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PubMed2004

Effects of quetiapine and haloperidol on prepulse inhibition of the acoustic startle (eyeblink) response and the N1/P2 auditory evoked response in man.

Contraction of the orbicularis oculi muscle in response to a sudden loud sound (acoustic startle response) and the N1/P2 component of the auditory evoked potential are both attenuated when a brief low-intensity stimulus is presented 30-500 ms before the 'startle-eliciting' stimulus (PPI). Here, we report the effects of the 'atypical' antipsychotic drug quetiapine and the 'conventional' antipsychotic haloperidol on these responses. Sixteen males (aged 19-38 years) participated in four sessions at 7-day intervals, in which they received quetiapine 12.5 mg, quetiapine 25 mg, haloperidol 3 mg and placebo, according to a balanced double-blind design. Electromyographic (EMG) responses of the orbicularis oculi muscle and N1/P2 auditory evoked potentials were recorded in a 20-min session, 2 h after treatment. Subjects received 40 trials in which 1-kHz sounds were presented: (i) 40 ms, 115 dB ('pulse alone' trials) and (ii) 40 ms, 85 dB, followed after 120 ms by 40 ms, 115 dB ('prepulse/pulse' trials). Mean amplitudes of the EMG response and the N1/P2 potential were derived from the pulse-alone trials and, in each case, percentage PPI was calculated. Serum prolactin was measured after each treatment, and autonomic (heart rate, blood pressure, salivation) and psychological (visual analogue self-ratings of mood and alertness, critical flicker fusion frequency) measures were taken before and after each treatment. Quetiapine 12.5 mg and 25 mg significantly reduced the amplitude of the EMG response without altering its inhibition by prepulses; haloperidol had no effect on EMG response amplitude or PPI. Neither drug affected N1/P2 amplitude or PPI of this response. Quetiapine, but not haloperidol, reduced subjective alertness and critical flicker fusion frequency. Haloperidol, but not quetiapine, elevated serum prolactin level. The ability of quetiapine to attenuate the startle response may reflect its sedative action.

Acoustic Stimulation↗
PubMed2005

Actions of antipsychotic drugs on pancreatic beta-cell function: contrasting effects of clozapine and haloperidol.

The use of antipsychotic drugs is known to be associated with a number of adverse metabolic side effects, including diabetes mellitus. These side effects could be, at least in part, the result of impaired islet cell function, although the underlying mechanisms are unknown. We have studied the effects of the atypical antipsychotic clozapine and of the conventional drug haloperidol on electrical and secretory activity in rat pancreatic beta-cells. At a low glucose concentration (4mM), clozapine (5microM) had little or no effect on membrane potential. However, at a stimulatory glucose concentration (16mM), clozapine was found to hyperpolarize the cell membrane potential, resulting in a complete inhibition of electrical activity. In contrast, haloperidol (5microM) was found to cause a marked depolarization of the membrane potential in the presence of both low and high concentrations of glucose. Clozapine and haloperidol were found, respectively, to increase and decrease-cell input conductance, an index of K(+) permeability. Single channel recordings indicated that changes in K(ATP) channel activity contributed towards these effects. Neither clozapine nor haloperidol affected basal insulin release, although clozapine inhibited glucose-induced insulin release. It is concluded that clozapine and haloperidol exert contrasting actions on electrical activity in rat pancreatic -cells as a result of opposing effects on K(+) permeability. These findings may relate to the increased incidence of diabetes associated with clozapine treatment.

Animals↗
PubMed1983

A comparison of the clinical effects of timiperone, a new butyrophenone derivative, and haloperidol on schizophrenia using a double-blind technique.

The efficacy and safety of timiperone, a new butyrophenone derivative, in schizophrenia as compared with haloperidol were assessed in a multi-clinic double-blind controlled study in a total of 206 patients. The patients were given timiperone (1.0 mg/tablet) or haloperidol (1.5 mg/tablet) in a daily dose of 1--3 tablets for the first day, then up to a maximum of 12 tablets depending on symptoms for 12 weeks. Timiperone was found to be significantly superior to haloperidol in the final global improvement rating and in the general usefulness rating. In the over-all safety rating there were no statistically significant differences between the two drug treatments. With regard to analysis by stratification timiperone was superior to haloperidol in improving abnormal experiences such as hallucination and delusion as well as deficiency of initiative and blunted affect. From these results it is considered that timiperone could be superior to haloperidol in the treatment of schizophrenia.

Adolescent↗
PubMed2002

Differential effects of haloperidol and clozapine on motor recovery after sensorimotor cortex injury in rats.

BACKGROUND: A variety of drugs impair motor recovery after sensorimotor cortex (SMCTX) injury in laboratory animals and may have similar effects in humans. METHODS: Rats (n = 142) underwent unilateral suction-ablation of the hindlimb SMCTX or sham lesion. After 24 hours, rats were given a single dose of placebo, haloperidol (0.1, 1.0, or 10.0 mg/kg, intraperitoneal), or clozapine (0.1, 0.5, 1.0, or 10.0 mg/kg, intraperitoneal), and motor recovery was measured. RESULTS: Neither haloperidol (analysis of variance [ANOVA] F[3, 12], P = 0.43) nor clozapine (ANOVA F[4, 19], P = 1.00) affected motor performance in controls. Haloperidol impaired motor recovery (ANOVA F[3, 42], P = 0.002) at each tested dose, with no differences between the doses. The effect persisted after 2 weeks. In contrast, although rats given a single dose of clozapine of 1.0 or 10.0 mg/kg had poorer recoveries (ANOVA F[4, 51], P = 0.014), only those given the highest dose differed from controls. The effect was no longer apparent after 2 weeks. CONCLUSION: Consistent with previous reports, haloperidol retards motor recovery after SMCTX injury in rats. In contrast, there was no detrimental effect of clozapine when given at low doses. The use of low doses of atypical antipsychotics such as clozapine may provide a safer alternative to haloperidol in the treatment of agitated stroke patients.

Analysis of Variance↗
PubMed2006

Intramuscular aripiprazole or haloperidol and transition to oral therapy in patients with agitation associated with schizophrenia: sub-analysis of a double-blind study.

OBJECTIVE: A sub-population analysis of 325 patients with agitation (Positive and Negative Syndrome Scale Excited Component [PEC] score > or = 15 and < or = 32; score of > or = 4 on > or = 2 items) associated with schizophrenia in a randomized, double-blind study investigating the efficacy and tolerability of intramuscular (IM) aripiprazole 9.75 mg, IM haloperidol 6.5 mg, or IM placebo and the transition to oral therapy. RESEARCH DESIGN AND METHODS: Over 24 h, patients could receive up to three IM injections; the second and third administered > or = 2 and > or = 4 h, respectively, after the first, if deemed clinically necessary. Following IM treatment, oral aripiprazole or haloperidol was administered for 4 days. The primary efficacy measure was the mean change in PEC score from baseline at 2 h. RESULTS: At 2 h, mean improvements in PEC scores with IM aripiprazole (-8.0) were significantly greater versus IM placebo (-5.7; p < or = 0.01), and similar versus IM haloperidol (-8.3). Secondary efficacy measures also significantly improved with active IM treatment versus IM placebo. Continuation with oral treatment provided continued efficacy with both active treatments. The safety profiles of IM and oral aripiprazole were similar. The incidence of extrapyramidal symptom-related adverse events was 0% with IM aripiprazole, 1.6% with IM placebo and 16.5% with IM haloperidol. CONCLUSION: Intramuscular aripiprazole is effective in patients with acute agitation associated with schizophrenia, comparable to IM haloperidol, and enables convenient transfer to oral aripiprazole therapy.

Administration, Oral↗
PubMed2001

Subjective response to antipsychotic treatment and compliance in schizophrenia. A naturalistic study comparing olanzapine, risperidone and haloperidol (EFESO Study).

BACKGROUND: In order to compare the effectiveness of different antipsychotic drugs in the treatment of schizophrenia it is very important to evaluate subjective response and compliance in patient cohorts treated according to routine clinical practice. METHOD: Outpatients with schizophrenia entered this prospective, naturalistic study when they received a new prescription for an antipsychotic drug. Treatment assignment was based on purely clinical criteria, as the study did not include any experimental intervention. Patients treated with olanzapine, risperidone or haloperidol were included in the analysis. Subjective response was measured using the 10-item version of the Drug Attitude Inventory (DAI-10), and treatment compliance was measured using a physician-rated 4 point categorical scale. RESULTS: A total of 2128 patients initiated treatment (as monotherapy) with olanzapine, 417 with risperidone, and 112 with haloperidol. Olanzapine-treated patients had significantly higher DAI-10 scores and significantly better treatment compliance compared to both risperidone- and haloperidol-treated patients. Risperidone-treated patients had a significantly higher DAI-10 score compared to haloperidol-treated patients. CONCLUSION: Subjective response and compliance were superior in olanzapine-treated patients, compared to patients treated with risperidone and haloperidol, in routine clinical practice. Differences in subjective response were explained largely, but not completely, by differences in incidence of EPS.

Adult↗
PubMed2004

Haloperidol in palliative care.

Haloperidol is one of 20 'essential' medications in palliative care. Its use is widespread in palliative care patients. The pharmacology of haloperidol is complex and the extent and severity of some of its adverse effects, particularly extrapyramidal adverse effects (EPS), may be related to the route of administration. Indications for the use of haloperidol in palliative care are nausea and vomiting and delirium. Adverse effects include EPS and QT prolongation. Sedation is not a common adverse effect of haloperidol. It is important that palliative care practitioners have a comprehensive understanding of the indications, doses, adverse effects and pharmacology of haloperidol. This review is intended to address these issues.

Antipsychotic Agents↗
PubMed1985

Sulpiride and haloperidol in schizophrenia: a double-blind cross-over study of therapeutic effect, side effects and plasma concentrations.

In a double-blind cross-over trial, 20 chronic schizophrenic patients were treated with sulpiride and haloperidol in two 12-week periods. The final median dose of sulpiride was 2000 mg/day (range 800-3200) and of haloperidol 12 mg/day (range 6-24). Sulpiride had an antipsychotic effect and therapeutic profile not significantly different from that of haloperidol. In spite of the high doses of sulpiride, extrapyramidal side-effects were seen less frequently during the first four weeks of the sulpiride period than during the corresponding haloperidol period (P less than 0.05), whereas autonomic side-effects were equally rare for both drugs. A positive correlation was found between daily dose and plasma concentration of both sulpiride (P less than 0.001) and haloperidol (P less than 0.05), but no correlation could be established between clinical effects and plasma levels of either neuroleptic.

Adolescent↗
PubMed1998

Oral olanzapine versus oral haloperidol in the maintenance treatment of schizophrenia and related psychoses.

BACKGROUND: Three studies compared olanzapine and haloperidol given orally in maintenance therapy for schizophrenia and related psychoses. METHOD: Data were from double-blind extensions of acute studies. The subjects met criteria for schizophrenia, schizophreniform disorder or schizoaffective disorder. Subjects had responded to acute therapy (Brief Psychiatric Rating Scale total score decreased > or = 40% from baseline (Studies 1, 2, and 3) or was < or = 18 (Studies 1 and 2)) and were out-patients at their last acute phase visit. Relapse was defined as hospitalisation for psychopathology. Subjects treated with olanzapine in the three studies were pooled to form the olanzapine group and subjects treated with haloperidol were pooled to form the haloperidol group. RESULTS: Olanzapine-treated subjects experienced less relapse (P = 0.034). The Kaplan-Meier estimated one-year risk of relapse was 19.7% with olanzapine and 28% with haloperidol. CONCLUSION: Olanzapine was superior to haloperidol in the maintenance therapy of schizophrenia and related psychoses. DECLARATION OF INTEREST: This work was sponsored by Eli Lilly and Company.

Administration, Oral↗
PubMed1999

Olanzapine versus haloperidol in the treatment of schizoaffective disorder. Acute and long-term therapy.

BACKGROUND: The effectiveness of antipsychotic monotherapy in schizoaffective disorder is limited, and further constrained by safety concerns. AIMS: We aimed to compare the efficacy, tolerability and safety profile of the new pharmaceutical, olanzapine, with haloperidol. METHOD: Data were assessed from 300 DSM-III-R schizoaffective subjects from a larger double-blind prospective international study. Subjects were randomly allocated to six weeks of olanzapine (5-20 mg) or haloperidol (5-20 mg) treatment; responders were followed for up to one year of double-blind, long-term maintenance therapy. RESULTS: Olanzapine-treated patients achieved a statistically significant greater improvement than haloperidol treated patients on overall measures of efficacy, including clinical response. Significantly fewer olanzapine patients left the study early, and fewer adverse events were observed among those receiving olanzapine. During maintenance, olanzapine-treated patients continued to experience additional improvement, with fewer EPS but more weight gain than those on haloperidol. CONCLUSIONS: Olanzapine demonstrated substantial advantages over the conventional antipsychotic haloperidol in the management of schizoaffective disorder.

Acute Disease↗
PubMed1982

Chronic haloperidol treatment increases the level of in vitro translatable messenger ribonucleic acid coding for the beta-endorphin/adrenocorticotropin precursor proopiomelanocortin in the pars intermedia of the rat pituitary.

Chronic treatment of rats with haloperidol (1.5 mg/kg, once daily) over a period of 7--21 days resulted in a 80--100% increase in the tissue levels of immunoreactive beta-endorphin and in the in vitro release of immunoreactive beta-endorphin from the neurointermediate pituitary. Incorporation of [3H]phenylalanine into isolated neurointermediate pituitaries of haloperidol-treated rats revealed an increase in the amount of label incorporated into the beta-endorphin/ACTH precursor proopiomelanocortin (POMC) to a similar extent (about 80%) but had essentially no effect on the conversion of the precursor into beta-lipotropin and beta-endorphin. Extraction of messenger (m) RNA from neurointermediate pituitaries followed by cell-free translation in a reticulocyte system showed an increase in the total level of translatable mRNA (about 25%). The content of translatable mRNA coding for POMC, however, was increased by 100-150%. Time-course studies revealed a parallelism between the effect of haloperidol on the level of in vitro translatable mRNA coding for POMC and the ability of the drug to increase the concentrations of beta-endorphin in the neurointermediate pituitary. A complete reversal of the effects of haloperidol was seen 2 weeks after discontinuation of the drug. These findings suggest that the chronic blockade of dopaminergic receptors by haloperidol causes a reversible increase in the beta-endorphin biosynthesis in the rat intermediate pituitary at the pretranslational level by markedly increasing the level of translatable mRNA coding for POMC.

Adrenocorticotropic Hormone↗
PubMed1999

A randomized trial of risperidone, placebo, and haloperidol for behavioral symptoms of dementia.

OBJECTIVE: To compare effects of risperidone with placebo (efficacy and tolerability) and haloperidol (tolerability) for treating demented patients with aggression and other behavioral symptoms. METHODS: A 13-week double-blind study involving 344 patients with dementia randomly assigned to receive placebo or flexible doses (0.5 to 4 mg/d) of risperidone or haloperidol. Behavioral symptoms were assessed by the Behavior Pathology in Alzheimer's Disease Rating Scale (BEHAVE-AD), the Cohen-Mansfield Agitation Inventory (CMAI), and the Clinical Global Impression (CGI) scale. Tolerability assessments included the Extrapyramidal Symptom Rating Scale, sedation levels, Functional Assessment Staging, Mini-Mental State Examination, and incidence of adverse events. RESULTS: The mean dose at endpoint was 1.1 mg/d of risperidone and 1.2 mg/d of haloperidol. Although not significant, a higher percentage of patients receiving risperidone than those receiving placebo showed clinical improvement (> or =30% reduction from baseline to endpoint in BEHAVE-AD total score) at endpoint and week 12. Reductions in the BEHAVE-AD total score were significantly greater with risperidone than with placebo at week 12. In a further analysis of aggression, the most dominant symptom in these patients, BEHAVE-AD and CMAI aggression cluster scores were significantly reduced compared with placebo at endpoint and week 12. CGI scores were also significantly reduced at endpoint and week 12. Severity of extrapyramidal symptoms with risperidone did not differ significantly from that of placebo and was less than that of haloperidol. A post hoc analysis showed significantly greater reductions in the BEHAVE-AD aggressiveness score with risperidone than haloperidol at week 12. CONCLUSION: Low-dose risperidone (mean 1.1 mg/d) was well tolerated and associated with reductions in the severity and frequency of behavioral symptoms, particularly aggression, in elderly patients with dementia.

Aged↗
PubMed1981

Alteration in dopaminergic and muscarinic cholinergic receptors after subchronic treatment with haloperidol in the developing rat brain.

Influence of subchronic treatment with haloperidol (0.5 to 5.0 mg/kg for 10 days, twice a day) on sensitivity of both central dopaminergic (DA) and muscarinic cholinergic (ACh) receptors was behaviorally and neurochemically investigated 4 days after withdrawal stage of the drug in the developing rat aged 28 days. An i.p. injection of apomorphine 0.2 mg/kg induced locomotor stimulation more effectively in haloperidol-treated animals than in controls. Scatchard analysis of the specific [3H]spiperone binding to the striatal membranes showed that haloperidol treatment produced an increase in the maximal number of binding sites (Bmax) without alteration in a dissociation constant (KD). Pilocarpine (100 and 150 mg/kg) was less effective in inducing catalepsy in the treated animals than in controls, although the treatment did not induce any alteration in saturation parameters of specific [3H]quinuclidinyl benzilate ([3H]QNB) binding to the homogenates of striatum, mesolimbic area and hippocampus. It is suggested that a decrease in Bmax in the striatal [3H]spiperone binding by chronic haloperidol treatment underlies DA receptor hypersensitivity in developing rats. Behavioral muscarinic hyposensitivity caused by chronic haloperidol may not to be due to alteration in the striatal [3H]QNB binding.

Animals↗
PubMed2004

Thermodynamic consideration of the charge transfer interaction of the donor: acceptor type between chloranilic acid and haloperidol.

The thermodynamic parameters of the charge transfer complex between chloranilic acid and haloperidol were studied. Haloperidol in pure form and in dosage form was assayed in this study. The method was based on charge transfer complex formation between the drug, which acted as an n-donor, and chloranilic acid, which acted as a pi acceptor in a non aqueous solvent. The complex stoichiometry was found to be 1:2 (haloperidol: chloranilic acid) with the maximum absorption band at a wavelength of 576 nm. The complex obeyed Beer's law. The thermodynamic parameters investigated included stability constant, molar absorptivity, free energy change, enthalpy, and entropy. The method was successfully applied in the analysis of commercially available haloperidol tablets without interference from its excipients, with good precision and reproducibility, compared with the official assay method (non aqueous titration) described for haloperidol in the compendium.

Benzoquinones↗
PubMed1978

[Studies on circadian susceptibility rhythm to haloperidol (author's transl)].

Rats were given haloperidol in a variety of doses and time combinations and the sedation period were then measured. A clear-cut daily fluctuation in the sedative effect was observed, and the pattern of fluctuation differed depending on the dosage. In an attempt to elucidate the mechanism of this phenomenon, haloperidol was administered at two different times between which there was a significant difference in the sedation period. No difference was found. Thus it is presumed that daily fluctuation in the sedative effect of haloperidol may be ascribed not to the daily fluctuation in the levels of absorption, excretion, metabolism, or distribution of this drug, but rather to the daily fluctuation at the level of catecholamine receptors in the brain. There was a daily fluctuation in the antiapomorphine effect of haloperidol in a variety of doses and time combinations, and the pattern of fluctuation almost equaled that of the sedative effects of haloperidol. The daily fluctuation of the sedative effect is probably due to effects of circadian rhythm in brain dopamine receptors.

Animals↗
PubMed1987

Effect of long-term dosing with tiapride on brain dopamine receptors and metabolism in rats. Comparative study with sulpiride and haloperidol.

The effects of long-term dosing with tiapride for 21 days on barin dopamine receptors and dopamine turnover were compared with those of sulpiride and haloperidol. Haloperidol caused an increase in both antagonist (3H-spiperone) labeled receptors and agonist (3H-N,n-propylnorapomorphine) labeled ones, whereas tiapride acted on the agonist binding sites and sulpiride acted on the antagonist binding sites. The increases induced by sulpiride were only observed in the striatum, while those induced by tiapride and haloperidol were observed in both the striatum and limbic area. Dopamine and dopamine metabolites in the brain tissues were measured at 2 hr and 3 days after long-term dosing with the drugs as an indicator of dopamine turnover. They were higher at 2 hr and lower at 3 days than those of the saline treated controls; however, the increase at 2 hr was much less than that after single acute dosing with drugs. This suggested that all drugs induced tolerance with regard to dopamine turnover. In these studies, tiapride and sulpiride were less active than haloperidol in the effects on brain dopamine receptors and dopamine turnover. This generally weaker activity of sulpiride and tiapride suggest that the benzamide drugs have fewer side effects such as a tardive dyskinesia, than does haloperidol, even after long-term dosing. Furthermore, a slight difference between the effects of tiapride and sulpiride on the dopamine receptor subtypes in the brain subdivision was suggested.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2003

Torsade de pointes associated with the administration of intravenous haloperidol:a review of the literature and practical guidelines for use.

Haloperidol is the most commonly used medication for the treatment of delirium and psychosis in the critically ill patient. Whilst generally considered to be safe, haloperidol has been associated with a number of important cardiovascular side effects. The major toxicities include hypotension, cardiac arrhythmias and prolongation of the corrected QT (QTc) interval. In particular, torsade de pointes, a polymorphic ventricular tachyarrhythmia, has been associated with both intravenous and oral haloperidol administration. The management of torsade de pointes consists of discontinuation of the possible offending agent(s), correction of electrolyte abnormalities, administration of magnesium sulfate and, if necessary, overdrive pacing. Although clinicians should be aware of this potentially lethal complication of intravenous haloperidol therapy, it should not deter clinicians from using intravenous haloperidol to treat acute agitation in the critically ill patient with a normal QTc.

Antipsychotic Agents↗
PubMed2004

Chronic haloperidol promotes corticostriatal long-term potentiation by targeting dopamine D2L receptors.

Reduced glutamate-mediated synaptic transmission has been implicated in the pathophysiology of schizophrenia. Because antipsychotic agents might exert their beneficial effects against schizophrenic symptoms by strengthening excitatory transmission in critical dopaminoceptive brain areas, in the present study we have studied the effects of acute and chronic haloperidol treatment on striatal synaptic plasticity. Repetitive stimulation of corticostriatal terminals in slices induced either long-term depression or long-term potentiation (LTP) of excitatory transmission in control rats, whereas it invariably induced NMDA receptor-dependent LTP in animals treated chronically with haloperidol. Haloperidol effects were mimicked and occluded in mice lacking both D2L and D2S isoforms of dopamine D2 receptors (D2R-/-), in mice lacking D2L receptors and expressing normal levels of D2S receptors (D2R-/-;D2L-/-), and in mice lacking D2L receptors and overexpressing D2S receptors (D2L-/-). These data indicate that the blockade of D2L receptors was responsible for the LTP-favoring action of haloperidol in the striatum. In contrast, overexpression of D2S receptors uncovered a facilitatory role of this receptor isoform in LTP formation because LTP recorded from D2L-/- mice, but not those recorded from wild-type, D2R-/-, and D2R-/-;D2L-/- mice, was insensitive to the pharmacological blockade of D1 receptors. The identification of the cellular, molecular, and receptor mechanisms involved in the action of haloperidol in the brain is essential to understand how antipsychotic agents exert their beneficial and side effects.

Animals↗