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Pharmacology haloperidol

In noncancer-related pharmacology, GSK3 is inhibited by lithium at therapeutic concentrations, implying that the long-established effectiveness of lithium in the treatment of psychiatric mood disorders (and more recently as a neuroprotective agent) may be linked to GSK3 inhibition. Antipsychotics such as haloperidol... [Pg.1321]

Other drugs such as the neuroleptic, haloperidol, inhibit the induction of hsp70 mRNA in rodent neurons (Sharp et al.. 1992). Although this observation needs to be confirmed in the human population, it raises the possibility that an age-dependent defect in the production of HS proteins is exacerbated by a drug which is commonly used in demented elderly patients. The potential for certain pharmacologic agents to inhibit the HS response could increase the risk for untoward effects of atherosclerosis and hypoxia. A similar concern may be raised with certain calcium channel blockers which also have been found to reduce the synthesis of HS proteins in cardiac myocytes (Low-Friedrich and Schoeppe, 1991). [Pg.447]

There is, however, a unique risk in the bipolar form that antidepressant treatment may trigger a switch into mania. This may occur either as the natural outcome of recovery from depression or as a pharmacological effect of the drug. Particular antidepressants (the selective serotonin reuptake inhibitors) seem less liable to induce the switch into mania than other antidepressants or electroconvulsive therapy. Treatment for mania consists initially of antipsychotic medication, for instance the widely used haloperidol, often combined with other less specific sedative medication such as the benzodiazepines (lorazepam intramuscularly or diazepam orally). The manic state will usually begin to subside within hours and this improvement develops further over the next 2 weeks. If the patient remains disturbed with manic symptoms, additional treatment with a mood stabilizer may help. [Pg.71]

The biplots show which binding tests are predictive for which pharmacological tests. Binding to the haloperidol and apomorphine labeled receptors corresponds with inhibition of agitation and stereotypy in rats, binding to the spiperone receptor... [Pg.413]

The relative selectivity of drugs such as haloperidol for the higher affinity (+)SKF-10,047 labeled sites allowed the determination of the pharmacological profile of the low affinity sites, which was very similar to that of 3H-TCP labeled sites. PCP and... [Pg.22]

Zhou, M., Liu, P., Zhang, H. Y. et al. (2002). Double-blind comparison between risperidone and haloperidol in the treatment of schizophrenic patients. Chinese Journal of Clinical Pharmacology, 18(5), 341. ... [Pg.96]

Suessbrich, H., Schonherr, R., Heinemann, S.H., Attali, B., Lang, F. and Busch, A.E. (1997) The inhibitory effect of the antipsychotic drug haloperidol on HERG potassium channels expressed in Xenopus oocytes. British Journal of Pharmacology, 120, 968-974. [Pg.80]

Saha N, Datta H, Sharma PL. (1991). Effects of morphine on memory interactions with naloxone, propranolol, and haloperidol. Pharmacology. 42(1) 10-14. [Pg.530]

Cyclo(His-D-Leu) acts as a hydrolytic catalyst. Cyclo(Leu-Gly) blocks the development of (1) physical dependence on morphine, (2) tolerance to the pharmacological effects of /3-endorphin, (3) tolerance to haloperidol-induced catalepsy and hypothermia, and (4) dopaminergic supersensitivity after chronic morphine administration. Cyclo(Tyr-Arg), a synthetic analogue of kyortorphin (an endogenous analgesic peptide), and its A-methyl tyrosine derivatives are more potent than kyotorphin in the mouse tail pressure test. ... [Pg.683]

A number of different compounds of the piperidine and piperazine series with p-fluorobuty-rophenone group substitutions at the nitrogen atom display significant neuroleptic activity (haloperidol, trifluperidol, droperidol, methorin). There is a considerable interest in butyrophenone derivatives as antipsychotic agents as well as in anesthesiology. They exhibit pharmacological effects and a mechanism of action very similar to that of phenothiazines and thioxanthenes in that they block dopaminergic receptors. However, they are more selective with respect to D2 receptors. [Pg.91]

In terms of pharmacological action, pimozide is similar to haloperidol. It is used in hospitals as well as in outpatient settings for supportive therapy of patients suffering from schizophrenia, paranoid conditions, and mental and neurotic disorders with paranoid characteristics. It is unfit for use in severe psychoses because it does not possess psychomotor-sedative action. It is used for treating patients who suffer from Turretts s syndrome. Pimozide has a number of side effects, many of which are similar to those of phe-nothiazine and a number of others. A synonym of this drug is orap. [Pg.97]

Among the difficulties in pharmacological treatment is the frequent non-compliance. The biggest determinant of compliance is the quality of a patient s relationship with his doctor. But a further way to handle the issue has involved the development of long acting products (depot neuroleptics), even though their effectiveness in the absolute or compared to oral preparations has not been adequately explored. The most commonly used depot agents are fluphenazine and haloperidol decanoate (see David et al., 2004). [Pg.679]

FIGURE 50.3 Childhood aggression or agitation pharmacological approach. DPH, diphenhydramine CLON, clonidine LZP, lorazepam CLZ, clonazepam HAL, haloperidol DRO, droperidol. [Pg.681]

Pharmacodynamics, antipsychotics also differ in their pharmacodynamics, i.e. their pharmacological and clinical profiles of action. A rough distinction is made between highly sedative, hypnotic antipsychotics (e.g. clopenthixol, levomepromazine) and other products with weaker initial sedative action (e.g. fluphenazine and haloperidol). Sedative antipsychotics are prescribed for states of major unrest, often combined with insomnia, whereas the less sedative antipsychotics are preferred for patients suffering from delusions and hallucinations but in whom heavy sedation during daytime is undesirable. [Pg.6]

For example, withdrawal of haloperidol in one patient revealed little change in either mental status or involuntary movements 3 weeks after discontinuation ( 478). In contrast, there was a marked deterioration in mental status and involuntary movements in this same patient 1 week after clozapine withdrawal. This rebound psychosis was attributed to increased dopamine release, a mechanism suggested by earlier observations made after withdrawal studies in humans and animals. For example, a study of the effects of abrupt withdrawal in rats showed increased and decreased striatal basal dopamine release with discontinuation of clozapine and haloperidol, respectively ( 479). The exacerbation of dyskinesia after clozapine withdrawal suggests that human nigrostriatal dopamine receptors (putatively involved in the emergence of dyskinetic movements) may be altered pharmacologically by this drug. [Pg.86]

The biochemical basis of ballismus is unknown, but the pharmacologic approach to management is the same as for chorea. Treatment with haloperidol, perphenazine, or other dopamine-blocking drugs may be helpful. [Pg.616]

The pharmacologic basis of these disorders is unknown, and there is no satisfactory medical treatment for them. A subset of patients respond well to levodopa medication (dopa-responsive dystonia), which is therefore worthy of trial. Occasional patients with dystonia may respond to diazepam, amantadine, antimuscarinic drugs (in high dosage), carbamazepine, baclofen, haloperidol, or phenothiazines. A trial of these pharmacologic approaches is worthwhile, though often not successful. Patients with focal dystonias such as blepharospasm or torticollis often benefit from injection of botulinum toxin into the overactive muscles. The role of deep brain stimulation for the treatment of these conditions is being explored. [Pg.616]

AccessMedicine Print Chapter 28. Pharmacologic Management of Parkinsonism Other Movement Disorders Haloperidol, other neuroleptics Sometimes helpful... [Pg.620]


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