Haloperidol is a typical antipsychotic drug belonging to the butyrophenone class. It has been widely used since the 1960s and remains a cornerstone in the management of psychotic disorders. Its primary mechanism of action involves potent antagonism of dopamine D2 receptors in the mesolimbic and mesocortical pathways, reducing hallucinations, delusions, and disorganized thought processes. However, because dopamine blockade is not selective, haloperidol also interferes with dopamine transmission in the nigrostriatal and tuberoinfundibular pathways, leading to side effects such as extrapyramidal symptoms (EPS) and hyperprolactinemia.
Haloperidol is available in oral tablets, oral solution, intramuscular (IM), intravenous (IV), and long-acting intramuscular depot formulations (haloperidol decanoate). This wide range of preparations makes it versatile for both acute and chronic treatment. The oral form is typically used for maintenance, while intramuscular or intravenous injections are reserved for emergencies such as acute agitation, severe psychosis, or delirium.
The drug has been particularly valued in psychiatry for its rapid calming effect in acute agitation and aggression, making it a mainstay in emergency settings. In neurology, haloperidol has also been used for conditions such as Tourette syndrome, refractory hiccups, and nausea associated with chemotherapy, though its use for these is less common today due to newer agents.
Despite being an older antipsychotic, haloperidol’s efficacy in controlling positive symptoms of schizophrenia is well-documented, and it remains in clinical guidelines worldwide. The introduction of atypical antipsychotics has reduced its use for long-term therapy in some patients due to a lower risk of movement disorders with newer agents. Nevertheless, haloperidol continues to be relied upon in acute care, in resource-limited settings, and in patients who respond particularly well to it.
Treatment is individualized, with the lowest effective dose used to minimize side effects. Gradual titration is standard, and monitoring for side effects is critical, especially early in therapy.
Most side effects can be minimized with dose adjustment, switching formulations, or adjunctive medications (e.g., anticholinergics for EPS). However, long-term risks such as tardive dyskinesia require careful risk-benefit analysis.
Patients and caregivers should be educated about early warning signs of serious reactions, such as sudden fever, muscle rigidity, or uncontrolled movements.
Patients should always provide a full list of medications and supplements to their clinician to avoid harmful combinations.
Overdose: Symptoms include severe EPS, profound sedation, hypotension, cardiac arrhythmias, and coma. Management is supportive: secure airway, monitor cardiac rhythm, administer fluids, and consider activated charcoal if recent ingestion. There is no specific antidote.
Missed dose (oral): Take as soon as remembered unless close to the next scheduled dose. Do not double up. For depot injections, contact the healthcare provider promptly if a dose is missed, as timing is crucial for therapeutic levels.
Accidental double dose: May increase drowsiness, muscle stiffness, or tremors. Monitor and seek medical advice if symptoms are significant.
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