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PubMed1975

Haloperidol parenterally for treatment of vomiting and nausea from gastrointestinal disorders in a group of geriatric patients: double-blind, placebo-controlled study.

Twenty-eight geriatric residents of a nursing home participated in a double-blind study to compare the 12-hour therapeutic effectiveness of a single intramuscular injection (1.0 mg) of haloperidol with that of placebo for the relief of vomiting and nausea due to gastrointestinal disorders. Significantly fewer episodes of vomiting occurred in the haloperidol group than in the placebo group. Nausea also was less frequent in the haloperidol group. After four hours, symptoms recurred much more often in the placebo group. Global evaluations showed that a significantly greater number of haloperidol patients improved markedly than did those given placebo. There were no clinically significant changes in vital signs throughout the study in the haloperidol group. In 1 placebo patient the pulse rate was significantly increased; otherwise no adverse reactions were reported for this group. Thus, in a nursing-home population of geriatric patients who experienced vomiting and nausea due to gastrointestinal disorders, haloperidol administered parenterally proved to be a safe and highly effective antiemetic agent.

Age Factors↗

PubMed2005

Haloperidol prophylaxis for elderly hip-surgery patients at risk for delirium: a randomized placebo-controlled study.

OBJECTIVES: To study the effectiveness of haloperidol prophylaxis on incidence, severity, and duration of postoperative delirium in elderly hip-surgery patients at risk for delirium. DESIGN: Randomized, double-blind, placebo-controlled trial. SETTING: Large medical school-affiliated general hospital in Alkmaar, The Netherlands. PARTICIPANTS: A total of 430 hip-surgery patients aged 70 and older at risk for postoperative delirium. INTERVENTION: Haloperidol 1.5 mg/d or placebo was started preoperatively and continued for up to 3 days postoperatively. Proactive geriatric consultation was provided for all randomized patients. MEASUREMENTS: The primary outcome was the incidence of postoperative delirium (Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, and Confusion Assessment Method criteria). Secondary outcomes were the severity of delirium (Delirium Rating Scale, revised version-98 (DRS-R-98)), the duration of delirium, and the length of hospital stay. RESULTS: The overall incidence of postoperative delirium was 15.8%. The percentage of patients with postoperative delirium in the haloperidol and placebo treatment condition was 15.1% and 16.5%, respectively (relative risk=0.91, 95% confidence interval (CI)=0.6-1.3); the mean highest DRS-R-98 score+/-standard deviation was 14.4+/-3.4 and 18.4+/-4.3, respectively (mean difference 4.0, 95% CI=2.0-5.8; P<.001); delirium duration was 5.4 versus 11.8 days, respectively (mean difference 6.4 days, 95% CI=4.0-8.0; P<.001); and the mean number of days in the hospital was 17.1+/-11.1 and 22.6+/-16.7, respectively (mean difference 5.5 days, 95% CI=1.4-2.3; P<.001). No haloperidol-related side effects were noted. CONCLUSION: Low-dose haloperidol prophylactic treatment demonstrated no efficacy in reducing the incidence of postoperative delirium. It did have a positive effect on the severity and duration of delirium. Moreover, haloperidol reduced the number of days patients stayed in the hospital, and the therapy was well tolerated.

Aged↗

PubMed1990

Remoxipride and haloperidol in schizophrenia: a double-blind multicentre study.

Ninety-two patients with schizophrenia were included in a double-blind multicentre parallel-group trial comparing remoxipride and haloperidol. The mean daily dose during the last week of treatment was 316 mg (range, 150-600 mg) in the remoxipride group and 8.7 mg (range, 5-20 mg) in the haloperidol group. The study period was six weeks with at least one day of washout. Both Clinical Global Impression (CGI) rating, and Brief Psychiatric Rating Scale (BPRS) total scores declined at the end of the trial compared with pretreatment values in both groups. No significant differences were found between the remoxipride and haloperidol groups with regard to the treatment outcome. Treatment-emergent extrapyramidal symptoms were statistically more frequent and more severe during haloperidol than during remoxipride treatment. Haloperidol-treated patients reported also significantly more concentration difficulties. Severe extrapyramidal side effects in the haloperidol group and clinical ineffectiveness in the remoxipride group were the most frequent reasons for premature discontinuation of treatment.

Adolescent↗

PubMed1990

A double-blind comparative study of remoxipride and haloperidol in schizophrenic and schizophreniform disorders.

The antipsychotic effect of remoxipride was compared to that of haloperidol in a randomized double-blind study with parallel group design comprising 98 patients with schizophrenia or schizophreniform disorder according to DSM-III. After a 3-7 day placebo washout period, patients received either 150-600 mg of remoxipride or 5-20 mg of haloperidol daily for 6 weeks. No significant differences in efficacy were found between the two treatments. Treatment-emergent checklist symptoms such as hypokinesia, rigidity, and tremor occurred more frequently and were more severe during haloperidol than during remoxipride treatment despite a significantly higher concurrent use of anticholinergic drugs in the haloperidol group. Haloperidol-treated patients reported greater increases in sleep and salivation than remoxipride-treated patients. Shoulder shaking and tremor were reported as occurring more frequently in the haloperidol group according to the Simpson and Angus rating scale for extrapyramidal symptoms. In summary, the two drugs seemed to be equally efficacious, though the tolerability profile favoured remoxipride.

Adult↗

PubMed1988

Haloperidol and metabolite concentrations in the rat after concurrent isotretinoin administration: a preliminary report.

Blood and tissue haloperidol concentrations can be altered by the concurrent administration of a number of other drugs. Here we describe effects of concurrent administration of the vitamin A metabolite, isotretinoin, on haloperidol and reduced haloperidol concentrations in the rat. Isotretinoin increased the concentrations of both haloperidol and reduced haloperidol in serum, red blood cells, and brain. However, the dose dependence and degree of the effect varied significantly across tissues. Further study is called for to elucidate the interaction of neuroleptics such as haloperidol with the vitamin A acids such as isotretinoin.

Animals↗

PubMed1988

Effects of acute haloperidol treatment on regional catecholamine levels and utilization in rats exposed to toluene.

The aim of the present investigation was to evaluate whether the responses of central catecholamine (CA) neurons to CA receptor blockade by haloperidol are altered upon toluene exposure. Male rats were exposed to air or toluene (80 ppm) for 5 and 4 days, 6 h day-1. CA levels and utilization were determined in discrete regions of the forebrain and hypothalamus as well as in the substantia nigra (SN) and anteromedial frontal cortex (AMFC). Serum levels of corticosterone, thyroid stimulating hormone, luteinizing hormone and prolactin were determined by radioimmunoassay procedures. Toluene exposure led to increased dopamine (DA) utilization in the AMFC and increased CA utilization in the paraventricular hypothalamic nuclei. In air-exposed rats haloperidol (1 mg kg-1, i.p., 2 h before killing) increased DA utilization in the marginal part of the nucleus caudatus putamen (CAUD). In toluene-exposed rats, haloperidol induced significant depletions of DA stores in the SN and in the medial and central parts of the CAUD. In the posterior nucleus accumbens (ACC) DA utilization was significantly increased. Combined haloperidol and toluene treatment selectively decreased DA levels in the ACC and SN, and significantly increased DA utilization in the CAUD, as compared with the air-exposed control group. Furthermore, after combined treatment, there was a specific increase in noradrenaline (NA) utilization in the SN and in CA utilization in the medial palisade zone of the median eminence. Serum prolactin levels were substantially raised in both the air and toluene groups after the haloperidol treatment. In conclusion, acute haloperidol treatment preferentially reduces DA levels and increases DA and NA utilization in the SN and in discrete tel- and diencephalic areas in rats exposed to toluene.

Animals↗

PubMed1985

Haloperidol-induced suppression of carotid chemoreception in vitro.

Effects of antagonism of endogenous dopamine with haloperidol on single-unit frequency, interspike interval distribution, and interval serial dependency of the cat sinus nerve were tested using an in vitro carotid body-sinus nerve superfusion technique. A dose dependency of inhibition by haloperidol (0.05-2.0 microgram/ml) was observed. Superfusion with 1-2 microgram/ml haloperidol significantly reduced frequency within 5 min (P less than 0.05) and caused a complete cessation of firing within 25 min in 5 of 10 chemoreceptor units. Frequency recovered to control during drug washout. Acetylcholine (10-micrograms/ml superfusion or 500-micrograms bolus) increased sinus nerve activity under control conditions but not during superfusion with haloperidol. No effect of haloperidol on impulse serial dependency was detected. However, interval distribution was significantly altered by haloperidol in five of six chemoreceptor units. Our results suggest an excitatory role for dopamine in carotid chemoreception.

Action Potentials↗

PubMed1996

Haloperidol affects guinea pig chewing burst durations.

Previous investigations have reported that most movement patterns in humans and other mammalian species are partitioned into 1-5-s units. This finding has led to the hypothesis that a highly conservative physiological system, common among mammalian species, segments ongoing movement patterns into 1-5-s 'chunks'. However, to date little or no work has been done to explore the physiological and neurochemical nature of this segmenting phenomenon; therefore, it is unknown whether the same evolutionarily conservative mechanism controls partitioning of all movement patterns. The literature suggests that central dopamine plays a key role in this 1-5-s partitioning. If this is so, then dopamine blockers should result in significant alterations in the 1-5-s segmentation of mammalian movement patterns. To test this hypothesis, the current study determined whether the neuroleptic haloperidol significantly affected guinea pig chewing burst durations, which reportedly average 1-3 s and are therefore considered to manifest this partitioning phenomenon. Seven male albino guinea pigs received daily 0.5 mg/kg i.m. haloperidol injections, and three male albino guinea pigs received comparable saline injections (controls). After either 3 or 11 weeks, injections were stopped, and 1 week thereafter the animals were starved for 24 h and then videotaped singly in an experimental arena. Animals inevitably fed on alfalfa pellets during the taping session, and the chewing bursts that occurred while the animals fed were timed. The results showed that control animals' chewing bursts had durations similar to those previously reported for free-roaming, non-drug-treated guinea pigs. However, haloperidol-treated guinea pigs' chewing bursts were significantly more variable in duration (p = 0.0013) than those of matched control animals. Inspection of the data from individual animals revealed that two haloperidol-treated animals had abnormally short chewing burst durations, whereas three haloperidol-treated animals had abnormally long chewing burst durations. The fact that haloperidol treatment was associated with either abnormally short or long chewing burst durations is reminiscent of neuroleptic-induced human movement disorders, which reportedly range from a 'paucity of movement' to 'perseverant movements'. This suggests that intact central dopaminergic systems may play an important role in modulating the duration of mammalian movement patterns, which normally ranges 0.2-5 s.

Animals↗

PubMed1989

Effects of treatment with various doses of haloperidol on the pituitary-gonadal axis in male schizophrenic patients.

Fifteen male paranoid schizophrenics underwent an initial 4-week therapy with haloperidol 7.5 mg/day, and a subsequent 4-week treatment with haloperidol 15 mg/day, p.o. (group I). Another 15 male paranoid schizophrenics received an initial 4-week treatment with haloperidol 30 mg/day, and a subsequent 4-week therapy with haloperidol 60 mg/day, p.o. (group II). In each group of patients, serum prolactin (PRL), luteinizing hormone (LH) and testosterone (T) levels were measured before treatment and at the end of the two consecutive periods of treatment. A dose-related increase in serum PRL levels was found in both groups of medicated patients. Serum LH levels were not significantly affected by haloperidol treatment. A significant decrease in serum T levels was detected only in group II medicated patients, i.e., in the patients who were treated with relatively high daily doses (30 or 60 mg/day) of haloperidol.

Acute Disease↗

PubMed1985

Pharmacokinetics and effects of haloperidol in the isolated mouse.

The pharmacokinetic behaviour of haloperidol (0.6 mg/kg s.c.) was studied in grouped and 4-week isolated male mice of the CF-1 strain (24 h observation; gas chromatography, NPFID). Maximal drug levels occurred in serum within 2 min and in whole brain after 15 min. The elimination from serum and brain was biphasic with larger t1/2 values for brain. There was an accumulation of haloperidol in brain up to 40 times of the serum level. Isolation resulted in a more rapid first phase of elimination from serum, provided the animals were tested for aggressivity immediately before the administration of the drug. The minimal effective (i.e. cataleptogenic) brain level of haloperidol was approximately 0.1 microgram/g wet weight. Haloperidol-induced catalepsy was (after 1 h) in isolated mice weaker than in grouped mice; this applied to animals of both the CF-1 and the NMRI strain. The catalepsy disappeared after 6 h. The antagonism by haloperidol of the stereotyped gnawing (induced by methylphenidate, 30 and 50 mg/kg, i.p., NMRI mice) likewise lasted for 6 h. Therefore, the cataleptic effects, but not the brain levels of haloperidol, are influenced by isolation and aggression in mice.

Aggression↗

PubMed1988

Differential alteration in striatal dopaminergic and cortical serotonergic receptors induced by repeated administration of haloperidol or centbutindole in rats.

Centbutindole is a new neuroleptic drug having a pharmacological profile similar to haloperidol, but it does not cause hypothermia and has a higher separation between doses causing catalepsy and neurolepsy. The interactions of centbutindole with striatal dopamine and cortical 5-HT2 receptors have been studied along with haloperidol following 3 weeks of administration. Rats received haloperidol (1.0 mg/kg, p.o.), centbutindole (0.5 mg/kg, p.o.) or saline daily for 21 days. Following drug withdrawal for 3 days, apomorphine (0.1-1.0 mg/kg, i.p.) or 5-hydroxytryptamine (5-HTP, 50-200 mg/kg, i.p.) was injected. Apomorphine-induced stereotyped behaviour was potentiated in the haloperidol-treated rats, while the 5-HTP-induced behavioural syndrome was increased in centbutindole-treated rats. Receptor binding studies indicated an increase in the maximal binding capacity Bmax of striatal dopamine receptor (29.4%) in haloperidol-treated and of cortical 5-HT2 receptor (17.8%) in centbutindole-treated animals. No change in the apparent dissociation constant Kd was observed. It is concluded that repeated treatment with haloperidol produced striatal dopamine receptor supersensitivity while centbutindole treatment produced cortical serotonergic receptor supersensitivity.

5-Hydroxytryptophan↗

PubMedDate not supplied

A randomized, double-blind, crossover comparison of risperidone and haloperidol in Korean dementia patients with behavioral disturbances.

OBJECTIVE: Behavioral disturbances in dementia are extremely prominent and distressful, and often result in serious physical, social, and economic consequences. The authors compared the efficacy and tolerability of risperidone and haloperidol in the treatment of behavioral and psychological symptoms of dementia (BPSD) in institutionalized elderly Korean patients with Alzheimer disease, vascular dementia, or mixed dementia. METHODS: This was an 18-week double-blind, crossover study involving 120 patients who were randomly assigned to receive flexible doses (0.5-1.5 mg/day) of risperidone or haloperidol. BPSD were assessed using the Korean version of the Behavioral Pathology in Alzheimer's Disease Rating Scale (BEHAVE-AD-K), the Korean version of the Cohen-Mansfield Agitation Inventory (CMAI-K), and the Clinical Global Impression of Change scale (CGI-C). Safety and tolerability assessments included the Extrapyramidal Symptom Rating Scale and the incidence of adverse events. RESULTS: Both risperidone and haloperidol were efficacious in alleviating BPSD. However, when receiving risperidone, patients showed significantly greater improvement than when receiving haloperidol in the total and subscale scores of the BEHAVE-AD-K, the total and subscale scores of the CMAI-K, and the scores on the CGI-C scale. Also, risperidone had an additional benefit on aggressiveness and anxieties/phobias. The risk of antipsychotic-induced parkinsonism throughout this study was significantly lower with risperidone than with haloperidol. CONCLUSION: Risperidone had a favorable efficacy and tolerability profile compared with haloperidol in the treatment of BPSD in this patient population.

Aged↗

PubMed2003

Comparative efficacy and safety of atypical and conventional antipsychotic drugs in first-episode psychosis: a randomized, double-blind trial of olanzapine versus haloperidol.

OBJECTIVE: Few long-term studies have compared the efficacy and safety of typical and atypical antipsychotic medications directly in patients with a first episode of psychosis who met the criteria for schizophrenia or a related psychotic disorder. This study compared the acute and long-term effectiveness of haloperidol with that of olanzapine in patients with first-episode psychosis in a large, controlled clinical trial. METHOD: Patients with first-episode psychosis (N=263) were randomly assigned under double-blind conditions to receive haloperidol or olanzapine and were followed for up to 104 weeks. Domains measured included psychopathology, psychosocial variables, neurocognitive functioning, and brain morphology and metabolism. This report presents data from clinical measures of treatment response and safety data from the 12-week acute treatment phase. RESULTS: Haloperidol and olanzapine were associated with substantial and comparable baseline-to-endpoint reductions in symptom severity, which did not differ significantly in last-observation-carried-forward analyses. However, in a mixed-model analysis, olanzapine-treated subjects had significantly greater decreases in symptom severity as measured by the Positive and Negative Syndrome Scale total score and negative and general scales and by the Montgomery-Asberg Depression Rating Scale but not as measured by the Positive and Negative Syndrome Scale positive scale and by the Clinical Global Impression severity rating. Olanzapine-treated patients experienced a lower rate of treatment-emergent parkinsonism and akathisia but had significantly more weight gain, compared with the haloperidol-treated patients. Overall, significantly more olanzapine-treated subjects than haloperidol-treated subjects completed the 12-week acute phase of the study (67% versus 54%). CONCLUSIONS: As expected on the basis of previous studies, both olanzapine and haloperidol were effective in the acute reduction of psychopathological symptoms in this group of patients with first-episode psychosis. However, olanzapine had several relative advantages in therapeutic response. Although the nature of adverse events differed between the two agents, retention in the study was greater with olanzapine. Retention in treatment is important in this patient population, given their risk of relapse. Longer-term results are needed to determine whether treatment with atypical antipsychotics results in superior outcomes for a first episode of schizophrenia.

Adolescent↗

PubMed2004

Comparative effect of atypical and conventional antipsychotic drugs on neurocognition in first-episode psychosis: a randomized, double-blind trial of olanzapine versus low doses of haloperidol.

OBJECTIVE: The effect of antipsychotic medication on neurocognitive function remains controversial, especially since most previous work has compared the effects of novel antipsychotic medications with those of high doses of conventional medications. This study compares the neurocognitive effects of olanzapine and low doses of haloperidol in patients with first-episode psychosis. METHOD: Patients with a first episode of schizophrenia, schizoaffective disorder, or schizophreniform disorder (N=167) were randomly assigned to double-blind treatment with olanzapine (mean modal dose= 9.63 mg/day) or haloperidol (mean modal dose=4.60 mg/day) for the 12-week acute phase of a 2-year study. The patients were assessed with a battery of neurocognitive tests at baseline and 12 weeks after beginning treatment. RESULTS: An unweighted neurocognitive composite score, composed of measures of verbal fluency, motor functions, working memory, verbal memory, and vigilance, improved significantly with both haloperidol and olanzapine treatment (effect sizes of 0.20 and 0.36, respectively, no significant difference between groups). A weighted composite score developed from a principal-component analysis of the same measures improved to a significantly greater degree with olanzapine, compared with haloperidol. Anticholinergic use, extrapyramidal symptoms, and estimated IQ had little effect on the statistical differentiation of the medications, although duration of illness had a modest effect. The correlations of cognitive improvement with changes in clinical characteristics and with side effects of treatment were significant for patients who received haloperidol but not for patients who received olanzapine. CONCLUSIONS: Olanzapine has a beneficial effect on neurocognitive function in patients with a first episode of psychosis. However, in a comparison of the effects of olanzapine and low doses of haloperidol, the difference in benefit is small.

Adolescent↗

PubMed2004

Comparison between olanzapine and haloperidol on procedural learning and the relationship with striatal D2 receptor occupancy in schizophrenia.

The striatum is known to play a primary role in procedural learning. In this study, the authors simultaneously assessed the effects of two antipsychotic drugs on procedural learning and on striatal dopamine (D2) receptor occupancy. Twenty-seven patients receiving either olanzapine or haloperidol as antipsychotic medication were assessed with the Computed Visual Tracking Task (CVTT) and Single Photon Emission Computed Tomography (SPECT) following the administration of Iodine 123-IBZM (123I-IBZM), a radioligand with a high affinity and specificity for the D2 receptors. The results showed poorer procedural learning in the haloperidol-treated patients than in normal control subjects, while no difference could be found between olanzapine-treated patients and normal control subjects. In the haloperidol but not the olanzapine group, significant correlations were found between procedural learning deficits and striatal D2 receptor occupancy. However, there was no significant difference in D2 receptor occupancy between olanzapine- and haloperidol-treated patients, and this may be related to the high doses of olanzapine and low doses of haloperidol administered. The authors concluded that: 1) striatal D2 receptor blockade may alter procedural learning in humans; and 2) olanzapine may have a protective effect on procedural learning, even at doses that produce striatal D2 receptor occupancy as high as that found with haloperidol. This protective effect of olanzapine may be related to its atypical pharmacological properties.

Adult↗

PubMed2004

Intramuscular haloperidol or lorazepam and QT intervals in schizophrenia.

The objective of this study was to estimate the effects of intramuscular haloperidol and lorazepam on the QT interval in volunteers with schizophrenia. Intramuscular haloperidol and intramuscular lorazepam are standard treatments in the acute management of agitation and aggression. Although prolongation of the QT interval and sequelae, including torsade de pointes and death, have been reported for haloperidol (but not lorazepam), formal studies have been lacking. Volunteers with schizophrenia (n = 12) were administered a single intramuscular injection of 7.5 mg haloperidol or 4 mg lorazepam in a blinded, randomized, placebo-controlled crossover design. Serial EKGs and concurrent blood samples were obtained over 6 hours following each injection. Changes in the QT interval were evaluated, as were plasma drug and prolactin concentrations. Haloperidol injection increased the heart rate-corrected QT interval an average of 5.1 msec using Bazett's correction (QTb 90% confidence interval [CI]: 0.3, 9.8), 3.6 msec using Fridericia's correction (QTf 90% CI: 0.02, 7.2), and 4.2 msec using an empirically derived "baseline correction" (QT(ii) 90% CI: 0.3, 8.0). Effects of lorazepam on QT were nullified by correction for the heart rate elevation (QTb 3.8 msec, 90% CI: 0.6, 7.1; QTf 0.0 msec, 90% CI: -3.2, 3.4; QTii -2.3 msec, 90% CI: -6.6, 2.0). An association between QT prolongation and occurrence of extrapyramidal symptoms was observed. On average, intramuscular haloperidol led to minimal prolongation of the QT interval. This propensity is of theoretical concern in individuals with risk factors for torsade de pointes but seems unlikely to be a problem in the vast majority of patients.

Adult↗

PubMed2002

Effects of ketanserin 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 (prepulse inhibition). Here, we report the effects of the serotonin (5-HT)2 receptor antagonist ketanserin and the D2 dopamine receptor blocking antipsychotic drug haloperidol on these responses. Fifteen males (aged 18-35 years) participated in four sessions at 7-day intervals, in which they received ketanserin 20 mg, ketanserin 40 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, 3 h after ingestion of haloperidol or 1 h after ingestion of ketanserin. 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 prepulse inhibition 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. Ketanserin 40 mg significantly reduced the amplitude of the EMG response and both doses of ketanserin significantly suppressed prepulse inhibition of the response; haloperidol had no effect on EMG response amplitude or prepulse inhibition. Neither drug affected N1/P2 amplitude or prepulse inhibition of this response. Ketanserin, but not haloperidol, reduced subjective alertness and critical flicker fusion frequency. Haloperidol, but not ketanserin, elevated serum prolactin level. These results confirm that prepulse inhibition of the startle response and of the N1/P2 complex have different pharmacological sensitivities. The ability of ketanserin to attenuate the startle response may reflect its sedative action, as other drugs with sedative properties have also been found to attenuate the startle response in man. The ability of ketanserin to suppress prepulse inhibition of the startle response is consistent with previous evidence for the involvement of 5-HTergic mechanisms in the regulation of prepulse inhibition in man.

Acoustic Stimulation↗

PubMed1998

Effects of bromocriptine and haloperidol on prepulse inhibition of the acoustic startle response in man.

Experiments with animals have shown that D2 dopamine (DA) receptors are involved in prepulse inhibition of the acoustic startle reflex (suppression of the reflex response evoked by a loud sound by prior presentation of a low-intensity stimulus). The present experiment attempted to extend this observation to man. Twelve healthy males (18-30 years), screened for normal hearing thresholds, participated in four sessions in which they received oral doses of placebo, bromocriptine 1.25 mg (a D2 receptor agonist), haloperidol 3 mg (a D2 receptor antagonist) and combined treatment with bromocriptine 1.25 mg+haloperidol 3 mg, according to a balanced double-blind protocol. Thirty-minute electromyographic recordings from the orbicularis oculi muscle of the right eye were carried out 120 min after ingestion of haloperidol and/or 90 min after ingestion of bromocriptine. Subjects received 36 40-msec sound pulses (115 dB), separated by variable intervals (mean 25 sec); in 24 of the trials the pulse was preceded by a 40-msec prepulse (75 dB in 12 trials and 85 dB in 12 trials; prepulse-pulse interval, 120 msec). The amplitude of the startle response was not significantly altered by any of the active treatments. Under the placebo condition, both 75- and 85-dB prepulses inhibited the startle response. Bromocriptine significantly attenuated this prepulse inhibition; haloperidol also produced a small but statistically significant attenuation of prepulse inhibition. Haloperidol significantly antagonized the attenuation of prepulse inhibition produced by bromocriptine. Neither drug altered self-rated alertness, physiological finger tremor, systolic or diastolic blood pressure or salivation. Bromocriptine significantly suppressed and haloperidol significantly elevated serum prolactin levels, these changes being absent when the two drugs were given in combination. The results provide evidence for the involvement of D2 DA receptors in prepulse inhibition of the startle reflex in man.

Acoustic Stimulation↗