be in a direct relationship with the disease duration, character of the attacks, presence or absence of epileptic chandes of personality. The effect was the best in cases of a short duration of the disease and absence of gross epileptic personality changes, when the paroxysmal disorders were confined mostly to grand mals. A new scheme for arresting the epileptic status with didepil solution is offered. For the first time the efficacy of tempalgin in the treatment of patients suffering from alcoholic abstinence syndrome was substantiated. Optimal doses of the drugs have been determined with regard to the disease nosology and the leading syndrome. Contraindications to the use of the drugs have also been formulated.

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1. A variety of atropine-like drugs effective in the treatment of drug-induced extrapyramidal syndromes have been investigated with regard to their interaction with dopamine-containing neurones in rat brain.2. Under some conditions benztropine, trihexyphenidyl, atropine and ethopropazine significantly antagonized the chlorpromazine-induced increase in subcortical concentrations of homovanillic acid.3. Most of the atropine-like drugs investigated also decreased the turnover of dopamine in the subcortex as measured by following the disappearance of dopamine after administration of alpha-methyl-p-tyrosine.4. These findings are suggestive that an imbalance between a dopaminergic and cholinergic system might be closely linked to the pathogenesis of extra-pyramidal movement disorders.

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

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kemadrin injection dose 2016-05-23

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 buy kemadrin 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.

kemadrin generic name 2015-07-31

Both fine motor activity (reflecting smaller movements) and ambulatory activity (reflecting larger movements) were recorded for 23 buy kemadrin h following drug administration in food-restricted rats. All drugs were administered during the light period of the photocycle.

dose of kemadrin 2016-01-18

Various concentrations of atropine, pirenzepine, dexetimide, scopolamine, tropicamide, benztropine, dicyclomine, gallamine, mepenzolate, oxyphenonium, propantheline, procyclidine, 4-diphenylacetoxy-N-methylpiperidine (4-DAMP), hexahydro-sila-difenidol (HHSiD), p-fluorohexahydro-sila-difenidol (pf-HHSiD), methoctramine, AFDX-116, and quinuclidinyl benzilate (QNB) were injected into goggled eyes of Leghorn cockerels three times at 48-hour intervals. Fellow control eyes received saline. Control animals received saline buy kemadrin in both eyes. Twenty-four hours after final injections, refraction, eye weight, and axial length were measured, and eyes were prepared for microscopy.

buy kemadrin 2017-06-01

The nature of the antagonism by anticholinergic compounds of nicotine-induced convulsion in mice has not been defined clearly. Although, because they do not compete effectively for agonist binding to brain tissue in-vitro, these compounds are thought to be non-competitive antagonists in the brain, pharmacological evidence is lacking. This study describes the anti-nicotinic properties of the clinically used anticholinergic antiparkinson drugs, benztropine, biperiden, caramiphen, ethopropazine, procyclidine and trihexyphenidyl. Nicotine-induced convulsion and arecoline-induced tremor in mice were effectively prevented by these drugs. The concentrations of benztropine, biperiden, caramiphen, ethopropazine, procyclidine and trihexyphenidyl affording 50% prevention of nicotine-induced convulsion (ED50 values) were 7.4, 4.6, 7.8, 4.9, 3.1 and 3.3 mg kg(-1), respectively. The classical muscarinic receptor antagonist atropine had potent anti-muscarinic effects but very weak anti-nicotinic activity. The classical nicotinic receptor antagonist mecamylamine had potent anti-nicotinic activity but no anti-muscarinic effects. The pattern of shift of the dose-response curve for nicotine-induced convulsion in mice was determined in the presence of increasing concentrations of the buy kemadrin anticholinergic antiparkinson drugs. These drugs were found to increase the ED50 (0.49 mg kg(-1)) of nicotine-induced convulsion in a dose-related manner. The maximum effect of nicotine and the slope of nicotine dose-response curve were not significantly influenced by either low or high doses of benztropine, procyclidine or trihexylphenidyl, which suggests competitive action. Biperiden, caramiphen and ethopropazine, at low doses which significantly increased the ED50 of nicotine, did not affect the maximum effect of nicotine or the slope of the nicotine dose-response curve; at higher doses, however, they reduced the maximum effect and the slope, which suggests that these drugs have both competitive and non-competitive properties in antagonizing nicotine-induced convulsion in mice. The experiments demonstrate that the anticholinergic antiparkinson drugs and mecamylamine effectively antagonize nicotine-induced convulsion, but atropine does not; some of these drugs have competitive properties whereas others seem to have both competitive and non-competitive properties in antagonizing nicotine-induced convulsion in mice.

kemadrin 5mg tab 2015-10-25

Irritable bowel syndrome (IBS) is a functional disorder, which has recently been 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 buy kemadrin .

kemadrin medicine 2017-03-30

The interaction between various neuroleptics and antiparkinsonian drugs was analyzed by measuring the neuroleptic plasma level before and after withdrawal of antiparkinsonian drugs. The population completing the study consisted of 32 chronic schizophrenics treated with chlorpromazine (8), levomepromazine (14), thioridazine (6), or haloperidol (4). Twenty-five were also receiving benztropine; 4, trihexyphenidyl; and 3, procyclidine. During the first 4 weeks patients remained buy kemadrin on neuroleptics and antiparkinsonians, the latter being withdrawn during the 5th week, and the neuroleptics alone being administered during 16 following weeks. The plasma level of neuroleptics was assayed by gas liquid chromatography, once weekly in the morning at two different times. The analysis of variance showed a significant difference in neuroleptic plasma level when patients took neuroleptics only versus the period they had received neuroleptics and antiparkinsonians. The multiple comparison based on Studentized range Q0-05 revealed a significant progressive increase of neuroleptic plasma level during 12 weeks after withdrawal of antiparkinsonian drugs after which a plateau was reached. The hypothetical mechanisms of action of antiparkinsonians on neuroleptic plasma level are discussed.

kemadrin overdose 2015-07-07

Forty-nine schizophrenic outpatients stabilized on oral antipsychotic medication and procyclidine received 12.5 buy kemadrin mg or 18.75 mg of fluphenazine enanthate or fluphenazine decanoate and were examined for extrapyramidal side effects one and two weeks later. Extrapyramidal side effects were present in 30 patients (61%) but were clinically significant in only 11 (22%). Fluphenazine enanthate produced more clinically significant extrapyramidal symptoms, particularly akathisia, than did fluphenazine decanoate.

kemadrin medication 2015-10-20

Current treatment of nerve agent poisoning with ionotropic drugs proves inadequate, and buy kemadrin alternative treatment strategies are searched for. Based on positive findings with metabotropic glutamate modulators in microinfusion studies, the present study was initiated to examine anticonvulsant effects of MPEP (2-Methyl-6-(phenylethynyl)pyridine hydrochloride), a metabotropic glutamate receptor 5 antagonist, and DCG-IV ((2S,2'R,3'R)-2-(2',3'-dicarboxycyclopropyl)glycine), a metabotropic glutamate receptor 2/3 agonist, when administered systemically in combinations with HI-6 (1-[([4-(aminocarbonyl)pyridino]methoxy)methyl]-2-[(hydroxyimino)methyl]pyridinium) and procyclidine or HI-6 and levetiracetam relative to the combination of HI-6, procyclidine, and levetiracetam. The results showed that MPEP or DCG-IV combined with HI-6 and procyclidine resulted in substantial antidotal efficacy when administered 20 min after onset of seizures elicited by soman. MPEP or DCG-IV combined with HI-6 and levetiracetam did not terminate seizures and preserve lives. When given 20 min before challenge with soman, DCG-IV in combination with HI-6 and procyclidine provided protection, whereas MPEP combined with HI-6 and procyclidine did not. Combinations with metabotropic glutamate receptor modulators did not achieve the same high level of antidotal efficacy as the combination of HI-6, procyclidine, and levetiracetam. MPEP alone inhibited pseudocholinesterase activity in the brain markedly. A positive correlation was found between latency to seizure onset or full protection and level of pseudocholinesterase activity in brain. MPEP and DCG-IV can serve as effective anticonvulsants against nerve agent poisoning when combined with HI-6 and procyclidine. Metabotropic glutamate receptor modulators may represent an alternative or supplement to treatment with ionotropic drugs.

kemadrin dosage 2015-08-31

Platelet-rich plasma from healthy controls was pre-treated with neuroleptics of the phenothiazine, butyrophenone or benzamide variety before aggregation with one of the following agonist agents: ADP, adrenaline, 5-HT, collagen, platelet activating factor or ristocetin. All compounds effective as antipsychotics, except sulpiride, depressed aggregation. Unmedicated schizophrenics showed aggregation responses indistinguishable from healthy controls. However, within days of treatment with either trifluoroperazine or haloperidol responses became abnormal in acutely psychotic patients. Increased responses to 5-HT and depressed responses to platelet activating factor were detected. After 4 weeks of treatment responses tended to return to normal. Aggregation responses were normal in those buy kemadrin patients on long-term depot neuroleptics.

kemadrin drug classification 2015-12-31

It has been demonstrated that a triple regimen consisting of procyclidine (6 mg/kg), diazepam (10 mg/kg) and pentobarbital (30 mg/kg) can effectively terminate soman-induced (1 x LD50) seizures/convulsions in rats when administered 30-40 min following buy kemadrin onset. However, convulsive activity lasting for only 45 min can result in marked neuronal pathology. The purpose of the present study was to examine potential cognitive impairments of such brain lesions. The results showed that the neuronal pathology (assessed with Fluoro-Jade B) varied from none at all to 30% damage in the index areas (hippocampus, amygdala, piriform cortex). Cognitive deficits were seen in a novelty test (11 days post-exposure) and retention of a brightness discrimination task (28 days post-exposure) among the rats with neuropathology. Furthermore, significant correlations between neuropathology scores and behavioral measures were found for the animals that convulsed. Among these rats, the mortality rate was relatively high (60%) compared with rats in a previous study that had undergone implantation of hippocampal electrodes (17%). Neither the soman poisoning in the absence of convulsions nor the triple regimen alone affected behavior. It is concluded that early management of soman-induced convulsions is of major importance in preventing neuropathology and accompanying cognitive impairments.

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A treatment regimen consisting of HI-6, scopolamine, and physostigmine (termed the physostigmine regimen) has been based on the serendipitous discovery that it exerts powerful antidotal effects against high levels of soman poisoning if it is administered 1 min after exposure. A medical therapy with corresponding efficacy, but without the time limitation of the latter regimen, has been developed through studies of microinfusions of anticonvulsants into seizure controlling sites in the forebrain of rats. From these studies procyclidine emerged as the most potent anticonvulsant, and its potency was further enhanced when being combined with the antiepileptic levetiracetam during systemic administration. In the present study, the capacity of HI-6, levetiracetam, and procyclidine buy kemadrin (termed the procyclidine regimen) was tested against that of the physostigmine regimen. The results showed that both regimens were very effective against supralethal doses of soman (3, 4, 5 × LD₅₀) when given 1 and 5 min after intoxication. When the treatments were administered 10 and 14 or 20 and 24 min after soman exposure, only the procyclidine regimen was able to terminate seizures and preserve lives. When used as prophylactic therapies, both regimens protected equally well against seizures, but only the procyclidine regimen provided neuroprotection. The procyclidine regimen has apparently capacities to serve as a universal therapy against soman intoxication in rats.

kemadrin generic 2015-09-28

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 buy kemadrin studies demonstrate novel inhibitory actions of TCAD and phenothiazine derivatives at the NMDA receptor complex that are apparently mediated by the Zn++ binding site.

kemadrin 5 mg 2015-06-27

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

kemadrin tablets 2015-02-17

Two cases are described of chronic schizophrenic patients maintained on depot neuroleptics, who developed severe extrapyramidal symptoms following a period of heavy betel nut consumption. A mechanism for this effect is proposed based on the pharmacological buy kemadrin antagonism of the anticholinergic agent, procyclidine, by the active alkaloid ingredient of the betel, arecoline.

kemadrin maximum dose 2017-10-05

It is important that prophylactics used to protect military and emergency personnel against lethal doses of nerve agents do not by themselves produce impairment of cognitive capability. The purpose of the present study was to examine whether physostigmine, scopolamine, and various doses of procyclidine might reduce rats' innate preference for novelty. When these drugs were tested separately, the results showed that physostigmine (0.1 mg/kg) and procyclidine (3 mg/kg) did not affect preference for novelty, whereas scopolamine (0.15 mg/kg) and procyclidine in a higher dose (6 mg/kg) resulted in a preference deficit (Experiment 1). In Experiment 2, the combination of physostigmine and scopolamine or physostigmine and procyclidine (6 mg/kg) caused a marked deficit in preference for novelty. A much milder deficit was observed when physostigmine was combined with lower doses (1 or 3 mg/kg) of procyclidine. Zetia Reviews The latter combinations also had milder adverse impact on the animals' interest in the test environment and activity measures than the former combinations. By combining physostigmine with anticholinergics, a potentiation of adverse effects on behavior was seen. It is concluded that a slight cognitive impairment might be unavoidable with effective prophylactics.

kemadrin tab 5mg 2015-12-08

Dystonia is usually a lifelong condition with persistent pain and disability. Focal dystonia affects a single part of the body; generalised dystonia can affect most or all of the body. It is more common in women, and some Avapro Generic Name types of dystonia are more common in people of Ashkenazi descent.

kemadrin tablet 2015-01-05

It has been proposed that serotonin (5-HT) antagonists counteract neuroleptic-induced extrapyramidal symptoms by disinhibition of dopamine activity. The effects of the 5-HT antagonist mianserin, the anticholinergic drug procyclidine and placebo were evaluated in 16 psychiatric patients with chronic neuroleptic-induced parkinsonism in a double-blind cross-over Imodium Max Dosage trial. The patients received each drug in random order in 3-week periods separated by washout periods of 2 weeks. The effect of mianserin did not significantly differ from that of placebo, while parkinsonian symptoms were significantly reduced during treatment with procyclidine (P less than 0.05). Although mianserin was ineffective in chronic neuroleptic-induced parkinsonism, it cannot be excluded that 5-HT antagonists may be effective in the treatment of acute extrapyramidal side effects.

kemadrin reviews 2017-06-23

Changes in the hippocampal theta rhythm were used as a model in which anticonvulsant drugs may be screened for their potential to antagonize soman-induced (1xLD(50)) seizures. The zinc chelator, ethylenediaminetetra acetic acid (EDTA) (300mg/kg), and the NMDA receptor antagonist, HA-966 (60mg/kg), both disrupted the theta rhythm, but did not antagonize soman-induced seizures, neither separately, nor in combination. The anticholinergic and antiglutamatergic procyclidine (6mg/kg) did not influence the theta activity. The GABAergic agonists, diazepam (10mg/kg) and pentobarbital (30mg/kg), both reduced the theta frequency. Procyclidine, diazepam, and pentobarbital did not stop soman-induced seizures when administered separately, but both convulsions and seizure activity terminated when these agents were given together, and the rats slept through the critical convulsion period. This triple therapy was 100% effective, when administered 30-40min following onset of convulsions, and the rats displayed apparently normal behavior the next day. A screening model of potential anticonvulsants cannot be based on alterations in hippocampal EEG activity. Procyclidine, diazepam, and pentobarbital in combination disrupted the theta rhythm like the combination of EDTA and HA-966, Voltaren K Gel but the latter combination did not have anticonvulsant effect. It is concluded that a triple regimen consisting of procyclidine, diazepam, and pentobarbital can effectively terminate soman-induced seizures that have lasted 30min or more.

kemadrin storage 2016-11-22

The antidotal, anticonvulsant and neuroprotective effects of physostigmine (PhS) and procyclidine (PC), the combinational prophylactics for organophosphate poisoning, were evaluated. For the investigation of dose-response relationship in rats and guinea pigs, various doses (0-6 mg/kg) of PC in combination with a fixed dose (0.1 mg/kg) of PhS were pretreated subcutaneously 30 min prior to subcutaneous poisoning with soman. Procyclidine in combination with Effexor Brand Name PhS exhibited remarkable synergistic effects in a dose-dependent manner, leading to 1.92-5.07 folds of protection ratio in rats and 3.00-4.70 folds in guinea pigs. On the other hand, a low effect (1.65 fold) was achieved with the traditional antidotes atropine (17.4 mg/kg) plus 2-pralidoxime (30 mg/kg) treated immediately after soman poisoning, compared with a marked protection (5.50 fold) with atropine (17.4 mg/kg) plus HI-6 (125 mg/kg) in unpretreated rats. Noteworthy, the combinational prophylactics greatly potentiated the effect of atropine plus 2-pralidoxime to 6.13 or 12.27 folds and that of atropine plus HI-6 to 12.00 or 21.50 folds with 1.0 or 3.0 mg/kg of PC, respectively. A high dose (100 μg/kg, 1.3×LD(50)) of soman induced severe epileptiform seizures in rats pretreated with HI-6 (125 mg/kg), resulting in brain injuries in discrete brain regions under histopathological examination in 24 h. Interestingly, such seizures and excitotoxic brain injuries were fully prevented by pretreatment with PhS (0.1 mg/kg) and PC (1 mg/kg). Taken together, it is proposed that the prophylactics composed of PhS and PC could be a promising regimen for the prevention of lethality, seizures and brain injuries induced by soman poisoning.

kemadrin alcohol 2017-10-30

The anticholinergic antiparkinsonian drugs biperiden, benztropine, trihexyphenidyl, methixene, and procyclidine were compared with atropine and pirenzepine, as well as with orphenadrine, amantadine and some standard antidepressives and neuroleptics in their ability to inhibit the binding of tritiated quinuclidinyl benzilate (QNB) to the muscarinic receptors in rat brain cortical tissue. Most of the antiparkinsonian drugs studied were potent inhibitors of (-)3H-QNB binding, when compared to atropine (IC50-value = 0.22 microM), the IC50-values ranging from 0.0084 microM (biperiden) to 0.07 microM (procyclidine). Orphenadrine had a low and amantadine no evident affinity for muscarinic receptors. With the exception of pirenzepine and biperiden the inhibition curves were steep and parallel, giving linear Hill plots with coefficients close to unity. The binding profile of atropine, pirenzepine, and biperiden was further studied in heart and lung tissues, atropine showing only small divergences in its binding to the different tissues, but biperiden and pirenzepine having five to ten times lower affinity in the peripheral tissues than in the brain. The results confirm the high affinity of most of the antiparkinsonian drugs for brain muscarinic receptors. The dissociation Hyzaar Buy constants agree with the average clinical doses of the drugs. It must be remembered, however, that the binding data may represent multiple events at receptor sites because most of the drugs used are mixtures of stereoisomers. Thus further studies using individual enantiomers are needed to compare more directly binding data between the compounds.

kemadrin dose 2015-11-10

The case described here is that of a 34-year-old woman with a psychiatric disorder who was referred to the local surgical receiving unit with abdominal pain and vomiting. She remained well and fully mobile but refused blood investigations until the day following admission. At that time the tests showed a picture of acute renal failure. With the development of increasing abdominal tenderness and pyrexia she was persuaded to have a laparotomy which demonstrated a small tear at the dome of the bladder. Her deranged blood biochemistry returned to normal within 11 h following surgery. The important points demonstrated in this case study are the special clinical difficulties encountered in psychiatric patients, which may consequently lead to delay in diagnosis. This delay allowed significant peritoneal reabsorption of urea and creatinine, which masqueraded as 'acute renal failure' on biochemical testing. The case also highlights the use of procyclidine, commonly used in patients with psychiatric disorders; urinary retention is a recognised side effect of this drug--and it is possible that such retention together with a minor and hence easily overlooked episode of trauma, may have contributed to the patient's condition.

kemadrin tablet cost 2017-02-07

Current treatment of nerve agent poisoning consists of prophylactic administration of pyridostigmine and therapy using atropine, an oxime and a benzodiazepine. Pyridostigmine does however not readily penetrate the blood-brain barrier giving ineffective protection of the brain against centrally mediated seizure activity. In this study, we have evaluated donepezil hydrochloride, a partial reversible inhibitor of acetylcholinesterase (AChE) clinically used for treating Alzheimer's disease, in combination with procyclidine, used in treatment of Parkinson's disease and schizophrenia, as prophylaxis against intoxication by the nerve agent soman. The results demonstrated significant protective efficacy of donepezil (2.5 mg/kg) combined with procyclidine (3 or 6 mg/kg) when given prophylactically against a lethal dose of soman (1.6 x LD(50)) in Wistar rats. No neuropathological changes were found in rats treated with this combination 48 h after soman intoxication. Six hours after soman exposure cerebral AChE activity and acetylcholine (ACh) concentration was 5% and 188% of control, respectively. The ACh concentration had returned to basal levels 24 h after soman intoxication, while AChE activity had recovered to 20% of control. Loss of functioning muscarinic ACh receptors (17%) but not nicotinic receptors was evident at this time point. The recovery in brain AChE activity seen in our study may be due to the reversible binding of donepezil to the enzyme. Donepezil is well tolerated in humans, and a combination of donepezil and procyclidine may prove useful as an alternative to the currently used prophylaxis against nerve agent intoxication.

kemadrin drug 2016-02-28

A 51-year-old gentleman was admitted with a history of severe depression with marked agitation in the background of cocaine abuse. He had multiple medical problems like deep vein thrombosis, hepatitis C and tardive dyskinesia. Besides him being on antidepressant medication, risperidone was prescribed by his previous physician for a period of 2 years. Since commencement on this medication, he developed tardive dyskinesia that was never recognised and managed. This side effect caused additional anxiety to the patient and affected his social life. Upon admission, his medications were reviewed, risperidone was gradually withdrawn and procyclidine 2 mg twice daily was added. After being discharged from hospital, he was regularly seen in the out patient clinic. Within 3 months, his tardive dyskinesia improved tremendously, his quality of social life got better and by virtue of this, there was a faster remission in his depression and anxiety symptoms.

kemadrin injection dose 2016-07-29

In recent years, the complex treatment of schizophrenia has been extended by the neuroleptic large-dose therapy. Our investigations carried out so far, which reflect the experiences gained in several years with this form of treatment, include 30 schizophrenic patients admitted in an acute psychotic condition. They were treated for six days running with 40 to 120 (average 65) mg of Haloperidol daily. The results of our studies show that the large-dose therapy with Haloperidol as an initial phase of a combined pharmaco-therapy represents a safe, rapid and effective method.

kemadrin generic name 2017-02-27

In this 12-week study of anticholinergic discontinuation in 20 outpatients with schizophrenia or schizoaffective disorder, gradual decrease and discontinuation of anticholinergics led to a positive effect on cognition. There were no adverse consequences on general psychopathology and no significant differences for 18 of 20 subjects on movement disorders.