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Kemadrin (Procyclidine)
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Kemadrin

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.

Description

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.

Dosage

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.

Overdose

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

Storage

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

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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.

Contraindications

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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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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A pretreatment for organophosphorus (OP) anticholinesterase (e.g., soman) intoxication should prevent lethality and convulsions (CNV) at 2 LD50s and be behavioral-decrement-free when given alone. Behavioral-deficit-free pretreatment regimens (PRGs) for guinea pigs consisted of Physostigmine (0.15 mg/kg, im) and adjunct. Adjuncts [mg/kg, im] tested were akineton [0.25], aprophen [8], trihexyphenidyl [2], atropine [16], azaprophen [5], benactyzine [1.25], cogentin [4], dextromethorphan [7.5], ethopropazine [12], kemadrin [1], memantine [5], promethazine [5], scopolamine [0.08] and vontrol [2]. PRGs were given 30 min before soman (60 micrograms/kg, sc; 2 LD50s) or other OP agents. Animals were then observed and graded for signs of intoxication, including CNV at 7 time points and at 24 hr. Physostigmine alone reduced the incidence of CNV and lethality induced by 2 LD50s of soman by 42 and 60%, respectively. All of the PRGs tested abolished lethality and 12 shortened recovery time to 2 hr or less. Also, PRGs including azaprophen or atropine prevented CNV. When selected PRGs were tested against intoxication by sarin, tabun or VX, the efficacy was generally superior to that for soman. The data show that several PRGs are effective against soman intoxication in guinea pigs.

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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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During treatment with thioxanthenes or phenothiazines of schizophrenic patients non-protein nitrogen in urine was measured. The values were calculated in relation to the excretion of creatinine. a) Flupentixol or fluphenazine applied in optimal dosage, increased the excretion of urea and the amino acids asp, glu + gln, and gly. b) Moreover, if the drug induced a parkinsonoid (thioridazine) the excretion of ser and thr was increased, too. The usual desalting procedure by ion-exchanging resins before chromatography increases the contents of several amino acids, e.g. asp, asn, ala, gly, cys, ser, thr, indicating a breakdown of some instable products.

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In order to facilitate direct comparisons of anticholinergic drug effects on activity, nine drugs were tested in one laboratory using a standardized procedure.

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Based on currently available information, no confident statement can be made about the effectiveness of anticholinergics to treat people with neuroleptic-induced tardive dyskinesia. The same applies for the withdrawal of such medications. Whether the withdrawal of anticholinergics may benefit people with neuroleptic-induced TD, this should be evaluated in a parallel-group, placebo-controlled randomised trial, with adequate sample size and at least 6 weeks of follow up.

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Eighteen of twenty patients successfully discontinued their anticholinergic medication; two did not because of akathisia. Repeated measures analysis of variance did not show a significant effect of anticholinergic discontinuation on total Extrapyramidal Symptoms Rating Scale score or on the Parkinsonism, Akathisia, Dystonia or Tardive Dyskinesia subscales. However, significant improvement was found on the Brief Assessment of Cognition in Schizophrenia composite z score at weeks 6, 8 and 12 compared with baseline. Significant improvements were seen on the motor and the symbol-coding tasks. No significant effects were observed on the Positive and Negative Syndrome Scale, Clinical Global Impression - Severity and Clinical Global Impression - Improvement scales.

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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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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 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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The classification of muscarinic receptors into M1 and M2 subtypes and the involvement of guanine nucleotide binding proteins (G-proteins) as major mediators of receptor information transduction in the cholinergic and other neurotransmitter systems have prompted us to undertake studies both at receptor and postreceptor levels that may shed light on the importance of these new findings to the pharmacotherapy of manic-depressive illness and of extrapyramidal syndromes. We searched for patterns of muscarinic selectivity among the commonly used anticholinergics (biperiden, procyclidine, trihexyphenidyl, benztropine, and methixen) through radioligand receptor studies in various rat tissues. The drugs showed a range of selectivity, from the totally nonselective methixen to the highly M1-selective biperiden. Sinus arrhythmia measurements were undertaken in psychiatric patients treated with different antiparkinsonian anticholinergics. The extent of sinus arrhythmia suppression was inversely correlated with the degree of M1 selectivity of the drugs used, advocating the use of M1-selective antiparkinsonian anticholinergics like biperiden in the treatment of extrapyramidal side effects. The implications of muscarinic receptor subclassification were further extended to include postreceptor phenomena. We have directly studied G-protein function by measuring cholinergic agonist-induced increases in guanosine triphosphate (GTP) binding to these proteins. This cholinergic agonistic effect was shown to be exerted by G-proteins other than Gs (the adenylate cyclase stimulatory G-protein), i.e., Gi (the adenylate cyclase inhibitory G-protein) or Gp [the G-protein activating phosphatidylinositol (PI) turnover], as ribosylation by pertussis toxin abolished this cholinergic effect, whereas it was unaffected by cholera toxin. Pertussis toxin-blockable, carbamylcholine-induced increases in GTP binding capacity were found to be mediated through M1 muscarinic receptors, as M1-selective antagonists were 100-fold more effective than M2 selective antagonists in blocking carbamylcholine effects. Moreover, carbamylcholine effect was exclusively detected in tissues predominantly populated by M1 receptors. Our results thus suggest that carbamylcholine-induced increases in GTP binding are exerted through M1 receptors interacting with Gp. At therapeutically efficacious concentrations, lithium completely blocked carbamylcholine-induced increases in GTP binding capacity in both in vitro and in vivo experiments.(ABSTRACT TRUNCATED AT 400 WORDS)

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1 Procyclidine resembles hyoscine in enhancing the effects of amphetamine on ipsiversive turning by mice with a unilateral central dopamine lesion. 2 The stereospecific index for procyclidine is not greater than 10, in contrast to 173 for acetylcholine receptors in ileum from the same mice. 3 This suggests that although the central effects of procyclidine in this test involve acetylcholine receptors similar to those at peripheral sites, they cannot be identical with them unless there are differences at some secondary site, for example, if the weaker enantiomer were a stronger inhibitor of dopamine uptake or if there were a stereoselective uptake process for procyclidine itself.

kemadrin drug classification

Individuals with schizophrenia, compared to healthy individuals, are known to exhibit deficient prepulse inhibition (PPI) of the startle response as well as reduced performance on the antisaccade task. There is evidence for genetic transmission of both PPI and antisaccadic abnormalities in schizophrenia. It has been suggested that PPI and antisaccade measures identify separate endophenotypes, on the basis of a lack of relationship between PPI and antisaccade deficits in patients with schizotypal personality disorder. However, given that patients with schizotypal personality disorder are unlikely to manifest all the abnormalities associated with schizophrenia, it is important to determine that there is no relationship present between these two abnormalities in people affected with schizophrenia. The main objective of this investigation therefore was to establish the lack of the association between PPI and antisaccade deficits in schizophrenia in two independent studies. Study 1 involved 39 patients with schizophrenia and 14 healthy controls and study 2 involved 35 patients with schizophrenia and 22 healthy controls. PPI (uninstructed paradigm) of the acoustically elicited startle (eye blink) was measured electromyographically. Antisaccadic eye movements (standard, non-overlap version) were measured using infrared oculography. Patients displayed reduced PPI and a lower percentage of correct antisaccades relative to healthy controls in both studies. As expected, no relationship occurred between PPI and the percentage of correct antisaccade responses in either group. It is concluded that PPI and antisaccade abnormalities in schizophrenia represent separate endophenotypes, reflecting the functions of different genetic aetiologies and different or only partially overlapping neural systems.

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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 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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buy kemadrin 2017-10-21

Atropine, pirenzepine, and himbacine prevent form-deprivation myopia (FDM kemadrin buy ) when administered intravitreously. The mechanisms and sites of action of these drugs against myopia are not clear. To shed further light on whether this mechanism is muscarinic, several other muscarinic antagonists were tested.

buy kemadrin 2016-02-12

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 kemadrin buy biochemical abnormality responsible for this uncontrolled heat production might be muscular rather than hypothalamic.

buy kemadrin 2015-06-26

1. We studied the effect of temperature on the binding to rat heart M2 muscarinic receptors of antagonists related to the carbon/silicon pairs pridinol/sila-pridinol and diphenidol/sila-diphenidol (including three germanium compounds) and six structurally related pairs of enantiomers [(R)- and (S)-procyclidine, (R)- and (S)-trihexyphenidyl, (R)- and (S)-tricyclamol, (R)- and (S)-trihexyphenidyl methiodide, (R)- and (S)-hexahydro-diphenidol and (R)- and (S)-hexbutinol]. Binding affinities were determined in competition experiments using [3H]-N-methyl-scopolamine chloride as radioligand. The reference drugs were scopolamine and N-methyl-scopolamine bromide. 2. The affinity of the antagonists either increased or decreased with temperature. van't Hoff plots were linear in the 278-310 degrees K temperature range. Binding of all antagonists was entropy driven. Enthalpy changes varied from large negative values (down to -29 kJ mol-1) to Propecia Generic Brand large positive values (up to +30 kJ mol-1). 3. (R)-configurated drugs had a 10 to 100 fold greater affinity for M2 receptors than the corresponding (S)-enantiomers. Enthalpy and entropy changes of the respective enantiomers were different but no consistent pattern was observed. 4. When silanols (R3SiOH) were compared to carbinols (R3COH), the affinity increase caused by C/Si exchange varied between 3 and 10 fold for achiral drugs but was negligible in the case of chiral drugs. Silanols induced more favourable enthalpy and less favourable entropy changes than the corresponding carbinols when binding. Organogermanium compounds (R4Ge) when compared to their silicon counterparts (R4Si) showed no significant difference in affinity as well as in enthalpy and entropy changes. 5. Exchange of a cyclohexyl by a phenyl moiety was associated with an increase or a decrease in drug affinity (depending on the absolute configuration in the case of chiral drugs) and generally also with a more favourable enthalpy change and a less favourable entropy change of drug binding. 6. Replacement of a pyrrolidino by a piperidino group and increasing the length of the alkylene chain bridging the amino group and the central carbon or silicon atom were associated with either an increase or a decrease of entropy and enthalpy changes of drug binding. However, there was no clear correlation between these structural variations and the thermodynamic effects. 7. Taken together, these results suggest that hydrogen bond-forming OH groups and, to a lesser extent, polarizable phenyl groups contribute significantly to the thermodynamics of interactions between these classes of muscarinic antagonists and M2 muscarinic receptors.

buy kemadrin 2016-10-07

This Noroxin Pill study determined the effects of procyclidine, an anticholinergic drug, on PPI in healthy male volunteers, employing a double-blind placebo-controlled cross-over design.

buy kemadrin 2017-02-22

Fifty-one Cost Of Retrovir healthy volunteers were given haloperidol 5 mg in two consecutive pharmacokinetic studies.

buy kemadrin 2017-01-11

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 Amoxil Suspension patient.

buy kemadrin 2017-05-02

Low volatile organophosphorous nerve agents such as VX, will most likely enter the body via the skin. The pharmacokinetics of Atarax 25mg Tablet drugs such as oximes, atropine and diazepam, are not aligned with the variable and persistent toxicokinetics of the agent. Repeated administration of these drugs showed to improve treatment efficacy compared to a single injection treatment. Because of the effectiveness of continuous treatment, it was investigated to what extent a subchronic pretreatment with carbamate (pyridostigmine or physostigmine combined with either procyclidine or scopolamine) would protect against percutaneous VX exposure. Inclusion of scopolamine in the pretreatment prevented seizures in all animals, but none of the pretreatments affected survival time or the onset time of cholinergic signs. These results indicate that percutaneous poisoning with VX requires additional conventional treatment in addition to the current pretreatment regimen. Decontamination of VX-exposed skin is one of the most important countermeasures to mitigate the effects of the exposure. To evaluate the window of opportunity for decontamination, the fielded skin decontaminant Reactive Skin Decontaminant Lotion (RSDL) was tested at different times in hairless guinea pigs percutaneously challenged with 4× LD50 VX in IPA. The results showed that RSDL decontamination at 15 min after exposure could not prevent progressive blood cholinesterase inhibition and therefore would still require additional treatment. A similar decontamination regimen with RSDL at 90 min showed that it still might effectively increase the time window of opportunity for treatment. In conclusion, the delay in absorption presents a window of opportunity for decontamination and treatment. The continuous release of VX from the skin presents a significant challenge for efficacious therapy, which should ideally consist of thorough decontamination and continuous treatment.

buy kemadrin 2015-02-10

Resolution is enhanced with the new technique since it allows measurement of multiple doses on cells from the same batch. It has advantages to cuvette techniques because cells have intact dendritic tree and synaptic function and it Uroxatral Medication is a convenient method to obtain reliable dose-response curves for NMDA channel modulators on differentiated neural cells.

buy kemadrin 2015-10-11

During treatment with thioxanthenes or phenothiazines of schizophrenic patients non-protein nitrogen in urine was measured. The values were calculated in relation to the excretion of creatinine. a) Flupentixol or fluphenazine applied in optimal dosage, increased the excretion of urea and the amino acids asp, glu + gln, and gly. b) Moreover, if the drug induced a parkinsonoid (thioridazine) the excretion of ser and thr was increased, too. The usual desalting procedure by ion-exchanging resins before chromatography increases the contents Prednisone Maintenance Dose of several amino acids, e.g. asp, asn, ala, gly, cys, ser, thr, indicating a breakdown of some instable products.

buy kemadrin 2017-06-26

1 Procyclidine resembles hyoscine in enhancing the effects of amphetamine on ipsiversive turning by mice with a unilateral central dopamine lesion. 2 The stereospecific index for procyclidine is not greater than 10, in contrast to 173 Cymbalta Migraines Reviews for acetylcholine receptors in ileum from the same mice. 3 This suggests that although the central effects of procyclidine in this test involve acetylcholine receptors similar to those at peripheral sites, they cannot be identical with them unless there are differences at some secondary site, for example, if the weaker enantiomer were a stronger inhibitor of dopamine uptake or if there were a stereoselective uptake process for procyclidine itself.

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

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The case history presented illustrates that, following an overdose of 'Whizz' and alcohol, Feldene Piroxicam Gel 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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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 Zovirax Acyclovir Review 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.

buy kemadrin 2016-05-10

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.

buy kemadrin 2017-08-12

Forty-nine schizophrenic outpatients stabilized on oral antipsychotic medication and procyclidine received 12.5 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.

buy kemadrin 2016-01-26

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.

buy kemadrin 2017-11-05

The prophylactic efficacy of a combinational patch system containing physostigmine and procyclidine against soman intoxication was evaluated using dogs. Female beagle dogs (body weights 9-10 kg) were shaved on the abdominal side, attached with a matrix-type patch (7x7 cm) containing 1.5% of physostigmine plus 6% procyclidine for 2 days, and challenged with subcutaneous injection of serial doses (2-10 LD50) of soman. Separately, in combination with the patch attachment, atropine (2 mg/dog) plus 2-pralidoxime (600 mg/dog) or atropine plus 1-[([4-(aminocarbonyl)pyridinio]methoxy)methyl]-2-[(hydroxyimino)methyl]pyridinium (HI-6, 500 mg/dog) were injected intramuscularly 1 min after soman poisoning. The LD50 value of soman was determined to be 9.1 microg/kg, and high doses (> or = 1.4 LD50) of soman induced salivation, emesis, defecation and diarrhea, tremors and seizures, and recumbency of dogs, leading to 100% mortality in 24 h. The prophylactic patch, which led to mean 18.5-18.8% inhibition of blood cholinesterase activity by physostigmine and mean 7.9-8.3 ng/ml of blood concentration of procyclidine, exerted a high protection ratio (4.7 LD50), in comparison with relatively-low effects of traditional antidotes, atropine plus 2-pralidoxime (2.5 LD50) and atropine plus HI-6 (2.7 LD50). Noteworthy, a synergistic increase in the protection ratio was achieved by the combination of the patch with atropine plus HI-6 (9 LD50), but not with atropine plus 2-pralidoxime (5 LD50). In addition, the patch system markedly attenuated the cholinergic signs and seizures induced by soman, especially when combined with atropine plus HI-6, leading to elimination of brain injuries and physical incapacitation up to 6 LD50 of soman poisoning. Taken together, it is suggested that the patch system containing physostigmine and procyclidine, especially in combination with atropine and HI-6, could be a choice for the quality survival from nerve-agent poisoning.

buy kemadrin 2015-09-27

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.

buy kemadrin 2017-06-27

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 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.

buy kemadrin 2017-05-04

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.

buy kemadrin 2015-05-14

Identification of critical receptors in seizure controlling brain regions may facilitate the development of more efficacious pharmacological therapies against nerve agent intoxication. In the present study, a number of drugs with anticonvulsant potency were microinfused into the perirhinal cortex (PRC) or posterior piriform cortex (PPC) in rats. The drugs used exert cholinergic antagonism (scopolamine), glutamatergic antagonism (ketamine, NBQX), both cholinergic and glutamatergic antagonism (procyclidine, caramiphen), or GABAergic agonism (muscimol). The results showed that in the PRC anticonvulsant efficacy against soman-induced seizures (subcutaneously administered) was achieved by procyclidine or NBQX, but not by ketamine, scopolamine, caramiphen, or muscimol (Experiment 1). Hence, both muscarinic and glutamatergic NMDA receptors had to be antagonized simultaneously or AMPA receptors alone, suggesting increased glutamatergic activation in the PRC before onset of seizures. In the PPC, anticonvulsant effects were assured by scopolamine or muscimol, but not by procyclidine, caramiphen, NBQX, or ketamine (Experiment 2). Thus, muscarinic and GABA(A) receptors appear to be the critical ones in the PPC. Microinfusion of soman into the PRC or PPC resulted in sustained seizure activity in the majority of the rats of both infusion categories. The rhinal structures encompassed in this study apparently have critical functions as both control and trigger sites for nerve agent-evoked seizures.

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Eighteen of twenty patients successfully discontinued their anticholinergic medication; two did not because of akathisia. Repeated measures analysis of variance did not show a significant effect of anticholinergic discontinuation on total Extrapyramidal Symptoms Rating Scale score or on the Parkinsonism, Akathisia, Dystonia or Tardive Dyskinesia subscales. However, significant improvement was found on the Brief Assessment of Cognition in Schizophrenia composite z score at weeks 6, 8 and 12 compared with baseline. Significant improvements were seen on the motor and the symbol-coding tasks. No significant effects were observed on the Positive and Negative Syndrome Scale, Clinical Global Impression - Severity and Clinical Global Impression - Improvement scales.

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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 the associated movement side-effects.

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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.

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Among 266 chronic inpatients receiving neuroleptics, six of the 137 (4.4%) receiving neuroleptics alone and none of the 129 receiving concomitant anticholinergics manifested the rabbit syndrome. Procyclidine resolved the signs of all affected patients. The syndrome's potential prevalence remains unknown.

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A systematic review of the treatment options available for stuttering priapism is presented combined with our own experience in managing this condition over a period of 25 years.

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In a 12-week controlled study ethopropazine was compared to benztropine in the treatment of parkinsonism induced by fluphenazine enanthate in 60 schizophrenic outpatients. Ethopropazine and benztropine were found to be equally effective in controlling parkinsonian symptoms and were as efficacious as procyclidine, their previous antiparkinsonian drug. However, benztropine treated patients had a significant increase in tardive dyskinesia compared to their condition during procyclindine treatment, and significantly more anxiety and depression than ethopropazine treated patients. This suggests that benztropine is not the anticholinergic drug of choice in the treatment of neuroleptic-induced parkinsonian symptoms, because of its more toxic central and peripheral atropinic effect.

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In order to shorten the list of candidate drugs with anticonvulsant potential against nerve agents, critical subreceptors in seizure controlling brain regions should be specified. Epileptiform activity does not spread randomly throughout the brain, but appears to be generated and propagated by specific anatomical routes. Nerve agents evoke seizure activity in the forebrain that progresses to the hind brain resulting in tonic-clonic convulsions. In some recent studies, it was shown that lesion of the area tempestas (AT), medial septum (MS), perirhinal cortex (PRC), or posterior piriform cortex (PPC) produces anticonvulsant effects (prevention of convulsions or delayed onset of convulsions) in rats exposed to soman, whereas damage to nucleus accumbens, nucleus basalis magnocellularis, amygdala, hippocampus, or entorhinal cortex does not cause anticonvulsant impact. These results are in compliance with findings that seizures can be generated in AT, MS, PRC, and PPC by means of nerve agents, chemoconvulsants, or kindling. Results from microinfusion studies show that anticonvulsant efficacy is obtained by GABA(A) modulators or cholinergic antagonists (M1-M5) in AT, cholinergic antagonists (M1-M5) in MS, combined glutamatergic (NMDA) and cholinergic antagonist (M1-M4), AMPA antagonist, or modulators of metabotropic glutamate receptors (mGluR5, mGluR2/3) in PRC, and cholinergic antagonist (M1-M5) or GABA(A) agonist in PPC. Calculation of impact factors for the most potent drugs (percentage of positive effects in the seizure controlling sites) showed that scopolamine and procyclidine were ranking highest (75) followed by muscimol (50), NBQX (33), and caramiphen (33). Potential strategies for prophylactic and post-exposure treatments are discussed.

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Granulomatous amoebic encephalitis (GAE) is caused by two protist pathogens, Acanthamoeba spp., and Balamuthia mandrillaris. Although rare, it almost always results in death. In the present study, amoebae were treated with various combinations of clinically-approved drugs, targeting vital cellular receptors and biochemical pathways. The results revealed that among the seven different combinations tested, three proved highly effective against both Acanthamoeba castellanii as well as B. mandrillaris at a concentration of 100μM. These combinations included (i) prochlorperazine plus loperamide; (ii) prochlorperazine plus apomorphine; and (iii) procyclidine plus loperamide. In viability assays, none of the drug-treated amoebae emerged as viable trophozoites, suggesting irreversible amoebicidal effects. Four combinations of drugs tested showed varied potency against A. castellanii and B. mandrillaris at 100μM. The combination of haloperidol and loperamide was highly effective against A. castellanii at 100μM, but potent effects against B. mandrillaris were observed only at 250μM. Digoxin and amlodipine were effective against A. castellanii and B. mandrillaris at 100μM and 250μM, respectively. In contrast, the combination of apomorphine and haloperidol was effective against B. mandrillaris and A. castellanii at 100μM and 250μM, respectively. At 100μM, the combination of procyclidine and amiodarone was effective against neither A. castellanii nor B. mandrillaris. In this case, amoebicidal properties were observed at 750μM for A. castellanii, and 950μM for B. mandrillaris. As these drugs are used clinically against non-communicable diseases, the findings reported here have the potential to be tested in a clinical setting against amoebic encephalitis caused by A. castellanii and B. mandrillaris.