Haloperidol effects

K tt individualize dose for each patient. Transient dyskinesias may be caused by abrupt withdrawal. Enhances actions of CNS depressants, alcohol, anticonvulsants. Decreases actions of amphetamines. Severe hypotension with alcohol, epinephrine, antihypertensives. Antimuscarinics Increase intraocular pressure and reduce haloperidol effects. Lithium encephalopathic syndrome. ... 

Unknown mechanism (betel nut worsens the side-effects of flupentixol and fluphenazine). Ginkgo may t haloperidol effects. Kava kava t side-effects of haloperidol and risperidone... 

The interaction between haloperidol and rifampicin would appear to be established and clinically important. Be alert for any evidence of reduced haloperidol effects if rifampicin alone is used, and possibly increased effects if isoniazid alone is used. Adjust the haloperidol dosage if necessary. 

CJ-Receptors are localized ia the brain stem and limbic stmcture, regions associated with endocrine function (76). In the periphery, CJ-receptors are found in the Hver, heart, ileum, vas deferens, and on lymphocytes and thymocytes. Although there is insufficient evidence to clearly define the functional role of CNS CJ-sites, based on the effects of PCP and the interaction of haloperidol with CJ-sites, CJ-receptor ligands may be antipsychotics or used for the treatment of substance abuse. Several CJ-receptor ligands have shown neuroprotective effects in vivo. Ifenprodil (315) and CNS 1102 (316) are being developed for treatment of stroke (Table 18). 

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... 

There is an increased central nervous system (CNS) depressant effect when the skeletal muscle relaxants are administered with other CNS depressants, such as alcohol, antihistamines, opiates, and sedatives. There is an additive anticholinergic effect when cyclobenzaprine is administered with other drugs with anticholinergic effects (eg, antihistamines, antidepressants, atropine, haloperidol). See Chapter 30 for information on diazepam. 

Administration of atropine with meperidine (Demerol), flurazepam (Dalmane), diphenhydramine (Benadryl), phenothiazines, and the tricyclic antidepressants may increase the effects of atropine. There is a decreased effectiveness of haloperidol when administered with the anticholinergic dragp. 

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). 

There are few reports on the effects of nitrous oxide on dopaminergic neurotransmission. A study in mice showed that nitrous oxide inhalation produced a significant increase in locomotor activity that was antagonized in a dose-dependent fashion by the dopamine synthesis inhibitor a-methyl-/)-tyrosine (Hynes and Berkowitz 1983). Moreover, administration of the D2 antagonist haloperidol also reduced the locomotor activity induced by nitrous oxide (Hynes and Berkowitz 1983). These results suggest that excitatory effects induced by nitrous oxide may be also mediated by dopaminergic neurotransmission. However, other studies have reported that exposure to nitrous oxide resulted in decreased dopamine release by neurons in the striatum (Balon et al. 2002 Turle et al. 1998). 

Only two randomized, controlled trials have been completed, and neither provides anything like compelling data (Table 2.6). Chouinard and Albright (1997) conducted a unique evaluation of a subset of patients from a previously conducted clinical trial. Subjects were categorized and profiled at baseline and end point according to clinical severity, and a group of psychiatric nurses were asked to rate various aspects of likely outcome and quality of life to each profile (mild, moderate or severe symptoms). Health state utilities were then calculated risperidone was found to provide more than double the number of quality-adjusted life years compared with haloperidol. Csernansky and Okamoto (1999) conducted a rather more conventional trial, but included no economic analyses. However, they did find that the use of risperidone substantially reduced relapse rates compared with haloperidol—an outcome likely to have a positive impact on cost-effectiveness. 

Coley KC, Carter CS, DaPos SV, et al (1999). Effectiveness of antipsychotic therapy in a naturalistic setting a comparison between risperidone, perphenazine, and haloperidol./ Clin Psychiatry 60, 850-6. 

Davies A, Langley PC, Keks NA, et al (1998). Risperidone versus haloperidol II. Cost-effectiveness. Clin TherlO, 196-213. 

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. 

Amisulpride is a substituted benzamide, which acts as a highly selective blocker of D2 and D3 receptors (Kerwin, 2000). As with all the other drugs, it can easily be demonstrated to be effective compared with placebo and haloperidol, with a lower extrapyramidal symptom profile (Moller et al, 1995). The strength of amisulpride lies in the quality of the evidence to show that it is effective against primary negative symptoms and affective symptoms. Two studies have shown convincing superiority for negative symptoms... 

DA neurons in this nucleus, that not all the effects are elicited by the release of DA. Most neuroleptics block the inhibitory effects of applied DA but some, e.g. haloperidol, are less active against SN-evoked inhibition. Generally these studies lacked specific agonists and antagonists used microintophoresis which is not really quantitative and with extracellular recording gave little information on the state of polarisation of the neuron. 

In view of the known cellular actions of DA, such as increased K+ efflux and reduced Ca + currents associated with Dj receptor activation in cell lines, inhibition would be the expected response to DA, especially as cyclic AMP, which is increased by Dj receptor activation also inhibits striatal neurons. In fact although many DA synaptic effects are blocked by Dj antagonists like haloperidol, the role of Di receptors should not be overlooked. 

Figure 7.5 Rate recording of the dose-dependent inhibitory effects of apomorphine (pg/kg) on the spontaneous activity of a neuron in the medial prefrontal cortex of the halothane anaesthetised rat and its antagonism by haloperidol (HAL, 0.5mg/kg). Time scale is 50 min intervals. Reproduced by permission from Dailey (1992)...

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