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PubMed2006

Fyn is required for haloperidol-induced catalepsy in mice.

Fyn-mediated tyrosine phosphorylation of N-methyl-D-aspartate (NMDA) receptor subunits has been implicated in various brain functions, including ethanol tolerance, learning, and seizure susceptibility. In this study, we explored the role of Fyn in haloperidol-induced catalepsy, an animal model of the extrapyramidal side effects of antipsychotics. Haloperidol induced catalepsy and muscle rigidity in the control mice, but these responses were significantly reduced in Fyn-deficient mice. Expression of the striatal dopamine D(2) receptor, the main site of haloperidol action, did not differ between the two genotypes. Fyn activation and enhanced tyrosine phosphorylation of the NMDA receptor NR2B subunit, as measured by Western blotting, were induced after haloperidol injection of the control mice, but both responses were significantly reduced in Fyn-deficient mice. Dopamine D(2) receptor blockade was shown to increase both NR2B phosphorylation and the NMDA-induced calcium responses in control cultured striatal neurons but not in Fyn-deficient neurons. Based on these findings, we proposed a new molecular mechanism underlying haloperidol-induced catalepsy, in which the dopamine D(2) receptor antagonist induces striatal Fyn activation and the subsequent tyrosine phosphorylation of NR2B alters striatal neuronal activity, thereby inducing the behavioral changes that are manifested as a cataleptic response.

Animals↗
PubMed1989

Striatal homogenates from animals chronically treated with haloperidol stimulate dopamine and GABA uptake in cultures of rostral mesencephalic tegmentum.

The effect of pharmacologic denervation of striatal tissue on the production of growth promoting factors was examined in a cell culture system. Relative to saline-treated controls, rats were rendered behaviorally hypersensitive to a subsequent apomorphine challenge by 2 months of chronic treatment with haloperidol. Four days following chronic treatment, the animals were killed and the striata and cerebella were homogenized in Hank's Balanced Salt solution. The supernatants of these crude homogenates were then added to E-13 rostral mesencephalic tegmentum cultures for 6 days. Within 24 h, the haloperidol-treated striatal supernatants induced an overt increase in culture growth relative to all other supernatants. After 6 days, cultures incubated with haloperidol-treated striatal supernatants exhibited a significant increase in dopamine and GABA uptake relative to cultures incubated with all other supernatants. This effect was observed in the presence and absence of glia. The relative degree of this increased uptake was dependent upon the amount of haloperidol-treated striatal supernatant added. Boiling the supernatant removed the growth promoting effect. These results suggest that pharmacologic denervation of striatal tissue leads to a "target-specific" increase in growth promoting activity that may play a role in the pharmacologic and behavioral effects of haloperidol.

Animals↗
PubMed1992

Synaptic plasticity in the rat striatum following chronic haloperidol treatment.

Administration of the dopamine (DA) antagonist haloperidol leads to the development of behavioral hypersensitivity as well as enhanced neuronal growth when striatal extracts from these animals are incubated with mesencephalic cultures. For determining if alterations in neuronal growth also occur in vivo, the ultrastructure of the neuropil in the dorsolateral quadrant of the striatum from rats treated (24 days) with haloperidol (1.25 mg/kg) was examined by electron microscopy. Haloperidol-treated rats developed statistically significant behavioral hypersensitivity relative to vehicle-treated controls (p < 0.01). Evaluation of the neuropil revealed that haloperidol treatment enhanced, relative to vehicle-treated controls, the overall number of synaptic boutons by 9% (p < 0.01). The number of perforated synaptic profiles as well as the number of double synapses was increased by 20 and 50%, respectively, although this increase was not statistically significant. The number of myelinated axons remained unchanged, while the number of dendritic spines was increased by 21% (p < 0.05). These data suggest that chronic haloperidol treatment enhanced the growth and possible sprouting of presynaptic neurons and also induced postsynaptic plastic changes. These ultrastructural changes may contribute in part to hypersensitivity behaviors.

Animals↗
PubMed1981

Effects of lithium carbonate and haloperidol on cognition in aggressive hospitalized school-age children.

A comparison of the effects of lithium, haloperidol, and placebo on cognition is reported for a sample of hospitalized school-age children with a behavioral profile of aggressiveness and explosiveness. In this double-blind study, patients were randomly assigned to one of three treatment conditions. The cognitive battery was administered at the end of a 2-week placebo baseline period and again after 4 weeks of treatment. It included a simple reaction time (RT) task with preparatory intervals of 1, 4, and 8 seconds, the Porteus Mazes, and the Matching Familiar Figures Test. Drug effects on cognition, when found, were mild. Slower and more variable RTs were found on the RT task in the haloperidol group (mean dose, 3.1 mg/day), particularly at the 4- and 8-second preparatory intervals in comparison to placebo. This appeared to reflect decreased ability to hold a preparatory set. No other effects of haloperidol on cognitive performance were found. Lithium carbonate (mean dose, 1150 mg/day) caused a deterioration in qualitative performance on the Porteus Maze Test when compared with haloperidol but had no effect on test quotient scores or on the other cognitive measures. Results are discussed in terms of dose effects and the influences of task demands. This is part of a study critically assessing the effects of lithium and haloperidol on behavioral symptoms and other parameters.

Aggression↗
PubMed1997

Economic and health state utility determinations for schizophrenic patients treated with risperidone or haloperidol.

The current study uses utility analysis to assess economic and quality-of-life benefits of risperidone in patients with chronic schizophrenia. A retrospective analysis was performed on Positive and Negative Syndrome Symptoms (PANSS) data obtained from the published Canadian multicenter risperidone trial (part of the North American trial). Cluster analysis applied to endpoint PANSS scores, including all patients (N = 135), identified three clusters representing 130 patients with mild, moderate, and severe symptomatology. A narrative health state profile was written for each cluster, and 100 psychiatric nurses from Washington, DC, were asked to assign preference ratings to each one using linear analog and standard gamble (SG) methods. Mean utility values (confidence interval 95%) obtained from the SG ratings for the three health state profiles were 0.61 +/- 0.069 (mild); 0.36 +/- 0.073 (moderate); and 0.29 +/- 0.071 (severe). The mild health state (including the majority of risperidone 6 mg-treated patients) was rated by nurses to have a 0.25 +/- 0.0501 greater utility than the moderate health state (composed of the majority of haloperidol-treated patients). The results of these utility evaluations (SG) by the nurses were related to the clinical outcome for three of the six drug treatment groups (N = 65) by multiplying the percentage of patients in each of the three clusters, both at baseline and end-point, who were receiving risperidone 6 mg/day, haloperidol, or placebo, by the utility value for the health state assigned to that cluster. The gain in utility for risperidone-treated patients was 2.6 times higher (0.125) compared with haloperidol-treated patients (0.049), and 7 times higher compared with placebo (-0.021). After multiplying the gain in utility of each treatment by the remaining expected life span for men and women, it was found that risperidone-treated patients obtained more than twice as many quality-adjusted years as haloperidol patients. The incremental drug treatment cost divided by the incremental benefit of risperidone versus haloperidol was found to yield a favorable, generally accepted cost-utility ratio.

Adolescent↗
PubMed1999

Psychomotor, Cognitive, extrapyramidal, and affective functions of healthy volunteers during treatment with an atypical (amisulpride) and a classic (haloperidol) antipsychotic.

The primary objective of this study was to compare the objective and subjective effects of amisulpride with those of a classic antipsychotic, haloperidol, when both were given to healthy volunteers in representative therapeutic doses over 5 days. The secondary objective was to compare the effects of relatively low and high doses of amisulpride to confirm the suspected duality of its pharmacologic activity. Twenty-one subjects participated in the four-way, randomized, double-blind, crossover study with repeated daily doses of amisulpride 50 mg, amisulpride 400 mg, haloperidol 4 mg, and placebo. Subjects were institutionalized during treatment periods and were under 24-hour medical supervision. They underwent a series of psychomotor and cognitive tests 1 hour before and 3 and 6 hours after dosing on days 1 and 5. Their extrapyramidal disturbances and drug-related feelings were assessed at the end of each replication. Psychiatric interviews and ratings of depression, subjective well-being, and negative symptoms occurred on day 4. Amisulpride 50 mg had no significant effect on any parameter. Amisulpride 400 mg had several adverse effects on psychomotor and, although less severe, on cognitive performance on the fifth day only. Amisulpride 400 mg produced no significant extrapyramidal disturbances in the group as a whole, although it may have in some individual subjects. Also, it produced no signs of mental disturbances on clinical rating scales or during a structured psychiatric interview. Haloperidol ubiquitously impaired psychomotor and cognitive performance in a similar fashion after the first and the final doses. It produced extrapyramidal disturbances in nearly every subject, the most common being akathisia and the most severe, in the case of one individual, being acute dystonia. Unlike amisulpride, haloperidol produced a number of mental disturbances, the most noteworthy being negative symptoms. Amisulpride seems to be a well-tolerated drug. Its side effects should be much less troublesome to patients using the drug on a long-term basis than those of classic antipsychotics, like haloperidol.

Adult↗
PubMed2001

Divalproex sodium augmentation of haloperidol in hospitalized patients with schizophrenia: clinical and economic implications.

Divalproex sodium has been approved for use in treating bipolar disorder. Its usefulness in schizophrenia has yet to be adequately assessed. Three days after initiating haloperidol treatment, patients who were hospitalized for an acute exacerbation of schizophrenia received either valproate augmentation (early-augmentation group) or continued to receive haloperidol alone (no-augmentation group). Patients in the no-augmentation group who failed to respond 14 days after the dose of haloperidol reached 20 mg/day received valproate augmentation (delayed-augmentation group). By day 14, the early-augmentation group improved 32.4% more than the no-augmentation group. Fifty percent of the patients in the no-augmentation group failed to respond to haloperidol alone for 2 weeks. They improved by 29% upon the addition of valproate. Compared with those who received no or delayed augmentation, the early-augmentation group required 44.8% fewer inpatient days from the initiation of haloperidol treatment. Patient response to treatment was particularly noted in suspiciousness, hallucinations, unusual thought content, and emotional withdrawal. Early augmentation with valproate may reduce the length of inpatient stays and provide substantially better therapeutic outcomes. It is, however, premature to recommend changes in the standard clinical management of schizophrenia on the basis of the data provided herein, in view of the small sample and open-label nature of the report.

Adult↗
PubMed2002

Shifting from haloperidol to risperidone for behavioral disturbances in dementia: safety, response predictors, and mood effects.

For agitated dementia showing insufficient response to conventional antipsychotics, the feasibility of transition to atypical agents remains unknown. Sixty-two Chinese inpatients with dementia and disruptive behaviors were recruited into an 8-week screening trial of haloperidol. Thirty-five (56%) of them responded insufficiently. They then entered a prospective, 16-week, open-labeled study. Haloperidol was abruptly shifted to risperidone 0.5 mg/day at weeks 1 to 4 and then 1 mg/day at weeks 5 to 12. At weeks 13 to 16, the regimen was shifted back to haloperidol at previous doses, mostly 1 mg/day. Safety, efficacy, cognition, and moods were evaluated at least every 4 weeks. Generalized estimating equation methods were used for determining the effects of the prognostic variables on the outcome values. Risperidone, particularly at 0.5 mg/day, was generally tolerable. The Brief Psychiatric Rating Scale (BPRS) score decreased progressively under risperidone treatment; at week 12, 16 (46%) patients showed response (>or=25% reduction in the BPRS). Patients with vascular dementia were more likely to respond than those with Alzheimer's disease ( p = 0.02). Haloperidol reinstitution resulted in no further improvement, except trend increments in motor symptoms. Risperidone also tended to benefit the performance on the Behavioral Pathology in Alzheimer's Disease Rating Scale. Six (17%) patients improved on moods and self-care with risperidone. These preliminary results suggest that crossover from haloperidol to risperidone is generally safe and effective and may produce favorable moods in agitated dementia patients. Vascular dementia is a predictor of treatment response. In contrast to the dose (1 mg/day) recommended for most white individuals, 0.5 mg/day could be tried at first in Chinese patients. Because of the design's limitations, further controlled studies are warranted.

Activities of Daily Living↗
PubMed2002

The safety and pharmacokinetics of quetiapine when coadministered with haloperidol, risperidone, or thioridazine.

The effects of haloperidol, risperidone, and thioridazine on the pharmacokinetics and side-effect profile of quetiapine were investigated in 36 patients with schizophrenia, schizoaffective disorder, or bipolar disorder in a single-center, two-period, multiple-dose, open-label, randomized trial. Over a one-to two-week period, quetiapine doses were escalated to 300 mg twice daily (bid). Patients were then treated for at least 7 days at the target quetiapine dose and subsequently entered into the combination therapy period, receiving haloperidol (7.5 mg, bid), risperidone (3 mg, bid), or thioridazine (200 mg, bid) for 8.5 days (after 3 days of dose escalation). Key assessments included the pharmacokinetics of quetiapine at steady state (area under the curve within a dosing interval [AUCtSS], maximum [CmaxSS], and minimum [CminSS] observed plasma concentrations, and oral clearance [Cl/f]), as well as the UKU Side Effect Rating Scale scores and safety evaluations. Neither risperidone nor haloperidol had significant effects on quetiapine pharmacokinetics. However, thioridazine produced statistically significant changes, decreasing the least squares means values of the AUCtSS, CmaxSS, and CminSS by 40%, 47%, and 31%, respectively, and increasing Cl/f by 68%. Increases in the following adverse events were noted during coadministration: somnolence (risperidone), insomnia and dry mouth (all three coadministered therapies), and dizziness (thioridazine). UKU side effect items that became worse in >or= 25% of patients during each coadministration period included sedation and increased sleep duration. Results of laboratory tests, electrocardiograms, and vital sign measurements revealed few clinically important changes. Clinical stability can be maintained with good tolerability during the transition from quetiapine monotherapy to periods of coadministration with haloperidol, risperidone, or thioridazine. Coadministration of either haloperidol or risperidone did not have any important effects on the steady-state pharmacokinetics of quetiapine. Thioridazine significantly increased the oral clearance of quetiapine. Increased doses of quetiapine may be necessary to control psychotic symptoms when thioridazine is coadministered with quetiapine.

Adolescent↗
PubMed1995

Remoxipride versus haloperidol in healthy volunteers: psychometric performance and subjective tolerance profiles.

The aim of the present study was to evaluate the psychometric effects of equivalent clinical doses of remoxipride and haloperidol in comparison with placebo in healthy volunteers. In a double-blind design, either 3 mg haloperidol, 150 mg remoxipride, or placebo were administered to 36 healthy male volunteers ranging in age from 19 to 39 years. Performance was assessed using time estimation, critical flicker fusion, and choice reaction time tasks. In addition, self-ratings on subjective well-being were obtained. In healthy subjects, an acute dose of 3 mg haloperidol caused more severe alteration in cognitive functioning, cortical arousal, and psychomotor performance than a clinically equipotent dose of 150 mg remoxipride. Also, self-rating scales showed that subjective tolerance of remoxipride was partly superior to haloperidol. In general, the results of this study strongly suggest a difference between the psychometric profiles of remoxipride and haloperidol. This difference may be essential for maintaining a high level of compliance, especially in the long-term treatment of psychotic patients.

Adult↗
PubMed1976

The influence of various factors in the in vitro distribution of haloperidol in human blood.

Haloperidol is 89.6+/-0.3% bound (mean+/-s.e. mean) in human plasma under in vitro conditions and the free drug distributes rapidly between the plasma and the cellular elements of blood. The cell/plasma partition ratio was 1.12+/-0.06 (mean+/-s.e. mean). Alteration of plasma binding by dilution with buffer showed that uptake of haloperidol by the cellular elements of blood was proportional to free drug concentration. Bishydroxycoumarin (95 ot 286 mug/ml) reduced plasma binding of haloperidol and the displaced haloperidol was taken up by the cellular blood elements. The experiments indicate that the cellular compartment of blood as well as the plasma compartment may act as a sink for haloperidol and drug displacement interactions should therefore be interpreted with a knowledge of both of these compartments.

Female↗
PubMed1989

Substantial rise in sparteine metabolic ratio during haloperidol treatment.

A sparteine test was carried out in 14 patients suffering from acute schizophrenic psychoses before and 1-2 times during oral haloperidol treatment in doses of 10-40 mg day-1. In patients classified as extensive metabolisers (sparteine MR less than 20 before treatment), haloperidol treatment resulted in a rise in sparteine MR that correlated with the serum-haloperidol concentration both within and between patients. At the highest serum haloperidol concentrations (60-80 nM) an increase in sparteine MR by a factor 15-50 was seen, but no patients were transformed into phenotypically poor metabolisers. The steady state concentration of haloperidol on the initial standard dose of 10 mg day-1 was the same in one patient classified as a sparteine poor metaboliser (MR = 112) as in eleven patients classified as extensive metabolisers (MR:0.22-1.47).

Adult↗
PubMed1990

A comparison of the central nervous system effects of haloperidol, chlorpromazine and sulpiride in normal volunteers.

1. Twelve healthy male volunteers participated in four experimental occasions during each of which they were dosed with one of the following anti-psychotic drugs: chlorpromazine (50 mg), haloperidol (3 mg), sulpiride (400 mg) and placebo. Drugs were allocated to subjects in a double-blind, crossover fashion. 2. The subject's mood state, psychometric performance and electroencephalogram (EEG) were assessed pre-dose, and at 2, 4, 6, 8, 24 and 48 h post-dose. Mood states were assessed using 16 visual analogue scales and psychomotor performance was measured using the following tests: elapsed time estimation, tapping rate, choice reaction times, a rapid information processing task, flash fusion threshold, a manipulative motor task, digit span, body sway and tremor. 3. Chlorpromazine and haloperidol significantly reduced subjective ratings of 'alertness' and 'contentedness', and haloperidol significantly reduced feelings of 'calmness'. Sulpiride did not significantly affect any of the visual analogue scales. 4. All three anti-psychotic drugs had similar EEG effects with peak effect 2 to 4 h postdose. The profile was characterised by an increase in the proportion of slow wave activity (delta and theta) as well as decreased alpha (8-14 Hz) and faster (beta) wave activity. 5. Chlorpromazine reduced tapping rate and increased choice reaction movement times. Haloperidol reduced the flash fusion threshold frequency at 6 h post-dose. Sulpiride prolonged the duration of the manipulative motor task, particularly at 48 h post-dose. 6. All three anti-psychotic drugs impaired performance on the rapid information processing task. Chlorpromazine significantly reduced the number of correct letter pair identifications at 2, 4 and 6 h post-dose, haloperidol at 4, 6, 8, 24 and 48 h post-dose, and sulpiride at 24 h post-dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2004

Comparative cardiac safety of low-dose thioridazine and low-dose haloperidol.

AIM: To compare the rate of ventricular arrhythmia, sudden death and unexplained or unattended death among users of thioridazine and haloperidol. METHODS: Observational cohort study of thioridazine and haloperidol users in the UK General Practice Research Database (GPRD) using data from 1987 through 29 June 2000. Patients were followed for 30 days following each study prescription. The event of interest was a diagnosis of ventricular arrhythmia, sudden death, or unexplained or unattended death. Cox regression was used to calculate rate ratios (RRs) and 95% confidence intervals (CIs), to examine potential confounding factors, and to examine dose-response relationships. RESULTS: Use of thioridazine and haloperidol in the GPRD was primarily in older patients, at low dose (median daily dose 31 mg thioridazine, 1.8 mg haloperidol). There was no association between thioridazine use and the rate of ventricular arrhythmia, sudden death, and unexplained or unattended death (adjusted RR 0.9, 95% CI 0.7, 1.1). The rate did not appear to increase with dose for either drug over the range observed. CONCLUSIONS: These results suggest that low-dose thioridazine and haloperidol have similar cardiac safety.

Adolescent↗
PubMed2006

Identification of a new functional target of haloperidol metabolite: implications for a receptor-independent role of 3-(4-fluorobenzoyl) propionic acid.

Haloperidol, a dopamine D2 receptor blocker, is a classical neuroleptic drug that elicits extrapyramidal symptoms. Its metabolites include 3-(4-fluorobenzoyl) propionic acid (FBPA) and 4-(4-chlorophenyl)-4-piperidinol (CPHP). Until now, the biological significance of these metabolites has remained largely unknown. Here, we report that the administration of FBPA to mice effected a suppression of locomotor activity and induced catalepsy in a manner similar to that observed with haloperidol, whereas CPHP had no significant effects. Neither of these two metabolites, however, exhibited any ability to bind to the dopamine D2 receptor. FBPA blocked dopamine-induced extracellular signal-regulated kinase 1/2 phosphorylation, and it specifically affected mitogen-activated protein kinase kinase (MEK)1/2 activity in hippocampal HN33 cells. Moreover, FBPA was capable of direct interaction with MEK1/2, and inhibited its activity in vitro. We demonstrated the generation of haloperidol metabolites within haloperidol-treated cells by mass spectrometric analyses. Collectively, our results confirm the biological activity of FBPA, and provide initial clues as to the receptor-independent role of haloperidol.

Animals↗
PubMed1991

Muscarinic antagonists attenuate the increase in accumbens and striatum dopamine metabolism produced by clozapine but not by haloperidol.

1. The effect of the muscarinic antagonists, scopolamine and atropine, were examined on the increase in extracellular 3,4-dihydroxyphenylacetic acid (DOPAC) in the nucleus accumbens and the striatum induced by haloperidol and clozapine by use of in vivo differential pulse voltammetry with carbon fibre electrodes in anaesthetized rats. 2. Animals received saline (1 ml kg-1, s.c.), scopolamine (1 mg kg-1, o.p.) or atropine (20 micrograms, i.c.v.) followed 15 min later by saline (10 microliters, i.c.v.), haloperidol (1 mg kg-1, s.c.) or clozapine (30 mg kg-1, i.p.) and extracellular DOPAC was simultaneously recorded in the nucleus accumbens and the striatum every 5 min for 60 min after drug administration. 3. Scopolamine or atropine alone had no effect on the DOPAC peak height but attenuated the increase in extracellular DOPAC induced by clozapine in both brain regions. Neither scopolamine nor atropine altered the haloperidol-induced increase in accumbens or striatal extracellular DOPAC. 4. The present results demonstrate that muscarinic antagonists attenuate the increase in accumbens and striatal dopamine metabolism in vivo produced by the atypical neuroleptic clozapine but not the haloperidol-induced increase in dopamine metabolism. The results indicate that central muscarinic receptors are involved in the actions on dopaminergic function of clozapine but not haloperidol.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1993

Effect of haloperidol on measures of craving and impaired control in alcoholic subjects.

We recently proposed that alcoholics suffer from a functional defect within the basal ganglia/limbic striatum or its modulation by dopaminergic projections from the ventral tegmentum, and that inhibition of striatal output caused by the prodopaminergic effects of alcohol ingestion induces or exacerbates craving and impaired control over alcohol consumption in alcoholic individuals. To test this hypothesis, 16 subjects with a diagnosis of alcohol dependence or abuse were studied in a double-blind, placebo-controlled experiment in which the effects of the D-2 antagonist haloperidol on measures of craving and impaired control were assessed before and after administration of a priming dose of alcohol. Subjects were pretreated with 0.015-0.025 mg/kg haloperidol (experimental condition) or 2 ml normal saline (control condition), and subsequently consumed 0.4-0.6 g/kg ethanol as their preferred alcohol-containing beverage. Significant increases in subjectively rated craving for alcohol and perceived difficulty resisting additional alcohol consumption occurred following the priming dose of alcohol when subjects were pretreated with saline. In contrast, no significant changes in reported ability to resist additional alcohol occurred when subjects were pretreated with haloperidol, and reported levels of craving decreased relative to baseline following haloperidol pretreatment. Subjects also consumed about 25% less optionally available alcohol when pretreated with haloperidol than when pretreated with saline. These findings support the hypothesis that craving and impaired control are induced or exacerbated by the prodopaminergic effects of alcohol consumption.

Adult↗
PubMed1984

Sulpiride versus haloperidol, a clinical trial in schizophrenia. A preliminary report.

Sixteen out of 25 hebephrenic and paranoid schizophrenic patients completed a double-blind cross-over study with sulpiride and haloperidol. The patient sample was relatively chronic: Median age was 35 years (range 26-53 years), median duration of illness 10 years (4-35 years), and median duration of neuroleptic treatment 5 years (1-28 years). Each patient was treated with sulpiride/haloperidol in random order for 12 weeks with a drug-free period before each treatment phase. Mean total BPRS (Brief Psychiatric Rating Scale) score was reduced from 25 to 15 (P less than 0.05) during sulpiride (800-2800 mg/day, median 1600 mg/day), and from 28 to 15 (P less than 0.01) during haloperidol (6-18 mg/day, median 12). There were no significant differences between the groups with respect to total BPRS score, single items or symptom clusters. However, in a few, very "chronic", disturbed, and long-term treated patients, haloperidol appeared more beneficial than sulpiride. Autonomic side effects and parkinsonism tended to occur more frequently during haloperidol than during sulpiride, but no significant differences were found. It is concluded that sulpiride, a specific dopamine-2 receptor blocker, has antipsychotic effect, not significantly different from haloperidol, but may produce slightly less side effects.

Adult↗